DIP Episode 500 - USMLE Rapid Review Series 108 (For Step 1-3)

Welcome. This is Divine. This is episode 500 of the Divine Intervention Podcasts. Into these podcasts we're going to be continuing the Rapid Review series for the US Emily Step 2 C Can Step 3 exams. And this is going to be series 108. You know, this is a very meaningful podcast. And I feel like a lot of people have gotten a lot of benefit from this podcast over the years. And I'm just really grateful to God for how far we have come. I mean, I never like thinking back to when I made episode one. And now this is basically 500 episodes later. I'm just really grateful for the impact that this podcast has made in many people's lives. So today, the game plan is to make this a pretty high-youther, rapid review to go over a lot of very pertinent stuff for the US Emily exams. And the thing that's going to happen is I'm going to try to spend some time, again, really going into some things that are probably fall under the more technical aspect of things for people. But again, I think you're going to get a lot from this, like you have from many of the other podcasts that I have made. Okay. So let's start off with a few questions on cardiac pressures. So what if they give you a question about a patient, they tell you that two weeks ago, you know, this patient had motor rineria and had some, you know, had a productive cough.

But that now this person over the last two days, his legs have swollen and your toe that he has been having shortness or breath and that he now requires like two or three pillows to sleep comfortably at night. And then your toe that on cardiac or scotation, you can hear a lot of pulmonary crackles and you can hear a new S3 heart sound. If you see something like this, first things first, what's going on? Well, this person clearly has viral myocarditis, viral myocarditis. What's the thing that tells us this is viral myocarditis? Again, you see recent URI symptoms and then after that, you're seeing heart failure symptoms. You've seen a lot of crackles in the lungs. You've seen evidence of peripheral edema. You've seen an S3 heart sound. Remember, an S3 heart sound, many times on the USML Es, is codeword for the systolic dysfunction. This person has heart failure symptoms. It's going to be viral myocarditis. And again, what causes viral myocarditis? There are many causes of viral myocarditis, but when you examine, the big one you want to think about is coxache B, coxache B, right? And if you do a biopsy of these people's hearts, you're going to see like, you know, inflammatory infiltration of your heart. Again, a good number of these people completely recover with time, but you're going to treat them the way you're going to treat heart failure. So again, you see heart failure symptoms after URI. I want you to think of coxache B, viral myocarditis.

Now, in terms of cardiac pressures, right? So let's assume they're trying to ask you to imagine what the portal pressures will look like in this person. What the hepatic venous pressures will look like in this person. What the juggle of venous pressures will look like in this person. What the central venous pressure will look like in this person. What the pulmonary capillary rich pressure will look like in this person. So let's kind of put all these things together. Oh, they look like it. So the thing is, if a person has viral myocarditis, the hearts are not working. It's literally not working. So since the heart, the left ventricle, the right ventricle things like that are not doing very well. Blood is going to stop backing up in the heart. So all the cardiac pressures will be elevated. The pulmonary capillary rich pressure, which is a surrogate for left-itral pressure, is going to be elevated. Why? Because again, remember, by the way, left-itral pressure and pulmonary capillary rich pressure are pretty much the same thing, right? The reason it's called pulmonary capillary rich pressure is because the pressures are measured by waging something in the pulmonary capillaries. And then it gives you a surrogate of the left-itral pressure. Many of us know this as the swan-guns catheter. Okay? So whenever you see the term pulmonary capillary rich pressure, it's a surrogate on your exams for like pulmonary venous and left-itral pressures.

So these people are going to have increases in their left-itral pressures. That is very, very high up to no for you exam because again, the left ventricle is not contracting. So blood is going to back up in the left-itram, which is going to be increased. Okay? But think about it as well. These people's hearts are not contracting well. So since blood is backing up in the left-itram, it's going to back up in every other part of the heart. So they're going to have back up as well in the right-itram. So their central venous pressure, which is a surrogate for the right-itral pressure, will also be increased as well. Remember, your right-itram is where most of the venous in your body ultimately drain into. So since that's where most of the venous in your body ultimately drain into, your right-itram is like a central hub for your venous. That's why right-itral pressure is also called central venous pressure. So these people's central venous pressure is going to be elevated. Okay? So what's going to happen to their jugular venous pressure? Where their jugular venous pressure is going to be elevated as well. These people are going to have jugular venous distension. Why? Because again, the SVC and the IVC, right? More especially the SVC, cannot drain properly into the heart. So these people are going to have jugular venous distension. And then what's going to be true of their portal pressures and their hepatic venous pressures?

Well, I would hope you're saying while divine, those things are both going to be elevated as well. Because again, if your heart is not pumping well, fluid is going to back up into your IVC. And then it's going to back up because remember, your hepatic vein is what ultimately becomes the inferior vein that gave us. So this is not going to have an increase in their hepatic venous pressures. And their portal pressures are going to be elevated as well. If they want to be weird with you and your exams, how can they make a hepatic venous or portal pressure question hard? Instead of calling it hepatic venous pressure or portal pressure, like portal vein pressure, they can just call it liver sinusoidal pressure. They can literally just call it liver sinusoidal pressure. Again, that's a very classic pathway taken by the USNL Is. They'll take what you know and just express it in somewhat different terms that are closely related, but are not exactly that thing that you're looking for. So just be mindful of that. That's why I understand and really does matter on these exams. So because remember, your portal vein ultimately, if you look at the way the portal system works, your portal vein is going to drain ultimately into some sinusoidal capillaries. And then those sinusoidal capillaries are then going to ultimately drain into your hepatic vein. And then your hepatic vein is what's going to create your inferior venocative. Right? That's why the liver is called a portal system.

A portal system is basically when you have a system of capillaries that are fed by a kind of vessel and drained by the exact same kind of vessel. I'm going to say that again, a portal system is formed by a capillary network that is fed by a certain kind of vessel and is drained by the same kind of vessel by kind of vessel, I mean an artery or a vein. For example, the liver has sinusoidal capillaries. Those sinusoidal capillaries can be fed by a network of veins. Those are the portal veins. And then those sinusoidal capillaries are drained by a network of veins. That's the hepatic vein. Right? That's why it's a it's a portal venous system. If you're looking for another portal system, go and check the kidneys. The kidneys have an arterial portal system. Right? The glomerular capillaries are fed by the offering arterial because normally if you go all over the body, capillaries are fed by arterials and drained by venous. But that is not the case in the kidneys. The glomerular capillaries have fed by the offering arterials and the glomerular capillaries are drained by the effray arterials. That's an arterial portal system. Right? The next list you can find another portal system is if you go up to the hypothalamus, I'll let you kind of do the research on that on your on your own. But basically, most times you invent portal systems in the body when you want to really regulate how things move around.

When you when you have a capillary system that has a lot of regulation with it on a serial or a venous system with a lot of regulation, you love to put those things around portal systems. Just something I kind of want to throw in there. I'm kind of a useful point to know for for exams. Right? So again, hepatic venous pressures, portal pressures will be elevated for this person that has viral micrograditis. And if you really think about it, you have liver sinusoidal pressures, right? Because the sinusoidal are a go between between the portal vein that feed them and the hepatic vein that drains them. So just something to kind of keep at the back of your mind for exams. Okay, what if they give you a question about a patient? And you tell you that this patient is a 45-year-old male. And you know, for the past six months, he has had a lot of paritis. And you tell you that he has this plethora appearance to his skin. And then you're told that this person, over the last 24 hours, he has been having progressively worsening abdominal pain and swelling. And in detail, you that this person has a fluid wave, right? They have a fluid wave on palpation of the abdomen, right? And you're told you're giving some labs. This person's white blood cell count is like 7,000. So that's normal. The person's platelet count is like 550,000. So a little bit elevated. But this person's hematocrit is like 75%. That's super elevated. Clearly, this person has polycythemia vera.

And that polycythemia vera has led to botchiaric syndrome. Botchiaric syndrome. Remember, in botchiaric syndrome, you have thrombosis of the hepatic vein. You have thrombosis of the hepatic vein. When you thrombosis, the hepatic vein, everything that is proximal to it, blood is going to back up in those things. So those people are going to have an increase in the hepatic vein of pressures. They're going to have poor oconjession. They're going to have an increase in their liver sinusoidal pressures. They're going to have an increase in the appodovino pressures. If your podovenous pressures increase, especially if it's a high-grade obstruction, you can develop a sideys very, very rapidly. Although it's not everyone that has botchiaric syndrome that develops a sideys. They can just have very sharp, very significant right-over quadrant pain. Again, you're going to see in a person that is pretty spools to botchiaric syndrome, like a person that has polycythemia there, or a person that has a PNH paroxysmone-neutrional hemoglobinary. But let's focus on the person that has P-veira. Why would a person develop? Because if something you may have heard many times that, oh, people that have polycythemia there, they have a very high risk of thrombotic episodes. Well, why me that be the case? Well, it all comes down to this. It all comes down to the facts that these people's blood is very viscous. These people's blood is very, very viscous.

Whenever you have something that is viscous, that thing does not flow as well. It's like, for example, think about it if you're trying to pour water out of a jug versus you're trying to pour oil or like grease out of a jug. The grease is going to flow slower because it's a more viscous fluid. Just trying to think about it intuitively. Let's not make this thing more complex than it needs to be. So the thing is, normally, a person's hematocrit, especially for a guy, should be under like 45% of their about. Again, I'm just giving rough numbers. You can look up the exact numbers in your own time. But a hematocrit of 75%, that tells you that this person's hemoglobin is like 25. That's really high. That's really, really high. Whenever your blood is that viscous, it is not going to flow very well. And think about it. If blood is not flowing very well, what's going to happen? Ask yourself, what's going to happen? You're going to have blood steases. What does blood steases sound like that you've probably heard of before? It sounds like something that comes out of a vehicle's triad movie. Remember, in vehicle's triad, you have steases, you have hyperclineability, and you have endothelial dysfunction. That blood that is not as viscous is going to be more static because it's more static. It's going to have a higher risk of forming thrombi and embolite. And the person can get in trouble. These are why people that have polycythemia vera.

They have a very, very high risk of thrombotic episodes. They can get strokes. They can get my cartilage infarctions. They can get P Es. They can get DV Ds. But in this case, we're focusing more on the butchery syndrome that you can get thrombosis of the hepatic. That's why they have all these problems. Okay. That's why they have all these problems. And I guess as another tidbit, I can kind of throw in for you before we start talking about the pressures. You may wonder, why is it that people that have pivare? Why is it that many of them tend to be hypertensive? Well, again, think about it. It all goes back to oneself as well. That's a wonderful way they can take the stuff that you've learned from step one and throw it on a step two and a step three exam. That's a very simple way they can accomplish those goals. Why? Because if you think about it, total peripheral resistance is directly proportional to the length of the vessel. If directly proportional to the viscosity, right? And it's inversely related to the radius to the fourth power. So if you think about it this way, think about it this way. This person has blood that is very viscous. So because the person has blood that is incredibly viscous, the total peripheral resistance is going to go up. And if that total peripheral resistance goes up, then that's going to make it hard for blood to flow. That's going to cause the vessels to be congested. So the person's blood pressure is going to be high.

In fact, to be honest with you, this is probably going to be one of those rapid reviews that I'm going to leave as a rapid review for step one or the way to step three. Because there are just many things that I imagine that step one takeer will find to be quite helpful in this podcast. So let's go ahead and continue. So what is going to be true of this person's hepatic venous pressure? Well, this person's hepatic venous pressure is clearly going to be elevated because the hepatic venous blocked. So the hepatic venous pressure is going to be elevated. What's going to be true of the liver sinusoidal pressures? It's going to be elevated as well because again, all these things come before the obstruction. What's going to be true of the aportal venous pressure? It's going to be elevated as well. But ask yourself, what's going to be true of these people's jugular venous pressure? The jugular venous pressure is going to be normal because again, the blockade is in the hepatic vein. So blood is not really flowing into the inferior vein of the keva as much anymore. So these people are not going to have jugular venous distension. That's one. Another thing you're going to notice is that all the acardic pressures are going to be low. So they're left-itro pressure, which is the pulmonary capillary wedge pressure. It's going to be low or normal. And the right-itro pressure, which is the central venous pressure, is also going to be low or normal.

You may wonder, divine, why would this be normal if I'm not sending blood to the heart? Well, this may be normal because again, remember, there are all these other things that can send blood to the heart through different pathways. Just something you kind of want to keep at the back of your mind, for example. But it'll be low or it'll be normal. It'll be lower. It'll be normal. Okay, now let's give another situation. What if they give you a question about a person? Let's say it's a female and she's like 38 years old and she smokes and she's on OC Ps and she has this sodden onc sharpness or breath. And you're told that she has this sodden jugular venous distension that develops what's going on there. I hope you're saying, oh, divine, this sounds an awful lot like a pulmonary embolus, which it is. This person literally has a PE, right? Again, if you kind of think about the backdrop here, this person is over 35 and the smoke and then there are no C Ps. These people are pretty much like begging for pulmonary embolus. Well, again, remember, if you have a pulmonary embolus, what has been occluded? It's going to be your pulmonary vessels, especially your pulmonary arteries or pulmonary capillaries. That's where the obstruction is going to be, right? So, again, whenever you're getting these cardiac pressure questions, the smart police ask yourself ways to root block. And then ask yourself, everything before the root block is going to have higher pressures.

Everything after the root block is going to have low or normal pressures, low or normal pressures after the root block. So what are the things that come before the root block? The things that come before the root block are things like your right ventricle, your right atrium, your hepatic vein, your podo vein, your liver sinusoid. So all those things are going to have elevated pressures, right? So your liver sinusoidal pressures, podo pressures, hepatic vein loss pressures, jaw blood vein loss pressures, central vein loss pressures, which is a surrogate for the radio-trial pressure, those things are all going to be elevated. But everything that comes distal is going to be normal or decreased, right? Like your pulmonary capillaries pressure is going to be diminished. In fact, if we throw in a few more things, we're also going to be throwing these people's cardiac output. The cardiac output is going to be low, right? Because venus return for the left atrium is diminished. And if we were to see an acute kidney injury in these people, what kind of acute kidney injury would they likely have? They would likely have a pre-renome acute kidney injury, why? Because again, their kidneys are completely fine, the kidney is just not getting enough gas. The kidney is not being profused adequately. So this will be all going to have a pre-renome acute kidney injury, which on your example they can call a pre-renome is otemia. In fact, they can make another question out of this.

What will be true of these people's urinosemolarity? Their urinosemolarity is going to be extremely high because the body sees that wow, gee, this person is not profusing the kidneys very well. So since you're not profusing the kidneys, well, your afrin arterial, the GG cells are going to freak out. They're going to make a ton of reigning. You're going to make a lot of, you're going to convert angiotensinogen to angiotensin 1. And then angiotensin 1 is going to be converted to angiotensin 2. And then angiotensin 2 is going to go to the hypothalamus and cause you to release ADH. When you release that ADH, it's going to cause you to reabsorb a ton of water from your urine. So urine is going to be very, very concentrated. Again, you can see how the USML's can test material in many different dimensions. Okay, what if they give you a question about a person last three days, person has been coughing up a lot, having a lot of shortness of breath is not able to take many steps without feeling short of breath. And they give it like a chest x-ray and you notice that man, this person's lungs are huge, huge, huge, huge. And this person is like 70 something years old and this person has smoked like two packs of cigarettes per day since they were 30. This person probably has like an 80 pack years smoking history or something ridiculous. Obviously, this person has like a COPD, right? This person probably has core pulmonality.

Remember our friends at the USML is they really love this term of core pulmonality where you pretty much develop right heart failure from a pulmonary cause. Because if you think about it, what is the most common cause of right heart failure? It is left heart failure, left heart failure is in fact the most common cause of right heart failure. But you can have right heart failure because you have a pulmonary issue like cystic fibrosis or COPD or you pathic pulmonary fibrosis or something like that. That's called core pulmonality. When you have core pulmonality, you have pulmonary hypertension. So again, you can already imagine that, oh gee, wait, divine. All the labs you said for a person that has a large PE will literally be the exact same labs you see for a person or hours. You see for a person that has core pulmonality. You see for a person that has core pulmonality. Again, that's pretty high up to make sure you know and understand for example. And again, if you love this multi-dimensional thinking and let's say or teaching, unless you are studying for step one or step two or step three, have a bunch of classes coming up next month. I have a separate podcast on that. So I'm not going to spend time delivering that. But all my classes are pretty much based on scenarios. I use scenarios and then I really help you understand what the phase. So I'm not just throwing information at you.

And again, those scenarios are presented in exam-like formats like a wheel likely present on an exam. So you're actually getting a lot from that. And then you're also going to see how things integrate across multiple disciplines. I study on the eighth of January. I have a step one class. The 25-hour class is for people taking step one or complex one. If you're taking step two or step three or complex two or three, you have a poor step one foundation. The class will be perfect for you. And then I have a series of other classes during the month of January. I have a five-hour social sciences class for step one to step three, a four-hour biostat class for step one to step three. And I have an MB Me testing strategy class as well for step one to step three. And then I have a 20-hour step two step three review. And also have a 100-hour step two step three class actually taking place in May. If you're interested in any of these classes, listen to the podcasts I made where I talked about them or just read me an email and I can give you some more information. Okay, so let's go ahead and continue. Now, what if they give you a question about a patient? They tell you that this person is brought to the clinic by his wife because she has noticed he has passed out four times over the last week. I heard told that he has passed out every time that he was. You're in need of that the inside of the event seems to be your nation and you're in need.

And then a few minutes after a few seconds after his urinary string starts, this person completely passes out. So you're still at presentation, right? What should we be thinking about? What should we be thinking about? So here's the thing. Our friends at the USML is they can supply many different kinds of answers for this problem on your exam. If they want to be nice, they can call it like maturation induced syncopy, which makes sense. This person wants to be in this syncopyced. Now, what are some other ways they can present this answer on the exam? They can call this visovigal syncopy. They can call this overactive, corroded reflex. There are many things they can call this. Right? So we'd be like, define how do all these things relate? Well, first things first, this person has visovigal syncopy. But let's talk about how all these things kind of come together. The thing is the USML is they love to test the kinds of syncopy. And the one that they really want, one that they love to test a lot is visovigal syncopy. Now, here's the thing. There are many ways that visovigal syncopy can present on your, on your exams. It can present as a person that, or before they pass out, their face turns white, right? They have facial power. And you also notice that this person is sweating a ton and then they pass out. That's when we can test visovigal syncopy. But under when they can test visovigal syncopy is in the context of situations, is in the context of situations.

And what are the situations they love to test? They love to test situations that increase pressures on your corroded arteries. Increased pressures on your corroded arteries, right? Like think about it. Again, you can go to a restroom, sit on the toilet and try to pee with force. If you pee with force, do you notice that your neck kind of tenses up? That tensing up of your neck is literally compressing the corroded artery. If you have an overactive corroded artery receptor reflex, that's going to, because when you press on your corroded heart, when you press on it that hard, then your corroded artery receptor starts to fire like crazy. It tricks the body into thinking that this person's blood pressure is elevated. So your body is like, I need to send a par sympathetic discharge to the heart, to lower the blood pressure. So you send this par sympathetic discharge to the heart. It's going to cause profound brydicardia. It's going to cause a profound decrease in cardiac output. And that can cause you to become singable. It can make you singopies. So the thing is, that's the concept. But again, the way you get to that concept, again, the USML is, you can almost imagine that they can go in many different directions with this. They can give you a person that passes a wipe while peeing, right? That's that's viso-vigil syncoping. They can give you a question about a person that passes out while pooping. That's also viso-vigil syncoping. Again, think about it, right?

I'm not saying poop on yourself, but again, you're trying to poop really hard as you poop. Ooh, you're exreging all those pressures. You're going to be tensing up on your neck. You're going to be increasing your intra-thoracic pressures. All those things are going to compress your corroded arteries. You're going to get in trouble, right? Obviously, it's not everyone that does that that gets in trouble. But it's not everyone that does that that gets in trouble. But people that have overactive reflexes can get in that trouble. Or if they give you a question about a person that syncopies this while they're in labor, they can literally make that an uby-guin-shelf question. Or they can make that just a straight-up USMLD question. Again, it's going to be from parasympathetic stimulation of the heart. Because again, if you're in labor and you're pushing, oh, push, push, push, as you're pushing, pushing, pushing that heart, right? Your neck is going to tens up. You're going to compress the corroded, you're going to get in trouble, right? Another way they can even apply this principle is they can tell you about a person that's wearing a neck tie. And the tell you that this person keeps syncopies in whenever they wear a neck tie. So they've stopped wearing neck ties. Well, guess what? If you're wearing a neck tie and you tie it too tight, right? Again, you can have this extrinsic compression of the corroded artery.

You compress the corroded artery, you're going to stimulate that bar receptor reflex. You can get a parasympathetic discharge, you're going to pass out, right? So again, you can see that they are many wheeze they can test this concept. I mean, think about it. Why do you think that many times, if you try to pull pretty hard, you start feeling a little nauseous, a little dizzy? Well, it's because again, you're not, you're having that parasympathetic discharge to the heart, right? So, and even why do you think we tell people, why do you think we massage the corroded's in people that have superventricular tacky cardias? It's for that reason, because again, if you massage the corroded's, you're stimulating those cardiac bar receptors, that's going to cause the heart, that's going to cause the brain to send a parasympathetic discharge to the heart. It's going to slow conduction down the EV node. That's going to break that tacky arrhythmia, right? Or you may wonder, why do we tell these people to blow into a straw? Again, it's for that same reason. It's for that same reason. If you're blowing to a straw, think about it. Think of yourself blowing a balloon. That's like doing like a, like a valve solver. Again, don't do it because we do it well enough, you could actually pass out. Nothing, please. So, FYI, this podcast is just for educational purposes. This is not, is, is, is not for clinical decision-making or anything like that, right?

And putting out that disclaimer before you do anything, console your physician, blah, blah, blah, blah. Okay, so when you're blowing to a straw, right? Again, you're, you're raising your in-child thoracic pressures, you're raising the pressures in your neck, you're compressing those crudits, you're going to get a massive presence of any discharge to the heart, you're going to slow conduction down the EV node. That's going to terminate that person's tacky arrhythmia. Okay, it's going to terminate that person's tacky arrhythmia. Again, you can see all these things, they just love to test it on exams. And again, how do we diagnose viso-vigose therapy? You're going to do a tilt table test. You're going to diagnose it with a tilt table test. Okay, you're going to diagnose it with a, with a tilt table test, right? Again, these are all high old things. You want to make sure you know, you know, you know very well for your, for your exams. Okay, now what if they give you a question about a patient and they tell you that, let's see, how do I frame this question? So the tell you that this patient is a newborn and this newborn was born at like 31 weeks gestation and this person has profound respiratory distress. I know many of you are like, oh, divine, boohoo, this is respiratory distress syndrome. Of course, yeah, I know you know that, that's not the, that's not the concern here. But let's, let's talk about arrows that they can through with this, right?

In fact, this is almost like an arrow podcast, right? What are the arrows they can through with this? Okay, right? So first thing's first we know, see a child, the respiratory distress and the newborn prematurely is probably going to be from respiratory distress syndrome. It's pretty straightforward. It's going to be pretty straightforward. Okay, so what are the arrows they can test with this stuff? Well, the first already can test is compliance. What happens to your long compliance? Okay, well, think about this. When you're born that early, you don't have enough surfactant. Remember, surfactant by the way is made by your type two normal sites. Again, you may think that this is only something they care about for step one. Once you take step two or step three, you see this as a question and you're like, whoa, where did that come from? Well, that's where it came from. You got to know the stuff for your exams. Okay, so surfactant is made by your type two normal sites. So if you have a surfactant deficiency, normally what surfactant does is that it reduces surface tension. It reduces surface tension. It reduces surface tension. It reduces surface tension. It reduces surface tension. So because surface tension wants your lungs to collapse. So if you're reducing surface tension, you're going to make it harder for the lungs to collapse. You're going to make it easier for the lungs to be kept open. So think about it.

Since these people lack surfactant, they're going to have increased surface tension. So because they have increased surface tension, the lungs are more likely to collapse. Because they are more likely to collapse. They are less likely to expand. So because they are less likely to expand, what do you think is going to happen to the compliance? The non-compliance is going to go down. The non-compliance is going to go down. That's very high-youtuberant. The non-compliance is going to go down. Okay, what's going to happen to the elastance of the person's lungs? Or the elastance of their lungs is going to increase. Well, there are two ways you can think about this. Compliance and elastance are inversely related. So obviously, if your compliance is going down, then your elastance is going to be going up. But elastance is just a measure of the ability to snap back. So if you're not very good at expanding because you have increased surface tension, you're going to have an increased ability to snap back. So that means your elastance is going to be going up. Elastance is going to be going up. Okay, and then to another way they can even test this compliance thing is, they can test it instead of putting compliance as one of the arrows. They can just put volume, they can just put volume increase for a defined pressure change. You're going to have a smaller volume increase with applying the same amount of pressure if your lungs are not very compliant.

Again, because remember, compliance is volume of a pressure. Compliance is volume of a pressure. So because these people's lungs are more likely to collapse, you're going to need higher pressures to obtain the same kind of volume increase compared to a normal situation where you have adequate amounts of surfactant. Again, be careful. I'm telling you this. I don't know why I'm repeating this a lot to cup off the year. But the USMLE is a big thing they do these days. They take what you know and explain it out in a key step or explain it out as an answer choice. And they see they will begin to massively struggle with those things. Even if they've memorized all the honky decks known to one kind. So just be kind of careful about careful about that. Okay, what's another thing they can ask? They can ask about collapsing pressures of the our view like or be sure of the collapsing pressures of the our view like in a person that has a new need or respiratory distress syndrome. Well, clearly the collapsing pressures are going to be increased. Closing pressures are going to be increased because again, that surface tension is increased. Okay, now let me ask you this. What will be true of these people's long volumes? Would it be a pretty not high long volumes? Or would it be a pretty not low-long volumes? Or is it going to be a pretty not low-long volumes? Because again, they are longs have an increased tendency to collapse.

They are longs have an increased tendency to collapse, increased tendency to collapse. So they are longs are going to be a pretty not lower-long volumes. And again, they can just throw in some volume just to mess with your head. They can give you a question about like functional residual capacity or residual volume or whatever. Those things are going to be low. Okay, those things are going to be low. This is why many of these kids, you know, you're going to treat them with, you know, you're going to give them surfactant, right? Many of them are going to need oxygen therapy because you want to keep the longs open. You're counteracting many of these problems with increased surface tension in these people's longs. Now, one tip bit I think I'm going to throw in, you know, since this is a rapid review series and I kind of stop this here sooner. But one thing they may throw in you may see a child that is born at term and has new residual respiratory distress syndrome. And then they may ask you a somewhat unique question. They will say this patient's pregnancy and delivery was most likely associated with which of the following maternal medical histories. And they will put a bunch of things they will put hypertension, they'll put diabetes, they can put like heart failure, they can put like a bunch of stuff, they can put like full maternal fully deficiency, they can put exposure to a cut later or something ridiculous, right?

If you see this, I'll really hope you're saying, oh divine, I'm going to pick the diabetes as the answer. So I want to say something here before I address this concept. This is actually more like a testing principle or just to give you an idea of how the USMEL is love to test information. One classic way the USMEL is love to test information in this day and age is that you'll write a question on some pathology. You'll be reading a question and you're like, oh, I know exactly what this is. But then you ask almost like bizarre cues them and put bizarre answers. Like they'll give you a pathology and say, oh, this person most likely has which of the following medical histories or this person most likely will have which of the following findings on physical exam or this person will have which of the following findings in XYZ or which of the following things on exam make it more likely that this person has this disease and not this, right? So you see a child born a term and you have a new neuro respiratory distress syndrome and then you'll be asked for the evaluation of this pregnancy labor and delivery process is most likely as relevant to the following which of the following maternal medical histories. And again, sorry, I'm kind of coming off with this of the top of my head. But you're going to pick the answer that says diabetes. You're going to pick the answer that says diabetes. So how does diabetes time to a new neuro respiratory distress syndrome?

Well, the link is being an infant of a diabetic mom, right? So think about if your mom has diabetes, she has high blood glucose. Well, as the fetus, you're going to get access to that high blood glucose. Well, the fetus is going to be like, man, I don't like having this high blood glucose problem. It's not very good. I don't like this at all. So what is this fetus going to do? This fetus is going to be like, you know what? Beta cells, let's undergo high rupture. So I can make a term of insulin. And then that insulin that high insulin will help us deal with with the blood glucose problems that we're getting from mom. Well, one of the things that insulin does is insulin inhibits surfactant production, right? So factants is not going to be produced well when you have hyper insulinemia. Well, this fetus has hyper insulinemia. So guess what? This fetus is going to be pretty supposed to a new neuro respiratory distress syndrome. So if you see a child that is born on term and has NRDS because most times NRDS is going to be in a preterm child. Well, you see a child that's child is born on term and child has NRDS. That child is almost I can I'm not going to say guaranteed. No, but very likely that child is the child of a mom that has diabetes. That's an infant of a diabetic mom. Right? I'm telling you infants of diabetic moms, there are so many things they can test with those on exams. They can test polyhydramneus with that on exams, right? Because that child has hyperglycemia.

So they're going to have glucose or they're going to appear ton. They're going to have polyhydramneus. That's another way they can go with that on exams. Right? So there are just many things they can go with an infant of a diabetic mom, right? Or that child may need a c-section right? Because the child is too big. The risk of cephalopelvic disproportion is too high. So those kids have to be delivered by c-section, right? They're not going to feed in the pelvis, right? So, or they can even give you a shorter dystochial question, right? They can give you your herb to shame palsy, right? And they can ask, oh, what maternal medical history? Again, I'm just trying to tie all these things back. Oh, what maternal medical history most likely increased this child risk of X, Y, Z, right? Again, it's going to be that diabetes history. Okay, I think I should go ahead and stop here. This is going on almost 40 minutes. But again, I'd go for one or one tutoring for all the USML exams, step one to step three, and pre-clinical exams, 30-ish-off exams. And I also tutor for some of these residency exams, right? Like the internal medicine boards, I do certainly tutor for that. Internal medicine boards, family medicine I tutor for those exams. And then again, I have review courses for all the USM Ls and all the complex exams. I have this podcast on Apple Google and Spotify, I have a You Tube channel, you can check out that's where I have the videos that I have.

And then I also have another website called divine intervention life lessons.com. I mean, if you know of my Christian, so every week I post two podcasts and from a biblical perspective, I address a life lesson. We actually have 240 episodes, I meet the 240 year one this morning. So there's actually an Apple podcast associated with that, it's called the divine intervention life lessons podcast. So check that out, I think you're going to get a lot of benefit from it. Now, the one thing I'm just going to say, you know, this episode 500, I think it's a reasonable episode to give a life lesson. But honestly, my life lesson to you today is just going to be to be patient, be patient. Many people make me speaks in their lives because they're just not patient. You can trace many issues of people's lives to not being patient. You see people losing their tempers because they're not patient. You see people not getting enough from the dedicated period because they're not patient because a patient person is going to have a lot of staying power. If you have a lot of staying power, then you're going to toff it out through challenges to get to what you want to get to. You have a six week dedicated period. If you're a person that is patient, you put in the work to get there. A person that is in patients is not going to put the requisite amount of effort to get the goal that they want to achieve. Just encourage you to be a person that is patient.

You'd be amazed by how far patients can take you in your relationships with your significant other, with your kids, with your coworkers, or with patients, or in studying, or in taking exams. I'm telling you, patients is a virtue. Patience is in fact a virtue. I don't know if I kind of feel like that's something I want to push out to the audience. Be a patient person. I promise you it can really take you far in life. People that are patient, they tend to go a lot farther and a lot faster than people that are impatient. Sometimes you may think that a person that is patient is slow. No, those people actually fast because their actions are measured. They don't take random actions. They take measured approaches to life. They notice that man, this person makes a firm mistake because those people that are impatient that seem to be going fast. They are going fast but they actually slow because they're making so many mistakes. They spend a few chunks of their lives overcoming those mistakes that they meet from impatience. The person that is patient is making fewer mistakes. They don't have to spend copious amounts of time overcoming errors that they've made and they able to just make very, very rapid progress. Again, I'll just encourage you, as you cup of the year, as you go into the new year, just make up your mind to be a person that is patient. Be a patient person. Be a calm person. Be a person of a patient, quiet and calm spirit, and be a means that how far you can go.

I'll see you in the episode 500 and one. God bless you. Have a wonderful holiday. Have a happy new year and bye for now. Thank you.

Recent URI symptoms followed by signs of heart failure (S3 gallop, crackles, edema). Think Coxsackie B virus.

Both hepatic venous pressure and portal sinusoidal pressure will be elevated due to outflow obstruction.

Increased intra-thoracic/abdominal pressure compresses the carotid arteries, triggering a baroreceptor reflex that causes profound parasympathetic discharge and bradycardia.

Pressures before the root block are elevated; pressures after the root block are low or normal.

Maternal diabetes (Infant of Diabetic Mother). High glucose leads to fetal hyperinsulinemia, which inhibits surfactant production.

The blood becomes highly viscous, leading to sluggish flow and stasis, which promotes thrombus formation.

Coxsackie B virus.

Hepatic sinusoidal pressures and portal pressures.

Compression of the carotid arteries, triggering a baroreceptor reflex leading to parasympathetic discharge and bradycardia.

Compliance decreases (due to increased surface tension), and collapsing pressures increase.

In PE, CVP/JVP are elevated due to systemic backup; in BCS, CVP/JVP may be normal or less dramatically affected because the obstruction is more central/hepatic outflow.

The kidneys (glomerular capillaries fed by afferent arterioles and drained by efferent arterioles).

Maternal hyperglycemia leads to fetal hyperinsulinemia, which inhibits surfactant production.

Coxsackie B virus.

Hepatic sinusoidal pressures and portal pressures.

Compression of the carotid arteries, triggering a baroreceptor reflex leading to parasympathetic discharge and bradycardia.

Compliance decreases (due to increased surface tension), and collapsing pressures increase.

In PE, CVP/JVP are elevated due to systemic backup; in BCS, CVP/JVP may be normal or less dramatically affected because the obstruction is more central/hepatic outflow.

The kidneys (glomerular capillaries fed by afferent arterioles and drained by efferent arterioles).

Maternal hyperglycemia leads to fetal hyperinsulinemia, which inhibits surfactant production.