DIP Episode 622 - USMLE Step 2/3 Rapid Review Series 130

Welcome, my name is Divine, this is episode 622 of the Divine Intervention Podcast. In today's podcast we're going to be continuing the Rapid Review series for step 2, CKN Step 3. This is going to be series 130. So one thing I want to say for those that have been listening to my MSK series, I did make a podcast a while back on the knee. So if you're trying to look for a good podcast on the knee, just literally go do a search on my website for knee. There's a podcast I made a couple of podcasts ago that really addresses knee pathologies. Alright, so let's jump right into it. So what if they give you a question about a patient and they tell you that this patient three weeks ago was started on pharmacotherapy for seizure disorder. And that now the patient over the last two days has been having like, has had like three rounds of seizures. And then they give you some labs and you notice that the person's sodium is 124. And then they ask you which of the following, which of the following is the most likely theology of the patient's presentation or what is the cause of the person's new seizures. They will put an answer choice that talks about worsening seizure disorder. They will put an answer choice that talks about medication side effect. I really hope that you're picking the answer that talks about medication side effect. Right. So this person has SIDH from carbamazepine. Right. This person has SIDH from carbamazepine.

So remember that carbamazepine is a drug that can be used to treat certain seizure disorders. But beyond treating seizure disorders, you can also use carbamazepine as a drug to treat tick-diloroo. Right. So if a person has tried, even on a rarge where you have like this fleeting, lancinating pain on their face, like in a basically not trige, even on nerve distribution. So typically like that's what carbamazepine is used for. But there are two toxicities you want to make sure you know for your exams with carbamazepine. Right. Uh, carbamazepine can cause SIDH. It can cause SIDH. Right. I remember we have SIDH. You're sucking up a lot of free water from your urine because you have a lot of ADHD around anti-diarrytic hormone. So that order your sucking up is going to dilute your serum. So that's going to cause you to have hyponitrivia. So then that's going to cause your urine to be more concentrated. So you're going to have a high urinous malarity. Um, another way they can express that is you have a high urin specific gravity. Right. So again, when people have SIDH, you're going to see hyponitrivia, they're going to have a low sermosmalarity. They're going to have a high urinous malarity. Right. And if you really think about it, the urinous sodium is going to be high. Right. The urinous sodium is going to be high. Why? Because again, you're really, really sucking up a ton of water from the, from the urine. So the urine is very, very concentrated.

Now remember that carbamazepine can also cause a granulose itosis. It can cause fibroinitripe pine. Right. So if they give you a question about a person that is studied on a drug for seizure disorder, and then the person now presents with a fever, right. And the person is absolutely neutral. Feel count is super low. You want to think about fibroinitripe. Right. And don't forget the other causes of SIDH, especially small cell lung cancer. All right. Now what if they give you a question about a patient, you know, they tell you that, you know, this is like a 16 year old male. And that is parents bring him to the physician's office because he has been having a lot of, you know, that whenever he rises out of bed, he feels dizzy, right. And he has been having like some bouts of chest pain that last for a few minutes at a time. And then they go away. And then they tell you that this patient, that, you know, he's just 16 years old, you know, but that he has no other medical history that he was delivered, you know, at like 39 weeks. He's up to date on his vaccinations, blah, blah, blah, blah, blah. Right. And then they tell you that, you know, that the patient when he lays down in a supine position in the office, that a murmur is heard, and that when he then stands here, you know, stands and he's been standing for about 30 seconds, that the same murmur is heard, but the murmur has increased in intensity.

When you see something like this, what kind of concept should you be thinking about? What kind of concept should you be thinking about? I really hope you're thinking about hocoma. I really hope you're thinking about hypertrophy cardiomyopathy. So notice what I did here. And this is something our friends at the MBA me has been doing a lot of in recent times. Here, I didn't give you the classic presentation of an athlete that passes out during a game or something like that. What did I do? I decided to bring it from a different perspective of, oh, this person's having like pressing copa episodes, youngish person, pressing copa episodes, and not just pressing, syncopal episodes, the person, you know, rising out of bed, they're having all these symptoms and they have these bouts of chest pain. See, the thing is, you may wonder, how could I see how good in that this was hocoma? Well, if you put the overall thing together, you'll see that this is hocoma. And I'm going to explain as we go, but please, I'm just trying to use this scenario to emphasize something. The USML is, they've got been very big on not giving necessarily giving you, like they'll still give you the classic presentations, but they just move certain things around, right? Just to see if you can think and if you can reason. So let's kind of break this down, right? So why does this person have these problems? Right? So if you think about it, right?

While the person was laying down, you could hear a murmur, but then once the person rolls, the murmur became louder, right? In a youngish person should really make you think of hocoma. Right? So what's the deal with hocoma? Well, hocoma, many times it's a nozoro, orzomo dominant disorder, and you have issues in myocene proteins. But the critical thing I think that's very helpful to know here is that they are murmur maneuvers that will temporarily worsen the murmur and the murmur maneuvers that would improve the murmur and make it like less loud, right? Because really like in hocoma, you have this thing called asymmetric septal hypertrophy. And with this asymmetric hypertrophy of the intraventricular septum, that causes a levventricular afloat tract obstruction. When you have a levventricular afloat tract obstruction, that's going to make it hard for blood to come out of the levventricle. And that can cause you to have syncopal or presyncopal episodes. Right? So the thing is, when you go from a supine to a standing position, what exactly are you doing to preload? Well, think about this. When you're supine, you know, blood is layering from your legs and going back to your heart, your preload is great. But when you stand, gravity does the job. It keeps blood in your legs, prevents it from going back to your heart, that reduces your preload. Whenever you reduce preload, you're putting less blood back in the heart.

And whenever you put less blood back in the heart, you actually worsen that levventricular afloat tract obstruction. Right? The way I like to think of it is as follows. It's like whenever you put blood in the levventricle, it almost like pushes the intraventricular septum away from the walls of the levventricle. Separate stints, mixed up, is almost like it clears the traffic. Okay? So think of more blood in the heart as clearing the traffic out of the levventricle. Think of less blood in the heart as worsening the traffic out of the levventricle. When you're worsening the traffic out of the levventricle, right? When there's a big traffic jam, people are going to be honking a lot and all those things. You're going to get an louder remember. That's the way I think about it for purposes of the USML exams. Right? So whenever there's less blood in the heart, it worsens the levventricle afloat tract obstruction. We see in hookum. And by worsening that, you're going to have a louder murmur. But when you have more blood in the heart, that's going to reduce the effects of that levventricle afloat tract obstruction. And you're going to get a more blood in the heart. You're going to get a less louder murmur. Right? That's something that's pretty high you to know for your exams. Okay? Another manover that could be thrown in on your exams that will make it louder is the valve solvermanover. Right? Remember the valve solvermanover? You're pretty much blowing against the closed glottis.

Don't try that if you know you probably pass out. Right? But you're blowing against the closed glottis as you blow against the closed glottis. The thing that's going to happen is that you're going to raise your intra-thoracic pressures. When you raise your intra-thoracic pressures, you're going to be compressing the SVC and the IVC. You're going to also be compressing the heart. That's going to decrease feeling of the heart. You're going to reduce preload. Right? And that's going to worsen the murmur because there's less blood in the heart. Right? So again, pretty high yield to know these things for your exams. Right? These things are going to increase the intensity of the ho-com murmur. And remember, people that have the ho-com, that have ho-com, they should be on beta blockers. Right? Beta blockers are the primary medications that should be given to people that have ho-com. Now, since I'm talking about beta blockers, I think you'll be helpful to just talk about beta blockers in general for the USMELIS. Let's just do a quick drive-by of what are the different ways they can come after me with beta blockers on the exams. Well, the thing is, number one, we know that beta blockers, right, they improve survival in heart failure. Right? The improved survival in heart failure, especially metoprolol, carvidi-lol, and besoprolol. Right? So that's one indication you're certainly going to see on your exams with beta blockers.

Now, the second thing you need to know with beta blockers is, like we've said, they're useful for ho-com. That's how you manage ho-com. Third thing to know with beta blockers is to be honest with you, on your exams, think of them as the first line from aotherapy for stable angina. Okay? Think of them as the first line from aotherapy for stable angina, which makes sense, right? Because basically, they increase the systolic feeling of the heart. Why? Because they are negative chronotropes. They make the heart go at a slower rate. When your heart goes at a slower rate, you're going to give more time for dastily. That makes sense. And then also, they reduce by your cardiovascular oxygen demand because they are negative vinyl tropes. They make the heart contract with less force. And if the heart is contracting with less force, it's almost like conserving energy. So they're negative vinyl tropes and they are negative chronotropes. And then another factor to know about beta blockers is that they are very amazing for treating glaucoma. They're very amazing for treating glaucoma. Because again, the thing is the sympathetic glaucoma, the problem is you have too much ekeous humor. So one way you can kind of help because that increase ekeous humor is causing you to have increase in drug pressure. And then that's putting you in a lot of trouble. Well, if you had a situation where you could decrease ekeous humor production, that would be really helpful, right?

Because the sympathetic system promotes ekeous humor production. And maybe like divine, can you make that make sense to me? Well, think about it. What does your sympathetic system do to the eye? It causes popularity dilation, right? When you have popularity dilation, the thing that's going to happen is to have that to achieve that dilation, so that you can see that lion that is chasing you. You need to have bulging your eye. And that bulge comes by way of ekeous humor. So your sympathetic system wants your eyes to have more ekeous humor so that your eyes can bulge so that you can have popularity dilation. So if you have increased in drug love pressures, because you have too much ekeous humor, if you shut down the sympathetic system in the eye, you'll make less ekeous humor, you'll have less of that bulge, you'll have a reduced in drug love pressure, right? You'll have a reduced in drug love pressure. So just something you want to keep at the back of your mind for your exams. You can use beta blockers to treat glaucoma, especially like the open angle closure, like the open angle, sorry, the open angle glaucoma. And then another thing you can use beta blockers for your exams is for pressing the hazeotic dissection, right? So, eoteach dissection, which makes sense, right? Because remember in the eoteach dissection, you have a tear in the intima and that tear in the intima is ripping through into the media of the yoder. Now, the thing is you don't want that tear to get worse.

And one of the ways you can prevent that tear from getting worse is by reducing the shear stress exerted on the walls of the yoder. And that shear stress is a function of the force with which blood is living the left ventricle. That shear stress is a function of the force with which blood is living the left ventricle. So if you could reduce the force with which blood exited the left ventricle, that'd be very helpful in that circumstance. So what's the agent that can help you with that? It's a beta blocker because again, they are negative vinyl tropes, right? So they make the heart contract like in a very gentle fashion. So the blood that's coming out of the heart is not coming out with as great force. So that's going to reduce the shear stress on the walls of the left ventricle because the thing is many people that get into a yoder dissection are people that have hypertension. Remember, hypertension is the biggest risk factor for yoder dissection. When you have hypertension, right? When you have hypertension, it induces the blood in the left ventricle to come out with greater force like the shear stress of blood that comes like the shear stress on the walls of your yoder in a person that is hypertensive is very, very high. Why? Because the ventricle has to contract with great force to expel that blood from the heart because hypertension increases after load. You may wonder divine how? Well, how does hypertension increase after load? Well, the thing is think about this.

Let's say your blood pressure is 1.80 over 100. Your systolic blood pressure from what I just said is 1.80. Remember that flow happens from areas of high pressure to areas of low pressure. If you have such high systolic blood pressures, if you want blood to come out of the left ventricle, then the left ventricle has to generate pressures, has to generate systolic pressures that exceed 180, right? So obviously for your left ventricle to generate pressures that are that high, that blood has to come out with great force with great pizzas from the heart, right? That's going to put a lot of strain on the walls of the yoder, right? On all that strain is what causes aneurysmal dilution. All that strain is what can cause a tear in the intima that leads into the media, right? So that should hopefully kind of give you some context on what I've been saying about this shear stress, shear stress, shear stress with theotic dissection, right? Okay, so what else can beta blockers be useful in the USMEL exams? Remember, you can use them for essential tremors, right? You can use them for essential tremors, you can use beta blockers for acathesia, right? You see a person that starts an anti-psychotic and then a few days later, I'm just having all this motoristlessness, right? Kind of group those two things, motoristlessness of acathesia with essential tremors, group those two things together in your mind. Beta blockers are pretty good for that purpose.

And then another psychiatric use of beta blockers you may see on your exams. Is it for a person? Is about to give a speech and they're kind of worried, they're concerned, they're anxious, right? That's stage fright. That's the performance-up type of social anxiety disorder. In those circumstances, the smart play to go with for your USMEL exams is to give them beta blockers, right? To give those people beta beta blockers. All right, what else can beta blockers be useful in the USMEL exams? Beta blockers really do have a lot of use, right? You can use them. Actually, let's maybe talk about them in the context of side effects, right? So if a person has an acute CHF exacerbation, giving them a beta blocker during that acute phase, right? It's not a good idea, right? If a person has a few chromosytoma, right? It's a terrible idea to give them a beta blocker, you know, if you're trying to explore pharmacotherapy, you want to give them alpha blockade first before beta blockade, right? Because you don't want that on a post alpha stimulation. Same thing also applies with cocaine intoxication, and then also if you look at the context of arrhythmias, remember beta blockers are the way to go. If a person has aphab, right? If a person has aphab, you can use them as a form of a rate control. You can use a beta blocker or you can use a non-dihydroperidine calcium channel blocker, like Vera Pamelo, they'll tie us in, right? That's pretty high you to know for your exams.

All right, so I think of kind of a heat beta blockers and also you can use beta blockers for migraines, right? You can use beta blockers for migraines. They like to give you this scenario on your exams where a person has migraines, but they also have a lot of um, they have migraines, but they have also have another reason why they may do it with beta blockers, right? And that's her constant. Beta blockers will be the great chronic medication for their migraines. All right, so let's, let's keep going, right? So what if they give you a question about a patient and they tell you that this patient comes to the emergency room with a two hour history of severe flung pain, right? Left flung pain and you're told that this patient, you know, has a history of HIV. And for the last three weeks, this patient has noticed like increased swelling of the legs and increased swelling of the arms, right? And then they tell you that as you're listening to this patient's chest, you can hear, you know, crackles at the base of the lungs, right? And that you're told that, you know, when this, when the person on the goals, uh, CT of the abdominal pelvis with IV contrast, that you can notice, uh, positive flow, right? A positive flow within renaul vasculature. When you see something like this, what should you be thinking about? I really hope you're seeing divine. This is a renaul of intromboces. What? Yeah, this is renaul of intromboces.

So let's put it all together because again, the name of the game with the USMLA exams is not about how much you've memorized is about how much you can integrate, right? It's about how much you can integrate. So let's break this down. First things first, this person has HIV. If a person has HIV and they have a lot of edema, what should you be thinking about on your exams? I really hope you're saying divine. This sounds an awful lot like an aphrodix syndrome. Okay. So if you have HIV, what kind of an aphrodix syndrome should you be thinking about? What kind should you be thinking about? What kind should you be thinking about? Well, I hope you're thinking about FSGS or these days, I think the name is FSGN, right? Focuse segmental glomerulus sclerosis or Focuse segmental glomerulonephropathy, right? So FSGS is pretty common in HIV patients, right? At least let's not let me know. See it's pretty common in HIV patients. If you see a HIV patient with an aphrodix syndrome, you want to be thinking about FSGS, right? And the thing is, there are many kinds of FSGS, but one of the ones that has the worst prognosis is colapse in FSGS. colapse in FSGS is the kind that you find very commonly in HIV patients, right? So remember, in a phrodix syndrome, you're peeing out a lot of albiumin in your urine. When you pee out a lot of albiumin in your urine, that's going to cause you to lose on cortic pressure in your vasculatory.

And if you lose on cortic pressure, you don't have any impetus to hold onto water in your vasculatory. When that happens, you're going to have a lot of fluid extroversation. And that fluid extroversation is going to cause you to have a demon, right? So that's why this person has swelling of the legs. That's why the asswelling of the arms. That's why they have a plural effusion, right? They're going to have a trans-uditive plural effusion. But why is it that this person has renauvin thrombosis? Why? Well, let's talk about this because this is very high yield to know for you exams. Again, the USML is these days. Mechanisms, mechanisms, mechanisms is the name of the game, right? So there are three reasons why a person that has nephrodix syndrome will have renauvin thrombosis. Number one is that when you have nephrodix syndrome, it's not just abusing your losing your urine. You're also losing antithrombin three. Antithrombin three is an anticoagulant protein. It inhibits factors two and factor ten. So when you lose that anticoagulant protein in your urine, you become hyperquagulable. That hyperquagulability is going to cause you to get into trouble with thrombotic episodes like renauvin thrombosis. That's number one. Number two, people that have nephrodix syndrome tend to have hyperliplidemia. Hyperliplidemia can make you hyperquagulable. Why is it that people that have nephrodix syndrome develop hyperliplidemia?

Again, it all goes back to the reduced oncotic pressure they have because they've lost a lot of protein, a lot of argument in their urine. When you lose all that protein, when you lose all that argument in your urine, the thing that's going to happen is the following. It's the following. It's the following. It's the following. Okay? Your liver is going to try to be like, man, I've lost all this protein that's so useful from my bloodstream. What is one way I can try to augment my oncotic pressure? Okay, let me just start making a ton of lipid. Your liver makes a ton of lipid. Mix a ton of lipid, a ton of lipid. Just to try to keep some stuff in the bloodstream that can hold fluid in the bloodstream. Even that ton of lipid, some of it makes its way to your urine. That's actually the mechanism behind the lipid cast, behind the fatty cast that we find in a thrombotic syndrome. Now, what's a third reason why people that have a thrombotic syndrome could have renauve intranbozes could have these thrombotic episodes is because again, they have reduced oncotic pressure in their bloodstream. When you have reduced oncotic pressures, you don't have enough fluid in your vasculotry. That almost introduces like a slow flow state in your body. That slow flow state, remember Verko's triad, stasis, hyperquagulability, and endothelial dysfunction. You're going to have a lot of blood stasis.

That blood stasis can make you hyperquagulable because when your blood is not flowing fast, then that causes more interactions between your clotting factors. When you have more interactions between your clotting factors, that can make you hyperquagulable because you can stuff from in all these clots. Now, the final thing I want to say about renauve intranbozes, look at the way it presents it, flang pain, and then they can even give you CT of the abdomen and pelvis results with IV contrast. You notice that they is reduced flow within renauve acculature. Notice how it was kind of non-specific reduced flow within renauve acculature because it will make no sense for the USM used to throw you a bone and see reduced flow within the renauve. Well, hello, of course that's renauve intranbozes. They will make it a little more vague and see reduced flow within the renauve acculature. Now, one final thing I want to say about renauve intranbozes before I tap the surface, what is the nephrodite syndrome that has the strongest association with renauve intranbozes? I really hope you're saying divine. That nephrodite syndrome is membranostephropathy of all the nephrodite syndromes. membranostephropathy is the one that has the strongest association with renauve intranbozes. Remember, membranostephropathy is something I'm going to find in people that have, the thing you're going to find in people that have solid organ malignancies like colon cancer and things of that nature.

Alright, so I think I've made a lot of integrations today. So I think I'm going to go ahead and stop here. But again, I really hope that you found this podcast to be helpful. And if you love the way I teach, you love the way I make integrations, I have a bunch of classes coming up this month. I have a 20-hour step two, step three class that sticking place at the end of this month. And then I have a test-dicking strategies class, a 20-hour test-dicking strategies class that's for step one, all the way to step three. And then I have a biostatistics class that is four hours long that's also for step one, all the way to step three. I have a social sciences and ethics class also for step one to step three to five hour class. The thing is step one to step three these days about 10 to 20 percent of the questions you see are going to be centered around biostatistics and social sciences and ethics. So those classes really help. And then I have a three hour last minute review for step two, second step three. Again, these classes are updated very frequently to keep up with the vagaries of the US Emily exams. And there's many people that are taking these classes and don't extremely well on their tests. I've literally had people take these classes recently and getting the 250's, the 260's on their exams. I'm not saying everybody gets that score, but many people get those scores from these classes. And then I also offer one on one tutoring for the US Emily and Cummlex exams.

And I also help with Eras applications, personal editing of personal statements, recommendation letters, my help with marketing reviews. And then I have these podcasts on Apple Google and Spotify. And then I also have another website called divine intervention life lessons.com, divine intervention life lessons.com. Every week I post like one or two podcasts from a biblical perspective, address a life lesson. I mean, if you know I'm a Christful or in this podcast, I'm a Christful or a Christian. So I make these podcasts every week to kind of break down the Bible. I actually have almost 360 episodes on there. There is an Apple podcast that actually call the divine intervention life lessons podcast. All right, so thank you for listening to me today. I will see you God willing episode 623. Have a wonderful day. God bless you and bye for now. Thank you.

Hyponatremia with low serum osmolality, high urine osmolality/specific gravity, and high urine sodium.

The murmur increases in intensity because reduced preload worsens the left ventricular outflow tract obstruction.

1) Loss of Antithrombin III (hypercoagulability). 2) Hyperlipidemia. 3) Reduced oncotic pressure leading to blood stasis (Virchow's triad).

Membranous Nephropathy.

They reduce shear stress on the aorta by decreasing left ventricular contractility and lowering blood pressure.

Glaucoma (open angle), essential tremors, migraine prophylaxis, or performance anxiety/stage fright.

Hyponatremia and low serum osmolality.

Decreasing preload (e.g., standing up or Valsalva).

To compensate for the loss of plasma proteins (albumin) and maintain oncotic pressure.

Reducing shear stress on the aortic wall by decreasing left ventricular contractility.

Open angle glaucoma (by reducing aqueous humor production).

Hypertension, which increases afterload and forces the left ventricle to contract with greater force.

Hyponatremia and low serum osmolality.

Decreasing preload (e.g., standing up or Valsalva).

To compensate for the loss of plasma proteins (albumin) and maintain oncotic pressure.

Reducing shear stress on the aortic wall by decreasing left ventricular contractility.

Open angle glaucoma (by reducing aqueous humor production).

Hypertension, which increases afterload and forces the left ventricle to contract with greater force.