DIP Ep 622: USMLE Step 2/3 Rapid Review Series 130

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 uh three weeks ago was started on pharmacotherapy for a seizure disorder. And that now the patient over the last two days has been having like uh has had like three rounds of seizures and then they give you some labs and you notice that the person's sodium is one hundred and twenty-four.

uh and then they ask you, uh, which of the following um Condition, you know, which of the phone is the most likely etiology of the patient's presentation or what is the cause of the person's uh you know new seizures? You know, they will put an answer choice that talks about um, you know, worsening seizure disorder. They will put an answer choice that talks about medication side effects.

I would really hope that you're picking the answer that talks about medication side effect, right? So this person has SIDH. from carbamazapine, right? This person has SIDs from carbamazapine. So remember that carbamezepine is a drug that can be used to treat certain seizure disorders. But beyond treating seizure disorders, you can also use carbamezepine as a drug to treat

Um tick de la rou, right? So if a person has trigeminal neuralgia where they have like this fleeting, lancinating pain on their face, like in a basically in a trigeminal nerve distribution. So typically like that

what carbamazepine is used for. But there are two toxicities you want to make sure you know for your exams with carbamazepine, right? Uh carbamezapine can cause SIDH. Can cause SIDH, right? And remember when you have SIDH, You're sucking up a lot of free water from your urine because you have a lot of ADH around, antidiuretic hormone. So that water you're sucking up is gonna dilute your serum. So that's gonna cause you to have hyponutremia.

But then that's gonna cause your urine to be more concentrated. So you're gonna have uh high urinosmolarity. Um another way they can express that is you have a high urine specific gravity. Right. So again, when people have SIDH you're gonna see hypodytramia, they're gonna have a low serum osmolarity, they're gonna have a high urine.

Right. And if you really think about it, the urinary sodium is going to be high. Right. The urinary sodium is going to be high. Why? Because you 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 caramezapine can also cause a granulocytosis. It can cause fibronutropenia, right? So if they give you a question about a person that is studied on a drug for a seizure disorder,

And then the person now presents with a fever, right? And the person's absolute neutrophil count is super low. You want to think about febral neutropenia, 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 his parents bring him to the physician's office because he has been having a lot of uh you know that whenever he rises out of bed um 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 um uh this patient Just sixteen years old, you know, but that he hasn't all the 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 uh you know, that the patient when he lays down in a supine position in the office. Um that a murmur is heard.

And that when he then stands, he or you know, stands and he's been standing for about thirty 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'd really hope you're thinking about hookum. I'd really hope you're thinking about hypertrophic cardiomyopathy. So notice what I did here, and this is something our friends at the MBMEs have been doing a lot of in different 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 ooh, this person is having like pre-syncopel episodes, youngish person, pre-syncouple episodes, and not just pre-syncouple episodes. Uh 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 stay upgotten that this was Hokum?

Well, if you put the overall thing together, you'll see that this is Hokum and I'm gonna explain as we go. But please I'm just trying to use this scenario to emphasize something. The USML is they've gotten 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 rose, The murmur became louder, right? In a youngish person should really make you think of Hokum. Right? So what's the deal with Hokum? Well Hokum

Many times it's an orosomal dominant disorder, and you have issues in myosin proteins. But the critical thing I think that's very helpful to know here is that. There are murmur maneuvers that will temporarily worsen the murmur and they are murmur maneuvers that would improve the murmur and make it like less loud. Right? Because really like in Hokum, you have this thing called asymmetric septal hypertrophy.

And with this asymmetric hypertrophy of the interventricular septum, that causes a left ventricular outflow tract obstruction. When you have a left ventricular outflow tract obstruction, that's going to make it hard for blood to come out of the left ventricle. And that can cause you to have syncopal or presyncopal episode. 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.

Left ventricular outflow tract obstruction, right? The way I like to think of it is as follows: is like whenever you put blood in the left ventricle, it almost like pushes the interventricular septum away from the walls of the left ventricle. Separates things, makes that it's almost like it clears the traffic. Okay. So think of more blood in the heart as clearing the traffic out of the left ventricle. Think of less blood in the heart as worsening the traffic out of the leaven.

When you're worsening the traffic out of the left ventricle, 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 a louder murmur. That's the way I think about it for purposes of the USMLE exams, right? So whenever there's less blood in the heart, it worsens the left ventricular outflow tract outflow tract obstruction. We're seeing Hokum.

And by worsening that, you're gonna have a louder murmur. But when you have more blood in the heart, That's going to reduce the effects of that level ventricular flow tract obstruction. And you're gonna get a uh more blood in the heart, you're gonna get a less loud murmur, right? That's something that's pretty high yield to know for your exam. Okay, another maneuver that could be thrown in on your exams that will make it louder. Is the Val salva manover?

You're pretty much blowing against the closed glottis. Uh don't try that if not you probably pass. Right. The thing that's gonna happen is that you're gonna raise your intrathoracic pressure. When you raise your intrathoracic 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. Um so again pretty high yield to know these things for your exams. Right. These things are gonna increase the intensity of the whole murmur. And remember, people that have uh the hokum that have hocum, they should be on beta blockers, right? Beta blockers are the primary medications that should be given to people that have hocum.

Now, since I'm talking about beta blockers, I think it will be helpful to just talk about beta blockers in general for the USMLs. Let's just do a quick drive-by of, hmm, what are the different ways they can come after me with beta blockers on the exam?

Well the thing is, number one, we know that beta blockers, right, they improve survival in heart failure, right? They improve survival in heart failure, especially metoprolol, uh, carvidolol, and bisoprool, right? So that's one indication you're certainly gonna 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 Holcomb. That's how you manage Hokum.

Third thing to know with beta blockers is to be honest with you, on your exams, think of them as the first line pharmacotherapy for stable angina. Okay? Think of them as the first line pharmacotherapy for stable lungina, which makes sense. Right? Because basically they increase the diastolic feeling of the heart. Why? Because they they're negative chronotropes.

They make the heart go at a slower rate. When your heart goes at a slower rate, you're gonna give more time for diastole. That's that makes sense. And then also they reduce myocardial oxygen demand because they're negative inotropes. They make the heart contract with less force. And if the heart is contracting with less force, right, it's almost like conserving energy, right? So there are negative inotropes and they are negative chronotropes.

And then another factor to know about beta blockers is that they are very amazing for trading glaucoma, right? They're very amazing for trading glaucoma, right? Because again, the thing is the sympathetic in glaucoma, the problem is you have too much ICO humor. So one way you can kind of help, because that that increased the Q tumor is causing you to have increased intraocular pressures, and then that's putting you in a lot of trouble.

Well, if you had a situation where you could um decrease ACOS humor production, that would be really helpful, right? Because the sympathetic system promotes ACOS humor production. I may be 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 populary dilation, right? When you have populary 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 bulge in your eye. And that bulge comes by way of acheous humor. So your sympathetic system wants your eyes to have more acheous humor so that your eyes can bulge, so that you can have popular dilation. So if

You have increased intraocular pressures because you have too much acheous humor. If you shut down the sympathetic system in the eye, you'll make less acheous humor. You'll have less of that bulge. You'll have a reduced intraocular pressure. right you have a reduced intraocular pressure so just something you want to keep at the back of your mind for your exams you can use beta blockers to treat uh 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 in your exams is for a person that has aortic dissection, right? So aortic dissection, which makes sense, right? Because remember in aortic dissection, You have a tear in the intima, and uh that tear in the intima is ripping through into the media of the yodor.

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 sheer stress exerted on the walls of the yard. And that shear stress is a function of the force with which blood is leaving the left ventricle. That shear stress is a function of the force with which blood is leaving 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 in neutral. Right. So they make the heart contract gent 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 aortic dissection are people that have hypertension. Remember, hypertension is the biggest risk factor for aortic 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 sheer stress of blood that comes like the sheer stress on the walls of your yodor 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 afterload? Well, the thing is, think about this. Let's say your blood pressure is 180 over 100. Your systolic blood pressure from what I just said is 180. 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 live 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 gonna put a lot of strain on the walls of the yodor, right? On all that strain is what causes aneurysm dilation, all that strain is what can cause a tear in the intima that leads into the medium. Right. So That should hopefully kinda give you some context on what I've been saying about this shear stress, shear stress, shear stress with aortic bisection.

Right. Okay, so what else can beta blockers be useful on the USMLE 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 antipsychotic and then a few days later and they start having all this motor restlessness, right? Kind of group those two things, motorestlessness 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 exam. is if a person uh is about to give a speech and they're kinda worried, they're concerned, they're anxious, right, that's stage fright. That's the performance subtype of social anxiety disorder.

In those circumstances, the smart play to go with for your USMLE exams is to give them beta blockers, right? To give those people beta blockers. All right. What else can beta blockers be useful in the USMLE exam? B bit of blockers really d they do have a lot of use, right? Um you can use them Um 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 bit of blocker during that acute phase, right, is not a good idea, right? Or if a person has a pheochromocytoma, 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 unopposed alpha uh stimulation. Same thing also applies with cocaine intoxication, right?

And then also if you look at the context of arrhythmias, remember beta blockers are the way to go. If a person has um AFib, right? If a person has AFib, you can use them as a form of uh rig control. You can use a beta blocker or you can use a non-dihydropyridine calcium channel blocker, like Virapa Melodiltiasm, right? That's pretty high you'll know for your exam.

Alright, so I think I've kind of hit beta blockers and also you can use beta blockers for migraines, right? You can use beta blockers for migraines. Uh they like to give you this scenario on your exams where a person has migraines, but they also have a lot of uh They have migraines, but they have also have another reason why they may do it with beta blockers, right? In that circumstance, beta blockers will be the great chronic medication for their for their migraine.

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 flunk pain? right, left pl flank 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 leg.

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 uh you know crackles at the base of the lung. Right. And that you're told that, you know, when this when the person on the goals uh C T of the abdomen and pelvis with IV contract

that you can notice uh positive of flow within renovasculature. When you see something like this, what should you be thinking about? I'd really hope you're seeing divine. This is a renovin thrombosis.

What? Yeah, this is renoving thrombosis. So let's put it all together. Because again, the name of the game with the USML exams is not about how much you've memorized, it's about how much you you can integrate, right? It's about how much you can integrate. So let's First things first, this person has H I V.

If a person has HIV and they have a lot of edema, what should you be thinking about on your exams? I'd really hope you're saying divine, this sounds an awful lot like nephrotic syndrome. Okay. So if you have HIV, what kind of nephrotic syndrome should you be thinking about? What kind should he be thinking about? What kind should we be thinking?

But I hope you're thinking about FSGS or these days I think the name is FSGN, right? Focosegmental glomerulosclerosis or focusegmental glomerulome nephropathy, right? So FSGS is pretty common in HIV patients, right? At least let's not let me not say it's pretty common in HIV patients. But if you see a HIV patient with nephrotic 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 collapsing FSGS. Collapse in FSGS is the kind that you find very commonly in HIV patients, right? So remember in nephrotic syndrome, you're peeing out a lot of albumin in your urine. When you pee out a lot of albumin in your urine, That's going to cause you to lose oncotic pressure in your vascular tree. And if you lose oncotic pressure, you don't have any impetus to hold on to water in your vascular tree.

When that happens, you're going to have a lot of fluid extravasation. And that fluid extraversation is going to cause you to have edema, right? So that's why this person has swelling of the legs. That's why they have swelling of the arms. That's why they have a plural effusion, right? They're going to have a transuditive plural effusion.

But why is it that this person has renovin thrombosis? Why? Well, let's talk about this because this is very high yield to know for your exams. Again, the USMLEs these days. Mechanisms, mechanisms, mechanisms is the name of the game, right? So there are three reasons why a person that has nephrotic syndrome will have renovin thrombosis. Number one,

is that when you have nephrotic syndrome, it's not just albumin you're losing in your urine, you're also losing anti-thrombin 3. Antithrombin 3 is an anticoagulant protein. it inhibits factors two and factor ten. So when you lose that anticoagulant protein in your urine, you become hypercoagulable. That hypercoagliability is gonna cause you to get into trouble with thrombotic episodes like renovine thrombosis. That's number one.

Number two, people that have nephronic syndrome tend to have hyperlipidemia. Hyperlipidemia can make you hypercoaglible. Why is it that people that have nephrotic syndrome develop hyperlipidemia? Again, it all goes back to the reduced onchodic pressure they have because they've lost a lot of protein, a lot of albumin in their urine. When you lose all that protein, when you lose all that album in your urine.

The thing that's going to happen is the following. Is the following. Is the following. Is the following. Okay, um your liver is gonna 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. So your liver makes a ton of lipid. Makes 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, right? And even that ton of lipid, some of it makes its way to your urine. That's actually the mechanism behind the lipid casts, behind the fatty casts that we find in nephrotic syndrome. Now, what's a third reason why people that have nephrotic syndrome could have renovin thrombosis, could have these thrombolic episodes? It's because again.

They have reduced onchodic pressure in their bloodstream, right? So when you have reduced onchodic pressures, you don't have enough fluid in your vascular tree, right? So that almost introduces like a slow flow state in your body. And that slow flow state, right, remember Vircose Triad. stasis hypercoagulability and endothelial dysfunction you're going to have a lot of blood stasis that blood stasis can make you hypercoagulable because when your blood is not flowing fast

Then that causes more interactions between your clotting factors. And when you have more interactions between your clotting factors, that can make you hyperquaglable because you can start forming all these clots. Now the final thing I want to say about renovin thrombosis, right, look at the way you presented, right? Flank pain, right? And then they can even give you CT of the abdomen and pelvis results with IV contrast, and you'll notice that there is reduced flow within renovascular.

Right. Notice how it was kind of non specific, reduced flow within renovasculature. Um because it will make no sense for the USMLs to throw you a bone and see reduced flow within the renovin. Well, hello, of course that's renovin thrombosis. So they will make it a little more vague and say reduced flow within the renal vascular.

Now, one final thing I want to say about Rinovin thrombosis before I cap this off is what is the nephrotic syndrome that has the strongest association with renovine thrombosis? I really hope you're saying divine. That nephrotic syndrome is membranos nephropathy. Of all the nephropic syndromes, membranos nephropathy is the one that has the strongest association with renovin thrombosis. Remember membranos nephropathy is something you're gonna find in people that have

um like solid organ malignancies like colon cancer and things of that nature. All right. So I think I've made a lot of integrations today. So I think I'm gonna go ahead and stop here. Uh but again I really hope that you found this podcast to be helpful. Um And if you love the way I teach, you love the way I make integrations, um, I have a bunch of classes coming up this month.

I have a um a twenty hour, step two, step three class that's taking place uh the end of this month. Um and then I have a test taking strategies class, a two and a half hour test taking 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. Um I have a social sciences and ethics class also for step one to step three. It's a five hour class.

Um the thing is step one to step three these days, about ten to twenty percent of the questions you see are gonna 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, CK, and step three. Again, these classes are updated very frequently, right, to keep up with the vagaries of the USMLE exam.

And there's many people that have taken these classes and done extremely well on their tests. Like I've literally had people take these classes recently and getting the 250s, the 260s 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 children for the US MLE and Complex exam.

And I also help with Eras applications, personal editing of personal statements, recommendation letters. Um, I help with mock interviews. And then I have these podcasts on Apple, Google and Spotify. Um And then I also have another website called Divine Intervention Life Lessons dot com. Divine Intervention Life Lessons dot com.

Every week I post like one or two podcasts where from a biblical perspective uh address a life lesson. Many of you know I'm a Christ follower in um in this podcast. Um I'm a Christ follower, I'm 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's an Apple podcast actually called 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.