DIP Episode 618 - USMLE Step 2/3 Rapid Review Series 128

All right, welcome to episode 618 of the Divine Intervention Podcast. In today's podcast, I'm going to be continuing the Rapid Review series for the USMELIS step 2 CK and step 3 exams. This can be series 128. If you notice, I've been trying to pump out a ton of these recently because it's just a very efficient way to throwing the material that again is just popping up a lot on the USMELIS these days. So what if they give you a question about a patient and they tell you that this person is a 76-year-old male and that over the last three hours, his wife has noticed that he has been out of it. He has been out of it and that he symptoms started very suddenly and that she notices that whenever she, that on his left side, he says that his left side feels very, very weird. And that the right side of his face also feels weird. And then they tell you that on physical examination, this person was, you know, that the person has like no pain or a pain-prick sensation in the left upper extremities, left lower extremities. And they ask you for the most likely diagnosis. Well, I would really hope on your exams, you're picking an answer that talks about right point in stroke or right AI, right? So this person has a brainstem stroke and one of the classic ways you know that a person is dealing with a brainstem stroke is that you're going to see pain and temperature loss. You're going to see the upper and lower extremities are fact-fed together, right?

That pretty much rules out a cortical stroke as the etiology of the person's problem, right? Because if you wear cortical stroke, then you'll see there an MC distribution stroke, the upper extremities or an AC distribution stroke, just the lower extremities. But we see that here, the upper and lower extremities are affected, right? Especially when they give you cranial nerves that are impacted. That's going to be some kind of stroke that is below the cortex, right? It's going to be like some kind of brainstem stroke, especially when they throw in cranial nerves. So for this AI-Cast stroke question that I'm talking about, what cranial nerves should they throw in? Well, typically on the USM list, they're going to throw in something related to cranial nerve number seven, right? The facial nerve. Because remember, the facial nerve is in the lateral ponds. I'm going to say that again, the facial nerve is in where? It's in the lateral ponds. It's in the lateral ponds, right? So how does this explain all these findings? Well, the thing is the spinal phalamic tract fibers, remember, they run in the lateral brain stem, right? So if your right lateral brain stem is infarcted, right? Like you write lateral ponds, for example. Then those spinal phalamic tract fibers are going to be impacted, right? And why is it the left side that the person has symptoms on?

Well, remember, those spinal phalamic tract fibers that are running on the right side of the brain stem, the right lateral brain stem, where did they come from? They literally came from the left side of the body. Because remember, the spinal phalamic tract crosses in the anterior white commissar in the spinal cord. So those fibers you're seeing on the right side of the brain stem, the right lateral brain stem, they actually came from the left side of the body, right? So where did they come from? They came from the left side. So if they are impacted, it's the left side of the body that's going to suffer. Now another thing to also know is that the fibers that control pin and temperature sensation for the face, they run in the lateral brain stem as well. They run in the lateral brain stem, but they typically do not cross. They typically do not cross. So this is why if you have an AIK stroke, you're going to have pin and temperature loss. On the same side of the face, on the same side of the face, on the same side of the face as where you have the stroke. So that's why this person has pin and temperature loss on the right side of the face and pin and temperature loss on the left side of the body, right? And again, typically a nice signature for a brain stem stroke is going to be the presence of cranio nerve symptoms. This person will have cranio nerve symptoms, especially cranio-7 symptoms, right? The person may also have issues with balance and hearing, right?

The vestibulococlinin of cranio nerve number eight, because that cranio nerve also runs in the lateral brain stem, right? So it's going to be a lateral-pointing stroke. It's going to be a lateral AIK stroke, an anterior inferior cerebellar artery stroke, right? And then what if our friends at the MBME's give you a question about a patient and they tell you that this patient has a history of non-healing wounds, right? Let's say it's like a 36-year-old female, that she has a history of poorly healing wounds. She has like a history of pelvic organ prolapse, right? And you're told that you can hear the stomach murmur at her left strewnal border. And that she presents with a very sodium onset severe headache, right? Sodium onset severe headache and that she is barely responsive. Well, if you're seeing this kind of question, I would really hope you're saying, oh, divine, this person, it looks like this person has a hemorrhagic stroke, right? You may be wondering, divine, how did you jump all the way to hemorrhagic stroke in this person? Well, let's put the facts of this case together. First things first, what genetic disease do you think this person in this question that I just highlight it has? But I'd really hope you're saying, oh, divine, this sounds an awful lot like Euler's down low syndrome. Well, how did I get there? Well, first things first, this person has the dastolic murmur at the left strewnal border, right? That's probably going to be aortic regurgitation.

Remember, whenever you have dilation of the Euler, right, that can typically cause a person to have the murmur of Euler's regurg. Right? So, what a half-crisis down low syndrome, they can have aortic aneurysms, right? So as those, as the aortic dilates, dilates, dilates, dilates, right? It's almost like you're pulling the aortic valve liftlets apart. That can cause you to have aortic regurg. That's number one. All right. Number two, how does this person have, I remember, aortic regurg is a dastolic murmur, right? So dastolic murmur. Please, I hope you're not seeing this dastolic murmur. So dastolic murmur, right? Because you feel the effects of the murmur when the left ventricle is trying to feel with blood from the left e-trum, blood is literally regurgitated, right? So number one, number two, I said that, ooh, this person has poorly healing wounds, right? Remember, people that have Euler's down low syndrome, they have like hyperextensible skin, hyperextensible joints, right? Again, these people have not great collagen. So because the collagen is not great, right? They can have wounds that do not heal quickly, right? Or just don't really heal very well, right? In fact, our friends at the MVM Es believe it or not, they can give you a question on the exams about a person that has Euler's down low syndrome. And this person in the Q-stem, this person literally in the Q-stem, this person what literally in the Q-stem, right, has like pressure of sorts, right?

Those people again, because their wounds don't heal well, right? They can have like next level pressure of sorts. Something you want to keep at the back of your mind for your exams, right? Okay, and then I said this person has pelvic organ prolapse. Pophic organ prolapse is a pretty classic thing you may find in females that have Euler's down low syndrome, right? Because again, the collagen is not good. So their pelvic floor doesn't have a lot of support. So their organs can be falling out, right? Again, the thing is the USM hellizio, you're not going to be getting these stents based on just one thing. No, if you notice, there are multiple pieces of evidence I put together to arrive at these diagnoses that I'm talking about, right? And then we see the sodium onset severe headache. Remember, these people can have aneurysms in the circle of willis, right? And those aneurysms, right, they can rupture, they can rupture. And when those aneurysms rupture, you can get in big trouble, right? Typically, wait till these people tend to form aneurysms in the circle of willis. These are usually going to be in the anterior communicating artery, right? Remember your A-com, your anterior communicating artery, that is the most common location in the circle of willis where people tend to form these a barrier aneurysms. Those aneurysms, they can pop and get a hemorrhagic stroke, okay? Now, what's the pathophysiology behind Euler's down low syndrome?

Well, Euler's down low syndrome, remember, is an Orozomodominant disorder where you have mutations in type three and in type five collagen, right? Now, let's assume our friends at the MBM is, they give you a question about a patient. And they tell you that this is a 10-year-old male, right? And they tell you that, you know, that he was brought to the emergency room by his parents two days ago, because he had very severe headaches and very high fever, right? And you're told that this child is an immigrant, right? And his vaccine status is unknown, that he just immigrated to the US. He was adopted by his parents, like six weeks ago, or like two months ago, something like that. And then we're told that this child is now profoundly hypotensive. This child has PIT-KI, proper echimosis on the skin, right? And you're told that this child is extremely hypoglycemic. And then, they tell you which of the following, which of the following would be expected with co-synchropin administration to this child? Well, I really hope you're saying that, which of the following expected responses will be, you know, will be seen in this child with co-synchropin administration. I really hope you're picking the answer that shows they can actually make this an hour, right? Or they can say, which of the following cortisol responses will be seen with co-synchropin administration?

And they will put, like, you know, no effect on co-synchropin, on cortisol levels, increase, decrease, these, the same or whatever, right? Pick the answer that talks about, pick the answer that talks about no change, right? Pick the answer that talks about no change. So what exactly am I talking about in this question? I really hope you're like, ooh, divine. Sounds like you're talking about waterhouse fridric syndrome. You're like, wait, what? Divine, how did you get there? Yeah, this person has waterhouse fridric syndrome, right? Again, let's put the facts of the case together. Number one, again, see, the USM is all about integration, right? Integration, integration, integration, right? So the theory is if you think about it, right? Waterhouse fridric syndrome. First things first, this person came in with severe headache and high fever, right? And then this child also, we don't know about his vaccine status. Chances are this child has meningitis. From some meningitis causing bulk, right? Like strep pneumo on isoerm meningitis, right? And then now we see this child having like PTKI, a chemosis on the skin, right? Kind of like a DIC picture. And then you also notice that this child is hypoglycemic, right? Very hypotensive, right? In fact, sometimes they can slap in some detail that, oh, they're trying to give this child fluids, they're trying to give this child pressures, and it's not working, right?

That tells you that, oh, this child is dealing with some kind of adrenaline and sufficiency, right? Because again, remember cortisol exerts a permissive effect on the sympathetic nervous system, right? So whenever you're in a low cortisol state, your vasculotune is trash, literally. Your vasculotune is trash, right? So the thing that's going to happen in those circumstances is that those people when you give them fluids, when you give them pressures, they won't really respond, they won't really respond, right? They won't really respond very well, right? Because they're in a cortisol deficient state, right? These people need like this person, I'm going to talk about the management here shortly. But this person is not doing very well, right? This person is not doing very well. Because again, remember sometimes when you have meningitis, you can, that's sepsis that you have can spread to the adrenals, and you can have adrenal hemorrhage as a result of that. And when you have that adrenal hemorrhage, you're in big, big, big, big trouble. You're pretty much going to have a primary adrenal insufficiency, right? And that's also part of why the person has hypoglycemia. Again, many people do not realize this, but one classic telltale sign of hypodontal insufficiency on the US Emily exams is hypoglycemia. Because remember cortisol is a diabetes genic hormone. One of the rules of cortisol is to raise your blood glucose levels, right? But if your cortisol is working, right?

You're not going to be able to raise your blood glucose levels very effectively. That's going to put you in quite a bit of trouble. That's going to put you in quite a bit of trouble. And you can have hypoglycemia. Another weird organ disease on the US Emily is just as a quick sidebar that can cause hypoglycemia. It's when a person has liver disease, right? When you have liver disease, because gluconeogenesis is not going to work. Okay? So we see why this person is hypotensive. We see why this person has hypoglycemia, right? So the thing is, what's this whole deal with causing tropium? Why will the person's cortisol stay the same? Well, the thing is causing tropine is an ACTH analog, right? Cosine tropine is literally an ACTH analog. So the thing is, if you give a person causing tropine, right? You need an intact adrenal cortex for you to make cortisol. And no more person like me, if I give you a cause in tropine, your cortisol is going to rise in response if your adrenal cortex is intact. But if your adrenal cortex is not intact, and I give you a cause in tropine, an ACTH analog, guess what? Your cortisol is not going to rise, right? The thing is, the US Emily is, they know that everybody that has the job description, US Emily exam, US Emily exam ticker. You've probably memorized, you know, although waterhouse Friedrichsen is something that many people don't know about. But your chances are if you're a decent student, you probably memorized it, right?

So it's like, hey, how can I test this same knowledge? And just see if this person really has an understanding of pathophysiology. Instead of having memorized like a bunch of just random stuff from like some Ankydeck. Just, hey, test the cause in tropine stimulation test with waterhouse Friedrichsen syndrome. So just going to keep that at the back of your mind as you're preparing for your exams, right? So this person, because they don't have an intact adrenal cortex, this person is going to have a lot of issues responding to cause in tropine. So the cortisol will fail to rise, right? You know, hopefully many of you can kind of make this connection that way. This sounds a lot like the way we diagnose adicence disease, right? Primary adrenal insufficiency, right? You do the cause in tropine stimulation test. Because remember, this is like a principle in endocrinology. Whenever you're having hypocycrician of something, the way you diagnose, the way you confirm that diagnosis is to do a stimulation test, right? So like, for example, if a person has, if a person has adicence disease, right? The adrenochrotect is not working. You do a cause in tropine stimulation test, right? So in this case, right, we give cause in tropine. And you notice that cortisol fails to rise. That's pretty diagnostic of adicence disease. But again, the USML Es, one thing they like to do on the exam is to bring in novel scenarios like what else? Critics in syndrome.

And it's a concept they know you know, right? But they won't test it in the variation that you're familiar with. They will test it in a different variation. Again, the USMLE is when they're doing all these pool changes from year to year. These are classic ways that they change the question pools. Is the same concept as previous years that they're still testing? They just tested in a somewhat different variation. That's just the truth, right? So just something you want to keep at the back of your mind as you're preparing for your exams. Okay, please. That is something you want to do. What? Keep at the back of your mind as you prepare for your exams. All right? You want to keep at the back of your mind as you prepare for your exams. So how are you going to manage this person? Obviously, this person is probably on fluids, probably on pressors, probably on antibiotics. But this person is going to need a stress dose of steroids. This person in waterhouse, Friedrichs, in syndrome, to counteract that primary adrenochrotect in efficiency that they have. All right. So please keep that at the back of your mind as you're studying for your exams. All right. Now, what if they give you a question about a 75-year-old female? And you're told that over the last six months, she has been declining, she has been losing her way, she has been losing, she has been having trouble getting back home after she goes back to a grocery store or whatever. Right?

And then they ask you that she's now beginning to have trouble remembering her name and her children's birthdays and things like that. And then they ask which of the following brain regions is most likely responsible for the memory deficits found in this patient? And then our friends at the MBM is they give you an answer that talks about like the hippocampus, they give you an answer that talks about the basal nucleus of main art, they give you an answer that talks about the arachnoid granulations, they give you an answer that talks about the ventricles, they give you an answer that talks about the codic nucleus. Which answer should you pick here? I know some people are like, divine. You said two things that are correct here. No, I didn't say two things that are correct. I only said one thing that is correct. Remember, your assembly exams don't have two correct answers. It's going to have one answer. The right answer is going to be the hippocampus. It's going to be the hippocampus. So this is where you need to be abundantly careful. What in the world is going on in this question? First thing is, first is, first thing has Alzheimer's. Right? Dispracing Alzheimer's. And this really reflects why you should read your questions very, very carefully on your exams. Right? Because many people I can almost promise you picked the answer that talks about the basal nucleus of main art. And ignore the hippocampus answer.

See, this function in the basal nucleus of main art is associated with Alzheimer's dementia. It is. It is. Right? Because remember, that's a brain region that produces acetylcholine. Right? This is part of why people that have Alzheimer's, they have low levels of acetylcholine in their brain. And this is why when a person has Alzheimer's, we treat them with acetylcholine estuaries inhibitors that are centrally active, like d'unepe zeal, or galantamine, or revastigment. But the memory problems that you have in Alzheimer's is because your hippocampus is damaged. Remember, your hippocampus is your memory center. Is your memory center. Is your memory center. Right? So please be careful about this. People that have Alzheimer's, they have dysfunction as well of the hippocampus. Now you know some of you are like devoid of never heard this before. Well, sorry. Right? Now you know. Now you know. Okay? Now you know. But this is something you absolutely, positively need to know for your exams. It's something you need to do what absolutely, positively need to know for your exams. Okay? So please keep this at the back of your mind as you're studying for your test, right? Your hippocampus is your memory center. Right? So if you notice, this question that I just presented was focused on the memory memory memory problems. That's why you see me saying, oh, big answer that talks about hippocampus. Right? Now, so I would pick that over the Bizonucleus of Maynard issues. Right?

Because remember, and again, see, see, see, right? If for example, in really know of these answers, I didn't talk about the hippocampus. They should pick the answer that talks about the Bizonucleus of Maynard, because that's the one that has the closest relationship to Alzheimer's as an answer. Right? So what's the thing that's going on here? Right? Well, how does the Bizon, how does the hippocampus get damaged in Alzheimer's? Well, one of the things that is believed to happen is that you have neuronal damage. Well, what causes that neuronal damage? The thing that causes that neuronal damage is something known as glutamate excido toxicity. Right? Glutamate excido toxicity. Glutamate excido toxicity. Glutamate excido toxicity. Glutamate excido toxicity. Right? Glutamate excido toxicity. Right? And that usually happens because you have glutamate, just slamming, slamming, slamming, slamming NMG receptors. And as it slams those NMG receptors, it overexcites the neuron, and that leads to neuronal damage. Right? We call that phenomenon glutamate excido toxicity. Okay? Glutamate excido toxicity. I just like to think of it as like, let's say for example, you take too much cocaine. I mean, you should never take cocaine, right? But let's say you take cocaine and then you just take too much of it and then get too excited, your blood pressure rises, you get an M.I. and die. Right? You got like cocaine, cardio toxicity, like cocaine excido toxicity.

Well, think of glutamate excido toxicity in this case. Right? Too much glutamate, right? Your brain uses glutamate. Glutamate is an excitatory neurotransmitter. But when there's too much of it, just slamming, slamming, slamming the neuron, that can cause the person to have problems. So in fact, this is why a second line treatment for Alzheimer's is to give NMG receptor antagonists, like Mee Mantin, right? NMG receptor antagonists like, like Mee Mantin. Mee Mantin is an NMG receptor antagonist that you can use after, you know, these are stereotypical anesthries, inhibitors like Dunepe, Zio Galantamine and Rheverstigmin, and no longer working. And then just to real quick examine the other answers that I kind of propounded with this vignette, right? The, the codec nucleus remember that, that atrophies, right? That becomes smaller in a person that has hauntings disease, right? And then the arachnoid granulations, that's where CsF is reabsorbed, right? So if you have a CsF reabsorption defect at the level of the arachnoid granulations, you can have a buildup of CsF. For example, like an impression that has normal pressure hydrocephalus or an impression that has a diopathyk intracranial hypertension, right? That's something you want to keep at the back of your mind for your exams, please. That's something you absolutely want to keep at the back of your mind for your exams. All right. Now what if they give you a question about a two-month-old child?

And you're told that this child is brought to the physician by his parents, the pediatrician by his parents, because, you know, he has been having just recurring fevers, right? And the notice that this child is profoundly short of breath. And they tell you that, you know, that, you know, the, you know, when the child's vitals are measured, that the child is profoundly hypotensive, right? The child has a very high fever. And they tell you that this child, you know, has like a, has like a milky, that the child is more breastfeeding, but that this child has like a milky, you know, like a white milky consistency substance on his tongue, right? If you see, you know, you're told that this child that before the child left the hospital, that the child had to receive a course of antibiotic therapy. For, for a long infection. If you see something like this, and then they ask you like which of the following is the most likely theology of the patients are symptoms? Well, and then let's say they put an answer that talks about BCL maturation defect, and then they put an answer that talks about accelerated lymphocyte hipoptosis, and then they put an answer choice that talks about field-fiming development, and then they put an answer that talks about failed phagolisosom fusion. If you see that, I really hope you're picking the answer that talks about accelerated. lymphocyte hipoptosis, right? So what does this patient have? This patient has scared, right?

The person has severe combined immunodeficiency, scared, scared, scared, scared, right? Remember, severe combined immunodeficiency, right? A classic course you're going to see on your exams is when you have an adenosine deaminase deficiency, right? When you have an adenosine deaminase deficiency, you're going to have a buildup of a lot of deoxy substances that will lead to premature lymphocyte death. You have very rapid lymphocyte hipoptosis, right? That can cause problems, right? If you ingot lymphocyte, you're going to struggle with a lot of bacterial infections, viral infections, fungal infections, right? Like for example, this person on their mouth has throsh, right? This person has throsh, has a candidil infection, right? And again, we know that it's scared because their problems are just popping up so early in life, right? This child is like a two-month-old kid, and they're already having all these problems, right? In fact, the child probably had some kind of pneumocystis-jurveti infection. That's why they got antibiotics before they left the hospital after birth, right? So something you want to keep at the back of your mind for, for example. I remember another cause of skid is the interlooking two receptor defects, the gamma chain, right? That's actually another cause of skid. That's a cause of excellent recessive skid, right? Excellent recessive skid, interlooking two receptor gamma chain, right? Doesn't work, right?

That interlooking two receptors found on pretty much all lymphocytes, right? So if that lymph... If that receptor is not working, you're not going to be able to stimulate your lymphocytes, your lymphocytes are going to be in trouble, right? That's going to cause you to get in trouble. Again, that's excellent recessive, right? This adenosine-diamonins business I talked about, that's autosomor recessive skid, autosomor recessive skid, okay? Autosomor recessive skid, right? Look at that. The other answer is I talked about, right? Field-fogult lysosom fusion. That's going to be something I'm going to see in Chidiaki Gashi syndrome, right? Or, you know, field-fiming development, you're going to see this in a person that, for example, has the George syndrome. Remember in the George syndrome, you'll throw down your fourth-fiming geopouches field to form, so you don't have a thymus and you do not have paraphiroid clat. So you don't have a thymus and you don't have paraphiroid clat. And then issues with B cell maturation, that's Burton's right? Burton's a chemical bulimemia, right? But again, that's a B cell problem. Most of these B cell issues, you're going to be fine for a couple weeks, couple months of life, right? It's when those maternal antibodies that you go through the placenta, those IgGs, they start going down. Then you're going to start getting in trouble. You're going to start getting in trouble. All right, so rapid review series. Let's go ahead and stop here.

Again, if you love the way I teach, if you love the way I make integrations, you're going to love my classes. There's many people that have taken my classes recent times, got in 260's, right? Got in 270's on the exams. And these classes are all over Zoom. They're very well put together. And again, these classes are heavily updated on the regular. I think of it as software that has to be updated regularly, just to make sure that I'm presenting the most relevant information for you exams, okay? Presenting the most relevant information for you exams, right? So if you're interested, I have a test-taking strategy class for step one to step three, a four-hour bio-statistics class for step one to step three, a five-hour social sciences quality improvement, hospital medicine, and healthcare systems class. That's five hours long also for step one to step three. And then I have a three-hour last-minute review for step two and step three, and a 20-hour step two step three review. Many people have taken these classes from them to be extremely helpful. I have them later in the month of August. So if you're interested, there's still sports remaining. Shipping an email through the website or you send me an email at Divine Intervention Podcasts, Divine Intervention Podcasts with an S-A-Gmail.com, right? And the thing is these classes, it's not some other person that's teaching them. It's me that is teaching is not AI teaching is me that's teaching it, right?

So you're going to get the benefit of Divine. I also going to get the opportunity to ask Divine questions, right? And to interact with Divine, and get your questions answered. And then also offer one or one tutoring for all the USMELY exams. I know a lot of people are trying to get their tests in now. I offer one or one tutoring for all the USMELY exams, for all the complex exams, for 30-year medical school shelf exams, for pretty clinical exams, even for CBSC exams, I offer tutoring for all those things. And then also help with ER As applications, more interviews, personal statements, rec letters, right? I edit those things again, I've done this with numerous people over the years. Many of those people are even attending right now, or residents in many programs all over the country. And then I also have this podcast on Apple Google on Spotify. So check those out. I have a You Tube channel, Divine Intervention, USMELY Podcasts and videos. That's where I post the videos that I make. And then I also have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Many of you know I'm a Christ follower, I'm a Christian. So every week I post like one or two podcasts from a biblical perspective, I address a life lesson. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. So thank you for listening to me today. Again, I really hope you find this podcast to be helpful.

Listen to it, share with your friends, share with your colleagues. And I will see you God willing in episode 619. Have a wonderful rest of your day. God bless you and bye for now. Thank you.

Ipsilateral facial pain/temperature loss combined with contralateral body sensory loss (due to crossing tracts).

Cranial Nerve VII (Facial Nerve), as it runs in the lateral pons.

A diastolic murmur, due to blood leaking back into the left ventricle during diastole.

The Circle of Willis (especially the anterior communicating artery).

Failure of cortisol levels to rise.

Rapid lymphocyte apoptosis.

The anterior communicating artery (A-com).

Body sensation is lost contralaterally because the spinothalamic tracts cross in the anterior white commissure; facial sensation is lost ipsilaterally because the trigeminal tract fibers do not typically cross.

Type III and Type V collagen.

Cortisol deficiency (Cortisol is diabetogenic).

The Hippocampus.

Adenosine deaminase (ADA) deficiency.

The anterior communicating artery (A-com).

Body sensation is lost contralaterally because the spinothalamic tracts cross in the anterior white commissure; facial sensation is lost ipsilaterally because the trigeminal tract fibers do not typically cross.

Type III and Type V collagen.

Cortisol deficiency (Cortisol is diabetogenic).

The Hippocampus.

Adenosine deaminase (ADA) deficiency.