DIP Ep 582: USMLE Step 2/3 Rapid Review Series 120

about a patient and you're told that um you know this patient they give you like an image and they tell you that this patient you know for the last uh you know is a is a newborn and This newborn, you know, had a lot of seizures, you know, within the first few hours of birth. And they give you a chest x-ray. And you notice on the chest x-ray that

It's just all black, and you notice that you they tell you that oh you see uh reduced uh uh supramediastinal or radial density. What should you be thinking about? Well I would hope you're saying Ooh Divine, this is a De George syndrome, right? So remember in De George syndrome, your third and your fourth uh pharyngeal pouches do not form. So if your third and your fourth pharyngeal pouches do not form, You do not form a parathyroid gland and you do not form a thymus.

Make sure you can recognize a thymus on a newborn chest x-ray. You know, many of you know it as the sales sign. It's not enough to just know the sales sign. Make sure you can recognize it. And one thing I've always encouraged people to do is when you see a newborn chest x-ray, just always look at the very tippy top.

Because I don't know for whatever reason the tippy top of chest x-rays is like one region that many people just ignore. But many times our friends at the MBMEs have some very interesting things that they love to hide there. So just be careful. Get in the habit because many of us when we it's almost like a human bias. When we see a chest x-ray, the first thing we want to look at is, oh, look at the heart.

Try to look for the yodor and all those things. There are many things you should be looking for when you're looking at a chest x-ray, right? But I encourage you because it's an often missed region, look at the top, look at the apex of the lung. Because there's a lot of things that could be there. You know, they could hide no thymus being there. Right. This case is about the George syndrome. But there are many things that can cause a person to have no thymus.

Right. So for example, if a person has severe combined immunodeficiency, They will also have an absence cell sign, right? So it's just something you want to keep at the back of your mind on exams, right? So this person obviously that has the George is gonna have recurrent infections because there's they they have basically no T cell. Right? Remember your T cells really help with cell mediated immunity.

So if you don't have that, then that's a that's a problem, right? You're gonna struggle with uh a lot of cell mediated immunity problems. A lot of issues with viral infections, a lot of issues with fungal infections. You know, many times you'll see these kids that have pneumostis, girl Vetsi, pneumonia. Uh sometimes you'll notice that they have um you know oral candidiasis, thrush and all these problems.

So your next question may be divine, why is it that this child had several seizures after birth? Well this child had all those seizures because of hypocalcemia, right? Because if you think about it, people that have the George syndrome, they have primary hypoparathyroid. And if you have primary hypoparathyroidism, you will not make PTH. So if you don't make PTH, you will not have the ability to raise your serum calcium level. And hypocalcemia can absolutely cause seizure.

You know, and they may not just give you that, they may even give you like an EKG from the child, and you may notice that the QT interval is prolonged. When you see all those things, think of the hypocalcemia, right? Think of the hypocalcemia. Right. Because the child will you know, probably have other problems like they may have like technique and all those things, you know. So just something you want to keep at the back of your mind for for exams, right? They may have like muscle weakness.

Because remember you need calcium for muscle contraction, right? They may have cardiac arrhythmias because your heart literally needs calcium to contract. So it's just something you want to keep at the back of your mind as you're studying for your exam. And one thing I also wanna say is they may give you a picture of a child that has a D George syndrome, right? They may because you know like all these sometimes they either give you a picture or video, these video based questions.

And you may notice that, oh wow, okay, I see clef lip uh clef palette, right? So again, make sure you can recognize cleflip and clef palette. You know, sometimes they will give you a picture. The USMLEs, they never cease to amaze me. They can give you a picture and then ask you, uh, which of the following additional findings will be found? Uh so which of the following will be found on further diagnostic testing of this patient?

And I really hope that you're thinking of the answer or you're picking the answer that talks about congenital cardiac disease. This is actually very high yield to know. The thing is the USMLEs, they are not stupid, right? They recognize that many people are unkey warriors these days. So what do they do?

They will test something and then they will ask you about something related to it that you're like, wait, I'm not really thinking about this thing. Because think about it. I'm showing many onky decks. You're like, oh, DJorge syndrome, third and fourth pharyngeal parties fail to form. No thymus, no parathyric gland. Great, awesome.

But they can give you a follow-up question, and many times they can make these things like two part questions, right? Those questions where you gotta click on something before you see the next one. Right? And they can say oh which of the following should be uh which w what else should the patient be examined for? You should examine this person for congenital cardiac disease.

Or they may even say which of the following additional forms of diagnostic testing should be performed. You want to pick the answer that says echocardiography.

Because remember people that have De George syndrome, De George Syndrome has a very, very, very solid association with congenital heart defects, right? They can have things like tetralogy of the low They may have things like uh tronchos atteriosus, right? Remember in tronchos arteriosus is almost like you have like this common drainage from the heart.

Right. Tetralogy of the law. Remember they have four findings, right? They have like the uh pulmonic stenosis. That pulmonic stenosis basically and you may wonder what what causes it. Well the thing that causes it is basically Your membranous interventricular septum, it doesn't grow down proportionally to meet the muscular interventricular septum. So it's almost like

It's just one of these things I have to kinda diagram out. But it's something you m you can also kind of imagine. But basically I just like to think of it this way. The pathophase of Dejor syndrome is uh of uh tetralogy of a low is as follows. There's a part of your interventricular septum that is supposed to come down and is supposed to give, you know

Appropriate amounts of space to the auditor and appropriate amounts of space to the pulmonary arteries, but it does not, right? It ends up giving too much space to the odor. And too little space to the pulmonary arteries, right? To your pulmonic vein uh your your you know your your pulmonic system. So because you're getting too little space for your pulmonic system, you're gonna get pulmonic stenosis.

And then after you get pulmonic stenosis, well, think about it. It's gonna be hard for your right ventricle to pump out blood. So you're gonna get right ventricle hypertrophy. And also just because of the way that division happened.

You have a VSD, you will have a clear vious communication between your right and your left ventricles, right? And then you also have an overriding aorta. It's almost like your auditor is like picking up from both your right and left ventricles, right? Those are the four findings of inter trilogy. or for law. These things are all common. So just something I wanna keep in mind. So please don't don't neglect these things. Don't neglect these

Where they will give you a pathology and then ask what else should you screen the person for or whatever, right? It's just like for example, if a person, you know, presents with like muscle weakness that is worse by the end of the day. You know that oh you're dealing with myastenia gravis. And then they ask you, uh, which of the following is the which of the following additional diagnostic tests should be done?

Then you want to get like a chest x-ray or some kind of chest CT, right? Because we know that my stinal gravis is associated with thymomas, right? Myastinial gravity is associated with thymomas. In fact, some people when you reset those thymic masses, then you notice that their myastenia symptoms improve tremendously.

So please be mindful of these things where you're asked about one thing and you're supposed to check for something else. Right? Or sometimes instead of using the word thymoma, they may actually say uh which of the following is strongly associated with the patient's on the line condition. Right, they may put thymoma as an answer or they may put anterior mediastinal mass. Remember thymoma is an anterior mediastinal mass.

Right. So again, just to summarize, the George syndrome, don't forget that they can have these congenital cardiac problems like tronchos arteriosis, tetrology of low. Don't forget that they can have cleft lip and cleft palate. Don't forget that they can have hypocalcemic seizures because they basically is a congenital cause of primary hypoparathyroidism.

Like literally, don't be surprised if our friends at the MBMEs, they give you a Dejorge syndrome question, and then the one of the the the the right answer ends up being something like congenital primary hypoparathyroidis. The thing is, as I'm saying it now, it's something that seems pretty obvious to people that are listening to this podcast. But in the heat of an exam, congenital primary hypoparathyroidism you're like.

What? Divine, that doesn't make any sense. But no, it does make sense because that's literally what they have. Right? That's literally what they have. Again, the see, and this is something I share a lot in my test taking. Tell people this that C, be comfortable with hearing the MBMEs talk about things in other terms that you're not used to. Get comfortable with that. Because that's the reality of your exam.

Right? Your exam is not gonna be a buzzword heavy, buzzword f buzz phrase field exam. No. That's not how your exam is gonna be. They're gonna take what you know and just put it in other terms. And honestly, that's a good way to see if people really understand what's going on.

So please just be careful about that. Just be careful about that. Right. And then we've talked about myastenia gravis and how it may be associated with thymomas, right? It may be associated with uh thymomas. All right. And we've talked about how thymomas, anterior mediastinal mass.

Now, what if they give you a question about a person that is diagnosed with polymyositis or dermatomyositis, especially dermatomyositis, right? And then you are asked, oh, which of the following additional screenings need to be done? Well the thing is that person is gonna need some kind of age appropriate cancer screening, some kind of age appropriate cancer screening.

Right? If a person gets e b because remember polymyositis and dermatomyocitis have very strong associations with people having like malignancies, like lung cancer, or breast cancer, or colorectal cancer, or things of that nature. So based on the age of that patient, that should guide you as to, okay, these are other things we need to screen you for.

Because many people think that just by memorizing the screening guidelines, they're home-free on the exam. No. No. That's not all that's gonna save you on your test. You need to know those screening guidelines, but you need to know them in what? In what in context.

Context really really matters on the USMLEs. I'm gonna say that again. Context really really matters on the USMLEs. So it's just something I wanna keep at the back of your mind as you're prepping for your exams, right? They can literally make a screening guideline question out of Dermatomyositis, for example, right? Or what if they give you a question about a patient and they tell you that oh for the past four weeks.

This patient has been having like very significant pain in his hands, very significant pain in his knees. Right. And you know, they tell you that oh, they get an x-ray of one of these joints, and you see like a lot of reactive bone formation. And then you're told that this person has a two-pack per day smoking history for the past thirty-five years. And then they ask which of the following is the most appropriate next best step in diagnosis or screening or whatever.

You should go ahead and get a chest CT for this person. Why? This person has lung cancer. What? Divine, how did you get there? Well, I got there because this person has a perineoplastic syndrome. The person has hypertrophic osteoath uh you know, pulmonary osteoathropathy, right? You see this, you know, basically athropathy that develops over a few weeks or whatever.

It's a common perineoplastic syndrome we see associated with lung cancer. So for those people, they're going to need some kind of pulmonary imaging in the form of some kind of chest CT so you can see exactly what is going on. Right? You can see exactly what is going on. All right.

Now, what if they give you a question about a patient and you're told that this patient uh you know, was recently started on, you know, the this this patient has a long history of diabetes. And you're told that this patient, you know, has been on metformin, but his uh A1C did not decrease. And then two weeks ago he was started on a new draw. And that for the past two days the patient has been having trouble sleeping.

And you're told that when you listen to the person's chest, you can hear uh you know bibasilar crackles in the person's lungs. What should you be thinking about under those circumstances? What kind of drug was this person placing? I'd really hope you're saying divine, it sounds like this person was placed on a TZ.

It sounds like this person was placed on a thiazolidine diion. So what's a thiazolidine dien? Well a thousand thiazolidine dion, thiazolidine dion, let me spell that. So t-h i. Fire Zolidin Z O L. Zolidine, D-I-N-E, dion, D-I-O-N-E, thyazolidine dion. Right? These drugs all end in glidazone, rosiglidazone, pyogliazone, and things like that. The diabetes drugs, and how do they work? They work because they are agonists at the P PAR gamma receptor. They are P PAR gamma receptor agonists.

Now, they work like P par gamma receptor agonists, but and so they help you utilize sugar better, right? That's why they're diabetes drugs. But the thing is these PPAR gamma receptors, we also find them in the kidney. And when they're stimulated in the kidneys because you're taking a TCD, it actually causes increased fluid and water reabsorption from the kidneys. And if you reabsorb more water from the kidneys, that's going to not be very good if you have heart failure.

Right? If you have heart failure. If you have heart failure. Now you may say, Divine, you didn't give us that this guy had heart failure in the question. Yes, I did not give that to you. But there's something our friends at the MBMEs love to do where sometimes They won't give you a person having a history of something, but they do something else that then triggers the discovery of that issue that they have.

Right. This is a very perfect example of that kind of question. I'm telling you this podcast, I'm I'm trying to see if I can hit on some test taking principle. That can be really helpful for your exam, right? Like literally, I did not give you a history of heart failure, but I'm trying to get you to deduce that this person may have some kind of cardiac dysfunction. Why? Because

The person took a T Z D and they are now getting this unwelcome side effect of pulmonary edema, right? So the thing is it's almost like this person had this predisposition. But you did not find out until, hmm, we tried something, you know, tried a new drug and then boom, this person's problem kind of showed itself. Right? So it's just a kind of mindset that the MBMEs often have in creating questions.

They will give you something that you throw on top of another thing and then now it then unmasks another problem that the patient has.

In fact, let's talk about a few of these unmasking scenarios you may see on your exam, right? So giving a basic one like you get a TZD. For diabetes, and then you notice all of a sudden that oh this person is having pulmonary crackles, and that tells you that oh gee, this person has heart failure, right? So this person probably needs some kind of echocardiography or something to screen them for cardiac dysfunction.

Right. But what if they give you a question about a person that is started on an ACE inhibitor or an ARP and then their creatinine rises like Spotnik? What should you think about under those circumstances? Well that person has renolateristinosis.

Right. Again, their issue was unmasked by you taking by you taking an ACE inhibitor and ARB. ACE inhibitor and ARB. So how does that happen? Well the thing is again ACE inhibitors are Because remember angiotensin two, its job is to constrict the Ephrine arterium.

But if you take an ACE inhibitor, right, you're inhibiting the conversion of angiotensin 1 to angiotensin 2, you're going to make less angiotensin 2. If you make less angiotensin 2, you will have less constriction of the Ephrine arterial. You're going to have dilation.

Alternatively, if you take an ARB, an angiotensin 2 receptor blocker, you're going to be blunting the effects of angiotensin 2 of the E-frain arterial. If that happens, ultimately from taking any of these drugs, you're basically going to dilate the E-frain arterial. If you dilete the Ephrine arterial, then that's going to reduce the hydrostatic pressure within your glomerular capillaries. If that happens, that's going to raise your creature.

The thing is for most people that don't have other comorbidities, it's not a big deal. It's really not a big deal. But if you already have another comorbidity or another risk factor that kills your GFR and raises your creatinine, then giving that ACE inhibitor or ARP can tip you over the edge and get you in trouble. Right? So like for example, uh If you have renal artery stenosis, right, you're not properly profusing your affrine arterial.

So because you're not properly professing your alpha material, you're not bringing adequate amounts of blood to your glomerular capillary. If you're not bringing adequate amounts of blood there, then the hydrostatic pressure within your glomerulapillaries are going down. And if it goes down, that's gonna kill your GFR, that's gonna raise your creature. So you already have that race factor, and then you then supplement that with taking an ACE inhibitor and ARB. That's gonna get you in trouble.

Or they can give you an analogous question about a person that, you know, let's say has a history of osteoarthritis. And then they also diagnose with hypertension. You know, let's say they also authorized the control with ibuprofen or endomethicine or naproxin or whatever. And then you throw an EC inhibitor and orb on top of that. You gotta be careful.

Because think about it, what will ibuprofen or whatever do? Well, or it can even be a person that has a history of a myocardial infarction that's on dual antipletly therapy, it's probably on aspirin. Well what do these aspirins and NSAIDs and whatnot do? Well they inhibit cycloxygeny. Remember, aspirin is an irreversible COX1 and II inhibitor, but your NSAIDs are reversible COX1 and 2 inhibitors. Ultimately, these things are going to reduce the production of prostaglandin.

If you make less prostaglandins, prostaglandines are vasodilators. You have less vasodilation and you have more vasoconstriction. That vasoconstriction will cause you problems because if you constrict the afferent arterial, then there's going to be less perfusion of the person's glomerular capillary. That's going to reduce the hydrostatic pressure within that person's glomerular capillaries. And if that happens, that's gonna lower GFR and raise creature.

If you then add another problem on top of that, like taking an ACE inhibitor or an ARB, that may tip a person over the edge. So I'm not coming out here to say that, ooh, never take ACE inhibitors or ARBs if you're on an NSAID or aspirin. No, that's not the point of this. But if a person has like or like already impaired renal function and they're already on an NC or aspirin and then you throw an a uh you throw an EC ab or an ARB, that may tip those people over the over the air.

All right, so let's go ahead and continue here. Now, we've talked about cleft lip and you know cleft lip, and I said that hey, it's associated with D. George St. ¿Es eso el único...? disorder that is associated with cleft lip? No. There are actually other disorders that are associated with cleft lip and one big one that is very high yield to know for your exam is trisomy 18, right? What is trisomy 18? That's Edward syndrome.

Remember, there are certain very classic features that we find in Edward syndrome that are very, very high yield to know for your exams, right? Like, for example, what can they have? they can have micrognathia, right? People that have DJorge syndrome, I mean sorry, Edwards syndrome, they tend to have very small jaws. They tend to have very small jaws, right? And the thing is these people tend to have abnormal developments of their wrists, of their digits.

So they may have issues like clenched hands, right? You may notice that they have like clenched hands, they may have like overlapping digits, right? Uh sometimes on your exam, they may even use the term that they have a rounded profile to the bottom of the foot, a rounded profile.

What do I mean by this rounded profile to the bottom of the foot? This rounded profile is rocker bottom feet. But again, our friends at the MBMEs, they know that everybody that has, or at least many people that have the job description, medical student have memorized. Rocker bottom feet. Rocker bottom feet. Rocker bottom feet. Right? So why use the term rocker bottom feet when you can just describe it and say, hey, this person has a rounded profile to the bottom of the foot.

And then as you're reading the exam question, you're sweating, you're like, rounded profile to the bottom of the foot, what is that? Well, that's literally a description of a rocker bottom foot, right? These are things we find in people that have Edwards syndrome, right? So round their profile to the bottom of the foot. That's rocker bottom feet. Right. And these people also tend to have a prominent calcaneus. The calcaneus is one of the bones of your of the foot.

Right, all those things can be found in trisomy 18. Most of these kids they don't really make it very long. You know, many of them die in utero. If they're born, they'll probably die within the first few days, max within the first year of life. They're they're gone, unfortunately. Right now.

What if they give you a question about a child? And they show you an a picture. The thing is for some of these congenital diseases, they know that many people have memorized the finding. But they don't actually know what those findings mean, right? Like for example, many people have memorized. Oh, people that have Down syndrome, they have a transverse palmer crease. Many people have memorized that.

But do you know that there's a lot of people that literally have no idea what that transverse palmer crease looks like? I will encourage you, pause this podcast right now. Well, if you're driving, don't do that. But pause this podcast right now and literally just look up what a transverse Palmer Chris looks like. Because instead of giving you those words, they may substitute that with pictures. See, the MBMEs define creative ways to put things in other terms.

Right? Instead of using the words transverse palmer crease, a very easy creative way to put it in another term is to just substitute that with a picture. Right? They will show you a child and you notice that there's just this. Straight horizontal line running from one end to the other across the apartment. Look at your palm. I can almost promise you that you don't see a straight horizontal line.

Running from one end to the next is kind of interrupted in most people, right? But when you see that transverse palmer crease, you really want to think about a child having down syndrome. Right. And you know, many times people that also have Down syndrome, they may have like this uh flexion creek.

on the fifth digit. This flexion creates on the fifth digit of the of the hand, right? So like they're they're pinky. Right. So you should again try to look that up. Try to look that up. Make sure it's something you can recognize for your test. All right.

Now, what if they give you a picture of a child? They tell you that, oh, that this is a newborn. And this newborn, you notice that the extremities of this newborn are fused. They're fused. Right, they have like fused extremities, you know, they they almost look like mermaids. What should you be thinking about on your exam?

I really hope you're saying, ooh, divine, it sounds like this child has something known as sirenomya. Cyromalia, right? Cyrinomyal is when you basically have fusion of your lower extremity. Right. And sometimes on the exam they can ask, oh, what's the on the line pathophysiology behind the observed physical exam findings? Well the pathophys there is that basically you you have a failure to establish vascular supply. You don't have good blood flow.

To your lower extremities in uterum. So because you don't have good blood flow, it does not develop properly, right? So those extremities stay fused, right? So again, they may talk about like a vascular anomaly in utero as the pathophase behind sirenomele. What's another high yield congenital issue that arises from vascular anomalies in utero? I would hope you're saying, ooh, divine, that's jeunal atresia. Remember, duodenal atresia is a failure of recanalization.

But jugenal atresia is from a vascular issuing utero. Right? It's from a vascular issuing utero. So cyrenomelea, where you have fusion of the lower extremities, it arises because you don't establish good vascular supply from the Lower yoder to your lower extremities, right? So that causes you problems, right? And what is cyrenomelea heavily associated with on the USMLEs? Well, I hope you're saying divine is very heavily associated with maternal diabetes, right? With maternal diabetes.

The thing is, maternal diabetes can cause so many problems for a fetus, right? It can cause this fusion of the lower extremities, it can cause cyrinomalia. But what else can it cause? Well, it can cause something called caudal regression syndrome. Right. Sometimes they call this sacral agenesis, where basically your sacrum fails to develop. Your sacrum fails to develop. Right? It can cause a myriad of problems for for a fetus. They want to make sure that you can recognize for your exam.

Right? And remember, maternal diabetes is also associated with a child having a VSD. Is also associated with a child having a VSD. What else can maternal diabetes cause? It can also cause seizures in the newborn. Hey, we've talked about seizures in the newborn already today with DeGeorge syndrome because they have congenital primary hypoparathyroidism. But you can also see hypoglycemic seizures in an infant of a diabetic mother.

What's the pathophysiology? It's pretty straightforward. Think about it. Your fetus in the womb, you're exposed to high sugar mom. High sugar mom. High sugar mom. Well, all those high sugars are gonna cross the placenta. I'm coming to the fetus. So the fetus is like, hey, I don't like having these high levels of glucose around. So the fetus beta cells are gonna be like,

Okay, okay, let's undergo some degree of hyperplasia, right? So that you undergo that hyperplasia, right? You undergo better eyelid cell hyperplasia. So you can make enough insulin to deal with that problem. You make all that insulin, it helps you deal with the problem, and that's amazing, right? It helps the fetus control their blood glucoses, their blood glucose. But after the fetus is born, this fetus has been disconnected from the source of high glucose, aka mom.

But hyperplasia is a genetic process, it's not something that just reverses quickly. So this child is now in a state where the source of high glucose mom is out of the picture because the child has been born. But the source of the high insulin, the hyperplasia d if there's an there's that that's wrong English, but Just work with me here. You have that those those hyperplastic. Okay, let's be more accurate, right? Those hyperplastic B-I let's sell.

It's not immediately that the hyperplasia will just resolve out of the blue. No, it's not just gonna resolve out of the blue like that. It's gonna take some time. So that child is still gonna be producing very steep amounts of insulin. And those steep amounts of insulin are gonna drive down the child's blood glucose. And if you have low blood glucose, that can cause hypoglycemia and that can cause what?

Seizures that can cause hypoglycemia and that can cause seizures. And let me ask you this: besides the hypoglycemia, what other electrolyte abnormality will you expect, you know, within the first few minutes, first few hours of birth in an infant of a diabetic mom? I'd hope you're saying divine, this child may have hypochilinea.

Again, that may be a question you see on your exams. Why? Because remember insulin increases the activity of the sodium potassium ATP spump. That's literally one of the reasons why you can do insulin plus glucose to manage Hyperkalemia. Remember the first thing you're gonna do obviously is to give calcium gluconate to stabilize the myocardium. But insulin plus glucose they increase the activity of the sodium potassium ATP spump. And what does this pump do? It takes three sodiums out of the cell.

and puts two potassiums into the cell. So if you activate it, you're going to redistribute potassium from the serum into the person's uh uh cells, right, to try to control those blood potassium levels. Right. So this child is in a state of hyperinsulinemia that can tank the child's potassium. And you can already begin to see that that may potentially cause arrhythmias and things like that.

Right. So being an infant of a diabetic mom is not great, right? It's associated with many, many, many, many different problems, right? Like for example, they can give you a shoulder dystocia question. Because think about it, if you're an infant of a diabetic mom, insulin many people

Forget this. But insulin is literally a growth factor. Insulin literally makes people grow. Have you noticed that many type two diabetics are pretty big, especially people on a lot of insulin? Insulin is a growth factor. I mean Have you ever heard of IgF one? What do you think IgF means? It means insulin like growth factor, right? So insulin is a growth factor, so it can cause fetal microsomia. That fetal microsomia can cause a lot of problems. It can cause shoulder dystocia.

right where the child's anterior shoulder is stuck under the pubic symphysis, right? It can cause An increased rate of Caesarean seconds.

Right. Like literally they can give you a biostatistics question and talk about a cohort study. Right. So it's almost like a biostats and PEADs and Obi-Gain question all roading to one. They can talk about some kind of cohort study involving moms that have like a BMI of thirty something or whatever.

And then they also talk about their A1Cs. They'll say, Oh, they got a cohort of 200 bumps. And then they then say, Oh, which of the following outcomes will be observed in this cohort? Right? And they can say, Oh, increase and the right answer will be something like increase relative risk.

of uh c Cesarean sex of caesarean deliveries or increase relative risk of congenital abnormalities, right? They know that these are all things you know. They know that you know that or being an infant of a diabetic mom or being a diabetic mom increases your risk of your child having VAs. or you having C-sections or your labor being prolonged. Or you having a

shoulder dys uh you know, having labor where shoulder distosia is a problem, right? But again, why ask it as a direct question where you can just reframe it. It's all about reframing. And make it like a cohort study question where you ask about the most likely outcomes of this cohort study over like five years or ten years or whatever. Right? Again, these are just all forms of what? Of reframing. Of reframing. So please just be conversant with these methods of questioning on your exams. Please.

I'm saying this not because I like to hear myself speak, but because I'm trying to help you see how the US MLs love to test information. So since this is a rapid review series, I'm gonna go ahead and stop here. Um if you're interested in any of my classes, if you like the way I teach, you like the way I make integrations, you like the way I show people how the USML is test information.

You're gonna be very interested in the classes I offer. I have a class starting tomorrow, right? I have a test-taking class starting tomorrow. It's for step one to step three. On Wednesday, I have a biostats class. four hour class also for step one to step three and Thursday I have a social sciences quality improvement healthcare system

Also for step one to step three, right? And then on Friday I have a last minute review just for step two and step three. And then next week I have a twenty hour step two, step three review. And then first week in May, I have a step one class that's for people taking step one or level one. Or if you are taking step two or step three or level two and three, and you have like a poor basic science foundation, I think you'd find that uh that class to be extremely helpful.

One of a kind class, 50 hours, step two, step three review, taking place in the first two weeks of June. If you're interested in any of these classes, just shoot me an email and I can give you some more information. I've also made podcasts where I talk about the Again, these classes, many people have attended them and done extremely well on their exams. And then I also offer one on one tutoring for all the USMLEs, all the Complex exams.

I also help with like Eras applications, personal statements, mock interviews, and things of that nature. And then I have these podcasts on Apple, Google, and Spotify. I have a YouTube channel you can check out. And then I also have another website called Divine Intervention Life Lessons.com. Divine Intervention Life Lessons.com.

Um any of you that listen to this podcast, you know I'm a Christian. So every week I post like two or three podcasts where, from a biblical perspective, I address a life lesson. Uh there's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. So just listen to those. I have like more than 310 podcasts on there. Uh again, many people have found those to be really, really helpful. So thank you for listening to me today. Please.

Quick summary. Pay attention to the pathologies I discussed here, that's number one. Number two, pay attention to the methods of questioning I talked about here and the test taking principles I talked about here. It can be very, very helpful for your success on the exam. So I will see you in episode 583. Have a wonderful rest of your day. God bless you and bye for now. Thank you.