DIP Episode 220 - USMLE Step 2CK Rapid Review Series 34

Good morning. Welcome. My name is Devine. I'm a resident. This is episode 220 of the Divine Intervention Podcast. And in this podcast I'll be continuing the Rapid Review Series for the US Amelistabone exam. This series will be focused. This will be episode 34. And I'll focus on a bunch of high-yoda classic presentations that tend to pop up frequently on the exam. So let's get right into it. I guess maybe the first thing I'll see is with this Coronavirus business. You know, just some basic roles. Wash your hand regularly. Try to not touch your face as much as possible. Try to avoid non-essential public meetings. That's it. If you can follow those three roles and you know, just pray, trust God, you should be fine. Okay, so let's begin. So what if they give you a question about a patient? And this patient has like a droopy face, the tailor that they cannot smile on one side of their face. They can close their eyes on one side of the face. What are you thinking about? I'll really hope you're thinking about bells balls when you're exam. Remember, that's a cream under seven problem. And if they give you a question and ask, oh, what is the most likely infectious association with this? You want to choose HSV1. That's a very classic thing that tends to pop up on exams. Now, let's assume they give you a question about a patient. And they tell you that this patient has a history of chronic heuric regurgitation. What kind of live ventricular changes would you expect?

So here's the thing. Whenever you have chronic heuric regurg, the live ventricle will be exposed to a lot of volume overload on a chronic basis. Whenever you're exposed to volume overload on a chronic basis, the live ventricle responds in a certain way. Because think about it. If you know that your receiving more volume than it's typically normal, you would want to increase your capacity to deal with that volume. So the way the live ventricle increases its capacity to deal with that volume is by undergoing a phenomenon known as eccentric hypertrophy. And on the ghost eccentric hypertrophy. In eccentric hypertrophy, sacrameres are being added in series. So essentially think of eccentric hypertrophy as turning the patient's heart to like a shopping bag. We know shopping bags are awesome because they can take a lot of stuff. You can squish, squish, squish, a ton of stuff into them. But those shopping bags, you see that they have almost no ability to snap back. So that person essentially gets into trouble with sisterly. Those people's hearts will not be able to contract very well. So those people will have a heart failure with a reduced ejection fraction. So they are able to take more volume, but they're essentially given of the ability to contract the ability of the myocardium to contract as a result of that. So eccentric hypertrophy happens with chronic volume overload. That causes a systolic heart failure. Right? The presence heart essentially again becomes a shopping bag.

So that's one thing I want to keep in mind. And the heart sound associated with that will be like an esteric heart sound. And essentially that's the pathophysiology behind many cases of dilated cardiomyopathy. Right? Let's see. Is there any other thing I want to see there? So esteric heart sound dilated cardiomyopathy, heart failure with reduced ejection fraction, volume overload. And yeah, just not a good thing to be in. Right? And the thing that could potentially also cause that, right? It's safe for example. If a person has like a VSD, one ESD, the right ventricle will get chronic increases in volume that can cause a dilated cardiomyopathy. Right? And then on the flip side, if a person has the erotic stenosis, right? It's like it's just harder for blood to get out of the left ventricle. Right? So because it's harder for blood to get out of the left ventricle, your left ventricle has to, it's primary concern is not that, oh, I have to deal with much volume. No, it doesn't have a volume problem. The problem it has is that you're like, hmm, I need to be able to get this blood out so that the rest of the body gets enough blood supply. So your left ventricle is like, okay, well, I got to get bigger and be here. If you get bigger and be here, you know, it starts having a lot of muscle, muscle, muscle, muscle, muscle. Right? Yes, it gets a lot of muscle. The injection fraction will be awesome. Right? So you'll have like, you know, preserve the injection fraction.

But the unfortunate thing is, because there's so much muscle in the way, there's not enough space for the left ventricle to feel with a blood. Right? So it's like, okay, I am going to be able to contract better, but at the expense of volume. Right? It's almost like your heart can either, I mean, if you have a normal heart, you can accept adequate amounts of volume and give great amounts of our contraction. But essentially, if a person gets into one of these cardiovascular entities with these little volume overloads, in the case of these sensory hypertrophy and the systolic heart failure or pressure overload, chronic pressure overload, as you have a periodic stenosis, right? And the stolic heart failure. Essentially, you give up one thing for the other, right? In systolic heart failure, you give up your ability to contract or you gain the ability to take on more volume. In the systolic heart failure, you give up your ability to take on more volume, but you then now have this new ability to contract really well. Right? So whenever you see that, again, think of the systolic heart failure, the second example I'm mentioning, right? So chronic pressure overload, for example, like your periodic stenosis, if a person has hypertension, member hypertension, increases after load, right? It increases after load. So whenever you see those things, think of concentric hypertrophy, the associated heart sound is an S4 heart sound, right? And those people have the systolic heart failure.

They'll have problems with feeling, feeling of the heart with blood. And I know some of you may be saying, oh, divine, this stuff you're seeing is very basic science, so low yield. I promise you it's not, I really do. Like I'm not making this up. Just again, if I've taken many of these exams, I've treated, think for the thousands of people for these exams. This stuff I'm explaining to you is floridly high yield to know for the exam. So that's something I want to know. Now one other thing I want to mention and talk about is high outboard heart failure, right? I've got to talk about it in some of my podcasts, but let me give you like essentially the different scenarios that you'd likely see on your test. So the thing is high outboard heart failure. Let me set it up this way. If, whenever you work out to really heart, your heart is leaving away, right? Your heart is like bam, bam, bam, bam, working super hard, super well, right? But that's for a limited period of time. Most people do not work out for the whole day, right? So after a while, your heart kind of gets a breather. Doesn't have to keep working, working, working so hard. But if you're in a situation where your heart is always working so hard, remember the heart is made of muscle, you know, muscle burns out after a while if it's overworked. That's essentially what happens in a person that has high upboard heart failure. So you may say, okay, divine, give me some examples. What can cause high upboard heart failure?

Well, let's think about this, right? The common example they've read me talk about in many podcasts is having like an EV Festual, right? Having an EV Festual. Because the thing is, if you really think about it, blood goes from arterial to capillaries and then to veins. The problem is, if there is no direct conduit between arteries and veins and those capillaries are gone, then that's a problem for the heart. Why is it a problem for the heart? The thing is when blood gets at least the way I think about it, the way I try to explain to you to help you take up this information is. When blood is in capillaries, you know, it's been exchanged, you know, you have exchange of nutrients, oxygen and everything. It's almost like that blood is slowing down for a bit. Right? And the thing is, when that blood is slowing down, the heart is like, okay, you know, there's a small traffic jam ahead. Let me just get some rest for the, you know, few micro or picoseconds or something. At least blood is slowing down in the capillaries. I don't have to like get blood going again. Let me just rest a bit before I pick up again. Right? But if that's slow down, mechanism of capillaries are gone. Blood is going, zup, from the other to the veins, right back to the heart. The heart is like, oh, come on, I literally just send this blood out like a moment to go, I need to come right back so quickly, right? So the heart never has any time to rest.

So it gives us leaving, leaving, leaving, leaving, leaving, leaving. That's one thing that can cause higher blood heart failure. Another example may be like, say for example, they can give you a question about a person that was recently studied on dialysis. And then the person is having like shortness or breath volume overload symptoms. And they will try to trick you into like, oh, maybe the dialysis is not working or the person has like volume overload from kidney or whatever. But typically in the question, they'll give you that, oh, this person's creatinine is good and all that stuff. And then they will tell you that, oh, you'll hear crackles in the lungs and all that stuff. Strongly, strongly considering those situations, high output heart failure. Because think about it, for a person who's been studied on dialysis, what do you think they do first? They establish an EV Festula to increase the efficiency of dialysis. Those things can throw those dialysis patients into high output heart failure. Another thing that can cause high output heart failure is when, again, your heart is just doing more work on a regular basis than it's normally used to, right? So say for example, if a person has Pajet's disease, in Pajet's disease, the bone becomes hypervascular. If the bone becomes hypervascular, then the way I think about it is, again, I like giving simple analogies that can help you understand these things.

Let's say normally your heart is supposed to send blood to 10 million blood vessels. But let's say because a person has Pajet's disease, the bone becomes hypervascular, you're now sending blood to 15 million blood vessels for the same heart, right? The heart is like, come on, are you giving me all this extra work? Like how am I supposed to handle this? So it keeps working hard and hard and hard and hard and hard to meet those extra demands, right? And then after a while, the heart crops up. That's high output heart failure. Another example you'll miss on your exam is, say for example, if a person has really bad anemia, right? Let's say this person's hemoglobin is like in the single digits. Well, why is anemia? Because many people think one anemia is not a huge deal. People live with hemoglobin of sex all the time. It's not a big deal. It's not a big deal until they develop higher heart failure, right? Because think about this work with me here for a second. Normally, the body tasks, let me maybe set it up this way. Let's say you want a company that employs a hundred people, you know, to meet the demand for that company. But let's say you're like, yeah, you know, I want to pay just 10 staff so that I can make more profit as the person in charge. You know, as always happens in many companies, the downsides, downsides, downsides, let's say, oh, I want to increase our profits, give more whatever's to shareholders. Okay, fine.

So instead of a hundred people handling the workload is not just 10 people handling the workload. Those 10 people, they can only handle the workload of a hundred people for so long. After a while, they'll probably crop out and die or something, right? So that's the exact same thing that happens when a person has really bad anemia. It's like before you had 14 grams per deciliter of hemoglobin handling the workload of carrying oxygen, right? But now, because let's say your hemoglobin is like six, well, your body is like, oh, your body stages are like, we need oxygen, we need oxygen, we need oxygen, we need oxygen. You literally just don't have enough stuff to get that oxygen around. So your heart is like, okay, okay, I'll pump the blood a little faster so that the hemoglobin's make the, instead of maybe making the round like 60 times a minute, you know, let me just pump a little faster so that those limited hemoglobin's I have will make the round like 150 times a minute, right? So that you can keep up with the hypoxic needs of the body. Well, if your heart keeps leaving away at those kinds of rates, after a while, the person will get high up or heart failure, right? So these are all, I mean, there's this thing called tagic cardio-induced cardiomyopathy, right? It's almost like a high up or heart failure kind of business, right? So that's, those are essentially all the ways that your friends at the MBM will throw in a high up or heart failure kind of situation on an exam.

So those are things you just want to watch out for. Now, what if they give you a question about a patient? They tell you that, oh, this patient has, you know, she's, she always feels dizzy. She has like these episodes where she feels dizzy and she also has like, ready-go, you know, feeling like they're spinning around her and they tell you that, oh, this person has since her neurochairs and they may even tell you that, oh, this person has nice tagmas on physical exam. If you see that, what are you thinking about? I really hope you're thinking about mannier's disease, right? Mannier's disease, right? It's a triad on MBM exams of ready-go, denied us and here in loss. And sometimes one thing your friends at the MBM like to do is they may ask you, what's the path of physiology behind this disease? The both of you are looking for your test is something known as endolimphatic hydrops, okay? Endolimphatic hydrops, it's just way too much endolimph and then it causes all these problems, right? And the thing is in general, if they ask you for lifestyle changes that could be used to combat mannier's disease, you want to pick the answer choice that involves giving like a low salt diet, but the permanent treatment in general is to ablate the presence of creatinine each with gentle miceen, right? Remember, the amino glycosides are auto-toxic, so you just take advantage of auto-toxicity, essentially the person is going to be getting a permanent here and loss with that.

So not an ideal situation, but you know, sometimes that's all a person has. Now, what if they give you a question about a patient and they tell you that this one should be easy, right? They tell you that, oh, this patient has like, you know, like castrable moving, has like a resting tremor, has like cochlear agidity, what do you want to think about on your test? I really hope you're thinking about Parkinson's, right? And again, classically in Parkinson's, right? You'll typically ask you, what is the neuro-atomic unassociation? You want to associate this with the pigmentation of the substantione migra, right? And don't forget that people that have Parkinson's, right? They tend to have Louis bodies in neurons, right? And they have low dopamine. That's why you use drugs like carbidopalivodopa or amantadine or the contain inhibitors like entakapun, entokapun, or the MAP inhibitors like cellulogen, rassagelin, right? Or the dopamine agonist like bromocryptine, cabrigoline, epomorphine, right? To treat that disorder. Now, don't forget to drug-induced Parkinsonism, though there are some things that people can take that can cause Parkinsonian-style symptoms on an MDM exam. For example, they can give you a question about a patient on chemotherapy, right? That's taking clopromazine for nausea. Clopromazine is an anti-psychotic, essentially. It's one of those low potency, fresh generation anti-psychotics. It can certainly cause Parkinsonian-style problems, right?

So just something you want to watch out for. Watch out for an exam. They can give you a question about a person that has diabetic astroperesis, right? Remember, you can treat that stuff with beta-clopromide? Well, the problem with beta-clopromide is that, again, it's a dopamine receptor antagonist, so it can cause those kinds of problems. It can cause Parkinsonian-like features, or essentially any extra pyramidal side effect, you'll see what anti-psychotics, right? So like acute dystonia, where they have almost like these tonic contractions of like, usually muscles like the face of their extremities. I remember for that, you give an anti-colonogic agent like Diffin Hydramine, or you can give Ben Stropin, right? But Diffin Hydramine is probably the answer is shown exempts like 99% of the time. You're essentially taking advantage of its anti-colonogic effects. And then they could have like acathesia, right? We really feel like they keep pacing around. They feel like they want to jump out of their bodies. For there you go, along and give those people a beta blocker, right? That's first line. If that's not correct, you should give them a benzo, right? And then the Parkinsonism, right? Ben Stropin is what you're going after in your test. And then they can have Tardiv, dyskainisia. Obviously, you want to go ahead and stop the drug, right? You want to go ahead and stop the drug. So just one of those big things you want to keep in mind.

Although if a person has like, you know, like legit schizophrenia, and they have Tardiv, dyskainisia, unless they take like halopyrido, you know, go ahead and stop the halopyrido. Your next step in management after that is to switch to an etypical anti-psychotic, right? And then if they remember that Parkinsonism is also something that could happen when people take MPTP, right? Basically, like if a person is, you know, not very smart and prudent at cooking opioids, there's a nasty, nasty, nasty side, side product that can pop up MPTP. It can cause a permanent destruction of the person's a substantial Niagara. And then the person gets into trouble, right? And shouldn't be using opioids, probably not a prudent life decision to start with. And then what if they give you a question about a patient? And they tell you that, oh, this patient had an opyrus-perture infection like two weeks ago. And now this patient has like lower extremity weakness and is beginning to have shortness or breath. If you see that, I would hope you're thinking about Guillain-Berry syndrome, right? Again, it can follow like an opyrus-perture infection, a GI infection, right? And again, it's the shwan cells that are being destroyed, right? In this disorder. For the most part, these people you want to go ahead and do plasma exchange therapy, as quickly as possible. And then you monitor the FEV1 pretty well, right? Because these people they can, their diaphragms can feel, right?

And if their diaphragms feel, then they won't be long for this work from a respiratory perspective, right? So once you notice that the FEV1 is beginning to tank, you don't want to go ahead and into be these people as quickly as possible, right? Take over their earways so that they don't have to lose it fairly quickly. And then one thing I'd also like you to keep in mind, what if they give you a question about a patient? Let's say it's like a 53-year-old female, she tells you that for the past two weeks, whenever she gets out of bed or she sways ahead in a particular direction, she feels very out of it, feels like the room is feeling all around her. And they tell you that, oh, the performance physical exam and the notice that she has nice stagmas, right? But she doesn't have any hearing loss, doesn't have any ringing in the ears, none of that stuff. If you see that, I would really hope you're thinking about BPTV on your exam, right? So benign, paroxysmal, positional, ready to go, right? It's actually the most common cause of ready to go. And for the most part, the pathophysiology again, if they're asking you about this, is this person, essentially the Odochonia in the ear, where you can see them refer to as Odolyts, so O-T-O-L-I-T-H-S, they are being displaced in the inner ear, right? And that can cause problems, right? We've already go. And really, the way you make the diagnosis, you need to kind of remember the manovars on your test, right?

So don't forget the Dix Hall pipe manovar, right? Just look up videos of this because sometimes, instead of actually telling you the manovar, they may describe the manovars as a series of answer choices and they have to pick out the right one, right? So that Dix Hall pipe manovar is how you make the diagnosis, but to actually treat the disorder, you need to perform something called an Eplemonovar, so EPL, EY, an Eplemonovar. And then another one is like a sum, a sum, month manovar is something else you can also do to establish, I mean, to treat, to treat to treat BPPV, right? Essentially, these manovars just help you like displace the odorless to the right spot so that the brain stops having these vertiginal symptoms. And then, what if your friends at the MBM may give you a question about a patient that has like cataracts, has hypertrophy cardiomyopathy, is having like marital problems because he cannot have kids with his wife. And this is a 25-year-old guy and he's like very bald. What are you thinking about on the test? I would really hope you're thinking about my atomic dystrophy, right? So notice, I didn't put this physician has trouble releasing hand from grip, whatever, right? Yeah, those dastia pop-up on exams he does, but you know, your MBM is, your friends are the MBM, they become a little smarter, right? They know that every human being that is named a met student has, you know, kind of committed that to memory.

So, they're becoming more exotic these days or this stuff, right? So, the things, the association, I mean, again, you still know the physician has trouble releasing hand from grip or this person has trouble releasing hand from door, from door panel, so whatever, when he's trying to open doors, but there are some other things that I would really like you to keep by the back of your mind with my atomic dystrophy, right? You want to remember the early bald in, in a young man, right? Young man with cataracts, young man with heart disease, usually hypertrophy cardiomyopathy, or a young man that's having trouble with having kids, right? Because they're hypogonadol. If you see all those things, I only want you to think about my atomic dystrophy. And remember, my atomic dystrophy, right? Or the zoom-out dominant inheritance, it's one of those fancy schmancy, trinic lotharic beat disorders, right? Remember the trinic lotharic beat, in this case, is CTG. It's a CTG trinic lotharic beat, and the gene mutation right is the DMP-kg, right? The DMP-kg. You know, you may be saying, hmm, the vine that sounds low-yield, I promise you it's not. And the thing is, I foresee that in the very near future, with these changes in the US Emily to like passfield, step one to passfield, more basic science stuff, more like step one like stuff where things were here like, yes, only under the purview of step one, it will begin to pop up on step 12 would not be surprised.

If that's the general direction of the NBM has been for the last like seven, eight months. So again, just things to keep, to keep at the back of your mind. And then, I guess as a quick review, or let's talk about the four trinic lotharic beat disorders, I'll just mention them in pass-end, right? So again, my electronic dystrophy, CTG trinic lotharic beats, DMP-kg mutation, or the zoom-out dominant inheritance, right? The next one will be haunting tense, right? So be some present there, 40s or early 50s, that's actually in appropriately has query for movements, remember that's a chromosome four problem, right? Or the zoom-out dominant inheritance, CAG trinic lotharic beats, right? And you want to keep the neural anatomical association in my right, like atrophy of the codit, and you treat that stuff with anti-dopaminergic agents like alopyridone or tetrabenazine, which inhibits like the V-MATS transporter that dumps dopamine into vesicles. And then the third one, right, will be fragile X syndrome. In fact, your friends are the MBME, they're actually like the last two, because many people have kind of said, oh, you know what? All trying to repeat disorders and hear it in autosomodominant fashion, well, that is not true. These last two certainly do not obey that rule for sure, right? So, what do I mean by that? Um, fragile X syndrome is inherited in an X linked dominant fashion, right? And the trinic lotharic repeat is a CGG trinic lotharic repeat, right?

And again, you know, be a person that has a boy that has big ears and big testicles. They may not put big testicles on your exam, they may just say micro-orchidism, right? If you see that, think about fragile X syndrome. And then the final one, you'll give you a question about a patient that has like high arched feet, has a taxia, uses a ton of orthosis, right? To walk well, this person may have chai-fosis and all that stuff. If you see that, I'll hope you're thinking about like Phrygiaxia, right? Remember Phrygiaxia is inherited in an Orozomo recessive fashion, right? And the trinic lotharic repeat, there is a GAA trinic lotharic repeat. Again, you've got to know these four trinic lotharic repeat disorders for you, except. Now, what if they give you a question about a child that has been having visual difficulty? And they tell you that, oh, on imaging of the brain, you see like a supercella mass that contains calcifications. This one should be easy, right? This is very classically a craniofaringeoma, right? And remember the embryologic origin, does something your friends at the endemic really care about? It's descended from a rafky spout, or sometimes they may tell you the roof of the mouth, or sometimes they may tell you oral ectoderm, right? Those are all things you should keep at the back of your mind for exams.

And then another thing you may see on an endemic exam is they may tell you that a person has, you know, they're having like morning headaches, a lot of vomiting when they get up in the morning, they feel better as the digels on. And they tell you that on imaging of the brain, they see a mass in the frontal loop, so notice I didn't see a supercella anymore. A mass in the frontal loop that contains calcifications. If you see that, I really hope you're thinking about an oligodendroglioma, right? Classicly oligodendrogliomas, frontal loop mass, containing calcifications. That's the high-yield thing you want to keep at the back of your mind for exams. Now the final thing I want to say here, well, maybe not the final thing, because some stuff I still kind of have floating around in my brain I should probably discuss. So this block has probably go for a little over 30 minutes, my apologies, sorry. What if they give you a question about a patient and the tell you that this person has like a mass in the brain that's growing like in the middle of the cerebral hemispheres. Excuse me, if you see that you want to think about a meningioma, right? The thing is, again, many times the names of things are really pretty helpful in knowing what in the world is going on here, right? Look at the name meningioma, it's an oma, it's a mass that grows around the meninges, right? meningiomas on MDMA exams, almost like 95% of the time, they grow along dural foes, along meninges, right?

And classically, on MDMA is like the interhemispheric phasor, right? Along like the fox cerebra, essentially, right? So if you see those things, think about a meningioma, again, don't forget, it's B9, it doesn't grow within the brain parankoma, right? And it causes some, it contains some oma bodies on his starchy, right? Again, I hope you've not forgotten all those other tumors that have some oma bodies, right? So like a cirrhosis that occurs in the ovary mesophilia, right? You remember, like, peroplax on imaging, and there's one more, papillary thyroid cancer, right? That also has some oma bodies. I remember the biggest risk factor for mesophilia, is a history of asbestosis, and the biggest risk factor for papillary thyroid cancer is a history of radiation to the head and neck, right? Those are all things they love to test on exams, and the biggest risk factor for ovarian cancer is having a family history of ovarian cancer, right? So these are just all things you need to come into memory for your exam. Now, what if they give you a question about a patient? And they tell you that this patient has, you know, like a chronic diarrhea, and this patient has like, they give you a lab, you know, Jesus Christchurch, it is like 85, and this person has a bicarb of 17. You can clearly understand that when you notice it's normal. If you see that, what should you consider in your test? I would hope you're thinking about a vaipoma, right?

Again, if you notice, I'm not giving you like, a patient comes in with watery diarrhea, hypochyline, and acrohedria. No, right? The MBM is not they're smart, right? Again, these people have been in business for probably longer than you've been alive yourself, right? So again, they're not, they're, they're products. Let's put it that way. They're products, right? So these days, like I'll tell you this, like this is something that the MBM has been slowly doing over the years, but I'll say like last year's Wendy kind of like took like a very big step in this direction. Instead of giving you buzzwords, again, they still give buzzwords. Don't get me wrong. Like this white fixed bit of the S2 heart sound with an ASD, you know, these, I feel like most ASD questions still have that stuff, but they are becoming more descriptive, right? So notice, I kind of gave you like, low chloride. Told you this person has a watery diarrhea, right? Like a chronic diarrhea. And then I am giving you like, oh, the bicarb is this, and it's a normal anion, that whatever, right? This person has WDHC syndrome, right? With a vaipoma. Sometimes you may see them on exempts referred to it as a, as verna, more sincere syndrome, right? And essentially, these people have problems with it's a pancreatic neuroendocrine tumor. These people are making a ton of visual active intestinal peptide, right? And the vaip causes a lot of problems, right? Like, I mean, it can cause a secretory diarrhea, right?

Because it essentially works like an adenylid cyclist, right? So it will stimulate the production of cyclic AMP, kind of like the toxin that you find if you have like vibrocolor or people that have like, e-tech, right? Remember, like the heat, lebal toxin that increases the activity of a dentile cycle is a cyclic AMP, right? So you get a secretory diarrhea with that, right? And the thing is remember, whenever you have diarrhea, it's going to cause a metabolic acidosis. To be more specific, it will cause a non anion gap that a body acidosis. And to be even more specific, it will cause a normal anion gap that a body acidosis with a negative urine anion gap, right? Ooh, it's just like, you believe like, divine. What in the world do you mean by urinary anion gap? Well, the urinary anion gap is an anion gap, conclusion for the urine. It's essentially sodium, minus, basically adioprotassium and chloride. And then subtract that from the sodium, right? If the answer you get is negative, it's diarrhea. That's the cause of that presence, a normal anion gap metabolic acidosis on an ambient. Again, that's something we want to keep at the back of your mind, right? So versus a positive urinary anion gap that usually falls under the purview of an RTA, right? So you can see like, you know, again, it's essentially the same classic presentation, but they're just kind of stretching your knowledge a little bit with that, right?

And again, visual activity and testimonial peptide is shut down gastric acid production, right? That's why they have an acrohedria. So the chloride is really low. And the thing is, if a person has diarrhea, right? You're losing a lot of fluid from the colon, right? So whenever you lose a lot of colonic rich fluid, you're going to get a hypochylemia because the colonic fluid is very rich in potassium. And again, the way it should have aipoma, I mean, you can give the person like a true tired or something. And don't forget the associated on MEN1 syndrome, right? It's a pancreatic neuroendocrine tumor. So it makes sense that it's associated with MEN1 syndrome, right? And then what if they give you like a question about a patient and they tell you that this patient is like a 55-year-old guy, they give you glucose of like 250, right? And then they tell you that, oh, this person has, this person has like a rash, like a skin rash and diabetes, right? Obviously, they're going to try to trick you into picking cushions as an answer. Don't do that, right? It's kind of weird for a person to develop diabetes for the first time in their 50s, and then they have a rash. If you see that, that's a glucogonoma, right? It's a tumor of the of the pancreatic isleta alpha cells, right? Again, so the buzz word for the rash is a necrolitic migratoryorythema, right? And obviously, they will have diabetes because glucogon raises a presence of blood glucose, right?

So if you see that, think about a glucogonoma again. Don't forget the association with Amyin-1 syndrome. And then, what if they give you this question about a person that has like a chronic diarrhea? And they tell you that, oh, you perform endoscopy. And you find ulcers in the genus. Well, this one is pretty easy, right? This is a gastronoma, right? The gastronoma, basically it's a G cell tumor, right? So these cells are making a ton of gastro and gastroin stimulates acid production, right? If you stimulate acid production, whether you're going to get nasty peptic ulcer disease, so obviously these people respond well to BPI's. And in general, right, the diagnostic testing for this one kind of matters. So remember for every endocrine disorder, you always want to have some kind of screening test. And then after that, you need to have like some kind of biochemical confirmatory test, right? So, for example, if a person has a gastronoma, well, it will make sense to measure gastrointest, right? No, that doesn't seem like an unreasonable thing to do. So, you know, you measure the gastroint. It's more than a thousand year down. Presence gastronoma, endostore. But if you're like, hmm, this person's gastronoma is like less than a thousand, you're like, okay, let's do a second test, right? And the second test, you do is something called a secretive stimulation test.

So, the thing is, in general, when you give a person a secretive, they're, they're gastrin is supposed to suppress, right? They're gastrin is supposed to suppress. But the thing is gastronoma cells, they don't respond to those normal signals. If anything, when you give a person that has a gastronoma, or again, they can call it like Z-E syndrome, like Zolanger-Elicent syndrome, when you give them secretive, their gastrin levels will actually arise in response, usually like doubles. Once you see that, that's the agnostic of a gastronoma. But if they're sick, if they're gastrin barely rises, maybe like rises by like less than a hundred or something, that's not a gastronoma. That's probably like some secondary cause of an elevated gastrin. In fact, your friends at the Amy Mikan essentially write the question that looks a little like a gastronoma, but it's not really a gastronoma. Because again, think about it. If you take a PPI, what do you think is going to happen to you? You're going to kill acid production. So, negative feedback for the G cells will not be there. So, you're going to have elevated levels of gastrin, right? Or if, for example, your person has, takes these H2 blockers, right? Again, you kill acid production. So, your gastrin, there's no negative feedback, your gastronoma will go up. Or let's say your person has like a gastric outlet obstruction, right? Like they can make this a pediatric question even.

Like a person that has a pyloriostanosis that what should be true of their gastron? Well, their gastronoma will be elevated because the thing is, whenever you have a gastric outlet obstruction, right? The anchrom of the stomach is super, super, super distended. And when the anchrom of the stomach is super, super, super distended, it's almost like your body is like, this person just ate. So, we need to make acid so that this person's food can digest, right? Well, how do you make acid, you need gastric to make that happen, right? So, that can cause hypergastrinemia, right? So, then these are just all different things to keep at the back of your mind. Or let's say a person has like a, like an atrophic gastritis, right? Like the type A kind where you nuked the, nuked the body and the fondness of the stomach. Well, you've taken out acid production, right? If you take out acid production, then gastrin is going to rise in response, right? And again, don't forget gastronomalist, MEN1, right? Remember, these amiens symptoms, you know, the kind of high urinal for your test. There's like MEN1, there's a modem in it in heritins. I remember it as like parapanpit, they get parotheric problems that cause hypergastrinemia, right? So, that will show them the cutin, trival, and then engaging. They can have pancreatic problems, right? Like these pancreatic neuroendocrine tumors, and then they can help you to treat problems, right? Like a particular, they're normal, like a prolectinoma.

And again, I've talked about most of the pancreatic neuroendocrine tumors, right? Talked about glucogonomas, diabetes, they're called, they're called relidica, migratory rhythma. Talked about gastronomas and the genome ulcers and all that fun stuff. Talked about vipomas, right? With a non-anemic, that might have had a polychacidosis and a secretory diuretic, right? And my guess though, too, I've not talked about like insulinomas, right? Insulinomas, pretty classic, right? Those people have like neuro-glycopinic symptoms, right? So, you know, you'll have like sweating, hypoglycemia, you can even give you a seizure question. And it ends up being a person that has an insulinoma, they will give you a person that has like seizures, and then the hotel is that this person has hypoglycemia in the presence of an elevated insulin and elevated CPAP type, right? That pretty much seals the deal for you on a test, you know, that's an insulinoma. Remember there's this web-host triad, right? That I really hate because it's kind of obvious, right? It's like, oh, hypoglycemia, signs of hypoglycemia. Instead of seeing signs of hypoglycemia, you see the presence has neuro-glycopinic symptoms. It just means they have neurologic problems because they're hypoglycemia, right? And then they will tell you that these symptoms are relieved with like glucose administration, that's an insulinoma.

And an insulinoma right for the most part, you try to reset that stuff, you can reset it, you can give drugs like diazoxide, right? Because if you remember, insulin is made by bitersels of the pancreas, and if you're kind of thinking back to like basic signs step one, essentially the thing that happens is if you want to make insulin, you know, glucose will come in through the gluteus transporter, you make ATP, ATP will bind up potassium-dependent channel, like a potassium channel in the bitersel, and you know, you block that channel, the cell will depolarize, voltage-gated calcium channels will open, calcium will rushing, and then vesicles will come and pupe, squared out insulin. So, the zoxide, that potassium channel that I say is blocked by ATP, because if you think about it, if you block the potassium channel, right? Well, potassium is not going to be living the cell anymore, the cell will depolarize, and then, voted-gated calcium channel will open, right? So, calcium channel that, I mean, if it if a channel is voltage-gated, it means that it opens and closes in response to voltage changes, right? So, you know, that's essentially what will happen there, and then you squared out insulin, right? So, the thing is, diazoxide is a drug that opens up that potassium channel, so that will hyperpolarize the bitersel, and you know, you essentially stop making insulin.

So, that's again something to keep, keep the back of your mind, and then one rare, by a category, into a more than me, pop-up on a test, that most people probably will never get right, well, but you'll get right because you're listening to this podcast is, imagine they give you a question about a patient, and this patient's chloride is like 85, right? And they tell you that this patient has like, you know, like, neonce diabetes, and this patient has like Fatmonella absorption, and they tell you that this patient has had like four episodes of colilithiasis over the last year. That's kind of weird, right? Like, symptomatic colilithiasis. If you see that, you really want to think about like a Asomastatinoma, right? Or let me call it a Somarostatinoma. I think that's probably the more appropriate thing. Here we go. Yeah, what do I do? This find is a really odd. How does this stuff happen? Well, let's think about it for a second. The thing is Somarostatin shuts down the production of like everything in the GI tract, right? So, you may say, okay, why do they have a low chloride? Well, the thing is Somarostatin shuts down G cells. It basically decreases gastrointronduction, right? So if you're not making gastrointronduction, well, doesn't look like your Pridal cells are boosted by lethal, right? If you're not stimulated, you're not going to make an hydrochloric acid. So your chloride will be down. You may also say, okay, why do they have diabetes?

Well, one thing Somarostatin does is shuts down the production of a GIP, right? Gastroint inhibitory peptide. And normally gastroint inhibitory peptide, this job is to make you make more insulin, right? So if you shut it down, you're not going to stimulate insulin production. So you'll essentially be in like a glucogonal world, right? So you're not, you're going to have like diabetes, right? I mean, if you kind of think about this for a second with me, there's a reason why there's diabetes drugs that are GLP1 agonists, right? Those are drugs that essentially act like gastroint inhibitory peptide to stimulate insulin production. Those are your drugs like exenatide and lyragmotide, right? Remember, those drugs cause weight loss, right? Something you want to keep in mind. And those drugs are contraindicated in people that have a history of ME& syndrome. Yeah, just off-should there I wanted to. I just threw it in as bonus for you. And you may say, okay, why does this person have this Fatmala absorption? Well, the thing is, gastroint shuts down the production of colicis no kaini. So if C-Kid is not like around anymore, well, your gobladder is not going to contract. And if your gobladder isn't contract, the stuff inside you will be conconcene treated so you can get ghost stones. But also, the stuff inside is not getting anywhere like bowel, you know, you kind of need bowel to, you know, kind of like emulsify fats and all that stuff.

So if that stuff's not working, you're going to clearly get a Fatmala absorption. So I think that's all I'm going to say about that. And I know I didn't talk about ME&2e and 2b. So let me just talk about them real quick, right? So remember, ME&2e, it's like parathoric problems. They'll have fiochromocytomas and then they'll have medallary thyroid cancer, right? And then ME&2b is like marphanoid habitus, micosoninromus, fiochromocytomas, and they'll have medallary thyroid cancer. And remember, medallary thyroid cancer, right? Like, you can do congruent stint of the presence thyroid gland and you see like the upgreen birefringent because calcium toning the tumor microphones amyloid, right? In fact, we can give you a question about a person that has a neck mass and this person has like a prolonged cutin trouble on an e-chee. If you see that, that's medallary thyroid cancer, right? Because of the hypo calcium, coscalcytonin, tones down your blood calcium, right? And remember that ME&2, right? It's an autosomodominant disorder, right? From a red gene mutation versus ME&1 that's also autosomodominant, but it's from a many, ME&IN gene mutation. And whenever you notice the zone has, um, has a ME&2, you need to do like a prophylactic thyroidectomy because again, it's not a matter of, oh, will they get medallary thyroid cancer? No, it's not. Oh, when I think I'm going to get the medallary thyroid cancer, right?

So those people always get prophylactic thyroidectomy, cos medallary thyroid cancer actually has a pretty not so good prognosis. And then one last thing I just want to share here, cos it's just a common thing the ME&IN kind of likes these days is, if a person is diagnosed with a preferred cutinia, tarda, need to screen them for hep C, cos there's a very well established association between TCT and hep C. So again, I know this was supposed to be a rapid review podcast, but my apologies, I don't know, I'm just kind of determined to get through all the stuff I got through. There's a floridly high-yield podcast like you're going to get some questions right on your test from this. And one thing I will say for people that are taking step 2ck, if you want like in general, you'll get the vast majority of the information you need by going through my shelf review videos, right? But one thing I'll strongly recommend if you're working out, driving and all that stuff, listening to these rapid review series. Essentially, they're like add-ons to those videos and they are super high-yield and they are super helpful. There is a somewhat peculiar process I go through in making these rapid review podcasts, right? So I designed them to be super super super high-yield, right? And to incorporate like new and new information that the MBME is beginning to focus more on. So I'll encourage you to go through this.

And as I do, as I've been doing recent times, right, at the end of every podcast, I kind of give like a 30-second life lesson, right? So my life lesson for today is a statement that was made by Warren Buffet like a couple years ago, right? And it should be fearful when others are greedy. And it should be greedy when others are fearful. Well, what do I mean by that? Well, what I mean by that is you see all this coronavirus business, right? Like everyone is running, like there's almost like blood in the streets with the stock market, right? Everyone is fearful now. Well, it's probably the time to get greedy and invest, right? So because now no one wants to be in the stock market. It's not popular to be an investor at this point, but you know, it's probably a smart time to invest. Again, this podcast is not forgiving investment advice. In fact, those say, oh, do I made me invest? No. And just speaking my mind, right? Again, this podcast is not meant to give investment advice. If you're making games, you make losses, not me that laid you into that, right? I'm just giving you as a life lesson, right? Because being contrarian sometimes can really pay off a huge, right? So again, if you think about like the stock market crash of the 1920s, like 2008 or whatever, right? People that we're greedy, when everyone was fearful, then you know, they kind of make pretty big games. So I mean, I kind of have like very, I mean, I have strong interest in investing.

If I've actually been a pretty big investor in the past, I just don't have like an investment partnership when I used to put on that hat, but that's a story for another day, right? But again, just, you know, useful life lesson tends to panel pretty well for people that do those kinds of things. And then as I do at the end of every podcast, right? I do want to want to learn for many exams, right? Step one, step two, CK, step two, CES, step three, preclinical med school exams, 30-ish-off exams, if you're a medicine resident, I do that for the EBA import exam, or if you're a PEEDS resident, I do that for the PEEDS boards, also like the medicine in training exam, the PEEDS in training exam, I offer tutoring for those things. And then I do this thing called longitudinal tutoring, where essentially for your study now med school, you sign up with me, I'll tutor you all through your med school exams, and then as I'm tutoring for those med school exams, I tutor for your upcoming board exam, right? Like step one, unless you're a brand new 30-year med student, tutor you all through your 30-year, all your shelf exams. And again, as I'm doing that, I'll preppy for step two CK. Essentially, everyone I've done this with, they've been like wildly successful on their USMLE exams. And then also do these booster courses, where it's 20 hours for step one, step two CK, step three. And essentially, I review the most notes, the highest of the high yields for these tests.

Typically, whenever I do these things, what I usually do is, like the first session, I kind of feel a person out, because again, I think fully again, I've tutor for a while, so I kind of know like what would work best for a certain kind of person. So the course is not the same for every person, right? I kind of feel a person out, kind of see like, okay, these are the persons constitution is as like a learner or a test taker. And then after that, once I identify a sweet spot, I start going after that sweet spot. I keep hammering, hammering, hammering on the weaknesses. But after all is said and done, the high yields for the different subjects or different disciplines on that exam, they'll be covered in great detail during that course. It's rapid fire, it's Q&A, but people again find this to be super, super, super high yield, right? So if that's something you're interested in, I feel free to reach out to me. And then if your medicine or a plan to residency, so like an Amkass application, no, sorry, that's not Amkass, that's Eras. Or if you're calling to not plan to med school, so like an Amkass app, I draw for again, like consulting, or you can call it like coaching, you know, like personal statements, rec letters, mock interviews, editing applications, and all that stuff. Again, work with people, the vast majority of people have worked with a whole bunch that their first choice. And again, I've been on the admissions committee of a top two med school for a whole year, right?

So I've reviewed thousands of applications and I'm very particular with the way I review applications, but that process has very high fidelity, it's been very successful. Kind of like the same way, prepare people with step two CS. I have a very peculiar process, but again, it has, I've never treated anyone that has ever ended up feeling a step two CS. And then if you're a college student that you need to learn for like the Amkass or like your primates of this, like general chemistry or Danny chemistry, physics, biochemistry, histology, physiology of what you're doing for those things. So thank you for listening. Please like this podcast, especially if you're taking step two CK any time soon, I kind of recommend listening to this podcast. I suspect it will help you out a ton. So thank you for listening. God bless you. Stay safe out there and I'll see you in the next episode. Thank you.

Vertigo, nystagmus, and hearing loss.

Endolymphatic hydrops (excess endolymph).

Chronic volume overload, S3 gallop, systolic heart failure with reduced ejection fraction.

Concentric hypertrophy, associated with an S4 gallop and preserved ejection fraction initially.

Atrial septal defect (ASD)/Patent Foramen Ovale (PFO), chronic dialysis, Paget's disease, severe anemia.

Benign Paroxysmal Positional Vertigo (BPPV).

Watery diarrhea, low chloride ($\text{Cl}^-$), and normal anion gap metabolic acidosis with a negative urine anion gap.

CTG trinucleotide repeat expansion in the DMPK gene (Autosomal Dominant).

Eccentric hypertrophy.

Dix-Hallpike maneuver.

Hypoglycemia, neuroglycopenic symptoms (not just signs), and elevated insulin/C-peptide levels.

Meningioma.

Parathyroid problems (hyperparathyroidism), Pancreatic neuroendocrine tumors, and Pituitary adenomas.

Normal Anion Gap Metabolic Acidosis (NAGMA) with a negative urine anion gap.

CTG trinucleotide repeat expansion in the DMPK gene (Autosomal Dominant).

Eccentric hypertrophy.

Dix-Hallpike maneuver.

Hypoglycemia, neuroglycopenic symptoms (not just signs), and elevated insulin/C-peptide levels.

Meningioma.

Parathyroid problems (hyperparathyroidism), Pancreatic neuroendocrine tumors, and Pituitary adenomas.

Normal Anion Gap Metabolic Acidosis (NAGMA) with a negative urine anion gap.