DIP Episode 495 - USMLE Step 2/3 Rapid Review Series 107

Welcome, my name is Devine. This is episode 495 of the Devine Intervention Podcasts. And into this podcast we're going to be continuing the rapid review series for the US Emily, step-to-step, step-3 exams. There's going to be series 1, all-7. Again, these things are pretty high-yield things. I'll highly encourage you to make sure you can study them for your test. Okay, so what if they give you a question about a 26-year-old female? They tell you that she comes to the emergency room because she has noticed over the last 24 hours that she's only able to smile on one side of the face. And you notice that wow, the on physical exam, you notice that man on one side of the face, she can really wrinkle it properly both the forehead and the lower part of the face. And you know, they tell you that she recently visited Boston for conference or something like that. But what should we be thinking about? I hope you're saying divine. This sounds a lot further like a Bell's palsy. I'm like, wait, what? Yeah, Bell's palsy. Now what calls this person's Bell's palsy? Well, if you think that calls this person's Bell's palsy is a line disease, line disease, right? So you may wonder, why are you really focusing on this forehead business? Well, this forehead business is actually pretty high-yield to know. Well, why is that? Well, here's the thing. The thing is, when you have Bell's palsy, you have damage to the cranial seven nucleus.

We have Bell's palsy, we have damage to the cranial seven nucleus. So since it's a problem in the brain stem, you're going to see a facial muscle weakness in the upper and lower face. That's a very nice way to differentiate this from an MC stroke. Remember, when you have an MC stroke, an MC stroke is only going to affect the contralateral lower face. I'm going to say it again, the contralateral lower face. Why is that? Well, the reasoning behind that is that your the upper face has blood supply from both middle-servial otters. It has like collateral supply. So if you have a stroke in one otter, the other otter is going to pick up the slack. But the lower face has only one blood supply. It doesn't have a collateral, it doesn't have bilateral blood supply. So you can get in very big trouble there. So let's just make sure we can differentiate between line disease causing, if you have a cranial seven nucleus problem, which is a brain stem issue, or an MC stroke, which is a cortical issue. One, when you have the brain stem problem, that's called Bell's palsy. That's a cranial seven nucleus issue. You're going to get upper and lower facial paralysis, that is, if it's a lateral to the problem, that's very high you know, it's going to be if it's a lateral to the problem. But when you have an MC stroke, you're going to take the lower face only. You're going to take the contralateral lower face only. So the problem is going to be contralateral to the stroke.

That's very high you know, contralateral to the stroke. And the thing is, the USME leads the love to do this weird stuff on exams. When you give you a certain pathology and ask you or where, where is the lesion, right? It will be like a stroke or whatever or like something going on. And they will ask you where is the lesion and they will try to give you like different places they will see. They will give you a cortical sub cortical brain stem, myonero junction, peripheral nerve, blah, blah, blah, blah. Well, if you're thinking about a right, an MC stroke that's causing a contralateral lower face paralysis, that's obviously going to cause the person that's going to be a cortical lesion, right? It's going to be a cortical lesion. But if you have a problem with like Bell's palsy from like Lyme disease, for example, that's going to be a brain stem lesion. It's going to be a brain stem lesion. And I want to just throw in a bonus question for you real quick. What else on physical example help you differentiate Lyme disease causing Bell's palsy from an MC stroke? Well, look for upper extremity involvement. Because remember when you have an MC stroke, it's going to affect the face and it's going to affect the upper extremities, right? But if a person just has Bell's palsy, it's just a cranial seven problem. So the only thing that's going to be affected is going to be your face. You're not going to see any involvement of the upper extremities.

That's a pretty high yield thing to know. It's actually a very nice way to integrate microbiology with neurology. So just don't, if I were you, I would not mess this up on your exam. It's actually pretty high yield to know the stuff. Okay. Some other thing, one other thing I want to talk about because this is something that's becoming very important for the exams, is many people kind of ignore cirrhosis on the USM in the sense. cirrhosis is actually pretty high-yield stuff. It's actually pretty high-yield stuff. Do not ignore cirrhosis on your exams, right? Like literally there are many different ways they can throw cirrhosis to you, right? There are many different ways they can throw cirrhosis to you. Like for example, if the describe a person that has IST and LT from having sex without protection or you see potential maternal to fetal transmission or you see like needle stick and those circumstances you probably want to think about head B. Obviously that will easily be a head B serologic question. They'll give like a positive head B surface antigen, for example. Or, and obviously if you have chronic head B that can lead to cirrhosis or they can give you a question about a person that had like a blood transfusion back in the day. They're going to make it a blood transfusion from like, you know, like 30, 32 years ago.

So like early 90s, 80s and you know, basically like from like 1992 or earlier, you'll see a person that got a blood transfusion like years down the years prior. And then now we notice that man this person has cirrhosis. They want to think about head C. Although remember you can also have fine head C on your USM exams in IV drug users. And also in people that get needle sticking drugs, you can absolutely get head C from those circumstances. Or what if they give you a question and obviously that can lead to cirrhosis. What if they give you a question about a person that has elevated liver function tests, right? The ALT, AST and both elevated, but the ALT is more elevated than the AST. And they tell you that this person does not consume alcohol. This person is not a drug user. This person does not have any history of, basically, it doesn't have any hepatitis aviars. When you see something like this, don't you think about non-acorolic fatty liver disease? Maybe like, wait, what? Yeah, yeah, yeah. Something you definitely want to make sure, you know, it can be a cause of cirrhosis. In fact, this is one of the most common causes of cirrhosis in the US. And there's something that I said here that should hopefully catch your eye, that here the ALT is going to be greater than the AST. Many people just think that that relationship obtains for alcoholism only. Yes, it obtains for alcoholism, but also in the USML Es, it can obtain for non-acorolic fatty liver disease.

They're going to give you a person that has like a lot of fatty deposits in the liver, or you see these weird elevation in their LF Ts and again, ALT with greater than AST. And they don't have race factors for classic cirrhosis. Like for example, they won't have any history of head B. They won't have any history of hep C. They won't be alcoholics. I can totally see the USML Es giving you a question where while the ALT is greater than the AST, they'll tell you in the Houston clarity that this person is not an alcoholic, but they'll put alcoholism as an answer. They'll put an alcoholic fatty liver disease as an answer. Make sure you pick the answer that says non-acorolic fatty liver disease. Remember, non-acorolic fatty liver disease has two kinds. One is called non-acorolic fatty liver, which has a test of a better prognosis. And then the second one is the non-acorolic stiato hepatitis. That one is really bad. It hasitis and the name inflammation that's not happening in the liver. The person is going to get in a lot of trouble. Now, what if they give you a question about a person that like a female, she has all these neuropsychism thumbs. And they tell you that these neuropsychism thumbs have become more frequent since she started using a corporate UD. When you see something like that, you want to think about well-sense disease. Well-sense disease. Well-sense disease. Well-sense disease. Well-sense disease.

So you're going to see these people, they're going to have neuropsychism thumbs. And you're going to notice that they're going to have a low serum, seroloplasmic. When you see that combination, I want you to think of well-sense disease. Remember, it's almost like this, but we'll have like copper excess. That's why the copper UD is contraindicated in these people. That's why we noticed this person's neuropsychism thumbs, we came more frequent once they got the copper UD. Again, I know he may be like, man, the way this is a really bizarre presentation. But I promise you, the presentation is certainly want to know for you for your exams. So again, well-sense disease. Remember, it can cause a serosis. That copper deposition in the liver can ultimately mess up the liver. And remember, another disorder that's not liver related, which is neuropsychism thumbs. You see a young person, they have neuropsych symptoms and they have red urine. If you see something like that, I really hope you think about I could enter methane, poupharia. I don't know, you're just going to come to mind, just figure it out through this as a side point. You see neuropsych symptoms, you see red urine, think of acute intermissing poupharia. Remember, that's an autozomo dominant disorder. Will you have a deficiency of an enzyme known as a poffobili-no-gindiamines, poffobili-no-gindiamines, some of these hymns and facies pathway disorders? Okay, let's go back to serosis.

I really want to hit serosis hard because it's something that's having more and more increased emphasis on exams. So, what if they give you a question about a person that has been having a lot of breathing problems, they're really struggling to breathe, they have this chronic cough, and they tell you that you see a long hyperinflation on chest x-ray. And again, these people's LF Ts are elevated. When you see stuff like this, you want to think about off-one antitripsin deficiency. Remember, off-one antitripsin deficiency, the problem is when you have the mutation, you're off-one antitripsin is misforted. Whenever something is misforted, it can cause a poptosis of the cell that is not 14 properly. Well, in this case, off-one antitripsin is made in the liver, if it's not fully properly, it's going to cause a poptosis of your hepatocytes that can lead to serosis. And obviously, that means fully that off-one antitripsin that never mixes with to the lungs. Remember, off-one antitripsin is an anti-protease. It helps you deal with proteins in the lungs. If you don't have it, then proteins are going to tear apart your lungs, you're going to get a panaceinar and physema. That's pretty high yield to know, for example. You're going to see a person that has long liver problems, think of off-one antitripsin deficiency. That can absolutely positively lead to serosis. And then, what if they give you a question about a person that, you know, they have elevations in their LF Ts.

And you notice that, man, this person has like chronic fatigue. They have a thralgeas. You notice that their A1 C is pretty elevated. When you see stuff like this, that's going to be hemochromatosis. Hair-editri hemochromatosis. Again, I know I'm maybe giving you some presentations that seem bizarre, but that's actually my goal here. I want to give you some of these red herons that we pop up on exams. I probably not even see any resource. So this person has a heroditri hemochromatosis. They're going to see chronic fatigue. There are many things you can see. You can see a thralgeas. Remember, hemochromatosis has a very strong association with calcium pyrophosphate deposition disease. It has that pretty tight association. So they can have a thralgeas, they can have diabetes. Because remember, it's like an iron overload disorder. They have a ton of iron. That iron can incite the fainting reaction. When it incites the fainting reaction, it's going to literally explode in your organ. It's in deposit. It can deposit in the pancreas. Most of these people's beta cells that don't have diabetes. They can have skin bronzing. They won't call it bronzed diabetes. No, that's ridiculous. They're not going to call it that on your exams. They're going to tell you the person has diabetes. They have skin hyperpigmentation. And then you may think that, man, if I couldn't just be cushions, but no, it's not going to be cushions because they're going to give you other things.

You may see signs of hypo-petuitarism. Or you can also see cardiac issues. Because remember, hemocromatosis can cause restrictive cardiomyopathy. So the person can have like, that's not like this function of the heart. So many times, those people are going to have like an S4 heart sound. They're going to put all those things together for you. When you see that cluster of symptoms, you know that, yeah, I don't think I'm dealing with, I'm not dealing with cushion syndrome. This sounds an awful lot like a hemocromatosis. So kind of keep that in mind. I remember it's an Oluzoma recessive disorder. And typically, you're going to notice that they're going to have an increase in the afferating and an increase in the transverse saturation. You can actually use either or both as a way to kind of screen for hemocromatosis. And then what if they give you a question about a person? That's this, you know, rapid onset abdominal pain. It literally shows up very rapidly. They have like this rapid onset abdominal pain. They have societies. They have a pato-megal-y, right? And they tell you that, man, this person has a history of like an efferate syndrome. When you see something like that, I want you to think of what of bud-kiari syndrome, bud-kiari syndrome. And then maybe like, divine, bud-kiari, how did you get there? Well, let me explain. Again, that's the thing. See, let me tell you this folks. The people that write the USMLE is, they are all about integration these days.

Because again, they recognize, this is something I teach a lot in my testing and strategy scores. The USMLE is, and also in my review courses, the USMLE is, they recognize that many people are just memorizers these days. So they try to see if you understand, and then they try to see if you can see links across the spirit topics. Because think about it, how does nephrodite syndrome relate to a bud-kiari syndrome? Maybe like, divine, where is the link? Well, let me explain. Remember, bud-kiari syndrome, bud-kiari syndrome, bud-kiari syndrome is from bosses of the hepatic vein, right? We call it hepatic vein thrombosis, right? So typically, what is going to present is, you're going to see a person that develops rapid onset, rapid onset, because you're going to see rapid onset, abdominal pain, ascites, and hepatic vein thrombosis. Think about it, most times when people develop ascites, it's not rapid onset, it's going to be gradual onset. You should people that have like malignancy or people that have cirrhosis. The ascite is going to be gradual onset. When you see this rapid, rapid, rapid, rapid, rapid onset, ascites, severe abdominal pain, and hepatic vein thrombosis, we want to think about bud-kiari syndrome. And many people have learned the classic causes of bud-kiari syndrome on the exam. Things like paroxys someone knocks on him or the binaria, or you may have also heard of a polysiphemia variant. Those are the two classic causes of bud-kiari syndrome.

But the USML is these days. They're getting very inventive, very inventive. Usually, a person that's going to have bud-kiari syndrome is going to have an underlying hyper-quagulable disorder, right? So you may wonder, okay, divine, so how does the frotic syndrome fit in this picture? Well, the frotic syndrome fits in this picture, because in the frotic syndrome is more just obviously you're going to be losing your urine. And the thing you're going to be losing your urine is antithrombein 3. Antithrombein 3 is an anticoagulant protein. How is it an anticoagulant protein? Well, think about it. In the hippy's factor 2 and factor 10, when you lose something that hippy's factor 2 and factor 10, the factor 12 factor 10 are going to have a longer half-life. They're going to cause you a lot of problems. You're going to have four more clots, and that can cause you issues. So this will kind of have thrombosis of the hepatic vein. You may even wonder, divine, why does p-varium make you hyper-quagulable? Well, think about it. If you have polycythemia vera, because you have that japtum mutation, what do you think is going to happen to your hematocrypt? Your hematocrypt is literally going to what? Skyrocket. It's going to what? Skyrocket. If your hematocrypt is skyrocket, you have so many red blood cells, so much more glubing in your bloodstream. It's going to make your blood more viscous. Whenever your blood is more viscous, it does not flow as fast.

Think about the difference between pouring water and pouring oil. Oil is more viscous. It does not flow as fast. Whenever you have increased blood viscosity, if you remember, plus cells law that you probably learned studying for step one. If you increase the viscosity of blood, it's going to raise the total perfor resistance. That's going to cause bloodstakes. That's going to make your hyper-quagulable. If you think of paracysmon, noxional hemoglobinorium, these people have overactivation of complement medine pathways. Whenever you overactivate complement, it makes your hyper-quagulable. Literally, they can give you Bokyari syndrome in many different ways on your exams. They can make a factor of five lighting question out of Bokyari syndrome. They can make anti-phospholipinantibody syndrome question out of Bokyari syndrome. Just be mindful of that. I don't want you to get really one of my goals in making this rapid review, especially this series, is to give you bird's eye view into the way the USML Is love to test information these days. In fact, I think that's something I may make a separate podcast on. How the USML Is love to test information these days? Just to give people some idea. Maybe that's going to be a good idea for future podcasts. Syrosis, there are many other things. I don't necessarily have the time to discuss them today, but it can give you a question about some middle-aged female, has John Dis, has parietas, has positive anti-matter control antibodies.

That's going to be PBC, primary biliric colangitis. Back in the days, we call it primary biliric cirrhosis, both change the name. There's not primary biliric colangitis that can certainly lead to cirrhosis. When you see a person, he's supposed to be a colitis, inflammatory bowel disease. They have John Dis, they have parietas, they have yellowing of the skin. Many things you're going to have direct type of biliric minimia. Think of PSC, think of primary sclerosis in colangitis that can also lead to cirrhosis. When you see a person, it's a female, she's infertile, and she has this crazy elevation in the EST and ELT, and it tells you that she has positive anti-sport muscle antibodies, well, that's going to be autoimmune hepatitis. What do you mean hepatitis can certainly lead to cirrhosis? And again, remember, whenever a person has cirrhosis, they got to get hepatic ultrasound every six months to screen them for hepatocellula, carcinoma, hepatocellula, carcinoma, hepatocellula, carcinoma. So again, I just kind of wanted to use this rapid review to accomplish two purposes. I want to show you how cirrhosis presents, and also a few other high-altopics, but also to begin to train your brain, to begin to think more and more, like the way the USMEL is wanting you to think.

And again, I offer a bunch of review courses that can help with this, my review courses, they're not lecture-based, they're all going to be question-based, and they use a lot of integrations, a lot of explanation of pathophysiology, a lot of clinical situations and scenarios, an exam scenarios to really help you get the concepts down. For step one, to step three, have a two and a half hour MBA Me test-taking strategy scores, a four-hour bio-stats class, a five-hour social sciences, ethics quality improvement, healthcare systems, a communications class, and then I have a 25-hour step-on review. That's a three-taking place in January. These first three courses I mentioned are taking place next week. Then I have a 20-hour step two step-to-three review. That's going to be taking place the pretty much the third week of this month. And then I have a 100-hour super comprehensive step-to-step-to-three review. That's going to be taking place in May of next year. So if you're interested in any of these classes, you should be an email, I'll give you some more information. This podcast on the major apps Apple GoGoSpoly 5, I have a You Tube channel, Divine Intervention, you have somebody podcast and videos, check it out. You're going to find the videos that I have posted on there. Then I have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. It's a website that many people have used, found it to be extremely helpful.

From a biblical perspective, I try to go over a life lesson about two life lessons every week. There's actually an Apple podcast associated with that, called the Divine Intervention Life Lessons Podcast. So I'm going to stop here because this is our update review series. I like to keep these on the 20 minutes whenever I can. But I'll see you in episode 496. I'm a wonderful rest of your day. God bless you. Bye for now. Thank you.

Bell's palsy affects both upper and lower face muscles; MCA stroke only affects the contralateral lower face.

A brainstem lesion (e.g., cranial VII nucleus issue/Bell's palsy), as the upper face receives collateral blood supply from both sides.

Rapid onset abdominal pain, ascites, and hepatic vein thrombosis.

ALT > AST.

Neuropsychiatric symptoms combined with low serum ceruloplasmin.

Acute intermittent porphyria (AIP).

Bell's palsy affects upper and lower face; MCA stroke only affects the contralateral lower face.

Polycythemia vera (or other conditions causing erythrocytosis).

Non-alcoholic fatty liver disease (NAFLD).

Alpha-1 antitrypsin deficiency.

Low serum ceruloplasmin levels combined with neurological symptoms.

Primary biliary cholangitis (PBC) or other autoimmune liver diseases.

Budd-Chiari Syndrome.

Bell's palsy affects upper and lower face; MCA stroke only affects the contralateral lower face.

Polycythemia vera (or other conditions causing erythrocytosis).

Non-alcoholic fatty liver disease (NAFLD).

Alpha-1 antitrypsin deficiency.

Low serum ceruloplasmin levels combined with neurological symptoms.

Primary biliary cholangitis (PBC) or other autoimmune liver diseases.

Budd-Chiari Syndrome.