DIP Episode 449 - USMLE Step 2/3 Rapid Review Series 93

Okay, welcome. My name is Devine. This is episode 449 of the Divine Intervention Podcasts. In today's podcast, we're going to be continuing the Rapid Review series for the USM Listep 2 CK and step 3 exams. This is going to be series 93. Let's get right to it. So what if they give you a question about a two-year-old boy and the tell you that he has had multiple fractures and the tell you that they see all these cigarette marks on his skin and the tell you that he's brought into the hospital by his mom because she noticed that three days ago he had become less and less responsive and the tell you that on physical exam he has a retinohemorrhage and the tell you that brain imaging shows increased radio density. So obviously the increased radio density is going to be from bleed. If you see this, what should you think about? I really hope you're saying, um, divine. This sounds an awful lot like child abuse. Child abuse is something that you need to be able to recognize on exams and there are certain things that will tell you that this is child abuse in a question. One, parents that are very young, so like teenage parents for example, that's a very classic risk factor on the USM and the exams. Two, when does an unstable situation at home? Think also about potential child abuse. Three, they can write a military question involving child abuse on your exam where you see a person who just came back from deployment and then everything just goes downhill for their kids.

You see stuff like that you really want to think about child abuse and obviously if you suspect child abuse you're going to call child protective services. Another feature I'll say four is when you see parents coming to physicians for help with health problems in their kids on a delayed schedule. When you see something like that, that should tell you that, um, there's something kind of wrong with the care of these parents for their kids. That's probably going to be child abuse as well. Five, if you also see unusual patterns, fracture patterns, right, like spiral fractures or you see fractures of the sternum, you want to think about child abuse also going on. Six, if you also see one child's, to be honest with you, one child's by proxy where for example, parents are simulating diseases in their kids so that they can get that medical attention. That's a kind of child abuse. All those are indications for calling child protective services. Seven, the physical exam findings can be very, very helpful. When I see right now, hemorrhages in a little kid or you see like a subgirl, he might play in a little kid, these are all telltale signs of child abuse. In those circumstances, you need to consult child protective services. Then obviously in the case of one child's, by proxy, the parent is going to require some kind of psychiatric evaluation and help. That's pretty high yield to know for exams.

But what is another thing that our friends at the USMELIS can kind of throw in a question like this one I raised to try to mess with your head. They come through in osteogenesis imperfector. Osteogenesis imperfector is something that can absolutely cause many of these things that I'm discussing. But what are the things that are going to tell you that this person has osteogenesis imperfector? First things first, you're going to see multiple fractures. So kids that have osteogenesis imperfector with very little trauma, they have a ton of fractures, a ton of fractures. That's one. Two, many times you're going to notice that you're going to have a blue sclery because remember, in osteogenesis imperfector, it's a problem with type one collagen. When you have poor type one collagen because type one collagen is also found in the eye. You'll find it in the sclerer. So the thing is because the sclerer doesn't have adequate amounts of type one collagen, then the choroidal vessels that are below the sclerer, they become more visible. It's not like someone comes and adds blue pigments to their sclerer. No, that's ridiculous. The sclerer contains type one collagen, they don't have an optype one collagen in the sclerer. So the choroidal vessels that generally lie beneath the sclerer that you're not supposed to see, they become more visible. It's almost like you have a more transparent sclerer. That's why they have the blue sclerer. That's the pathophase in the blue sclerer.

So if you see a child, a lot of fractures with very little trauma, but you see blue sclerer is not child abuse. It's not child abuse. It's not child abuse. It's going to be osteogenesis imperfector. And remember again, it's a type one. Remember, OI, OI is the abbreviation that I should make you think of like a one. That's a type one collagen defect. It's a type one collagen defect. Pretty high yield to know that stuff, for example. And again, it's in Herithid and an Orozomodominant fascia. Right? And many types people that have osteogenesis imperfector, they're going to have hearing problems. Because again, remember your middle ear bones. Your middle ear has these ossicles, the malios, the incos and the steppes. Those things remember bones contain type one collagen. If those bones don't work, you're going to get what? A conductive hearing loss. You're going to get a conductive hearing loss. That's pretty high yield to know for, for example. Now, another thing that people usually, and many times I think is probably like smarts to know for exams, that if for example a woman has osteogenesis imperfector or her fetus has osteogenesis imperfector, C-section may not be a terrible idea in those people. Because if they come through the breath canal, that vagina is going to absolutely just do a number on those kids. You don't want that. So in that case, a C-section is not a bad idea. That's a very classic question.

I want to know for you, you have to use them in the exams, by the way. And then, you know, one of the disorder that people tend to confuse osteogenesis imperfector with is acondroplasia. So acondroplasia kind of presents similarly. But in acondroplasia, the critical things you're going to find is you're going to see a child that has a short stature. You're going to see frontal bossing. That's a very classic thing, right? So the ahead, it's kind of like the front of your head is like big and almost looks like a truck is looking, is almost like you're staring at a truck, right? So you're going to see frontal bossing, short stature. And many times they're going to have like bow legs and all those things. But typically you're not going to find a blue scler. Typically you're not going to find multiple fractures. When you see something like that, I want you to think of e-condroplasia. I want you to think of e-condroplasia. So what are some critical differences between e-condroplasia and osteogenesis imperfector? Well, I've given the differences in clinical presentation. That's something to know. But the genetic mutation, again, I said that in people that have osteogenesis imperfector, it's a type one collagen defect. But people that have e-condroplasia, the problem is in FGFR3, fibroblast growth factor, receptor 3, FGFR3. That's another key difference. Now, similarities that both of those disorders are in herithylin and in an orzomodominant fashion.

Although many times when people have osteo, when people have an e-condroplasia, most times it arises from a sporadic mutation. So that's how you can give birth to a child that has e-condroplasia. Well, you the parent doesn't have e-condroplasia. Many, many times e-condroplasia arises from a spontaneous mutation. And I don't know why this off-shoots is just kind of coming to my mind, but let me talk about it. There are certain diseases that are not really heritable. They arise more from spontaneous mutations and exams that are pretty high or to know for exams. Number one is see-vit. Comunovurable immunodeficiency is not like you pass it onto your kids. No, usually arise from a spontaneous mutation. Another classic one you may see, that many people think is a genetic disease, but it's not. Even if it has genetic underpinence, it doesn't mean it's heritable. It's paroxysmone-nautonal hemoglobinary. PNH, PNH is not a heritable disease. It typically arises from a spontaneous P-A mutation. Okay, let's go back to these things. So we said a similarity between OI and e-condroplasia is the presence of all those other dominant inheritance for both. But now one way thing that our friends at the USMLE and this one, they can absolutely drone step two, step three. Because it's a basic science detail, but it's kind of important. But it's something that people learn more for step one, but then it kind of gets shaved off of their memories for step two and step three.

It is the fact that Osteogenesis imperfecta is a problem with both endocondrial and intramembranos, as in term, membranose bone formation. Okay, OI is a problem with endocondrial and intramembranos, intramembranos, bone formation. Intramembranos is spelled INTRA, MEM, B-R-A, N-O-U-S. Andocondrial is spelled IND-O-C-H-O-N-D-R-A-L andocondrial bone formation. Osteogenesis imperfecta, because there are many mechanisms of bone formation, those are like the two major ones you want to know for your exams, right? Andocondrial intramembranos, I'm not going to go into the details of those, that's more appropriate for like a mainstream podcast, that's against a rapid review podcast. But Osteogenesis imperfecta is a problem with both endocondrial and intramembranos bone formation. But acondroplasia is primarily a problem with endocondrial bone formation. Again, it's one of those rare things where you know when you reach some of these USMD questions, you're reading the question and you're like, oops, I know exactly what they talk about. And then you look at the answers and you start scratching your head, that's a very classic thing they can do. You know, they can describe an acondroplasia question. And then they'll say, I mean, they won't tell you the person has acondroplasia, but they'll give you all the classic findings and then they'll say, which of the following is the most likely pathophysiology behind this clinical presentation?

And you'll be waiting for FGRFR mutation as an answer. Well, then you may see a problem with endocondrial ossification. And you see another answer that says a problem with both endocondrial and intramembranos ossification. Right? Acondroplasia, look at the name, condroplasia is a problem with endocondrial ossification. But in Ostegenesis imperfecta is both, it's a problem with both intramembranos and endocondrial bone formation. Okay? So make sure you can differentiate between those two things when you exams. Okay? Very, very important to make sure you can differentiate between those two things when exams. Okay. Now, what if they give you a question about a patient? The tell you that this patient is, you know, has been altered, hasn't been doing well for the last few hours, and it's going to be a young person. This thing I'm going to discuss now, can you happen in old people? Absolutely. But like 95% of the time on exams, many times he happens in the young. And he can even happen in kids. Believe it or not, this is something that he even like to throw slap on kids on exams. And they can say, you know, this person's heart rate is like 200 or 300 and something like some crazy high heart rate. And then they should be on EKG. You notice the QRS complexes are narrow. And the spaces between the QRS complexes are the same. When you see something like that, what should you be thinking about? I'll really be saying, oh, divine, this appears an awful lot to be an SVT.

This is a super ventricular tacky card. It's from above the ventricle, so it makes sense that the QRS complex should be narrow. And also, the fact that the spaces between the QRS complexes are equal tells you that it's a regular rhythm. It's not a regular like E-Fib, or anything like that. So this person has SVT, super ventricular tacky card. So how do you manage super ventricular tacky card on exams? The first thing you need to ask yourself is the presence stable or the presence on stable? Is the presence stable or is the presence on stable? If the person is stable, then you can start off with vagal maneuvers, you know, massage the carotids, put your head in water, tell them to blend to a straw. Why does that work? Well, that's going to work because if you think about it as you massage the carotids, that's going to tell the borrower receptors is going to trick the borrower receptors into thinking that there's a crazy, crazy high blood pressure. So when your borrower receptors, you know, through cradios 9 and 10, you know, the glysopharine gel nerve and the vagal nerve to top to the brain, the brain will be like, okay, well, let's send the prostate pathetic discharge. Typically, that's going to be through, again, cradios 9 and 10. You send that prostate pathetic discharge, it's probably going to be more cradios 10. You send it to the heart and that prostate pathetic discharge is going to slow the speed of conduction through the EV node.

It's going to slow that speed of conduction. If you slow that speed of conduction, you can terminate that tacky rhythm. However, if those vagal maneuvers do not work, then the next thing you need to consider is adenosine. Interconciter adenosine. Adenosine is a drug that can very quickly terminate SVT, it can basically break your EV node. You can essentially just shut it off for a very short period of time. And then if you shut it off, that can kind of give the heart a time to almost like restart itself, although it's a very short-lived drug. Many times, you know, after you do that, you need to put those people on some kind of negative, like some kind of negative coronal trope to keep them at a good heart rate. So you're going to like something like a beta blocker or a non-dihydroperiodine consumption channel blocker, like Vera Permail or Deltaism. Okay, so notice all these steps have talked about is for a person that has SVT and is hemodynamically stable. Okay, for a person who has SVT and the hemodynamicly unstable, you should not do any of these things I just said. So how do you know a person is hemodynamicly unstable because some people keep saying, wow, this resource says person that is hemodynamicly unstable, what in the world does that stand for? Well, if a person is altered or if you see a person that is very hypotensive, look at those people's vitals, the blood pressure is a dead giveaway. Persons is like very hypotensive and they'll be very to gippnic.

I noticed that they're like failure responsive. Oh, that person is probably hemodynamically unstable. In those circumstances, the smart play is synchronized, cardioversion is synchronized, cardioversion. This is something that many people fall for an example. They're like, oh, the only time we do synchronized cardioversion is when a person has VTAC and they're hemodynamically unstable. To be honest, we feel most tacky arrhythmias, mostly all, but most tacky arrhythmias when the person is hemodynamically unstable, the right step is synchronized cardioversion. And remember, synchronized cardioversion has many names that are friends at the USMELES can't go through on there. Right? So they can call it synchronized cardioversion, they can call it DC or direct core in cardioversion. Sometimes they can call it DC or direct core encounter shock. Those are all names you'll be seeing your exams for synchronized cardioversion. Remember, synchronized cardioversion is not defibrillation. That's a common error that many people that have this job description of being met students make. Again, synchronized cardioversion is not the same thing as defibrillation. Defibrillation is unsynchronized cardioversion. I'll say that again, defibrillation is unsynchronized cardioversion. That usually is done in two situations on USMELES. Either you have VFED or you have VTAC with no pulse. Those are the two classic situations where you defibrillate. Acistually is not defibrillated.

PEA, postless electrical arrest is not defibrillated. Because many people they think, again, you may even be deceived by the stuff you watch on TV. All these shows where a person goes into a sisterly and they start shocking the heart. That's literally the wrong thing to do. You're literally making it less likely that you're going to come back. It's just one of those weird things you kind of want to keep at the back of your mind, for example. Again, if you want more information on ACLS, go to my ACLS podcast. It's one of my 7-O podcasts, super, super high yo to know for your exam. It's called the ACLS podcast, the ACLS podcast. So again, be careful. For pressing as SVT, the human and the human stable, your next step is synchronized cardioversion. Okay, your next step is synchronized cardioversion. The next step is synchronized cardioversion. Okay, now one other thing I kind of want to comment on today that I think it's pretty high yield, for example, but people don't be enough attention to it during PhDs. Right? And the one you probably care the most about are basic urine PhDs. So what are the pathologies you miss hearing, your USMEL exams? I can kind of whip you up into shape on. Hmm. Basic urine PhD. Well, there are two things you want to think about. Right? One, they can give you is a person that has flunk pain, they have hematuria, and they're just in so much pain. It just hurts so bad. They don't even know what to do.

When you see something like this, I'll really be saying, hmm, divine. Sounds an awful lot like this person has a kidney stone. Person has never been thesis. Obviously for person has never been thesis. The diagnostic test is, I mean, you're going to get a renunciation. You're going to see a lot of blood. You're going to see a lot of blood. Okay? You're going to see a lot of blood. So you'll see like three four plus blood, you're going to see a commensurate number of red blood cells. Right? So you're going to see like 30, 40, 50, 60 red blood cells per high power field. Again, comparing contrasts that would rub them my own six, where you see three or four plus blood. But you do the urine microscopy, and you're seeing like zero three red cells per high power field. You see no muscle red cells, because those things you thought was blood on your analysis is actually myoglobin. Something you want to be careful about. Right? Well, people that have kidney stones, they're going to have legit blood in their ear. Right? And many times you're going to get a non-contrast CT, a non-contrast. You don't want to get contrast. Contrast CT is kind of the abdomen is for is for pilot, not for kidney stones, because if you give contrast, then you're not going to see the kidney stone, because the contrast is going to obfuscate the stone. You don't want that. That's probably not a good thing. So I'll encourage you to get that non-con abdominal CT. You're going to see it.

You're going to see sometimes they call it a helical CT on exams. Just kind of keep that about your mind for tests. But again, let's talk about the urine pH. So they tell you that, oh, this was your page is like seven or seven point five or some crazy high number. When you see that, they ask, oh, what's the most likely geology of this kidney stone? I would really hope you're saying divine. Sounds a lot more like a like a ures positive bog, like a ures positive bog. So something like proteospinarabilus, that's probably like the big one. Right? Probably the big one. Remember, it's a ures positive bog. So it causes these staccorn calculus. So the person probably has ammonium magnesium phosphate stone. We call those things the staccorn calculus. Right? Many times you can see a picture on your USM exam like a radiograph. I'm going to see these things that look like antlers. When you see that, that's a staccorn calculus. When you see stuff like that, think about ures positive bogs. Typically proteospinarabilus is one of those things, if you're probably remember from step one, that it grows with a swarming motility, because with a swarming motility. It can cause that. But also do not forget staphsaprophidicus. So if you don't see proteospinarabilus as an answer, an answer you should consider is staphsaprophidicus. Remember staphsaprophidicus is the second most common cause of UT Is in sexually active young females. Remember the most common cause of UT Is is equal. Right?

But about 15 to 20% of UT Is are caused by staphsaprophidicus. So price, surprise, staphsaprophidicus is a ures positive bog. So if you see a person that has a UTI and they have very basic hearing and you don't see a proteospinarabilus as an answer, you probably want to consider staphsaprophidicus. So when you consider staphsaprophidicus. So remember normally your UMP should be less than 5.5. If you see a person's UMP and it's over 5.5, those people's URI, that person's URI is basic. Okay? That person's URI is basic. So they want to keep on the back of your mind for instance. So now, so if you may be like, hmm, divine. What is another thing that causes a basic hearing teacher? Say there are two things you should keep in mind. The second one you should keep in mind honestly is maybe think of a situation in your kidneys where your alpha-intercalated cells don't work. Remember those alpha-intercalated cells, they can have this thin coat of proton pump. That proton pump is like a proton hydrogene, I mean proton potassium. So hydrogen potassium ATP is pump. If that pump doesn't work, they're not going to be able to put hydrogen ions in your urine. So think about it. If you don't put hydrogen ions in your urine, those hydrogen ions are going to be stuck with them. They're going to sting your blood. If those hydrogen ions sting your blood, you better believe they're going to knock down your bicarb. So you'd be like, divine.

The cells are not full of like your describing the metabolic acid doses. Ah, yes, I am. Actually, to be a little more specific, I'm describing a normal anion gap, but a body got a sedosis. To get even more specific, I'm describing a renal tubular acidosis. To be even more specific, I'm describing a type 1 RTA, a type 1 renal tubular acidosis. Remember, that's the distal renal tubular acidosis. So in that, the primary pathophase behind a distal RTA is that you literally do not have a well-functioning alpha-intercalated cell. So you're not able to put protons in your urine because the thing is that alpha-intercalated cell, that proton pump literally helps you put protons in your urine and that acidifies your urine. It keeps that urine pH nice and solid below 5.5. But if that thing is not working, your impage is going to be really, really high. That's not the thing that can cause basic urine. In fact, if you ever see an RTA question, in person's urine pH is over 5.5, you're pretty much stopped reading the question. The person has a type 1 RTA. Again, remember, it's also called the distal RTA. The fact that it's a type 1 RTA does not mean that it's proximal. The proximal RTA is the type 2 RTA. That's the one where you have issues with bicarbary absorption from things like acetazolemine, for example. If you have like fancone syndrome, fancone syndrome is where you have like a global proximal covalerated tubular absorption defect.

And they don't forget that type 4 RTA at the ones where you have a like low out dust rune. It's the low out dust rune RTA. So if you see a person that has an RTA and they have like adicence disease, for example, all their teakine and adicence are antagonists for heart failure. So say, for example, they're taking like spermolactory and perino. Those things basically simulate a low out dust rune state. Those things are causing type 4 RT As. And one of the brilliant things that can tell you that you have a type 4 RTA is hyper chilemia. Because think about it. One of the jobs of our dust rune is that it causes you to put potassium in your urine. So if you have a low out dust rune state or you're blocking out those chile receptors, then you're going to put out those chilemia urine. Whatever you don't put in your urine, you're going to hold onto it in your blood. So you're going to have hyper chilemia. That is the only RTA that is associated with hyper chilemia. So hopefully I've kind of giving you like some very nice tips and tricks that can help you differentiate the three RT As. Right? There's type 2, there's type 4, and there's type 1 RTA. They are other kinds of RTA beyond those, but those are beyond the scope of the USML Is. So we're not going to discuss them at all. But a type 1 RTA is the distal RTA, the classic feature you're going to see that's going to make you think about that on exams. Again, it's going to be the presence of a higher NPT. Your NPT has over 5.5.

The two other RT As, the type 2, which is the proximal RTA and the type 4, which is the low out dust rune RTA, are associated with a normal urine peach. The urine peach in those situations is going to be less than 5.5. So I'll give you different shades of those to check the potassium. A present that has a type 2 RTA is not going to, generally you're going to have like hypochylemia, but a present that has a type 4 RTA, the low out dust rune RTA, is going to have hyper chilemia. And again, I've literally explained the pathophys behind all these things. If you know these unique features, you don't have to even dig like crazy, crazy, crazy deep to understand your RT As. So I think I'm going to go ahead and stop here. Again, I kind of like to keep these podcasts at a 20-minute mark. But again, I do offer review courses for step 1. I have some coming up in April for step 2 and step 3, also coming up in April. And I also have a bi-statistic class, social sciences, ethics, healthcare systems, quality improvement, communications, and professionalism review. That's a 5 hour review. Many people have taking these courses, funding to be extremely helpful. I've all wanted to do it for all the USML exams, pre-clincoma, school exams, 30-ish-elf exams. I have these podcasts on the major apps, Apple, Google, and Spotify. And then I have a You Tube channel to find intervention, USML, podcast and videos. That's where you're going to find some of the videos that I make.

And also post some versions of this podcast on there as well. And then I have a new website called divininginterventionlifelessons.com, divininginterventionlifelessons.com. Basically, I post two life lessons that are based on scripture, that are based on the Bible. And many people have found them to be extremely helpful, like post to every week. There's even an Apple podcast as a sheet of that called the Divining Intervention Life Lessons podcast. And then I also help people with eras applications, mock interviews, recliders, personal statements, and things like that. So thank you for joining me today. I will see you next time. I'll see you in a piece of 450. Have a wonderful week. God bless you. Bye for now. Thank you.

Blue sclerae, due to defective Type I collagen making underlying choroidal vessels visible.

Synchronized cardioversion (or DC cardioversion).

Struvite stones (staghorn calculus).

Type IV Renal Tubular Acidosis (RTA).

Staphylococcus saprophyticus.

Endochondral bone formation.

Defect in Type I collagen synthesis, affecting both endochondral and intramembranous bone formation.

Urine pH > 5.5 (Failure of alpha-intercalated cells to acidify urine).

Type II RTA typically causes hypokalemia; Type IV RTA causes hyperkalemia.

Adenosine.

Non-contrast helical CT scan.

It can worsen outcomes and is generally reserved only for V-Fib or pulseless V Tach.

Defect in Type I collagen synthesis, affecting both endochondral and intramembranous bone formation.

Urine pH > 5.5 (Failure of alpha-intercalated cells to acidify urine).

Type II RTA typically causes hypokalemia; Type IV RTA causes hyperkalemia.

Adenosine.

Non-contrast helical CT scan.

It can worsen outcomes and is generally reserved only for V-Fib or pulseless V Tach.