DIP Episode 487 - USMLE Step 2/3 Rapid Review Series 104

Welcome, my name is Divine. This is episode 487 of the Divine Intervention Podcast. In this podcast I'm going to be continuing the Rapid Review series for the USMELIST of 2 CK Step 3 exams. This is going to be series 104. Let's get right into it. So, what if they give you a question about a 25-year-old male and the teller that he's 6'5", tall and for the past 12 hours he has had very significant chest pain. And then they tell you that his blood pressure is 115 over 80, his heart rate is 85 beats per minute and his respiratory rate is 19 breaths per minute. Now you have an axe for the next best step in diagnosis. Well, I really hope you're saying, oh Divine, sounds like we're going to get a chest CT angiogram with contrast. This person clearly has an aortic dissection. I may wonder, Divine, how do you know this person has an aortic dissection? Well, pretty straightforward. Number one, the person is 6'5", tall. The USMELIST is not just going to give heights of people for no great reason. It's kind of ridiculous, right? The pretty more teller the person has a morphine syndrome. So the person likely has a morphine syndrome and morphine is a member that can have a cystic medionicosis, which we call cystic medionic generation of the aortic media. And because of that they can have dissection. And if you look at the vitals that I give you, because this person is totally fine from a vitals perspective, you know, they have the chest pain, but they don't seem to be very important.

Then it makes sense to do a CT chest angiogram with contrast. That's how you diagnose aortic dissection when a person is stable. But for persons who are aortic dissection and they're hemodermic here on stable, they're going to do a TEE, going to do a transist of a gel echocardiogram, going to do a transist of a gel echocardiogram. Now, so what you may see, Divine, is there something else that could be the right answer in this question? Absolutely. Something else that could be the right answer in this question is the person having some kind of pneumothorax, pneumothorax. But the thing is, if they want you to think pneumothorax, they will give you something along the lines of decreased breath sounds somewhere. They will give you something about maybe the person having like, you know, jog lavenos distension or whatever, right? Or, you know, just something that goes along the lines of, wait, wait, wait, this person is not doing very particularly well. So that's one thing they can easily test on your exams, right? But, you know, if you give me a more transparent patient, you'll probably go in after aortic dissection. That's probably the first thing I think about if I were you. And again, real quick, what are the key details to not about morphine syndrome? Remember, first things first, it's an Orozomo dominant disorder, right? So if, since it's an Orozomo dominant disorder, most people that are born with it, they have one of the bad genes, right?

Usually they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, they're born with a lot of morphine syndrome. So, you know, how many of their children or what percent of their children are going to have, are going to have problems? Well, I would really hope you're saying, oh, divine, like 50% of their kids are going to have problems. Well, how did I do that math? Well, big A little A, multiplied by little A little A. If you work it out, you have big A, little A, you have big A, little A, you have little A, little A, you have a little A, little A, right? So, basically like 50% of their children will be completely normal. And 50% are going to have morphines, right? I remember morphines, the problem is with a, it's a fibrillin defect. Fibrillin is like an extra cellular protein. Basically, if it's messed up, then your euric media has not got a hold up very well on your test, honestly. And then you're going to end up getting a lot of, a lot of trouble. So, they can have things like euric dissection, they can get my trovaf prolapse.

And remember, they can also get, like aneurysms in the circle of willis, they'll be more like a headache presentation. It'll be like a cured headache, be like a cured headache presentation in those, in those folks, right? So, something you kind of want to think of, keep at the back of your mind as you're studying for your exams. And I remember, put a half a morphine, they probably shouldn't be doing contact sports. Kind of seems like a wonderful way to rupture the order. So, those people, contact sports are not a good idea for those people. And honestly, something I'm sure is pretty, pretty high to know for your exams. So, again, chromosome 15, fibrillin defect, autosomodominant inheritance, they will have a mitrovav prolapse, aneurysms in the circle of willis that can pop rupture, cost a brain, brain bleeds, they can give it the euric dissection. And again, I've kind of worked out the genetics of it. If the mario-son that does not have marphans, basically, they're going to have a 50% of your kids that don't have marphans, and 50% will be completely normal. Okay? I remember, when you're dealing with an autosomodominant disease, careers is not really a big thing. If you have the bad gene, you're going to get in trouble, simple and straightforward as that. Okay, now, another thing I want to kind of go over here are the different kinds of hemoglobin. I feel like many people kind of watch these hemoglobin, and they just pop up often enough on the exam.

You kind of know what they represent. So, what's the first hemoglobin I'm going to discuss? Well, I'm going to discuss regular adult hemoglobin. Regular adult hemoglobin has two alpha genes and two beta genes. That's literally how it works, right? It's normal adult hemoglobin is two alpha genes, two beta genes. Now, what if they give you that, oh, a person has anemia? And you notice that in the midst of that anemia, they have an elevation in their hemoglobin A2. If you see a person that has a hemoglobin A2 elevation, you easily want to think of a person that has beta thalacemia on your test. Maybe like divine. What in the world is hemoglobin A2? Let me explain. Hemoglobin A2 is alpha 2 delta 2 alpha 2 delta 2. The thing is, if you have beta thalacemia where your beta-globin gene is almost stopped, then you're not going to have enough to make regular adult hemoglobin, which is hemoglobin A. You won't have enough to make alpha 2 beta 2. So, your body's going to be like, okay, well, what's the next best thing? Let's find these deltas and pair with our alpha. So, you have alpha 2 delta 2. That's going to be hemoglobin A2. If I let me tell you this right now, if you have an increase in hemoglobin A2, I'm going to say that again, if you have an increase in hemoglobin A2, that's almost pathonomonic on the US Emily exams for a person that has beta thalacemia. Person that has beta thalacemia. Now, okay, how about hemoglobin F?

Hemoglobin F, right, is the one that we find in the fetus. That's alpha 2 gamma 2 alpha 2 gamma 2 alpha 2 gamma 2. That's hemoglobin F. That's hemoglobin F. I remember regular adult hemoglobin of alpha, which is hemoglobin A alpha 2 beta 2. We don't really use it much until we kind of come out of the womb, until you pop out of the womb. But hemoglobin F alpha 2 gamma 2, remember, that's the one we use in year-end, that's pretty high year to know. And also, it's pretty high year to know that the drug that can increase your hemoglobin F is going to be hydroxyurea. Hydroxyurea is a drug that we used to treat sickle cell disease. Believe it or not, hydroxyurea is an anti-cancelor drug. It works by inhibiting the enzyme ribonucleotide reductase, ribonucleotide reductase, which converts ribonucleic acid to deoxyribonucleic acid. But it raises hemoglobin F. The mechanism I have never found a good explanation in the literature. I don't think anyone really knows how. I'm sure there's probably some handwavy stuff out there. But again, I've never really said a good explanation as to why. Okay, so if you see a asking for a drug that raises hemoglobin F, think of hydroxyurea, which leads to a tricycle cell disease. Okay, now I want to know another hemoglobin I want to talk about is hemoglobin Barts. Basically, if you see hemoglobin Barts, a person clearly clearly has alpha phallusemia. They have the really nasty one where they literally have all four genes in common.

Because remember for your alpha-globin gene, you have four genes. If all four are messed up, you're not going to be born alive, basically. That's the only kind of phallusemia where the child will die in uterine hemoglobin Barts. So, ultimately hemoglobin Barts, hemoglobin Barts is gamma four. Well, how in the world do you get hemoglobin Barts? Well, think about it. If you have alpha-thal, you know, alpha-thalusemia has like many different gradations, you know, because again, there are four genes that are called phallus-globin. So, if you mess up to, basically if you mess up three or less, you're going to be born alive. But if you mess up all four, you're not going to be born alive. Because you literally don't have any alpha-globin genes. If you have alpha-globin genes, that's going to be problematic. Literally, that's going to be problematic. Why? Because basically, basically, phyto-hemoglobin is alpha-2 gamma-2. Well, if you don't have alpha-s at all, then the gammas are going to be like, man, I don't see any alpha-s to get married to. So, the gammas are going to all pair up together. They're all going to pair up together. And if the gammas all pair up together, you're going to have gamma-4. Gamma-4 is literally hemoglobin barbs. That is not compatible with any kind of meaningful life. So, those kids are going to die in Europe. It's really sad, really sad to say, but those kids are certainly going to be dying in Europe. Okay.

Now, what's the next thing I want to talk about here? Let's talk about hemoglobin H. Hemoglobin H disease is something you'll find also in alpha-thalacemia. We find that in people that have four copies of the, I mean, people that have alpha-thalacemia and three of the genes don't work. Remember, I said if you have three or less of the genes affected, you'll be born in life. But if you have all four affected, you're not going to be born in life. Those kids are going to die in Europe. Those kids are going to die in Europe. Those kids are going to die in Europe. They're going to die in Europe. So, what hemoglobin H disease is something we find when people have alpha-thalacemia and three of the genes are messed up, right? So, basically, three are messed up and one is still functioning. So, 75% of the genes are pretty much gone, but 25% work. But the thing is, again, these people have a very severe depletion in their alpha-globing chains. They don't have enough alpha. So, since they don't have enough alpha, but they've been born, right? If you're born, you need an adult hemoglobin, hemoglobin A, which is alpha-2 beta-2. But, man, because they're like, she doesn't have enough alpha. The beta is going to stop pairing up with each other. The beta is going to stop pairing up with each other. So, they're going to have beta-4. Beta-4 is hemoglobin H. Many times people that have hemoglobin H disease, they tend to be very transfusion-dependent.

They tend to be very, very transfusion-dependent. That's pretty high, you'll know, for example. Now, I know some people may be like, define, can't hemoglobin A2 be increased in alpha-thalacemia? The answer to that question is going to be no. And again, you don't have to take my word for it. You just have to literally understand the mechanism. Think about it. What is hemoglobin A2? And literally, you just said that hemoglobin A2 is alpha-2 delta-2. What globin chain does hemoglobin A2 seem to contain? Contains alpha and delta. But if you ingot alphas, I don't know how you're going to be raising your hemoglobin H2. Right? So, in fact, this question I posed explains why beta-thalacemia can be diagnosed with hemoglobin electrophoresis. But alpha-thalacemia cannot. Wait, what? Yeah, you heard me correctly. Beta-thalacemia can be diagnosed with hemoglobin electrophoresis. But alpha-thalacemia cannot. In fact, I will strongly encourage you on your USMD exams. Vowsha will not peak. Hemoglobin electrophoresis as the way you want to diagnose alpha-thalacemia. Hemoglobin electrophoresis is largely going to be normal in a person that has alpha-thalacemia. Why is that? Well, let me explain. The thing about alpha-globin is that it's like a very pervasive kind of hemoglobin. We find it in almost every hemoglobin of note. We find in adult hemoglobin alpha-2 beta-2. We find in hemoglobin A2 alpha-2 delta-2. We find in hemoglobin F alpha-2 gamma-2. We find in many hemoglobin.

So the thing is, hemoglobin electrophoresis is like a test of relative difference, right? Like, oh, is this one more than the other? So because all these hemoglobin is all quantine-offers, they are all going to be proportionally decreased. So because they are all decreased roughly in the same proportion, you will not see any relative difference. But in beta-thalacemia, you absolutely will see a relative difference because why? The thing is, there is only one major plus of hemoglobin that has beta-globin chains in it, right? Adult hemoglobin alpha-2 beta-2, right? So you're going to notice that why? If a person has beta-thalacemia, the adult hemoglobin is going to be decreased. Well, the others are going to be increased, things like hemoglobin A2, right? You're going to see that relative difference. That's why we can use hemoglobin electrophoresis to diagnose beta-thalacemia. Again, many resources don't talk about this point. What is a very, very high point to know for the purposes of the USMLE exams? All right. Now let's go ahead and continue. So what if they give you a question about a person that has a testicular mass? And then they tell you that the person's beta-hcg is markedly elevated. What may you see? What mass should you be thinking about? We're going to really hope you're saying, oh, divine. Sounds a lot like this person has a semi-noma. Sounds a lot like this person has a semi-noma, right?

Remember, these beta-hcg raisin lesions are pretty high to know for the exams, right? So let's talk about actually just a quick review. What are the causes of an increased beta-hcg on our friendly USMLE exams? So remember one, it's going to be pregnancy, right? For a person's pregnant, your beta-hcg is going to be pretty, pretty high. And remember, your beta-hcg, I think is kind of important to know this. Kind of tops out around like 10-ish or just a little above that in terms of weeks. It's basically tops out after the first trimester. It's also supposed to keep rising, rising, rising, rising, rising, rising, rising, rising, after the first trimester, right? I usually tops out at around like, let's say 110. Just look up the exact number, but I think it's like 110, 120-ish, 1000 roughly. Again, that's like a good ballpark figure to know for your exams, right? Well, if you're starting to see a beta-hcg, so again, the first cause is going to be pregnancy. But if you're starting to see a beta-hcg that are like insane and astronomical, you're like, man, it's basically a beta-hcg, like 400 grand, 500,000, 600,000, 700,000. When you start seeing it going the multiples, multiples of hundreds of thousands, there are basically two things you need to think about on your exam, especially in a woman. Number one, you want to think about this woman having some kind of molar pregnancy, molar pregnancy, right? Justation of probabilistic disease.

That's one thing that causes a very high beta-hcg. And I think that when it causes a very high beta-hcg, it's going to be a choral carcinoma. Choral carcinomas have beta-hcg as their tumor marker, right? But again, if you're looking at a very beta-hcg in a guy, don't you think of a semi-noma. Semi-noma's tend to have a very beta-hcg, okay? Semi-noma's tend to have a very beta-hcg, okay? So what do you think of your question? About a 25-year-old female, they tell you that she delivered healthy newborn through a crash cesarean section, let's say five minutes ago. And then this person is now chemodynamically unstable, right? The person has a blood pressure of like 90 over 75, or let's say 90 over 70, the person's heart rate is 160 beats per minute, the person's temperature is 99.4 degrees Fahrenheit. What should we be thinking about here? This person probably has post-partum hemorrhage. So what in the world do we do for post-partum hemorrhage? Well, the thing is, first was the most common cause. The most common cause of post-partum hemorrhage is already at me. You know, you literally have no tone, right? Usually we have this in many situations. One, actually, it's going to hide you to know the risk factors for you during at-me. Again, you're in at-me just means your myomychrom just is kind of cooped out. It's like, man, I can't contract anymore. Well, what can cause these things on exams? Number one, it can be if you're carrying just multiple kids.

Let's say for example, you're carrying on twins or triplets or whatever. Basically, like, your uterus has had to work harder than the average uterus in the process of being pregnant. So it's almost like, man, it's used up all his energy and carrying all those kiddos. So when he's trying to actually push them out, it's a problem. That's one. Second cause of this is if, for example, a person is, oh, it's the other side I'm thinking about here, if, for example, the person has had a very prolonged labor. So you've been pushing for a very, very, very long period of time. You know, again, myomychrom is a muscle. It's going to get tired and that can cause a urine acne. So when I'm pressing, how's urine acne? Which is the, you know, most common cause of postpartum hemorrhage? What's the first thing I'm going to do? You're going to do a urine massage. Basically, a no-be-line doctor is going to stick her hand in your vagina and be compressing your uterus from the inside and then she's going to be pressing on two of your pubic symphysis, you know, just above it and also squishing your vagina. That's the first thing I'm going to do, urine massage. A urine massage, you almost never put it as an answer on the USM. So let's go to what you do next. But really, that's the first thing you're supposed to do. You're supposed to do the urine massage. Okay, what do you do? Number two, one, number two, if your urine massage is not working, you're going to go to oxytocin.

You're going to go to oxytocin. You're going to give the person the tosin. It's going to contract down the uterus, contract down the myomychrom and that's going to be very, very helpful. And that can help the bleeding. Maybe be like, divine. How does that help bleeding? Well, think about it. Many of the blood vessels that we see in the uterus, they're on in between the myomychrom. So if you squish on the myomychrom by compressing an oxytocin, then that's going to cause those blood vessels to be basically tied off. If they are tied off, then you're not going to bleed any more. But if that does no work, you can begin to try other things like a trinacamic acid. You can try trinacamic acid. Trinacamic acid is actually, you know, many people in the hospital, I think they call it TXA. It's something that's actually very, very helpful for reducing postpartum hemorrhage. Okay, very, very helpful for a gene postpartum hemorrhage. Basically, the way trinacamic acid works is that it's like lysine and it has like anti-fibrenal lytic properties. It basically prevents fibrenolysis. Remember, fibrenolysis has a stronger sejuone bleeding. If you want to bleed, you want to start busting clots. But it basically prevents, it's like the anti-cloth boster. So it's pretty good for that purpose. But it's really easy for a lot of things these days in medicine. Well, if you don't see that as an answer, you can begin to try exotic things like, you know, like it's a prostal.

It's a prostal can help you contract down the uterus as well. Or you can use things like copper prost. Copper prost can also help you, you know, because it's a prostaglandin analog, it can help the uterus contract down. If you're like, why will copper prost help? Well, let me explain something here. Prostaglandins can cause uterine contraction. Prostaglandins can cause uterine contraction. I mean, think about it. How do you think we treat primary dysmeneoria? Well, remember, primary dysmeneoria is when you have a painful period. It's painful mences. Well, why do you get all that pain? It goes to uterus is contracting violently. My armature is contracting violently. So for primary dysmeneoria, we're going to give an inset. An inset is a cycloxygenase inhibitor. And give a coxene inhibitor. That's going to decrease a prostaglandins emphasis. And that's going to prevent the uterus from contracting like crazy. So it doesn't hurt. But in the key supposed bottom hemorrhage, you'll want the uterus to contract down. So you're going to go ahead and give copper prost. You're going to go ahead and give copper prost. If you give copper prost, it's a prostaglandin. It's going to contract down the uterus. It's going to be very, very helpful. Now, the one thing I want to keep you in mind, your prostaglandin is that prostaglandin is bronchospastic. It is bronchospastic.

So if you have a reactive airways, you know, like asthma, for example, a couple of pros, maybe not the best idea in the world. You can also use her. God, I mean, but honestly, these days, people just try to know how to use that stuff because it just has quite a number of problems. You can jack up your blood pressure. Well, it's probably a good thing in this person we have. And that's pretty high potency, but you can jack up your blood pressure. And if there's so many contraindications, right, let's say you have a hysterox strokes, can't really use it because it is a very powerful visual constrictor, right? So it's not good. You can give you strokes. We have a history of MI's. Basically, if you're a person that has like very tenels vessels, or got agents or not, maybe a particularly good idea. Okay, so let's go ahead and stop here. This is going on for 20 minutes. I do offer review classes. I have a bunch of review classes for step one, all the way to step three coming up in November. If you're interested, just shoot me an email and give you some more information. I'll follow on on one to your room for step one, all the way to step three, you know, pre-clean comments, good exams, 30-ish off exams. I have these podcasts on the major apps. Apple Google Spotify. And then I have another website, divineinterventionlifelessons.com. Basically, on that website, I post two podcasts every week that uses a biblical perspective to address a life lesson.

So if you're interested in any of these, just shoot me an email and also have a podcast I made on my website, divineinterventionpodcast.com, where actually have the dates. You know, you can listen to the podcast, but the dates also in the comment tree below the podcast. So thank you for listening to me today. Have a wonderful first of your day. I'll see you in the episode 488. God bless you. Bye for now. Thank you.

A fibrillin defect (specifically affecting connective tissue).

It is an autosomal dominant disorder, meaning there is a 50% chance that offspring will inherit the condition.

Aortic dissection (due to weakened aortic media).

Beta-thalassemia.

Hydroxyurea.

It has anti-fibrinolytic properties, preventing the breakdown of clots (fibrinolysis).

Carboprost or Methylergonovine.

Uterine atony (lack of uterine tone).

Hemoglobin Bart's ($\gamma_4$).

Pregnancy (general), Molar pregnancy/Choriocarcinoma (female), Seminoma (male).

Beta-thalassemia shows a relative difference (e.g., high Hb A2, low Hb A); Alpha-thalassemia does not show a relative difference because all globin chains are affected proportionally.

Fundal massage/Uterine compression.

Prostaglandins (like Carboprost) because they are bronchospastic.

Uterine atony (lack of uterine tone).

Hemoglobin Bart's ($\gamma_4$).

Pregnancy (general), Molar pregnancy/Choriocarcinoma (female), Seminoma (male).

Beta-thalassemia shows a relative difference (e.g., high Hb A2, low Hb A); Alpha-thalassemia does not show a relative difference because all globin chains are affected proportionally.

Fundal massage/Uterine compression.

Prostaglandins (like Carboprost) because they are bronchospastic.