DIP Episode 415 - USMLE Step 2/3 Rapid Review Series 84

Okay, welcome. My name is Divine. This is episode 450 of the Divine Intervention podcasts. And into these podcasts, we're going to be talking about the Rapid Review Series. We'll be continuing our Rapid Review Series. And this is going to be Series 84. So let's jump right into it. What if they give you a question about a newborn? And they tell you that this newborn has seizures. You know, that we're controlled after, you know, they gave appropriate to electrolyte replacement. And in detail, the this child that's age six months, you know, has had like two bolts of pneumonia with a pneumocystis adiorevetsi. And in detail, you want the most likely finding on a chest x-ray. If you see stuff like that, I really hope you're thinking about a de-George syndrome. And the most likely find you on a chest x-ray will be the absence of the cell sign of the thymus. Right? That's pretty classic for de-George syndrome. So what's the battlefield phase? Remember de-George syndrome happens when you're third and you're fourth, far angel pouches do not form. Your third and your fourth far angel pouches do not form. So if they do not form, you'll have no thymus. That's why you have no cell sign on a newborn chest x-ray. And also they have no parathyroid. Right? If you have no parathyroid, you'll not make pteach. If you don't make pteach, you're going to have a lot of problems with low calcium. And that can cause seizures. I remember low calcium on an EKG would show up as a prolonged QT interval.

As you've heard me say many times in the past, most of these notable electrolyte anomalies that have high bull in the name are all associated with a prolonged QT interval. Like hypocalcemia, hypokillemia, hypomagnesemia. Hyponytremia, though, does not belong. Remember hypercalcemia is kind of weird in that it causes a short QT interval. It's one of these weird notable EKG anomalies that causes a short QT interval. And then another thing I think that's kind of imperative to keep in mind here is that if you think about these things with the far angel pouches and stuff, I feel like these, these brinkel clefts and far angel pouches and da, da, da, da, da. You think that it's kind of high you to know but many people just ignore them. It's not to your advantage to ignore them. Right. I will say that in general there's a couple of pathologies that are related to the brinkel clefts that are kind of high you to know. The brinkel clefts, sometimes they call them far angel clefts, the far angel pouches. So let's kind of break this down. So the thing is there's such a thing as a brinkel cleft and there's such a thing as a far angel cleft. They're literally the same thing. They're right from ake dooderm. And then there's such a thing as the far angel pouches or the far angel groves. Again, it's the same thing. If you see the word far angel pouch, you see the word far angel grove. It's literally the same thing. Those are the right from end dooderm.

Now if your third or your fourth far angel pouches do not exist, that's how you get the George. Now if you notice that your second to your fourth far angel groves, I mean, sorry, your second to your fourth far angel clefts, right? Okay, let me, I think let me backtrack a little bit so I don't confuse myself. So the far angel clefts are derived from ake dooderm, simple and straightforward. And then there's the far angel groves or the far angel pouches they're derived from end dooderm. So if your third or your fourth far angel groves or your third and fourth far angel pouches do not form or they're not around, that's how you get the George syndrome. Remember, that's the chromosome 22, Q11 problem where they have again, no thymus, no parathyroid, cleft lip cleft palate and stuff like that. But your second to your fourth far angel clefts, which are ake dooderm derived, you know, there's supposed to disappear on your room if they don't, that's how you have a brinkel cleft cyst. Remember, it's those cysts that are lateral to the, they're lateral to the neck, right? And they do not move with swallowing, right? That's probably a good contrast distinction with the the thyroid glossodoxist, you know, where it's in the midline, because remember normally your thyroid will start from the back of your tongue and from your back of your tongue, thyroid glossodoxo grow down, ballonaut from your thyroid and then the thyroid glossodox disappears.

If it doesn't, that's how you get a thyroid glossodoxist. It's going to be assist in the neck and it's going to move with swallowing because it retains a connection to the tongue and it's in the midline, right? It's in the midline and don't forget your thyroid glossodox again is, is endoderm derived, right? So again, let's just summarize again just to make sure you're really good on this stuff. Your thyroid glossodox comes from endoderm, thyroid glossodoxist is an endodermal issue. Your brinkel cleft cysts come from ectoderm, it's an ectodermal issue. The George syndrome, your third and your fourth far angel grooves, far angel pouch is not being around, that's an endodermal issue. I think another thing I want to talk about that they love to bring with embryology, especially the head and neck, is this whole concept of a craniofarinjoma, right? So it's going to be a supercelemas, it's going to contain calcifications, that's pretty helpful. I mean, some other sometimes you can also present as a person that may have signs of a, they may have signs of a bite temporal hemianopsy, right? Like, basically, a ton of vision. When you see stuff like that, again, think of a craniofarinjoma, again, it's going to be a calcified supercelemas, remember they love to test, that is the right from the roof of the mouth, right? Sometimes they call a rathkis pouch, it's an embryonic derivative of rathkis pouch.

And don't forget that craniofarin jomas, they're especially notable for the fact that again, on histology, you see this mudo-well fluid that they leak, right? But again, it's pretty high you to know that stuff, so just going to keep that in mind. So since we're talking about a lot of neck masses, what kind of imaging do you want to use in general? So this is not a road that works all the time, but in general, it's pretty accurate. When a presence of neck mass, I was strongly encourage you to consider for those people using an ultrasound. Ultrasounds are amazing for neck masses, something you kind of want to keep at the back of your mind for, for example, ultrasound's fine needle aspirations to get tissue, they're very helpful for neck related masses. Again, it's not always the case, right? But it's pretty helpful. Now, what if they give you a question about a patient, and they tell you that this patient, you know, has a histrothcrenic pancreatitis, but that now for the past three days, this person has had an altered mental status, but you notice the person's temperature is normal, the person has like asterisks and all those problems. Obviously, this person has a, this person has a complication of alcoholism, right? Remember alcoholism can really damage your liver, colisptophypertension, you know, you can get cirrhosis, like you can get hyper, hyperamonymia, right? So in this case, this person very likely has like hepatic insephylopathy.

So I know some people may be like, oh, divine. Come on, how do I differentiate this from SBP? Let me explain. People that have hepatic insephylopathy, they don't have abdominal pain, and they typically may not even have a sideys, right? But the thing is SBP typically presents with a triad on exam, a triad on exams. Let me tell you what that triad is. So usually they'll have abdominal pain, they'll have a sideys, and the abdominal pain doesn't have to be severe, but they'll have abdominal pain, they'll have a sideys, and they'll have altered mental status. But if you see altered mental status alone, and you see very literally in the world of abdominal issues, I really want you to think about hepatic insephylopathy. Many times they'll tell you that people that have an hepatic insephylopathy, I forget for, they tell you they're pretty confused. When you see that, they can think of hepatic insephylopathy. And how do you treat that on exams? You can treat it with lactolose, right? That lot because it's the high ammonia that's causing all these problems, right? So that lactolose is converted to lactic acid, and then that lactic acid, acidifies the ammonia, that is being generated in your GI tract and all those things. And that, you know, that lactolastic acid binds to ammonia, and form ammonia, and then that ammonia will come to be excreted. But you may not see lactolose on exams, right? You may see refaxamine, right?

Refaxamine is something that's pretty helpful as well for treating hepatic insephylopathy, right? So lactolose refaxamine, right? Forgetfulness, confusion, no abdominal issues, in a patient that's like a liver patient, has a bad liver issue from alcoholism. And then if a person has liver disease and they're bleeding, what's something that may be helpful in those people as treatment? Well, I'll really hope you're saying, hum, divine, strongly, strongly consider FFP, you know, think about FFP. FFP is very helpful for bleeding, especially in a liver patient. Because again, if you're a liver patient, you're not making clotting factors very well at all. And if you're not making clotting factors, that's problematic. So FFP will really help you with replacing those clotting factors that you're missing. But I guess maybe to bring a bring a bring a good parallel here, what if a person has a renal disease and they're bleeding? What's helpful in those people? Desmopressin is a very unusual but pretty helpful answer on exams. Because the thing is when your kidneys don't work, you have a lot of euremia. When you have euremia, then you're going to have this huge massive issue with your platelets degranoletin and like doing their jobs properly. So the thing is, the smopressin is an agent that makes platelets work better. So you give the smopressin in those circumstances and it's really, really helpful to those people. Now, what is the most common infectious complication of cirrhosis?

I really hope you're saying, oh, divine, it's SBP. It's SBP. And let me tell you this. One of the reasons that when people have like a lot of assidence, we try to drain that acidic fluid is, we're trying to lower the risk of SBP. Literally, this can be an imping question for you. They'll give you a question about a person that has a way, whatever wave, they have this massive wave on exam, like this abdominal fluid wave, and the alcoholics, blah, blah, blah, blah, blah, blah, blah, you know, and they have assidence. And then they can ask you, which of the following are useful approaches for reducing the risk of this patient developing infectious complications? The smart thing you want to do is one, you want to drain that assidence. And two, if you don't see draining the assidence like scina parts and diseases as an answer, and nothing that may be a good answer is to give those people a fluoroquine alone, right? When people are like big-time liver patients, especially when they have a history of like a syphagiotrheal disease, or if had SBP in the past, it's usually prudent to give those people SBP prophylaxis. Usually on MBM Es, when we're giving SBP prophylaxis. So again, for those ones, we're going to do what you mean by SBP. SBP literally means spontaneous bacterial parotonitis. SBP prophylaxis on exams is usually with a fluoroquine alone. For SBP treatment, right?

When we were trying to mention earlier, SBP treatment is usually with a third generation of syphilospory, like syphtriaxone or syphotoxin, right? And again, remember the pathophys behind SBP is like bacterial translocation. That's like a very good keyword to remember for your exams. And how do we diagnose SBP? We actually diagnose SBP by doing a paracent thesis. So you drop a bunch of fluid from these liver patients, and they incendiate for analysis. And if you see more than 250 neutrophils, so you see 250 or more neutrophils, you don't even have to see bugs. Persia has SBP, right? And again, SBP treatment is a third gen syphilospory, like syphtriaxone or syphotoxin. But SBP prophylaxis is with a fluoroquine alone. That's a pretty useful thing to keep in mind on one example. Okay, and then what if they give you a question about a patient and they tell you that this patient has been having like, has been sweating a lot, has a hyperhydrousis, a person has a lot of hair on their skin. And then you notice that this person, they just have all these dermatologic manifestations. And they tell you that this person recently took like a set of group B-415 inducer or something like that. And then you notice that while the HIPC is positive, what should you be thinking about? Well, I really hope you're saying, ooh, divine. Sounds like you're talking about prophyracutinatarda. Yes, prophyracutinatarda, PCT. Remember, it has a very close-ass region on HIPC.

It's about 30% of people that have prophyracutinatarda, half hepatitis C infection. In fact, let me tell you this. For persons that knows, we prefer prophyracutinatarda. Many times the next one example is to screen them for HIPC, you know, just basically doing a HIPC RNA study, like a PCR, basically. And again, remember, PCT, it arises because you have a deficiency of a urod, a uro-pofereinogenic carboxylase. It's actually not a heritable disorder, something that arises spontaneously, because they can give you more of inheritance, put all these modes of inheritance, and it's not a heritable disorder. It's just kind of something to keep in mind. It's the close causing acute intermithin porphyria that is hereditary. And I think one other thing I'll also say would help see. For persons that have see, you want to treat it as direct, active, anti-viral, right? Like, so, force-bovere or leadipazvere. Those drugs, they reduce the mortality, they reduce your need for transplant, they reduce your risk of developing hepatocelular carcinoma, they reduce your risk of having hepatic decomposition, right? So again, it's just pretty smart to keep these things. They can literally ask you like a prognosis question that, but mainstream so force-bovere, what is the most likely effect on this person?

And the liver patient is going to reduce mortality, going to reduce your need for transplant, going to reduce your risk of hepatic cellular carcinoma, go to reduce your risk of decompensating, right? Hep atically, right? So it's pretty, pretty helpful. So I think I'm going to go ahead and stop here. Again, as I do at the end of every podcast, I offer one and one, two, three, four, many exams, step one, just step three, pretty clear and combing your school exams, 30-ish-off exams, for a 20-hour review course for step two, step three. And it's also useful for people that want to get a good overview of what you'll see on their shelf exams. And then I offer an NBME Testicking Strategies class and I offer a biostatistics class. I have some this October, like the Testicking courses on the 21st, 20-hour courses from the 24th to the 28th, and the biostatistics board campus on the 20th. So if you're interested in sending them for any of these things, just shoot me an email and I'll be happy to give you some more information. So thank you for listening to this podcast. Have a wonderful rest of your day. God bless you. Bye for now. Thank you.

Spontaneous Bacterial Peritonitis (SBP).

Fluoroquinolone alone (e.g., Ciprofloxacin) is used for prophylaxis, while third-generation cephalosporins are used for treatment.

Thyroglossal duct cyst.

A neutrophil count $\ge 250$ cells/mm$^3$.

Desmopressin (DDAVP).

Abdominal pain, ascites, and altered mental status.

Defect in the third/fourth pharyngeal pouches (DiGeorge Syndrome).

Brinkel cysts are ectoderm-derived, lateral, and do not move with swallowing. Thyroglossal ducts are endoderm-derived, midline, and move with swallowing.

Deficiency of uroporphyrinogen decarboxylase.

IV amino-aryl drugs, such as Flagyl (metronidazole) or Leucovorin (folinic acid).

Prolonged QT interval.

Lactulose (or Rifaximin).

Defect in the third/fourth pharyngeal pouches (DiGeorge Syndrome).

Brinkel cysts are ectoderm-derived, lateral, and do not move with swallowing. Thyroglossal ducts are endoderm-derived, midline, and move with swallowing.

Deficiency of uroporphyrinogen decarboxylase.

IV amino-aryl drugs, such as Flagyl (metronidazole) or Leucovorin (folinic acid).

Prolonged QT interval.

Lactulose (or Rifaximin).