DIP Episode 130 - USMLE Step 2CK Rapid Review Series 10 (Peds)

Okay, welcome. My name is Devine. I am a PQI-2 resident. This is episode 130 of the Divine Intervention Podcasts. And in this podcast, I'll be continuing our Rapid Review series for the USML Step 2 CK exam. This will be series 10 and I'll be focusing on Peds. So, and again, I'll try to knock this out fairly quickly because again, I want to keep this short. So let's assume you'll get a question about, you know, like a two-year-old kid. And this kid had like Rhinorrhea for the past had like Rhinorrhea for the last two days. And this kid, you know, has like a mouth fever, Lissy's temperature is like a hundred point nine or just like a one-oh-one, so like very low grade fever. And then they tell you that this kid has been having like a Barkey cough. What are you thinking about? Well, I hope you're really thinking about CROPE, right? Remember CROPE? Remember CROPE is caused by what bug? I hope you're telling me the power influence of virus, right? The power influence of virus, the power influence of virus causes a causes CROPE, right? And the thing you want to keep at the back of your mind is that CROPE is an upper-airway problem. So in the NVME question, they're gonna give you something along the lines of strider, okay? They will give you a most strider less reason on your exam. So I'll tell you this on Pete's questions, you really want to pay attention to the wording.

If you're seeing a lot of striders, striders, striders, striders, striders, think about an upper-airway problem like bacterial tracheitis, right? Or like CROPE or like epiglotitis, right? But if you're telling you a reason, you want to think about asthma and you want to think about areas of pneumonia, okay? Although, right, if you see a kid in the first month of life that has pneumonia, you want to think more about group B strep. But most times on NVME exams, it's kids that are less than two years old that tend to get like areas of pneumonia. RSV is probably one of the most common causes of pneumonia in a kid that's less than a year old or thereabouts. But more than 20 days old. If you see within the first 20 days of life, you're thinking more about group B strep or strep agalactia. So CROPE is caused by the parian influenza virus. Again, remember, it's an upper-airway problem so you see strider, right? And those kids tend to have, it's a sub-glotic problem. This is something your friends at the NVME can expect you to know, right? Because remember, epiglotitis is like above the glottis, right? But if you're seeing sub-glotic problems, you want to think more about group or you want to think more about, uh, uh, bacteria, tracheitis, right? And CROPE obviously will have that steeple sign that is classically found on radiography, um, in patients that are affected with, uh, with the disease, right?

And really for the most part group, you just supportive care, the kid should be fine. But I said again, if you see, um, like sodium onset, so notice for this group question, I give you like this program of like ryanorea and like so throat and all that crap. But if you see a kid that like within a very short period of time, like over hours, they feel like crap, right? They just feel like super sick. They have very high fevers, their temperatures like 103. They're having like grunting. They are, um, they tell you that, um, the kid is like tripod in or like his mouth is like open and he's like trying to catch air, right? If you see that, I really hope you're thinking about epiglotitis, right? Epiglotitis, uh, back in the day was caused a lot by H-fluty B. But now we have like a conjugate vaccine against H-fluty B, right? So we don't necessarily have many of those problems anymore, right? So uh, strapping you more can cause, um, can cause epiglotitis, staphores can cause epiglotitis. And the good thing is, um, oh, I guess not necessarily a good thing, but a unique thing I want you to keep in mind is don't just think of kids as the only ones that can get epiglotitis on an MB in, right? The thing is your friends at the MBME have realized that, oh, many people have seemed to memorize this association. Oh, oh, if you see a kid high fever, uh, strider, um, sudden onset, think about epiglotitis, right? So remember, people in their 20s can have epiglotitis.

People in their 60s can have epiglotitis on an MBME exams. So that's something you sort of kind of want to keep at the back of your mind. And then, um, one last thing I just want to say is if they give you a question about a kid, right? That has like really bad bouts of cough, right? Like this kid, like coughs, coughs, coughs of tongue, right? And then they tell you that, oh, after this kid coughs, this kid has like vomiting or the kid like looks cyanotic, like becomes blue or basically they have like any change in the color of their skin with the cough because it's that severe. Um, you should really be thinking about like pertosis, right? Like birdytillipartosis. So what are the high yield things you want to keep in mind with birdytillipartosis for you? Exactly, right? You want to remember that one, it's a bacterial infection. That's one. But it, because think about it, if a person has a bacterial infection, how does the immune system classically respond? Right? You have a leukocyteosis, but what is the cell type that will be predominantly elevated in most bacterial infections? Will I hope you're telling me you'll be neutrophils, right? But pertosis is kind of special in the sense that it causes, uh, it's a bacterial infection, but the way your body actually responds to it is with lymphocytes. That's a higher thing you want to keep in mind.

And the thing is pertosis is one of those rare things where it's an infection, but these people's white counts are like crazy, high, like 70,000 sort of deal. So that's again, some, that's like some high yield bit of trivia you want to keep in mind with, uh, with, uh, pertosis, right? And again, obviously something that is a vaccine preventable. And if you want to treat it, right, you want to give the kid a macrolid, like is it throw my skin or erythro my skin or whatever, right? Although remember erythro my skin, your macrolids can prolong the QT interval, right? And if you're a close contact rate, this is actually very high yield to know. If you're a close contact of a person that has, um, that has, um, pertosis, right? You want to also go ahead and get a get a macro little cover yourself. Okay. Now, what if they give your question about, uh, newborn, um, that has billions vomited, a newborn that has billions of them. This is a way the mbimi gets people all the time. So I'm going to spend like probably like three, four minutes on this, a newborn with billions of them. What are the three things you should keep on your differential? You want to keep my rotation with volvulus as one thing on your differential. You want to keep broadener Latreia as another high yield thing on your differential. And then you want to keep gejunal Latreia as a third thing on your differential, right?

So my rotation with volvulus, broadener Latreia, gejunal Latreia, those are the three things you want to think about. So how do you get these things right on exams? Well, here's the algorithm you should basically follow. They try to, whenever the, your friends at the mbimi write these, um, billions of them in questions, you always write them to be like very non-descript so that it's hard for people to like get towards the answer. So here's the trick you should use. If you see videos about it in a newborn, if they give you a picture on the exam, ask yourself these two questions. Do I see a double bubble or do I see a triple bubble? If you see a double bubble, obviously you should go ahead and pick broadener Latreia. If you see a triple bubble, you should obviously go ahead and pick gejunal Latreia. If you don't see a double bubble or triple bubble, then you should go ahead and pick marotation with volvulus. Here's why. The thing is your friends on the, the, at the mbimi, whenever they give marotation, right? And they give a picture. They always put that picture to mess with people's heads. The thing is should have you been a radiologist, it's usually very hard to pick up what marotation with volvulus looks like on an mbimi exam. So just use almost like a picture process of elimination and you'll get these questions right a lot of the time. If not all the time, okay?

If you don't see the fancy double bubble or the fancy triple bubble, you know it has to be marotation and you go with that answer. Okay? Because again, I promise you most times for most people, I'll see probably for like 90% of people taking the USML Es, you will not be able to diagnose marotation of volvulus just based on the picture. And it's usually like a crappy picture that will give you on the mbimis. So, so what are the again, the big things you want to keep in mind with this pathologies, right? Marotation with volvulus again presents as billions of amitting. It's a very non-specific presentation, but that's about as much as you can do on an mbimi exam and still finagle your way to the answer, right? And you can do like an upper GI series to try to make the, to try to make the diagnosis. Even if the upper GI series is not super, it's not super, super, super specific. But the thing is it's one of those can't miss the diagnosis because it can be rapidly fatal if it's not treated, right? That's one. Now, the Dorena Latrizia, you already know this, it's classically found in kids with downs, right? And remember that the buzz word pathophysiology, you want to remember for your test, is a failure of recolonization, right? Failure of recolonization, that's the buzz phrase of pathophys. And then for the general Latrizia, right? It's the one that's associated with a vascular problem, right? Your friends at the mbimi will try to trick you by seeing failure of recolonization.

Failure of recolonization is not the pathophysiology behind general Latrizia, okay? And for the one Latrizia, you'll find your fancy double bubble, right? Because remember, right? You'll find your stomach bubble and then you'll find the bubble distal to the pyloric sphincter. So that's your double bubble, right? So, but if you see a triple bubble, you know you're dealing more with a general Latrizia. So that's how you always get those questions right on exams. Now, what if you get a question about a kid that, you know, has like, is like at the, I don't know, like 10th percentile for weight. This kid always has like false mailing stools. And this kid is having problems with like bone development. And their stools always like float. The kid is just tiny, doesn't seem to be developing, has failure to thrive. What are you thinking about? I hope you're thinking about celiac disease, right? I really hope you're thinking about celiac disease. Remember, celiac disease, right? You know, raises when you have like problems with like your, your microbiology, right? Like you have like immune-mediated destruction of your microbiology, right? And obviously, if you want to go ahead and make that diagnosis, right? You want to check for antibodies against like tissue transgletaminase or anti-gliadine antibodies or like anti endomysial, endomysial antibodies, right? And obviously, the way you treat is by, by we're drawing gluten from the diet, right?

So those are some key things you want to keep with celiac disease. The thing that can cause a malabsorption. So why does this kid have these bone problems, right? Remember, if you have fat malabsorption, what are the vitamins you will not be able to reabsorbed? Well, I hope you're telling me like vitamins A, D, E, and K, right? If you can already absorb those vitamins, right? Like vitamin D, for example, you have like a, you essentially have like, uh, rickets, right? The kid will have rickets. Or if you're dealing with an adult, you're thinking more about like osteomalacia, right? So under those circumstances, they will have like a secondary hyperparthiaidism where, because they're not reabsorbing vitamin D, right? They are not reabsorbing calcium and phosphating near guts. So the calcium will be low, right? But because the calcium is low, the apthit will go up. If the apthit goes up, you'll trash your phosphate. So the phosphate will be low, okay? So they can get a secondary hyperparthiaidism with that. With the vitamin K deficiency, they will have like recurring bleeds, right? Remember vitamin K is kind of like an anti-quagulant, if you may, because it helps with the gamma-capoxylation, right? Of like factors 279 and 10 and aportines as CNS, right? And then, um, they can also have like acanthocyteosis on a blood smear, because they have that vitamin E deficiency. Remember vitamin E is required for the maintenance of like appropriate membranes of stuff in your body, right?

So if you're not maintaining your red blood cell membranes appropriately, you can have acanthocyte with that, right? And then obviously if the person has like the vitamin A deficiency, they can have like, like, my blindness sort of deal, right? So that's all I'm going to say about celiac disease. Well, actually, maybe not all of that, right? But what's the dermatologic manifestation of, of a celiac disease? I hope you're telling me about like some fancy rash on extensor surfaces, right? So like, you're classically described as dermatitis, uh, her pediformis, right? So that's one thing to know. Now, also remember, right? If the describe a person that has a history of like celiac and then they tell you that, oh, like over the past three months, they've lost a ton of weight, they have abdominal distension and all that crap. Uh, what are you thinking about? I hope you're thinking about like some kind of malignant generation, right? Remember that celiac can cause a kind of like a lymphoma. It's like they call it like an enteric associate associate theta lymphoma. I usually I think it's like a T cell lymphoma. So EATL, enteric associate theta, associate theta T cell lymphoma, that's one thing you want to keep in mind with a celiac disease. Now, what if they give you a question about a kid that has like intermittent? So this is the high-o thing you want to remember. Not constant intermittent abdominal pain. And then between episodes of that abdominal pain, they feel good.

They feel okay. What are you thinking about? Well, I hope you're thinking about interception, right? Interception, again, remember, it arises when you have like telescoping or bow. And the thing is your friends at the MBM already tend to give you certain clues that, oh, hey, you're dealing with interception, right? You'll give you clues like, um, I don't know, like recent operator infection or recent like J.A. infection, right? Those are things that can all predispose a person to having interception. Or alternatively, right, they can give you questions about like a person that has like a mechal's diverticulum. Remember mechal's diverticulum can provide a leap point for interception, right? So if a person actually has a history of mechal's diverticulum, you'll actually want to go ahead and avoid the rotavirus vaccine in those people because that can increase the risk of interception, right? Another one you may see on the example is if a person has a history of like, um, like I.J.A. in a property, again, you also want to avoid the rotavirus, um, vaccine in those people because again, you can raise the risk of of interception. And obviously before interception, right, your treatment is you want to do like an air or contrast NMR, right? That is both diagnostic and therapeutic, right?

Now, what if you get a question about a kid that has, um, you tell you that this kid has, um, they tell you that this kid has like a demiverware and this kid had like an upper respiratory infection like a few days ago and they tell you that this kid has four plus proteinuria. What's your diagnosis? I really, really hope you're telling me minimal change disease. I know that's why I kind of paused. I know many people like, I do, it does this essentially what I try to do. Try to trick you by saying, oh, upper respiratory infection. So I'm sure the thing that your mind went to first was either posting post-triptococcal, uh, glomerulina fritis or, um, or IGNF-ropathy. Remember, post-triptococcal glomerulina fritis and IGNF-ropathy examples of nephritic syndrome, right? So those people will not have four plus proteinuria, right? You have like a non-nephritic range proteinuria. So it'll be like two plus or three plus or whatever. And then they'll tell you that they have like red blood cell casts, right? Or like this morphic erythrocytes in the aurel. If you see that you're like, oh, okay, this is an epritic syndrome. So you want to think more about IGNF-ropathy or post-triptococcal, or also called a post-infectious or glomerulina fritis, right? So how do you differentiate between those two things? You differentiate between those two things by looking at, uh, when they have the upper respiratory infection, right? If they had it like two to six days ago, that's IGNF-ropathy, right?

If they had it like two to six weeks ago, you're thinking more about, post-triptococcal glomerulina fritis. Or if you tell you that this person had like a skin rash, right? Like that's typical of a groupase trap, right? And then they have like this hematuria. Again, you want to think about post-triptococcal glomerulina fritis, right? And hopefully, remember for the PSGN, remember like the ASO titers, right? Or the anti-DNESB antibodies, especially when you have like a strep-as-skin infection, right? So this case that have upper respiratory infection has four plus proteinuria, you're thinking about nephrodite syndrome, right? So remember, nephrodite syndrome, those people pee out more than like three and a half grams of your, uh, for a protein in a 24-hour period. And minimal change disease is the most common cause, very high you to know that it's the most common cause of nephrodite syndrome in kids. And it has a bunch of associations, right? So it has associations with like upper respiratory infections, it has associations with like liquid malignancies, so what do I mean by liquid malignancies? More like your hematologic malignancies, right? So like leukemia, lymphoma and all that stuff, those are all associated with a minimal change disease, right? And remember in nephrodite syndrome, right? Like minimal change disease, for example, by peeing out all that protein in your urine, what's happening to your oncotic pressure?

Well, with that oncotic pressure on your, that low oncotic pressure, you're getting like, uh, like a dimi everywhere, right? So they can get like facial edema, they can get arm edema, they can get leg edema, like peripheral edema, they can even get a sideys, right? That a sideys can become infected, they can get many problems with that, they can get like SBP, where you have to do like a pass and T Cs to find the more than 250 neutrophils and treat with like a third gen cephalosporin, like cephotaxine, for example, right? They can have DV Ts from the nephrodite syndrome, right? Because as the PL data antithromic in three in their urine, right? Remember, antithromic in three is an inhibitor factor, 10 and two. So if you waste that antithromic in three in the urine, you no longer inhibit factor, 10 and two, you become hyper-quagulable, right? Or those kids, right? They can have like a botcaric syndrome, where they can get like a thrombosis of the hepatic vein, right? Or they can get like a thrombosis of the reno vein, right? Or they can get like a splining vein thrombosis, although remember, usually when you see botcaric syndrome, they really ask that in the setting of like polycytemia vera, whenever you see a splining vein thrombosis, they really ask that in the setting of pancreatitis on NBM exams, right? But if you see reno vein thrombosis, you really, really want to think about some kind of nephrodite syndrome.

You can arise in any kind of nephrodite syndrome, but classically, on NBM is the guapter membranous nephropathy, as the inciting agent with reno vein thrombosis. And then, just I guess sort of like a quick association review here. What if they give you a question about a kid that's getting like recurrent like staff abscesses, or they're getting like recurrent like condibel infections or aspergillus infections? What are you thinking about there? We're like, I hope you're thinking about CGD, right? Chronic or Lomato's disease, where they have like an NEDPH oxidase deficiency, right? So the oxidative burst mechanism that operates in neutrophilus is all screwed up. Okay, now what if you get a question about a kid that has like an anaphylactic reaction with like blood transfusions, or the tell you that this keeps getting like recurrent like G-adial diarrhea, or like recurrent opus vitro infections? What are you thinking about there? I really hope you're thinking about IGD efficiency with that, right? Now what if they give you a question about a kid that's having recurrent, um, operasperture infections, recurrent g-adial infections, and it's a boy. So how you'll to know this, it's a boy, and all these things seem to have started after six months of age. What are you thinking about there? I hope you're thinking about Breton's Igama Global Lememia, right? Remember, it's like a problem with like B cell maturation.

So those kids will tend to get recurrent bacterial infections, and if they give your G-A infection, it's almost always g-adial, on an MDMI exam, right? And obviously for those people, you give them monthly IVIG as a treatment, and again, they will have mostly bacterial infections, not viral, not fungal, okay? Mostly bacterial infections. Now what if they give you a question about a kid that's born, this kid has seizures, and they tell you that oh, on an EKG, you see like a prolonged Q-team interval, and the kid is getting like recurrent infections with like new mosesis, gerovetsis. What are you thinking about? Well, I hope you're really, really telling me about, I hope you're telling me about the George syndrome, right? Remember, that's where your third and fourth pouches don't form, right? So your thymus doesn't form, so your t-cells are gone, right? So you have like a recurrent viral and fungal infections, and then because your parathyroid is gone, right? You get hypocalcemia, hypocalcemia can cause seizures, right? Or you can also present as a prolonged Q-team on an EKG. Remember that infants of diabetic moms can also get hypocalcemia, right? So if you say like seizures in an infant of a diabetic mother, right? You want to think about like hypoglycemia seizures or hypocalcemia seizures. So I think I'm going to maybe go ahead and, you know, let me talk about this, these two other immunodeficiencies.

So what if you get a question about a kid that has, you get a question about a kid that has like recurrent like infections, and they tell you that they give you like a CBC, and you find that his platelet count is like 40,000, and they tell you that this kid has like pigmented lesions on his skin. What are you thinking about? I really hope you're thinking about Whiskotovotrich syndrome, right? Remember, though the association like thrombocytopenia, right? So like low platelets and eczema, right? And again, it's going to be in a boy on an MBME. Basically, the boy immunodeficiencies, syndrome on an MBME, things like Whiskotovotrich, CGD, and Brutonzeigama, Globalinemia, those disorders should not show up in groups. They are all inherited in an ex-linked, processifation on an MBME. So again, very high-yout to know those states. And I think I guess I'm going to go ahead and stop here. Again, I really want to give this short. I want to kind of make up for the very long podcast time media yesterday that is very high-yout. And then as I say at the end of every podcast, I'd offer one or one tutoring for a ton of exams, right? So like step one, two CK, two CS, step three, the pre-clinical medical exams, 30-ish-off exams, if you're a medicine resident, like the intranin exams, the ABI-emboid exams, I'd offer tutoring for all those states.

And then if you're a college student, then you need tutoring for like Gen CAM, O-CAM, Physics, Bio CAM, Physiology, Histology, offer tutoring for all those states. And then if you're a med student, applying to residency, right? So like an ERAS application, or a college student applying to a med school, so like an AMCA's application, I'd offer like advising and consulting for those on a one-on-one basis, right? So things like personal statements, mock interviews, prepare you out to the application, letters of recommendation, I assist with all those states. So just reach out to me through the website or you can send out an email, a divine intervention podcast with an S at the end at gmail.com. I'd be happy to point you in the right direction. So have a wonderful rest of your day. I will see you in the next podcast. God bless you. Thank you.

Parainfluenza virus.

Bacterial tracheitis or Epiglottitis.

The "steeple sign."

Duodenal atresia.

Bruton's Agammaglobulinemia (B-Ag).

Deficiency in NADPH oxidase, impairing the oxidative burst mechanism.

Malrotation with volvulus, Duodenal atresia, and Jejunal atresia.

Jejunal atresia.

Coagulopathy/bleeding due to impaired synthesis of clotting factors II, VII, IX, and X.

Minimal change disease (MCD).

IgAN occurs 2-6 days after an upper respiratory infection; PSGN occurs 2-6 weeks later.

Chronic Granulomatous Disease (CGD).

Malrotation with volvulus, Duodenal atresia, and Jejunal atresia.

Jejunal atresia.

Coagulopathy/bleeding due to impaired synthesis of clotting factors II, VII, IX, and X.

Minimal change disease (MCD).

IgAN occurs 2-6 days after an upper respiratory infection; PSGN occurs 2-6 weeks later.

Chronic Granulomatous Disease (CGD).