DIP Episode 121 - USMLE Step 2CK Rapid Review Series 5 (IM/Peds)

Okay, welcome. My name is Define. I am a PGY2 resident. This will be the 121st episode of the Divine Intervention Podcast. And this podcast I'll be continuing my my rapid review of the USMLSTEP 2 CK exam. So let's begin. So what if you get a question about a patient that is a chronic alcoholic and this patient has like this patient is kind of like altered. His body temperature is like a 100.9 so kind of like a low grade fever. And then they tell you that he's reporting some vague abdominal pain. And his abdomen is mildly distended. What are you thinking about? I really hope you're thinking about SBP, right? So like spontaneous bacterial epiatoritis, right? So we'll be your next step in diagnosis, right? So I'll resume that you want to go ahead and perform a parasyntesis, right? And after you perform a parasyntesis, right? You basically counts the number of of white blood cells, right? If it's more than 250, that helps you make your diagnosis of of SBP. Or alternatively if you perform like a gramsthen of that parasyntesis fluid. And you notice that you'll find actual bugs. Again, that's positive for SBP, right? And obviously if you want to treat SBP, you go ahead and give drugs that cover gram negatives, right? You go ahead and give drugs that cover gram negatives pretty well, right? So you'd potentially give a drug like like safe tracks on for example, or you can give like a fluoroquine alone.

And remember that if a person has SBP, you kind of need to perfect lock them for the future, right? Against future episodes of SBP. And you do that with a with a fluoroquine alone as well. And one kind of like sneaky with your friends at the MBME can present SBP. It can be in a patient that's kind of like that has some kind of like instrumentation in the bowel, right? So it can be a person that is on like on dialysis, right? Remember some people do like periodoneal dialysis. That's when we can present. And although we this same phenomenon can also present is in a person that has like a VP shunt, right? So a ventricleopyrotonin shunt. So let's say a person that has like a history of like bad hydrosephalus or whatever, right? You can that shunt, you go basically go from the from the brain to the to the periodoneal cavity, right? That can be another presentation of of of spontaneous bacterial periodonitis on MBME exams. And that's kind of something you want to keep at the back of your mind. Okay. Now what if you get a question about a person that that you know had an infection a few days ago, got a drug and then now they're telling you that this person, you know, the temperatures like a hundred and one point five, they have like a like a small rash on their face and on their trunk and then they show you a CBC and you notice that the person's your synophilic count is quite elevated, right? What are you thinking about? I really hope you're thinking about AI, right? AI, right?

So remember AI is basically the triad of fever, rash and your synophilia, right? So they'll have a high fever, they'll have a rash and their your synophiles will be elevated even the blood when the urine when both. Okay? Those are high your things you want to keep at the back of your mind. So what are kind of like some other things? You want to keep at the back of your mind with your synophilia because the thing is your synophilia is a very high ill thing you want to know for your MBME exams, right? So I mean I've said this at NOS and in many podcasts, right? So the moment that I've kind of like come out from like resources and all that stuff from all my taking exams over the years is DN quadruple ACP, right? So DN quadruple ACP. So the distance for drugs, right? The N stands for Neoplasms, right? So like cancer, the first A stands for asthma, right? The other A stands for Adesence Disease, right? And in terms of drugs, right? Again, like it's like your classic antibiotics, Neoplasms pretty much any Neoplasm can cause your synophilia. Well, classical your name, BME exams, it's the hematologic malignancies, especially like Hodgkin's lymphoma. The first is asthma, right? Asthma, reactive or a disease. The second is Adesence Disease, right? So if they give you an Adesence Disease question, it'll be in a patient that has like hyperchilemia, hyponitremia, right? And the patient will like have like a relatively low blood pressure and they will have skin hyperpigmentation, right?

And then acute intestine of right? This is the next one, right? EIN again fever rash, your synophilia or your synophilia or both, right? And then, um, so asthma, allergies, acute interstitial nephritis and Adesence Disease, so I don't think I've measured that energy. So allergies the fourth A, right? And then the C is for collagen, vascular disease, right? So any disease like scleroderma, like lupus, basically all those autoimmune things that you've learned about and then the piece for parasites, right? Those things are all associated with your synophilia. And I just said that in acute interstitial nephritis, if you take a look at the urine, you'll find elevated your synophilms. What if they give you an NVME question and in the urine they found white blood cell casts? What are you thinking about? I really hope you're thinking about pylonophritis, right? These like urinary findings in selected diseases are kind of high you to know for example, what if you see like pigmented epithelial casts or like the classic lead described moody brown casts? What are you thinking about? That'll be ETN, right? A cutiblerne process. And remember that rabdom Iolosis, the kind of AKI causes is acute to learn a crosses, so like an intra-renol acute kidney injury.

Okay, what if a person has, what if a person has like reddish urine and it tells you that the urine looks really red, that it's like positive for blood by urine dipstick, but when you spin it down and do the urine microscopy, you don't see any red blood cells. What are you thinking about? I'll be thinking about rabdom Iolosis, right? Remember, rabdom, that's the classic description positive for blood by dipstick negative for cells by microscopy, right? Because remember in rabdo it's the myoglobin that is essentially torching your kidneys, right? And again, remember, rabdom Iolosis is an example of acute to learn a crosses. Okay, I remember the things that will cause rabdo in an NV Me exam is a person that has some kind of risk factor that makes them up ton dead, right? So they are alcoholics and they pass out or it's an old person fell down and couldn't get up for a couple of hours or it could be a person that's the recent victim of like some kind of curfew injury, right? That can also cause a rabdom Iolosis and then also don't forget if a person combines two drugs that are myotoxic, right? So if a person combines like a static and a vibrate, right? So like a static like atovastatin or prevastatin or suvastatin or cymbastatin and a vibrate like Jim Fibrezel or phenophibrate and stuff like that. And also remember, right? Drugs like, what is it called? A drug like datomycin that covers MRSA, remember it's also myotoxic, okay? So again, those are all high your things.

You want to keep at the back of your mind for exams. Okay, now what if you find red lot cell castes in a person's urine? What are you thinking about? I hope you're thinking about glomerulina frightens, right? So I'm kind of a nephrodite syndrome, right? So like either like post-infectious glomerulina frightens or iginephropathy, right? Those are things you want to, or even lupus nephrodis, right? Those are things you want to keep at the back of your mind. And then what if you get a question about a person that has like fatty casts in their urine? Fatty casts in their urine? What are you thinking about there? Well, I hope you're thinking about again some kind of nephrodite syndrome, right? Remember, nephrodite syndrome classically they tend to have like four plus proteinuria, or they have like the classically described three and a half grams per day of a protein greater than three and a half grams per day of protein in their urine, right? And again, they will have like the fatty, like the overall fatty casts in their urine. Remember that can be either like minimal chain disease. If it's a pediatric question dealing with with nephrodite syndrome, especially after like let's say they have like some kind of like hematologic malignancy, or it can be like FSGS. So for that you want to think about a patient with a history of HIV or a patient that is a drug user, like an IV drug user, or a patient that is African-American or a patient that is obese, right?

You want to think about that, especially like the colapse in FSGS. That's the one that has the worst prognosis. And then if you're thinking about, if you're thinking about, if the describe a person that has like some solid cancer, right? So let's say the person has like colon cancer, ovarian cancer, or whatever they have nephrodite syndrome, you certainly want to think about like membranostinopropathy, right? And then remember that diabetes can also cause a kind of nephrodite syndrome, right? It's just called diabetic nephropathy. We do classically observed chemo-steel Wilson nodules, right? On his stology. And remember the way you sort of like slow down the risk of like complete kidney failures by giving some kind of a ACE inhibitor, because remember your ACE inhibitor sort of causes or they slow down an intra-glomerial hypertension, right? Again, I've explained that mechanism in multiple podcasts, so that's something I want to keep at the back of your mind. Okay. So I think those are all the casts I specifically want to talk about, but again, those urinary findings and diseases, oh, wait, I forgot one last one. So what if you tell you what if a person is dehydrated? What kind of cast would you observe in the urine? I hope you're telling me higher-ling casts, right? High-ling casts. Those things are kind of made of like tam-hose 4 protein. It just happens whenever you have like a person that is super dehydrated, because think about if you're dehydrated, right?

Your afrin arterial will no longer be well-prefused. And if your afrin arterial is not well-prefused, well, the activity of your renein and your tensin outosterone system will increase. And when your renein and your tensin outosterone system activity increases, right? So one of the things, right? For example, like outosterone, right? It goes up, that we absorb sodium in the distal, distal an effrin and water goes along side, right? So urine becomes more concentrated. Also, EDH, remember, one of the jobs of adjutancing too, is to go to the, is to go to the super optic nucleus of the hypothalamus. So that you release more EDH when you release that EDH, that increases the reabsorption of water at the principal cell of the nephron, right? So urine becomes more concentrated. Under those circumstances, if you look at those people's urine, you're going to find higher-ling casts, okay? So that's something you want to keep at the back of your mind. Okay, now let's talk about, let's talk about some, yes, presentations of back pain on NV Me's because the NV Me's, the law of questions about back pain, back pain, back pain, back pain, right? Okay? So what if they give you a question about a patient that, you know, has like low back pain, but in addition to that, they have, they've kind of like lost their situation around their body, and then they tell you that this person is having trouble, having kids or maintaining an erection, like has a erectile dysfunction.

What are you thinking about? There's a classic surgery NV Me question. What are you thinking about there? I hope you're thinking about lyrish syndrome, right? It's basically peripheral arterial disease, but it's so bad that it does involve like the odor, like the distal ayodor and the iliac arteries, okay? That's what's known as lyrish syndrome, L-E-R-I-C-H-E, okay? It's like bad, bad, bad p-E-D that has involved distal ayodor and the iliac arteries. And remember, what is the biggest risk factor for peripheral arterial disease on NV Me exams? That will be smoke it, right? I get very high iliac to know that. Okay, now what if the describe a person that was, you know, lifting heavy boxes and then they have like sodium onset severe back pain and then they tell you that on physical exam, you observe paravertibral muscle tenderness. What do they want you to go after there? I hope you're thinking about just a muscle strain, okay? And you don't need to do anything heroic, just NSAI Ds, activity modification, right? Stuff like that. Okay, now what if they tell you that a person was again lifting heavy boxes or let's say it's a person with osteoporosis, right? So maybe like a compression fracture kind of deal. And then they have low back pain and they tell you that when you do a straight leg wrist test, it is positive. What are you thinking about on that those circumstances? I hope you're thinking about like a herniated disc, right? Like a herniated disc, right?

So remember that you know, the part of the disc, right? That tends to her knee is the part that's known as the nucleus proposis, right? So as it herniates, you can begin to impinge on nerves that are exiting this spinal cord and the person will essentially have a radical lapathy, right? Remember in my neuro podcast, I was very careful in distinguishing between my lapathy or radical lapathy, a plexopathy, right? Those different things, those are all kind of high your things. You want to keep on the back of your mind and be able to distinguish Oh, is this a problem at the level of the nerve or problem at a nerve root or problem at the spinal cord or problem at the neuromuscular junction or problem with muscle or a cortical problem or sub cortical problem or brain stem problem, right? I know you may see define, well, these are all different levels of different things. Again, I promise you, especially if you're taking a neurology shelf, it's very high, you know, if you're taking step two CK, it's one of those things that you can test. That is one nice way to contest a neurology on step two. So again, I'll encourage you to go back and maybe listen to those neuro podcasts, those are things that I feel strongly would help on an exam. Okay, and again, her needed this again, activity modification rest usually recover within like six, six weeks, like you can take and say, but that doesn't mean that you should just rest at home for six weeks. No, that's not what that means.

They rest for a while, activity modification and all that stuff, but yeah, they can resume like physical activity just with care. Okay. Now, what if this back, you get this low back pain question and it's kind of like a sodium onset severe back pain, like it's something that started notice, notice the just Trump attention to this question. So it's like sodium onset super severe and it's a person that, how do I put this? So it's sodium onset, it's severe. It's a person that has, they tell you that like they give you that this person's blood pressure is like a hundred over 50, right? And this person is complaining of severe back pain, but they also complain of like severe abdominal pain. And let's assume this person is a big time smoker. What are you thinking about on that those circumstances? What are you thinking about on that those circumstances? Lower back pain, relatively low blood pressure, sodium onset, smoker, severe abdominal pain with that. What are you thinking about? I hope you're thinking about like a ruptured triple A, right? A ruptured abdominal leorica and yours, right? A ruptured triple A. Remember, many people are used to like, oh, hypertension, abdominal pain, pulse, a talab, abdominal mass and all that crap. The thing is the end game is beginning to stare away from those classic presentations of like a triple E that's about to rupture or has already ruptured. And they are beginning to go after the more exotic clinical presentations, right?

Kind of like the low back pain, sodium onset, abdominal pain. In fact, sometimes they may ask, they may give you this classic presentation where they tell you that on imaging, the person has this thing known as the draped a yoder sign, right? The draped the yoder sign is just one of those things where I mean, it's like a classically described sign in radiology where you kind of see like some almost like some calcifications in front of your vertebral bodies. It's just remember people that have a triple A, right? You tend to have like a calcified a yoder, right? The problem there is that if that yoder ruptures, if it's like a contained rupture, like the posterior wall of the yoder, remember the yoder is like your descending yoder, especially is a retroperitoneal structure, kind of like your vertebral bodies. Your vertebral bodies are like in the posterior abdominal wall, right? So can you already envisage that if a triple A has ruptured is about to rupture, the posterior wall of the yoder can sort of like just lie over the vertebral body. That's what creates the imaging finding known as the draped a yoder sign, okay? That is classic for ruptured or an almost ruptured or like a contained rupture of a triple A, okay? So those are always ruptured triple A can can present, right? And again, hopefully remember the screening guidelines for a triple A. I talked about it in my risk factors and preventive medicine, podcasts.

Remember that the biggest risk factor for a triple A is smoking. Okay, so let's see, I want to talk about one more thing. Okay, let's talk about some, let's talk about some quick things with, with, let's see, let's talk about some quick things with, with peets, right? So what if you get a question about a kid that is beginning to lose motor milestones and they tell you that let's say it's like a kid that's like six months old, beginning to lose motor milestones and this kid, they tell you that he has like fasciculations on the exam. What are you thinking about? That will be spinolecular trophies, right? Remember if you have mentioned this again, multiple podcasts, very high you to know. If you see like the kid with fasciculations, again usually is less than a year old, under those circumstances you want to think about spinolecular trophies, if you see an adult like an older age person with muscle fat sequelsions, you want to think more about an ALS, right? A myotrophic and lateral sclerosis, also known as a lugeuric disease. Okay, so, so this kid has an SMA, right? Remember it's an Orozomer recessive disease, right? So believe it or not, they want you to still know these weird genetics things on step two, right? So it's an Orozomer recessive disease and remember that it tends to arise from mutations in chromosome five, right? In like the SMA and 1 G, right? So the survival motor on your own 1 G. Okay, now wouldn't they give you a question about a kid?

Let's say it's like a 12-month old and they say that you know since he was born, especially since like six months of age, he's been having like, he has had like three bolts of like numococcal pneumonia, like numococcal sepsis and he's had like like gastroenteritis from like GRD or whatever and they tell you that some other members of his family like his uncles or his dad or whatever, they've also had like multiple severe infections. In fact, like one or two of them have died from severe infections. What are you thinking about there? Again, a kid. I hope with that you're thinking about some kind of B cell problem, right? Like Bretons, E. Gamma Globulinemia. So a real long name there. Bretons, E. Gamma Globulinemia. I do it to say that 10 times. Okay, back to this. So Bretons, right? Remember, it's an excellent disorder, right? So it should not show up in a girl on an NV Me exam, right? It should not show up in a girl. It's show up more in a guy, right? And remember that it's basically a problem with like B cell like maturation. So those people will have like a lot of B cell or like antibody or like humoral immunity associated diseases, right? So primarily bacterial infections. The thing is on NV Me is if you ever get a question that is an immunodeficiency question, you can usually finigle your way to the right answer by just sort of taking a look at what kind of bog pattern do you see in the question, right?

So if you notice that the person is having a lot of like bacterial infections, you know it has to be a B cell problem, right? It has to be like, and I mean, they may use different analogous words, B cell, antibody-mediated immunity, humoral immunity defect or whatever, right? Those are all words these for that. But if it's a T cell problem, right? They will have like recurring viral infections or fungal infections or they may have like new assistive gerovetiae, so like PCP, right? If you see any of those things, think more about like a T cell or a cell-mediated immunity kind of problem. Okay, so that's what I, so this kid has a brutance, right? And those kids will have like low levels of essentially every immunoglobulin. And really the way you treat that is almost like with like monthly injections of IVIG, okay? Again, that's high yield to no for exams. And if you notice kids with brutons, right? Their symptoms tend to crop up after the age of like six months, right? Because remember, they kind of have that protective IGG effect from mom remember, IGG is the only antibody that sort of crosses the, crosses the placenta, right? So it sort of persists for a while. So it tends to protect those kids in that circumstance. Okay, now what if you get a question about a kid, you know, that has like, he's had like recurrent infections and they tell you that he has like the TTI on his skin and that he's had like some, some like bleeds when mom tries to brush his teeth.

I need to tell you that he also has like a history of like exama. What are you thinking about? I hope you're thinking about a Whiskotol-Drich syndrome, right? Whiskotol-Drich syndrome. And remember, again, that's also an excellent problem, right? It's also an immunodeficiency disease and classically, right? So those people tend to have like low pleclets, right? So they have like a thombocytopenia. That's when describing like the PTI. And then they also tend to have like eczema, right? Eczema. That's something you want to keep at the back of your mind. Okay, now what if a kid has like recurrent like abscesses with like stuff or is what is the disease you're thinking about? Again, I hope you're thinking about CGD, right? I hope you're thinking about CGD. CGD is like chronic granolomatosis disease. Remember that classically, I summarizes from a problem with any DPH oxidase, right? So if you have mutations in any DPH oxidase, you'll have a CGD. And basically, right, it's the thing that is kind of gets all screwed up, right? It's like your oxidative burst of mechanism, right? So since I assume it's a person that's taking step to seek it, that's listening to this, I would assume that you remember like this, I don't know if you remember if you all remember from step one like this whole process of acute inflammation, where you have like any DPH oxidase work. And then after that, you have like myeloperoxidase work and all that stuff, right?

So if the oxidative burst doesn't happen, right? Like in neutrophils, for example, you then begin to have problems with with catalyst positive organisms and classically on NBM is it is stuff-urious that it tends to go after. Okay, and then what if you get a question about a patient that has like an immunodeficiency disease and they tell you that oh, when this kid was born, this kid had seizures, right? And they tell you that oh, that so this kid had seizures, this kid has been getting like recurrent like like this kid has had like recurrent paren-frontal infections. And they tell you that when the kid had seizures when he was born, they got an ekegen, they notice that the acute interros prolonged. What are you thinking about on those circumstances? That's the George syndrome, right? The George syndrome, remember, the George syndrome, the third and fourth of pharyngeal pouches do not develop, right? So those people's thymesis don't develop, remember that's where your T cells form. I mean those are where your T cells complete their growth. Everything ultimately starts in the bone marrow. Where your T cells, T cells, they kind of like complete their puberty in the thymus if you may, right? So those people's T cells don't work basically, right? So they have recurrent, again viral and fungal infections on like TCP pneumonia, right? And then the reason they have that prolonged acute interros and seizures is from hypocalcemia, right?

So remember those people, right, they are parathyroid glands, like they're inferior parathyroid glands, they're not developed. So they don't make pt.ge. If they don't make pt.ge, guess what? You're not going to be able to activate vitamin D or reserve bone. So your calcium will be low and your phosphate will be high, right? Because there's no more phosphate trashing hormone. Those people can have hypocalcemic seizures and remember hypocalcemia when an eGG can present as a prolonged acute interval. And it's actually kind of high yield to know that infants of diabetic mumps also have a hypo can also get a hypo calciumic seizures. So if you see a baby that's like 10 pounds, 9 pounds or some crazy weight and they have seizures after they're born, think about an infant of a diabetic mom. They either have those seizures from hypocalcemia or they have those seizures from hypoglycemia, right? From hypoglycemia because remember, infant of a diabetic mom in utero, he's seen high blood sugars, high blood sugars, high blood sugars coming, coming down the pike from the placenta. But after the, in utero, the infant's blood is like, oh crap, there's too much glucose in blood, too much glucose in blood. So the kids pancreatic eyelid cells, beta cells in the eyelids of longer hands, they make a crap ton of insulin to deal with that high sugar load. But when the kid gets born, right? That high sugar load is gone.

But it's not like the pancreatic eyelids instantly, shrivel down and stop secreting that much insulin. No, they still have like the hyper insolimemia. And with that hyper insolimemia, right, they can get hypo glycemia and get seizures. Okay, so that's another thing you want to keep at the back of your mind. I remember that in front of the diabetic moms, they tend to have, they can have like a hypertrophy cardiomyopathy, right? And they can have like a VSD on MBS. So those are things you want to keep at the back of your mind. Okay. And then the final thing I'll say is right. And if you're again also thinking about like a neonatal seizure, they can or like a pediatric seizure. So not necessarily in a neonate. But if they give you a question about like a patient that was on Desmopressin for like nocturnal and uricis, right? Like a six year old or whatever, I think about a hyponitremic seizure. I remember, Desmopressin is an ADHD channel lock, right? So you can cause a hyponitremia. Even the intranisal kind, believe it or not. Okay. Or if the described a kid that has been like vomiting and all that crap and then you've been given the kid like just like distilled water or like just straight up water, not like oral rehydration therapy to sort of like repeat the electrolytes that can also again cause a hyponitremica seizure. Okay. So I think I'm going to go ahead and stop there. Again, I've gone for like 30 minutes. This is supposed to be a rapid review.

And again, as I usually do when I run the podcast, I do offer one on one tutoring for the USMAD step one, step two CK, step two CS and step three exams, right? And I also offer tutoring for like the medicine, internal medicine, training exam, the ABIM or board exam. And also the like preclinical exams in med school and like the third year show of exams. And then if you really have an acquaintance that is in college and needs to do it for like physics, general chemistry, organic chemistry, physiology, histology, biochem, pretty much most of the stuff that's tested on the MCAT, you can have them reach out to me and then if you're met student applying to residency so like an ERAS application or a college student applying to med school so like an AMCA's application, I do offer like one on one advice and I'm consulting for that like personal statements, interview prep, application prep and all that stuff. So again, I've advised tons of people over the years and many of those people have matched to their first choices. So take that for what you will and again, I've also been on an admissions committee at a top two med school for like a year, right? So again, I have a lot of experience with these things. So feel free to reach out to me through the website or a divine intervention, podcasts with an SIVN at gmail.com. So have a wonderful day. I'll see you in the next podcast. God bless you. Thank you.

Fever, rash, and eosinophilia (or elevated peripheral blood/urine eosinophils).

DNQACP: Drugs, Neoplasms, Asthma, Adenosine Disease, Allergies, Collagen Vascular disease, Parasites.

Urine dipstick positive for blood, but urine microscopy shows no red blood cells (myoglobinuria).

Low back pain, severe abdominal pain, hypotension, and smoking history.

Bacterial infections suggest a B cell (humoral) defect; viral/fungal infections suggest a T cell (cell-mediated) defect.

Fasciculations in children (<1 year) suggest Spinal Muscular Atrophy (SMA); fasciculations in adults suggest Amyotrophic Lateral Sclerosis (ALS).

Drugs, Neoplasms, Asthma, Adenosine Disease, Allergies, Collagen Vascular disease, Parasites.

Hyaline casts (due to increased ADH/RAAS activity concentrating the urine).

The draped azyder sign (calcifications overlying the vertebral bodies).

Bruton's Agammaglobulinemia.

Smoking.

Hypoglycemic or hypocalcemic seizures; due to transient hyperinsulinemia/hypoparathyroidism respectively.

Thrombocytopenia (low platelets), Eczema, and recurrent infections.

Drugs, Neoplasms, Asthma, Adenosine Disease, Allergies, Collagen Vascular disease, Parasites.

Hyaline casts (due to increased ADH/RAAS activity concentrating the urine).

The draped azyder sign (calcifications overlying the vertebral bodies).

Bruton's Agammaglobulinemia.

Smoking.

Hypoglycemic or hypocalcemic seizures; due to transient hyperinsulinemia/hypoparathyroidism respectively.

Thrombocytopenia (low platelets), Eczema, and recurrent infections.