DIP Episode 187 - USMLE Step 2CK Rapid Review Series 25

Okay, welcome. My name is Divine, I'm a resident. This is episode 187 of the Divine Intervention Podcasts. And in this podcast I'll be continuing the rapid review series for the US semily step 2 CK exam. If I'm not mistaken, I am fairly certain that this is the 25th in the series for the US semily step 2 CK exam. And those things are all very high. Those are rapid reviews. They are very high to know for the US semily step 2 CK exam. So again, I will encourage you, especially if you're again towards the end of your dedicated period, even at the beginning of your dedicated period, just go through a bunch of these. Most of them are like half an hour long, but they are very good, high-yield, rapid reviews. Okay, so when if you get a question, and this one is not going to have any particular focus, I'm just going to kind of touch on most of the major subjects, but again, it will be a short and sweet podcast. So when if you get a question about a child, let's say you know it's like a six month old, and this kid you know has been hypoxic, and then you get a chest next to him. You see, he's in testically infiltrated. And let's assume they do some kind of bronchovular lavash. And you notice that this kid is found to have what is it called? Neumocystis Jerovesi. And then they give you labs. And you notice that this person's at levels of IgG, very low, IgA, very low, IgE, very low, but you notice that their IgM levels are super, super high. What's your diagnosis there?

I hope you're thinking about something on this hyper IgM syndrome. Okay, hyper IgM syndrome. The thing is hyper IgM syndrome. It's an immunodeficiency disease that arises when a person has problems with class switching, right? Because remember, the first immunoglobulin you make to an infection is IgM. Remember that you know you're going to class switch at least for like IgG, IgG and IgG you need interlooking for that for IgA. You need it to look in five for that. So if you are, but the thing is for that class switching to happen, you need to have an interaction between something on a CD40 and CD40 ligand. So if you have any problems with that CD40, CD40 ligand interaction, then that can cause a lot of problems, right? Then you won't have class switching. So you only have IgM. So those kids tend to have like, you know, a ton of like really, really nasty infections. And I'll say probably like the post-to-child one you should look out for on the USM list of 2 CK exam is Neumocystis Jerovesi. If you see a child that has Neumocystis Jerovesi within the first year of life, the things you want to think about, you want to think about the child having you want to think about the charge having the George syndrome. With another one you certainly want to think about is the child having hyper IgM syndrome as well. And again, don't forget it. It raises from problems with class switching.

Now, what if they give you a question about a child and they tell you that, oh, this child, you know, seems to get all these recurrent infections like lymphodonopathy. And you notice that, you know, this child tends to have, you know, a lot of and from this like lymphodonopathy and these like, I don't know, like abscesses, they grow a lot of stuff for years. What disease are you thinking about? Well, I would hope under those circumstances you're thinking about the George, I mean, sorry, about CGD. So chronic, chronic, chronic, chronic, chronic, rheumatoid disease. Remember, CGD is an ex-linked recessive disease, right? So, it will show up in a boy on an MBA exam. And it classically arises in the setting of having an NEDPH oxidase deficiency, right? And it's actually very high yield to remember that the cell that is affected in a person that has CGD is the neutrophil, okay? Knowing the kind of cell that is affected in a particular disease is typically very high yield to know for the USML exam. So, in a person that has CGD, it's the neutrophil that's affected in CGD. Now, another thing you may also see on an MDM exam is how do you diagnose CGD? Well, you diagnose CGD right by doing either the nitroblutetrius only of tests. That was the test that was done back in the day. So, you may not see it very often on MDM exams anymore. Another test you may see is something known as the, like the oramin oramin test, okay? That's a test you can use these days to make the diagnosis of CGD.

And the way you treat CGD is actually to give interferon gamma. Interferon gamma is the drug of choice for the treatment of CGD. Although, please do not forget the uses of interferons on MDM exams. Interferon alpha is used to treat hemp C and it's also used to treat hemp B. Although remember, interferon alpha, right? Therapy. Having a history of major depressive disorder is a relative contraindication because it makes you feel like crap for a prolonged period of time. And then interferon beta on MDM exams, you want to think of it as a treatment for multiple sclerosis. And then interferon gamma, you want to think about it as a treatment on MDM exams for CGD. And then IVIG, I mean IVIG, you can use it for many things. You can use it for protons on MDM exams. You can use it for, you can use it for hyper IGM syndrome. You can use it for as like second line, like temporizing therapy. And a person that has Guillembris syndrome. There are many things you can for sure use IVIG for on MDM exams. Now, what did they give you a question about, you know, like a newborn, and you know, this newborn has has like hypokalcymic seizures, right? And then they tell you that this kid has like tetralogy of phono. What disorder are you thinking about? But I hope you're thinking about the George syndrome, right? Remember, the George syndrome, it arises when the third and fourth foreign geopalaches fail to form.

The thing is, if the third and fourth foreign geopalaches fail to form, the thing that happens is you will not develop like your thymus, right? So these people get like a T cell problem, okay? They will get a T cell problem. And these people will also have hypokalcemia from hypoprothyroidism because their thyroid glands fail to form. Now, remember, right? Because they have like a T cell defect, they will have like recurrent viral and fungal infections, right? So again, the specific cell type, like again, I kid you know, these immunodeficiency diseases, you better know your cell type that are affected. So the specific cell type that's affected in a kid with the George syndrome is the T cell. Remember your T cells, like your CB3, CB4 positive T cells, okay? And again, they tend to have problems with like the thymus and then they also tend to have problems with the pyrophirus, right? So the George syndrome is actually one of those things that can cause the absence of a thymus shadow on a newborn chest x-ray. The other thing that can also do that on a name-beaming exam classically will be skid, severe combined immunodeficiency. Now, what did they give you a question about a child, right? And you know, this child, when this child gets infections, the child's white count is typically pretty high.

But you notice that the child forms like these like cold abscesses and then maybe they tell you that, oh, you know, this child, it took like six weeks for the umbilical cord to fall off after the child was born. What are you thinking about under those circumstances? Well, I'll really hope you're thinking about um nucleoside adhesion deficiency, right? LED, right? So LED, right? The classic presentation in the name-beaming exams, you'll see the least depression of the umbilical cord, right? And again, the cell type that is affected in a child with LED is the neutral film, okay? It's a problem with adhesion. You have like a mutation in like beta-2-integrane or like CD-18, right? Those are things that on the light, the pathophysiology behind lucoside adhesion deficiency. And it's actually very high to remember that lucoside adhesion deficiency is inherited in an autosomal recessive fashion, right? And again, the step in uh, like acute inflammation that's all screwed up is the adhesion step, is the adhesion step because when you lock CD-18 and when you lock um like beta-2-integrane, then the neutral film will not be able to adhere to the endothelial cells. And one of the bizarre thing you mission an ambient exam that actually ends up being very high-yield is that when a person has lucoside adhesion deficiency, they can, they also tend to have a lot of like bleeding episodes.

And the reasoning behind that is they actually have a glans month from bastemia like bleeding defect that just cause kind of causes problems with primary hemostasis and then they tend to bleed. So again, all high-yield things to keep at the back of your mind for tests. And then what if they give you a question about a patient, they tell you that, oh, this patient was recently given an allopryl, uh, you know, for, I don't know like for some like high blood pressure thingy. And then this person is now complaining of like severe abdominal pain. If you see that, what are you thinking about? Well, I hope you're thinking about hereditary dima, okay? Hereditary dima, remember that classically arises from a C1 S3's inhibitor deficiency, right? Remember C1 S3's inhibitor, it's essentially like shuts down something known as calycrane. So the thing is if you have a deficiency of C1 esterase inhibitor, right? Then you will not be able to shut down calycrane and calycrane will lead to an increased production of bradykainin. And when you have increased production of bradykainin, you have increased vasculoprimability, you have a ton of edema. So the thing that will happen with that is that those patients, you'll have like a dim of many things, they can have like early edema so that can cause respiratory compromise, they can have a dim of the lips, they can have a dim of the GI tract, right? So that's why classical your nbimix ams, those people will present with abdominal pain.

Basically, any mucus of surface is susceptible to a dim in a patient that has hereditary dima. And the thing is again, when you, if you want to do like some diagnostic testing, you can check their levels of compliments, their levels of C2 and C4 will be low. And if your friends at the nbimidine ask you how do you treat hereditary dima, you want to think about drugs like ecalantide? Ecalantide is a direct inhibitor of calicrine, it's spelled as ECA, WLATIDE. Ecalantide is an inhibitor of calicrine, so it prevents the formation of bradykainin. And then another drug emission, an nbimix ams known as i-catiband, so i-ca-at-i-b-a-n-t, i-catiband, i-catiband is a not-pant, bent. i-catiband is a bradykainin receptor antagonist that can be used in the treatment of hereditary and your dim. Now, what did they give you a question about a child? And they tell you that this child when he was born, this child was hypotonic, and then they tell you that now it's like a 15 year old boy, and this boy eats a ton, he's like super obese, he's being like, I don't know like, in the 99.9% towel, or let's say maybe it's like 50 or something crazy, right? And then they tell you that this child has almond eyes. If you see that, what are you thinking about? Well, I hope you're thinking about pre-davillis syndrome, right?

Pre-davillis syndrome, the classic presentation would be a child, it would be a boy, not a girl, it would be a boy that has obesity from hyperfigia, like it's a ton, and these kids usually tend to have like some mild amounts of intellectual disability, right? So, and they may also have like an almond eyes, like almond shaped eyes on nbimix ams. Now, what is the chromosome that's all screwed up in a child that has pre-davillis syndrome? Well, I would hope you're telling me chromosome 15, chromosome 15 is the chromosome that does not work in a kid that has pre-davillis syndrome, right? And very high yield to know that on nbimix, like actually, like the nbimix, they love you to know like the two genetic mechanisms that potentially on the lie, the development of pre-davillis syndrome, and also I guess it's close causing injury, remember, injury one syndrome would be in a girl, okay? And that girl is, you know, some people call it like the happy puppet syndrome, it would be like a girl with like inappropriate laughter and things of that nature, right? So, if you see that think about a think about a pre-davillianjoman. So, the two genetic mechanisms I'm talking about, the first one, probably the more common one you see on exams is something known as genomic imprinting, because the thing is the gene, let's just call it some gene, okay?

Some gene that controls pre-davillis syndrome and in joman, the thing is if you're a boy, I mean every human being regularly had inheritance from mom and dad, the thing is if you're a boy, the gene that is active in you is dad's gene, you're also inherit mom's gene, but you turn it off with genomic imprinting. So, I mean, that's the normal situation, you know, dad's gene works well, you use genomic imprinting, you shut down mom's gene, but if for example dad's gene has a mutation, but you already still have this genomic imprinting already shutting down mom's gene, then you're gonna have a lot of problems like pre-davillian, right? Now, in the situation of a girl, right? Again, girl inherits gene from mom and from dad, right? Well, the thing is that's gene is shut off like genomic imprinting, but mom's gene, if you have a mutation in that then you get injurement syndrome. Now, another genetic principle you want to think about that underlies pre-davillis syndrome and injurement syndrome is something known as a uniparental dicemium. So, what we've been here for a second, I just explained that if you have a mutation in dad's, let's say you're a boy, right?

You inherit that some gene that I'm referring to, you inherit some gene from mom and dad, but because you're a boy, mom's gene is shut off by genomic imprinting, and then that's gene, if you have a mutation in it that you get pre-davillian syndrome, well, think about it, you can also actually get a similar problem if instead of getting both genes, let's say like, oh, you get one gene from mom, one gene from dad, let's assume you're a boy, and then let's say you get both of your some gene chromosome 15 from mom, then you're kind of screwed, right? Because because they are both mom genes by default, both of them will be turned off genetically, right? By genomic imprinting. So, a boy can have pre-davillian syndrome if he inherits both of some gene chromosome 15 from mom, and a girl can have injurement syndrome if she inherits some gene chromosome 15, if she inherits both of them from dad, that is why that phenomenon is known as uniparental disome, disome means two genes, uniparental means you're getting it from one parent, okay? Again, I promise you these are all very high-eal things, you want to keep at the back of your mind, for example, and then what are the drugs that have been shown to improve survival in a person that has heart failure? What are the drugs that improve survival in heart failure?

Well, I hope you're thinking about drugs like your ACE inhibitors, remember your ACE inhibitors, the cleavondutensin-1, so you have, you know, like decreased, I mean sorry, your ACE inhibitors they inhibit and your tensing convertion enzyme, so if you inhibit and your tensing convertion enzyme where you have less cleavage of and your tensing one to form and your tensing two, right? So, ACE inhibitors, your AR Bs, they've been shown to improve survival in heart failure. Another group of drugs are your audosterone receptor antagonists, right? So, drugs like Spirino lactone and Eplarylon, remember, Spirino lactone can cause, Spirino lactone can cause kinachomastia, right? It can cause kinachomastia because it's also an adrogen receptor antagonist in addition to being an audosterone receptor antagonist. Remember that kinachomastia is not something you'll find with Eplarylon, and then I'll not prove that in pro-survivolence HFI or beta blockers, right? So, drugs like metoprolone, cavedolone, and extended release B-soprolone, okay? Those drugs also improve survival in CHF. And then in African-Americans, right? The drug bibl, which is the combination of hydrozene and isosobidinitrate, has also been shown to improve survival in the setting of CHF. So, those are all high-yield things to keep at the back of your mind with drugs that improve survival in CHF.

And then, if they give you a question about a patient that's on an anti-psychotic and this patient gets a diluted cardiomyopathy, what drug should you be thinking about? Well, I hope you're telling me about clasping. Remember, clasping can cause a myocarditis, and that can ultimately lead to a diluted cardiomyopathy. What if you get a question about a patient that's placed on an anti-psychotic and this patient develops hyper-prolactinemia? What are you thinking about? I hope you're thinking about a respiratory donor, right? And remember that arises from the tuberum from developed pathway. And another thing you should also think about is are repyprozo. Remember, a repyprozo is a partial agonist at dopamine receptors, or G-soids, essentially, acting as an antagonist, but it's actually a very good, it's actually a fairly common cause of hyper-prolactinemia as well on endemic exams in the setting of using an anti-psychotic. Now, what if they give you a question about a patient that's placed on an anti-psychotic and this person now has to resound the point? What are you thinking about? Well, I hope you're thinking about the proceed, don't remember the proceed, don't can prolong the cutie interval and not prolong cutie interval, can then predispose the pressing to getting to resound the point and then they die.

And then, it wouldn't they give you a question about a patient that was placed on an anti-psychotic and this person has like now has an increased, um, um, chemotherapy A1 C, what are you thinking about? But I hope you're thinking about o'lanzapine, okay? Remember o'lanzapine can cause the metabolic syndrome and it can cause obesity, right? So that's a higher thing to know on exams. Now, what if you get a question about a patient that was placed on an anti-psychotic and this patient now has a ultrasonic fever? What should you think about? Well, I would really hope that you think about something along the lines of clasapine, remember clasapine can cause a granular cytosis. And then my final question, what if you get a question about a patient that was recently placed on an anti-psychotic and now this patient has visual difficulty and then they tell you that oh, on fondoscopic exam, you notice a classification of the lens. Well, I would hope on that those circumstances, you're thinking about quithiapine, remember quithiapine can cause a cataract, right? There's this numonic that quithiapine causes quinaurex, that's a classic thing you will see tested on end-earning exams. Now, what if they give you a question about like a 55-year-old guy? Let's say this guy has smoked like two bucks of secrets every day for the past 40 years. So maybe stay smoked at 15. Yeah, that's a pretty, that's a pretty durable.

I mean, not legally, but you know, people smoke pretty early in life, it just happens unfortunately. So if you get a question about that person and then this person, they tell you that for the last three months, he has been having like, you know, like cough, like this chronic cough, and then you also notice is that he has a hard time rising up from a seated position. If you see that, what should you think about? Well, I hope you're thinking about like Lambert, it in my astenic syndrome, right? Remember, Lambert, it in my astenic syndrome is a primal plastic phenomenon that classically I resist in the setting of small cell lung cancer, right? Remember, the other part of your plastic phenomenon, phenomena, not phenomenon. So that's awful English. Phenomena, right? That can arise in the setting of small cell lung cancer is, you can have like the topic easy teach production. Remember, that's the one that does not suppress with the administration of high dose dexamethasone, right? So that's one. And then the next, the other one is a SID, right? So like SID, where the person will have like a high urine or similarity and a low serum or polarity, right? So that in addition to Lambert, it in my astenic syndrome, at the classic primal plastic phenomena that are observed in the setting of small cell lung cancer. Now remember, what is the pathophysiology? What is the mechanism behind Lambert, it in my astenic syndrome?

Well, the mechanism is that you make autoantibodies against something known as the pristine optic voltage-gated calcium channel, okay? You make autoantibodies against the pristine optic voltage-gated calcium channel, right? So the thing is, so you may say, okay, divine, how do I make the diagnosis of Lambert eating? Well, actually, the way you can make the diagnosis is, you can actually do like EM Gs, you can also do like a nerve conduction study. So your friends at the MDMA, they tell you that, oh, you know, they expose this pristine in the course of a nerve conduction study, so like a 10 hertz stimulus. And then you get like a certain amplitude of muscle contraction. And then they tell you that, oh, they expose this patient to, you know, like 20 hertz, right? And then you get like a, like a bigger amplitude of muscle contraction. Or they tell you that, oh, this patient keeps rocking, like this patient, you know, it tells you that it's hard for him to get up from a seated position. But if he rocks himself back and forth and forth in a chair, he then finds it easy to get up. If you see that, think about Lambert eating my astenic syndrome, okay? Think about Lambert eating my astenic syndrome. The thing is, and I mean, I literally made a really post about this, maybe like a couple of minutes ago. But there's this thing I want to encourage you to do as you're studying for the USMLE step 2 CK exam. Back in the day, it was just okay for you to just memorize associations.

And you'll be set for step 2. The more associations, you need the better. But our luck truly encourage you to take a step beyond that these days and try to actually understand the pathophysiology behind the diseases. You're trying to study, okay? Why do I say that? The reason I say that is these days, the NBM is now almost making the step 2 CK exam like kind of like a step 1 like exam, where they actually expect you to actually understand pathophysiology behind what you're studying. So that those are all actually very important things to keep at the back of your mind, right? So make sure you actually understand pathophysiology because you, I mean like a common complaint, I mean you see I'm ready on SD Ns, people will say that, oh, like this exam looked, I studied so hard for this exam, but I don't know what's going on, like I don't seem to get what, like it's like I'm getting questions that are completely out of the blue. The thing is, it's not like the NBM is testing pathologies that they've never tested before. No, that's not what they're doing. The NBM is still in the business of testing classic pathologies, but the way they're doing these days is they are testing them in ways that you would not think to prepare for, right? So they can test like stuff that's you know, pretty classic, but they'll put it in a fashion where you're like, yeah, this thing looks really bizarre, right? So again, these are just all things to watch out for on exams.

Now the last topic I want to talk about today is Coriocarcinoma, I'm not going to freeze it as a question, I'm just going to go ahead and talk through it. It's a high old malignancy, I want to make sure you understand for purposes of the USM Ls. But the thing is the Coriocarcinoma, right? Obviously it's a malignant new plasma. So what are some key things that your friends at the NBM need test in the context of Coriocarcinoma? Well, one thing they can test is what is the biggest risk factor for Coriocarcinoma? Well, the biggest risk factor for Coriocarcinoma is gestitional trophoblastic disease, okay? The biggest risk factor for Coriocarcinoma is gestitional trophoblastic disease. And I mean, this cancer, right? It's regarded as like a germ cell tumor, okay? And remember that it has beta-HCG as its tumor marker. And this cancer loves to be testicized to the lungs. Like if you see a person that has a histrovalaggestitional trophoblastic disease, or they have a histrochoric arcinoma, and then they're now completing no shortness of breath. You want to think about that person potentially having long vets, okay? And the good thing about this cancer is it responds extremely well to methyl-tract site, okay? It is very sensitive to methyl-tract site. And again, like I said, the biggest risk factor you can see, the most common cause of Coriocarcinoma is having a history of a high-duty deformal. And again, remember this cancer arises from Prophoblastic tissue.

That is one of those step one-like pieces of information that your friends at the NBM need test in the context of Coriocarcinoma. That's one. Another thing you also want to keep in mind is you may actually get a question about a patient that has Coriocarcinoma. And the person is having like E-Fib, and the person is having like Taki-cardia, and having like Hyperreflexia, and having like Lidluck, right? That patient actually has Hyperthyroidism. Remember, beta-HCG, if you remember from step one, beta-HCG and TSH, they actually have fairly similar subunits. They actually differ by I think like maybe like one of my nosey dose, like some very many school difference, right? So the thing is when a person has Coriocarcinoma, those elevated levels of beta-HCG, believe it or not, can actually trigger hyperthyroidyptoxicosis, okay? So the thing that will happen under those circumstances is that the person will have like elevated levels of T3, T4, because beta-HCG can have like some again, some agonist activity at TSH receptors. So the person's T3, T4 levels will be elevated, but the TSH will be depressed, okay? Those are all high-youth things you want to keep at the back of your mind with Coriocarcinoma. So I'm going to go ahead and pause here. There are many other things I want to talk about, but again, this is supposed to be a rapid review podcast. So I'll make another podcast and finish up the high-youth things I want to talk about.

And as I say, again, of every podcast, I'd love for one or one to join for many exams. Step one, step two CK, step two CK, step three, pre-clinical medical exams, third-year shelf exams, the EBIM board exam for medicine residents, the internal medicine, intruding exam that you take in residency. I also do like comprehensive step two CK, step three, step one courses, although you need a group of five for that to happen. And then I also do this thing called longitudinal tutoring, where if you're like a first, second or third-year medical student, now tutoring for like your block exams or your shelf exams, and then at the same time, I'll concurrently tutor you for your upcoming USML exams. Most of the people have done that, we've found that to be like wildly, but many people that have done that with, they've actually done extremely well on the USML exams. And then I also offer these booster courses, like it's 20 hours for step one, and it's 10 hours for step two CK and step three, where if you at the end of your dedicated period of, or if you just want to again put most of the high-youth stuff that you'd like to see on your exam together, writing a very quick, very rapid high-youth format, like again, like the most news for this exam, just let me know again, you can either reach out to me through the website, or you can send me an email at divineintervention, podcasts with an SAD end at gmail.com.

And then I also offer something I call like a repair course, where if you have, like let's say you take a practice exam, unless your cardiology bar is very off to the left, right? These repair courses are like two to three hour courses, where I meet you, and I essentially go over pretty much all the high-youth stuff we expected to know for that subject area, for that US Emily exam. So that's again something you're interested in. I think I, I mean I do this mostly for people that are taking step two CK. Feel free to reach out to me, and I'll be more than happy to point you in the right direction with that. And then if you're, if you're a college student applying to Met School, so like an Amcass application, or a met student applying to residence, so like an ERS application, I offer like one-on-one like advice, you know, coaching for those things, right? So like rec letters, personal statements, editing applications, mocking reviews, I have worked with tons of people on that and again, most of the people have worked with, they've marched into their first choices with residency. So again, if you're interested in any of those things, or if you have like a college buddy that needs to learn for like Gen CAM, O Cam, Physics, Bio Cam, Histology, Physiology, I'm offered to learn for all those things. So have a wonderful rest of your day, I'll see you in the next podcast. God bless you. Thank you.

The neutrophil. CGD results from a defect in NADPH oxidase within the neutrophil, impairing their ability to generate reactive oxygen species necessary for killing certain pathogens.

Hyper-IgM Syndrome. Patients have low IgG, IgA, and IgE, but high IgM.

T cell deficiency (due to thymic hypoplasia), hypocalcemia (due to parathyroid gland failure), and hypothyroid symptoms (due to thyroid gland failure).

Autoantibodies against presynaptic voltage-gated calcium channels. This is often associated with SCLC.

Quetiapine. Mnemonic: Quinaurex (Quetiapine $\rightarrow$ Cataract).

A history of Gestational Trophoblastic Disease (GTD).

Deficiency of C1 esterase inhibitor, causing Hereditary Diffuse Musอาการ.

Interferon gamma ($\text{IFN-}\gamma$).

Absence of a thymus shadow.

ACE inhibitors/AR Bs, Beta-blockers, and Aldosterone receptor antagonists (e.g., Spironolactone).

Loss of function due to a mutation on chromosome 15 that affects the paternal allele, which is normally active in this region.

Risperidone (and other dopamine receptor partial agonists).

Deficiency of C1 esterase inhibitor, causing Hereditary Diffuse Musอาการ.

Interferon gamma ($\text{IFN-}\gamma$).

Absence of a thymus shadow.

ACE inhibitors/AR Bs, Beta-blockers, and Aldosterone receptor antagonists (e.g., Spironolactone).

Loss of function due to a mutation on chromosome 15 that affects the paternal allele, which is normally active in this region.

Risperidone (and other dopamine receptor partial agonists).