DIP Episode 394 - USMLE Step 2CK/3 Rapid Review Series 76

Okay, welcome. My name is Divine. This is episode 394 of the Divine Intervention Podcasts. Into this podcast, I'm going to be continuing the Rapid Review series for the USME Li step 2 CK-SL Step 3 exams. This is going to be Series 76. If you're taking step 2 or step 3 or complex level 2 or 3, anytime within the next, I'll say like four weeks, I have a 20 hour review course taking place starting on Monday. There are going to be four hours every day from Monday to Saturday. We're going to be skipping Wednesday. So, it's going to be on Monday, Tuesday, Thursday, Friday and Saturday from 5 to 90 and Pacific Standard time for our day. Again, if you're interested, just shoot me an email through the website. I'll give you some more details on cost and registration. And then I have the second version of the disc school is the 75 hour step 2 CK school. Obviously, that also applies to step 3 and complex level 2 or 3 taking place within the first weeks of July. Again, also over Zoom, that one has a cap on the number of people that can attend. So, shoot me an email through the website. I'll give you some more information and you'll be able to sign up. Okay. So, what did they give you a question about 36 year old male? They tell you that he was brought to the emergency room because he was ataxic. And then they tell you something about how he has like optic disc hyperemia on physical exam. He has like some kind of visual impairment.

And they tell you that you know, he lives in a rural area and he consumes homemade whiskey or whatever. What should you be thinking about? Well, I really hope you're saying, oh, the varnish. It sounds like this guy has methanol intoxication. Again, the key that they give away clue here that, oh, this is probably something of methanol is the problem with the optic disc. Whenever he's optic disc hyperemia, I really, really want you to think about methanol intoxication. So, remember that methanol can ultimately be converted to formic acid. It can be converted to formaldehyde. That's probably not a good thing, right? I mean, think about it. We literally use formaldehyde to preserve biological specimens, maybe not the best idea in the world, to have something that preserves biological specimens be the exact same thing that is forming in your body, right? So, again, once you see problems with the optic nerve, once you see problems with kidney nerve too, I really want you to think about methanol intoxication. So, what are we usually going to do for these people? Typically, what we're going to do for these people is we're going to give them a drug known as formepizol, right? So, remember, formepizol is a drug that inhibits alcohol dehydrogenase. So, by inhibiting alcohol, dehydrogenase, you prevent the formation of the nasty, nasty byproducts of methanol metabolism. Remember, we can also use formepizol for treating ethylene glycopoysen.

Remember, ethylene glycopoysen is something you're going to find in people that consume antifreeze. Again, that antifreeze can be converted to toxic metabolites that can be problematic. So, typically, on imbim exams, it's pretty high you to remember that these people should get formepizol, right? Formepizol. And don't forget that people that have ethylene glycopoysen, they can also go into renal failure because they have a very powerful nephrolithiasis. They can form these calcium-oxalate stones. Now, who is the other person that can get calcium-oxalate stone problems, some exams? I really hope you're saying, oh, divine, it's going to be the people that have Crohn's disease. Because remember Crohn's disease, those people tend to have issues with the terminal elium. When you have terminal elium problems, the thing that's going to happen is you're going to reabsorb too much oxalate. So, that's going to be pretty spozile forming oxalate stones. And you can absolutely, positively get calcium-oxalate crystals as a result of that on exams. Okay. Now, what if they give you a question about a 32-year-old male? They tell you that, you know, for the last two days, he has been having a lot of vomiting, he has been having a lot of bloy diarrhea.

And the tell you that he was admitted to the hospital, actually, like he came into the hospital like three weeks ago for the management of Pylon of Ridesh and he was given a septriac zone and he got better and he was then placed on an outpatient floor when the lung regimen. And then now he has this diarrhea. When you see something like this, right? Obviously, this is going to be seeded, right? Again, whenever you see a person having diarrhea, and you see a recent association with them taking some kind of antibiotic, you really, really want to think about C-Death, right? C-Death. Remember, sometimes on exams, instead of calling it C-Death, they call it pseudo-membranos colitis because you may see pseudo-membranes on colonoscopy. In fact, I would encourage you to be able to identify pseudo-membranes on imaging for your test, okay? It's something I would encourage you to be able to identify. And then, sometimes, they can even call it, again, like an antibiotic-induced diarrhea or something like that. So just something I want to keep in mind. And so, what we mean is, oh, divine, used bloody diarrhea for C-Death. Yes, I did. So, why is that important to know? Here's the deal. C-Death does not only cause watery diarrhea. It can cause both watery diarrhea and bloody diarrhea. So that's something I want to keep at the back of your mind, for example. It can cause both watery diarrhea and bloody diarrhea, right? And remember, how do we treat this stuff? Or how do we diagnose it?

Well, you're going to look for the toxin in the stool, right? And then, besides that, remember, in terms of tripping, you can treat with oral vancomycin, or you can treat with oral fidaxomycin. Remember, metronidousol is no longer a first-line agent for the management of C-Death on exams. That's something you want to keep at the back of your mind study-wise. Okay. Now, what if they give you a question about a person that has C-Death and they tell you that, you know, the person is being treated in the hospital and then they have the sodium onset, CV abdominal pain, and they tell you that the person is having like a very powerful fever, a very powerful lucositis. Whenever you see stuff like that, I want you to think of toxic makeup colon. Many times, your next step in those people is to get an abdominal x-ray because if you get an abdominal x-ray, chances are you will see that the transverse colon is more than 6 centimeters in diameter. And that tells you, huh, this person has toxic makeup colon, right? Toxic makeup colon, most times you can treat it conservatively, but if you see that there are signs of like balischemia, malincrosis, or bowel perforation, obviously, in those circumstances, that person is going to proceed to some kind of exploratory laparotomy, okay?

Now, what if they give you a question about a 29-year-old male and they tell you that, you know, for the past two weeks, he has noticed, or let's say for the past five days, he has been having like a rash, so they tell you that he has a rash on his strong, on his extremities, and then they also tell you that they give you some laps and you see that wow, okay? His white count is a little bit increased, or his white count may be normal, but he may notice that, huh, he has like 10% of your synophilus, and his scrapping is going to be a little bit elevated. If you see that, what should you be thinking about? I really hope you're saying, oh, divine, this sounds an awful lot like AIN, I could interstitial, now for right, this, right? To remember, it's many times he's going to be a triad, although you may not see every part of the triad in exams, right? But these people are going to have fever, right? They're going to have a rash, and they're going to have your synophilia. They may have your synophils and they're bleeding their blood, or your synophils are bleeding in their urine. That's AIN, again, it's a triad of fever, of rash, and of your synophilia. And again, remember, it tends to have a very nice association with taking antibiotics, especially those antibiotics that are useful for my stitis, so things like naff, saline, things like oxaselin, that's something you want to keep at the back of your mind for, for example.

Okay, now what did they give you a question about a patient? And they tell you that, oh, this patient is a 29 year old guy, and they tell you that he has been having polyurea for the past three days, and they tell you like a serum, they show you like a serum, osmolarity, you see, serum, osmolarity, or less sodium, he's serum sodium is like 150, right? So he has hypernatrhymenia, and then they tell you that, oh, he has a hypotonic urine, so his urine osmolarity is like 300. And then they tell you that, oh, the administer, you know, this patient gets a, this mopressant, right? Or the administrative agent, they may not tell you this mopressant, but the administrative agent, and they tell you that he is urinus molality, quadruples, and he's hypernatrhymerous, if you see that, what do you want to think about? Well, I really hope you're saying, oh, divine, something like this guy has diabetes in sypitus, more importantly, this guy has central diabetes in sypitus, right? So again, the fact that the patient has polyureia does not always mean that they just have like straight up diabetes militaries. Again, on endemic exams is always helpful to make sure that you're reviewing context, and you know the context behind something that you're discussing, right? Like one thing I always tell people in my review courses is that you can just say, oh, if you see this, it's always this on exams, that's, that's a pretty bad way to take exams.

You always gotta look at not just or a key fact, but you need to look at the context around that key fact. Like literally, I can, as a as a question writer, I can literally write an NVME question where a person has polyureia, and they have type 1 or type 2 diabetes, or they have polyureia, and that polyureia is because they have psychogenic polydipsis, or that polyureia is because they have diabetes in sypitus. So there are many questions I can write, right? So like, obviously, like if you see a person having like polydipsis and polyureia, and you notice that, wow, these people have really high glucose, that really high glucose context, or let's say they tell you that, oh, they have a history of some kind of autoimmune disease, like Hashimoto's or Adescent's disease, then that tells you that you know what this person probably has type 1 diabetes, right? Because again, remember many times when the NVME is a testing an autoimmune disease, they should give you a pass medical history of some other kind of autoimmune disease, right? But if I give you like, oh, polydipsia polyureia, and you see this person is having like a tough situation at home, like the appearance recently got a divorce, or the person has like some psychiatric thing going on, then that's going to be psychogenic polydipsia. But obviously, if a person has psychogenic polydipsia, they're also going to have hyponitremia at the same time, right?

Many times those people are going to drink so much water, they're going to dilute their serum, so they'll have hyponitremia. But the body is like, hold up, what's this with all this free water? I'm not going to deal with this, so they're going to dump a lot of free water in the urine. So the urine of the polarity is going to be low, right? But alternatively, if you see a person they have polydipsia, they have polyureia, and let's say they have a history of like meningitis, or they have like some kind of breeding jury or something, they want to think about diabetes in sepidus. In the original veneer that I gave, this person, when we give an agent, an oral agent, most times the NVME is not going to tell you what the oral agent is, but FYI, the oral agent is going to be a descompressant, right? Did the EVP? So you give descompressant, you notice that, wow, they're in a polarity quadruples, then that tells you all you need to know. The person has central diabetes in sepidus, right? So central diabetes in sepidus is the kind of diabetes in sepidus that arises because you literally have an ADHD efficiency. You literally have an ADHD efficiency. So you give, if you give ADHD, like if you have an ADHD efficiency, well, literally ADHD is anti-diarrytic hormone. You're not going to be able to hold on to any kind of water from the urine, right? So you're going to be dumping all your free water in the urine. That's why you have polyureia.

But you're going to have polydipsia because you're going to be like, man, I'm really hypernatrhypidus, I kind of need to dial down my body sodium concentration. So you're going to be drinking a ton of fluid, you're going to be drinking a ton of fluid. So those people, they're going to have hypernatrhypidus in trinia, right? But they're going to have polyureia with it. So if you see hypernatrhypidus in the presence of polyureia, think about diabetes in sepidus. But if you see hypernatrhypidus in the presence of polyureia, think about psychogenic polydipsia. But if you also see a person having polydipsia, polyureia with a very high glucose, then think about some kind of diabetes. Usually it's going to be type 1 diabetes or type 2 diabetes on exams, right? So again, in central diabetes in sepidus, these people just have an ADHD efficiency. So since they have an ADHD efficiency, if you give them an ADHD analog like this one person, they're going to respond, right? If you see that this person in the veneer that I gave, the person is urinous molality, a quadriple with the administration of decimal person. I want to say something about that. If a person is urinous molality rises by like 50 or 100 or 200 with the decimal person administration, that's not a response. A good response to the small person is when your urinous molality goes up multiple forward. So if it goes up by like 50 or 100, 200, that's not a positive response.

That person has the fortunate diabetes in sepidus, right? So again, central diabetes in sepidus is where you have an ADHD efficiency. So if you give the small person, that's actually the primary treatment for central Di, you're literally giving them what they're missing. Now remember for nephrogenic diabetes in sepidus, the way we're typically going to, the things that cause nephrogenic Di and exams, they have varied, right? So you can have lithium so they can give you a person that has bipolar disorder, is an immutableizer, and the person has a polyurea. You want to think about nephrogenic Di from lithium use, right? Remember if you have hypercalcemia, hypercalcemia can absolutely cause a person to have a nephrogenic diabetes in sepidus. In fact, this is one of the primary reasons when people that have hypercalcemia, when they present, on USMLE exams or in the real world, they tend to have a lot of volume depletion because they just lose an autonomous fluid because they literally cannot hold onto it. When you have high serum levels of calcium, that prevents your body from being able to respond to ADHD. So you're going to have a nephrogenic diabetes in sepidus. Also do not forget, the mechlocycling, it's an anti-biotic, it's a tetracycline, it can absolutely also cause nephrogenic diabetes in sepidus. Most times, nephrogenic diabetes in sepidus, you're going to stop you on the line-drog, right?

Or you can try to give those people thazide diuretics, you may be like, divine, why will thazide diuretics help? But if you think about it, the body reabsorbs a certain amount of the water that you get into your kidneys, into your renal tubules, early in the tubules. But then your reabsorbs, a good chunk of it, not all of it. Let me see more of a minor percentage of it in more distal parts of the nephron, like your principal cell or your distal-convoluted cell or your collecting ducts. So the thing is, because when people have nephrogenic diabetes in sepidus many times, it's a problem with the inect channel. The inect channel in the principal cell of the collecting ducts. Let me not say problems with the inect channel. Sorry, let me take a step back. They have more problems with the collecting ducts. Let me put it that way. Let me simplify things so that I don't get confused myself or confuse people. But they have problems with the collecting duct. Okay? They have problems with the collecting duct because that's where EDH does a lot of its job. So they cannot respond to EDH in the collecting duct. So if you give a thazide diuretic, the thing that's going to happen is, when you give that thazide initially, you're going to be volume depleted. Your body is going to be like, why in the world am I taking this thazide and volume depleted? So the thing is, whenever you induce volume depletion in a patient, the way the body is going to respond to that is by saying, you know what?

Let me start being a little wiser at reabsorbing water earlier in the nephron. So reabsorb more water at like the proximal trivilo whatever, since you're like, you know what the collecting ducts are not doing your job? Well, let me make more proximal parts of my nephron, reabsorb free water. So if you start reabsorbing the more proximal parts of your nephron, then that EDH activity you don't have is not going to matter as much because again, it's almost like you've induced a state, that state is being volume depletion, that just makes all the parts of the nephron that are earlier than the collecting ducts to become wiser and start reabsorbing more water. But if a person has nephrogenic diabetes in syabes from lithium, you can try to prevent it by giving an in-each channel blocker because we know that lithium, the way it causes this is nephrogenic diabetes in syabes is by literally entering through that in-each channel, we'll find in the principle of self of the collecting duct to mess up the sydmalinca skate of EDH. So if you block that in-each channel with an in-each channel blocker, like amylo-ride or triamterine, that's extremely helpful in preventing the nephrogenic diabetes in syabes that's associated with the use of lithium, right? So again, if you have nephrogenic D.I, many times you're going to stop the offendine medication or you can give thizideioretics.

But if you have central diabetes in syabes, since their problem is an EDH deficiency, go ahead and give those people an EDH analog like dysmopressant. So remember we can definitely use dysmopressant for the management of central diabetes in syabes. I guess since we're going to be wrapping up here soon, let's be able to talk about some other reasons why we may want to use dysmopressant on an in-beam exam. So remember you can use dysmopressant on an in-beam exam to also treat vomulibrands disease. Remember vomulibrands disease, it's a platelet disorder, right? So those people are going to have like the cosoblids, right? So a lot of nosebleeds, heavy menstrual bleeds, and things like that. It has all those omeldominantinheritans, right? And the problem there is that they literally have a deficiency of a vomulibrand factor, right? Remember since vomulibrand factor is involved in primary hemostasis, you know, that's formation of the platelet thrombus, you're going to have an increase in your bleeding time, your bleeding time is going to be up, right? But the thing is, your bleeding time is up in every other platelet disorder. So what are the tests can you use? Well, under the test you can use is to say, you know what? Huh? Let's use the Ristocetin Cofacteria C, because the Ristocetin Cofacteria C is a test of the adhesion step of primary hemostasis.

So blue-dahavon, wheelbrand disease, again, allosomol dominantinheritans, they're going to have an abnormal Ristocetin Cofacteria C, but they are also going to have an increased bleeding time. So it may be like, wait, but the fine, there's another disorder that also has similar labs. Yes, you're absolutely correct for something like Bernard Suleer, which is an orosomal recessive disease. There you have a deficiency of GP1 B. Those people are going to have an abnormal Ristocetin Cofacteria C, and they're also going to have an increased bleeding time. Again, the reason the Ristocetin Cofacteria C is abnormal is because GP1 B is involved in the adhesion step of primary hemostasis. So what is one further way you can differentiate vomulibrand disease from Bernard Suleer? Well, the way you're going to do that is by using the PTT, because remember, vomulibrand factor, one of its other job descriptions is that it increases the half-life of factor 8 in the circulation. So if you have deficiency of vomulibrand factor, factor 8 will have a much shorter half-life. So your PTT is going to go up, but the PTT is not increasing the person that has been a Suleer. So how do we treat vomulibrand disease?

We're going to give this more present because this more present is going to increase the release of vomulibrand factor from WIBL, from WIBL, from WIBL, Paladi, but it's PALA, so PALA, DEE is going to increase the release of vomulibrand factor from WIBL Paladi, but it's also if a person has hemophilia A, at least certain types of hemophilia A can be treated pretty well with this person, although most times when people have hemophilia A, you're just going to give them a factor 8 concentrates. But you can absolutely treat hemophilia A with desmo pressing because by increasing the release of vomulibrand factor, even if you have a partial deficiency of factor 8, you can increase the half-life of that little factor 8 that you have by giving desmo pressing. So since we're about 20 minutes, I'm going to go ahead and stop here. Again, I offer my review courses for all the USMLE exams, step 1, 2, step 3. I mean, step 2, you can't step 3 on complex level 2 and 3. That's the 20-hour review course, the MBME Testicking Strategy course, the 75-hour school, and then I also offer one on one tutoring for all the USMLE exams, step 1, 2, step 3. Preclinical med school exams, third year clerkship shelf exams. I do the same way I do longitudinal tutoring. So let's say you're studying off med school or you're just studying out third year. I can tutor you for all your shelf exams or I can tutor you for all your preclinical exams.

Many times as I do that, I'm also willing to be introducing you to a lot of USMLE concepts. So when it comes to your dedicated period for those exams, you already feel like pretty strong in terms of knowledge base. And then I also have these podcasts on the Minjo Podcasts apps, Apple Podcasts, Google Podcasts, Spotify, I have a You Tube channel, Divine Intervention, USMLE Podcasts and videos. That's where I post the videos that I make. And then I also have a new website called Divine Intervention Lifelessence.com. Actually, there's a podcast associated with that. It's on Apple Podcasts. It's called the Divine Intervention Life Lessons Podcast. And I post like two podcasts every week. Most of it is Bible-based teaching on common problems that are just faced by humanity or conundrums that people face. So if you're interested in any of those, just check out those resources. So thank you for listening to me today. I will see you in the next podcast. Have a wonderful weekend. God bless you. Thank you.

Optic disc hyperemia (due to formic acid toxicity).

Formepizole.

Fever, rash, and pyuria.

Ristocetin Cofactor C.

Crohn's disease.

In vWD, Factor VIII has a shortened half-life, prolonging the PTT; this effect is absent in BSS.

Inhibits alcohol dehydrogenase (ALDH), preventing the formation of toxic metabolites like formate and formaldehyde.

Urine osmolality quadrupling after administration of desmopressin (ADH analog).

Lithium use or Hypercalcemia.

Desmopressin (an ADH analog/vasopressin V2 receptor agonist).

Inducing volume depletion causes compensatory water reabsorption in the proximal nephron, bypassing the defective collecting duct mechanism.

Deficiency of vWF factor, which impairs platelet adhesion and increases the risk of bleeding.

PTT (Partial Thromboplastin Time). In vWD, Factor VIII half-life is shortened, prolonging PTT; this does not happen in BSS.

Inhibits alcohol dehydrogenase (ALDH), preventing the formation of toxic metabolites like formate and formaldehyde.

Urine osmolality quadrupling after administration of desmopressin (ADH analog).

Lithium use or Hypercalcemia.

Desmopressin (an ADH analog/vasopressin V2 receptor agonist).

Inducing volume depletion causes compensatory water reabsorption in the proximal nephron, bypassing the defective collecting duct mechanism.

Deficiency of vWF factor, which impairs platelet adhesion and increases the risk of bleeding.

PTT (Partial Thromboplastin Time). In vWD, Factor VIII half-life is shortened, prolonging PTT; this does not happen in BSS.