DIP Episode 270 - USMLE Step 2CK Rapid Review Series 43 (and upcoming 2CK Course 11/6-7)

Okay, welcome. My name is Divine. This is episode 270 of the Divine Intervention Podcast. And in this podcast, I'll be continuing the Rapid Review series for the USMELIS step 2 CK exam. This is actually going to be series 43. And really, into this podcast, one thing I want to focus on, just like weird stuff, but you don't see covered in many resources, but the end of the new, usually high yield for purposes of the step 2 CK and step 3 X. They just pop up a lot. So, I'll just encourage you really pay attention here. This is probably one of those ones you probably want to take notes with, because there are just many things that I will discuss here that you may not necessarily have heard of before. Or like, there are so-to differences, you may not think about. Well, those things, you see some of these NV Me questions. You're like, why is the answer this way? I've never thought about it this way. Again, that's something you want to know. And then for those of you that are taking step 2 CK anytime soon, I am offering a step 2 CK class, like a series of classes, from the 5th to the 7th of November. So, on the 5th, we have the Testikin Strategies class. And that Testikin Strategies class is going to be from 2 to 430, Mountain Standard time. So, that's 2 hours behind the Eastern time. And basically, we use again a bunch of well-written questions to Botress, Testikin Strategies that are helpful for the US Emily exams, especially step 2 CK and step 3.

And then on the 6th and the 7th of November, from 11 a.m. to 4 p.m. Mountain Standard time. So, that's again 2 hours behind Eastern Standard time, or have the 10 R course. It would just basically be split into 2 days. And we'll cover about 800 concepts from all the disciplines. So, P, Surgery, I, M, O, B, G, G, S, I, K, Neur. Over that period again, tons of people have taken this course. Tons of people have found it to be very useful. I have a very large list of people that have done really well on the step 2 CK exams after taking this course. So, if it's something you're interested in, just shoot me an email. And I'll be happy to point you in the right direction. So, what if they give you a question about like a soldier or, you know, like an athlete that was maybe running around, you know, 100 degree day or something like that. Let's say like in Arizona or Texas or New Mexico or something like that. And in detail, you that this person has ultra mental status, is confused, doesn't know where he is. And this person's temperature is like 104. What should you be thinking about on those circumstances? I would really hope you're thinking about a heat stroke, right? I really hope you're thinking about a heat stroke. A heat stroke is something that can happen in many different settings, right? But, classically, you'll be a person that's working around outside on a very hot day, right? It can be a soldier, it can be an athlete.

And typically, when a person gets heat stroke from this kind of cause, right? Because if you notice, the person was engaging in some kind of physical activity before they go into trouble. And if you notice a person having heat stroke from like some kind of physical activity, I will strongly, strongly encourage you to consider treating them with like immersion in ice water, right? Emersing those people in ice water is usually the prudent thing to do on MBM exams. And one thing that people routinely ask me is, define how do I differentiate between a heat stroke and heat exhaustion? The way you differentiate between both pathologies is people that have heat stroke. Look at the name, it has a stroke in the name. They usually have ultra mental status in the question. People that have heat exhaustion, they usually don't have ultra mental status in the question. Again, that's not a setting stone difference, but it's a difference that often helps you pick one apart from the other on an MBM exam. So, it may be like, okay, define why you highlighting all this physical activity. And saying, oh, if you see a person having a heat stroke from physical activity, you should treat them with ice water immersion. Well, let me explain. There are other things that can cause heat stroke that do not involve you engaging in physical activity.

So, for example, if a person is taking like over the counter-code medication, basically, diving hydramy, remember that can exert an anti-cule energy effect, right? Also, remember some of these same pathomimetic drugs, right? So, some of these drugs that have produced like adrenergic tones, some of these pressures, they can absolutely cause hypothermia, right? And again, that should make sense, because these drugs in some situations can increase your metabolic rate. Remember, fight-of-flight response so they can absolutely cause those kinds of problems, right? And also, some thanks diuretics in some cases, because again, if you're dried out, you're almost not able to distribute fluid very nicely around the body, right? So, those things can all cause heat strokes, right? But you're not engaging in any kind of physical activity when you arrive at those kinds of problems, right? So, whenever you see stuff like this, it's usually being an old person, because what are the people that take pressures, like usually super-seeking the hospital, or what are the people that take an anti-cule energy and all that stuff? It's gonna be an old person, right? And again, these people, they'll have the altered mental status, they'll have the high-feevers. But in this case, you want to actually cool these people down with evaporative cooling mechanisms, right? You basically want to cool them from an external perspective, right?

So, like, evaporative cooling, or, you know, you can put them on a fan, under like a fan or something like that. But in general, again, when physical activity is not involved, again, I know you may be like, divine, I don't care about this thing, you're saying, I promise you, you will care if you sit on an MBM exam. When a person has a heat stroke from taking like some kind of medication, you want to use evaporative cooling techniques. For a person that has heat stroke from physical exertion, you absolutely want to immerse those people in ice water, right? Emersing people in ice water that have like anti-colonage toxicity as the cause of the heat stroke is contraindicated on MBM exams. Again, very high you to know that. Against a subtle difference, but I promise you, this is something that, especially the newer MBM exams, like the stuff from 2020, they love this concept a ton, right? And then, what if they give you a question about a patient, and they tell you that this patient, you know, had to be paralyzed, right, for surgical procedure. And then they notice that during the course of the procedure, the patient is becoming harder and harder to ventilate, the patient's PCO2 is going up, right? And then they tell you that the patient has like a glucose etosis, right, and again, has a very high fever. If you see stuff like that, right, you absolutely want to think about what? You want to think about malignant hypothermia, right?

Remember malignant hypothermia, it's actually an autosomal dominant disorder. And usually it arises from mutations in calcium channels, right? It can usually be like the ryanidine receptor, right? So remember, that's a calcium channel. And in some cases, it can also be the dihydropyredine receptor. But usually it's a ryanidine receptor mutation that causes malignant hypothermia. And again, what's the thing that puts you in that position, right? If you're exposed to like anasthetic, right? So like, if you're exposed to like all these inhaled anaesthetics, I mean, all these volatile anaesthetics, like halothane, although no one uses halothane anymore, probably like in some developing countries, they still do that. But for the most part in the US, you really find that anywhere, anymore, right? Or you know, stuff like isofluorine, all those anaesthetics that end in A, right? And also don't forget succinocholine. Soxinocholine can absolutely trigger malignant hypothermia on an end beam exam, right? So again, the classic presentation, high fever, leukocyteosis, the person will have an increasing PCO2. They can make it like a surgery question, where the person is becoming hard to ventilate a few minutes to hours after the surgery was started. If you see that, you think about my ligand hypothermia. And again, you want to go ahead and stop the drug, right?

Remember, if a person is suffering from toxicity from any drug, the first thing you always want to do is go ahead and stop that drug, right? You want me giving someone something that's kind of crushing their, crushing their lives, right? So you stop the drug, and then the other thing you want to do on an end beam exam is to give them dantrullin, right? Remember dantrullin is a ryanodin receptor antagonist, although if your friends at the end beam wanted to get cute, instead of putting dantrullin as an answer, what you will do is you'll put calcium channel blocker as an answer. Because it's a ryanodin receptor antagonist, and the ryanodin receptor is a calcium channel, okay? So it's a ryanodin receptor antagonist that's very awesome for the treatment of... For the treatment of malignant hypothermia. And one thing your friends at the end beam can do with malignant hypothermia is they can ask which of the following represents the most likely electrolyte and normality in this patient? I hope you're telling me that it's going to be hyperchilemia, right? Because these people, they're having a lot of death of muscle cells. As those muscle cells die, right? They're going to release their cell soup into the surroundings, right? That's going to be hyperchilemia. So again, in some cases, they can literally give you a hyperchilemia question in the context of malignant hypothermia.

Obviously, you're going to give those people calcium and gluconeid first, you know, to stabilize the myocardium. You're going to give them insulin plus glucose, right? So they can drive potassium into cells. You want to give them like sodium by carbonate because that will create a metabolic alkalosis that will draw hydrogen ions out of cells. Potassium will go in reverse. You can give them a bit or two agonist like a bit or all right, that can again increase the activity of the sodium potassium ATP is pump. And that will drive because remember the sodium potassium ATP is pump gets three sodium out of cells and puts two potassium into cells, right? So you can give them that you can give them that a bit or all bitter to agonist and increases the activity of the sodium potassium ATP is pump now drives potassium into cells and that will help those patients, right? And also that insulin plus glucose business remember insulin loves to activate that right can activate the sodium potassium ATP is pump and also give you a similar effect, right? And also remember you can potentially give these people like vigorous fluids, right? And then accompany that with fluorescent light, right? So you're giving them a ton ton ton ton ton ton of fluid that fluid will cause them to pee a lot and if you're giving them fluorescent light, you can accelerate the rate of that pee.

Because remember if you're somebody is a lube diuretic and lube diuretics cause you to dump a ton of water because they make you volume depleted, they increase the activity of urine and your tensin, our dose-turing system, right? And our dose-turing if you remember the principle of the collecting duct, it will cause you to dump potassium in your urine, right? So you can essentially get like a potassium diuresis that way. And another thing you can also do obviously in hyperclinia, right? You can give Kxcel it, right? Remember Kxcel it makes K exit out of the body, right? So it's sometimes you may see it instead of calling it Kxcel it on an exam to mess with your head, we can call it sodium polystyrene sulfonyl. Try to see that again, sodium polystyrene sulfonyl, right? So it's a potassium by near as in binds of the potassium and you pop it out safely. Although remember it actually increases the presence risk of bowel and the crosses, that's why they are beginning to think twice about using it in many hospitals across the US. And then remember that people that have malignant hyperthermia, these people can absolutely get rubbed on myoluses, right? They can get rubbed on myoluses, they can, so if you see a rising creatine in the setting of malignant hyperthermia, right? It's going to be myoglobin that's collecting in those people's urine causing an acute tubular necrosis, right? Essentially just crushing these people's are reno tubules.

Again, this is one of those reasons why giving a ton of fluid is very helpful in these people, right? Giving a ton of fluid is extremely helpful in these people because you are washing away that myoglobin in those circumstances. And then please also do not forget is actually important to remember the findings in the urine, right? In a person that has a rapidomyelosis, remember they will have this thing where you're looking at the urine, you're like, woo, this urine has four plus blood, right? But then you notice you're like seeing like zero to two or three red blood cells per high power field. That makes absolutely no sense. If a person has like four plus blood in the urine, you're going to be seeing like a ton of red blood cells, you're going to be seeing like 50 to 100 red blood cells per high power field, right? So if you're seeing four plus blood, but you're not seeing a commensurate number of red blood cells per high power field, then that should tell you that you are very, very, very, very likely dealing with some kind of rapidomyelosis, right? In fact, to be honest with you, I think of rapidomyelosis as almost like the albiuminol, cytologic dissociation of the urine. Remember, albiuminol, cytologic dissociation is a phenomenon that we find with Guillain-Barré syndrome, right? But in Guillain-Barré syndrome, the thing we notice is that the presence, you check their CSF and they will find that you'll find a ton of protein, right?

But normally when you see a ton of protein, you should find a lot of white blood cells, right? So if you see a ton of protein, like five plus protein in the CSF, and then you're seeing again zero to two white blood cells per high power field, that makes no sense, right? So there's a dissociation between the protein counts, that's the albiuminol part of things, and the white blood cell counts, that's the cytophane, right? So that's like albiuminol, cytologic dissociation, right? So that's what we find with Guillain-Barré syndrome. We find an analogous thing, right? In a person that has, with this time in concerns, blood and red blood cells in the urine of a person that has a rapidomyelosis. And then, what if they give you a question about a patient, and they tell you that this patient has a history of like diabetic gastroparases, a person was recently studied on a drug, and then no, this person has like, confused, has altered mental status, has like a ton of muscle rigidity, is super tacky-cardic, has a very high blood pressure, right? And they tell you that this person has no myoclonus, right? And this person's deep tendon reflexes are decreased, pay attention to that decreased deep tendon reflexes. If you see this, what do you want to think about? Well, I hope you're telling me that this person likely has NMS, right? So this person almost certainly has some kind of neuroleptic malignant syndrome, right?

So neuroleptic malignant syndrome, remember, it's something that can happen when you're exposed to a drug that blocks dopamine receptors, right? Although there's one new scenario that your friends at the emb amnesia have studied going after, I'll talk about that in a second. But basically, this person has the diabetic gastroparases, obviously you're giving a prochaineetic agent like metal clopromide. So the clopromide, right, is a dopamine receptor antagonist, right? So you can absolutely cause neuroleptic malignant syndrome. The key thing that you'll find in your, that helps you differentiate NMS from malignant hypothermia is the predisposing factor, right? People that have NMS, these are people that have taken, you'll see a temporal association with exposure to some kind of dopamine blocker, some kind of anti-psychotic, right? So like, olandsapine, alopereidol, quityapine, stuff like that, right? But in malignant hypothermia, the exposure will be to some anesthetic-based agent, right? Again, all those fluorines, succino-coline, things like that. Now, the one weird exposure that you may see, especially on the newer NBMS, in a person that has NMS, it will not be a person that has taken any kind of dopamine antagonist, but it will be a person that is withdrawing from exposure to a dopamine energy agent. Let me give you an example, right? So they can give you an NMS question in a person that is being treated for Parkinson's disease, right? What do I mean by that?

So let's say, for example, a person is, you know, taking carbidopa-livo-dopa for Parkinson's, and then for some reason, the person is not able to fill the prescription, and then, if not taking the medications for like two weeks, and then, in detail, that this person has a leukocyteosis, has a leukocyteosis, has a lot of rigidity and all that stuff. If you see that, you absolutely want to think about NMS, right? You absolutely want to think about NMS. And again, how do you treat NMS? Stop the badness, right? Stop the bad bad bad drug that's causing their problems, right? And go ahead and give those people down trolling. Again, don't forget that Rianodine receptor antagonist, although NMS is not a genetic condition, unlike malignant hypothermia. In general, I will just say that in general, right? So for NMS, you're going to give down trolling, and then usually, you can also give a dopamine agonist, right? So you can give something like bromo-cryptine or carburegoline, right? Although, pick down trolling first as treatment, if you don't see that, then you can go ahead and give like a dopamine agonist. If you don't see a dopamine agonist as an astray, you can give a benzo, you can give a benzo-daisy pain, right? And then, remember, something that may look a lot like NMS is serotonin syndrome, right? And again, serotonin syndrome can have many triggers on NBM exams. Basically, they'll give you a bunch of drugs that can cause those problems, right? So like SSR Is, right?

SNR Is, right? So remember, SNR Is like vanilla vaccine, duloxetine, melmacipran, desvenal vaccine, right? Don't forget your limizolid. Limizolid is an antibiotic that's used to treat MRSA, right? But remember that it also has some weak monominoxidys inhibitor properties, so it can absolutely cause serotonin syndrome. Don't forget, so much trip time, your migraine meds, your migraine meds, the serotonergic agents, right? The serotonin receptor agonist, so it can absolutely cause those kinds of problems. And then also don't forget, like some of these have our preparations, like St. John's Wart, St. John's Wart, basically is an SSRI, right? So he absolutely has serotonergic properties that can cause serotonin syndrome. Another classic drug emission you examine is MDME, XDC, right? XDC is a serotonergic agent, so they can make a serotonin syndrome question based on that. And then also don't forget your other psych medications, right? So like TCA's, you know, tricyclic and anti-depressants, don't forget your MEO Is, your monominoxidys inhibitors, right? So drugs like phenylzene, tranelcypromine, isocarboxazid, right? Those are all examples of monominoxidys inhibitors, those things can all trigger serotonin syndrome. And the thing is, many people are classically used to seeing that, oh, you're in two serotonergic agents, so it caused problems, fine, whatever. But the thing is your friends at the MDME, they're getting smarter. So what do they do these days?

So give you a question about a person that's taking like one serotonergic agent. But they recently just discontinued another serotonergic agent. Again, if you see that, that can predispose a person to getting serotonin syndrome. I mean, like for example, if you're taking an SSRI or an SNRI, you're supposed to wait for two weeks. Before you start a patient on like a TCA or an MEOI, if not, you are raising that patient's risk of serotonin syndrome. And one key critical thing actually, now I help you differentiate between NMS and serotonin syndrome on MDME examples. People that have NMS, they have no myoclonus. What people that have serotonin syndrome will have myoclonus. People that have NMS, they'll have a decrease in their deep tendon reflexes. What people that have serotonin syndrome, they'll have an increase in their deep tendon reflexes. So basically, just think of it as the double negative for NMS and the double positive for serotonin syndrome. The double negative for NMS is the absence of myoclonus and a decrease in deep tendon reflexes. The double positive for serotonin syndrome is the presence of myoclonus and an increase in deep tendon reflexes. And in general, when a person has serotonin syndrome again, go ahead and stop the offending agents. But actually, serotonin syndrome, the first line treatment for serotonin syndrome on MDME examples is a benzodiazepine.

This is super high, you'll know the first line treatment for serotonin syndrome on an MDME exam is a benzodiazepine. So if they give you a benzodiazepine as an answer and see proheptidine as an answer, pick a benzodiazepine over see proheptidine. The only time you should pick see proheptidine is if a benzodiazepine is not given as an answer choice. Again, you may be like, hmm, the wind is kind of weird. I'm not buying what you're saying. I promise you, you really should buy everything I'm selling right now. It's extremely high yield to know the stuff, especially for the newer exams. If you remember, if you compare, because again, this is one of those things that you pick up on as a tutor and as a teacher for a long period of time. I mean, I've been making podcasts now for quite a while. Right? So the thing is the character of MDME exams between 2017 to 2019 is vastly different from the character of MDME exams in 2020. The MDME exams in 2020, they test the same pathologies that you're used to, but they test more subtle things with those pathologies. And they're letting go essentially of all these buzzwords. And they're giving you, they're beginning to give more descriptions of these buzzwords or usual presentations of common pathologies that you've previously learned. Because other than like these risk factors, prognostic factors, most common causes of death and all the stuff with the military and healthcare systems, the MDME still tests in the exact same knowledge.

They're just testing it in new ways. Right? So again, when you see me emphasize unusual presentations of things, pay special attention to those things, because those things in general are very high yield to know for purposes of exams. And I'm going to be writing them up soon, since this is a rapid review series. Right? But so what are some things that I think I want to throw in here. Right? So again, let me talk about some quick, hypertensive syndroms. Like some quick, let me call them almost like acute hypertensive syndroms that you should recognize and be able to treat on an enemy me exam. Right? So obviously they give you a question about a person that has a history of morphine or a history of like Turner syndrome. And then this person has like sodium onset severe chest pain. Right? And the person is very hypertensive. If you see that, I really hope that you're thinking about the audit dissection. Remember, a audit dissection, what you always want to give those people, you want to give them a bit of blocker first. Right? You can give them any kind of bit of blocker. You can even give them a bit of law, which is an alpha bit of blocker. Right? So you give them a bit of blocker. A classic fake out answer on MDME exams is hydrozene. Never pick hydrozene for your dissection. It worsens morbidity in the audit dissection. If you pick that answer, I guarantee you will get it wrong. Right?

There are many studies that are proven that hydrozene is an awful option in a person that's being treated for for your dissection. Right? And then what if they give you a question about a patient and a patient is going through like some kind of CFF exacerbation. Right? For patients going through like a CFF exacerbation and you know, they have like pulmonary gima and they are hypertensive. If you're seeing hypertension in the setting of a CFF exacerbation, what kind of drug do you want to give those people? Want to give them something like nitroglycerin and want to give them something like nitroperside. Right? Those things will help in those circumstances. What? Well, those things are vinyl dilators. Right? So because they have vinyl dilators, they're going to pull that blood in the legs where it will kill you. Right? And take it away from the lungs where it will kill you. Right? So you give again a nitrate based compound, those are vinyl dilators. Right? And those things will also decrease by your cardiovascular oxygen demand. Right? So you give nitroglycerin or nitroperside in those circumstances. Right? And then if a person is very hypertensive, right? And let's say those people have like they have like very thick skin, they have like a long history of good. Obviously that person has clear dermarino crisis. Right? When a person has clear dermarino crisis, you absolutely want to give those people like an E-synhibiter on ER, like on ERB, a stripping board.

First one should be an E-synhibiter enalapril, like cyno-pril, stuff like that. Right? And then if a person has a hypertensive emergency on ERB, let's say these people tell you that this person has a history of ETB code depression or started a new drug and then started having like an altered mental status at a restaurant and then the presence block pressures like 250 over 130, like crazy high blood pressure. If you see that right, you're thinking about some kind of tyramine food crisis, right? If you see the thyroid hypertensive crisis, because remember tyramine is a sympatomymetic, it's broken down by monominoxidics. Right? So if a person is on an MEOI, again something like trinocypromine or isocraboxazid or phenolzine, that's going to inhibit the MEOI. If MEOI is taking out of commission, then guess what? You're not going to be able to break down all, you know, metabolize. Tyramine, right? So tyramine will go and do it, sympatomymetic stuff and that can cause some pretty significant problems for the patient, right? That can cause some pretty significant problems for the patient. So just again, something you want to keep on the back of your mind for these exams, right? So when a person has that kind of situation, I want to give that person phentolamine. Phentolamine is the drug of choice in those circumstances, although you can also use mitroperside, but almost certainly the first thing you'll like to see on an MEOI exam is phentolamine.

Phentolamine is a reversible, non-selective alpha blocker, right? That can help with treating those kinds of hypertensive emergencies. And then obviously if a person has hypertension in pregnancy or some kind of hypertensive emergency in pregnancy, you know, usually in the setting of like, preeclampsia or a clumsy, what do you want to give those people? Typically on MEOI exams, you want to give those people like labidolol, you can give labidolol, you can give my cardiopine or you can give hydrozine, right? This is one of those rare hypertensive emergency problems where given hydrozine is fine, okay? Pregnant women, hypertension, preeclampsia, clumsy, if you're trying to cut down their blood pressure, go ahead and give those people hydrozine, right? Or labidolol or my cardiopine, right? Remember, you cannot give ACE inhibitors or AR Ps to pregnant people or those direct training inhibitors, like, so drugs like a list screen, for example, you can do that, right? On an extra per side, those things are bad for the baby, right? So you want to give those things on that little circumstances, right? So I think I'm going to go ahead and stop here. So thank you for listening. I hope you find this to be helpful. For those of you that, again, I'm going through the ERAS process. I wish you all the very best. If you need help with mock interviews, feel free to reach out to me. And then please subscribe to the website, right? It's a Word Press website, divininginterventionpodcasts.com.

And then I also have a You Tube channel, Divine Intervention, US Mly Podcasts and videos, right? So please subscribe to that. And then I also have this podcast on Apple Podcasts and Google Play. I think it's not called Google Podcasts and also Spotify, right? So, you know, please subscribe, leave any feedback. So it's helpful. And then one other thing I think I want to mention is the most recent 150 podcasts I make at the things you will find on the podcast apps. If you want to find all the podcasts, including the old ones, go to the website, right? It's something that's completely out of my hands. It's like a Word Press rule, essentially, that I cannot circumvent. Trust me, I have track. So thank you for listening. God bless you and have a wonderful evening. I'll see you next time. Thank you.

Exertion involves intense activity; drug toxicity often occurs in older adults without recent strenuous activity.

Evaporative cooling (e.g., fans/misting), as ice water immersion is contraindicated.

NMS has decreased deep tendon reflexes and no myoclonus; SS has increased deep tendon reflexes and myoclonus.

Benzodiazepine.

Dantrolene sodium (a ryanodine receptor antagonist).

Labetalol, Hydralazine, or Nicardipine.

Dantrolene sodium (a ryanodine receptor antagonist).

Volatile anesthetics (e.g., halothane) or succinylcholine.

Myoglobinuria leading to acute tubular necrosis (AKI).

Hyperchilemia.

Benzodiazepine.

Finding a high protein level (CSF) or positive dipstick blood (urine) without a commensurate number of white blood cells or red blood cells, respectively.

Phentolamine (a reversible, non-selective alpha blocker).

Dantrolene sodium (a ryanodine receptor antagonist).

Volatile anesthetics (e.g., halothane) or succinylcholine.

Myoglobinuria leading to acute tubular necrosis (AKI).

Hyperchilemia.

Benzodiazepine.

Finding a high protein level (CSF) or positive dipstick blood (urine) without a commensurate number of white blood cells or red blood cells, respectively.

Phentolamine (a reversible, non-selective alpha blocker).