DIP Episode 390 - USMLE Step 2CK/3 Rapid Review Series 74

Okay, welcome. My name is Devine. This is episode 390 of the Divine Intervention Podcasts. In today's podcast, we're going to be continuing the rapid review series for the USM Listep 2 CK step 3 exam. That's going to be episode 7-4, but this is episode 390 of the podcast. Now, the thing I'm going to go ahead and say is if you're studying for step 2, see here step 3, I do have two courses that may be of interest to you. I have the MBME Testic and Strategy Scores, I guess maybe three courses. So the MBME Testic and Strategy Scores is going to be taking place this Friday from 5 to 7, 30 p.m. Pacific Standard Time. And then on Saturday, I'm going to be having the first of the two parts, 20 hours step 2, see case step 3 course. We're going to do 10 hours this Saturday and 10 hours the following Saturday. Basically, we're going to be meeting for 10 hours each day. We're going to cover a Neuro IM, OBGYN, PSYCH, Surgery, FX, Bios stats, multi-systems, persists and disorders, and a host of other subjects, communication, FX, healthcare systems and things like that. And then I have the second version of the disk school taking place in the first two weeks of July. Basically, we meet for eight hours, for a day for 90s, and then the final day we meet for three hours. I made a pretty detailed podcast on that about two days ago. That school has limited attendance. There's not a limited number of people for that. So if you're interested, just shoot me an email through the website.

If you want to sign up for any of these courses, again, any of these courses will help you tremendously for your exams. I've had tons of people take these courses and live done ridiculously well on their tests. So if you're interested, shoot me an email. They're definitely testing monos on my website. So just let me know. Again, if you see the way I teach on these podcasts, there'll be a very clear indication of what you're going to learn as we go through material during any of these courses. Okay, so what if they give you a question about a 45-year-old female? They tell you that for the last three weeks, she has had a dry cough and she's had some malchartness or breath and exercising tolerance. And then they tell you that on physical exam, she has a rash on her cheeks that spares the neisolibial folds. And then they tell you that of course the MBM is in their wisdom. They'll give you some answers. They'll give you an answer that says, and they'll give you an answer that says, so I'll go to the right answer, we start with doses. But you know some people, they will focus really hard on the rash, on the cheeks, especially the neisolibial folds. And that's what they will focus on. Right? We remember on these exams, we want to pick more encapsulating answers. This is going to be so I'll go to the next one. So let's talk about so I'll go to the next one. What in the world is happening with this patient? Well, again, you see a female dry cough.

Although remember, the MBM's can give sarcoid to men, but classically it's a female disease on exams. Right? So what are the key things you want to know for your exams about sarcoid doses? Well, remember sarcoid, they can have certain dermatologic manifestations. One of them is lupus perneal. Lupus perneal is the one I just described. It's literally a Miller rash just like regular lupus. We're going to find that in people that have sarcoid doses. Right? So lupus perneal is a dermatologic manifestation of sarcoid. And they don't forget that on sarcoid, these people can also have a rhythmanoidosam. A rhythmanoidosam is usually going to be on some extremity and it's going to be tender. Right? It's a form of subcutaneous tissue inflammation. Right? It's a form of panicolitis. Right? So the two dermatologic manifestations don't forget inodosam and don't forget lupus perneal. And actually those dermatologic manifestations are prognostic indicators. People that have lupus perneal with sarcoid, they tend to do worse than people that have a rhythmanoidosam with sarcoid. So sarcoid doses are pretty high yield to know. Right? These people typically they're going to have like hyaluronic phytonapathy, they're going to have sometimes in testicially infiltrates, sarcoid because it ends in ulcers. Right? So sarcoid doses. That means they have a restrictive pattern of long disease.

Remember, I've said this so many times, many times whenever you have a disease that ends in the word ulcers, you have a restrictive disease of said organ of that organ. Right? So like, you know, sarcoid doses causes restrictive disease in the heart. Right? I mean, in the lungs. So obviously those people are going to have an FV1 to FVC ratio that is normal or going to be increased. Right? And you know, since sarcoid can cause phybrotic lung disease, it would make sense that the Ae grid end should be increased. Because if you think about it, when you have fibrosis of the lungs, then the oxygen that's inside the alveolar looming isn't going to be able to equilibrate with the oxygen that is in the pulmonary capillaries because there's an increased diffusion distance because of the phybrotic disease in the way. So that can certainly increase the Ae gradient. Right? And you should know, right, that the DLCO, the diffusion capacity should be decreased. So why is that? Again, you're not going to be able to diffuse whenever you increase diffusion distance. Right? When we increase diffusion distance, remember, there's this role that says that I think of it as the DAT role. For people that have dental school buddies, you know, probably have to take the DAT. They probably have to take the DAT Wendy to get into medical school, the dental admissions test. Right? So the D's the diffusibility. It's directly proportional to the Ae. That's the surface area for diffusion.

And it's inversely proportional to the T. That's the thickness of diffusion. Right? The thickness of the surface available for diffusion. Right? So we know that diffusion can be affected by those things. And also, diffusion is also directly related to the pressure gradient, directly related to the pressure gradient. That's kind of high you to know. So if you think about it in a disease like, in a fibrodeclone disease like sarcoidosis, the thickness is bigger. And we know that the thickness is inversely related to the diffusibility. So the thing that's going to happen is, since the thickness goes up, the diffusibility is going to go down because they are inversely related. But you think of a person that has been a heavy smoker, an alpha-1 antitripsin patient, where they have a ton of proteins just chewing off their lungs. Well, your lung perenchema is pretty much gone. When your lung perenchema is gone, the surface area available for diffusion is going to be markedly decreased. Okay? So if you notice that the visibility on surface area are directly related, as the surface area goes down, then your diffusibility is going to go down. Right? They are directly related. So the mechanism behind the hypoxia or the reduced DLCL in a person that has emphysema, right, is a decrease in diffusion surface area. That's pretty high you to know, for example. Again, the MBM Es these days, especially for step two, they're very big on these physiological scenarios.

That's actually something I focus on pretty heavily on my courses. So let's go back to sarcoidosis though. So the DLC is going to be decreased. The A-grade is going to be increased. Right? And remember, again, people that have sarcoidosis many times, they can have this thin weird, they can have a thritis, erythema nodosum and the lung problems. So it's almost like a triad. So you see the person, they have erythema nodosum, they have a thritis, they have the lung issues like hyalur lymphatic and whatever. And that's what's called Lothgren syndrome, L-O-F-G-R-E-N, Lothgren syndrome. So how do we typically treat sarcoidosis on exams? Well, don't forget sarcoidosis. We're typically going to treat it with steroids. You give steroids, steroids can literally melt away a person's sarcoidosis. I mean, it doesn't mean it cannot recur, right, but it's pretty treatable when you give a steroid. And you know, by the way, sarcoid is a pretty high value subject, right, because there's so many integrations. It's one of these things that can easily slot into the multi-systems processes and disorders section of the exam. Because you can slot it into so many things, right, like I'll give you a classic example. They can give you like for example, a person that has sarcoidosis and they have like right-upocodian pain. Well, that's sarcoid that has involved the liver. Remember, sarcoidosis, many times it involves the lungs, right, but it can absolutely involve a person's liver as well.

They can have granulomas from in the liver, right? And those granulomas, we all know, not just the ones in the liver, the ones anywhere in the body, they contain macrophages. And those macrophages, surprise, surprise, express one alpha hydroxylase. Well, we know that one alpha hydroxylase is a job. It's to convert inactive vitamin D, that's calcium dial from the liver, to active vitamin D, which is calcium trial from the kidneys. Remember, another name for calcium dial is 25 hydroxy vitamin D. And calcium trial, another name for edimation exam is 125 dihydroxy vitamin D. So if you notice, well, from the liver, we get 25 hydroxy from the kidneys, we produce 125 dihydroxy. That means something must have happened at the number one position to form that vitamin D. Well, enter one alpha hydroxylase. So that one alpha hydroxylase causes you to make active vitamin D, right? And it's going to cause you to increase the reabsorption of calcium from your gut. So you're going to have hypercalcemia. So remember, hypercalcemia is a pretty classic feature of sarcoidosis on endemic exams. Again, because they have hyper vitaminosis D, a very classic question they can ask you. And typically, right, people that have sarcoid, you're going to have an increase in their LDH. The electid dehydrogenase is going to be increased. Well, again, if you think of why, if you think of why, maybe you have so much inflammation and cell death, right? Remember, lactid dehydrogenase is an interesting enzyme.

So whenever a lot of cells are dying quickly, right, you're going to have an increase in your LDH. So that's just like a concept. Instead of just memorizing that while increase LDH is specific for sarcoid, you can just try to get out many other things, right? Like if a person has tumor-licised syndrome, for example, the LDH is going to be up. Why? Because you're killing a lot of tumor cells, especially with these leukemias and lymphomas, like brackets, for example, is a pretty, pretty prime candidate. You're killing a lot of cells. As you're killing them, they're going to spill the lactate dehydrogenase into the, into the serum. And also remember, a sarcoidosis, you're going to have an increase in your ACE, your angiotensin-confertine enzyme. Again, these things are all high yield to know. And don't forget, people that have sarcoid, they can absolutely get heart block on exams. Because again, they can form granulomas in the conductance system. And those granulomas in the conductance system can absolutely cause them to have a heart block. Remember, when people have heart blocks, they are certain drugs that you should not give them. Because if you have heart blocks, your EV node is not working well already. It doesn't make any sense to give any drug that's going to block your EV node. Again, these are ways they can make these integrations on your exams, right? So, for example, they can give you a person, right? You shouldn't put those people on beta blockers, right?

Don't be a stellar idea at all. Because beta blockers are going to slow conduction down the EV node. Remember, those are class 2 anti-rhythmiics. You also don't want to give these people the non-dihydroperidine-custom channel blockers, right? So, drugs like Phyrapa-Mail or the Altayazem, because you're going to slow conduction down the EV node. That will not be a good idea as well, right? Remember, those are your class 4 anti-rhythmiics. You don't want to give them something like dejuoxin. Because if you give them something like dejuoxin, dejuoxin, yes, it increases cardiac contractility by inhibiting the sodium potassium ATP as pump. But dejuoxin also increases vagal tone. Dejuoxin is a monstrosynecrycector agonist. It will not be good for people that have again EV node disease. And remember, when people have EV node blocks, you know, Mobids 2 and type 3 heart blocks to spoil get pacemakers, but Mobids 1, which is the first kind of, that's the winky block. Mobids 1, which is the first type of a secondary degree heart block, and the first degree heart blocks, those people don't get a pacemakers. They will only get pacemakers if they are symptomatic as a result of the heart block. So again, just make sure you know as many things as you can about steroidosis. It's something they love to test, right? Or they can even give you a question about a person that has steroidosis and they have like eye pain or visual difficulty. Then what's going to be your next step?

Well, your next step is going to be a pharmacologic evaluation. Because remember, people that have steroid, they can absolutely get U Vitis. They can get anterior U Vitis. This is very high eo to know. They can get anterior U Vitis. They can get anterior U Vitis. Right? An anterior U Vitis is absolutely a manifestation of steroidosis. In fact, our friends at the MDM Es, they can easily give you a question on the exam. And they can say, oh, you know, in a person that has just gotten a new diagnosis of steroid, what's the next best step? Well, the thing is, when people get a new diagnosis of steroidosis, there are a few tests you're supposed to get in these people, right? So you're supposed to get a chest x-ray because you know, these people, again, they can have the high-level infotain apathy. You can just hope you see whatever long disease they have. And for these people as well, not a bad idea to get an EKG because, again, they can have heart blocks because you don't know if the granulomas have involved your conductive system. Right? They can even get restrictive heart disease. Believe it or not, people that have steroid, again, remember, it ends in osis, so it can cause restrictive heart disease because those granulomas can deposit in the myocardium. You can deposit amongst the myocardial cells. And that can absolutely cause problems for those people. Right? So people that have a new diagnosis of steroidosis, they're going to get a chest x-ray, they're going to get an EKG.

You're going to get PF Ts on those people. You're going to get PF Ts on those people. And those PF Ts, again, because you just want to see if they have, if they've gotten all the way down to restrictive long disease. And then you will also be helpful to get LF Ts on those people because, again, steroid has a very good predilection for a person's liver. It can cause LFT and evations. Another disease, so I guess I'll say I'm officially don't with steroid, but another disease that has like a similar set of, huh, you got to keep this in mind when you're starting, there is probably more medication is if you're starting a person on a muterone, not about a day to get PF Ts. Look at the with your, the lungs work, LF Ts, look at the with your liver works and TF Ts because remember, I'm your the name, I'm your the wrong right? Ayodot, it contains Ayodine. It can cause both hypothyroidism and it can also cause hyperthyroidism. If you're remembering past podcast, I've described this whole your base down your base down, JOD base down, base down is B A S E D O W like the Dow index for the stock market. So your base down and then there's the wolf chikof, chikof is spelled C H A I K O W F wolf chikof the wolf is W O L double F the wolf chikof effects, those are effects that explain how steroidosis can cause both hypo or hyperthyroidism, right? I mean, I'm a muterone whoops not steroidosis, I'm a muterone can cause both hyper or hypothyroidism, right?

I remember a muterone is one of these high values drugs, used for many things on example, you can use it for a feb when you're posturing a rhythm control strategy, remember you can use either a rate control or rhythm control for a feb, right? But again, we're using the rhythm control strategy. So for suck, you know, for for a muterone, you're going to do PF Ts, you're going to do LF Ts, you're going to do TF Ts when you're starting people on those medications. And then remember, you also want to get like these like eco-cardiograms when you're starting people on these cardio toxic medications, right? So things like donaldoxo-revisin, those anti-cancer agents, remember those things they can precipitate the fentin reaction so they can cause free radical damage of your myocardial and all those badness, right? But also these like eco-cardiograms not a bad idea as well. And people that have been placed on trust to zoom up, remember trust to zoom up is a breast cancer medication. It's something we're using people that have those who are two mutations, her two new, right? You want to use trust to zoom up trust to zoom up is extremely helpful in those people because again, it blocks those receptors as a more plural antibody. But unfortunately trust to zoom up can cause a reversible dilated cardiomyopathy or like doxodontarobysin that cause an irreversible dilated cardiomyopathy, right?

So before you put people on those medications, you need to put them, you need to get these like eco-cardiograms in those people. And then don't forget if we're going into the world of psych, not a bad idea to check to check CB Cs quite frequently in people that are on clasoping. Remember clasoping is a third line agent for the management of schizophrenia. You're going to give it to a person that you've tried all the usual stuff of schizophrenia, none of those things are working, right? And you're going to go for clasoping. But remember, clasoping can absolutely cause igranonocytosis, igranonocytosis. So be a person that can present with like nontropenic fever on NBME exams. In those circumstances where you want to, when people are placed on clasoping, you got to put those people on, you got to check their CB Cs regularly. Because again, they can have really, really bad igranonocytosis and that can be pretty life threatening. Right? So and just remember anticycotics in general, again, you don't always have to do this. But on exams, a potential question could be that you want to get an EKG before you start people on anticycotics, especially Ziprasi don't, right? Of all the anticycotics, remember Ziprasi don is the one, that's the one I think that's called geodong in the hospitals. As Ziprasi don't has the very unique ability to prolong your acute interval. But remember, pretty much any anticycotic can prolong your acute. Right?

So again, you may be surprised you can just get this month-descript question on your exam where you're like, huh? Okay, this person is being studied on an anticycotic. And then they ask for like the stuff you're expecting with anticycotics as answers, you're not seeing any of it, right? And the answer may just be, oh, get an EKG, right? Because again, those things prolong the acute interval. So again, these are just all kind of high-yield things you want to make sure you know and know well for for your exam. And then what if they give you a question about a patient? And they tell you that this patient, you know, for the last five weeks, he has become more and more, uh, forgetful. And they tell you that he has been having like intermecan shortness or breath. So he's become more and more forgetful. They have been intermecan shortness or breath. Um, he has been having a lot of diarrhea. And then they tell you that he has been having this rush. They can even show you an image that he has a rush on the palms, has a rush on the souls and you see all those things, right? And then you read the question like, man, how I put all of this together? Well, let's put it all together. Um, and they can even tell you that you, you hear a murmur in this heart that increases your inspiration. When you see stuff like that, you should really think about this person having pelagra as a result of cross noise syndrome. So let's explain. Now the thing is pelagra, right?

It's a nice inefficiency, okay? Well, we know that nice is also known as vitamin B3, okay? Well, we know that nice is not made out of thin air. Nice thing is made from a compound called triptofan, right? Nice thing is made from a compound triptofan. So we know that triptofan is a pretty ubiquitous molecule. I'm used to make many things on exams. You can use it to make nice thing, right? Which is vitamin B3. You can use it to make serotonin. In fact, another name for serotonin is 5 HT, 5 hydroxy triptofan. Right? So, in fact, there is this thing that I believe is known as triptofan hydroxylase that converts triptofan to serotonin. So when a person has a deficiency of vitamin B3 and nice, they're going to have what we call pelagra. Pelagra, the classic findings are going to be diarrhea during a tightest and dementia. So if you notice, this person has diarrhea, although they have diarrhea, but also just be caused by them having carcinol syndrome, which we'll talk about in a bit. But you can have diarrhea, they have dermatitis, right? So they'll have a rush. Again, it can be a rush that you see on the extremities, right? So they can have diarrhea, they can have dermatitis, they can have dementia, right? They can have dementia as a result of this problem, right? So those are all things you can see in a person that has B3 deficiency. And obviously, if he goes on for long enough, and you don't treat it, the person is going to die, which is unfortunate.

So how does carcinol syndrome cause a person to have pelagra? Well, remember, in carcinol, you have a tumor that is most commonly be appendix that produces a lot of serotonin. So because you're making so much serotonin, you're going to divert pretty much all the triptophine you're taking to the body into producing serotonin. So there is less available, right? If you're thinking in terms of the low shot, please principle, this is something probably learning general chemistry back in the day in college. As you're driving more triptophine, you know, through triptophine hydroxylistore serotonin, then you don't have enough triptophine available to make niacin. So you're going to have a niacin deficiency, right? So that's how people that have carcinoid, they can get a niacin deficiency. So carcinoid, remember, these people, the classic symptoms you find in carcinoid syndrome, you can remember them with the mnemonic BFDR, BFDR. FDR was a pretty famous present in the US, if I'm not mistaken, I believe it's Franklin Delano Roosevelt. So FDR, so the B stands for Bronco Spasim, right? The B stands for Bronco Spasim, the F stands for Flushing, the D stands for Direa, and the R stands for Right Side at Heart Legions, right? So this person I described in this question, though, for them to be having like the Bronco Spastic features, that means the tumor is no longer in the appendix, that means the tumor is metastasized to the liver.

Because remember, if the tumor is in the appendix, you're not going to be symptomatic because the liver has the ability to break down serotonin, so that you don't get the deleterious effects all over the body. I remember the appendix has the ability to drain into the liver through the porovina system. When the tumor metastasizes to the person's liver, then you can start elaborating those masti, you can start elaborating the serotonin, they can have the systemic effects, right? So you know, they can get Bronco Spasim, right? So they can get the Bronco Spasim, they can get the Flushing, they can get the Direa. And the right side at Heart Symptoms they get is again, because the agent released from the carcinol tumor can absolutely torch the right side of a person's heart. Many times, it can cause vascular problems, it can cause like tricospidian sufficiency, right? That's tricospid regurg and pomenic stenosis. You can remember that with the nomonic tips, right? Try cospidian sufficiency pomenic stenosis. So you may wonder, divine, why does this thing not go after the left side of the heart? Well, it doesn't because your pomenary capillaries are heavily metabolic organs. They have the ability to break down serotonin, so they will break it down, so you're not going to get that active metabolite in the person's left side of the heart. So that's why these people, classically, not going to have any problems in the left side of the heart. That's very high yellow to know.

So how do we diagnose our carcinolate? Well, on exams, typically, you're going to look for a breakdown product. You're going to look at 5-HIEA. I believe it's like 5-hydroxyendol ascetic acid, 5-HIEA. It's a breakdown product of serotonin. It's going to be elevated in the serum of people that have of people that have carcinolate syndrome, right? It's going to be elevated in serum of who the have carcinolate syndrome. And obviously, for a person who has carcinolate syndrome, you want to treat it by getting rid of the mass. But another drug emission example is telotrysthat. Telotrysthat is a triptophane hydroxylase inhibitor. So you're going to prevent the conversion of triptophane to serotonin, right? And again, just one last thing I'll say with 5-HIEA level. So remember, it's going to be low. If you check, if you do a long-term pump, who would have like suicidal ideation, people that have depression, right? Those people are going to have low serotonin, right? That's one of the reasons why we give SSR Is, SNR Is for the management of our depression. These people, if you check their CSF, they actually have low levels of serotonin, or it's metabolite, 5-HIEA. That's just a very nice psychiatric integration there. So I'm going to go ahead and pause. Again, as I do at the end of every podcast, I'll for one or one tutoring for all the USML exams, although that's much more limited now. If you want one or one tutoring with me, something you have to book like weeks and advance.

I tutor for step one, step two CK, step three, pre-clean home medical exams, 30-ish off exams. I do offer the review courses for step two CK and step three. And also obviously, the applied to complex level two and three. That's the 20-hour course, the MBME testing and strategy course on the disk school, the 75-hour school that I mentioned at the beginning of the podcast. And then I do also offer consulting with ERAS applications like personal statements, recommendation letters, mock interviews, and things like that. Editing your ERAS application, your supplemental application, if that's something you're interested in, just shoot me an email through the website and give you some more information on any of these services. And then I have the podcasts on all the major podcast apps, Apple podcasts, Google podcasts, Spotify, at least the most recent 150. If you want everything from episode one, all the way to a 390, which is this present podcast, you have to go on the website, divineinterventionpodcasts.com. And you'll see everything you don't have to do any sign up. Although, if you have a Word Press account and you sign up for my website, you'll get an email notification whenever I make a new podcast, which for some people is quite helpful. And then I have a new website called divineinterventionlifelessens.com. On that website, I make some life lessons podcasts that are Bible-based, about 10 minutes long for most of them.

And I discuss like a common problem that fits this humanity, or would very likely be applicable to a medical student from a biblical perspective. In fact, I have the podcasts on Apple podcasts, called the divine intervention life lessons podcast. So if that's something you're interested in, again, just check that out. Again, I suspect you're going to find it to be pretty helpful. So thank you for listening to me today. Have a wonderful rest of your day. I'll see you in the next podcast. God bless you. Thank you.

Dermatitis, Diarrhea, and Dementia (the 3 Ds).

Neuroendocrine tumors, often originating in the appendix.

Elevated 5-hydroxyindoleacetic acid (5-HIAA) in the serum.

Granulomas can deposit in the cardiac conduction system, causing conduction abnormalities.

Beta-blockers (Class II antiarrhythmics) and non-dihydropyridine calcium channel blockers (Class IV antiarrhythmics).

Anterior uveitis.

Erythema nodosum, arthritis, and bilateral hilar lymphadenopathy (or pulmonary infiltrates).

Lupus pernio and erythema nodosum.

The tumor must metastasize to the liver, allowing for sufficient metabolism of serotonin into active metabolites.

CXR (for pulmonary involvement), PF Ts (for restrictive lung disease), and LF Ts/TF Ts (for hepatic/endocrine axis disruption).

Decreased DLCO (Diffusion capacity) because the thickness increases, reducing the rate of gas exchange.

Beta-blockers and non-dihydropyridine calcium channel blockers (e.g., verapamil).

Erythema nodosum, arthritis, and bilateral hilar lymphadenopathy (or pulmonary infiltrates).

Lupus pernio and erythema nodosum.

The tumor must metastasize to the liver, allowing for sufficient metabolism of serotonin into active metabolites.

CXR (for pulmonary involvement), PF Ts (for restrictive lung disease), and LF Ts/TF Ts (for hepatic/endocrine axis disruption).

Decreased DLCO (Diffusion capacity) because the thickness increases, reducing the rate of gas exchange.

Beta-blockers and non-dihydropyridine calcium channel blockers (e.g., verapamil).