DIP Episode 370 - USMLE Step 2CK/3 Rapid Review Series 71

Okay, welcome. My name is Divine. This is episode 370 of the Divine Intervention Podcast. And into this podcast we're going to be continuing the Rapid Review Series for the USMEL step 2, CK slash step 3 exams. And that's going to be Series 71. So let's just get right to it. So what if they give you a question about a researcher? And this researcher decides to increase the diagnostic rate. Like he says, you know what? To make the diagnosis of diabetes, we're going to make it a fasting blood glucose. So after an in-hour fast, a fasting blood glucose of 200 milligrams per deciliter, right? After an in-hour fast. What is that going to do to, I guess, your diagnostic parameters for the diagnosis of diabetes? Well, if you really think about it, we know that right now to say that a person has diabetes. After an in-hour fast, we say if your blood glucose is 126 milligrams per deciliter or higher, right? So the number 126 is included. You have diabetes. So if you increase that number to 200, well, think about it. Think about it. You're going to now start missing a lot of people, right? That have diabetes, right? So if you're missing a lot of people that have disease, you can see that that test is not very sensitive anymore, right? So your sensitivity in those circumstances is going to be going down, right? But your specificity is going to be going up, right? Your sensitivity is going to be going down, but your specificity is going to be going up.

Remember in general, as your sensitivity as sensitivity and specificity of many tests, you're almost going like reverse directions. Like the more sensitive a test becomes, the less specific it becomes, but the more specific a test becomes, the less sensitive it becomes, right? So this test is getting less and less sensitive, right? Because again, you have essentially missing out on that population, on the population of people that previously, we would say, oh, you have diabetes that have a fasting blood glucose between like 126 and 200, right? So the sensitivity of the test will go down, but the specificity will absolutely go up, right? And then remember, the negative predictive value, right? The negative predictive value is going to go down, right? And the positive predictive value is going to go up. Just don't forget that in general sensitivity and NPV, remember the ends match the sensitivity and NPV, they're going the same direction. So since sensitivity is going down, NPV is going to go down. And specificity is going up, the PPV is going to go up, right? Again, let's just kind of maybe logically look through this, right? So the thing is we said that, oh, fasting blood glucose now 200, right? I mean, if you say that, right? Again, you're missing out on so many people that have diabetes, right? So your test is not very sensitive. Remember sensitive tests are supposed to detect disease, right? They're supposed to detect people that have disease.

Well, if you're missing out on so many people that have disease, right? You're no longer very sensitive, right? So if you get a negative test result from that, where he says, oh, you know, your test shows negative, you know, you don't have diabetes. Well, because we've just increased the value, the diagnostic criteria for the test, you don't really believe those negative results because you're like, oh man, I've just missed people that are between 126 to 200. So those negative tests, you don't believe them very much, right? So your negative predictive value is actually going down. You can again, make very similar arguments. This is actually a very good exercise if you can reason through it for specificity and positive predictive value. Now, what if they give you a question about a patient and they tell you that, oh, this patient, you know, she was, she's a 32-year-old female and she just delivered a newborn, right? But she's unable to lactate, right? And they tell you that she has like hypoglycemia and she has, you know, she's unable to lactate, she has hypoglycemia, she has code intolerance. What should you be thinking about? I really hope you're saying, oh, divine, this patient has shihan syndrome, right? This person has shihan syndrome, right? Now remember, shihan syndrome is an ischemic stroke of the pituitary gland, right? Basically, the thing that happens is, remember, as you get pregnant, you anterior pituitary, like triples in size.

So if you lose a tumor blood during the process of liver and delivery, let's say from like placenta, privia, visoprivia, you know, brubtube placenti, some weird stuff, right? You can cause an, you're like, systemically hypotensive, you can cause an infarction of your pituitary gland, right? So they can have a pan-hypopituitary as a result of that, right? So why does this person have code intolerance? Well, they're no longer making TSH, right? So they're not stimulating the thyroid glands, right? So those people are hypothyroid. So they are T3 and they are T4, it's going to be low, and their TSH is going to be low. The only thing that's going to be high is going to be the TRH, right? The TRH, they're dropping, releasing a hormone because that's meeting the hypothalamus. And then if we look at it from the perspective of the hypoglycemia, why don't she have the hypoglycemia? Well, the reason she has the hypoglycemia is because she has a cortisol deficiency, right? This person essentially in this case has what we call a secondary adrenaline deficiency, right? Because again, ACTH, adrenalcotropic hormone is literally made in the anterior pituitary. So if your anterior pituitary is dead, you're not going to be able to make ACTH. If you're not making ACTH, then your zona fasciculata and your zona reticularis are not going to be stimulated, right? Remember, the zona fasciculata of the adrenal cortex is the part of the cortex that makes cortisol, right?

The zona reticularis is the part that makes sex steroids. Now, let me ask you something here actually, this offhand question. What do you think will be true of the austere in this person? I would really hope you're saying that the austere levels will be normal. Some of you may be like, what? But I thought the adrenal cortex wasn't working, yeah, that's true. The thing is the adrenal cortex has three sections, right? There's the glomerulosa that makes our dosturant. There's the fasciculata that makes cortisol. And then there's the reticularis that makes sex steroids. Okay. Now, the fasciculata and the reticularis under the control of ACTH, but the glomerulosa is not under the control of ACTH. The glomerulosa is under the control of the renian and your tensin out dosturant system, right? The renian and your tensin out dosturant system. Okay. So, if you have a secondary adrenal insufficiency, which is an ACTH problem, the fasciculata reticularis did not work as well, but the glomerulosa is going to be just choking along just fine, because it's been controlled by hormones that are regimeing in the kidneys, in the GG cells, of the afferent arterials of the kidneys. The only time that an adrenalins insufficiency will cause you to have your outdoor levels being low, right? Is when you have a primary adrenalinsufficiency, right?

Where you have like your actual adrenal cortex dead from, you know, like autoimmune disease, like adescent disease, or let's say you have like meningococcal infection, right? What a house, Friedrich Sensen syndrome. We have like a TB infection of the adrenal cortex, right? Then your actual anatomical adrenal cortex is going to be dead, right? So, the glomerulosa is going to be dead, so your industrial and will be low. The fasciculata is going to be dead, so your cortisol is going to be low. My reticularis will also be dead, right? Remember, in general, when you see that a person has primary adrenalinsufficiency or adrenalinsufficiency, they're not referring to any problems with the medulla, they're just referring to problems with the cortex. The reasoning there is that the adrenal gland is essentially two organs that are almost like just whatever bizarre is a mashed into one, right? Remember, the adrenal cortex is very different embryologically from the adrenal medulla, right? The adrenal cortex is very high, it's very different embryologically from the adrenal medulla. The adrenal cortex is different. The adrenal medulla is actually derived from neurocressels, right? The adrenal medulla remembers like a modified postganglionics and pathetic neuron, right? If you actually look at the adrenal medulla grossly, you know, on the installgie, which I actually didn't call it back in the day, you'll see all these cell bodies there, okay?

So, again, remember, in primary adrenalinsufficiency, those are going to be low, but in secondary adrenalinsufficiency, those are going to be normal, right? Because in secondary adrenalinsufficiency, the problem is your ACT switch is not working well, right? But there is nothing wrong with your glomerulosa, because it's under the control of raining. Okay, now, what if they give you a question about a 73-year-old guy, you know, they tell you that he has a history of CHF, he's been on diuretics. But then over the last two days, he'll be having syncopal episodes, right? And they tell you that the Russian to the ED during one of these syncopal episodes, and they notice that he has a white QRS arrhythmia. And then they tell you that, oh, this man was recently started on a positive Ionotro. If you see this, then what should you be thinking about? I really hope you think about dig toxicity, right? Jocsin toxicity, right? So, what's the story here? Well, don't forget, this guy has CHF. Well, we know that input ACF take water pills, right? A.K.A. diuretics. Well, what is one of the most common side effects of diuretics? Well, remember, diuretics love to cause hypochyline. Now, the thing is, the Jocsin works by binding to the potassium pocket of the sodium potassium ATP spot. So, if you're taking a diuretic, like a hypochylemic, you have very little potassium around. So, there is even more binding spots available for the Jocsin, right?

So, that the Jocsin can accumulate and cause really bad toxicity, right? So, this person has been on a diuretic. He had hypochylemia as a result of being on said diuretic. And then you added a positive Ionotro, which in this case will be the Jocsin, right? And then they go into trouble, right? So, remember, hypochylemia and dig, it's not a good mixture at all, right? That's something that our friends at the NBM is, they love to test a lot, right? The thing is, very few people use the Jocsin these days, but the NBM is still love to test them, right? So, remember, the Jocsin is not something you want to give to a person that has WPW, because remember, the Jocsin is also a most chronic receptor agonist. So, he slows conduction down the EV node, right? For potassium as wolf Parkinson white, right? You don't want to block the EV node. Basically, in general, if you have WPW, you don't want any EV node blocking agent on board, because if you do, then you're going to be encouraging more flocks of stuff through that bundle of Kent, and that can be problematic for the patient, right? You don't want them to, you don't want to convert their WPW to like a bad ventricular arena like V-Fib, for example, right? So, dig is contraindicated in people that have WPW, right? And for potassium also has like the EV node not working well from the get go. Let's see, they have like some kind of hard block, then putting those people on Jocsin is maybe not the smartest again in the world, right?

Again, dig is can cause a profound breeder cardio, right? Because again, it's a most chronic receptor agonist, right? So, again, this person that had this white QRS Aridmia, from, you know, they were already on diuretics, but the positive vinyl tropols added, right? The fact that it's a white QRS Aridmia tells you it's a ventricular Aridmia, right? This person basically is suffering from dig is in a toxicity, right? Remember dig is can cause these after depolarizations that can cause like V-Tag V-Fib, you know, bad stuff like that. Okay, now what if they give you a question about a 75 year old guy and they tell you that, you know, for the last three months, actually, for the last six months, he has been having pain in his left thigh. But then you also tell you that, you know, over the last three, four weeks, he has been having these chronic headaches, he's been having like hearing difficulties and they tell you that physical exam shows some cranial nerve deficits. What should you be thinking about? I really hope you're saying all divine, looks like this guy has Pudge's disease of the bone, right? Now the thing is, if a Pudge's disease, right, it's going to be again, the classic, heart stone fit, cranial nerve deficits. Most times it's cranial nerve seven and eights that get messed up, right? So they can have like hearing problems, they'll have all these cranial nerve issues. And many times they'll have like bone and joint pain, right?

Now remember, Pudge's disease is essentially like a metabolic bone disease, right? And there are many antecedents of Pudge's disease that our friends at the NBM is love to test, like for example, you know, Puda have Pudge's disease, they are pretty supposed to osteosircoma, right? Right? Pudge's disease can increase the presence risk of osteosircoma, right? So again, Pudge's disease can cause osteosircoma, right? Remember, you know, with terryparatide as well, or if you have an RBG mutation, those things can all cause osteosircoma. But Pudge's disease can also cause high up or heart failure, right? Remember high up or heart failure is something you get because think about it, people that have Pudge's disease, they have bone marrow, they become hypervascular, right? So it's almost like the heart is working to supply like a larger number of blood vessels, right? And again, the heart is a muscle, right? You can work heart forever, right? I mean, even if you go workout, a hard workout, your body can atick some time to recuperate, your heart can slow down after a while, right? If you keep putting your heart through all those motions, right? That chronically elevated cardiac output can cause you to go into heart failure, right? And then remember, Pudge's disease, how do we diagnose it? Well, again, don't forget that alkaline phosphatase could actually be elevated in Pudge's disease of the bone, right?

So this is why alkaline phosphatase elevations don't always mean obstructively for disease, right? That's where GGT comes in, gamma glutamol transfer is, you know, so how do we diagnose Pudge's disease? Remember, you're going to use a bone scan, right? You're going to use a bone scan. But again, as we know, our friends at the NBN Es, they like to do this thing where, you know, they give you different name that you're not used to, right? So the thing is a bone scan is a nucleomedicine test. So because a bone scan is a nucleomedicine test, sometimes you may see it refer to as bone syntography on NBN Es, right? Bone syntography on NBN Es, let me just tell you this, whenever you see the word, syntography, they're referring to some kind of nucleomedicine study, right? So like, for example, bone syntography means bone scan on NBN Es, and remember, a bone scan is not the same thing as a dexascan. That's a common mistake many people make. The dexascan is an x-ray. The bone scan is actually an actual legit nucleomedicine test. I've read a lot of these studies. And then, you know, a rai-use scan, radioactive aerodynamic scan, right? That's what's called firex-integrity, right? So again, just be careful of what you see, what you see with those things. Okay, so, right? So this person has Pudge's disease, you're going to diagnose it on a bone scan, right? And how do we treat Pudge's disease? We're going to treat it with a bisphosphonite, right?

Pudge's disease is treated with a bisphosphonite on exams. Okay, now, what if they give you a question about, you know, like a 76-year-old female, and they tell you that, you know, she has been a chronic smoker, right? And that over the last six months, she's lost like 30 pounds, and they tell you that, you know, she, like her daughter tells you that her mom is not being eating much at all, right? And that her mom just always has really bad abdomen open after meals. I mean, if you see that, what are you thinking about? Well, I really hope you're thinking about some kind of mesentericus chemia, right? In this case, once you think of chronic mesentericus chemia, right? To be honest with you, I like to call this the solder intestinal angina, right? Basically, the pathophysiology behind angina in the heart is what essentially causes chronic mesentericus chemia, right? Again, it's pretty common in smokers, right? Because again, remember, smoking is a very big risk factor for atherosclerosis, right? So what is people losing all the sweet? Well, the thing is, think about it. When you eat, there's increased blood flow in your GI tract, right? Through those cilia arteries, supermaisenteric arteries, inferior mesenteric arteries, right? There's increased blood flow, right? But if you have like really bad atherosclerotic disease of your cilia arteries, or your SMA, or your IMA, right?

The problem that is going to essentially crop up for you is that whenever you eat, because those things have atherosclerosis, there's not going to be a non-blown flow, right? So eating literally hurts. So because eating hurts, these people are going to stop eating and they're going to lose a ton of weight. And of course, knowing the NBM Es, they're going to be smart about this. They're going to try to make you think that, hmm, this person has like cancer or some whatever. No, right? You don't have some cancer, right? If you see a person that is like not eating because they have a lot of pain with meals, right? It's not cancer. They have chronic mesenteric ischemia. Again, especially if the person is a vascular path, let's say they've had M Is in the past, or they've had peripheral arterial disease. Again, many of the things that cause M Is and PD, are the things that cause chronic mesenteric ischemia, right? Remember like the biggest risk factor for an M Is smoking for PD is smoking, right? So chronic mesenteric ischemia. Again, it's usually found in people that have a lot of atherosclerosis. And many times, if you want to establish the diagnosis, you can perform some kind of angiography to make the diagnosis. Now, what if they give you a question about that 76-year-old guy? They tell you that over the last three weeks, he has had like two syncopal episodes, right? And then they tell you in the question that, oh, they obtain an ekeg and he shows like living trucolahypertrophy.

And then they ask, what is your next best step in diagnosis? Well, I'll really hope you're saying, hmm, divine. Let's go ahead and get an echocardiogram, right? Let's go ahead and get an echocardiogram for these people. And let me just say something about echocardiograms, right? There's a common question I get from students all the time, you know. You know, there's such a thing as a TTE transporacic echocardiogram and a TEE, a transistophageal echocardiogram, right? But let me tell you this, many times you can use pretty much any kind of echolue wand, right? Although there are certain specific circumstances where TEE is preferred, right? So say, for example, if a person has like endocraditis, you want to use a TEE, right? A transistophageal echocardiogram, because that's just more sensitive. Literally the ultrasound probes in the presence of a soft august, right? Remember, the soft august is posterior to the left-d-trem, right? That's like, I'll hope, you know, some anatomy is to remember from step one. So you can get much better, just much better resolution there, right? So here's the rule I'll tell you, right? If you are taking an ambient exam and you put TEE and TTE as answers, just pretty much always speak TEE. TEE is pretty much always a better study than a TTE, right? But if they give you TTE and that's all they put, you know that an echocardiogram is the right answer. Big TTE, right? That's the way I approach these on exams.

That's actually what I teach people when I do my one-on-one tutoring, or when I teach any of my courses. And it's a pretty reliable rule, right? So this guy, you're going to get an echolue, right? Because again, we see an old guy, EKG, Schoenliving, Trucola hypertrophy, right? This guy has eardics stenosis. That's what's happening, right? He has eardics stenosis. That eardics stenosis is causing pressure overload, right? So the person has concentric hypertrophy of the living trichord. That's what you pick up as LVH on an EKG, right? Levantric hypertrophy on an EKG. Now, right? Because it's a structural problem with the heart, again, it will make sense that you want to use an echocardiogram. Remember, echocardiograms are useless for detailing electrical problems in the heart. Well, let's not say the entire useless, but I'll say probably for like medical students, it's not going to help you much. If you go into cardiology, that's a different story. But in general, for structural problems in the heart, on end-beaming exams, echocardiograms are the things you want to use, right? And again, the person basically is not getting enough blood out of their left ventricle, right? So they're not profusing the brain. That's why they have all these syncopal episodes, right? This person probably has severe eardics stenosis. Really, this person, what they need is an eotic valve replacement, right? Remember, there's not really many drugs that it's going to help you much.

Eardics stenosis is a valve replacement that's going to do the trick for you. I remember, again, it's calcification of the valve. That's the underlying pathophysiology, right? But again, if you saw eardics stenosis in a much younger person, like a person in their 40s, right? Especially people that have like Turner syndrome, for example, right? I really hope you think about bicospediotic valve, right? Remember, bicospediotic valve, the reason that they developed that calcification early is you have a valve that normally is supposed to have three cossips, but now has only two cossips. So two cossips are doing the job of three cossips, right? If two people are doing the job of three, those two people get tired just a long quicker, right? So that's why people that have bicospediotic valves, that's a perfect setup for early onset eardics stenosis, right? And again, remember eardics stenosis, you're going to hear it best at the right of personal water. So it's going to be a systolic ejection murmur, right? They'll have a pulse of sparrows, they'll say tartus, right? So the acarctic pulse is going to be delayed, you know, just stuff like that, right? You know, the classic buzzwords that I'm sure you're probably, you're probably used to have this point, right? Probably used to have this point. Okay. Now, what if they give you a question about a 63-year-old male, you know, he has been in the ICU for the past like, you know, two weeks because he has like a Eurosepsis, right?

But then he's not as tells you that, you know, over the last two days, he has been having a lot of poop accidents, right? So he has been having a lot of stool, making a lot of stool, right? If you ask him for the diagnosis, what are you going to go with? Well, I really hope you're saying, definitely, it's not like this person has c-diff, right? So just kind of walk backwards here. This person has Eurosepsis, okay? Well, if you have Eurosepsis, I would really hope that the hospital chose to give you, give you, not give you, chose to give you some kind of antibiotic. Well, if you're taking antibiotics, and they are now making a ton of poop, right? That's diarrhea, right? You're just basically as c-diff. Remember, c-diff, the biggest risk factor for c-diff, right, is exposure to, you know, antibiotics, especially clean the micecene, right? But pretty much any antibiotic you take can increase your risk of c-diff because again, you take antibiotics, you're no-cure GI-g-i-flora. If you're no-cure GI-flora, the thing is going to be happening is you're going to be building up a lot of over some things that normally keep c-diff in check, we're not giving it in check anymore, right? And then you get into trouble, right? So how do we diagnose c-diff? Remember, c-diff, you're going to diagnose it by, you know, looking for the toxin in the stool, right? You're going to look for the c-diff toxin in the stool, right? So let's say the test comes back positive, or what are you going to do?

Well, the thing is you're going to give vancomycin, you're going to give Euro vancomycin. Remember, the thing about vancomycin is it is polyreabsorbed. So if you give it early, it stays in the GI tract and kills the c-diff, right? So you give Euro vancomycin, right? Another drug you miss you on exams is that of vancomycin, if the MbMe is trying to get cute, is fidaxomycin, FIDA, fidaxo, FIDA, XO, MIC, I-N, right? Fidaxomycin, that also works just just as well, right? Or all fidaxomycin, right? And you know, sometimes the patient can have just very severe disease, right? If you're having like terrible, terrible, terrible disease, sometimes in addition to that vancomycin, you know, they can add in some metronidazole, right? Now, one thing you just want to be aware of when exams shows up pretty well, whenever it shows up, it's going to hide you to know is what if they give you a question about a person that has c-diff, a person is just vomitting a ton, right? So they can't, they don't seem to tolerate any kind of oral intake. In those cases, you can actually, again, the thing is, I-V vancomycin is not going to do squat for them. Because remember, I-V vancomycin is not ideal, right? Again, you want Euro vancomycin if you can for these people. So the thing that you're going to do is you want something that will touch the mucus of the GI tract. So if you can't go from the top, which is the mouth, you're going to go from the bottom, which is the butt, right?

So you can actually give a vancomycin erectile. That's something you want to keep at the back of your mind for, for exams. And then, what if they give you a question about an IV drug user that over the last, you know, two weeks has developed like a lot of a demon. And they tell you that his urine has looked like very white, like had this whiteish discoloration. If you see this, I would really hope you're thinking about like the Freudic syndrome, right? And what's the Freudic syndrome here? It's going to be FSGS, Focal segmental glomerulus sclerosis. Remember, FSGS, right? Is the most common cause of nephrodite syndrome in IV drug users, right? I mean, FSGS, you also find it in, you know, who that will be, people that have HIV, people that have African Americans. I mean, to be honest, with you, if you're looking at the most common causes of nephrodite syndrome in adults, FSGS and membranous nephropathy at the top two, that's for sure, right? The one that is number one, the one that's number two kind of keeps changing every time, right? So, but FSGS, I want you to know the populations of people that get FSGS, right? IV drug users, African Americans, Hispanics, obese people, and then people that have HIV, right? People that have HIV, they actually tend to get the, the variant that's called a colapsina FSGS, right? Colapsina FSGS, right? And you remember, since it's an ephrodite syndrome, right?

Those who are going to have more than three and a half grams of protein, extruded from urine every day, right? Although sometimes instead of putting that, they'll just put like, they have four plus or more proteinuria, that tells you that, you know, they have, they have, they have FSGS, right? And again, there isn't, they have this a deep, I remember, they are, they are basically getting rid of all the, all the, all the, been, forget it all, while you mean, I don't know how you're going to have anything that can keep in cardiovascular fluid, right? The oncotic pressures are going to be in the toilet, so, they're not going to have adequate oncotic pressures, right? So, that's why they're going to get into trouble. Now, what if they give you a question? I know some of you may be like, well, the one you're, you know, rapid review series is usually 20 minutes. I just kind of want to get through a few important topics today. So, let's maybe dig it to like 30 minutes, how's that? Or just learn a little more information, right? So, what if they give you a question about like a 13-year-old male, you know, the tell you that he just returned from a class field trip to North Carolina, and then the tell you that his mom brings him to the emergency department because he's been very short of breath, right? And they tell you that on physical exam, you notice that he has like particular lesions on his, on his hands and on his legs, right?

And, you know, they tell you that, you know, you have like headache and really high fevers for a few days before he's bumpered him into the ED. If you see this, I really hope you're saying, ooh, divine. This kid has a Rocky Mountain spotted fever, right? RMSF, right? Rocky Mountain spotted fever, right? It's a disorder caused by a re-cat's hair, a cat's eye, right? And really, how do you treat this? I got a treat with a dog's cycling. Remember, Rocky Mountain spotted fever is one of those things that can cause a rash on the palms and so on. But again, to be honest with you, the MbMe is almost not going to say rash, right? It'll be ridiculous for them to do that. Make the question a little too easy there, right? The smart thing that our friends at the MbMe's would likely do to you is they will say something along the lines of PTKI or proper, right? Like PTKI or proper lesions, you'll see them in stats on the palms, on the soles, and then in stats coming inward toward the body, right? That's Rocky Mountain spotted fever. And let me just make your life easy. The way we treat Rocky Mountain spotted fever is with a dog's cycling for everybody, doesn't matter, right? The thing about Rocky Mountain spotted fever is one of those things that you kind of want to take seriously. If you don't eat seriously, that child is going to die, basically, right? If you don't treat it and treat, catch it early and treat it well, the child is going to die, right? The child is going to die.

Because the thing is, you know, we get here, we get side. And you do this thing where it breaks up blood vessels, right? It makes them more leaky, makes them more permeable. So, we're going to just with you, that's actually one of the mechanisms behind the PTKI and the proper, uh, proper lesions that they get on their skin, right? So, you know, on the skin, it's not that big of a deal. But if you're rupturing blood vessels, making more blood vessels more permeable, right? Especially like in the lungs, that can certainly be a problem, right? We're kind of inching into ERGS territory at that point. So, you want to be careful actually. That's probably like one of the primary things that kills people that have a Rocky Mountain spotted fever is that ERGS they get, right? Because again, we get here, it gets a lot to cause leaky blood vessels, right? So, if you cause leaky blood vessels in the lungs, that's going to be problematic, right? So, the person is going to have like ERGS, really bad pulmonary edema, right? And they're going to die, right? So, remember, ERGS just as a side point, right? It's a non-cardiogenic pulmonary edema, right? ERGS is a non-cardiogenic pulmonary edema, right? So, the pulmonary coupler which pershobe will less than 18, right? Contrast that with like a person that has pulmonary edema from like CHF, right? That'll be kind of a cardiogenic pulmonary edema, right?

I mean, that case, the pulmonary coupler which persho, which is a surrogate for your left-inch operation, is going to be over 18. Now, what if they give you a question about like a 34-year-old female IV drug user, the tell you that her mom brings her to the physician because for the last three weeks, her mom just tells you that, you know, this child, this 34-year-old child of mine, has been deteriorating, praying it's not going to be a child's portion in Jesus name. But basically, you know, they tell you the physical exam shows like the fused motor weakness, again, having a person's sickness and the family is not always ideal, right? This is always tough on the family, right? But let's continue, right? So, they say that physical exam shows like the fused motor weakness and they tell you that this person is not even able to participate in a mini mental status exam or they give you like some really low score, like I don't like 5 out of 30, right? Something like that, right? And then they tell you that, oh, you know, they do some brain imaging and they see all these non-enhancing lesions, right? Just multiple non-enhancing lesions, right? And they tell you that this person, the last so physician like 10 years ago, right? Because they had like oral candidacies and a lot of weak loss, right? You can already begin to see me build a story here, right?

This person is an IV drug user, you know, 10 years ago, they had candidacies or really how many of those usual oral candidacies, you know, oral candidacies with loss, right? You probably have HIV, right? And then you see now, you know, they're just deteriorating pretty quickly, right? It's not like, oh, they're deteriorating over years, no, this one they're deteriorating over like weeks, right? And then you see all these lesions in the brain, right? If you see this, I'll really hope you're saying that this person has a PML, right? Remember PML is progressive multi-focal, look whencephalopathy, right? Progressive multi-focal, look whencephalopathy, right? Remember it's caused by the GC virus, right? And there are certain things that can cause you to have this kind of problem, right? Like again, for example, if you have like really bad HIV and you see four counties like nothing to write home about, crazy, crazy love, right? You can get GC virus reactivation. You can also get this if you're taking certain MS drugs, right? The multiple sclerosis drugs are one of their big problems. It's rare when it happens, it's pretty bad. It's a PML, right? Again, from GC virus reactivation, especially the MS drug, not at least your map. Remember, that's like an integrated inhibitor that can absolutely cause a PML, right? So I think I'm going to go ahead and stop here. Unfortunately, there's no real good treatment for PML.

Again, I do offer one or one two different for all the USMLA exams, step one, step two, see case, step three, preclinical medical exams, 30-ish off exams. And I also offer review courses. Again, I have like the MBAB test taking strategy scores. I actually have one coming up on the 21st of this month. It's through zoom is two and a half hours. Tons of people have taken it. They've done extremely well on the exams. I've had people like literally improve like 30, 40 points on their tests, you know, as a result of the course. You even see people they say, wow, you work two bank percentages of jump by like 20, 30 percent, right? So it's a very tried and true course. Tons of people have taken it, very useful course. I think you'd really find it to be helpful. And then I offer a 24 hour, you know, step two, see case, step three review course. Again, also over zoom, you know, most people have about 130 to 140 pages of notes from the course. We go over like thousands of scenarios from most of the subject areas that are tested on step two, see case step three. And then I have a USMLA at least step two, see case school, but that's going to be in the summer. That one actually has a couple of 40 people on it. I said 75 hours long. It's going to be the first two weeks of main. I mean, if you want to register for any of these courses, just shoot me an email through the website and I'll give you some more information.

Again, the testing and strategy scores February 21st, 24 hour review courses from the 22nd to the 25th of February as well. And then the disk school is going to be it's going to be in May. And then I have all these podcasts on Apple podcasts, Google podcasts, Spotify, right? At least the most recent 150. If you want everything from episode one to episode three, 70, you're going to have to go on the website, divine intervention podcasts.com. If you have a Word Press account and you subscribe, then you'll actually get an email notification whenever I make a new podcast. And then I have a You Tube channel, Divine Intervention USMLA podcasts and videos. That's where I post the videos that I make periodically. And then finally, I have a new website because you know, I get all these emails from people, oh, divine. I love the life lessons you put at the end of these divine intervention podcasts. So I started, many of you know, I'm a Christian. So I started a new website called divine intervention life lessons.com. In fact, there's a, it's actually an Apple podcast as well. It's called the divine intervention life lessons podcast. And I, you know, use the Bible in, you know, series of short podcasts like, you know, 10, 15 minutes long. And I go over like some topic from a biblical perspective and just give you some encouragement. It's almost like a devotional for people. So again, if you're interested in that, you can feel free to hit that up. I have almost 60 episodes right now.

And I'll keep adding like new episodes, you know, about two episodes every week. Okay. So thank you for listening to me. Have a wonderful day. The encouragement I'll just give you today is just keep moving forward. Right. Keep moving forward. Don't stay in one place. Let me tell you this when you stay in one place, you're already falling behind because other people are moving forward relative to you. Right. Keep moving forward. Right. Again, press on toward that mark. Right. Instead of staying in the same place or moving backwards, just move forward. Right. As long as you're moving forward, especially if you're moving forward in the direction of your dreams or your calling, you're going to be making progress in life. So thank you for listening to me. Have a wonderful rest of your day. This probably one of my longest, uh, um, rapid review series. But I think we reviewed a lot of high yield information today. Okay. I'll talk to you later. God bless you. Thank you.

Primary involves failure of the adrenal cortex itself (e.g., Addison's); Secondary involves pituitary failure (ACTH deficiency), leaving the mineralocorticoid axis intact.

A bone scan (or nucleomedicine test/bone syntography).

LVH (Left Ventricular Hypertrophy) on EKG; a systolic ejection murmur best heard at the right upper sternal border.

Any AV node blocking agent, such as digoxin or calcium channel blockers.

IV drug use, African American descent, and HIV infection.

Atherosclerosis of the superior/inferior mesenteric arteries (SMA/IMA).

Zona Glomerulosa (Aldosterone, controlled by RAAS); Zona Fasciculata (Cortisol, controlled by ACTH); Zona Reticularis (Sex steroids, controlled by ACTH).

Because the zona glomerulosa is regulated by the Renin-Angiotensin System (RAAS), not ACTH.

Non-cardiogenic pulmonary edema (ARDS/non-cardiogenic).

Rectal enema or rectal administration (to bypass the GI tract).

Neurological deterioration over weeks/months; non-enhancing lesions on brain imaging; caused by JC virus reactivation, often in immunocompromised patients.

Transesophageal Echocardiogram (TEE), as it offers better resolution, especially when visualizing the soft palate/posterior structures.

Zona Glomerulosa (Aldosterone, controlled by RAAS); Zona Fasciculata (Cortisol, controlled by ACTH); Zona Reticularis (Sex steroids, controlled by ACTH).

Because the zona glomerulosa is regulated by the Renin-Angiotensin System (RAAS), not ACTH.

Non-cardiogenic pulmonary edema (ARDS/non-cardiogenic).

Rectal enema or rectal administration (to bypass the GI tract).

Neurological deterioration over weeks/months; non-enhancing lesions on brain imaging; caused by JC virus reactivation, often in immunocompromised patients.

Transesophageal Echocardiogram (TEE), as it offers better resolution, especially when visualizing the soft palate/posterior structures.