DIP Episode 633 - USMLE Step 2/3 Rapid Review Series 132

All right, welcome. This is episode 633 of the Divine Intervention Podcasts. And today's podcast will be addressing rapid review for the US Emily Step 2 CK, Slash Step 3 exams. And this is going to be series 132. A lot of actually pretty high-yield things I'm going to be discussing today, biosstatistics, just a few ideas I've kind of had in my head. So I kind of figured today will be a good day to hit those. So what if they give you a question about a patient? They tell you that this patient works as an air traffic controller. And then you're told that the patient, you know, the patient's an air traffic controller. And then you're told that the patient that he's police of work because of excessive noise exposure. He's enrolled in a hearing conservation program that involves annual audiometry. And then they ask you, these actions taken by the patient's employer most likely represents which of the following levels of prevention. I really hope you're picking the answer that says secondary prevention. I really hope you're picking the answer that says what secondary prevention. The US Emily is the love to do stuff like this, right? And this is something that basically falls under the purview of social sciences and ethics, right? There's a reason why that material, you know, together with bio statistics ends up in about 15% of the exams. So if you're interested in that material, I do have a class coming up this week. Actually on Wednesday, I have a social sciences and ethics class.

Taking place on Wednesday, you know, QIO, those things we covered that in that class, a five hour class, covered like almost like 300 scenarios. And then on Tuesday, which is basically tomorrow, I have a four hour bio statistics class. The class I have today this evening is the test taking strategies class. But let's continue with that. So basically like this person is in a career, is in a job where they have excessive exposure to noise. When you have a lot of exposure to noise, that can cause hearing loss. That can typically cause a sensory neuro hearing loss. Let me ask you this. Will this sensory neuro hearing loss in this patient be unilateral or bilateral if they were to have it? It's going to be bilateral, right? It's going to be bilateral. That's pretty high you to know for your exams. So if the person is in a hearing conservation program and we're trying to screen them for hearing loss, that screening is going to be secondary prevention. Remember secondary prevention is when you screen to catch disease early, to figure out if a person has a disease earlier or not. But what if they give you a question and they tell you that, you know, the employer decides to institute the use of earplugs and earmuffs, and the patient has no history of hearing loss on audiometry. Then that would be an example of primary prevention, right? You're literally trying to prevent them from developing hearing loss in the first place.

You're literally trying to prevent them from developing hearing loss in the first place, right? But what if they give you a scenario and the person has already developed some mild hearing loss? And then in the hearing conservation program, you institute that, hey, this person should be getting, this person should have earmuffs and earplugs, you know, that they should be fit tested for it and they should use it regularly. Then in that circumstance, that's going to be an example of tertiary prevention. We already know that you have the pathology. Now we're just trying to minimize, we're trying to prevent it from worsening, we're trying to prevent it from getting worse, right? So guys, it's very high you to know these things for exams, right? Because they like to do these blended questions where they will give you a scenario and really depends on the scenario that then tells you the level of prevention, right? So you have to analyze the context of the situation that they're giving to you on your exams, right? So like, for example, if you're a person that is a resident and you work at a, you know, you're working on ICU and you're in an N95 mask, again, that's primary prevention, right? We're trying to prevent you from getting COVID-19 or TB or measles or whatever, right? Or, you know, from people that are, you know, kind of infected. All right. So what if they give you a question about a patient? So the second we need today, right?

So they give you a question about a patient that was started on semagglutide three months ago. And the patient, upon initiation of therapy, the person's BMI was 35. But now this person's BMI is 29. The person comes for follow-up, right? And during the visits with the physician, during the patient physician encounter, the patient complains of, you know, having like a thinning, you know, the person is complaining of that he, he's, he's hair no longer looks uniform. That's his shift complains to the physician, right? And then they ask you which of the following is the most likely diagnosis? The thing you're going to be picking on your exams are really hoping is a telogen effluvium, telogen, T-E-L-O-G-E-N, effluvium, E-F-F-L-U-V-I-U-M, telogen effluvium, effluvium, or telogen effluvium, right? Bring your warrior from, right? But again, they like to again blend things. See, the USML is these days, they are not very big on linear questions. They are very big on integrations, right? The goal of your, the goal of your exam is for them to integrate a question to you, and for you to figure out that integration and picking your answer, right? So this person has telogen effluvium, and telogen effluvium basically is just a loss of hair, right? And you just notice over a very short time period, the person just loses a ton of hair, and it's like a diffuse hair loss, is not like concentrated in one region of the scalp, right? They have like this just acute diffuse hair loss, right?

And typically we're going to see this when the body is like shocked. What do I mean by when the body is shocked? Well, if you lose a lot of weight very quickly, that can cause that problem. They can also give you the same thing in a person that is pregnant or a person that, you know, was just, you know, has been living with cancer for a bit, right? Or the person just underwent like very big surgery or had a myocardial infarction or something like that, right? Or the person had like very severe, like mental trauma, you know, unless the person was raped or whatever, right? That puts the body under very intense amounts of stress, right? When you see people that are recently on the gone, very intense levels of stress, and you notice that they have hair loss, right? Just diffuse hair loss. Then in that circumstance, I really want you to think of a person having telogen effluvium, right? So typically, I've got to notice that their hair is just going to thin out, right? So the person typically on the USML is the classic vignette, will be the person saying that his hair no longer looks uniform, and that he has noticed that his hair looks patchy, right? When you see something like that, that's telogen effluvium, right? That's telogen effluvium. And the thing is sometimes our friends at the MVM Es again, because they love prognosis. I mean, this is something I address a lot in my classes. I tell them that I tell people that, hey, prognosis do not ignore it for you exams, right?

But they can ask you which of the following is the most likely outcome of this patient's presentation? Well, I hope that you're going to say like a self-limited, right? Or pick the answer that says eventual resolution, right? The thing is telogen effluvium is going to resolve, right? Many times, once that stressor goes away, when the body gets used to that stressor, the person is going to grow their hair back. The person is literally going to grow their hair back, right? Again, it's pretty high you to know that for your exams, right? So these people, their scalp, their hair shafts are completely fine, right? But they will lose all that hair. Sometimes you can take up to a year for the hair to come back, but they will come back, right? So just where I show those people, right? So again, classic vignette on your exams is to blend it with a GOP1 agonist, right? Because again, remember, this GOP1 agonist like semagglutide or trazepatide, or lyragglutide or exenatide, right? They are very, very good at causing fairly rapid weight loss, right? Especially if you're basically like taking them and doing the things, right? Like you're doing strength training, you're doing some cardio, you're counting your calories, you know, stuff like that. All right. Now let's go ahead and continue here. So what if they give you a question about a patient? And they tell you that this patient is brought to the, you know, that this person has a history of hepatitis C infection, right?

And that over the last three months, he is, he is wife, has noticed change in behavior. You know, notice a change in behavior that he has been having a lot of mood swings and he has been sometimes having these very angry outbursts, right? And then we're told that this patient on physical exam has a white exudate on he in his oral cavity, right? And we're told that the patient has like mild weakness in his bilateral or extremities. If you see something like this, what should you be thinking about on your exams? What should you be thinking about on your exams? Well, I really hope you're saying, oh, divine, this is hand. No, I don't mean your real hands. What exactly do I mean? I mean, HIV associated neurocognitive disorder, HIV associated neurocognitive disorder, right? So maybe like, come on, divine, like this is kind of mean. How do you expect me to have figured out that this person has HIV? Well, I give you too many clues. I was actually a little too nice with this question, right? Like literally this person has a history of hepatitis C. You know, IV drug use, right? That's a way to get HIV. Okay, person has a history of hepatitis C. What are the clues that I give? Okay, I give that. Hmm, hmm, hmm. This person has a white exudate on the oral cavity. This person has oral candidaeosis. Right? That's pretty classic in people that have HIV, right? Again, please, they're not going to give you every single thing known to mankind for you to properly answer a question.

No, they literally will not give you every single thing known to mankind. Right? So just be careful about that. They may not necessarily give you every single thing known to mankind. Please keep that at the back of your mind as you prepare for your exam. So this person has HIV associated neurocognitive disease. Right? So how is this going to present on you exams? Well, this is typically going to present in a person that is immunocompromised. Right? And it's going to be a person that is probably not on antiretroviral therapy. I can almost promise you the person will almost certainly not be on antiretroviral therapy. The person will not be on antiretroviral therapy. Right? So their HIV will be poorly controlled. Right? It will be poorly controlled. Many times their CD4 count is going to be under 200 on the US Emily Exam. So it's going to be very, very low. And you're going to notice that they're going to have, again, there's a reason it's called a neurocognitive disorder. Right? There's literally a reason why it's called neurocognitive disorder. Right? So they're going to have like issues with cognition. They're going to have like these neuro psych symptoms. You're going to notice that they have, um, they're beginning to have like signs of like dementia. Right? In fact, before these to call this HIV dementia, but again, these days, the more official term is HIV associated neurocognitive disease. Right? So they'll have like mood problems. They'll have behavioral problems.

They may have these angry outbursts. They may have these dementive symptoms. Right? Again, if you see something like that, and I can almost promise you, they're going to try to confuse you with Alzheimer's or your exams. Do not be call-zymers. Right? If you see a person that has demented style symptoms and their CD4 count is very low, it's hand that they have. They don't have Alzheimer's disease. Right? They don't have Alzheimer's disease. And then sometimes on the exams, they will ask which of the following represents the greatest risk factor? Right? Or which of the following patients specific risk factors is the biggest risk factor for this problem in this patient? Well, I hope you're picking the answer that talks about like a low CD4 count. Right? If the person's CD4 count is low, then that's going to really, really increase your risk. In fact, let me show you how the USM is going to try to put you in trouble with this kind of prognostic factor or risk factor question. Right? So say, for example, they give you a person that has hand and they end their 30s and the person has a low CD4 count. Right? If you see something like that, I will strongly encourage you to pick the answer that talks about the low CD4 count. Right? I will strongly encourage you to pick the answer that talks about the person's low CD4 count. Low CD4 count in that situation will be a bigger risk factor. Okay? Don't get me wrong. As you get older and you have hand, you don't worst your prognosis.

But the thing is typically like the lower your CD4 count, the more opportunity HIV has to replicate in your brain and if you can't replicate in your brain, it's going to cause problems. Again, remember, HIV can mess up your brain matter. It can mess up your microglia. Right? It can cause a lot of problems. Right? This is why once a person is diagnosed with HIV, go ahead and put them on an antiretroviral therapy. You know, sometimes we call that highly active antiretroviral therapy. All right. Now, what if they give you a question about a patient? And they tell you that this patient is a 32-year-old female and that for, you know, she has a history of like a shortness or breath and dry cough. Right? And that for the last 24 hours, she has been having like very significant eye pain, very, very significant eye pain. Right? Very significant pain in her left eye, very significant pain in her left eye. And she tells you that she has had a lot of tearing and the eye looks very red on physical exam. And then you're told that visual acuity is, so this is the right eye. Okay? She has all these problems in the right eye. And they tell you that visual acuity is 20 over 40 in the left eye and 20 over 80 in the right eye. Right? And they then tell you that, you know, this, you know, patient has a required cortical steroid therapy in the past for her chronic cough and shortness or breath. Right? If you see this, what's going to be almost likely diagnosis here?

I hope you're saying, oh, divine, this looks like antireuvitis, anterior uviitis. You're like, wait, what? If I had you arrived at this? Well, let me explain how I arrived at this. Right? So let me ask you this first. First things first, what systemic disease does this patient have? Well, this person has a steroidosis, right? Like think about it. A woman that is relatively young, right? And not just relatively young. She has a history of like dry cough, shortness or breath. Right? And she has requires therapy in the past. Let me ask you this. How do you think steroidosis is treated? I hope you're saying steroids. Right? So this person probably has a steroidosis. This person probably has a steroidosis. So whenever you see a person that has a steroidosis and then they have like eye pain, they have eye inflammation, I will strongly encourage you to think about antireuvitis on your exams. I strongly encourage you to think about antireuvitis on your exams. So typically, the way this is going to present is going to be an acute presentation. Right? And the person is going to have like very bad visual acuity. The person is going to have redness of the eye. They're going to have tearing. They're going to have a meiosis. So they're going to have a public constriction. Right? When you see something like that, think about anterior uviitis. And the thing is, you know, there are many different ways they can test this on the exams.

I decided to test it in the context of steroidosis for this question. But there are many other ways they can test this exact same thing. Right? They can test it in the person that has osteoarthritis. They can test it in the person that has Crohn's disease. They can test it in the person that has any of the HLEB27 Spondyl Oathropathies. Right? Like, you know, ankylocin Spondylitis, psoriatic arthritis. Right? Or reactive arthritis. Those people can certainly have an anterior uviitis. Right? And then, another way they can also test this, they can test it in the context of a person that has like an infection. Right? An anterior uviitis can literally arise from an infective process. It can literally arise from an infective process. Right? Now, the thing is sometimes on the USML Es, actually, there are two ways they can, two other ways, besides what I've said, that they can use to try to screw you over with anterior uviitis on your exams. So, one of the ways they can try to screw you over, let me kind of walk you through these so that you're not gimped on your exams. Right? So, first thing they can do is they can literally give you an anterior uviitis question. Right? They can literally give you an anterior uviitis question. Right? And then, ask which of the following represents the most likely theology of this patient's presentation? And of course, they're not going to tell you the person has anterior uviitis. They'll expect you to decipher that the person has anterior uviitis.

And then, they'll ask you which of the following represents the most likely theology of this patient's presentation. Right? And then, they'll put an answer that says, for a Cerdosa, they'll put an answer that says inflammatory bowel disease, they'll put an answer that talks about the seronegative spondyloathropathesis. Right? They'll put an answer that says infection, they'll put an answer that says idiopathic. If you see these things, then you want to go ahead and pick the answer that says idiopathic. Right? The most common cause, very high of the most common cause of anterior uviitis, is an idiopathic, it just arises idiopathically. We don't know what causes it. Right? Although some people can also have it from just trauma. Right? But typically it's going to be idiopathic on your exams. And another disorder that you should know, and they're going to obviously put this in a pediatric patient or a teenager on your exams, is going to be a person that has oligua-ticula-djuvenarumathoid arthritis. Right? Remember, oligua-ticula-jra has a very, very strong association with anterior uviitis. In fact, this is precisely why, when a person has oligua-ticula-jra, those people are subjected to anual eye exams, anus-letlamp-i-exams, anus-letlamp-i-exams. Pretty high up to know that stuff for your test. Okay. Now, what is the second way they can try to screw you over with anterior uviitis on your exams? Again, the USM is they're not stupid. They realize that most people have memorized.

And till you, uviitis. Right? So, they know many of you have memorized that term. Right? So, what is one way they create new questions from the same concept? Is to literally just switch up the name. So, what other name may you see on your exams for anterior uviitis? Well, they may call it iridocyclytis. I write this. I write this. I-R-I-T-I-S, or they may call it iridocyclytis. Iridocyclytis. Right? So, what are two other names for anterior uviitis on your exams? Think of iridocyclytis. Right? I-R-I-D-O-C-Y-C-L-I-T-I-S. I readocyclytis. Very high u to know those for your exams. Now, what if they give you a question about a patient? And they tell you that this patient, you know, this is just a factoid thing. I just want to go over. Just one of these simple things. Probably say this in other podcasts. Right? But remember, if a person, if a person's, if you do the poor cohort calculations, what is the threshold that makes us say, okay, let's go ahead and put you on a starting. I hope you're saying divine 7.5%. Right? If your risk, if your 10-year ASCVD risk is more than 7.5%, over the next 10 years, they were going to go ahead and put you on a starting. We're going to go ahead and put you on a starting. Alright, let's maybe hit a few things that are bio statistics related as we begin to wrap up this podcast. Right? So, what if they give you a question about, you know, it's a confounding question.

Again, if you're kind of confused on confounding, if confounding is confounding you, you should go on losing to my confounding podcast. I literally have a podcast on confounding and have a separate podcast on effect modification. Right? So, if you get a question about confounding and then they tell you that auto control for this factor, the researchers decide to do performance stratification. And then a classic thing they'll ask you is, this mode of controlling for the confounder is will most likely be done in what fees of the research study. Well, I'd really hope you're saying that if the person's this stratification is going to be, is something that is done in the analysis phase of the person's research study. Right? This is just one of these strange things that almost no research talks about but is very, very high yield to know for the USMLA exams. Right? And what do they do? They know that you have memorized, again, see, let me tell you something guys. Right? Before I introduce this concept because it's going to make it make more sense to you, make it more meaningful. The thing is our friends at the NBM Es, they realize that a lot of people use Anki these days. They recognize that a lot of people just blindly, blatantly, flagrantly memorise things without any form or degree of understanding. Right? So these days, the stuff you know, yes, you still need that foundation but you'll extend beyond it a little bit, just to see if you can think beyond just the basic stuff.

You've memorized from some on king or on queen or whatever deck that you're memorising. Again, there's nothing wrong about using Anki. Just make sure you actually understand what you're memorising. Right? Make sure you actually understand what you're memorising. Right? So the thing is, if you're doing stratification to control for confounding, it's going to be done at the analysis phase of the study. Right? It's literally going to be done at the analysis phase of the study. That's when you do stratification. You don't stratify people before the study has started. Right? But what if the mode that you, what if the method that you used to control for confounding is randomisation? Right? Because remember, you can use randomisation. By randomising, you pretty much spread out the confounder equally between your two groups, your experimental group and your control group. Well, that's done during the selection phase of the study. Right? So make sure you know what can be done during the selection phase of the study. That's randomisation versus during the analysis phase of the study. That's stratification. This concept is actually pretty simple, but again, you can just see people kind of getting to trouble with this. Right? And again, another thing I want to discuss with bio statistics, is again, what kind of information can you get from a cross-sectional study? Literally, what kind of information can you get from a cross-sectional study?

Well, the key thing to know is that you can give you prevalence information. Right? They can try to trick you on your exams and put an answer that says that you can get incidents or whatever. You can not get incidents information from a cross-sectional study. Right? A cross-sectional study is literally a point in time study. Right? You literally get a snapshot. So because you're studying people at one point in time, you cannot see new cases developing. You want to see new cases developing. They have to use something like a cohort study, for example, because that's a longitudinal study. Okay? So remember, a cross-sectional study is a snapshot study. It's a point in time study. But a cohort study on the other hand is a longitudinal study. It's a longitudinal study. Again, very high you to know those things for your exams. Right? So a cohort study can give you prevalence and incidents information. But a cross-sectional study can only give you prevalence information. It can only give you prevalence information. Right? Now, just real quick run through to wrap this podcast up. I just want to run through 10 high-yield drugs to know for your exams. And the way it's going to be tested on your exams. Right? This is just going to be literally a quick run through. Right? Preparal law need a law. Think of those. You can use those non-selective beta blockers to manage S of Agile as perphylaxis for a subagile varicides. Right? So as perphylaxis. Right?

We don't want you having a subagile varicides. You give them chronically. You take it regularly. So you don't have a bleed in a varicides. Okay. Let's talk about proponent law. That's number two. Proponent law is also used on the USML exams for the management of thyroid storm. Why? Because it inhibits that peripheral 5-prime diodeine, that converts T4 to T3. All right. Next, we're going to talk about cell dynaphyl. What is cell dynaphyl used for on the USML exams? It's used for two purposes. Number one, it can be used for the management of erectile dysfunction. Right? It can be used for the management of erectile dysfunction. Because it works at the level of the copper carbon. And also remember, it's a phosphodized freeze inhibitor. So it's going to increase your levels of cyclic GMP. That's going to cause more muscle relaxation. So your penis is going to be engorges with blood. Right? And then it's also used for pulmonary hypertension. It's also used for pulmonary hypertension. For pulmonary hypertension. Because it can cause pulmonary vessel dilation. And remember, be careful about combining cell dynaphyl with a nitrate or another powerful viso-dyliter, like an alpha-1 blocker. Right? Or even something that may not be an alpha-1 blocker, but indirectly has alpha-1 effects. Like a tricyclic antidepressant. Right? Those things, you combine them with a cell dynaphyl that can cause a big time drop in blood pressure and cause orthostatic hypertension. Right?

So you can give you a question about a person that has erectile dysfunction. And then the person is placed on the neutral for BPH. And then the person has, like, all these syncopal or presyncopal episodes. Well, basically what happened is you combine the person's alpha-1 blocker with a cell dynaphyl that they're taking. All right. Next, what we're going to talk about, dorsolamide. Right? Dorsolamide. What would dorsolamide be used for on the USML exams? Well, dorsolamide or its close cousin has said a zolamide, they're carbonych and hydrates inhibitors. Right? So what do we use them for? Well, we use them for things like, we use them for mounting sickness. We can certainly use them for mounting sickness on the USML exams. Right? And they can also use for the moneymen of chronic glaucoma. Right? They can use them to manage open-ung glaucoma. Right? Because by inhibiting carbonych and hydrates, you're going to decrease the production of a caes humor. All right. Let's go to another drug. So what if they give you a question on your exams about a dynosumap? Well, remember, dynosumap is a rank ligand inhibitor. Remember, your osteoblasts express the rank ligand that then binds to the rank receptor on osteoclasts, to activate those osteoclasts. Right? So the nossumap is a monoclonal antibody against rank ligand. It binds to rank ligand. And when you bind to rank ligand, you're going to prevent the interaction with the rank receptor.

And if that happens, your osteoclasts will not be activated. You're not going to drop your bones. So what do we use dynosumap for? We use dynosumap for the management of hypercalcemia of malignancy, remember, you can also use b-sphosphonis for that purpose. Okay. Drug number six that we're going to talk about is terryparatite. Terryparatite. T-E-R-I-P-A-R-A-T-I-D-E. What is terryparatite? How does it work? Well, it's a PTH analog. It's a PTH analog and you give it intramithantly. Remember, PTH works differently for a thyroid hormone. Works differently depending on if you give it intramithantly. Or if you give it constantly. If you give it constantly, osteoclasts are going to be activated. You're going to reserve your bone. But if you give it intramithantly, kind of like G-N-R-R-H, kind of like lupor light, you give it intramithantly. That's going to cause bone buildup. So we occasionally use it for the management of osteoporosis. We occasionally use it for the management of osteoporosis. But the thing is, you cannot give it for more than two years. Because think about it, you're literally given a stimulating factor for bone that can increase the presence risk of osteosterochor. All right. Now, drug number seven, let's talk about b-sphosphonis. What do we use b-sphosphonis for on the US Emily exams? Well, we use b-sphonis for the management of osteoporosis, right? That's pretty high up to know for your exams. We also use them to manage hypercarcymia of malignancy.

That's also pretty high up to know for your exams. And we can also use them to manage budgets, disease of the bone. We can also use them to manage what budgets, disease of the bone. That's pretty high up to know for the purposes of your test. Okay. Now, drug number eight, amylo-ride or triumterin. What do we use amylo-ride or triumterin for? Well, those are potassium-sparing diuretics, right? But typically on the US Emily exams, they are really used for their anti-hypertensive purposes. We typically use them in one of two variations on the exams. Well, one is to prevent the nephrogenic diabetes in sepidus that is caused by lithium. Because remember, how does lithium cause nephrogenic Di? Well, if you go to the principal cell of the collecting duct, lithium enters through the inek channel, right? On the urine side of the principal cell of the collecting duct, and then it goes and disrupts the vituris signaling cascade, the vituris-separous signaling cascade, right? So that prevents the insertion of aquapouring channels on the urine side of your tubules to go ahead and reabsorb water, right? So you can prevent lithium from doing those dirty deeds by literally blocking that inek channel with potassium-sparing diuretics like amylo-ride or triumterin. They literally work by blocking the inek channel. Now, those diuretics also remember their potassium-sparing diuretics.

So since they are potassium-sparing diuretics, if a person is taking another drug for the management of their high blood pressure, and those people have hypochylemia as a side effect of that drug, and the person is having some mild symptoms, right? One way you can actually just fix that hypochylemia problem is to just give them potassium-sparing diuretic like amylo-ride or triumterin, right? It's going to help with even better blood pressure control. But because the potassium-sparing diuretics they cause a hyperchylemia, you can use that to counterbalance the hypochylemia that the other diuretic that they're taking like a thazadiretic, for example. All right, now drug number nine. Drug number nine, I'm going to talk about is a dobidamine. So dobidamine, remember, it's a beta-1 agonist. It's a positive anal trope. We can use it for cardiogenic shock. We can use it for cardiogenic shock, because remember, it's going to stimulate beta-1 receptors. And if you stimulate beta-1 receptors, that's going to increase your cardiac output, your cardiac contractility, right? So your heart rate, your stroke volume, is going to go up. Right? And one thing that they can test on the USMD exams with regards to dobidamine is they can ask you, which of the following will be most likely observed, you know, like 12 hours after a person is given a bolus of dobidamine. In terms of GFR, remember, the GFR is going to rise and creatinine is going to fall, right? Well, why is that?

Well, the thing is, again, it's a positive anal trope. So it's going to basically stimulate the heart. As you stimulate the heart, right? You're going to be collecting fluid in your body. That fluid, you're able to push it forward. You're not able to have forward fluid to your kidneys. And once it gets to the kidneys, right? You're sending more blood to the kidneys, right? Delivering more blood through the afrin arterial, right? You're going to send more blood to the glomerular capillaries. If more blood goes to the glomerular capillaries, you're going to have an increase in hydrostatic pressure within those glomerular capillaries. If that happens, you're going to have more fluid extravisation, you're going to have more filtration. So your GFR is going to rise, and that's going to bring your creatinine down. All right. And that's also going to be able to make urine. And that's going to help you get rid of all that excess volume. That's one of the reasons why we like to use dobidamine when people have a cardiogenic shock. All right. Now, the final drug I am going to talk about here today is going to be amlodipine, right? So amlodipine, what context do they use it from the USML exams? Well, they use it in the context of the fact that it's a dihydropyredine calcium channel blocker, right? Amlodipine is a dihydropyredine calcium channel blocker. So how exactly does it work? Well, the way it works is that it is an arteriola dilator. It's an arteriola dilator.

So because it dilates arterioles, right? It's very, very good for managing blood pressure. It literally reduces your systemic vascula resistance, right? If you reduce systemic vascula resistance, you're going to lower the presence of blood pressure. But what is one big side effect with amlodipine? Well, it's going to be that peripheral edema. Again, go back to the mechanism of action. It dilates arterioles, right? When you dilate arterioles, you're going to send more blood to the vessels that are next in the vascular tree. That's going to be your capillaries. If you send more blood to your capillaries because you're dilating arterioles, you're going to increase the hydrostatic pressure within those systemic capillaries. When you increase those hydrostatic pressures, you're going to have more fluid extraversation. As you have more fluid extraversation, that's going to literally cause you to have peripheral edema. Now, how can you fix that peripheral edema? Well, you can give an ACE inhibitor. Because again, divine. Why would ACE inhibitors work for this purpose? Well, easy. Look at the next vessel in the vascular tree, right? Remember, after arterioles, we have capillaries, after capillaries, we have venuals. Well, what do ACE inhibitors do to venuals? ACE inhibitors dilate the post-capillary venuals. They literally dilate those post-capillary venuals. If you dilate those venuals, then you're going to be pulling blood away from those systemic capillaries.

If you remove blood from those systemic capillaries, you're going to reduce the hydrostatic pressure within those systemic capillaries, and that's going to basically shut down that peripheral edema. All right. So that's it. Again, if you love the way I teach, you're going to love my classes, right? I love to... And it's not like some TA that teaches my classes. It's literally me that teaches my classes. So if you love the way I teach, you love my classes, you love one or one tutoring with me, right? I have classes that literally start this evening. I have a test-taking strategy class. It's two and a half hours long. It's first step one, two, three. It's from like 745. It starts at 745 PM Eastern. And it's over Zoom. And then tomorrow Tuesday, I have a four-hour biostatistics class. That's at 545 PM Eastern time. And then... Sorry, that's... Sorry. So the class tonight starts at 745 PM Eastern. The class tomorrow starts at 645 PM Eastern, right? And then on Wednesday, I have a five-hour social sciences quality improvement healthcare systems ethics class. It's a five-hour class. The thing is that class has gotten bigger over time because there's just so much of that material covered on the USML EC. It's almost like an arms race to make sure we're keeping up with them, which I really make very strict efforts to do. It's a five-hour class. These first three classes I mentioned there first step one, two, step three.

And then on Thursday, God willing, I have a three-hour last minute review. It's for step two and step three. And then on Saturday and you know, basically counting Saturday and the five days after that, I have the 20-hour step two, step three class, right? And then in June, I have the 50-hour, step two, step three class, the 500-multiple-choice-question class. And it's not just 500-multiple-choice questions. We have a lot more stuff that happens in that class. The people that are taking that class, the alumni of that class, they've done extremely well on their exams. Literally, extremely well on their exams. In fact, I've had somebody that took the class, right? The class is a two-week class. And again, there's limited spots for that. It's a two-week class. The person took the first week of the class and went and took their real exam. It just happened to have to take their real exam. I think it was like they're... I think it was like step two or something like that. The person got like in the 250's just from half the course. Obviously, the person came back to take their mini-5 D's because I think they had a complex exam or whatever that they also had to take. But that class is very, very good. It is extremely high. Just imagine, for 50 hours, you're working through content, very comprehensive coverage of content. And then you're working through like test-taking strategies out of the wazoo.

Like literally, you'll be like an extremely confident and extremely good test-taker after that class. And then I also offer one or one tutoring for all the USM Lian complex exams. I also help with error's applications, personal statements, mock interviews, even discussing a ranking list with people I do all those things with people. And then I have another website called the Divine Interventional Life Lessons.com, many of you know I'm a Christ follower. So every week, I post like one or two podcasts where from a political perspective, I address a life lesson. Divine Interventional Life Lessons.com. There's actually an Apple Podcast associated with that called the Divine Interventional Life Lessons Podcast. So thank you for listening to me today. I will see you God willing in episode 634. So have a wonderful day. God bless you and bye for now. Thank you.

Screening to catch a disease early.

If the employer institutes them and the patient has no history of hearing loss on audiometry (preventing loss before it starts).

Self-limited; eventual resolution once the stressor is removed.

A low CD4 count (typically <200 cells/mm³).

Idiopathic.

Anus-letlamp-i-exams.

It cannot determine incidence because it only provides a snapshot in time, not longitudinal data on new cases developing.

Denosumab (a monoclonal antibody against RANK ligand).

Iridocyclitis or iridocyclytis.

Cyclosporine (or Nifedipine/Dihydropyridine CC Bs).

It is an arteriole dilator, which increases capillary hydrostatic pressure, leading to peripheral edema.

Potassium-sparing diuretics (by blocking the epithelial sodium channel).

GFR will rise, and creatinine will fall.

It cannot determine incidence because it only provides a snapshot in time, not longitudinal data on new cases developing.

Denosumab (a monoclonal antibody against RANK ligand).

Iridocyclitis or iridocyclytis.

Cyclosporine (or Nifedipine/Dihydropyridine CC Bs).

It is an arteriole dilator, which increases capillary hydrostatic pressure, leading to peripheral edema.

Potassium-sparing diuretics (by blocking the epithelial sodium channel).

GFR will rise, and creatinine will fall.