DIP Episode 509 - USMLE Step 2/3 Rapid Review Series 111 (MUST LISTEN for Step 2/3)

Welcome, my name is Devine. This is episode 509 of the Divine Intervention Podcasts. Into this podcast we're going to be going over the Rapid Review series for the USML step 2 CK, step 3 exams. It's going to be series 1-11. To this podcast is going to be a little different. I'm going to be focusing on quite a number of basic science things that are tested on the USM Ls. I think one thing people are going to realize pretty quickly this year is that the USM Ls for the step 2, step 3 level, don't get me wrong. I'm still going to be testing the clinical stuff absolutely. That's going to be the bulk of the exams. But there is going to be a big push for most step 1 related content on step 2 and step 3 starting this year. Just going to keep that in mind. Okay, maybe I'll talk about that in a future podcast. But one thing I think I want to hit with as a foundation before I start and I'll make integrations as I go along today. It's kind of talking about some of these receptors. I feel like it's something that people see from step 1 and they just kind of look like, it's gone forever. No, it's not really gone forever. No, it is important for step 2 and step 3. So I'll just try to make some integrations and review the high-yield receptors. I think it's just something that's always kind of helpful to know.

So what if they give you a question about a person that has an nasal congestion or they give you a question about a person that got anesthesia and the person's blood pressure dropped or they give you a question about a person that has BPH. What's the receptor that links all these ideas together? Easy. It's the alpha-1 receptor. The alpha-1 receptor is a high-yield receptor to go for a purpose of step 2 and step 3. It's a receptor that we find in a few places. One, we find it around the bladder neck. So if you activate it, then you're not going to pee. But if you block it, then you're going to pee better. That's why it's helpful for what I have BPH. We also find it on blood vessels. So if you activate it on a blood vessel, then you're going to get viso-construction. That's going to raise your blood pressure. What if you block it on a blood vessel, that's going to cause viso-dilation. That's going to crush your blood pressure. So how do all these stains factor in? Well, all these stains factor in in the sense that they can give you a BPH question. Remember, BPH is going to be in a person that is old. It's going to be in an old guy. It's not going to be like in some 30-year old man or something ridiculous. No. That doesn't make any sense, right? It's going to be in an old person. Persons are going to have urinary problems. Or they can give you whatever derivative that kind of catches the offancy. Like you can see like hydronophoresis in a person that's an old guy.

It's probably going to be BPH. Or they give you this question about like a chronic renophilian and old guy with urinary problems. That's probably going to be BPH. So your person has BPH. Remember, you can give them an alpha-1 blocker. You can give them something like time. So loosen. You can give them presence in a what-not. Those alpha-1 blockers, you block those alpha-1 receptors, you open up the bladder and make them. And the person will be able to P find. Although those are more short-term treatments, you know, long-term, one thing you can do that's very effective is to give a five-hour very doctorate inhibitor. So something like finasteride or dutasteride. And by inhibiting five-hour very doctorate, you'll make less D-H-T. If you make less D-H-T, then you're not going to be the person who is going to shrink. You can actually shrink quite well over time. Obviously, if that doesn't work, they need to be thinking about surgery of some sorts to resex the person's a prostate. Another alpha-1 association here, I kind of talked about blood pressure, right? So a person has a high blood pressure and you put them on an alpha-1 blocker. So let's say for example, they give you a question about a person that has like hypertension and LPH. An alpha-1 blocker is probably not a bad idea for those people. Because one is going to open up the bladder neck, but two is going to bring down the blood pressure. So you can give something like, again, like Prasosin and what-not.

But again, what one side effect they love to test on the US signal is with these alpha-1 blockers. Well, is this whole concept of orthostatic hypertension, especially like this first dose or thostasis? Pretty common problem with these alpha-1 blockers. Because again, if you think about it by causing visualization, your dropping of person's systemic vascular resistance is that if that happens, then you know, you'll bring me not get not perfusion as it should because you're not you're keeping more blood in your vessels. You don't have enough to go to the heart, go back to the brain, blah, blah, blah, blah. That can cause a person to have a orthostatic hypotension. And remember the definition of orthostatic hypotension. This is something that many people screw up a lot on the exams. So drop, you know, if you're going from from a supine position to a standing position, if your systolic blood pressure drops by more than 20 or more millimeters of mercury or your last-to-leg drops by 10 or more millimeters of mercury and going from a supine to a standing position. So lean back flat to standing up. Obviously, remember if you lean back flat, then your veins are going to send all their blood back to the heart. So your preload is going up, your credit card put is amazing, your blood pressure is phenomenal, proficiency to bring great. But once you stand, more blood is going to pull in your veins. Remember from step one, your veins are capacitance vessels.

They have the ability to hold very steep amounts of blood compared to arteries. So if blood is pulling in your veins, that's kind of going to be a problem for you. Because again, the blood that's pulling in your veins, where is it not going back to? It's not going back to your heart. So credit card put is going to go down, your blood pressure is going to go down. That's how people get orthostatic hypotension. Now, and I guess I don't know why this thing just going to drop to my mind, but it's just one of these things that our friends at the NBA means they can just throw on an exam and you're like, man, I never saw this in any resource. What happened is this whole concept of why orthostatic hypotension will be more common in the elderly, right? Maybe because they have like fibrosis or destruction of their virus sectors in their blood vessels. So they're not able to sense blood pressure changes because those virus sectors are like sensors. When you see your blood pressure is dropped, the compensate by, you know, reliance on information to the brain. Your brain will give a sympathetic discharge to your heart. Now, raise your credit card output, raise your blood pressure and now counterbalance things. But if those bar receptors, if the blood pressure sensors don't work, then things are going to be all over the place. Right? And then, you know, another alpha one relationship, right?

I said, not just, you know, for training hypertension, I've talked about the orthostatic hypotension business. But again, remember, if a person is getting anesthesia, they love to throw this question on exams. They'll make it like an acute care medicine question. Persons getting anesthesia, they have blood pressure plummets at the DC. One in the world, I supposed to do for these people. I want to give them an alpha one agonist. So something like phenolephyrene or effedrine, right? Phenolephyrene is probably a big one. Just going to give it to them IV and that will against an alpha one agonist is going to climb down on their vessels. It's going to raise your blood pressure. It's going to raise your system of hospital resistance, which is going to jack up their blood blood pressures. And then another business you may see on your exams with these alpha one receptors may be a person that, you know, is like a war veteran and the person is having trouble sleeping. They tell you that since the person who turned from the ploy main three months ago, the person has been having trouble sleeping, has been having a lot of nightmares, having a lot of bad dreams, that he always often wakes up in a, in breaking out, breaking out of sweat. That's going to be PTSD. Remember for you to see a person has PTSD straight forward. They got to be having, you know, they'll have, usually we hit like a military question or a first responder question.

And the person would have had some kind of trauma in the past or some stressful circumstance. And then what will then happen to those people's life, life, right? Their lives are just heavily distorted, right? They have these nightmares, intensified experiences, yeah, yeah, yeah, yeah, yeah. And again, remember, you got to have it for more than a month. We don't say, ooh, this person has, this person has PTSD. Remember, if it's less than a month, we call it acute stress disorder. This person has PTSD and PTSD, obviously, these people, they're going to get CBT, but SSR Is are a very big part of their treatment strategy. But we don't just live it at that, right? One other thing that the tend to have, as I said, a nightmares, those nightmares are controversial. Very well, Prasosin. That's a high level thing to know for your exams. Prasosin is the drug of choice on your USMD exams for nightmares in PTSD. I certainly know that if I were you. Okay. So now let's just start, I guess jump to another receptor. I like the way I'm talking about these receptors. I'll give you a bunch of different vignettes and they tell you like what's the receptor that links everything together. So let's think of this next receptor. So what if they give you questions that hit certain things like they talk about chemical stress tests or they talk about heart failure or they talk about ringing fluctuations or they talk about in prevents survival in heart failure.

If you see all these things, what should you really be thinking about? I'll be thinking about the beta one receptor. The beta one receptor is a pretty high-youtur receptor to know. And for the step two, step three level, just remember it has been into spots with your heart and your GG cells, your heart and your drugstore glomerular cells. So your heart, what does it do? Well, if you still a little bit of one receptor, you're going to increase your cardiac output, you're going to increase your cardiac contractility. And then if you stimulate the beta one receptors or your GG cells, that's going to cause them to make a ring. So all these vignettes I mentioned, how they relate it. Well, I started off with a chemical stress test. Cause remember, most times on the USM at least, if we're trying to do a stress test for a person, you generally want to try to do an exercise stress test, an exercise test because it just gives you a lot more information than pretty much every other kind of stress test. You can see a person's exercise capacity. It just gives you more functional information compared to other kinds of stress tests, really, like lean on a bed and then we're stressing out your heart with a bunch of drops. So that's why, you know, we like exercise stress test.

But you know, if a person cannot exercise, because they have some reason for not exercising, like they're, they have a lot of syncopal episodes because they have like a cardiac volume disorder, like the olex anosis or the legs having chopped off, right? A person has an amputee or the person has a, there's another classic one peripheral, a zero disease and they cannot exercise. Then in these situations, you've got to consider chemical stress tests. One thing you can use for that purpose is dubia. I mean, dubia means a bit of an agonist. It's really good. Basically, you're going to drop to stress out the heart. So it works pretty amazingly well for that purpose. And then in terms of heart failure, in prevention of having a heart failure, remember beta blockers, in personal, heavily heart failure, although remember, it's not every single beta blocker. For the most part, the big ones are metoprolol, which is a beta one blocker. It's a beta one specific blocker. And then don't forget a carvedi law. I think it's called quarring in the hospital and then be so per law, right? Those are classic beta one blockers that in personal, have a heart failure. Okay. It is actually not every beta blocker that in personal, have a heart failure. Just kind of throw that out there. I don't think you'll go that granular on your exams, but if they decided to, it'd be helpful if you heard it from this podcast. So we've talked about it again from the heart failure perspective, right?

And then again, remember from the raining perspective, right? Again, if you love to make these things arrow questions on the exams, if you give a person a beta one agonist, they can give you a bunch of arrows, right? So let's walk through a few arrows with these beta one agonist. So let's say you get the beauty of me. One in the world is going to happen to your cardiac output. Your cardiac output is going to go up, right? Because you're still leading those beta one receptors on the cardiac myocytes. All right. What's going to happen to your end systolic volume? Well, your end systolic volume is going to go down. Because remember, if you're a beta one, I can ask you to cause in the heart to contractive one better. If your heart contractive one better, well, you're going to be getting rid of as much blood as possible from your ventricles. If you get rid of a lot of blood in the process of the heart contracting, an aka systolic, and at the end of that systolic, the amount of blood I'll be left behind will be small. So your left ventricle line systolic volume is going to go down. Okay. What's going to happen to your reading production? Well, your reading is going to go up. Your reading will increase. Your reading will literally increase because again, of that direct stimulatory effect on reading increase on really release by beta one stimulation. And then what's going to happen to your rest of your reading and diagnostics in our dose system?

Well, all those things are going to get jacked up, right? So like, for example, you're going to have an increase in your 101 and increasing your 102. You're going to have an increase in your dose to your own, right? So all these things you're going to see from this beta one activity. And remember, for person over doses on a beta blocker, you know, let's say they take it and they have like severe bradycardia, you know, which is not good, obviously. What are you going to do in that circumstance? I really hope you're saying, hmm, divine. Sounds like something outropping can fix. You can certainly give outropping. You know, many people know the glucagon aspect. And that's true. They still test that glucagon because the beta one receptor is a stimulatory G protein coupled receptor. So if you block it with a beta blocker, you're having over it, like toxicity from that, then you can just try to use something else that works with a stimulatory G protein coupled receptor to achieve that stimulatory G protein coupled receptor second messenger cascade. I glucagon, the glucagon receptor is a stimulatory G protein coupled receptor. So you'll bang on that receptor, you're pretty much going to achieve the same effects as you'll get from stimulatory beta one receptor. Right. So, but again, another way to counter beta one blocker over dose is just to use atropping. Right. Atropping is a most great antagonist. So it's going to speed up your heart rate.

It's going to be very helpful for that purpose. Okay. So that's all I think I'm going to say about the beta one receptor. Those are kind of like the big things. Again, I'm not discussing this on a step two step. I mean, on a step one level, this is a step two step three level. So please, for those that are listening to my podcast, don't be shocked if you see me. Don't get me wrong. I'm going to be talking about a lot of clinical stuff. That's where I'm going to be investing the bulk of my time. But this year, you're going to be seeing some basic science things make their way to the step two step three podcasts. Don't be surprised. Okay. Don't be surprised. I'm literally doing this for your own good. It may not feel good. You're like, man, divine. These things are pretty detail heavy. But again, I'm literally trying to give you like the bare minimum in terms of what you need to know to conquer these basic science questions. I'm telling you this. If you're a person that is taking step two, step three this year and your basic science, at least like the basic basic sciences, you don't have those downpots. I kind of feel bad for you. You're sending yourself up on a very slippery slope, very, very slippery slope. The USML is I'm telling you this. And again, you don't blame them for doing this, right? With step one being pass fail. Well, how are they going to make sure that people surely learn that material and retain it? They're going to just don't get on step two.

That's the thing. That's why many times when people plead for pass fail exams, I kind of scratch my head because you're basically hurting yourself. You may think that, oh, this is great. No, it's really not. It's really not great at all. I kid you not. It is. It's really not great at all. Because the thing is one of the fundamental things about a score is that it gives a very objective way for you to be compared to another person, right? Yeah, you may be like, man, those are making my life more stressful. Yeah, it does. But the thing is having a score levels out the playing field. It really does. So if you go to a top five medical school versus a bottom 30 medical school, that score, like having like a real score is a good level. But many people are like, you know, I just feel like we live in a world where people do a lot of like virtue signaling. If you're a person at the school, you probably understand what virtue signaling is. If you don't understand it, just look it up on your own. I'm not going to talk about that. There's not a political podcast. But honestly, like these days, it's kind of annoying. You see people, they go on these virtue signaling tirades and they try to do like they're looking out for the common man, right? Well, then at the end of the day, the things that you're seeking for, it actually ends up harming people than helping them, right? So all this pass fail, push for pass fail, push for pass fail.

It has really honestly watered down the USM at least, but he has on the whole meet the exam a lot harder for people. I'm telling you this, since step one became pass fail, it's not as easy of an exam anymore. And that difficulty did not just still with step one, it just kind of spilled into order like step two, step three and things like that, right? So this would keep pushing for pass fail. I just be kind of careful what you wish for. Be careful what you wish for. Like I don't just be careful what you wish for. It's not as great of a thing as many of you think it is. Actually, maybe get off this front and let's control this podcast. Okay, so what is the receptor that links the following ideas together, right? So asthma, COPD, and that's pretty much it. Asma, COPD, and then we'll talk about fire out store. What's the receptor that links all these things together? I would really hope you're saying now, divine, the beta to receptor. And there's more stuff than what I'm mentioning that links with it. So let's kind of break many of these things down again. I'm not discussing every receptor. No, that's not my goal at all. I'm just discussing receptor pharmacology, but from a step two, CK step three perspective. So remember the beta to receptor, we find it in a few places, but the big place we find it is on the early. That's it. That's kind of like the big, big, big place, the beta to receptor.

If you activate it, you dial it your bronchial, you block it, you constrict your bronchial, bronchial. So it's no surprise that when people have asthma or like an asthma exacerbation or a COPD exacerbation or whatever, we like to give them a beta to agonist, like a beautiful, to show that tibetra to agonist, it's going to dial it your bronchial, it's going to open up your early, that's going to be amazing. Also, if you think of a person that is at a restaurant and in detail, that they become more responsive, if a person becomes more responsive at a restaurant and detail that you hear a lot of strider or your job is kind of done, that person has an affelactic shock. So if a person has an affelactic shock, you need to open up their early, but how bitter early is not going to be what you're going to be using. So please don't pick up bitter early as an answer for opening up her ways in an affelactic shock. That's not a very good idea actually. So what are you going to be using on your exams? You're going to use epinephrine. Epinephrine, it pretty much goes after every adrenergic receptor, but the one that it goes after very strongly is the beta to receptor. And that's the receptor where concerned about if you have an affelactic shock. So if you stimulate those beta to receptors, you open up the early and the person should start doing better just in general. And just remember for the purposes of the USML, I just figured I'll throw this out as a concept.

Let me see it on an example question, you're like, whoa, where does it come from? So for persons that have an affelactic shock, after you give them epinephrine, if you notice that they are still hypotensive, it's not a bad idea to give fluids. Fluid, giving fluids is actually not a bad idea in an affelactic, so you may wonder, divine, like, why are we doing this? Well, think about it in an affelaccess. Many times you've released a bunch of inflammatory mediators, you know, things like histamines and brachyneins. What do you think those things do to your vascular permeability? They're going to raise your vascular permeability. So your blood vessels, your systemic capillaries and whatnot, they're going to get more leaky. And they get more leaky than what happens to your intravascular volume. Intravascular volume is going to plummet. Basically, the fluid is going to be like people use the term third spacing. I really hate that term, but basically the fluid is going to go to your into the interstitial. So it's not going to be your vascular tree. So of course you're going to be hypotensive because literally your effective circulating volume is down, right? So fluids, that's really common. You give normal saline, normal saline, you're going to, you're basically pumping that fluid into the vascular tree. That's going to raise the presence preloads, going to raise the caloric hopper, going to raise the blood pressure.

At least it's going to increase your effective arterial blood volume. So that's just one benefit of that, right? And then I'll have alexis. So we've talked about the asthma angle. I've talked about the, I feel like this angle. And remember, you know, in terms of asthma, they're also the long-actin beta-twaginists. So things like salmererol and for morero, salmererol and for morero. Those things, they're things you use as the third wrong one, the latter for managing asthma on a chronic basis. Remember asthma, you know, we start off with a, should I think beta-twaginist like a beta-rol, the end. And then if that's not controlling the symptoms, in addition to that, add a, any helicoregosteroid. If that doesn't work, then go ahead and add a lava, right? Add a lava or you can add a luchotrine antagonist like Monte-Luca, those are for luchast. Although we prefer Monte-Luca, those are for luchast because are for luchast as a few more side effects than Monte-Luca. But if that's not working, then the fourth wrong one, the latter is going to be oral steroids. But again, that's not a point of this podcast. So let's continue. And then in terms of thyroid, so we need to be wondering, why thyroid store? Well, they can pretty much give you a question about a person. The activity of a person has a Hissro grills disease or something like that. And then the person's blood pressure is like insanely high, like 190 systolic, the heart rate is like in the 300s.

The person is some more lame, barely responsive. That's thyroid store right there. That's thyroid store. Remember, what is the drug of choice for Trillion Thyroid Storm? The first thing, and usually the only thing the graph throw of the exam, is a beta blocker. When you give a beta blocker, especially like per per normal. Although you can also give Esmo-Lal, but they love per per normal a lot on the USME Ls. Remember, per per normal is a beta one and beta two blocker. So you want to think twice about it in a person that has asthma, right? Because remember, before we go to the thyroid store issue, asthma, we treat asthma a beta to Agnes. So how do you think a beta blocker is going to do like a beta to a blocker? Do you think that's going to be a good idea in an asthma? Probably not, right? Because if you block those beta to receptors, you'll close up their ear when they can die. You don't want that, right? Well, why is per per normal low useful in thyroid store? Well, per per normal is going to be useful in thyroid store. Because it inhibits the enzyme we know as a 5-prime diodeonase. When you inhibits a 5-prime diodeonase, you're going to prevent the peripheral conversion of T4 to T3. Why do you want to decrease that conversion? You want to decrease that conversion because T3 is the more powerful moment, a more likely active form of thyroid hormones. So if you decrease the synthesis, that's going to be very helpful. So again, I'm going to tell you this.

The first line treatment for thyroid store is a beta blocker. Usually on the USMEL exams, they go per per normal low. If you don't see that as an answer, you can go with asthma low, okay? You can go with asthma low. But again, per per normal low is kind of a big one on the exams. And another weird thing to know about per per normal low. And I guess one of the weird thing I'll say as to why per per normal low helps in thyroid store is the hyperadrenergic effects associated with thyroid store. You can shut those down by giving per per normal low. Because again, remember many people forget this from step one. But one of the jobs of thyroid hormone is that it basically makes you stick more beta-1 receptors on the surface of a credit myocytes. So that's why people that have thyroid storm, they have like insane taggy cardio. They may even have a fib. Remember, a fib is the most common arrhythmia in people that have hyperthyroidism. So they may have like crazy taggy cardio insane e fib stuff like that, which can be very deadly. Actually, the mortality from thyroid so it's pretty high. It's just one of those things you want to recognize and treat pretty quickly. But essentially, if you give per per normal low knowing that it's a beta one and a beta two blocker, it's going to block those beta one-adrenergic receptors. So that's going to kind of tamp down those hyperadrenergic effects. Now, another place you may see per normal low, let me give you a question about a person.

And it's a thing that this person has chronic alcoholic and this person has been admitted to the hospital like three days ago because they were very hypotensive, they were altered and they were copious amounts of blood. And that the person had to undergo an endoscopic procedure and the person has since recovered doing well. And then you'll see which of the following should be done in terms of long-term management. Don't forget a beta blocker. What am I getting after here? I really hope you're saying, divine. This thing you just said sounds like an awful lot like a ruptured is over geoviruses. Yeah, right? So you see chronic alcoholic puking blood. Of course, that's going to be viruses. So, very sees, you know, you're going to manage it acutely with endoscopic therapy, you know, bandins, therapy, whatever floats your boat. But the thing that's kind of worrisome is that those things have a high risk of recurrence. So you need to try to lower portal pressures so that they don't keep having these problems because ruptured viruses are pretty, pretty deadly. Actually, quite a good number of people die from that stuff every single year. So what can we do to lower portal pressures? You can use a beta blocker. You can use a beta blocker like per per per hour law. They love per per hour law for that purpose on the USM in the exams. Every now and then you see them. So putting per per hour law, they're putting needle law.

But per per hour law is probably the most common one you're going to see on your test. Although remember, you all dost run antagonist like spurnal lactone. Those things also used to lower portal pressures. So, see for example, a pressing is a, you know, has a, you know, like portal hypertension and the half-heart failure. And how dost run antagonist is pretty good because it's going to help with the heart failure. And it's going to help with the portal hypertension as well, right? The buzz word you want to think about for your exams as to why per per hour law and spurnal lactone, lower your portal pressures is this term splanchning viso-construction because splanchning viso-construction, okay? Splanchning viso-construction, the term sounds counterintuitive. You may wonder like, how can viso-construction lower portal pressures? It's counterintuitive, but let's just leave it at that. It's just one of these things that you don't need to start sweating so much about first step two. Believe it or not, I have talked about that concept in a, I can't even remember the podcast from like way back. I actually described the mechanism behind how splanchning viso-construction can help with lower portal pressures. But again, don't sweat your head about that for step two-step three. So, another to talk about the mechanism. We just don't have the time for that. These are rapid review podcast. We're already at 27 minutes.

So, basically, because splanching viso-construction, that's the word you want to remember. By having that happen, you're decreasing portal pressures, okay? You're decreasing portal pressures, you're decreasing portal pressures. So, again, kind of keep all these things in the buckle of your mind as you're dealing with the beta-to receptor. Okay, so what if they give you a question about a person or what receptor links the following concepts together? So, you see a person that is depressed and the person is having trouble sleeping. And the person ditched the SSRI because it was affecting the average and whatnot. So, that's one question. I know the question is, a person that is in the hospital, the person is an IV drug user or drug user of some sort. And the person is in the hospital and they came in for some other thing. But then now, this person is having a lot of sweating, a lot of diarrhea, a lot of rain or diarrhea. And what's the thing that also links a 12-year-old boy that talks out of his turn at home and at school. And he was placed on pharmacotherapy. But this boy is losing a lot of weight. He's not eating enough and he's having trouble sleeping. So, what's the receptor that links all these ideas together? Well, these are the alpha-2 receptors. So, you can see why these receptors are kind of high yield. I'm kind of surprised by how much one can really ring out all these receptors for step 2, step 3. So, this may actually just be the point of this podcast.

I'll call it a rapid review series, but I'll put a small notation in the topic that, okay, receptor pharmacology for step 2, step 3. I would know this podcast if I were you, honestly. You're going to get a lot of questions right from this loan podcast. That's the truth. But basically, let's kind of hit the alpha-2 receptor. So, the alpha-2 receptor, the big thing to know about it is that it's a receptor that if you stimulate it, you're going to make less nerve and effort. That's kind of the big thing. You stimulate it, you're going to make less nerve and effort. You stimulate it, you're going to make less nerve and effort. Because it's a G-14-copyld receptor, but it's an inhibitory G-14-copyld receptor. So, you're still related, you're going to make less nerve and effort and make less nerve and effort. So, how does this relate? So, you know, we talked about the person that was depressed and was having trouble sleeping and whatnot. And then, you know, they were taking it, they were on pharmacotherapy for the depression, but they stopped because, you know, it was kind of affecting the emerge. Oh, let's kind of unpack the story. This person had depression and they were probably on an SSRI on SNRI of some sort. I remember those drugs cause sexual dysfunction. So, because those drugs cause sexual dysfunction, sometimes that can be like a limiting side effect for people and they're like, I'm not going to take this anymore. So, for this person, what do you want to try?

You want to try something like metasapine. Metasapine is actually a pretty amazing, anti-depressant. It's amazing that it's not prescribed more often, but again, disclaimer, disclaimer, disclaimer. None of this is for medical decision making. It's just solely for educational purposes. Okay. So, how does metasapine work? How does it work as an anti-depressant? Because if you think about it, you know, the monamine hypothesis of depression is that people that are depressed, they have low levels of neurobenefering, dopamine, serotonin and stuff like that. So, metasapine is an alpha-2 blocker. So, remember, I said if you stimulate the alpha-2 receptor, you make less neurobenefering. So, think about if you block the alpha-2 receptor, you're going to be making more neurobenefering. You're basically blocking your inhibiting and inhibitor. So, you're getting a net activation. You're going to make more neurobenefering. So, it's going to be a very helpful for that. Now, what does one of the benefits of metasapine? It doesn't have sexual side effects. So, it's great. So, to give you a question about a person on an SSRI, SNRI or TCA, and if we don't think about it, TCA is also called a sexual dysfunction. You should really consider metasapine for those people. Or double propion is also not a very bad gig for that. But metasapine is helpful for that. And metasapine also helps with sleep. It makes people sleep really well. It makes people sleep really, really well.

So, this person that is having depression and struggling with sleep metasapine, not a bad idea at all. Now, remember, metasapine also stimulates appetite. So, if you're a person that is depressed and you're not eating well, metasapine is not a bad idea for those people. Now, this person that's in the hospital, that's a drug user, has been in the hospital for some stuff. And then now they're sweating, they're everything. That's opioid withdrawal. That's opioid withdrawal. The person is going to have my dry ass issues on the exams. Remember, opioid overdose, you're going to have pretty cardiac, you're going to have respiratory depression, you're going to have pinpoint poopy, all spruppular amyosis, and you're going to have constipation. So, the reverse of that is you're going to be super, super leakier, right? So, those people are going to have diarrhea, ryanaria, everything. So, most times when a person has opioid withdrawal, somebody cares what they need, you know, give them fluids, whatever, they're going to be fine. But sometimes on the exams, they can try to request that you pick an actual drug for treatment. If they're wanting to pick an actual drug, pick a clonidin. Like, whoa, define what? Yeah, you're going to pick clonidin. Now, let's explain why. So, here's the thing. Again, the USMLE is one general class of concepts they love is where you have two different receptors that accomplish the same goals.

I'm going to say that again, two different receptors that accomplish the same goals. It's just one of these weird patterns that I've seen over my career, like teaching medical students. But basically, if there are two receptors that achieve the two different receptors that achieve the same goal, the USMLE is they love to use that as an integration. They love to test those things. Like, for example, I give, I've literally given one example already in this podcast where it's like, ooh, gee, better block her overdose. What are you going to do? And you give glucose gone? Why? Because the beta one receptor is a stimulator G protein coupled receptor. The glucose gone receptor is also a stimulator G protein coupled receptor. So, for pressing as a beta block her overdose, you need, you basically killed stimulator G protein coupled receptor activity, right? Stimulated, then lead cycle, so make more sickly KMP. So, we're just like, huh, we swap out and go to the glucose receptor. It gives us the same thing, but at least that glucose gone receptor has not been blocked by the beta blocker that are present over the dose time. That's one example. Okay, so what's the other example here with this opioid withdrawal thing? Why is cloning in helpful for opioid withdrawal? Well, if you think about it, the new opioid receptor is an inhibitory G protein coupled receptor. Let me say that again. The new opioid receptor is an inhibitory G protein coupled receptor.

Believe it or not, that new opioid receptor when you stimulate it is an inhibitory G protein coupled receptor at the adrenergic synapse because it's inhibitory. It's going to cause it to release less in the open effort. If you make less in the open effort, especially like in the eye, for example, you'll have less stimulation of the alpha one receptors in the eye. So, you're going to have meiosis, this is not my dry sense. I mean, people always memorize like, oh, opioids cause meiosis, pinpoint, opioids. Well, how do you think that happens? It's because you're making less in the open effort to stimulate the alpha one receptors in the eye. Okay, well, here comes the alpha two receptor. The alpha two receptor already said is an inhibitory G protein coupled receptor. So, it reduces the production of an inhibitory G protein effort at the adrenergic synapse. So, basically, it's a different receptor. Well, you actually get a pretty similar net effect to what you see with opioids. The only thing is that alpha two receptors are not distributed all over the body like we see with the mere receptor. That's why you can see the mere receptor having certain effects on certain things. We don't see that with alpha two agonist like clonidate. So, that's where clonidine comes in. It can help with many of the peripheral symptoms of opioid withdrawal because you're pretty much like achieving an opioid-like effect.

You're just using a different receptor and the thing is these alpha two agonist are not as addictive as opioids. That's why I remember like where I went to med school, you know, in Baltimore. Believe it or not, clonidine is a pretty popular street drug for that purpose. It's a pretty popular street drug. Why? Because it kind of makes your opioid, it's almost like, wow, it's going to make you not withdraw from opioids. What drug user is not going to love that, right? You can kind of add the rest of the story together yourself. So, okay. Now, another situation I talked about with these alpha two receptors, I pretty much talked about this boy that's talking out of his turn at home and at school, right? So, that's two settings. Remember, those two settings are kind of necessary. I mean, you know, it was placed on pharmacotherapy, but he's having trouble sleeping, he's losing weight, he's getting a lot of stuff. This child has ADHD, simple as that. This child certainly has ADHD. Remember, ADHD, you need the issues in two settings for you to make the diagnosis on your exams. It's kind of important to know for the USML Es. So, typically, when a person has ADHD, you're going to be placed on a stimulant, you know, something like method any date or a dixtramphetamine. With those stimulants, sometimes the cancer pressure person's appetite, person's going to be losing weight.

As a grown-up kid, you don't want to be losing, I mean, if you are obese, you probably want to lose weight, but if you're not obese, you don't want to be losing weight. As a kid, you want to get good sleep. As you remember, growth hormone is released a lot when you sleep. So, pediatricians kind of get very panicky. When they see kids on these ADHD meds, they're losing a ton of weight, they're not sleeping well. It's kind of affecting the child's future. So, in those situations, you're going to try out a non-stimulant. You can try something like a homoxetine. But what if they don't put an homoxetine on your exams? What can you use? We can use an offered to agonist like clonidine or guanfacine. Guanfacine is spelled G-U-A-N-F-A-C-I-N-E. I'm going to spell that again. G-U-A-N-F-A-C-I-N-E. That's an offered to agonist. It's going to be very helpful in treating a third-line treatment for ADHD. So, just something you want to keep out of the buckle of your mind for your exams. Remember, clonidine can also be used as a blood pressure drug. Again, it decreases no repinephrine production. So, if you make less no repinephrine, you're going to have less viso-construction. It's going to be very helpful for blood pressure. The only problem with that is that the dosing is not very good. It's not one of those things you can take once a day. You know, it's not one of those things you're going to have to take like multiple times a day.

And if you miss a dose, you can have a rebound hypertension. That's a high yield side effect of clonidine to know for your exams. Now, so again, I think I've hit a lot of the drugs and receptors I want to hit. I'm just going to mention some things in passing. Like the viso-pressing receptors, also important receptors to know, right? Is the V1 and V2 receptors? The V1 receptors, these receptors all respond to EDH, just something you want to keep in mind. The V1 receptor, the big place to think of them is blood vessels. Think of them as being on blood vessels. You stimulate them. You're going to get viso-construction. That's going to raise your blood pressure. That's why we leave it or not. For certain kinds of shock, we can use viso-pressing to treat that. The V2 receptor is in the kidneys. It's in the principal cell of the distal network. So that's where EDH works. That's where EDH works. It's going to help us absorb water from the urine. That's going to be helpful. Remember, lithium and demyclocycling, they have a lot of stuff to say about that. Lithium enters through the inech channel in the principal cell and shuts down the viso-pressing V2 receptor. So if you shut it down, then you're not going to respond to EDH. You're going to have an effiging diabetes in sepidos and all the things that come with that. Those are the viso-pressing receptors. The most grainy receptors, I feel like sweating out that M1, M2, M3.

That's more of a step one gig for the step two, step three level. I feel like that's not something that the make people sweat so much about. Just remember, though, you're most grainy antagonists. They are pretty high to know for step two, step three, like atropine. Remember, if a person has an atropine overdose, they're going to have an anticholinergic toxidrom. Don't forget things like atropine. We can use that for organophosphate poisoning. Remember, organophosphates, the inhibitor cellululinesterase, that's going to raise your levels of cellululin, you're going to get a cholinergic toxidrom. You can reverse that by giving an atropine first and then putting in toxin to be regenerated at cellululinesterase. Then remember, there are also some most grainy, you know, some of these anticholinergic drugs like Benadryl, Typhin hydramine, we can use them to treat some of these extra pyramidal symptoms, like a person having a cuteness to any of the taken an anticholic, or even Parkinsonism responds very well to these anticholinergic drugs like Benastropine, for example. Then don't forget that atropine is used to reverse beta blocker overdose, we've kind of talked about that. I'm sure of many of you are seeing the one you're talking about these most grainy can taginists. How about most grainy can I can as well?

I'll see the big most grainy agonist to know for you exams is things like Bethany call or carbacol, pylocarpine, pylocarpine, especially we use it for acute, like acute angle closure of glaucoma, it's going to constrict your poopyels and that's going to help with drainage of ectostumor. But also if a person has overflowing continents, whether the trusser muscles don't work, those the trusser muscles you can stimulate them to contract so the bladder can empty out, but even a most grainy can get it's like Bethany call or carbacol, or you can give an acylocolinesteris inhibitor like new steaming, new steaming and acylocolinesteris inhibitor. If you inhibitor, you're going to jack up your levels of acylocoline and that's going to be very, very helpful for trading overflowing in continents. Okay, so I'm going to go ahead and stop here. Okay fine. Not most grainy receptors, but remember many of these in your most club blocking drugs are nicotine receptor antagonists, like the vecoronium, rocoronium, pancoronium. The only one that's most nicotine receptor agonist is like succinocholine, but the thing is it stimulates the nicotine receptor that we find at the neuromuscular junction. It's going to stimulate it, but then it just kind of stays there. And once that thing is stimulated, it needs to be on stimulated, it will to be stimulated again. You're like divine, seriously, man. Hang on, hang on, hang on calm down.

Basically, the way the nicotine receptor works is that you stimulate it and then you on stimulate it so that you can have the next stimulation. So, succinocholine basically stimulates it and then does not leave. So that on stimulation that should happen before the next stimulation does not happen. And then it basically acts as a blocker that's it. Okay, that's we're going to leave it at that. We're going to leave it at that. Okay, I remember for my stenographies, right, we're going to use acylocolinestriase inhibitors like pyridolstigmin because it will shoot up your levels of acylocoline and that's going to help compete those nasty or anti-bodies against the nicotine receptor at the neuromuscular junction. Okay, so I think honestly, if you know these things, I discussed in this podcast, you're probably no like 95% of the receptor stuff that you need to know for your test, right? All the stuff with alpha 1 beta 1 beta 2 alpha alpha alpha 1 alpha 2 beta 1 beta 2 visual person V1 and V2 most great in receptors. If you know these things, again, I'm telling you step two, step three, you're going to see a lot of questions on this stuff on your exam. To be honest with you, I almost don't want to call this a rapid review series, but we'll see, we'll see, we'll see. Okay, so thank you for listening to me today. Again, I have these podcasts on all the major apps, Apple Google Spotify, our You Tube channel, and I have a bunch of courses coming up this month.

I have some classes for step one, two, step three. I have a four hour bio stats class, a two and a half hour NV Me testing strategy class and a five hour social sciences, all the team improvement, healthcare systems, ethics class. Again, many people have taken these classes, found it extremely helpful. For step two, step three, I have a 20 hour step two, step three review, coming up this month as well. And then the very first week in March, I have a step one review. I have a 25 hour step one review. Again, these courses are not lectures. If you expect to a lecture, you're shooting for the wrong course. Basically, I use a lot of vignettes, a lot of scenarios, a lot of exam style questions to one, help you understand the path of phase deeply, but also help you see how the material be tested on exams and show you integrations across many other disciplines. Like I'm telling you, these courses, many people have taken them, they've done extremely well on the exams. I kid you not. Especially again, on the USMEL is these these where understanding is beginning to matter a lot more than memorization. These courses are are very helpful and they're all over most times they're they're held in the evening. So if you interested, just ship me an email and give you some more information. And also for one or one two or in for all the USMEL exams and all the complex exams. And then I have another website called divine intervention life lessons.com.

Many people have found the website to be very helpful. We have 250 podcasts on there. There's actually an Apple podcast associated with that. And basically every week, I post two podcasts where from a political perspective, I try to address a life lesson. So thank you for listening to me today. Again, I do hope that you find this podcast to be helpful. And I do hope you actually studied this material. Please, I'm not making this podcast just for fun. Well, I have fun doing it, but it's also for your for your exam purposes. So see you next time. Bye for now.

The alpha-1 ($\alpha_1$) receptor.

Orthostatic hypotension (due to decreased systemic vascular resistance).

They cause bronchodilation by relaxing bronchial smooth muscle.

Epinephrine acts on multiple receptors ($\alpha_1$, $\beta_1$, and $\beta_2$), providing systemic support (vasoconstriction via $\alpha_1$) in addition to bronchodilation.

Rebound hypertension. Clonidine decreases NE release; missing a dose allows for excessive sympathetic rebound.

The alpha-2 ($\alpha_2$) receptor (it is an inhibitory G-protein coupled receptor).

It causes vasodilation (lowering BP) and relaxes the bladder neck/prostate smooth muscle (improving urinary flow).

Tamsulosin or Silodosin.

A drop in systolic blood pressure of $\ge 20 \text{ mm Hg}$ or diastolic blood pressure of $\ge 10 \text{ mm Hg}$ when moving from supine to standing position.

Non-selective beta-blockers (e.g., Propranolol). They block $\beta_1$ receptors (reducing cardiac workload) and inhibit the peripheral conversion of T4 to T3.

Inattention/hyperactivity in both home and school environments.

$\alpha_2$ agonists (e.g., Clonidine). They reduce NE release at the adrenergic synapse, achieving a similar net effect to opioids.

The V2 receptor.

It causes vasodilation (lowering BP) and relaxes the bladder neck/prostate smooth muscle (improving urinary flow).

Tamsulosin or Silodosin.

A drop in systolic blood pressure of $\ge 20 \text{ mm Hg}$ or diastolic blood pressure of $\ge 10 \text{ mm Hg}$ when moving from supine to standing position.

Non-selective beta-blockers (e.g., Propranolol). They block $\beta_1$ receptors (reducing cardiac workload) and inhibit the peripheral conversion of T4 to T3.

Inattention/hyperactivity in both home and school environments.

$\alpha_2$ agonists (e.g., Clonidine). They reduce NE release at the adrenergic synapse, achieving a similar net effect to opioids.

The V2 receptor.