DIP Episode 474 - Beta-1 Receptors and the USMLEs (Step 1-3)

Welcome my name is Divine this is episode 474 of the Divine Intervention Podcasts. And to this podcast we're going to be continuing the series on the Adrenergic Receptors. Again as we've mentioned the pretty high yield things to understand. So I've had a podcast already on the Alpha 1 receptor, a podcast on the Alpha 2 receptor. It is going to be a podcast on the beta 2 receptor. And the beta 1 receptor, sorry, and the beta 1 receptor is a pretty straightforward receptor. Just like again every adrenergic receptor it's a G-boughton compote receptor. And it's a stimulatory G-boughton compote receptor. So what happens basically if a ligand binds to it, so something like Norepinephrine or Ibanephrine, you're going to have an activation of adenylate cyclists. And adenylate cyclists as we know, its job is to convert ATP to cyclic AMP. And then that cyclic AMP is going to activate protein kinase A. And that's going to cause a lot of different things. And honestly, on the USML Es there are two high yield places to know as to, this is where the beta 1 receptors are. Because honestly there are many places you can find this in the body. Typically on the USMLE exams, there are kind of a few select places they love to go after. And what are those two places? Well, the one big place is going to be in your kidneys, at your drugstore glomerulose cells, and then the second big place is going to be in your heart.

Your cardiac myocytes, your AV node, your essay node, the beta 1 receptors in many places. And basically what's the effect? So maybe let's look at each organ. Again, you'll notice from the others what I've tried to do is to give a quick introduction and then it will start making some integrations here. But basically in the heart, these things, the beta 1 receptors job is to raise your cardiac output. So we're really going to see that this may be helpful in a person that has heart failure. But it increases your heart rate, it increases your contractility, right? It increases your conduction velocity. Those are like the major things. But then at the level of the kidneys with the GG cells, remember the GG cells are known as the Drockster glomerulose cells? And their job is to produce reining. So it increases reining in our production. So now that we understand this, let's maybe go ahead and consider some classic clinical vignettes that you may see on your exam. So what if they give you a question about a patient? And this patient has a history of diabetes that has been complicated by significant lower extruding infections that have required amputation. And then the total of the patient presents with two weeks of chest pain that's beginning to worsen your chest pain. Let's say this chest pain whenever they do any kind of physical activity after like 15 minutes it calms or when the arrest it goes away. What should you be thinking about here? Well, this person has an agenda.

Now the thing is when a person has certain cases of an agenda, especially those that are quite severe, you typically want to do some kind of stress test. Now the thing is in terms of stress testing, many times we love exercise stress test because the person's exercise capacity can give a lot of very good prognostic information concerning that. But if a person has been has is an amputee, then we have to use a drug. We used to need to do something along the lines of pharmacologic stress test like what? Well, we can use something like the beta mean. The beta mean is a beta one agonist. Again, we know that beta one receptors, as we said, increase cardiac output, heart rate contractility, conduction velocity. So like even a beta one agonist, I'm going to really begin to see that. Oh, you can chemically stress out the heart. So even if they are not working out on a treadmill, you can pretty much selectively put the heart through some kind of workout. And remember, we also use the vitamin in the management of heart failure, right? Especially when a person has like a cardiogenic shock, we have cardiogenic shock. Again, you want to use something a positive vinyl drop like the beta mean, for example. Remember, the other positive vinyl tropes, they just don't necessarily work as beta one agonists, right? So we have things like Mary known, which is a phosphodi series inhibitor. We have things like the juxtaposition, which is inhibitor of the sodium potassium ATP pump, right?

But do you know the big thing today is that it's a beta one agonist. Now friends at the USMAD is one classic question you can get is what should happen to your potassium balance? When a person is on a dobutamine, well, one of the things is supposed to be the potassium balance is think about it. We said that again, they are beta one receptors, not just in the heart, but also in the kidneys. So when you stimulate those beta one receptors, that's going to increase the production of raining. When you make more raining, then you're going to convert angiotensin, which in 2010, 2001, angiotensin, one is going to be converted to angiotensin 2. Angiotensin 2 is going to go to the zona glomerulosa of the general cortex. It's going to cause you to make our duster. That our duster is going to make you your unique, literally excrete my potassium. So you will get a hypochiline. You will in fact get a hypochiline. And I think that you can also test on your examinations what's going to happen to your end-sistolic volume when you take the dobutamine. Think about it. Your end-sistolic volume, I would hope you're saying, should go down. Think about this. End-sistolic volume literally means the volume of blood in your heart at the end of systole. Or what in the world of systole means? systole literally means contraction. So after your heart has contracted, after your liver and your liver has ejected blood, what's left behind?

Well, if you're taking a positive vinyl truck, right, and you're contracting with more force and whatnot, obviously that's going to cause you. Obviously, obviously, obviously, that's going to cause you to have a decreasing end-sistolic volume. Because your stroke volume is going up. So basically the thing that's happening is that with each heartbeat, with each leventricle ejection, you're getting rid of more of more blood. But that's a pretty high-yield thing to keep at the back of your mind for exams. Very very high-yield thing to keep at the back of your mind for exams. Just kind of keep that in mind. Okay, keep that in mind. So there are just many ways they can go with some of these things. Okay, now the next thing I don't want to consider is what if they give you a question about a patient? And, you know, I guess, honestly, there's not many beta-1 agonist. You know, the one I'll mention, but this one is more for step one purposes. I superterial. I superterial is a non-selective beta agonist. It's both a beta-1 and a beta-2. Beta-1 and a beta-2 agonist. So we're going to keep going from there. Beta-1 agonist, you know, it's just not much going on with them. Although I will certainly say that the beta blockers, there's a lot of stuff going on with those. So I think maybe let's focus more on those. I mean, like the very first area you can think about is, you know, they give you a question about a person that, you know, had an MRI a few months ago.

The ejection fraction is like 40% or something like that. And they're trying to get you to, you know, prescribe drugs that the person can take long term. Well, obviously one of the drugs the person should take long term is going to be a beta blocker. Because the beta blockers, three of the, you know, the beta-1 blockers, they do improve survival in heart failure. Many of them do, in fact, improve survival. But if you're like, ooh, divine. What are some specific ones that will be good to know for exams? You want to keep your mind drugs like metoprolol or a carvedilol. I think carvedilol is what's called corrig in the hospitals. So metoprolol, carvedilol, and that be so prolonged. Those ones certainly improve a survival. And then what if you see a question about a patient and, you know, the USMLA exams, you notice that they have like really bad e-fib. You know, they have really bad e-fib. Remember, e-fib, one classic thing to worry about on your exams is the chronic management. One of the drugs we use chronically in the management of e-fib is going to be a beta blocker. Beta blockers are actually pretty effective for the management of e-traumatic fever lesion. Right? Although remember, if you got a fib in addition to a beta blocker, what else should you be on? You should be on some kind of anti-qualglition. And honestly, you can pretty much be on any kind of anti-qualglition you want.

The only exception, obviously, is if you have like a valve-yellow problem, let's see, you have like my trosternosis. And in that case, the only option is going to be offered. But in general, if we would have a fib, they're going to be on a beta blocker and anti-qualglition. Although in lieu of a beta blocker, one other thing you can use is you can use a non-dihydroperidine constant channel blocker. So something like verapamele or dill tires it. And also remember, beta blockers, you can use them to keep a person that has just so less city, or question about a patient. And you tell you that this person has a narrow complex regular tacky arrhythmia. Obviously, that's going to be an SVT. It's going to be a super ventricular tacky cardio. Typically, when a person has an SVT, the very first thing you're going to be doing is you're going to be doing some kind of vagal maneuver. Some kind of vagal maneuver. So like for example, you know, massaging the carotids, half them blowing to a straw. Because remember, if you're blowing to a straw, that's going to almost like a raise your intra-thoracic pressure. And that's going to compress your blood vessels like your carotids. And if that happens, your virus efforts are going to freak out that way. There's a load too much going on here. So you're going to send the person with the discharge to the heart. So it's going to slow down the heart to be very, very helpful. I mean, a person has a SVT. If you try that, it doesn't work.

Then your next step in an SVT is to go to a denocene. We should give like three doses. It can vary rapidly, abort many kinds of SV Ts. But if they treat a person's SVT with a denocene, you can just say, okay, you're cured. Moving on, no. And to keep them at a good heart rate. So to give them at a good heart rate, you better believe. You better, better, better, better believe. They should be also kind of, again, bitter blocker. Or a non-dihydroperidine concentration of blocker. And they can maintain them at a good heart rate. Okay? So that's something that's pretty, pretty, pretty high yield to know for purposes of the exams. Now, one other thing I want to say here about bitter blockers is, what if they give you a question about a patient? And they tell you that this patient has a fib. And for the last 12 hours, this patient has had like significant or deferred mental status. Becoming less responsive. They give you some vital. So you see the heart rate is like 300 beats per minute. The patient is like very to keep Nick. And you notice that the person, the tell you that the person has like a profound, increasing deep tendon reflexes. And you know, the person's ejection fraction is like 70% or some crazy high number. And then they tell you that the TSEG is undetectable. Well, that's going to be pretty straightforward. I hope you're seeing all the behind. The thyroid store. The thyroid store is really bad. This then actually has a pretty, pretty awful, a prognosis.

What do you do when a patient has thyroid store? The first thing you want to do is to give a bitter blocker. And now friends at the USMD is the account of medical students saying, let's give an anti thyroid medication first. Please don't do that. I'm not smart at all. Keep a bitter blocker. A bitter blocker is what you're supposed to do first when a patient has a thyroid store. You can give for a part of the law. But on the drug, you can give that I kind of want to introduce. It's not something finding many resources, but it's actually quite abundant on the USM Ds. It's a drug known as Esmolol. Esmolol is a bitter one blocker. And it's a very good IV medication works very quickly. So we can use it for those purposes. We can also use, so they may not be prepared well as the answer for the thyroid store where you examine. They can put like IV Esmolol. So it's very, very helpful in that circumstance. Well, how will Esmolol actually help? Again, like any bitter blocker, it can inhibit 5 prime diodeonies. 5 prime diodeonies that peripheral one is the one that converts T4, which is not a super metabolic reactive form of thyroid hormone to T3, which is a very metabolic reactive form of thyroid hormone. So in doing that, it's going to really help infyroid, infyroid a store. That's one. And also remember that these bitter blockers, they're also pretty helpful in people that have, pretty helpful in people that have what am I thinking about?

Say, for example, maybe let me give this as a scenario. So they give you a question about a patient. And the patient, they tell you that they have significant chest pain, you know, that's going to their back. You see a left-sided plural of fusion. And the person is pretty tall and what not. Obviously, that's going to be a neotic dissection. A presence of neotic dissection. The first macotherapy you're going to be getting is a bitter blocker. Larry, the first macotherapy you're going to get is a bitter blocker. So you can again use Esmolol in that circumstance. Esmolol in that circumstance. So that's something that's pretty high-youtu-no. Because the thing is, you may wonder, why do bitter blockers help in a neotic dissection? One is, many times, you have a neotic dissection. Your blood pressure is pretty high. Because as it so happens, the biggest risk factor for neotic dissection is hypertension. So it's going to help. But one other way that it helps is that it specifically slows down your heart. We said that the bitter one receptor, you know, the thing that happens is your heart's going to speed up. Well, if you take a bitter one blocker, your heart is going to slow down. If your heart slows down, then the blood that's going to be coming out of it is not going to be coming out as much force. Because the thing is, the blood coming out of the heart, the force with which it comes out determines if your dissectional or worsened or improved.

Blood coming out with more force is going to be ripping through that intimate into the media with more like energy. So that's going to basically worsen your dissection. But if you give a bitter blocker, bitter one blocker, that's going to slow down the heart. That's going to make the heart not contract as strongly. So as the blood comes out, it's going to come out with less force. There's going to be less shear stress on the intimate of the aortic wall. And that would, you know, basically improve the dissection while you're trying to figure stuff out. So, you know, bitter one blockers are pretty helpful in the management of aortic dissection. Now, our friends at the USML is, can you even give you a question about an athlete that collapses during a game? And again, they tell you that what should you recommend for long term management? Well, the thing you're going to recommend for long term management is, you're going to very likely put him on a bitter blocker. Can bitter blockers are pretty helpful for these folks? Why is that? Well, bitter blockers are pretty helpful because, if you think about it, when people have hypertrophy cardiomyopathy in a hookah, you know, which usually are from a cardiac sacramir mutation, the thing you notice is, many of us have heard of this term asymmetric septal hypertrophy. Okay, fine. That asymmetric septal hypertrophy or includes the levventricular outflow tract.

That's one of the reasons why these people have these crazy syncopies, because these crazy syncopies happen because that asymmetric septal hypertrophy as the levventricle is contracting, that hypertrophy interventricular septum essentially almost like forms a blockade out of the levventricle, forms a blockade out of the levventricle. So, those people's cardiac couple can drop precipitously and that can cause a problem. But it so happens that if you made the cavity size of the levventricle bigger, then that's going to almost like stretch it out some more. So that even when it does contract, I just like to think of it this way. If you've made something bigger at this line, even if it contracts down, it won't contract down to a smaller size as if it was not bigger at this line. So let's say something had a volume of like one centimeter cube, that's his baseline, whatever. If you contract it down, it's going to end up at a smaller size than if its volume at baseline was three centimeter cubed. I believe centimeter cubed is a little volume. So that's the same thing. It's when you give a bit of blocker, your heart goes slower. So since your levventricle is going slower, it's going to have more dastolic filling. It's going to have more dastolic filling. So it's going to get bigger.

So even if it contracts because the cavity size is so much bigger, then when it squishes down, that hypertrophied interventricular septum is going to be less able to cause that levventricle outflow tract obstruction. In fact, if you notice, anyone over that puts blood in the levventricle makes the murmur of hockum sound softer because you're basically relieving that obstruction temporarily. Again, how you doing that by increasing the end-astolic volume, because by giving a bit of one blocker, the heart is going a lot slower. If the heart goes slower, that's going to be pretty helpful, because you'll basically have more time in dastily, when the levventricle fills with blood. The levventricle fills with more blood. That's going to be very, very, very helpful. It's going to be very, very, very helpful. So just something I want to keep in mind. That's what we use it for hockum. And I know some people may be like, oh, divine. So you kind of meet this big force about how we should use beta blockers in theotic dissection because they slow down the heart and decrease the contract. So this blood comes out less force. If you want to actually extend that concept a little bit, that's why we don't give many visual dialeders in a setting of theotic dissection, especially hydrolyzing. That's like a common medical student error. This year, a person, they have aortic dissection. Their blood pressure is pretty high. They're like, oh, let's give hydrolyzing. No, don't do it.

Again, the fact that something looks logical doesn't always make it right. That's why you need to understand pathophys. Because literally, if you give hydrolyzing to visual dialeders, when your visual dialeders going to bring down your blood pressures, you're like, oh, good. That's no good, specifically in that context. Because the bar receptors are going to see a low blood pressure. So you're going to send the sympathetic discharge to the heart. So those kind of color means, it's going to stimulate the beta-1 receptors on your heart. You're going to have a faster heart rate. So you're going to have a reflex-tagging cardio. You're going to have an increased force of contractivity. So you already think about this if you're following my discussion. The blood that's coming out of the left ventricle is going to come out with more force. That's going to rip right through that intima. That literally going to worsen the dissection. So hydrolyzing and many visual dialeders, just not a good idea. When a person has a new dissection, they're just not a good idea at all. So please don't do that on your exams. And remember, beta blockers can also be used to manage essential trevers. They're pretty good for managing essential trevers. If you're looking at another neurologic thing that beta blockers are good for. Say for example, they give you a question about a person that has these disabling headaches. They have to be in a dark room, sound mix it worse.

And now they tell you that they're having these symptoms like 12 times a month. That's a lot, right? That's a migraine. That's a migraine. They're having too many symptoms. So you've got to do something about said migraine. Right? Although remember the acute management of migraine is not the symptoms as the chronic management or chronic prophylaxis of migraines. Again, that's one thing that many people on the USML Es screw up. Not necessarily understanding that sometimes the USML Es are requesting acute management for something. And sometimes the USML Es are requesting chronic management for something. That's something that's kind of lost to many people. And in the end of getting a lot of questions wrong, right? Like when a person has a migraine, you're going to use something like sumatriptan. So much symptom is pretty effective. Some bulls migraines respond very well to NSAI Ds. Right? That's acute management. You cannot give a person sumatriptan forever. Or like every day, oh, take it for your migraine prophylaxis. No, it doesn't make any sense. Why? Because sumatriptan is a pretty powerful visual constrictor. It's probably not a good idea, you know, because it can cause problems. You know, it can cause like strokes, all these things. So it's more for acute management. You take it, you let it go. But if you want chronic prophylaxis against migraine, so on one kind of drug you can use is a is a bit of blocker. You can actually use bit of blockers. Why?

Because again, those things are pretty, pretty good at slowing down your. In fact, maybe let me give a little bit of a, of a pathophysiology here. Here's the thing. Visual dilation causes headaches. Just think of this relationship. Visual dilation causes headaches. Visual constriction fixes headaches. Sumatriptan is a serotonin receptor agonist. That in a sense kind of causes visual constriction. It's going to be helpful for headaches. Again, it's just a relationship I've noticed from my review of pharmacology, especially as we're, again, regards to the US and the exams. And again, please, none of these podcasts are for clinical decision-making and just for test-taking purposes. And again, obviously, my leg may be very, very, very, very, and since inhibits cycloccygenase, it's going to shut down for stagglondin synthesis. You're going to get a visual constriction. They help with headaches. So a bit of blocker, because many times when people have like migraines, you can use bit of blockers as prophylaxis. Why? Because essentially, what can happen is, you're something like propanolol. I guess I'm kind of deep into my next podcast, but propanolol is a beta one and a beta two blocker. So because it blocks beta two receptors as well. Remember, the beta two receptor normally when you stimulate it, you're going to get a visual dilution. When you block it, you're going to get a visual constriction. That's going to be good for migraine.

So that's why drugs like propanolol, especially when a patient has, many times, because there are many drugs you can use for migraine, migraine prophylaxis. You can use some anti-seizure medications. We'll see, for example, a patient has like migraines, and they have another disorder that can be attacked very beautifully with a beta blocker. In those circumstances, you probably want to go ahead and use a beta blocker. So let's say a person has a visual migraine and they have an antenna. A beta blocker will be indicated for the chronic prophylaxis, the chronic management of their migraines. Again, these are all things. These things may look like a divine, whatever, whatever, whatever. But the premise you just stuff is actually pretty, pretty important. Pretty, pretty, pretty important. I mean, what else do we use beta blockers for? We can use them for managing glaucoma. Although this is less commonly tested on the USMNE, but drugs like acabutolol, so acabutolol, acabutolol, pindolol, p-a-n-d-l-l, those are beta blockers, although they're more like partial agonists at beta receptors. But if you're a partial agonist, you're giving us less than full effect, so you're pretty much a blocker. So as a beta blocker, they're actually pretty good for managing glaucoma. Pretty good for managing glaucoma. And then remember that beta blockers, those that have the names A through M, are beta ones selective blockers. But those that are N through Z, they're non-selective.

So you kind of want to be careful with asthmatics, when you're taking certain beta blockers, especially if they're like, perprime law, they're not very solid again asthmatic, because it's a beta one and beta two blocker. I mean, there's a reason why we give our beta wrong, which is a beta twig in this for treating asthmatic. So it probably starts to reason that, maybe even a beta two blocker, they're not the hottest idea in the world. Now, beta blockers, again, also have some other where to use this, you may see on your exam, right? Like, they can give you a person that, you know, comes in with, they've been hearing voices for past few days, kind of acting out, you know, weird, social withdrawal, the works, right? Persia has like, you know, bad psychosis, bringing them to the hospital, they put them on a drug. I mean, person feels like they're kind of jumping out of their bodies out of their skin. These extra pyramidal side effects. Well, we treat acathesia absolutely, right? You can use a beta blocker for acathesia. Although, remember, I know the drug you can use for acathesia, probably more of a second-line agent. It's going to be a benzodiazepine. But the thing is, you know, benzos have side effects. Beta blockers also have side effects, FYI, but, you know, we like beta blockers more. Well, see, for example, you have like asthma. And you have acathesia. Maybe getting, um, preparing a law as your treatment of acathesia is not a good idea.

In that case, you maybe want to go ahead and consider your benzodiazepine. You want to go ahead and consider your benzodiazepine. So, you know, there's definitely psychiatric conditions that we use beta blockers for. We use ac- you know, manage acathesia. We also use beta blockers to manage, um, stage fright, right? So social anxiety and disorder, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, you know, like given a beta blocker, not very smart, right? Because those people, their AV nodes, already not conducting things properly, conducting at a super, super, super slow, slow rate. So since their AV nodes already conducting things that are super, super, slow rate, doesn't seem great to add something that was super, super, super, because remember, beta one receptors also found in the AV node, right? So if you give a beta blocker, it's going to slow things down even more. You can throw those people into like cardiogenic shock. Then it's not a, not necessarily a good idea, right? It's not necessarily a good, good idea. And to finish with, even if a person does in half-fireage storm, if a person just has like hyper-adrenergic symptoms with your hyper-firoidism, beta blockers again, not necessarily about, not necessarily about idea.

And remember, for a person, you know, overdoses on cocaine, beta blockers not the first thing you should give. Hmm, why is that? The reason there is, again, the beta tour, if you take cocaine, you know, cocaine is, you know, makes you have more cardiocolourmines in your synapses. So all those cardiocolourmines can stimulate many of the receptors. You can stimulate the other one receptor, get visual constriction that can jack up your blood pressure. But those cardiocolourmines can also stimulate the beta tour receptor, which is a visual dilatier receptor, which is kind of helpful, right? Because that's going to, you know, lower your blood pressure. But if you give a beta blocker first, I give a beta blocker in cocaine overdose. Then, you're going to block those beta tour receptors. And the alpha-malaric receptor is going to be the only adrenergic blood vessel-bees receptor that's around. So those cardiocolourmines are going to be smashing those alpha-malaric receptors, causing visual constriction, get a hypertensive cardioprosticism, probably die. So it's actually pretty high yield to know from the example that this is. The redose on cocaine, or if you're going to meth, beta blocker, not a good idea. Because you're going to have a hypertensive crisis with that.

In fact, that's also why when a person has a fiochromocytoma, that's why you typically want to give an alpha blocker first, an alpha-on blocker, you know, like Prisocene, or Phentolamine, or Phenoxybenzamine, before you give a beta blocker, before you give a beta blocker. And also beta blockers, you can use them, you know, in people that have like, asides, like, let's say they have cirrhosis, one way you can chronically reduce bottle pressures, is to give a beta blocker, or you can give an aldosterone antagonist like Spurnolato, or a player know. The mechanism you're looking for there on your example is that they promote splanchonic visual constriction. Splanchonic visual constriction. Splanchonic visual constriction is a very cool process to understand. But it has almost like extremely limited utility on the USML Es. So it's kind of a waste of time, so I'm not going to cover that today. I think I may have covered it in a previous podcast, if a moment is taking. But the exact podcast, even right now, I cannot remember. But just know that beta blockers, again, on a chronic basis, the lower bottle pressures. Again, on an acute basis, if you want a lower bottle pressures, that's where you're reaching for true tight. On true tight is an acute lower, if there's a term like that, I don't think there is, of bottle pressures. But long term beta blockers, your aldosterone antagonist, that's where it's at. Something that's, again, pretty high-youtu-no for exams.

And I remember beta blockers, they're not necessarily good. In the sense that they can cause erectile dysfunction. Because we do use them for angina. We do use them for angina. So that's another used to know. But they can cause erectile dysfunction. So just FYI, something you kind of want to watch out for, watch out for on an example. They can certainly, certainly, certainly cause erectile dysfunction. You know, certain drugs can just cause erectile dysfunction. Yeah, beta blockers are a pretty, pretty big one. Pretty big one there. Beta blockers are definitely a pretty, pretty big one there. Pretty, pretty big one there. And again, remember, I think I've said this already, but you should not use them for an acute C-chef exacerbation. It's not necessarily a good, not necessarily a good idea. Right? Undessertely a good, a good idea. And again, remember beta blockers are regarded as antirithmics, right? They're going to be the class two antirethmics. They're going to be the class two antirethmics. Okay, so I think I'm going to stop here. You know, a lot of the stuff is pretty, pretty high yield. I definitely know these things if I were you. For those that are taking any of the USMID exams, especially step one to three, I have a class on Thursday. It's the test taking strategies class. Many people have taken them for you to be very helpful. I've literally had people that just from the test, they take it and boom, their scores should have quite a bit.

Even the acute bank percentages get better. So it's for step one or the widows step three. It's on Thursday, 5 p.m. Pacific time. And then on Monday, starting Monday next week. So on Monday Tuesday, Thursday and Saturday, we have a four day, 20 hour step two, step three class. And it's also for people that want like a good bird overview before they jump into their shelf exams. The class, 20 hours, again, many people have taken the class out and done extremely well. I learned how to do the class pretty recently. And I got into the two seventies on their step two. And this is like the new step two with all these questions, pull out changes. The class I have did pretty regularly. And again, people find it to be profoundly helpful. Then I have like a biostatistics class that's four hours long. That's for step one to three. And the social sciences quality improvement and ethics class, you know, healthcare systems, communications, professionalism class. It's five hours long. Also for step one, just step three. Those are taking place on the belief 17th and 18th of August. So if you're interested, just shoot me an email. All these classes over Zoom. They're pretty much not traditional lectures. They're pretty much almost entirely based on scenarios. Because again, it's not just learning the concepts that matters. It's learning the context behind the concepts as well. And seeing integrations, right?

So that's one type of dimensional thinking super, super helpful for the, for the USML exams. So if you love the way I teach, you have a pretty solid idea of how I run these classes. And these classes, I spend a very good amount of time taking and answering people's questions. And then, you know, also for one or one two during fall, the USML exams and for medical school exams. And then I help with your applications, personal, steep men's rec letters, application editing and all those things. And then, you know, I have these podcasts on the major apps. Apple Google and Spotify. I have a You Tube channel, Divine Intervention, USML, podcasts and videos. And then I do have a website called Divine Intervention Lifelesses.com. From a public whole perspective, I address certain life lessons. I, you know, post two podcasts every week. I really have more than 200 podcasts on there. There's actually an Apple podcast associated with it called The Divine Intervention Life Lessons Podcast. So, if you're interested in any of these things, just check those out. I think you're going to find it to be pretty, pretty helpful. So, thank you for joining me today. I will see you in a episode I guess, 475. So, God bless you. Have a wonderful day. Bye for now. Thank you.

The heart (cardiac myocytes, AV node) and the kidneys (juxtaglomerular cells).

Increased cardiac output via increased heart rate, contractility, and conduction velocity.

Hypokalemia, because stimulation of $\beta_1$ receptors increases renin release, leading to aldosterone secretion and subsequent K+ excretion.

Beta-blockers (e.g., Esmolol), as they rapidly control life-threatening sympathetic overdrive and tachycardia.

They block $\beta_2$ receptors, which normally cause vasodilation; blocking them causes vasoconstriction, which is beneficial for treating vascular headaches.

Blocking $\beta_2$ receptors leaves unopposed stimulation of $\alpha_1$ receptors, leading to severe hypertension and crisis.

Beta-blockers (e.g., Esmolol).

Diastolic filling/volume, by slowing the heart rate and allowing more time for ventricular filling, thus reducing outflow tract obstruction.

They slow the heart rate and decrease contractility, thereby decreasing shear stress on the aortic intima.

Class II antiarrhythmics.

Blocking $\beta_2$ receptors, which prevents vasodilation and promotes vasoconstriction (beneficial for headaches).

An alpha ($\alpha$) blocker (e.g., Phentolamine), because the $\beta$-blocker would otherwise leave unopposed $\alpha_1$ stimulation.

Beta-blockers (e.g., Esmolol).

Diastolic filling/volume, by slowing the heart rate and allowing more time for ventricular filling, thus reducing outflow tract obstruction.

They slow the heart rate and decrease contractility, thereby decreasing shear stress on the aortic intima.

Class II antiarrhythmics.

Blocking $\beta_2$ receptors, which prevents vasodilation and promotes vasoconstriction (beneficial for headaches).

An alpha ($\alpha$) blocker (e.g., Phentolamine), because the $\beta$-blocker would otherwise leave unopposed $\alpha_1$ stimulation.