DIP Episode 255 - The Legendary Step 2CK/3 Pharmacology Podcast

Okay, welcome. My name is Devine. This is episode 255 of the Divine Intervention Podcasts. And in this podcast, I want to talk about a subject that seems to be given people quite a number of issues on step 2, and step 2, and in recent times, at least people seem to be worried about mechanism of action questions, people are like, oh, mechanism of action, mechanism of action. So I figured that make like a podcast or two, you know, or maybe like a few podcasts here and there. When I talk about like the major drugs and the key things that the USMLE will probably go after with those drugs, this is targeted specifically to those that are taking step 2, CK or step 3. If you want an in-depth treatment of pharmacology, I've pretty much covered all the pharmacology in first aid in different podcasts, but check on the step 1 tab on the spreadsheet that I highlight on my website. And then just as a reminder, if you're taking step 2, CK, I do have a course coming up this Saturday on the 22nd of August. I also have another one coming up on the 5th of September, and then I have a two-day option, right? So remember the 22nd of August one is a 10-hour class. It's 10 hours one day, and we basically review like 600 to 800 concepts from like, from IM, PEED, Surgery, Neural, OBGYN, Psych, and it's over a 10-hour period. We start at 6 a.m. Pacific time, go from 6 to 10 a.m. Pacific, take a to-a-break, not to 4 p.m. Pacific, take a to-a-break, and then 6 to 8 p.m. Pacific, and then we're done.

And again, many people have found this course to be pretty helpful. And again, I think of the course as software. I updated very regularly, very, very regularly, to meet the needs of the newer exam. Again, just trying to stay, stay in tune with the MBM and the Weedy test things. And most of these things I discussed, I discussed them in the context of clinical vignettes. And then, if you want to know how to take these tests and take them successfully, I'm offering a test-ticking strategy course. It's going to be on the 10th of September. It's going to be on the 10th of September. I made a post, like my most recent podcast, like the podcast before this episode, 254. I cannot talk about the times and stuff. So if you want to have all your questions answered, listen to those podcasts. Listen to that podcast. It's very short. You'll put it through on all these things. So, you know, I have a bunch of courses basically coming up over the next couple of weeks, because I know that ERAS is popping up on the 21st of October. So there's a ton of people taking exams this period. Okay. So let me just go and if you want to sign up for these courses, just basically fill out like the contact form on my website and just reach out to me and then I'll give you some more information. But again, I feel like most questions that people email me about, I pretty much answer them in the podcast. So just listen to episode 254.

It will just see what's from having to like go back and forth over email on something that I've already clearly described in a podcast. Okay. So, and again, this will be a freestyle discussion. They're freestyle discussion. But again, I'll try to hit on most of the major drugs. Again, I'll try not to meet this podcast as super long. Okay. So let's talk about the blood drugs. Right. That's probably like a good place to start. Right. So, you know, the blood drugs, there are essentially two big categories here. Right. There's the anti-plitlet agents and there's the anti-coagulants. Right. Again, remember the anti-plitlet agents. They're not the same thing as anti-coagulants. And for the most part on NV Me exams, what do we use anti-plitlet agents for? We use them for things like if a person has a stroke or a TIA, right, like Cardid stenosis, we give those people anti-plitlet agents, right. Like first line, if a person has Cardid stenosis, the first line drug is always going to be aspirin. If you don't see that as an answer, the second line drug you should go for is Copidogra. If you don't see that as an answer, the third line drug you should go for is Diperidomo. Right. And I'll talk about the mechanisms of actions of these drugs. Right. Another region on NV Me exams where we use anti-plitlet agents. Right. If you notice, I kind of have like a fairly different focus with discussing these drugs.

Another thing you may see on NV Me exams with these anti-plitlet agents is if a person has peripheral or peripheral disease, for a person has peripheral or peripheral disease, those people need to take an anti-plitlet agent, basically like aspirin for life. Right. Another group that also gets this is if a person, for example, has like a precutinous corner intervention, right, for like a myocardial infarction, those people are usually placed on some kind of dual anti-plitlet therapy. Right. For you know, a couple of months after they get the, after they get the stent, and obviously for a person is having an MI, right, I would hope that you're giving them an aspirin at the very beginning, right. Like you know, when they come in for therapy, that's the first drug. You should always give any person that presents with chest pain on an NV Me exam, right. You give them aspirin, right. And then remember, we also use aspirin for Kawasaki's disease, right. And some of those things we give, we give aspirin plus IVIG for Kawasaki's disease. And then finally, if a woman has had pre-eclumsia or the previous pregnancy and you're like, you know what, I don't want you getting pre-eclumsia or the later pregnancy, go ahead and give the woman aspirin. Aspirin is actually pretty good for philaxis. I guess while we're in it, if you see a woman that has had like, come on divine, think, if you see a woman that has had the cervical thing, cervical insufficiency, right.

Serviculin's efficiency, you can prevent it in future pregnancies by giving a progesting suppositories, right. So let's talk about these anti-plitlet agents, right. So what are the key things with these anti-plitlet agents, right. So we know that the platelet cascade, right, is primary, hemostasis, the secondary, hemostasis, right. So primary, hemostasis, what happens in primary, hemostasis. First thing we do is we have this adhesion step, right. You know, GP1 B binds to the wheelbend factor, right. You have that adhesion step. When those two things couple together, right, you then begin to eject the ton of adp from the platelet. The adp from the platelet will bind to an adp receptor. Remember that adp receptor is also known as the P2 L2 receptor, right. When adp binds to that receptor, it's a G protein coupled receptor, right. It will trigger some kind of signaling cascade that will then cause you to make a ton of GP2 B3 A, okay. GP2 B3 A. And then that GP2 B3 will bind with another GP2 B3 from another platelet, right. And that will be the aggregation step. So first step is adhesion with GP1 B binding to the wheelbend factor. Second step is the activation step where you're releasing a lot of adp from the platelet that will act on adp receptors on that same platelet. And then the third step is the aggregation step where again GP2 B3 A is kind of coexist bind to each other to form that platelet plug, right. So what are some key things you want to know here?

If you want to know that aspirin is a cox inhibitor, right. Aspirin is a cox inhibitor. Aspirin inhibits cycloxygen ease inhibits cox 1 and to its irreversible compared to all the other NSAI Ds that are reversible inhibitors of cox 1 and cox 2, right. And by inhibiting the production of cycl- by inhibiting cycloxygen ease, right. You're not going to make thromboxin A2. If you don't make TXE2, then you're not going to be able to have that aggregation step. You're inhibiting the aggregation step of primary hemostasis because TXE2 actually helps with platelet aggregation, right. That's one high-yield thing to know for example. Second high-yield thing you want to know with these agents, right. You remember like we have these GP2 B3 inhibitors, right. So things like abscessemab, right. Optifibatide, tyrophiban, right. Abscessemab is probably the big one you see on a test, right. It's a GP2 B3 inhibitor. By doing that, right. So you're preventing one GP2 B3 from binding to another GP2 B3. So you don't form the primary platelet block, right. And then if you go down this P2 Y12 receptor business, right. Remember drugs like clopidogrel, prestogrel, tycagrelar, right. Those are ADP receptor antagonists, P2 Y12 blockers, right. Because if you block that receptor, then ADP won't bind to it and you will not activate the platelet, right.

And then in terms of these drugs like diperidomol, celosterzol, those are actually anti-plitlate agents, but they are not classically used for platelet problems, right. So like celosterzol, for example, on NBN exams, is one of those things you give after you've tried a supervised exercise program for a person that has peripheral ulterior disease. If that's not correct in it, you can add a diperidomol, you can add celosterzol, right. Diperidomol, on the other hand, is one of those things that are used for pharmacological stress tests, right. Again, if you notice, maybe like divine, but I have the Sankey cut that said this and this and this and this and this. Again, this is a targeted review for pharmacology for who. People taking step 2 CK and step 3. Basically, I'm trying to give you the information that you need to get these questions right, right. So diperidomol, again, is used for pharmacological stress tests. Celosterzol is used to treat peripheral ulterior disease after you've tried a supervised exercise program, right. So how do those drugs work? So the thing is, these drugs, they are phosphodistorysterystery inhibitors, the inhibit PDE3. When inhibit phosphodistorysterystery, that will actually increase the amount of cyclic AMP.

When there are high levels of cyclic AMP inside a cell, that actually, inside a playclips, that actually inhibits that signaling cascade downstream of the P2 Y2 receptor because the P2 Y2 receptor, believe it or not, it's actually an inhibitory G protein coupled receptor. So when ADP binds to it, because it's an inhibitory receptor, that will quad down on the production of cyclic AMP, right. And that will then cause activation of the playclips. So less cyclic AMP equals more pleated activation, right. So if you inhibit phosphodistorysterystery, remember PDE3 breaks down cyclic AMP. So if you inhibit it, cyclic AMP will build up more cyclic AMP less pleated activation, right. Less pleated activation. And some of you may be like, divine. Why would se los dos corte for me if I have, if a person has peripheral ulterior disease? Well, think about it, right. Remember, cyclic AMP when it's low, that actually causes smooth muscles to relax, right. When cyclic AMP is high, whoops, when cyclic AMP is high, that actually causes smooth muscles to relax. I'll say that again, when cyclic AMP is high, it causes smooth muscles to relax, right. Remember, cyclic AMP does different things in different kinds of muscles. When it's in cardiac muscle, high cyclic AMP causes increased contraction. When it's smooth muscle, increased cyclic AMP actually causes muscle relaxation. So if you relax smooth muscle, that means you'll cause a blood vessel dilution, right.

So you feed more blood to the legs, right. So that's a higher thing to know with those, with those drugs. So those are the key mechanisms of action with those things. And then don't forget that if a person is on the offeling, right. Then a diapyredomo will probably not work, right. Or like a denocene will probably not work in those people, right. So remember, you use a denocene for pharmacological stress tests. You can also use diapyredomo for pharmacological stress tests. Why would that be the case? One, a denocene is a visual dilator, right. But the thing is diapyredomo actually boosts your levels of adenosine. Diapyredomo is an adenosine diaminase inhibitor. So if you inhibit adenosine diaminase, adenosine will build up, right. And if he builds up, right, that will cause visual dilution. Remember, the offeling antagonizes the actions of adenosine, right. So like they can probably give you like a question about a person that has like a, I don't know, like COPD or rebar asthma that's being treated with the offeling, right. And then you notice that, hmm, this person, we're giving this person adenosine for an SVT and not doing well, right. If you see that, right, then you should already begin to imagine that this person is taking some drug that antagonizes the actions of adenosine like the offeling, right. Now, if we're going to secondary hemostasis, the big things you want to know about these drugs, right. So let me kind of talk you through the key things, right.

So warfarin is a big time drug, right. What are the things you would see on step 2, CK with regards to warfarin? If a person has a prosthetic heart valve, they need warfarin, right. If a person has a prosthetic heart valve, they need warfarin. And remember warfarin, how does it work? It inhibits vitamin K, peroxide reductase, right. If you inhibit vitamin K, peroxide reductase, you will not be able to gamma caboxylate factors 279 and 10 and protein CNS, right. But remember that before you start a personal warfarin, you need to bridge them with haaprin. And how does haaprin work? Haaprin activates antithromine 3. If you activate antithromine 3, then you'll be able to inhibit factors 10 and factor 2, right. Because remember, factors 279 and 10 and protein CNS, protein CNS, those things actually anti... Those things actually pro-quagulable, but 279 and 10, if you inhibit... So, sorry, let me put it this way. Protein CNS, those are anti-quagulants, like natural anti-quagulants in the body. 279 and 10, those things promote coagulation. But the thing is, protein CNS, they have a shorter half-life than 279 and 10. So, when you give a person a warfarin, and you inhibit vitamin K, peroxide reductase, CNS, which are natural anti-quagulants, will fall out of circulation first, while 279 and 10, they are still living on for like a few more days, right. So, there is a temporary hyper-quagulable state when a person is placed on warfarin.

That's why you have to start haaprin first before you bridge them to warfarin, right. Now, what do we use warfarin for? Again, I said we use warfarin for people that have prosthetic heart valves, right. Remember that target INR, there is 2.5 to 3.5, right. Second, we use warfarin in people that have a fib from a valve-yular cause. So, let's say you have a person that has like microstenosis as their cause of a fib, and you need to put those people on warfarin, right. You need to put those people on warfarin. And remember that warfarin is a teradogen, right. So, you don't want to give it to a pregnant woman, right. And if a person is like supratherapeutic on warfarin, what are some bad things that can happen well, they can have like a doodinal hematoma, right. That can present us like a small bowel obstruction, right. Or they can have like a rectus sheath hematoma, right. Or those people can have an intracranial bleed. Those are all things you want to keep at the back of your mind on exams. And obviously, if a person is on warfarin, it doesn't seem like a very good idea to give them TPA, right. It's only if you want them to bleed out and die, right. That's probably not an ideal thing to do, right. And if a person, you know, just has a supratherapeutic in our, let's say it's like six or seven for whatever reason, but they don't. They're not bleeding anywhere. They're normal, right. Go ahead and stop the warfarin.

If they really want to do anything for those people, you can give them like oral vitamin K. But if for some reason the person is like bleeding out, bleeding out, bleeding out. I want to reverse that warfarin. Reverse warfarin these days with four FPCC, the four factor, the thrombin complex concentrate, right. And then heprin, right. Remember, you reverse heprin with predominance of it, right. Reverse heprin with predominance of it. And again, remember heprin is an activator of antithrombin three, right. Which causes it to inhibit factor 10 and 2. Low molecular weight heprin on the other hand, right. It also activates antithrombin three, but it activates it to only inhibit factor 10, right. It activates it to only inhibit factor 10. And then remember, as again, as we were talking about, remember again, the first group of drugs I talked about were antipyletal drugs. Antipylogolansal warfarin heprin, the factor 10 inhibitors. Remember, the factor 10 inhibitors all have XA in their name, a pixaban, a doxaban, riveroxaban, right. So those drugs, right, they all inhibit factor 10, right. And then we have the factor 2 inhibitors, right. We have things like dabigatran, bivaluridine, agatroban, right. So I'll say that again, agatroban, bivaluridine, dabigatran, right. Those are all factor 2 inhibitors. Those are all factor 2 inhibitors, right. And remember that the classic situation where you give people these drugs on exams, is if a person, for example, has hit, right.

So they give you a person, came in for surgery, got like lumolecular with heprin or heprin. And then you notice they give you two sets of labs. And notice that the platelet count has tanked, right. Like five days later, like dropped by like more than 50%. That's easy. That's hit. If a person has hit, stop the heprin product. Do not start them on lumolecular with heprin, dabigatran, absurd thing to do. Study monofactor 2 inhibitor, like bivaluridine, dabigatran, or agatroban. And remember that, classically, the classic teaching is, oh, we can reverse warfarin, oh, we can reverse heprin, but we can reverse any other drug, any other anticoagulant. That's not true. Dabigatran is now reversible, right. There's a monoclonal antibody known as a dioresisumap. I'll say that again, agadaroidaru, cizumab, agadaroisumap. It's a monoclonal antibody against the dabigatran, right. So dabigatran is reversible these days on MDM exams. So I think those are the things I'm going to say with the blood drugs, right. So let me maybe take a quick dive into some of these cardio drugs, right. So what are the big things with the cardio drugs? Let's start with the isine inhibitors, right. They all end in prel, lysinopril, anala prel, for synopril stuff like that. How do those things work, right? Those things, the inhibitor and retention converting enzyme, right. And if they ask for the site of action of these drugs, it's in the pulmonary capillaries.

They work at the endothelial cells of the pulmonary capillaries, right. Now, what do we use isine inhibitors for an exam, right. Again, isine inhibitors, if you don't know about them, you're kind of asking for it on the test, right. So what do isine inhibitors work for an MDM exam? Again, especially step two, see, can step three, right. We use them in people that have diabetes, right. So that their kidneys don't fall apart, right. We use them and remember those, that isine inhibitor story about how they are good for their headaches. The mechanism behind that is actually something that's high or to know, listen to the recent podcast I made on Starlin forces. That will very quickly point out those high or things to you, right. But basically, right, like isine inhibitors, we use them to make people that have diabetes, we don't want their kidneys falling apart. If a patient has heart failure, right. And we want to improve survival. Isine inhibitors are awesome for that. Remember, the other drugs that improve survival in heart failure, beta blockers, right. Arbs, right. And you're tensed receptor blockers, right. Remember, those are those strongly separate antagonists, right. Like Spurinolactone, right. And a player known, all the remember Spurinolactone is also an angiogen receptor blocker. So he causes guys to have boobies, right. So like, can a comastia. But a player known does not have that side effect, right.

And they remember if you're not, if a president is an African American, right. So let's say, president is African American. You can actually give them the combination of hydrolyzine and isosobadine nitrate, right. That actually improves survival in that population. And then there's also this thing known as cardiac synchronization therapy. Basically, on MB, this is like a newer MBME concept. But basically for a person, if a person has heart failure, their EF is less than 35%, and you're on maximum medical therapy. So let's say if we put them on ACE inhibitors, by the L, blah, blah, blah, blah, blah, everything, right. One thing you can actually do is, if the press, especially if the person has, like a, like a YQRS, you cannot really do this thing where you put an ICD. And they also perform something called cardiac synchronization therapy. It has actually been shown to improve survival in some people with, in some people with heart failure, especially if this population I just described, EF less than 35%. And then, so what drug was I talking about? I was talking about ACE inhibitors, right. So we'll say it again, diabetic. So the kidneys don't fall apart. People that have heart failure. And I don't mean for heart failure, I mentioned beta blockers. If I did not, beta blockers, right. Remember like my temporal lobe, carvidi lobe, sopor lobe, those things actually improve survival in heart failure. So again, ACE inhibitors, right.

Diabetic so the kidneys don't fall apart in pro survival in heart failure. Contrary indicated in people that have bilateral, bilateral, or other stenosis. So how does it show up on a test? They'll give you a question about a person. Oh, person has hypertension. They put them on an ACE inhibitor. The acronym was fine when they were studied on said ACE inhibitor. You're like, wait, come back for a checkup two months from now. You look at the acronym, you're like, whoa. How do you create an get to like three, right. Those people have bilateral, or in our list of stenosis. Usually for those people, go ahead and do some kind of angiography of the kidneys, right. And figure out what in the world is going on with those people's kidneys, right. So just figure out basically the renal aleristinosis that they have, right. And then remember, if a person is being treated for a CHF exacerbation, and you're giving them like fear or some height, you're giving them like a lube diuretic, you know, to try to kind of help their kidneys, I mean, try to help them with that fluid so they can get rid of that fluid. If you notice that, hmm, all the fluid is not going out. I want to go ahead and add in a drug at an ACE inhibitor, right. Because an ACE inhibitor will serve two rules. One, it's a diuretic. But two, the hyperchylemia associated with taking an ACE inhibitor will counterbalance the hypochylemia that's associated with a person taking a lube diuretic, right. For heart failure, right.

And then what else do we use ACE inhibitors for? If a person, for example, has a peripheral edema from taking like a dihydroperiodine calcium channel blocker, ACE inhibitors are the drugs of choice there. Again, the mechanism behind that, I discussed that in my Stalin-forcesa podcast, is one of those episodes in the 250s. Okay, what else do we use ACE inhibitors for? Sculidermorinocrysis. If a person has sclerodermorinocrysis and the acryctin is kind of like falafelene all over the place, go ahead and give those people an ACE inhibitor. It's actually the drug of choice for treating sclerodermorinocrysis. Remember, if a person has sclerodermorinocrysis, like sclerodermas, there is never the right answer ever for sclerodermas. Okay. Now, is there any other thing I want to see with ACE inhibitors? Oh, they are terrarogens, right. So don't give them to a pregnant woman. That will not be good, right. They can give you a question about a pregnant woman, you know, lost to follow up, taking ACE inhibitors for hypertension, and then they tell you that her child, like she has oligohydramineals, right. That's pretty classic, right. Like she took ACE inhibitors, crushed the child's kidneys, child basically has like powder-style problems, not making urine, not present as oligohydramineals, right. So it can be like, oh, the amniotic treating this is like two, like some astronomically low number, right. Those are always the contests, those things.

And obviously ACE inhibitors can cause a dry cough, right. From an increasing bradycaning, right. And also if a person has like a C1 S trace inhibitor deficiency, right. Those people should not be placed on ACE inhibitors, right. And also do not forget, for pressing has that dry cough from ACE inhibitors, go ahead and give them an ARB, right. Things that end in sartan, low sartan, can the sartan, tell me sartan, right. So those are big things there, right. And then again, our dose of receptor antagonists, what do we use those for, right. So we use those for, again, one in proven survival in heart failure, right. They work by blocking our dose of receptors, right. Remember, those are an example of a potassium-sparing diuretic, right. So they cause hyperchylemia as a side effect, right. And then remember that spermolactone, you can actually use it to treat the hersotism, associated with PCOS on a test, right. You can actually treat the hersotism as a zero PCOS on a test. And then don't forget that these are those who run on antagonists, you know, you can use them as to decrease portal pressures, right. You can actually use them to decrease portal pressures. So if a person has like a histro-like, as a geovaricist, this is not what you give acutely, but you can give it chronically to reduce portal pressures. For an olactone can actually be helpful for, for those purposes. Okay. And one of the things you may see spermolactone may use for is consendrum, right.

Especially when a person has bilateral and general hyperplegia, the cause of the consendrum, spermolactone or pleurinone is actually pretty good for those people. And again, as I said, spermolactone, been an adostron receptor antagonist, improves survival in heart failure, right. And then if we're going to the beta blockers, right. We use beta blockers for many things, hypertrophic cardiomyopathy, improves survival in heart failure. We use them for migraines, especially like proprenolol, right. Remember, we use them to treat acathesia, right. Acathesia, one of those extra pyramidocyte effects, from the tuberin-informed developed pathway, not working very well. We use proprenolol for that. Performance anxiety, we use proprenolol for that, right. If a person has a high command of I think, if a person has thyroid storm, right. The first drug, the initial drug of choice in thyroid storm, right. Is proprenolol, remember, he gives it that five-primed diiodin is that we find in the periphery. That's a high-yield mechanism of action thing to actually know for exams, right. So we use proprenolol for migraines, right. We use proprenolol for many, many things on exams, right. Another classic beta blocker emission of tests is labeta law. Remember, labeta law is an alpha beta blocker, right. Labeta law is an alpha beta blocker. It's an alpha beta blocker. We use it to treat hypertensive emergency on exams, right.

It's actually one of those anti-hypertensives that actually seep in pregnancy. Remember that mnemonic hypertensive moms love my fedipine. For those anti-hypertensives that are seep in pregnancy, right. Hydralazine alpha methodopal labeta law and my fedipine, right. And then what else do we use beta blockers for? You can use beta blockers, right. Again, to improve survival in heart failure, especially like metoprolol, carvidolol, and besoprolol. And remember, if a person has like a few chromositoma, you're going to block alpha receptors first, right. You can use an alpha one blocker like phantolamine, right. Or phenoxybenzamin to block those alpha one receptors first, before you then put them on a beta blocker, right. And again, remember, again, for a person comes in, they are all doptop on cocaine, right. It would be incredulous to give them a beta blocker first, right. It's only if you're looking for like on opposed alpha problems so that you can, you know, like get like a big stroke or a hypertensive crisis and die. You don't want to do that, right. So you give them an alpha blocker first before you give them a beta blocker. Although typically on mbim exams, the person comes in with cocaine intoxication. And you notice that the atroponins are elevated, they have ST elevations. You basically treat them like you treat any regular MI, right.

But if their blood pressure is just high, but they don't have like any severe problems, like their EKG is fine, their atroponins are fine. And IV benzo, that is a pin, is the drug of choice for those people on exams, right. But if you don't see an IV benzo, you can give them again, something that can bring down their blood pressures like clabitolol. Remember, labitolol, yes, it's described as a beta blocker, but it's an alpha beta blocker. So it's acceptable to give those kinds of people, right. So those are kind of like the big things I think I want to mention on beta blockers. Remember, you can use them in AFAB. If a person has AFAB, remember for AFAB, you can post you like a rate control strategy or a rhythm control strategy, right. So the rate control strategy involves a beta blocker. Remember, beta blockers are class 2 antarid mix or you can use a non-dihydroperidine calcium channel blocker like very fundamental of delta ism. Remember, those are class 4 antarid mix, right. You can use those to maintain a presence rate in effect, right. To try to keep people in like a normal retina in effect. And then, don't forget that beta blockers, we can also use them to treat glaucoma, you know, things like a pindolo, or that stuff you can use them to treat glaucoma. Okay, I think that's what I'm going to say about beta blockers. The alpha blockers, right. So the big things with alpha blockers, remember the alpha one blockers, right.

Like Prasocene, remember Prasocene, you can use it for the nightmares. And a person that has PTSD, right. But those alpha blockers, they have pretty awesome for BPH, right. BPH, right. Although remember, they can cause orthostatic hypotension as a side effect because they are very powerful viso-diiliders, right. But we can use them for BPH. But if you're like, you know what I just want to touch the person's BPH and not your hypertension, you can give Thamso-Losen, right. Remember Thamso-Losen is an alpha one blocker. But he blocks the alpha one AD. Remember AD as an Anthony Davis, right. You know, I'm a big liquor fan, obviously. Right. So he blocks those alpha one AD receptors. You find those mostly in the bladder. You don't really find those in blood vessels, right. So those are kind of like the big things you use alpha one blockers for. Alpha two receptors on MDM exams. You know, there's alpha two blockers. Alpha two blockers, probably the big one you want to remember is Mertazepine. Mertazepine, right. Remember, the alpha two receptor is a G-pertin-copyut receptor. It's an inhibitory G-pertin-copyut receptor, right. So when you activate it, you release less nerve in effron. So if you block it, you release more nerve in effron. That's one of the reasons why Mertazepine is awesome, right. It's an alpha two antagonist. It's used to treat depression, right. Remember, it causes like sedation and it causes weight gain. It actually kind of spurses up your appetite.

So it's probably not about IVF repressing that has like an overexender of osamlia depressed. And then don't forget, right. Alpha two agonist, right. So stuff like clonidine. Clonidine is, you know, it's an alpha two agonist, right. So it cuts down on nerve in effron release, right. So if you make less nerve in effron, that will lower your blood pressure. So, you know, it's pretty good for hypertension, right. But remember, most people don't prescribe it because it causes a rebounder, kind of hypertension. And remember, clonidine is also used on imbi-emixums for opioid withdrawal, right. Because again, if you think about it, this means perfect sense. How do opioids work? Opioids are mu receptor agonists. Mu receptors are inhibitory-g-pertine-copyred receptors. And we tend to find an abundance of them at adrenergic synapses, right. So if an opioid binds to a mu receptor, that actually causes less release of nerve in effron. So guess what? If a person takes clonidine, well, clonidine happens to be an alpha two agonist. And that alpha two receptor is an inhibitory-g-pertine-copyred receptor. So you release less nerve in effron, right. So surprise, surprise. Clonidine pretty much works like an opioid. It just uses a somewhat different receptor to achieve those problems. Right. So when they say opioid withdrawal, power plants, and hospitals, most of them pretty much always involve clonidine.

In fact, in some localities in the US, at least I remember where I went to med school, clonidine is now like a straight drug in that part of the US. But what else do we use clonidine for? Obviously, it's not just for hypertension. Clonidine is used a lot on psych for whatever bizarre reason, right. So remember, it can be used to treat ADHD. It's a third line drug for ADHD. Remember, ADHD, first line, like methylphenidates, dichromphetamine, second line is auto-moxetine, third line, right. Or your alpha two agonists, right. Like clonidine or one facin, right. And they remember clonidine, one facin, those alpha two agonists. You can also use them for Tourette's syndrome, right. You can also use them for Tourette's syndrome. Okay. And they remember your diuretics, right. Remember your lube diuretics, right. Like ferozomide, right. If a chronic acid, remember ferozomide is a sulfur drug. So if a person has like a sulfalurgy, if a chronic acid is a great idea for those people. Big, big, big use of ferozomide, right. It's a water pill, right. Lysix. We use it to treat peripheral edema in a person that has like an frotic syndrome, or a person that has like CHF, right. And remember that lube diuretics, right. They cause hypocalcemia, right. Remember lupes lose calcium, right. So they cause hypocalcemia, but they cause hypercalcyuria, because hypocalcemia, but they cause hypercalcyuria.

So if a person has like a history of like nephrolythiasis, lube diuretics are probably not the smartest I get in the book, right. Because they're basically putting more calcium in their urine. It's almost like, ooh, let's, you've had kidney stone before. Oh, let's give you some more, right. Again, that will not be a pretty thing to do on an MB example. And then don't forget that in contrast, thazideioretics, right. They tend to cause hypercalcymia, but hypocalcyuria, right. Hypercalcymia, but hypocalcyuria, right. So if a person has again, has a kidney, history of nephrolythiasis, thazideioretics are pretty good, right. And again, on MB exams, they may not put HCTZ as the thazideioreticumicidin. They put things like metola zone in that palmite, right. Those are things that people are not used to hearing on exams, right. You want to be aware of those, right. So remember how to look diuretics work. Look diuretics, the inhibits are transported that you find at the thick ascending length of the lube of Henley. The inhibits are sodium potassium, two chloride transporyls. See it again. The sodium potassium, two chloride transporyls that we find at the thick ascending length of the lube of Henley. And then the thazides, they work at the distal convoluted tubule. The inhibits are sodium chloride, same powder, right. The inhibits are sodium chloride, same powder.

Remember between lube diuretics and thazideioretics, thazideioretics actually have a stronger association with hyponic trimmium. Okay. And remember, thinking of lube diuretics, right, is like having butter syndrome. Taking a thazideioretics is like having a ghetto man syndrome, right. It's like having ghetto man syndrome. And then if you go further down in the nephron, right, especially like those, the principal cell, right. Remember the principal cell? That's where you have those potassium sparing diuretics working, right. So we have things like ameloride or triameterine. Remember those are inectional blockers. The inhibits that inectional that brings in sodium in the principal cell, right. Remember primarily those drugs, you know, again, they are potassium sparing diuretics. So obviously they'll have hypercalemia as a side effect. One thing you want to remember those drugs for is if a president has nephrogenic diabetes in sepidus and sociodelic lithium use, you can block those inectional so that lithium cannot get in the tree to mess up the signaling cascade of EDE train. And one thing I guess I suppose I forgot to mention a beta blocker is for a person like overdoses on a beta blocker and they need treatment. You need to actually go ahead and give those people a glucagon. It's the drug of choice to rescue people from beta blocker toxicity, right. To rescue people from beta blocker toxicity. Okay. And the aldosterone blockers, right.

You know, I've kind of talked about them from the context of like how they are used. But don't forget that we can also, those drugs can cause a type 4 RTA basically, right. Because if you're blocking aldosterone receptors, right. It's almost like you're inducing a high point of aldosterone state, right. So those people will have a type 4 RTA. And remember one of the key distinguishing factors on nbm exams. To tell you that you're dealing with an RTA is the anion gap will be normal, right. But to tell you that, ooh, this is a type 4 RTA. Just check that anion gap is normal. And person has hyper-kilemia. I'll tell you that you're likely dealing with some kind of type 4 RTA, right. And then one of the things that is kind of like diuretic related that your friends at the nbm, they love to, you know, kind of hit on his own. They love to hit on the fact that many of these diuretics, right. They love to cause like the auto toxic, right. So like your loop diuretic is a auto toxic, especially if the chronic acid, although remember if the chronic acid is not associated with suffer allergies, right. But your loop diuretic is those that auto toxic, what are the auto toxic drugs on test, right. Cisplatin is auto toxic. Vancomycin is auto toxic. You're a minoglaco side, right. Gentamysin, Tobramysin, all that stuff. Those are auto toxic medications. Those are auto toxic medications. And then amur the already is another nice cardiac drug you want to know about on exams.

Remember you can use it for rhythm control. And a person that has a fib. You can also give it to a person that has a attack. A person that has a attack and is immunodynamically stable deserves a mutorine, right. Deserves a mutorine. And remember we also use a mutorine for many of the ac LS algorithms, especially when a person has like a like V-fib, Postless V, V-fib, right. Postless V-tac were basically I'll say many times you alternate a mutorine with epinephrine for many of these ac LS algorithms, right. I remember amur the run can cause a pulmonary fibrosis. The mechanism of action there is it's a clastroid anteroidmic, it's a potassium channel blocker, right. It's a potassium channel blocker. Remember in terms of the anteroidmic, we have the clastone agents, right. Those are sodium channel blockers, right. So we have things like, I'll say probably like the biggest one to know there is proquinomite. Remember proquinomite is a type 1a anteroidmic. It's a sodium channel blocker. Remember we can use it for WPW. If a person has a fib with WPW, it's a drug of choice there. Don't forget that it can cause drug induced lupus with those antihistone antibodies, right. Clastroantheric mix, those are beta blockers, I've talked about those. Clast 3, those are potassium channel blockers. Big bad boy there is amur the run. I've talked about the mechanism of action. Don't forget that amur the run can cause pulmonary fibrosis, right. So you can cause restrictive lung disease.

Remember that it can cause hypothyroidism, it can cause skin hyperpigmentation, right. And all that stuff, right. And then clast 4, those calcium channel blockers, right. Calcium channel blockers, remember we have the dihydroperidine calcium channel blockers, right. Like I'm low-depean, fellowdepean and all that stuff. The big thing I want to know about those drugs is that those things cause peripheral adema, right. And then for them, and they can also cause constipation, right. Because basically if you're blocking calcium channels, you're relaxing smooth muscle, especially in your GI tract, right. But the non-dihydroperidine calcium channel blockers, like verapimilodotias, those are clast 4 anteroid mix. Remember we can use those for e-fib, right. We can use those for e-flotter, right. Those drugs are also pretty good as well for migraines, right. And then don't forget for pressing has prinsmedal angina. The drug of choice for prinsmedal angina on an ambiume exam is the calcium channel blocker, right. It's a calcium channel blocker. And remember that verapimilodotias specifically can cause hyperprolactinemia. That's just one of those weird bizarre side effects they love to test on exams. And then there's one more thing. Yes. Multi-focally trotachicardia. For a person who has MFAT, right. For a person who has MFAT, remember, those who have like three or more p-wave morphologies, the drug of choice is not a beta blocker.

It's actually a non-dihydroperidine calcium channel blocker, like verapimilodotias. Right. And then don't forget that this specific dihydroperidine calcium channel blocker, Nymodepine, we can actually use that to prevent a post stroke visospasm, right. After a person has like a hemorrhagic stroke, right. So after a person has a subarachnoid, if you want them to not have like a visospasm of their cerebral vessels, give them Nymodepine for that purpose, right. And then don't forget dig, digoxin, the love, love, love, digoxin on Nymodepine exams. Right. How does digoxin work? Digoxin is a sodium potassium ATP blocker, right. And he is a sodium potassium ATP pump. So if that pump does not work, remember that the pump, it's normal job is to take three sodiums out of the cell and bring in two potassiums, right. So if that pump is not working for whatever reason, they're not going to be able to bring potassiums into cells. So guess what? Digoxin causes hyper-kalemia as a side effect. I'll say that again, digoxin causes hyper-kalemia as a side effect. But the thing is for digoxin to work, right. We said, ooh, it inhibits the sodium potassium ATP pump. The thing the juxin does is, to inhibit that pump, it actually binds to the potassium binding side on that pump. So whenever a person is hypokylic, there are more binding sites available on sodium potassium ATP pumps for digoxin. So digoxin can accumulate and cause problems, right.

So whenever you're hypokylic, it makes you more susceptible to digoxin toxicity. But if you take the juxin, you can get hyper-kalemia as a side effect. Make sure you understand that I'll say that again. If you're hypokylic, the more binding spots are available on the sodium potassium ATP pump. For digoxin to bind. So the digoxin can accumulate and a person that's hypokylic, right. So when you're hypokylic, you are more susceptible to digoxin toxicity. When you take the juxin, you can get hyper-kalemia as a side effect. Again, maybe like divine, there's no way they test this on MIM exams. I wish all the best. These are things they classically test because think about it. Who usually takes the juxins, a person that has heart failure, right. Is usually a person that has heart failure that takes a dig, right. So a person that has heart failure that takes dig. So for a person, and what do most people that have heart failure also take at the same time. They take diuretics, they take water pills, right, to help them. Most diuretics cause hypokylic as a side effect, right. So you can imagine or imagine a person that has heart failure, right. That starts having palpitations, prolonged cutie intervals, problems with vision, like yellow vision and all that stuff, right. Abdominal pain, diureal, those things. Those are all signs of digoxicity, right. Those are all signs of digoxicity. And again, remember for a person who has WPW, giving digs is actually a bad idea as well, right.

Digs is a bad idea because digs is also a most caranic receptor agonist. So it actually slows conduction down the EV note. And remember, you can read rescue or present from digs toxicity with those anti-digia, fab fragments. With those anti-dig fab fragments, right. And then I've talked about a denocene, right. Again, we use a denocene for pharmacological stress tests. And then we use a denocene as the second line measure after we've tried V-Gome and over for a superventricular tacky cardio. For a superventricular tacky cardio. Okay. Let's see, well, this is a 40-minute podcast already. Let me just see. I feel like I've hit on many of these high-yield drugs all due. I suspect I may need to make another podcast in the future. This is the new drug I've not really talked about. That is high yield. I mean, I'm sure there are more, but are there more that are high yield that I've not talked about. Come on, divine think. They need big drugs. I feel like I've not hit. I feel like I've kind of hit most of them. Oh, I guess from a cardio perspective, right. Don't forget drugs that can cause diluted cardiomyopathy, right. As side effects, transstusium, right. They can give you a moment being treated for breast cancer or like a dry amicin, right. Like basically your doxodonal rubissin, right. Those things, those anthracyclics, those things can cause diluted cardiomyopathy. Remember myocarditis, right.

Myocarditis from a drug can also ultimately lead to diluted cardiomyopathy like clasapin, right. Closapin is a big-time drug that loves to cause myocarditis, loves to cause myocarditis. Okay, so I think I'm going to go ahead and stop here, but let me share a quick life lesson here. This is actually kind of important, right. So, you know, I check radi-periodically whenever I have the chance. And it's pretty saddening, right. Like, if anyone hears this and knows the person that has this problem or knows the particulars of this person, please check in on them and reach out to them. But there is a person on Reddit. Again, I'm putting this out publicly because this person posted on Reddit is a mess to them that was thinking of pretty much ending his or her life. I don't know the sex of the person, but the person has a girlfriend in Canada. So, please, if you know this person, if you're the girlfriend of this person or whatever, please reach out, reach out, reach out, reach out, please. This person posted already yesterday. He has not, this person has not responded to anyone. So, I guess it's probably a he since he first has a girlfriend in Canada. Again, I don't want to assume sex here, but you kind of get my point, right. So, please reach out to this person. This person has been studying for step one for like a year. Doesn't seem to have been making much of any kind of headwind. So, this person is thinking of a ending it all, right.

So, please, if you know this person, if you're a friend, if you're a colleague, if you're a parent, if you're a met student, please reach out to this person. Reach out to this person. That's like the big public service announcement I want to put out there. Just in case anyone is listening to this. But on that note, I want to talk about mental health, right. So, the thing is, I will say for sure, we definitely need mental health reforms in this country. In the US, especially, I feel like a medical education system really drives many people to the outweigh end from a mental health perspective. And to be honest with you, this is something I may make a podcast on in the future, like how to reform the medical education system in the US. But I just feel like many things. I feel like you can train great doctors. You can train excellent doctors without creating an environment that makes them mentally unstable, right. I'll give you some examples, right. Although, I should maybe kind of think twice before I start speaking here because I don't want to ruffle feathers. But, like, one easy one I can come up with is the way people are greeted in 30 year of med school, right. Med students, if attendants and residents knew the mental anguish, med students go through just to place people to get good evaluations. And the dirty games that many of them have to play to get good events, you'd be surprised. I feel like that is something that can easily be remedied.

I don't know, maybe like making 30 years, also like a pass fail system. That may not be the worst thing in the world. But I feel like that will help a lot from a mental health perspective with students, but also have like some punitive measure you can put in if a student is taken advantage of that kind of system, right. And then on the thing, right, with these US Emily exams, again, I have no problems with the US Emily exams, but again, again, I feel like there are things that can be done to not get people, like just get me to learn super neurotic, get them super depressed. Because basically the way the system is designed now is a score and a test can make our Mario future, which is really unfortunate, right, which is really unfortunate. Or like the pressures and the rigors that all like even pre-mends go through, because I mean I've been on the admissions committee. If you see the problems, primates need to go through like, oh, you need to take this six, seven hour exam or the MCAT to be able to get into med school. I need to do this and this and this and this and this and this. I just feel like people that I'm medicine, they almost never have any respite, right. They're pre-mends. They have to get almost like straight A's, crush the MCAT to get into med school. And then they get into med school, they have to do research into crush all these exams, need to do this, need to do that, right. Study for or limited hours every day to crush the exams, right.

Step one is what and eight hour exam if you include the break time. Step two, nine hour exam, step three, two day exam, right. And then you get into residency and then you have in training exams and then you're being evaluated by attendance. And then you have to take a board exams and then you need to live up to expectations of your colleagues, of your attendance. And people are gossiping about you that all your performance residency. And then this attending to scare you and to almost like shake you down, they use the word professionalism with you. They say, oh, I'm really concerned about your professionalism to freak out med students and all these things or residents just to make them like have like a fire hose on their ass. Again, I'm speaking, I'm saying this. I'm trying to not be angry here, but I'm just saying this. If you're involved in health care, look out for your fellow man. These little things you are doing like shaking down a resident by even if they didn't do something really bad. But let's say you want to get back at them, I want to scare them. I feel like it's like a buzz word that's used in medicine these days. If you want to shake a resident down or scare them, just slide in something. Oh, I am concerned about your professionalism to freak them out. Brethren, that's a bad thing to do. If a person has professionalism problems, don't get me wrong. Yes, you can chase them for that. But you don't always have to use that for every single thing that a person does.

Because that word professionalism concern, it can make a resident or a med student pin their pants. And when you begin to put those kinds of things in their evaluations, you essentially for closing those people's futures. So please, I'm seeing this. And again, I'm seeing this because again, I know I'm just a junior person in medicine. But I'm humbly, I'm begging, I'm appealing. If you're an attendant that's listening to this. If you're a resident that's listening to this. If you're a senior med student that's listening to this. If you're an admissions committee member that's listening to this. If you're involved in health care in any way, if you're a nurse, if you're a physician's assistant, anything. Be merciful. Be merciful. Just remember that medicine by the virtue of the widths constructed in this country puts people at very high risk of mental health problems. So anything you can do to look out for your fellow man, anything you can do to lessen that mental health burden. Do it, right? If for example, you see a student, you see this student is working hard, the students doing their best. And you see that there are no patients coming in in the afternoon or whatever if you're a resident. Send that medicine to their home. You don't need to keep them there, right? Or you don't need to guilt them into like, oh, if you don't stay long, I will give you about evil. No, sickly expectations at the beginning of a rotation like, oh, you know what?

And again, I'm sorry if this podcast is taking a long, but this is an important thing because things like this, where someone has been studying for a step one for a year and yeah, committing suicide, this thing should not happen in medicine. Where people that are supposed to take care of people that have health problems, where people that are supposed to be healers for other people. But then we're essentially eating our own young. That is not becoming of a profession, right? Like literally medicine has one of the highest recid rates of any carrier that you'll find in any part of the world, right? Look at during this COVID thing, right? During this COVID thing, you see med schools. You see that? Oh, they especially have the peak of COVID. We saw med schools trying to get medical students to come in. When most other med schools, AAMC and everything says, you know these people, their rotation should be so spending. You should try to find an online option. Is that med student like super, super again? I know a awful of you fed us on this and I'm seeing it right now. I'm sorry. I'm sorry. But the thing is, is that med student super, super, super vital to the healthcare team, like COVID and ICO whatever? Is that med student really vital at that point? No, no, you can find other activities where they can help, but you don't need to put them through that thing like, oh, okay. Let's say it's a class of 10 people and two people are going in. Eight people are not going in.

And then those eight people begin to worry, oh, although my evaluations look like, what will this look like? Again, all those things are not good. And one other thing I would also see is as a med student try to not compare yourself with other people. In fact, there is a part of the Bible that says comparing themselves with themselves. When you begin to compare yourself with another person, when you begin to try to do what the other person is doing, you are certain yourself are up one for neuroticism. And two, you are putting yourself in a high risk place. You are putting yourself in a high risk place to start getting mental health problems. To start getting anxious and, oh, no, my classmate has much of 30,000 on key cards, but I have not. Oh, my classmate is using all these textbooks, but I have not. No, do work hard, but do what works best for you. You don't have to do what every other person is doing. But again, the message I will throw out here today, please, if you're involved in health care, just check in on your fellow woman or woman. Just check in. Just check in. Like, if for example, you see like a new intern, this new, this intern is facing their first patient death. Right? Touch peace with the person. Sit them down. You know, tell them you know, how about you take the afternoon off? Come, let's debrief on this thing.

Please look out for your fellow man if you see another person struggling because I feel like, unfortunately, in this country, the way health care is set up is, we are trying to outdo each person. I want to be better than this other person. I want to outdo this other person. But I am begging you, I am pleased, please, please, please, please. If you see someone struggling, do what you can to pull them up. Within reason, do what you can to pull them up and med students, if you're having mental health problems, reach out to a confidential health care practitioner. Reach out to someone. If you need to be placed on medication, if you need psychotherapy, again, we really need psychiatrists in this country. Mental health is an epidemic. You're not just in this country, but in health care, in health care. So please, please, please, look out for each other, seek help, reach out to people, and you know, just look out for your fellow man. Look out for every person, if every med student looked out for just one or two other med students. That may decrease the number of suicides that are happening because when I read that post already yesterday, to be honest with you, my heart just dropped. I was like, wow, this is unbelievable, right? And this is not one, it's not two, it's not three. This thing happens almost every week, almost every week. So please, let's look out for each other, but I am really making a call.

I'm challenging med school administrators, hospital administrators, people in charge of health systems. Don't just create like some lecture, oh, watch this lecture on wellness, or do this on wellness. No, no, no, no, no, no, no, no, those things, frankly, don't do squat for a person's wellness. You need to take more tangible action that will help with ensuring wellness, right? I don't even want to get started on these physician health programs. That's like another kind of one that I really don't want to open in this podcast. But those things, many times, they don't accomplish, they don't accomplish the things that they are supposedly set out to do. But I'm not going to, I'm not going to see more thing because I feel like I've probably reaffored a ton of feathers here today. But this is an important topic. This is something we need to discuss. We cannot keep killing our young as healthcare professionals. It does just not the way life is supposed to be. So thank you for listening to this podcast. Again, my apologies that it's really long. But I think this message needs to be put out there. And I also, again, needed to talk about this, this person already that is basically said, yes, they will end their lives. So if you know this person, please reach out. Share this on social media. Please reach out. This is a very, very important thing. So thank you for listening. I'll see you in the next podcast. God bless you and thank you.

Aspirin.

Aspirin (a COX inhibitor).

They inhibit Angiotensin Converting Enzyme (ACE), reducing Angiotensin II levels, which lowers blood pressure and improves cardiac remodeling.

Propranolol.

They tend to cause hypercalcemia and hypocalciuria, which helps prevent calcium deposition in the urinary tract.

Clonidine.

Phosphodiesterase inhibitors (e.g., Citrate/PDE-3 inhibitors).

Warfarin.

Normal anion gap and hyperkalemia.

Nimodipine; it is a dihydropyridine calcium channel blocker.

1) Improving survival, 2) Protecting kidneys (especially in diabetes), and 3) Treating peripheral edema/scleroderma.

Loop diuretics (e.g., Furosemide).

Digoxin; Hypokalemia.

Phosphodiesterase inhibitors (e.g., Citrate/PDE-3 inhibitors).

Warfarin.

Normal anion gap and hyperkalemia.

Nimodipine; it is a dihydropyridine calcium channel blocker.

1) Improving survival, 2) Protecting kidneys (especially in diabetes), and 3) Treating peripheral edema/scleroderma.

Loop diuretics (e.g., Furosemide).

Digoxin; Hypokalemia.