DIP Episode 297 - USMLE Step 2CK Rapid Review Series 52

Okay, okay, welcome. My name is Divine. This is episode 297 of the Divine Intervention Podcasts. And in this podcast, which will be a really short one, I'll be doing the Rapid Review series for the USMLE Step 2 CK exam. And this will be Series 52. We will be discussing a host of vignettes on the USMLE exam. And again, I'll encourage you to kind of keep these in mind. They'll be really helpful to you as you study for your test. And again, basically all the stuff that I have on this website for Step 2 CK, it's pretty applicable to Step 3 as well, to be honest with you. Because really, Step 3 is essentially a Step 2 CK rehash, but with a lot of bio stats, a lot of ethics. And you know, they bring back some stuff from Step 1 with, you know, immunodeficiency diseases and whatnot. And by the way, I have a podcast on how to study for Step 3, right? So first thing, what if they give you a question about a patient, you know, they tell you that he's like a 22 year old guy and he's parents, you know, he's that has diabetes, his mom has hypertension and she has had one stroke. And you know, his BMI is like 24. What if they ask you like, what's your next best step, right? They love to meet these screening questions. And many times for whatever reason, the right thing is to go ahead and screen these people for hyperliplidemia. In fact, it's actually kind of high you to know the hyperliplidemia guidelines, right?

So remember that for hyperliplidemia, you can start screening at the age of 20, pretty much for everybody, right? Pretty much for everybody. And you can screen roughly every five years, right? And remember, you meet decisions based on people's LDL cholesterol, right? Not based on their total cholesterol. It's the LDL cholesterol you meet decisions based on, right? And again, if a person has really, really high LDL cholesterol, just go ahead and put them on a statin, okay? Go ahead and put them on a statin. Although if a person has hyper-tragilistorydemia, what should you be giving to those people? Well, I hope you're saying that, oh, divine, okay, let's give them a fibrate, right? Remember those fibrates like gem fibrosyl, phenofibrate, chlorophybrate, those drugs, right? They are the best that we're using triglycerides, right? And you may be like, oh, divine, how can hyper-tragilistorydemia present on an NB exam? Well, they can present as a person having like epigastric pain, right? And they will tell you that they don't have any, they don't take alcohol, and the person, you know, doesn't have any gold stones or whatever, stuff like that. If you see things like that, you really want to think more along the lines of hyper-tragilistorydemia causing the appendicititis. For those people, they can ask, oh, which of the following interventions will most likely reduce the incidence of these episodes, right? You want to think about giving those people a fibrate.

Again, fibrates are awesome for reducing a person's cholesterol, I mean, triglyceride levels, right? And one nice thing that your friends at the NBME love to do with step 2, CK step 3, is they like to bring some throwbacks again from step 1? In fact, they're bringing a lot of throwbacks from step 1, right? So what's the big thing I think I should mention here? Do you mean as you're like, oh, what's the mechanism by which are starting lowers a person's cholesterol? It's actually, again, you know, they know that most people know that all start-insign inhibitors of HMG query ducties. Great, right? Well, how exactly do start-insign free lower person's cholesterol? Well, the thing that you should be looking for in your exam is the answer that says increase the expression of LDL receptors, right? Or look for the answer that says increase clearance of LDL cholesterol from the circulation, right? By hepatic receptors, right? So why is that? Because if you think about it, the liver has the ability to synthesize its own cholesterol, right? It does that through HMG query ducties. Now, if for some reason you inhibit HMG query ducties, then the liver is not going to be able to synthesize its own cholesterol, right? So the intracellular concentration of LDL cholesterol in the hepatocytes will go down. So the hepatocytes will be like, okay, I can't make. So I guess I might as well go ahead and finagle some cholesterol from the circulation. So you begin to express more LDL receptors.

So you express more of those LDL receptors, you then go ahead and drum or LDL into the hepatocytes. And that will lower the person's LDL cholesterol levels, right? And then one other thing that I want to say that can be on unusual vignette on your exam is they can give you a question about a person that has like some kind of familial hyper-tragilist right? And then they tell you that all those person goes for surgery, you know, he's placed on their anesthesia is getting like an infusion. And then they can tell you that, oh wow, a few minutes or hours after surgery, the patient begins to have a lot of abdominal discomfort, a lot of epigastric pain radiating to the back. If you look at that, if you see a question like that, you want to think about the person having pancreatitis, so you may be like, hmm, define what trigger their pancreatitis, well think about it. If a person has a familial hyper-tragilist right? At baseline, those people's triglycerides are pretty high, right? So one of the most common things that I that I used to induce an anesthesia to kind of knock a person out is proper for. Well, what does proper for contain a ton of, proper for contains a ton of lipid, right? So it's something that you absolutely want to avoid in a person that has a high triglyceride level at baseline or has a familial hyper-tragilist right? I mean, I kind of deal.

To be honest with you, if a mom is speaking, this may have plead out in one of my, in a patient that I saw like back in the day. Actually, I won't say where or when, right? For HIPAA purposes. So just something to keep at the back of your mind, for example, right? So again, that's a very nice way that they can integrate pharmacology, right? With that whole pathology of having familial hyper-tragilist right? And I guess since we're talking about screening, right? If they, if they ever, if they, give you a question ever about a person that smokes and they see which of the following will most likely reduce, you know, in previous person's quality of life, reduce mobility, reduce mortality. If smoking cessation is an answer and they smoke, you should pick smoking cessation as your answer, right? I mean, smoking is the biggest risk factor for so many bad things, right? So many bad things, right? I mean, like one of the best things you can do for your patients is to get them to quit smoking, right? Because smoking increases the presence risk for many, many things, right? It's literally the biggest risk factor for myocardial infarction, right? Is the biggest risk factor for peripheral arterial disease, right? It's the biggest risk factor for renal artery stenosis. I'm telling you this, this may actually be something that shocker to some of you. When a person has renal artery stenosis, the biggest risk factor is smoking, right?

Because remember, people that smoke, they get a lot of essentially an accelerated atherosclerosis, right? Like they get accelerated atherosclerosis, they get M Is, accelerated atherosclerosis, they get PAD, accelerated atherosclerosis, they get renal artery stenosis, right? Smoking is the biggest risk factor for many other things, is the biggest risk factor for pancreatic cancer, biggest risk factor for bladder cancer, biggest risk factor for renal cell carcinoma, right? Is the biggest risk factor for so many things, right? So if you see smoking cessation, as I'll answer, they love to do these with like family medicine, MBME questions or internal medicine, MBME questions or emergency medicine, MBME questions. If you see stuff like that, you always, always, always, always want to go with a smoking, right? As the thing that they should quit, right? In fact, smoking can, it can just cause so many problems, right? So it's just one of those things you want to, you want to avoid in your patients, right? And then what if they give you a question about a patient and they tell you that all this patient comes to the emergency room, has very severe chest pain. And that chest pain is radiating to the jaw, whatever. So you know, obviously they have an MI and then they give you a bunch of labs, and you notice that wow, this person's heart, I mean a bunch of vitals, right? You see this person's blood pressure is low, right? You're like, oh, 60 over 50 or something like that.

And then you also notice that, hmm, this person's heart rate is like 30, right? What kind of MI can be associated with Brady Cardia? When an MBME exam or like an AV block, right? If you see MI's of that nature, you want to think about an RC infart, right? So our right corner, our right infart. Remember, that's associated with elevations, ST elevations in two, three and AVF, right? So maybe like okay, divine. Why does an RC infart cause Brady Cardia? Well, the reason it causes Brady Cardia is very remember, your essay nodal artery, right? The artery that literally supplies your pacemaker, right? Is a branch, is a derivative of the right corner artery, right? So when people have a right corner artery infarction, one of the mechanisms behind them going into cardiogenic shock is that they have a profound Brady Cardia, right? Because if you infarct the essay node, well, yes, some other pacemaker in your heart will take over, right? Because you know, they have the property of automaticity. But those things that take over have a lower intrinsic firing rate compared to your essay node, right? I mean, if, for example, is the ventricle that takes over as the pacemaker of the heart, the ventricle is beta than intrinsic rate of I think about 30 bits per minute, right? You're not going to get be getting much of a cardiac output from that because remember, cardiac output is the product of your heart rate and your stroke volume, right?

So if your heart rate is that down, no matter what your stroke volume is, you're going to be in big trouble, right? Person is not going to have much of any cardiac output, right? So that can cause Brady Cardia. But remember, there are many other things that can cause IV block, right? I mean, like there are certain drugs that can cause IV block, right? So say, for example, if a person is taking a beta blocker, right? Or a person is taking like a non-dihydroperidine calcium channel blocker, like verapamele or delta-ism, right? Those things can absolutely cause cause Brady Cardia. Even the joxin, right? Many people, the joxin is a positive hyinotropa. But the thing is, the joxin is also like a most chronic receptor agonist, right? So it actually has the ability to slow a person's heart rate down, right? That's why the joxin is something I want to think twice about using in a person that has an IV block, right? And that also explains why the joxin could be used in treating a fib, right? Because again, it literally by being a most chronic receptor agonist, slow-sconduction down the IV node, right? So again, many, many things that can cause Brady Cardia on IV, in exams. Also, Brady Cardia is associated with a person being hypothyroid, right? Brady Cardia is a relatively specific finding on IV, in me. So even if they are not all the way Brady Cardic, well your heart rate will be like pretty low. It's not going to be like 90-something if they have hypothyroidism, right?

Because remember, maybe like, okay, why might that be the case? Well, remember that when a person has high levels of thyroid hormone, right? So let's look at maybe the opposite case. Sometimes, some things in life, the best way to understand them is just to look at the opposite. When you look at the opposite, you're probably like going to be pretty, pretty good in terms of understanding what goes on with your other circumstance, right? So, if for example, a person has, remember, thyroid hormone, right? One of its jobs is that it increases the placement, right? Remember, it's a, you know, it's a steroid hormone, so it works through the, you know, like these response elements on DNA, right? So you basically put more, you put more beta-1 receptors, steroid hormone, one of the things it does is it puts more beta-1 receptors on the person's cardiac myocytes, right? So if you put more beta-1 receptors, you'll be more responsive to cardiac coulomines, like Narepinephrine, for example, right? And so your heart rate and your cardiac output and your contractivity will go up. So if you think about it, if you have like less thyroid hormone, right? It will then make sense that you should probably have less beta-1 receptors on the surfaces of cardiac myocytes. And if that happens, then you're going to be less responsive to cardiac coulomines, right? And if that happens, you're going to be pretty cardiac, right? So that's why people that are hypothyroid tend to be pretty cardiac, right?

Again, if you want to become a thyroid expert, and again, like, let's just say like, you really shouldn't be taking in here, similarly, exam if you're not a thyroid expert, right? You're going to land in a lot of hot water, because guess what? Your friends at the MBM, they love love love love love thyroid questions. In fact, they made a whole podcast just for the thyroid. That's a episode 251. You really should listen to that if you have a chance. Now, what if they give you a question about a person that, you know, has really bad headaches, prevents them from going to work? We have it like nine times a month, right? And they have like high blood pressure. What kind of drug should you consider giving those people? I really hope you're telling me that you want to give those people a bit of blocker, right? So this person obviously has chronic migraines, right? Remember when a person has the thing that puts you in the category of, oh, you have chronic migraines, right? Is if you have it or more episodes, right? So if you have it episodes among that included, right? So it or more episodes every month, right? That's what throws you into chronic migraine theory tree. For those people, you need to put them on some kind of drug, right? That can be some kind of, you know, migraine prophylaxis, right? So if you see a person though, the MBME, they love this, kill two birds with one stone philosophy, right?

So they will give you this question where a person has like multiple comorbidities and you're trying to get you to pick, you know, they'll give you many drug answers that can fix the same problem, right? But then they'll be one drug answer that can fix multiple problems at once, right? Whenever you see stuff like that, always go with that, right? So like, remember that perpranolol, right? Brita blockers, you have actually pretty good as migraine prophylaxis. So it actually makes sense if a person has migraines, right? And we have like hypertension, given a bit of blocker is not a terrible idea in those people, right? Given a bit of blocker is not a terrible idea in those people. Now one thing that your friends at the MBME though could do with beta blockers is they could give you like arrow questions. Again, for those of you taking step two against step three, don't think that those arrow questions just, you know, magically disappear because you're done with step one. Again, if anything, and again, you don't even have to believe me, you can look at it or you can look it up online. The MBME has started bringing a big focus of, you know, bringing back some step one material, right? So what is one classic thing that you can do with beta blockers on exams?

They can ask you like, oh, after a person gets a beta blocker, you know, they can give you arrow questions to see if you can figure out what happens to their levels of reigning and your tensing one and your tensing two stuff like that. Well, beta blockers will bring those things down pretty much, right? Because remember, one of the things that happens, I mean, beta blockers, right? Especially like a drug that's like a beta one blocker or a beta one and beta two blocker, they're a beta one receptor is at the GG cells, the juxtaglimarial cells of the afferent arterial. So if you smash those, if you smash those, if you block those are beta one receptors, you're not going to be making much of any random, right? So your reigning is going to go down. If your reigning goes down, your angiotensin one and two will go down, your dose will go down as a result of that, right? So just something high you to keep in mind. And with those migraine medications, I guess, since I'm kind of talking about it now, please do not forget, Topiramites is another drug that you can use as migraine profile access. But that Topiramite, remember that it's associated with nephrolithiasis. So they can give you a question about a patient was recently studied on some medication for migraine profile access and then they present with like hematuria, flank pain going down to the groin, right? Or in a woman, it will be flanked being going down to the labia, right?

If you see stuff like that, you know, think about nephrolithiasis with, with a Topiramite, right? Think about nephrolithiasis with Topiramite. And also remember for migraine profile access, you can also use a tricyclic and tady present, right? So if a, for example, a present has migraines and they have like a histone like neuropathic pain, right? Or they have a history of depression, right? Giving those people a tricyclic and tady present may not be the worst thing in the world. Although you also want to make sure that you're thinking about those tricyclic side effects, right? Remember, those things have anti-harm side effects, right? So they have anti-hitone effects so they can cause sedation, they can cause, they have anti-alpha one effects as well, right? So if they block off of one receptor, they can cause orthostatic hypotension, right? Because by blocking off one receptor, you'll cut down on the person's systemic vascular resistance and that can obviously cause problems, right? With blood pressure. And then they also have anti-muskaryneic effects, right? So if, for example, a person has, I don't know, like people can get delirious from those, they can get an anti-cholinergic toxic drone, and they also cardiotoxic, right? Because remember these TCA's, they have the ability to block sodium channels, right? So if that's one of the reasons why to rescue a person from TCE toxicity, give him a sodium, giving them a sodium channel blocker is not the worst idea in the world.

I mean, sorry, giving them sodium by carbonate, whoops, giving them sodium by carbonate is not the worst idea in the world, right? Because by giving a high amount of exogenous sodium, you can, you can basically like overcome that blockade that's already happening through those sodium channels, right? So remember, typically when a person has TCA cardiotoxicity, you'll have like a white carousel and an ekeg. For those people, the thing you really should be doing is going ahead and giving them sodium by carbon. Now what if a person has a hypertension and you have BPH, right? Obviously, you want to give them an alpha-1 blocker, right? Something like Prasosin or something of that sort, right? Don't pick the answer that says times elocin. Times elocin is an alpha-1 blocker, but it only works in the bladder, right? You block those alpha-1 AD, you know, AD-like Anthony Davis, right? Alpha-1 AD receptors are in the bladder, right? So if you, if you really want to help your blood pressure, you need to give them like a legit block every kind of alpha-1 receptor, right? Again, something like Prasosin, Doxazosin, Terazocin, right? It's not like that. Because again, the alpha-1 blocker by doing that, you open up the internal urinary sphincter in the bladder so their urine will flow better, but you also block those alpha-1 receptors, right? That will cause a decreasing systemic vascular resistance at lower their blood pressure.

Although one thing your friends at the Mbimilov to do is they can then ask, oh, what, you know, they can tell you that all this person just started an alpha-1 blocker and then they start having politicians. If you see that, you want to think about our reflex-tacky cardio, right? Because you really think about it, right? Like when you give an alpha-1 blocker, you crush the Prasin systemic vascular resistance. When you crush the systemic vascular resistance, right? That's going to cause their virus-eptus, right? Currently, cardiac sinus, theotic arch, they'll be like, whoa, okay, blood pressure, low, blood pressure, low. So they will signal, I believe, the nucleosolitarius in the brinstem, and that nucleosolitarius will cause you to release a ton of, you know, it will cause you to have like a sympathetic discharge, right? To raise your heart rate and your stroke volume. So they have a reflex-tacky cardio. So the thing is, if you actually want to blunt the reflex-tacky cardio, associated with taking some kind of viso-di-liter. So they can even make this question with not just an alpha-1 blocker, they can do it like a dihydroperidine calcium channel blocker, like a low-depean, fellow-depean, or even a drug like hydrolyzing, for example, right? Which is an atyrolovizodialidure, right? So if you see that, you can actually give a bit of blocker together, right? Because the bit of blocker will blunt that sympathetic response so that they don't have that reflex-tacky cardio, okay?

Now, I'm going to be wrapping up here soon. So what if a person has like diabetes and hypertension? This is easy, right? You want to give them an isinhibitor and ARP, right? Remember, isinhibitors and AR Ps, they are renal protective, right? So if you have a disease that predisposes you to having like renal problems, right? And you have hypertension, then you should really should be on some kind of isinhibitor in ARB, or if you even see a person that has hypertension and they are beginning to, you know, have like, arising their creatinine, and they say their creatinine is like 1.5 for those people, right? Even again, a diabetic, you really want to put those people on some kind of isinhibitor, or if you see a person that has hypertension, and they have a history of, again, like autosomal dominant polycystic kidney disease, right? Again, those people dig pharmacists in their kidneys, right? For those people, you want to put them on an isinhibitor, an isinhibitor is the drug of choice for hypertension, in that patient population, right? For presciense hypertension, and they have a history of like some kind of nephrodic on a phytixendrom, again, an isinhibitor is the drug of choice. I hope you're getting the point, right? Like, the thing is, these are extremely exams and not just about memorizing, memorizing, memorizing.

The key detail here is, if you have something that tortures kidneys, and you have high blood pressure, doesn't matter what the thing touching your, touching your kidneys is, go ahead and give that person an isinhibitor and ARB. You know, the big exception to that would be like, if those people have like hair detranger, a demon, you would don't want to do an isinhibitor, that'd be a bad idea. If you have like bilateral rhinolitis, don't know this. You also don't want to give an isinhibitor, right? That'd be a bad idea as well. And then, for presciense, he's sort of nephrodisiases and hypertension, right? Remember, you want to give a thiazide, right? You want to give a thiazide. Remember, thiazides, they are the razor-persistent blood calcium, but they actually crush the amount of calcium in the presciense urine, right? So they actually are very good for presciense, like nephrodisiases. And then, gout and hypertension, right? Like, you want to give it like a drug like a little sartan. A little sartan is actually your euricosteric drug, so it makes you don't put on of a urine cassette in your urine, right? So, it's actually good for hypertension, and people that have a history of gout. Okay, so I think I'm going to go ahead and stop here, as I do at the end of every podcast. I do offer one or one tutoring for many exams, right?

Step one, step two, CK, step three, preclinical medical exams, third year shelf exams, and if you're a medicine resident, actually tutor to the medicine boards, or you know, the medicine training exam, and then if you need application advice in, again, you see we're in a tricky cycle, see all the horror stories that happened like two weeks ago, something like that, right? So, if you need help in those areas, just script me an email, and I can give you some more information on pricing and things of that nature. And then I also offer courses, right? Right now I'm offering the step two CK course, and the MBA Me Testicking Strategies course. Again, I'll offer, I have another offer in the month of April, I will release some information on that, hopefully maybe sometime this evening, or maybe sometime tomorrow. So, you know, thank you for listening, and please subscribe to the website, divininterventionpodcasts.com. If you subscribe on the website, then whenever I make a new podcast, you'll get an email notification. And again, I also have these podcasts on Apple podcasts, Google podcasts, Spotify. So, you know, feel free to subscribe to those, and you get, you know, when you'll be able to listen to it on an app, although remember those podcast apps, they have like this most recent 150 podcast limit thing, right? Although it's also sort of kind of Word Press rule that I don't really have much control over sadly. So, in those circumstances, you'd have to go to the website.

All the podcasts will always be on the website. And then also for the videos I make, check out my You Tube channel, divinintervention, USMELY podcast and videos. And I just want to share short life lesson today. So, what's my short life lesson? My short life lesson is to be content, right? Be content. The thing is, I think I feel like we're living a world where we always want more, right? We always want the best of the best. We always want more, right? The thing is, if you're not content, then you will never truly be happy. I mean, like I feel like many people they attach their happiness and life to how much money they have or how prestigious the residency program they go to is or if they are using like all the famous resources to study for an exam. The thing is many times, I mean, like there's this part of my, you know, my Bible study recently that I read that, you know, Godliness with contentment is great gain, right? The thing is, many people, they draw their, like they draw their draw from things that are just change all the time, right? If something changes all the time, why do you want to be drawing your draw from that? Because if that thing changes, they won't get joy anymore. You'll not have to go for that next big thing, that next big thing, right? I mean, like for example, with med students, you see some med, this is actually the root cause of many, a lot of med students stress.

You see them, they come into a med school, they've done some reading online or whatever, they're like, you know what? I'm going to, you know, my first two years of med school, I'm going to study for a state, make my own flashcards, you know, maybe do like two, two pages a day, you know, not put myself on any kind of stress. Commit for a state to memory, make sure I understand if I don't understand something or look it up on Wikipedia, maybe do like a Q-bank five questions a day. But then they start med school and then they see someone using some famous Anki deck or they see someone using some video blah blah blah blah blah resource, right? And then they're like, hmm, instead of going to be content because the original plan was sold, it was smart from the get go, but no, that's that's not good enough, right? They want the next big thing, they want the next new fun gold item, right? So they go, they get it and then they find another friend, right? They think, oh, they'll get satisfaction when they start this new thing, but then they find another friend that always using this resource that is used by the best students at Hopkins and Harvard, and then the pff, the pivots to that, right? And then they notice that, wow, two years of the a mess will pass by and they've not settled on one thing, right? They always want to keep seeking that best, that best, that best. Let me tell you this folks, be content, the grass is not always greener on the other side.

Sometimes just stick with what you have, do it well and be grateful for it, right? Be grateful for it. So, you know, you should go on, you should, I'm not saying that you should not aspire to do better big things with your life, but only do those things when they make sense, right? There's some things you have now that do the job just fine, they do an amazing job, right? You don't always have to keep seeking for that shiny new blah, blah, blah, blah, blah, right? Because again, that concept of always wanting more, those people never get satisfied, right? They never get satisfied. I mean, even though there's a part of the book of Proverbs that says that there's it's better to have a little with the fear of the Lord than a great fist with a lot of strife, right? Because you see some people just buy that more, more, more, more that they want. They've essentially pierced themselves with many sorrows. There's a part of the Bible that says that, oh, you know, many in the quest for more, I think it's in like second Timothy chapter six or chapter seven, right? Many than in the quest for more, they've just pierced themselves with many sorrows, right? So, stop making your life sorrowful, right? Draw your joy and happiness from things that actually count, things that actually matter. I mean, like for me, you know, you, again, just from listening to the podcast, you won't see in the website, divineinterventionpodcast.com.

You can tell that, you know, I'm probably a person of faith, right? I draw a lot of happiness and fulfillment from my faith, right? Not necessarily from, oh, having gone to a prestigious medical school or whatever. Now, those things at the end of the day, those things, those things fade away, right? Those things fade away. Even if you had like the awesome SUSMLS scores, right? Those things fade away. I mean, think about it. Let's say you're a resident listening to this. Do you really care much about your USMLS tip two CK or step one scores now that you're like three, four years into residency? Probably not, right? Or your MCAT scores that were 99% out back in the day. Do you really care? No, you probably don't even remember what those scores were, right? So again, just be content, be content, and draw your excitement, your love, your joy from things that have more permanence. So thank you for listening to this podcast. I will see you next time. God bless you. Thank you.

Age 20 years old, for nearly everyone.

LDL cholesterol (Low-Density Lipoprotein), not total cholesterol.

Fibrates (e.g., gemfibrozil, fenofibrate).

They increase the expression of LDL receptors on hepatocytes, enhancing clearance of LDL from circulation.

Propofol (or other high-lipid agents).

Smoking cessation.

Right Coronary Artery (RCA) infarction/MI.

ACE Inhibitors or AR Bs, as they are the preferred agents due to renal protective effects.

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

Nephrolithiasis (kidney stones).

Hypothyroidism leads to decreased expression/responsiveness of Beta-1 receptors on cardiac myocytes, making them less responsive to catecholamines.

For gout + HTN, use an ARB or CCB (like losartan) because they are uricosuric; for general nephrodisdisease, thiazides may be used.

Sodium Bicarbonate, to overcome sodium channel blockade.

ACE Inhibitors or AR Bs, as they are the preferred agents due to renal protective effects.

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

Nephrolithiasis (kidney stones).

Hypothyroidism leads to decreased expression/responsiveness of Beta-1 receptors on cardiac myocytes, making them less responsive to catecholamines.

For gout + HTN, use an ARB or CCB (like losartan) because they are uricosuric; for general nephrodisdisease, thiazides may be used.

Sodium Bicarbonate, to overcome sodium channel blockade.