Cram The Pance - S1E20 Hypertension Medications

Episode Date: April 15, 2021

Hypertension medications review for your Pance, Panre and Eor’s.►Paypal Donation Link: https://bit.ly/3dxmTqlAffiliate links to support the podcast (Thank you!):1) Amazon Prime Student Membership- 6 month free trialhttps://amzn.to/3yMmH0i2) Audible Plus- Free Trial and 2 free Audiobookshttps://amzn.to/2SG3mNP3) Pance Prep Pearls V3https://amzn.to/3uxMUfC4) Paramount + Sign Uphttps://amzn.to/2R2EaAu--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so today we're going to be doing hypertensive medications. Now, I already went over on hypertension. I did a whole podcast on that, but this is just going to focus just on the farm side of the hypertensive medication. So we'll really dive a little bit deeper into that, but again, only focusing on the high yield things you need to know for your boards. Now, again, I always want to thank you guys for the comments, the reviews, everything. Thank you so much.

It makes my day when I see those. And if you haven't checked out the YouTube channel yet, please do. It's under cram the pants on YouTube. I think if you like the podcast, you'll definitely like the YouTube channel. I have a lot more visuals and things like that. So let's get started for hypertensive medications. There's really six classes you should be familiar with. It's going to be your ACE inhibitors, your angiotensin receptor blockers,

Guitensor 2 receptor blockers, your calcium channel blockers, beta blockers, and alpha-1 blockers. And then finally, your diuretics. Of those six classes, really should be familiar with the ACEs, the ARBs, calcium channel blocks, and your diuretics for hypertension, because those are the four. classes that are used as your first-line monotherapy for an uncomplicated hypertensive patient. So let's work our way through the classes. We'll focus, again, just on the high-yield stuff that you really need to know. Let's start with your ACE inhibitors. So ACE inhibitors are angiotensin converting enzyme inhibitors. These medications in this class all end in PRIL. So

catapril, analapril, enalapril, and Lacinapril are the ones in this class. Again, all ending in PRIL. The way they work, the mechanism of action, is that these medications inhibit the conversion of angiotensin 1 to angiotensin 2. They do this by inhibiting ACE. And what ACE does, Ace does a couple things. Ace both creates angiotensin 2. So it helps angiotensin 1 turn it to angiotensin 2. And then it also breaks down radokin, which I'll go over in a minute,

is going to be important for your adverse drug reactions. Now, what is the function of angiotensin 2? Why does it matter that we stop the conversion? of angiotensin 1 to angiotensin 2. Well, the primary function of angiotensin 2 is vasoconstriction. So if you don't allow angiotensin 2 to ever be made, you don't allow this vasol construction to occur. So this leads to vasodilation.

And because of this vasodilation, you have an increase in both your preload and your afterload. And that's really as much as you need to know. So the basic thing, again, mechanism of action for your ACE inhibitors is going to be, you inhibit ACE. This stops angiotensin 1. to turning into angiotensin 2. And by doing this, you allow, you decrease the vaso, the vaso constriction that angiotensin

2 would have allowed to happen. And now you're vasodilating, which is going to decrease both, a decrease in both your preload and your afterload. Now, indications, I'm going to go over for all of these. Obviously, I'll go over the hypertensive uses, but I'm also going to go over some of the other uses as well, because you should be familiar with these, even though it's a hypertensive medication one. So ACE inhibitors are going to be first.

line meds for hypertension. It's one of the four classes of the initial monotherapy that you'll use. Congestive heart failure, as well as patients with the previous MI, really big. These are going to be some of your first line meds. They decrease ventricular remodeling and things like that. And then, of course, absolutely have to know this. This is going to be your first line hypertensive medication in patients with diabetes and chronic kidney disease or nephropathy. So you have to know that one. So again, indications, hypertension, hypertension, first-line med, especially in your diabetic patients or patients patients with chronic kidney disease, and then congestive heart failure as well, as well as a previous MI. So really focus on that diabetic patient because that's what really seems to come up the most

with your ACE inhibitors. And in real life, you need to know that even in non-hypertensive, you're still going to use ACE inhibitors because of the effect of the progression, decrease the progression of diabetic nephropathy. All right, now your adverse drug reaction for ACE inhibitors, there's really five things I think you should know that are going to come up that you really need to know. So those five things, the first one is really your most important. That's hypercalemia. So you can have an increased potassium level in patients with ACE inhibitors. It's really big and you'll actually see it a lot in clinical practice. So you always want to look out for that. So hypercalemia. These patients can also have a cough, which is another common side effect from ACE inhibitors.

angioidema is another possibility. Now, the cough and angioidema, remember I talked about bradykine before and why this was important, the cough and angioidema are both related to bradycinine. Now, we stopped ACE from, we inhibited ACE's action. Now, Ace again, remember what we talked about before, Ace helped both angiotensin one become angiotensin, too, but it also had a function of breaking down bradycinine. So we're inhibiting ACE, so it can no longer, inhibit bradycinin or break down bradycinin. So because of that, we have this increased bradyquinine in the body. And bradychinine is a peptide that promotes inflammation through vasodilation.

So the cough, the angioidema are all because of this increased bradycinine. So just remember that. And then the last thing that you should know, or actually two more things that you need to know, is that ACE inhibitors can also cause hyperuricemia. So increase uric acid, gout, and then first dose hypotension. So they can cause orthostatic hypotension, normally within the first 90 minutes of the first dose, or any time you're increasing the dose, you may see this as well. So again, the five adverse drug reactions you should know, hypercalemia, cough, angioidema,

hyperurisemia, and first dose hypotension. They also do carry a black box warning for fetal toxicity, so you cannot use these impregnant women. Do not. So completely contraindicated an impregnant woman. Okay. So the, um, the arduous drug reactions are really important. I think you do need to know them. And you also need to know the indications for this drug. So what I came up with was you need to remember a guy named Chad. So there's a guy named Chad and he takes ACE inhibitors. Now, Chad takes ACE inhibitors because

they control hypertension and diabetes. But Chad doesn't like taking ACE inhibitors because they give him a cough, hypercalemia, hyperuricemia, angioidemia, angioidema and dose one hypotension. So Chad takes ACE inhibitors because, remember we're doing the letters here, control that they control hypertension and diabetes. That's Chad, C-H-A-D. But Chad doesn't like taking ACE inhibitors because they cause a cough. That's your C-N-Chad. They cause hypercalemia and hyper-Easemia.

That's your H in Chad. They cause angioadema, the A. And then dose one hypotension. That's Chad. Those are all of your adverse drug reactions. So remember, Chad takes ACE inhibitors. and you can remember both your adverse drug reactions and your indications, hypertension, diabetes.

Okay, so that's ACE inhibitors. We're going to go over something very similar, like the cousin of ACE inhibitors, and that's your angiotensin-2 receptor blockers. Now, angiotensin-2 receptor blockers are all going to end in Sartan, Sartan, Sartan, Sartan. So that's L-Sartan, Erbis Sartin, Kand-Sartin, VAL-Sartin. The one you'll see the most commonly used is going to be L-Sarton. But remember, you know, anything ending in Sarton is an ARB or angiotensin 2 receptor blocker. So the way these work is instead of inhibiting ACE and thereby stopping the

conversion of angiotensin 1 and angiotensin 2 like in ACE inhibitors, angiotensin 2's instead, they're receptor blockers. So like the name states, they simply block angiotensin 2 receptors, which blocks the action of angiotensin 2, which as we discussed in ACE inhibitors is mainly vasoconstriction. So it doesn't allow that to take place. So that leads to an increased blood pressure. obviously with vaso constriction. So again, same result in ACE inhibitors. You're going to stop the effect of the angiotensin 2. So you're not going to have the vaso constriction. Instead, you'll have vasodilation, which will decrease your preload and your afterload. So ACEs just stop angiotensin 2 from ever being made while ARBs allow it to be made but block its receptor so it can't work. And it's basically

two different ways of doing the same thing, but the same end result. But this is the key. The key difference in ARBs versus ace inhibitors, since ARBs don't inhibit or interfere with ACE, they don't stop ACE's breakdown of bradykine like in ACE inhibitors. So they don't inhibit ACE, so ACE can still be made and ACE can still do its job of breaking down bradycine. So what do you think happens in ARBs? Well, with ARBs, you're not going to have that cough and you're not going to have the angioidema either. Now, the thing of angioidema is kind of controversial for a while. they were saying, well, it doesn't produce the cough, but it can still produce the angiodema. Well, that's kind of gone by the wayside.

And most studies now are proving that ARBs do not produce angiodema like an ACE inhibitors, and they do not produce the cough. So really the main indication for ARBs are just going to be somebody who had a cough or angioidema related to the ACE inhibitors. And you can use an ARB as an alternative to produce the same effect. So a lot of things are really the same with angiotensin2 receptor blockers. the indications are pretty much the same. First line for hypertension. It can be used in heart failure. And again, remember, your diabetic patients, patients with chronic kidney disease, is going to be first line.

Now, the adverse drug reactions, there's a couple different things. Hypercalemia share in common with ACE inhibitors. This also carries the risk for hypercalemia. But remember, you're not going to have your cough. You're not going to have your angioedema. Now, hyperurisemia, it's a little different, and you're probably not going to be asked this because some literature states that ARBs don't really affect uric acid. Some say they can cause an increase. One thing that that's definitely certain that you should know is that LOSARTAN of all the ARBs, of all the angiotensin-2 receptor blockers, actually has been found to decrease uric acid.

So, lo sartin, remember that low sartin, I guess you could remember low, as in low sartin, low uric acid. That's the only one they found that actually decreases uric acid. So that's important to remember because they may ask you that. Now, it's also contraindicated in pregnancy for the same reason as ACE inhibitors. And that's really all you need to know about ARBs. For the most part, they're pretty similar to ACEs. Just remember, they don't have the cough.

They don't have the angioedema. But everything else is pretty similar in their indications and otherwise. Okay, so let's move on to our thyside diuretics. Our thyside diuretide like diuretics, hydrochlorathyde is going to be pretty much the most popular one. you'll always hear patients taking it. A lot of times it's used in combination with an ACE. Chorthalodone is another one. That one has a really long duration of action of all the thyside diuretics.

Ndapamide, metolazone is another one. But again, with the thysides, you're mainly going to hear about hydrochor thyside or HCTZ. Now, the mechanism of action, your thyside diuretics are going to prevent sodium and water reabsorption at the distal convoluted tubule. So they're going to prevent the reabsorption of water and sodium. at the distal convoluted tubule, which is going to decrease preload and essentially reduce blood pressure by just really decreasing the overall blood volume. So it's like a mild volume depletion.

And remember, anytime a patient is volume depleted, they become hypotension because of the low overall circulating volume of blood in the body. So that's basically what these are doing. They're kicking out all the sodium in the water. So you have this mild volume depletion and it decreases your preload, which decreases your blood pressure. So again, just remember they prevent sodium and water reabsorption at the distal convalued. convoluted tubule. Now, they, because of the ionic imbalance they cause because of the sodium loss and the distal convoluted tubule, the body tries to regain its equal erium. And you'll see a number of electrolyte abnormalities, which we'll go over in a minute once we get to the ADRs. As far as indications,

these are first-line monotherapy for hypertension. Remember, thysides, calcium channel blockers, aces, and arms are your first-line monotherapy in a non-complicated hypertensive patient. So first-line monotherapy. And then peripheral edema is another indication that you'll see for your thyside diuretics. Loop diuretirics are more commonly used, but hydrochlor thyside and some of the other thysides can be used as well. Now your adverse drug reactions, you're going to have some electrolyte abnormalities because of the changes that we saw with the mechanism of action.

Most of the changes, most of the electrolyte abnormalities are going to be an increase, like hyperglycemia, hyperuracemia, we'll go over those in a minute. There's only two that are going to decrease. And one of them is obvious. Remember, we said that it prevents sodium reabsorption. So hyponatremia is obviously a possibility. It's obviously preventing the kidney from reabsorbing sodium at the distalconvalututubule. So that one is common sense.

You can remember that. The other one is hypokalemia. It's aldostero-mediated action by the sodium potassium pump. I'm not going to go into it because it's not important for you to know. But just remember, the only two electrolytes that are going to decrease, hyponatremia and hypokalemia. Those are the going to need two that will decrease in thineineatrilema. Now, the four that are going to increase are going to be your glucose, your lipids, your calcium, and your uric acid.

So you may have hyperurisemia, hyperglycemia. Normally, it's a mild increase, but still can be careful in your diabetic patients. Hyperlipidemia, again, mild increase in cholesterol levels. And then hypercalcemia. So because we're exchanging calcium for sodium at the luminal membrane, we're actually decreasing the amount of calcium excreted in the urine. but putting more back into the blood. So less is going out in the urine, more is coming back into the blood.

And because of this, it actually makes thiozydes useful in patients with renal stones because there's less calcium in the urine. So less chance for renal stones. And then it's also useful because less in the urine, more in the blood, it's actually useful for patients with osteoporosis. So those are some indications. So remember four things that are going up, hyperurisemia, hyperglycemia, hyperlicemia, hyperlipedemia, and hypercalcemia.

So remember the only two that are going to be down are good potassium and sodium. And the way that I remember, at least the four ones that go up. So you just have to remember the two that are going to be decreased are going to be your sodium and your potassium. But the way I remember the four that are elevated is I remember glucose. Now, glucose is also elevated in thiozydes. Glucose also elevated in thiozides. Now, what is the word glucose stand for?

What are the letters in glucose stand for? So the first four, so glucose obviously spelled G-L-U-C-O-S-E. So the G stands for glucose, remember, hyperglycemia. The L stands for lipids, hyperlipidemia. The U-S-S-A-Uric acid, hyperurisemia. And then the C stands for calcium, hyper-calcemia. So that's the G-L-U-C. What is the O-S-E stand for in glucose?

That stands for O-So-E-E-Lovated. So glucose, lipids, uric acid, calcium, O-so-elevated. Remember the word glucose. You can remember the four things that are elevated, glucose, lipids, uric acid, calcium, oh, so elevated. So that's how you remember all the things that are elevated. You just have to remember potassium and sodium are down. Okay.

So let's move on to our potassium sparing diuretics. That's going to be triamterine, spirnalactone, amelioride, and eplurinone. So these are diuretics that increased diurecise without the loss of potassium. So remember in your thysides, we lost potassium. You can have potentially hypokalemia. But as this name states, these are potassium sparing diuretics. Now, the way they work is it depends on which medication we're talking about. So if we're speaking on triamterine and amelioride, these actually work by directly blocking the epithelio sodium channel and the cortical collecting duck.

And because of this, it leads to less sodium being reabsorbed and more being flushed out of the body. So you're getting sodium out of the body along with water. and it also leads to a decrease in potassium being excreted, so more retained. So more potassium being retained and more sodium being pushed out along with water, which again helps with your blood pressure. And that's how that works if we're talking about triumptorine and amelioride. Now, if we are speaking about spyrnalactone and apleranone, these work differently. We're going to be differently, and they're actually aldosterone antagonists.

So they decrease the effect of aldosterone. And if you're familiar with aldosterone, remember its principal effect is to balance sodium and potassium in the body. The more aldosterone released, the more the sodium the body retains and the more potassium the body loses. So as you can imagine, a drug like spyrinalactone or a pleranone that are aldosterone antagonists, which decreased the effect of aldosterone, would do the opposite. So they're going to increase sodium excretion, so loss of sodium in the body, and increase potassium retention. So increase potassium in the body.

So remember, again, these are going to be spirinalactone and epleranone. They're going to be aldosterone antagonists. So they're going to increase the sodium kicked out of the body and retain more of the potassium. So that's how those two drugs work. So they work differently. Now, as far as your adverse drug reactions, again, all of them are going to potentially cause hyperkillemia, which makes sense you're retaining potassium. So it's possible you retain too much.

And you can have an increased potassium hypercalemia. Now, spyrnalactone. mostly spiroinolactone, but also a plerinone to a lesser extent, due to their anti-androgen effects can actually cause gynochomasty, and that's a huge one. They always ask about spyrinal lactone and gynochomastia for some reason. It's a really popular question, but they can also lead to decreased libido, erectile dysfunction. So remember, those are only going to be in the spironal and the pleranone, more so with the the spyrinal lactone.

But overall, they can also, they can all produce hypercalemia. Now, as far as indications, they can be used in hypertension, but they're not first line, and they're generally pretty weak diuretics. They don't work that well. So they're normally combined with either a loop or a thyside to minimize potassium loss, but they're normally not used as monotherapy. So you'll normally see them combined with either most commonly a loop or even potentially a thyside because combining those, you'll minimize the potassium loss.

Now, as far as indications when we're talking about spyrinalactone and pleranone, These actually have some other uses because of their androgen effects. And these are one of the few drugs, the spirnal lactone and a pleranone, using heart failure that can actually improve mortality. So remember those two heart failure medications that can improve mortality. And spyrinal lactone is, it's really widely used in versatile. It can be using a lot of different things. It's used in PCOS for its anti-endrogenic effects.

It can be used in cirrhosis-related ascites, even in acne. because, again, because of the anti-endrogenic effects. So it has a lot of different uses. So remember that as well, some of the different drugs that you can use for different things in addition to the hypertension. Okay, so let's move on to loop diuretics. Loop diuretics, out of all the diuretic classes, loops are going to be your most potent. They work the best of the strongest, especially in patients with edema, peripheral edema,

they can pull fluid pretty dramatically out of the body. And patients who have like heart failure and things like that, you want to get all the fluid out of the lungs in the body. Loop diuretics are your way to go. Now, furosomide, also known as Lasix, is the most commonly used of the loops. It's the one you'll hear about the most. But there's also torsomide in this class and Bumetanide that you'll hear about as well. The way they work, the mechanism of action.

So within the nephron of the kidney, you have the loop of Henley. And coming off of the loop of Henley, you have this thick ascending limb. And within this ascending limb coming off of the loop of Henley, there's a co-transporter. And the job of this co-transporter is to reabsorbe and transport sodium, magnesium, calcium, potassium, and chloride back into the blood. So what loop diuretics do is they just shut down this co-transporter. And due to the sodium sting in the loop of Henley, this shifts the overall tonicity in the general area. And this leads to water instead of being reabsorped, getting flushed out. So you have this dilute urine and you flush out all this fluid, which can lead, which can help in edema.

and help in hypertensive patients to decrease the blood pressure. So simplified loop diuretics are inhibiting the sodium potassium chloride co-transporter of the thick ascending limb of the loop of Henley. This leads to dilute urine and fluid being pulled down to the body rather than reabsorbed. So that's a real simple way to kind of talk about what loop diuretics do. Now, as far as their indications, they can be used for hypertension. They're not going to be first line, but they do have hypertensive properties. But really, we're going to see these being used as for edema.

So to help decrease pulmonary your peripheral edema due to congestive heart failure, that's really the most common use of these medications. And you'll really see LASICs being used a lot for that, for that pulmonary peripheral edema to pull the fluid out of the body. You also can actually use these to treat patients with hypercalcemia. Remember, when we shut down the co-transporter, one of the electrolytes we stopped from being reabsorbed was calcium. So it's going to decrease the amount of calcium in the blood,

but it'll increase the urinary calcium. So you actually want to be careful in a patient's with kidney stones. But if a patient does have hypercalcemia, this is a medication that can be used for a patient with hypercalcemia. So you can remember that as well as another use for this class of medication. Now, as far as the adverse drug reactions, they're all going to be really related outside of a couple ones. I'll go over to the inhibition of the absorption of all the, all the, electrolytes that we spoke about. So all of the things that we stopped at the co-transporter, we can lead to hypokulemia, hypokalemia, hypokalemia, hyperchloremia, hypomagnosemia, and hyponatremia.

The only two things that you'll see go up in the body are going to be hyperglycemia and hyperurisemia, so gout. So everything else is going down. The only two that are going up, and I'll tell you wait or remember that in a minute, are going to be hyperglycemia and hyperurisemia, so gout potential. one of the ones you need to remember, the electrolyte's not so important, but you need to remember that loop diuretics can cause autotoxicity. So remember, these patients can have temporary hearing loss, especially if these meds are given intravenously and infused too fast. Autotoxicity is huge, and you're going to be asked that. So remember, loop diuretics can cause autotoxicity. Another thing, too, that I'll talk about, it's actually controversial, but sulfa allergies. So a lot of literature is actually

retracting this statement, but there's a potential, not definitive cross-reactivity between loop diuretics, as well as some of the thysides and patients who have sulfa allergies. It's possible, but as time goes on, more studies are showing that this may not be true, but you may be asked it. And if you are, for now, I would say, just to remember that loop diuretics, there is some cross-reactivity in patients with sulfa allergies. So remember again for your adverse drug reactions, autotoxicity, sulfa allergy, question mark and then a decrease in your five electrolytes, sodium, potassium, magnesium, chloride, and

calcium. The only molecules that are going up are the ones starting with a G. So if it starts with a G, think of G growing or gaining. That's going to be glucose and gout, so aka hyperuriscemia. So the only two that are going up in loop diuretics are the ones starting with a G. They're gaining or growing, and that's going to be glucose, hyperglycemia and gout, hyperurisemia. So remember that because everything else goes down. Just remember VCAG hyperglycemia or gout hyperuracemia.

It's going up, growing, or gaining. So that's how you remember that. Really, of all of those, I would say, just remember the autotoxicity. That's really important. One last note for loop diuretics in case you get a question on this because I remember I did. So if you see a question, it says you want to use a loop diuretic, why the patient has a history of gout or they have a sulfa allergy, which loop diuretic would you use. Now, ethocrinic acid is a loop diuretic, and it's safe to use in both these circumstances.

It's not commonly used, but like I said, I remember getting a question. So just be aware. Ethocrinic acid is a loop diuretic that is safe to use in a patient with the history of gout or sofa allergy. And again, I didn't list in the medications as we went over then because it's so rarely used, but because they like to ask these kind of, you know, rare questions like these sometimes just remember ethically acid if they have a history of gout or sofa allergies. Okay, moving on to calcium channel blockers. So the common calcium channel blockers you'll see are nicartapine, amloadapine,

varapamil, nipetapine, diltiasm. Those are some of the common calcium channel blockers you'll see. So you'll notice there's no common ending in the meds like prill and aces or sartan and arbs, but I still have a way for you to remember them. And I never forgot this. I hope this this works for you. It definitely worked for me. But the way that I remember the calcium channel blocker,

since they don't have a similar ending, is that I remember the three endings that they do have. So the three endings that they do have is pine, like an M-Lodotapine, or you could say P-N, but I say pine because it helps the mnemonic. So M-Lodotapine, P-I-L, and then Zem like in Verapa-M-I-L, and then Zem, like in Diltaya-Zem. So you have pine, P-I-N-E, M-I-L, and then Zem, like in Deltiazem. You have to think of a guy with an accent saying this.

But if you remember the sentence, cut down Zem Pines and put them in the sawmill, cut down Zem, Z-E-M-P-I-N-E-S, and put them in the sawmill, M-I-L. So you think about somebody cutting down like pines, like pine trees and putting them in a sawmill. So cut down Zem, Zem, like that's where your accent comes from instead of saying them.

So cut down Zem, like in Diltai Zem, pines, like in Lodotapine, and put them in a sarm. saw mill like in verapamil. So remember that sentence. You'll remember that's your endings in all your calcium channel blockers. Cut down zem pines and put them in the sawmill. Okay.

So hopefully that helps you. But it really did help me and I never forgot that. Now, the mechanism of action, there's two different subclasses in calcium channel blockers. And it depends on what subclass we're talking about. So the two different types, there's going to be dihydropyridines and non-dhydropuridines. And but the dihydropyrodines are mainly very very very. vasodilators, I'm sorry. So dihydropyridines like nipedipine amylopine are mainly vasodilators.

They have little to no effect on the cardiac contractility, and they don't alter conduction through the AV node. So they have no effect on heart rate. They really just vasodilate. That's their main effect. And they do this by binding to and blocking calcium channels in smooth muscle cells of the vessels. So no calcium enters the cell means no muscle contraction. So dilates of the smooth muscle of the vessel rather than constriction.

So vasodilation, that's going to be your dihydropyrodines. They're basically just vasodilators. Now, your non-dihydropyrodin, which are really just verapamillin dilatism, those are really the only non-diropyriene's you'll see talked about, rapamylidylidylidylidylidylidylidem. I'll tell you how you remember that in a minute. Their main function is to slow heart rate conduction through the avino. They also have effect on cardiac contractility,

which the dihydropyridines do not. They have an effect on vasodilation as well. But the key to the non-dihydropyrienes is the fact that they affect both cardiac contractility and cardiac conduction. So non-dihydropyrienes, and that's why you'll see some of these subclasses being used in arrhythmias like aphib, atrial flutter, because they can change the contriteity and the conduction of the AV node. The way I remember them, again, really the only two you'll hear about is dilettysm and varapamil.

I remember deltisem of varapum will start with the d and a v. D and a V stands for decreased velocity because you're decreasing the velocity of the heart, slowing the heart rate. So dv, deltizum, varapumil, decreased velocity of the heart. Now, the indications, these are first-line monotherapy for hypertension for the non-complicated hypertensive patient, along with your aces, your arbs, and your thiozydes,

first-line monotherapy for hypertension. They can also be used in arrhythmias, your non-dihydro-puridines, of course, like AFib, Atrial Flutter. Verapamil in particular can actually be used for migraine prophylaxis. They can also be used in esophageal spasms like your jackhammer esophagus, Raynaz phenomenon as well. So those are some of the things that you'll see as well.

Okay, as far as the adverse drug reactions, there's really, there's a few, but there's two that you need to remember. These are going to be the ones you'll be most commonly asked about. And these are also the two that you're going to. to see in real life in clinicals when you're seeing patients. So peripheral edema is a big one. And then constipation is another really big one. Those are the two that you have to remember.

Those are the adverse drug reactions that are very common that you may see on the question or in real life. So peripheral edema, constipation. And the constipation is actually all related to the same reason that it helps with blood pressure is the same reason it causes constipation because that smooth muscle relaxation. It also affects the smooth muscle of the bowel, which can lead to constipation. You also may, these patients also may experience dizziness and then headaches, which is kind

of weird because we said it works for migraine prophylaxis, but it can actually temporarily cause a headache too because of the vasodilation. Now, contraindications, if a patient's taking a beta blocker, you don't want to give them a calcium channel blocker as well. They're both decreasing the cardiac contractiline in conduction, and you have an increased risk of bradycardia and AV block. So patient taking a beta blocker, contraindicated to give them a calcium channel blocker. And then also in patients with congestive heart failure with left-fentricular dysfunction,

the non-dihydropiridines are contraindicated. They have a negative inotropic effect on the heart, meaning they weaken the force of the contraction, which obviously is not a good thing for a patient who already has weakened contraction. So non-dihydropyrodin's contraindicated in a patient with left-ventricular dysfunction, heart failure. And finally, patients with any history of sick sinus syndrome, Sick SIC-K sinus syndrome, severe bradycardia, heart block, particularly second and third-degree heart blocks, all conditions that can be exacerbated due to the effect of the non-dihydropyridines, again, the effect that they have on avino conduction, Sloan conduction, and these can all be exacerbated with those non-dihydropyridine calcium channel blockers.

So again, left ventricular dysfunction heart failure, you know, we use your non-dihydropyrodines, patients also taking beta blockers, and then patients. with any history of those heart, second and third degree heart blocks, severe bradycardia, or six sinus syndrome, avoid the non-dhydrupyrodion. So that's your calcium channel blockers. We're almost done. We just have a couple more classes left. So beta blockers, with beta blockers, you have three different types.

You have your cardio selective, your non-selective, and then you have your non-selective plus your alpha blockers. Now, let's start with your cardio-selective. So the cardio-selective is only going to affect the, the beta 1 receptors in the heart. So these are the patients, these are the class, the subclass of beta blockers that you're going to use in patients that have a history of COPD or asthma, other pulmonary conditions, because they only affect the beta 1 receptor, which is in the heart.

They don't affect the beta 2 receptors, which are in the lungs. So these are the ones that you can use in patients with pulmonary conditions, because if you use a non-selective that can affect the beta 2 of the lungs, this can lead to bronco constriction and exacerbation of their pulmonary disorder. So again, remember, cardio selective are going to be the ones that are mainly only affecting the beta-1 receptors in the heart, cardioselective. Now, what are the most common cardioselective beta blockers you need to know? How do you remember them?

So it's going to be bisoprolol, esmal, etymol, and metoprolol. Those are the four most common ones that you need to know that you'll see most commonly, again, bisoprolol, esmol, atenol, and metoprolol. And those first letters of those words spell beam. So, mesopalalosoth with a B, Esmalal with an E, tenelal with an A, metapalal with an M. So that spells beam. So when I see that, I think of a beam of light. And a beam of light is like very targeted, direct, it's very selective, it only affects one small area.

So you think beam, beam of light, very targeted, direct, cardio-selective. These are all your cardio-selective medications. That's how I remember those ones. Now, your non-selective beta blockers, these aren't used as commonly anymore. They're your first-generation beta blockers. So they affect not only beta-1, but beta-2 as well. So beta-1, the way you can remember it is beta-1, you only have one heart. So that's where your beta-1 receptors are.

Beta-2, you have two lungs. So two lungs means your beta-2 receptors. Now, when I say this, you know, technically beta-1 is also found in the kidneys. Beta-2 can be found in the uterus, the liver. But we're going over hypertension now. And we're going over beta blockers. So let's focus on the main things for those. So non-selective are going to affect both beta 1 and beta 2.

So both the heart and the lungs, meaning you want to avoid these in patients with pulmonary disorders. And like I said, they're not used as often. But there is one that you really need to know because this is the one that's most commonly used. And that's propranolol. It has a lot of different uses. It can actually be used in migraine prophylaxis, essential tremors, hyperthyroidism to treat with some of the symptoms. Natalol is another one that's used primarily for its anti-arhythmic properties. And then timelol is another one you may see.

This also comes and drops the timulol, but mainly focus on your propranolol. That's the one you're going to see most commonly, the one that you'll see most commonly use because it does have so many different indications. And then finally the last subclass, there's one known as the non-selective plus alpha blockers. So this one is going to be Labatal Law and Carveta Law. they not only affect the beta 1 and beta 2 receptors, but they also affect the alpha receptors as well. So you can think of these as extremely non-selective. They could care less which receptor they affect.

That's how I remember them too, because Carvetylol and Labelol, C and L care less. They could care less what receptor they affect. They'll affect beta 1, beta 2, even your alpha receptors. They could care less. So Carvatalol, Labelol care less. Now, the mechanism of action of all of these is the way they work is actually by blocking the action of endogenous catacolamines like epinephrine or epinephrine. And if you remember, the catacolamines, they have a number of actions in the body. But catacolamines, when they're released, they can increase your heart rate, they can increase your blood pressure,

and they can relax or vasodilate the bronchules, which makes it easier to breathe during a period of stress or exertion. So if you block these receptors with beta blockers, you're going to have the eye. opposite effect. So you're going to decrease your heart rate, you're going to decrease your blood pressure, you're going to vaso-constrict the pulmonary bronchials, which is why those non-selectives we don't use in pulmonary conditions. So that's how they work. It's mainly by blocking the action of endogenous catacolamines. Now indications, they do work for hypertension. You can use them for hypertension, but they are not first-line medications. They're only going to be used in patients who have pre-existing systolic heart failure, coronary artery disease. So these patients with those

comorbidities, you're not just going to have a patient walk in, you give them a beta blocker who have no other comorbidities. It's really only used if they have pre-existing systolic heart failure or coronary artery disease. And now, they also have some other uses as well besides the hypertension. They can be used, like I said, migraine prophylaxis, essential tremors, U-Coronary syndrome, and even some arrhythmia, these bed blockers can be used for as well. As far as your adverse drug reactions, they're mainly related to the catacolamine inhibition.

So a big one that you really need to know. And the reason why we try to avoid these in diabetic patients is because they can actually mask the symptoms of hypoglycemia. So one of the main symptoms of hypoglycemia when the blood sugar goes low is an increased heart rate. And beta blockers are going to prevent this, as well as blocking some of the noradrenergic or sympathetic system response that normally takes place in a diabetic patient once their blood sugar goes low. So they're going to be shaky, anxious.

They're not going to feel any of these things. They're not going to feel that increased heart rate, which is the main thing. They're not going to feel shaky or anxious. It's going to blunt all of those responses. So you want to be careful in prescribing beta blockers for diabetic patients. Now there's a few other ones you'll hear talked about. One is depression. And again, I like to give you the most up-to-date data.

but I also want you to be cautious because this is still potentially something they can be tested on. But depression is one that they've always listed for beta blockers. But new research is actually saying that this is not entirely true. You should probably know it for your boards. But in a few years, this may not longer be listed as a potential adverse drug reaction. But they have said that beta blockers can cause depression. Again, that's being questioned now. A couple of other ones that are less than they previously thought,

but still can be increased in beta blocker use. is fatigue and impotence, like sexual dysfunction, as well with beta blockers. So those are a few of the ones that you should know. I always like to put that side note about the most up-to-date info. So you're educated as well on it. Now, as far as your contradictions, just like in your non-dihadro period and calcium channel blockers, cannot use these in second and third-degree heart block. They're contradicted due to the depression of the AV, no conduction, which can lead to, of course,

serious perit arrhythmias. And while these drugs are great men's for patients with heart-filled, which are their first line along with ACE inhibitors, as soon as these patients have decompensated heart failure, so an acute episode of worsening heart failure with dyspnea, pulmonary edema, you actually want to stop your beta blockers. So when they have a decompensated heart failure, you stop the beta blockers because they can potentially worsen the acute heart failure due to the negative inotropic effects during acute heart failure. So you can't risk having the contractility of the heart decrease. So you stop the beta blockers when they have an acute attack of. of heart failure.

And then, of course, your non-selective beta blockers like propranolol should, of course, be avoided in patients with pulmonary disorders like COPD and asthma to avoid those potential exacerbations we talked about before. Okay, so the last one is going to be your alpha-1 blockers. It's going to be brief because these are not very commonly used. They're not first line. They're really only used with a patient who has coexisting BPH, so benign prosthetic hyperplasia. So only patients who have BPH.

These meds all end in zocin, so prazosin, doxazosin, terrazocin, these are going to be all the meds, you'll see in alpha-1 blockers. So the alpha-1 receptors that they're blocking, when activated, are mainly responsible for vaso-constriction of smooth muscle. So like those in the vessels, smooth muscle of the prostate, so if you block these alpha-1 receptors like the zocin meds do, this leads to the opposite effects. So you have vasodilation of the smooth muscles, of the vessels, decreased blood pressure, and relaxation of the smooth muscle of the prostate,

which decreases the obstruction and the pressure on the urethra, which leads to symptomatic relief in patients with BPH. Now, the adverse drug reaction is the big one you need to know is going to be first dose syncope or first dose, first dose hypotension. That's why it's actually recommended to give these patients, this medication at bedtime, particularly with the first dose, so you avoid this potentially having.

They take the first dose, they go to sleep, so it doesn't matter if they have orthostatic hypotension. They're sleeping. they're laying down. So it's not an issue. But that's the big one first dose syncope or first dose hypotension. You can also have dizziness headache. It's even possible to have nasal congestion due to the vasal dilation of the nasal mucosa. Now indications, really all you need to know is hypertensive patient with coexisting BPA. That's it. That's all you really need to know. It's really the only time you'll use this hypertensive agent is if a patient has a coexisting BPA because it can

treat both. You're never going to use this as a, uh, that's all you're going to use this as a, initial monotherapy. Now some caution. You really want to try to avoid these in elderly patients due to the hypotension, the synchopy that I just discussed. And then caution in patients who have cataract surgery. There's something known as floppy iris syndrome. And again, due to these meds that's effect on smooth muscle and vasodilation, it can cause a loss of the smooth muscle tone of the iris. And during surgery, the iris can actually prolapse and potentially tear a rip. So it's contraindicated before surgery of the eye. You can have something known as floppy iris syndrome.

Now, I always bring up these weird things like that because I remember being asked them. So I don't waste your time with that unless there was a reason. And it's because I do remember being asked that for some odd reason. Okay. So that's it for the hypertensive medications. That was very long, but there's a good amount of material there. So let's do five quick questions and then we'll wrap it up. So first question, which medication class should be used caution?

in a diabetic patient due to potentially masking the symptoms of hypoglycemia. Which medication class should be cautiously used diabetic patients due to potentially making the symptoms of masking the symptoms of hypoglycemia? That's beta blockers. Which medication class would be best to use in a patient with both hypertension and BPH? Medication class would be used in a patient with both hypertension and BPH. It's going to be your alpha blockers, your zosins, your tersosein, etc. describe the main difference between dihydropyrodines and non-dihydroperidine calcium channel blockers.

Main difference between dihydropyridine and non-dihydroperidin calcium channel blockers, it's going to be that non-dihydropyrodin's affect cardiac contractility and conduction while dihydropyrodines do not. And remember your non-dihydropiridines, decrease velocity, dilatizum, varapamil. Question four. What are the five main adverse drug reactions of ACE inhibitors? Five main adverse drug reactions of ACE inhibitors. Remember, Chad, it's going to be cough, hypercalemia and hyperuricemia, angioedema, and dose 1 hypotension. Okay, last question.

Bisoprolol, Esmalol, Attenol, and Metoprolol are what subclass of beta blockers and what receptors do they block? So, Bisopalal, Esmal, Attenal, and Metoprololol, remember your beam of light. Those are going to be your cardio-selective. They only affect beta 1. So beam of light, esopalal, esmol, tinaol, metopalalal. Okay, so that is your hypertensive medications. I hope that was helpful. As always, thank you so much for listening to the podcast.

If you're enjoying it, please leave me a review a like. Check out the YouTube channel as well. Thank you so much. And good luck on your pants, your panery, and your EORs, and good luck in PA school.