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Angiotensin Receptor Blockers (ARBs) - Hypertension Treatment - Cardiac Pharmacology

Medicosis Perfectionalis5:26

Transcription

In the previous video, I've talked about ACE inhibitors, the angiotensin-converting enzyme inhibitors. Today, we'll talk about angiotensin II receptor blockers, also known as ARBs. They are a famous antihypertensive medication that are good because they don't cause dry cough, and they don't cause angioedema. With that being said, now let's get started. [Music]

Ren comes from the kidney, converts angiotensinogen from the liver into angiotensin I. ACE comes from the lung, converts angiotensin I to angiotensin II. Angiotensin II has two receptors, angiotensin II receptor one and II receptor two. AT1 and AT2 are receptors for angiotensin II. Just because it says AT1, it doesn't mean angiotensin I; no, it means that number one receptor for angiotensin II. Please, please don't forget that. And angiotensin II does all of this crazy, bad stuff. Also, ACE inhibits bradykinin degradation; even if it's formed, it's going to degrade into inactive, ugly, useless metabolites.

Okay, now ACE inhibitors used to inhibit this enzyme. They used to increase bradykinin, causing dry cough and angioedema. Now, where are the angiotensin II receptor blockers, which is today's video—the famous ARBs? They are angiotensin II receptor blockers. Do they block AT1 or AT2? They block AT1 of the angiotensin II. Again, AT1 of the angiotensin II. Okay. If normally angiotensin II will lead to hypertension and increase sodium reabsorption, hypokalemia, and alkalosis, what do you think angiotensin receptor blockers will do? I'll tell you: they will treat hypertension; they will increase natural races, which will treat hypertension as well; and they will cause hyperkalemia and acidosis.

When should you use angiotensin II receptor blockers? Hypertension, CHF, diabetic nephropathy, and vascular disease such as atherosclerosis, atherosclerotic aortic aneurysm, and Marfan syndrome. We have talked about high molecular weight kininogen leading to bradykinin causing all of this stuff. Is this involved in angiotensin receptor blockers? Case: no, it's not. So let's forget about that. High molecular weight kininogen will be converted into bradykinin. When you use ACE inhibitors, you'll have lots of bradykinin causing cough and angioedema. But when you're using angiotensin receptor blockers, forget about this; it's not going to happen. Alright, you don't have an increased risk of dry cough or angioedema. Doesn't mean like zero percent of cases; of course, there are some cases, but it's not as relevant or as prevalent as using ACE inhibitors. Do you think bradykinin is going to be specifically relevant when you use angiotensin receptor blockers? No.

Side effects of ACE inhibitors, as we have discussed in the previous video, we have dry cough, hypotension, and angioedema; renal impairment; natural races; acidosis; and hyperkalemia. They have dry cough; they have angioedema. Fast forward to angiotensin receptor blockers: they will not touch the ACE, so bradykinin is normal; it's not increased; you're not going to have dry cough or angioedema. However, you're still going to treat your hypertension; it still can damage your kidney; and you will have other symptoms such as natural races, hyperkalemia, metabolic acidosis, and please add orthostatic hypotension as well as dizziness.

So, side effects of ARBs: we have hypotension, renal impairment, natural races, acidosis, hyperkalemia, orthostatic hypotension, dizziness, rash, dyspepsia, abnormal liver function tests, and insomnia. You can make me happy and make grandma happy by getting my 50 hematology cases. You can get them by going to patreon.com/medicalcases. These cases are awesome; I mean, come on, guys.

Examples of angiotensin II receptor blockers: they block the AT1 of angiotensin II. They include anything that ends in "-sartan": valsartan, irbesartan, candesartan, eprosartan, olmesartan, azilsartan, and tell me who named these things.

So, in brief, ARBs, angiotensin II receptor blockers, block the AT1 receptor of angiotensin II—AT1 of angiotensin II. They do not inhibit ACE; therefore, they do not inhibit bradykinin breakdown; therefore, there is no dry cough, or no—I don't mean no, I mean like very little and very unlikely. Thank you guys for watching. Subscribe, follow me on Facebook and Instagram. You can get all of my notes and all of my cases by going to patreon.com/metakosis, and I'll send you my bloody Dropbox links. Thank you for watching. As always, be safe, stay happy, and study hard. This is mini-coasters perfection. Yellow swear medicine makes perfect sense.