Transcription
Another day, another hematology video. In the previous videos, we have talked about bradykinin, hereditary angioedema, as well as acquired angioedema. Today, we'll talk about ACE inhibitors, the famous antihypertensive medication, and good for congestive heart failure. By inhibiting the angiotensin-converting enzyme, it causes dry cough, angioedema, hyperkalemia, and may cause kidney problems. So when you inhibit the ACE, good things happen, such as controlling your blood pressure, and bad things happen, such as cough and angioedema hyperkalemia.
Now let's get started. [Music]
Angiotensin-converting enzyme: let's talk about the enzyme before we inhibit it. Renin comes from the kidney, which converts angiotensinogen from the liver into angiotensin I. It's coming from the lung as well as the endothelium, converts angiotensin I into angiotensin II, which acts on its receptor—no kidding—which will lead to vasoconstriction of arterioles, raising the blood pressure, aldosterone release, reabsorbing sodium, secreting potassium and secreting hydrogen ions, increased thirst and ADH—this is very important—and increased sodium-potassium exchange at the proximal tubule. Okay. Now, the same angiotensin-converting enzyme is responsible for preventing the formation of bradykinin. And even if bradykinin is there, let's decorate it into an inactive metabolite. Cool. Angiotensin II will cause sodium reabsorption, hypokalemia, and alkalosis. What do you think ACE inhibitors will do? ACE inhibitors will treat the hypertension, absolutely, increase natriuresis, increase natural diuresis, okay, and cause hyperkalemia as well as acidosis.
Indications of ACE inhibitors: when should we use them? For hypertension—oh yeah, big time—CHF (congestive heart failure), myocardial infarction, and diabetic kidney disease, also known as diabetic nephropathy. It can also be used to decrease water intake in patients suffering from psychogenic polydipsia or schizophrenia. Why is that? Because remember, angiotensin II used to increase thirst sensation. So when you use an ACE inhibitor, there is no angiotensin II, so you decrease the thirst sensation. Brilliant, isn't it?
First things first: high-molecular-weight kininogen is converted into bradykinin. Things to collect written bradykinin will do all of this crazy, bad stuff, but there's an enzyme here called ACE (angiotensin-converting enzyme). Please don't produce bradykinin. Even if you did, I'm going to decorate it into an active ugly useless metabolite. So ACE takes bradykinin to the cleaners; that's why we call ACE a kininase. Thank you, ACE; you truly ace. So when you use ACE inhibitors, bradykinin is left free; it's uninhibited, it's undecorated.
Side effects of ACE inhibitors: first, let's talk about ACE. ACE takes bradykinin to the cleaners, cool. When you use an ACE inhibitor, bradykinin is left free; it's not taken to the cleaner. In fact, it's dominant; it's live and kicking, baby, and will lead to dry cough and angioedema, hypotension, etc. The same ACE enzyme used to convert angiotensin I into angiotensin II. Now you're using ACE inhibitors; there is no vasoconstriction, there is no hypertension; in fact, there is hypotension. That's why ACE inhibitors are antihypertensive medications. There is no increased GFR; that's why they could cause some kidney problems, at least in the beginning. And we have no increase in sodium reabsorption, leading to net renal loss of sodium; in theorem, increase potassium reabsorption, leading to hyperkalemia; and increase hydrogen ion reabsorption, leading to metabolic acidosis. So here are the adverse effects of ACE inhibitors: dry cough, angioedema, hypotension, and renal impairment, net renal acidosis, hyperkalemia, and N/V/D (nausea, vomiting, diarrhea). Because come on, it's pharmacology.
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Contraindications of ACE inhibitors: okay, hereditary angioedema, big time. Watch my previous video because when you use ACE inhibitors, you have lots of bradykinin, and people with hereditary angioedema already have lots of bradykinin. Don't add fuel to the fire. Complication: if there is a previous ACE inhibitor-associated angioedema, if you gave a patient ACE inhibitors, they develop angioedema, please don't repeat your mistake twice; you'll look like an idiot, and the patient could die. Pregnancy: ACE inhibitors are teratogenic; they are pregnancy category D; they can lead to congenital malformation of the CVS and CNS. LR3 because some ACE inhibitors contain sulfur, so sulfur drug allergy of the patients leads to sulfa. Don't use some of them.
Examples: okay, ACE inhibitors are drugs that I like because all of them end in "-pril," which is nice. We have three groups: the sulfhydryl group, which contains captopril; the dicarboxylate group, which contains enalapril, ramipril, lisinopril, quinapril; and the phosphate group, which contains fosinopril.
Some pro tips for the pros: ACE inhibitors are excellent, and I mean excellent, for treatment of kidney disease in cases of scleroderma, now we call systemic sclerosis. They are excellent to the point of being miraculous, and I'm not kidding; they are really good for nephrosis due to systemic sclerosis. If you're a patient with diabetes and hypertension, try ACE inhibitors; it's your first drug of choice because it treats hypertension, and it's good for diabetic nephropathy. I mean, two birds with one stone; it's a dream.
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