Renin-Angiotensin-Aldosterone-System (RAAS) – Pharmacology | Lecturio

now you have this really cool diagram in your notes so i want you to take a look at it it shows you where all the players of the raas what organs they come from what comes from the liver what comes from from the injection of glarular cells what comes from the lungs what happens in the capillaries and what happens it's really neat so i want you to pause the video for a second just take a look at it orient yourself to that picture and then restart the video when you're ready now let's break the raas down very simply okay some reason your body senses wow we need to raise the blood pressure maybe it senses a drop in the blood pressure maybe it senses um a low sodium whenever that alarm bell goes off the junctional glomerular cells in the kidneys now you may not be proud of me for saying that but that word scares me to death every time i have to say it juxtapolarial cells so i'm pretty impressed that i got it out but renin is excreted from these j cells in the kidney because why the body sensed a need to raise blood pressure so that's why renin that's squirted out through your kidneys now renin connects up with circulating angiotensinogen when you're looking at your downloadable section where does angiotensinogen come from what liver-colored organ does angiotensinogen come from when renin and the circulating angiotensinogen meet up you end up with a different product angiotensin one okay so i went from renin to circulating angiotensinogen well why did the renin appear because my body sense i needed to raise my blood pressure so renin connected to the circulating angiotensinogen i end up with angiotensin one now when angiotensin one meets ace or angiotensin converting enzyme you end up with [Music] angiotensin ii this is another bad mamma jamma this causes potent vasoconstriction and volume expansion so the raas is a system one of the five key players that my body uses to maintain blood pressure the renin can you remember the reason that renin appears why does the body put that out why do those j cells in the kidney put out renin renin connects with angiotensinogen then you end up with angiotensin one angiotensin one hits ace angiotensin converting enzyme pretty cool name right and you end up with angiotensin ii the end result of angiotensin ii my blood pressure is raised two ways with a potent vasoconstriction and volume expansion so what does that mean that reminds me of that little girl in willy wonka remember when she said i want it now she was the blueberry girl and she that volume blew right up so that's why i'll use that to remind you so look at the breakdown on the bottom of your screen why are we going over this over and over again because that's a great study tip for you repetition really helps your brain remember things it likes to see things that it's familiar so renin plus angiotensinogen equals angiotensin one then angiotensin one connects with ace and you end up with angiotensin ii now there's two ways the release of angiotensin ii raises your blood pressure can you remember the two ways and you don't have to do the sound effects but remember the two ways that angiotensin ii raises your blood pressure okay so we're not done with this we're going to keep going over and over this concept because this is the key to understanding multiple high blood pressure medications okay just understanding how the raas works will make it so much easier for you to understand these types of medications so the two reasons that your blood pressure elevates because of the end product of raas vaso angiotensin ii are volume expansion and vasoconstriction now you know the sound effects that go with that right vasoconstriction and volume expansion now the volume expansion comes from aldosterone the adrenal gland releases aldosterone now why would i say it like that because most normal people don't say aldosterone one it's pretty annoying and two it's something you didn't expect and will help it stick in your brain better so while you don't have to agree with the way things i do things anything you can do while you're studying that makes something stick in your mind then you'll say aldosterone i remember that i can be in the mall and i'll meet somebody who i had 10 years ago in pharmacology and they'll say hey brought flaws aldosterone and i think yes so anything that's weird or unexpected that helps you remember information go with it you might not want to say it in public but it'll definitely work in your studying so when the adrenal gland releases aldosterone that means the body hangs on to sodium those kidneys will hang on to sodium and you know the rule wherever sodium goes water follows so volume expansion comes from the release of aldosterone that means the body hangs onto sodium and wherever sodium goes water follows now the vasoconstriction that comes from angiotensin ii it is a very very potent vasoconstrictor like four to eight times as active as norepinephrine norepinephrine is a drug that we use usually in the critical care setting for someone who is desperately life-threateningly low blood pressure so this angiotensin ii which my own body is capable of making with the raas is four to eight times as potent as norepinephrine it's really impressive that's why i told you it is a bad mammogram so the raas the end products of that end up with volume expansion and vasoconstriction now without looking at the screen what i want you to do is to think through this diagram see if you can look in the margin of your notes and re-key recreate this diagram without looking at the notes okay now let's pretend that we have unlimited resources and finances and you and i are going to solve the problem of treating hypertension now if we look at this process like a flow chart so let's say this is how the ras works right we've got renin angiotensinogen angiotensin one ace and angiotensin ii okay so what kind of drugs could i design based on these steps how could i interrupt these steps or interfere with these steps and so i don't make it all the way down to the action of angiotensin ii now there is a point i want to point out angiotensin ii we know it is a really intense concept right it's really amazing what it can do in the body but it doesn't really do anything unless angiotensin ii has available angiotensin ii receptors so before i get that all that reaction that we get you want to make sure that the angiotensin ii can actually make it to an angiotensin ii receptor now that was a really big clue if we were in an escape room together that would have been a really big clue but let's walk through it because um what would happen if we for say used direct renin inhibitors if we could make a drug that would inhibit renin well look at that if i have less renin i'm going to end up with less angiotensin ii and i'm going to end up with less angiotensin one right because there won't be as much renin available to connect with the circulating angiotensinogen therefore i have less of every other product downstream okay cool so if i have less renin i'm going to end up with less potent vasoconstriction and volume expansion because there's just going to be less available so that would be cool if we could come up with a drug that would do that now what if i could come up with a drug that just made less ace available less angiotensin converting enzyme well i'd still have lots of renin angiotensinogen would be there i'd have angiotensin one but ah that's why i wouldn't have as much in her because if i have less ace i have less things available to convert angiotensin 1 to angiotensin 2. bueno that means i will have be able to lower my patient's blood pressure okay so we've talked about direct running inhibitors and we've talked about ace inhibitors so we've hit the inhibitors let's talk about the lockers okay so we've got a choice of angiotensin ii receptor blockers or aldosterone receptor antagonists or blockers okay so if i could create a drug that was an angiotensin ii receptor blocker that means that that is a drug remember we've got unlimited resources and money that's a drug that is so uniquely created that it will slide right into an angiotensin ii receptor and once that drug is on there it blocks off that receptor so let's walk back through our flow chart if i've given my patient an angiotensin ii receptor blocker will i have renin yes okay well then will i have circulating angiotensinogen yes well then will i have angiotensin one yes but if i've given them an angiotensin ii receptor blocker will i have ace yes so will i end up with angiotensin 2 yes you will but here's the deal it'll be all dressed up and no place to go because why because you were smart enough to give your patient an angiotensin ii receptor blocker look at this receptor down here it's all filled up so when your body squirts out those substances and angiotensin ii becomes available it can't connect to the receptor because you wisely gave your patient an angiotensin ii receptor blocker so without that angiotensin ii connecting to the receptor you're not going to have the potent vasoconstriction or volume expansion now we've got another blocker up there you can see that we called it an antagonist remember we used those terms interchangeably antagonist and blocker so an aldosterone receptor antagonist is the same thing as an aldosterone receptor blocker so if i have a med that's an aldosterone receptor antagonist that means that that medication is uniquely created that it will fit and block the aldosterone receptors without with the receptors not being available because you gave the patient a medication the body's not going to know to hang on to sodium right so you're not going to have that water that follows so your blood pressure will be lower so that's why understanding how the r a a s works before we ever talked about the drugs really can help you understand their mechanism of action if we have less renin we definitely have less angiotensin too if we have less ace angiotensin converting enzyme we're definitely going to have less angiotensin too if we have an arb an angiotensin ii receptor blocker we're going to have angiotensin ii but without its ability to connect to an angiotensin ii receptor we're not going to have that normal vasoconstriction or volume expansion if we try a patient on an aldosterone receptor blocker we're not going to have the body hanging onto us more sodium with water following for the volume expansion so understanding the ris is a really simple and straightforward way to look at four groups or categories of anti-hypertensive medications [Music] you

Channel: Lecturio Nursing

Views: 8,538

Keywords: NCLEX, Renin-Angiotensin-Aldosterone-System, nursing school, NCLEX review, medicine, health, Lecturio Nursing, NCLEX-RN, NCLEX-PN, nursing, RAAS, Cardiovascular Medications, Pharmacology, nursing students, nursing education

Id: -Jfcw8CkIrc

Length: 13min 50sec (830 seconds)

Published: Thu Mar 12 2020