RAAS agents Flashcards

1
Q

what are the ace inhibitors

A

fosinopril, captopril, benazepril, enalapril, moexipril, quinapril, ramipril

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2
Q

what is the mechanism of the ace inhibitors

A

they bind to and inhibit ACE; thus preventing the formation of angiotensin II from angiotensin I

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3
Q

when would we not see much of a response in patients taking ace inhibitors

A

if the patient has low renin levels

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4
Q

what are the 2 major things that account for the BP lowering effect of ace inhibitors

A

prevention of vascular smooth muscle constriction by angiotensin II, and reduction in the secretion of aldosterone

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5
Q

relaxation of arterial vascular smooth muscle results in decreased ___

A

TPR

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6
Q

the decrease in TPR with ACEi is seen ___

A

rapidly

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7
Q

how does blocking aldosterone secretion with ACEi decrease BP?

A

more sodium eliminated—> urinary output increases—> extracellular fluid volume decreases–> circulatory filling pressure decreases–> venous output decreases–> cardiac output decreases

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8
Q

ACEi red

A
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9
Q

ACE is also called ____

A

kininase II

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10
Q

ACE is also responsible for the metabolism of the vasodilator ____

A

bradykinin

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11
Q

increased bradykinin levels lead to what adverse effect

A

dry cough

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12
Q

clinical uses of ACEi

A

treat all stages of HTN, monotherapy or combo, used in heart failure, prevent pathological effects of angiotensin on blood vessels, prevent damaging effect of angiotensin which promote myocardial damage

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13
Q

adverse effects of ACEi

A

dry cough, angioedema, exaggerated fall in BP in hypovolemic patients

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14
Q

which drug combos work well with ACEi

A

thiazides, loops, vasodilators

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15
Q

drug interactions with ACEi

A

potential for hyperkalemia when used with potassium sparing diuretics, NSAIDs reduce the hypotensive effect of ACEi’s

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16
Q

what are the ARBs

A

losartan, candesartan, eprosartan, irbesartan, telmisartan, valsartan, olmesartan, azilsartan

17
Q

mechanism of ARBs

A

competitive antagonists of the AT1 receptor located on vascular smooth muscle that synthesizes and releases aldo and causes vasoconstriction

18
Q

as a consequence of angiotensin receptor blockade, vascular smooth muscle is _____

A

relaxed (decrease TPR, seen early)

19
Q

as a consequence of angiotensin receptor blockage, aldosterone secretion is blocked which decreases ____

A

cardiac output; takes time to develop effect

20
Q

use of ARBs in hypertension

A

used to treat all stages of HTN, can be used alone or in combo, cough is not an adverse effect and angioedema is even more rare

21
Q

name the renin inhibitor

A

aliskiren

22
Q

what is the mechanism of aliskiren

A

it binds to and inhibits renin, preventing angiotensinogen from binding to the enzyme in the blood. so there is no formation of angiotensin I and II

23
Q

the utility of aliskiren in treatment is similar to __

A

ACEis and ARBs

24
Q

name the Angiotensin-Receptor-Neprilysin Inhibitor (ARNi)

A

Sacubitril/Valsartan (Entresto)

25
Q

____ is an enzyme that degrades important vasodilator peptides and vasoconstrictors

A

neprilysin

26
Q

why is sacubitril not used alone

A

there is little effect on BP when used alone because it increases both vasodilators AND vasoconstrictors

27
Q

why can’t we combo an ACEi with sacubitril

A

increased risk for angioedema seen in trials

28
Q

clinical application of ARNi therapy

A

management of chronic heart failure