Flashcards in Intro to Antihypertensive Agents III Deck (46):
1
benazepril
ACE inhibitor
2
captopril
ACE inhibitor
3
enalapril
ACE inhibitor
4
enalaprilat
ACE inhibitor
-active metabolite
-used in IV
5
fosinopril
ACE inhibitor
6
lisinopril
ACE inhibitor
7
moexipril
ACE inhibitor
8
perindopril
ACE inhibitor
9
quinapril
ACE inhibitor
10
ramipril
ACE inhibitor
11
trandolapril
ACE inhibitor
12
azilsartain
angiotensin receptor blocker
13
canesartan
angiotensin receptor blocker
14
eprosartan
angiotensin receptor blocker
15
irversartan
angiotensin receptor blocker
16
losartan
angiotensin receptor blocker
17
olmesartan
angiotensin receptor blocker
18
telmisartan
angiotensin receptor blocker
19
valsartan
angiotensin receptor blocker
20
clonidine
block renin secretion
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propanolol
block renin secretion
22
aliskiren
renin inhibitor
23
renin
converts angiotensinogen to angiotensin I
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effects of ANG II
-kidney- Na/H2O retention
-brain - release of corticotropin and adiuretin, thirst
-adrenals - increased aldosterone secretion
-blood vessels - vasoconstriction
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altered peripheral resistance by ANG II
-vasoconstriction
-enhancement of peripheral noradrenergic transmission (NE release, vascular responsiveness, decreased NE reuptake)
-increased sympathetics
-catecholamine release from adrenal medulla
**rapid pressor response
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altered renal function by ANG II
-increase Na reabsorption in proximal tubules
-aldosterone from adrenal cortex (Na reabsorption and K excretion in distal nephron)
-altered renal hemodynamics (vasoconstriction, enhanded noradrenergic, increased renal sympathetic tone)
**slow pressor response
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altered CV function with ANG II
-non-hemodynamic effects - increased protooncogenes, increased GFs, increased ECM proteins
-hemodynamic-mediated (increased afterload, increased wall tension)
**vascular and cardiac hypertrophy and remodeling
**connection between HTN and cardiovascular disease
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meds that block RAAS
-diuretics
-aldosterone receptor antagonist
-ACE inhibitor
-ANG II receptor blocker
-renin inhibitor
-beta-blocker
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ACE inhibitor mechanism
-inhibit conversion of ANG I to ANG II
-also prevent degradation of bradykinin and other vasodilators
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indications for ACE inhibitor
HTN, heart failure, left ventricular dysfunction, prophylaxis for future cerebrovascular events, and nephropathy
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long acting ACE inhibitor
-ramipril (13-17 hours)
-lisinopril (12 hours)
-benazepril (12 hours)
-IV enalaprilat (11 hours)
-moexipril (12 hours)
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ACE inhibitor bonus activity**
-decreased ANG I to ANG II
-decreased bradykinin to inactive metabolites
**decreased vasoconstrictor (ANG II) and increased vasodilator (bradykinin)**
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benefits of ACE inhibitors
-lowers TPR, MAP, DBP, SBP
-SV and CO may increase slightly with sustained treatment
-baroreceptor and CV reflex not compromised
**-postural/exercise changes little impaired**
-younger active pt
-superior in pt with diabetes and HTN
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adverse effects of ACE inhibitors
hypotension
**cough** (variable with different ACE inhibitors)
angioedema
**hyperkalemia**
>stop aldosterone
acute renal failure
fetopathic
proteinuria
skin rash
dysgeusia
35
avoid in K sparing diuretics
ACE inhibitors
-bc of hyperkalemic effects
36
drug interactions with ACE inhibitors
antacids, capsaicin, NSAIDs, K-sparing diuretics, digoxin, lithium, allopurinol
37
renal considerations for ACE inhibitors
-prevent progression of renal disease in DM I
-vasodilate efferent > afferent (reduce glomerulus back pressure)
>reduced protein excretion
-improve renal blood flow and Na excretion rate in CHF
-rapid decrease in GFR, acute renal failure - rare cases**
38
ACE inhibitor risk factors
-MAP insufficient for adequate renal perfusion (poor CO/ low systemic vascular resistance)
-volume depletion
-renal vascular disease > B/L renal a stenosis**
-vasoconstrictor use
all can result in renal hypoperfusion*
39
ANG II receptors
GPCR
**AT1 - major in adults
-Gq > PLC > IP3 and DAG > smooth m. contraction
>blocked by ARBs
AT2 > production of NO and bradykinin > smooth m. dilation
40
ARB mechanism
block AT1 receptors
>decreased vasc smooth m contraction >decreased aldosterone secretion (hyperkalemia) > decreased pressor response > decreased cellular hypertrophy and hyperplasia
**no effect on bradykinin
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ARB clinical uses
HTN, diabetic nephropathy, HF, left ventricular dysfunction, prophylaxis or CV events
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adverse effects of ARBs
contraindicated - pregnancy
hypotension, hyperkalemia, proteinuria, skin rash, dysguesia
less cough and edema
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dysguesia
altered sense of taste
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ACE inhibitor vs. ARB
ARB permit activation of AT2
ACE inhibitors increase bradykinin
45
direct renin inhibitor mechanism
block renin - no angiotensinogen to ANG I
-contraindicated in pregnancy
**rise in plasma renin levels, but decreased plasma renin activity**
rebound HTN if withdraw quickly
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