Intro to Antihypertensive Agents III Flashcards Preview

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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

21

propanolol

block renin secretion

22

aliskiren

renin inhibitor

23

renin

converts angiotensinogen to angiotensin I

24

effects of ANG II

-kidney- Na/H2O retention
-brain - release of corticotropin and adiuretin, thirst
-adrenals - increased aldosterone secretion
-blood vessels - vasoconstriction

25

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

26

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

27

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

28

meds that block RAAS

-diuretics
-aldosterone receptor antagonist
-ACE inhibitor
-ANG II receptor blocker
-renin inhibitor
-beta-blocker

29

ACE inhibitor mechanism

-inhibit conversion of ANG I to ANG II
-also prevent degradation of bradykinin and other vasodilators

30

indications for ACE inhibitor

HTN, heart failure, left ventricular dysfunction, prophylaxis for future cerebrovascular events, and nephropathy

31

long acting ACE inhibitor

-ramipril (13-17 hours)
-lisinopril (12 hours)
-benazepril (12 hours)
-IV enalaprilat (11 hours)
-moexipril (12 hours)

32

ACE inhibitor bonus activity**

-decreased ANG I to ANG II
-decreased bradykinin to inactive metabolites

**decreased vasoconstrictor (ANG II) and increased vasodilator (bradykinin)**

33

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

34

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

41

ARB clinical uses

HTN, diabetic nephropathy, HF, left ventricular dysfunction, prophylaxis or CV events

42

adverse effects of ARBs

contraindicated - pregnancy

hypotension, hyperkalemia, proteinuria, skin rash, dysguesia

less cough and edema

43

dysguesia

altered sense of taste

44

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

46

contraindicated in pregnancy

-renin inhibitor
-ACE inhibitor
-ARBs