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RENAL II Exam 3 > Intro to Antihypertensive Agents III > Flashcards

Intro to Antihypertensive Agents III Flashcards

1
Q

benazepril

A

ACE inhibitor

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2
Q

captopril

A

ACE inhibitor

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3
Q

enalapril

A

ACE inhibitor

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4
Q

enalaprilat

A

ACE inhibitor

  • active metabolite
  • used in IV
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5
Q

fosinopril

A

ACE inhibitor

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6
Q

lisinopril

A

ACE inhibitor

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7
Q

moexipril

A

ACE inhibitor

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8
Q

perindopril

A

ACE inhibitor

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9
Q

quinapril

A

ACE inhibitor

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10
Q

ramipril

A

ACE inhibitor

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11
Q

trandolapril

A

ACE inhibitor

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12
Q

azilsartain

A

angiotensin receptor blocker

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13
Q

canesartan

A

angiotensin receptor blocker

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14
Q

eprosartan

A

angiotensin receptor blocker

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15
Q

irversartan

A

angiotensin receptor blocker

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16
Q

losartan

A

angiotensin receptor blocker

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17
Q

olmesartan

A

angiotensin receptor blocker

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18
Q

telmisartan

A

angiotensin receptor blocker

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19
Q

valsartan

A

angiotensin receptor blocker

20
Q

clonidine

A

block renin secretion

21
Q

propanolol

A

block renin secretion

22
Q

aliskiren

A

renin inhibitor

23
Q

renin

A

converts angiotensinogen to angiotensin I

24
Q

effects of ANG II

A
  • kidney- Na/H2O retention
  • brain - release of corticotropin and adiuretin, thirst
  • adrenals - increased aldosterone secretion
  • blood vessels - vasoconstriction
25
Q

altered peripheral resistance by ANG II

A
  • vasoconstriction
  • enhancement of peripheral noradrenergic transmission (NE release, vascular responsiveness, decreased NE reuptake)
  • increased sympathetics
  • catecholamine release from adrenal medulla

**rapid pressor response

26
Q

altered renal function by ANG II

A
  • 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
Q

altered CV function with ANG II

A
  • 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
Q

meds that block RAAS

A
  • diuretics
  • aldosterone receptor antagonist
  • ACE inhibitor
  • ANG II receptor blocker
  • renin inhibitor
  • beta-blocker
29
Q

ACE inhibitor mechanism

A
  • inhibit conversion of ANG I to ANG II

- also prevent degradation of bradykinin and other vasodilators

30
Q

indications for ACE inhibitor

A

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

31
Q

long acting ACE inhibitor

A
  • ramipril (13-17 hours)
  • lisinopril (12 hours)
  • benazepril (12 hours)
  • IV enalaprilat (11 hours)
  • moexipril (12 hours)
32
Q

ACE inhibitor bonus activity**

A
  • decreased ANG I to ANG II
  • decreased bradykinin to inactive metabolites

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

33
Q

benefits of ACE inhibitors

A
  • 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
Q

adverse effects of ACE inhibitors

A 
hypotension
**cough** (variable with different ACE inhibitors)
angioedema
**hyperkalemia**
>stop aldosterone
acute renal failure
fetopathic
proteinuria
skin rash
dysgeusia
35
Q

avoid in K sparing diuretics

A

ACE inhibitors

-bc of hyperkalemic effects

36
Q

drug interactions with ACE inhibitors

A

antacids, capsaicin, NSAIDs, K-sparing diuretics, digoxin, lithium, allopurinol

37
Q

renal considerations for ACE inhibitors

A

-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
Q

ACE inhibitor risk factors

A
  • 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
Q

ANG II receptors

A

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
Q

ARB mechanism

A

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
Q

ARB clinical uses

A

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

42
Q

adverse effects of ARBs

A

contraindicated - pregnancy

hypotension, hyperkalemia, proteinuria, skin rash, dysguesia

less cough and edema

43
Q

dysguesia

A

altered sense of taste

44
Q

ACE inhibitor vs. ARB

A

ARB permit activation of AT2

ACE inhibitors increase bradykinin

45
Q

direct renin inhibitor mechanism

A

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
Q

contraindicated in pregnancy

A
  • renin inhibitor
  • ACE inhibitor
  • ARBs

RENAL II Exam 3 (17 decks)

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