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PHRM 844 > ACEi, angiotensin antagonists, diuretics > Flashcards

ACEi, angiotensin antagonists, diuretics Flashcards

(62 cards)

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1
Q

RAAS pathway

A
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2
Q

where is renin produced

A

in the juxtaglomerular cells in kidney

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3
Q

what causes renin release

A

drop in BP in pre-glomerular arteries (systolic <90 mmHg)
low NaCl in kidney’s distal tubule
increased SNS activity (beta1)

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4
Q

where is angiotensinogen produced

A

liver

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5
Q

where is angiotensin converting enzyme (ACE) produced

A

kidney

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6
Q

what does angiotensin II cause

A

aldosterone secretion
vasoconstriction

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7
Q

what does angiotensin II mediated vasoconstriction cause

A

increased peripheral vascular resistance
–> increased BP

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8
Q

what does angiotensin II mediated aldosterone secretion cause

A

increased retention of Na and water –> increased BP

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9
Q

where does renin cleave angiotensinogen

A

between Leu-Val aa

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10
Q

where does ACE cleave angiotensin I

A

between Phe-His aa

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11
Q

where does aminopeptidase cleave angiotensin II

A

between Asp-Arg

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12
Q

what is the name of renin inhibitor drug

A

Aliskiren

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13
Q

aliskiren moa

A

direct inhibitor renin
decreases formation of angiotensin I from angiotensinogen

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14
Q

aliskiren clinical use

A

not 1st line tx for htn

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15
Q

aliskiren effect

A

drops BP bc it inhibits renin

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16
Q

aliskiren problems

A

do not use in pregnant and nursing mothers

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17
Q

what is common identifying factor of ACEi

A

all ACEi ends in -pril

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18
Q

what are the sulfahydryl-containing ACEi structurally related to Captopril

A

fentiapril, pivalopril, zofenopril, alacepril

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19
Q

what are the dicarboxyl-containing ACEi structurally related to Enalapril

A

lisinopril, benazepril, quinapril, moexipril, ramipril, trandolapril, perindopril, spirapril, pentopril, cilazapril

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20
Q

what are the phosphorous-containing ACEi

A

Fosinopril

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21
Q

ACEi action

A

inhibits angiotensin converting enzyme

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22
Q

ACEi effects

A

reduces vasoconstriction caused by angiotensin II
reduce Na and Cl retention caused by aldosterone
reduce total peripheral resistance
reduces myocardial mitogenic activity

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23
Q

ACEi clinical use

A

1st line tx for htn, hf

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24
Q

ACEi and ARBs in different races

A

particular useful in whites but not african americans as monotherapy for htn but appropriate for hf

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25
ACEi in pts with diff. diseases
better for pts with diabetes than thiazides better for pts with ischemic heart disease than direct vasodilators
26
ACEis AEs
cough, angioedema, hyperkalemia
27
why should ACEi not be used in pregnancy
can cause fetal hypotension, renal failure, mortality
28
what may reduce ACEi effectiveness
NSAIDs
29
what can ACEi/ARBs also be used in
renal artery stenosis, but not if GFR drops by more than 30%
30
bradykinin effects
causes vasodilation, in part mediated by PGI2
31
why can ACEi cause hyperkalemia
decreased production of aldosterone
32
why can ACEi cause angioedema of lips and tongue
accumulation of bradykinin
33
which race has bigger risk of angioedema from ACEi
black pts have a 4-5x higher risk than white pts
34
what is common identifying factor of ARBs
all ARBs end in -sartan
35
ARBs affinity
blocks angiotensin II receptors with higher affinity for AT1 than AT2 receptor
36
ARBs potency ranking
candesartan = omesartan > irbesartan = eprosartan > telmisartan = valsartan > EXP 3174 (active metabolite of losartan) > losartan
37
lisinopril info
t1/2 = 12h not a prodrug
38
enalapril info
prodrug, hydrolyzed to active diacid enalaprilat
39
captopril info
thiol-containing not a prodrug t1/2 <3h
40
what design is ARBs based off
carboxy terminus of angiotensin II
41
ARBs structure activity relationship
acidic group: o-phenylcarboxylic acid (or the tetrazole isostere) or carboxylic acid substituted imidazole or isosteric equivalent in some cases, a second carboxylic acid group
42
ARBs effects
decreased myocardial and vascular remodeling decreased cardiomyocyte apoptosis reduce total peripheral resistance
43
ARBs clinical use
1st line monotherapy for htn IN pts who cannot tolerate ACEi
44
ARBs AEs
hypotension, hyperkalemia, lower rate of angioedema, fetal pathologies, reduction in GFR
45
why do ARBs not cause persistent cough
ARBs do not inhibit breakdown of bradykinin
46
ARBs are particularly useful in pts with:
diabetes ischemic heart disease pts with CKD
47
what are the aldosterone (mineralocorticoid) receptor antagonists (aka potassium sparing diuretics)
spironolactone, eplerenone
48
K sparing diuretic moa
blocks reabsorption of sodium
49
what causes K sparing diuretic's effectiveness in hf
not primarily due to diuretic effect. increases production of aldosterone which promotes development of cardiac hypertrophy, remodeling, fibrosis. maintenance of normal K levels --> reduces risk of arrhythmias.
50
K sparing diuretic clinical use
chronic hf. aldosteronism. not monotherapy for htn but used to reduce hypokalemia.
51
K sparing diuretic AEs
hyperkalemia. spironolactone can cause gynecomastia and impotence due to interaction with other steroid receptors.
52
what is the thiazide diuretic drug
chlorthalidone
53
thiazides moa
diuretic blocking sodium-chloride symporter (NCC) on distal convoluted tubule
54
what does thiazide lower when used long term
peripheral vascular resistance --> lower BP
55
thiazide clinical use
1st line monotherapy for mild-moderate htn
56
what race is thiazides useful in
african americans
57
what pts do you not use thiazides for
pts with diabetes, hyperlipidemia, gout
58
thiazide AEs
hypokalemia, metabolic alkalosis, hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia
59
what does thiazides do initially
reduce blood volume and cardiac output --> decrease BP
60
which diuretic is not recommended as 1st line monotherapy for htn
loop diuretics
61
why are K sparing diuretics not recommended as 1st line monotherapy for htn
weak acting. associated with hyperkalemia
62
what htn meds can you use for pregnancy
methyldopa beta blockers (e.g. labetalol, metoprolol)

PHRM 844 (13 decks)

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