Intro to Antihypertensive Agents III Flashcards
1
Q
benazepril
A
ACE inhibitor
2
Q
captopril
A
ACE inhibitor
3
Q
enalapril
A
ACE inhibitor
4
Q
enalaprilat
A
ACE inhibitor
- active metabolite
- used in IV
5
Q
fosinopril
A
ACE inhibitor
6
Q
lisinopril
A
ACE inhibitor
7
Q
moexipril
A
ACE inhibitor
8
Q
perindopril
A
ACE inhibitor
9
Q
quinapril
A
ACE inhibitor
10
Q
ramipril
A
ACE inhibitor
11
Q
trandolapril
A
ACE inhibitor
12
Q
azilsartain
A
angiotensin receptor blocker
13
Q
canesartan
A
angiotensin receptor blocker
14
Q
eprosartan
A
angiotensin receptor blocker
15
Q
irversartan
A
angiotensin receptor blocker
16
Q
losartan
A
angiotensin receptor blocker
17
Q
olmesartan
A
angiotensin receptor blocker
18
Q
telmisartan
A
angiotensin receptor blocker
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
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
