antihypertensive Flashcards
(78 cards)
1
Q
what are the three main subclasses of diuretics?
A
- thiazides
- loop diuretics
- k sparing diuretics
2
Q
what are the four major classes of antihypertensive drugs?
A
- diuretics
- inhibitors of the RAA system
- vasodilators
- sympatholytic agents
3
Q
what are the two main subtypes of inhibitors of the RAA system?
A
- ACE inhibitors
- angiotensin receptor blockers
4
Q
what are the two main subtypes of vasodilators?
A
- direct acting
- calcium entry blockers
5
Q
what are the four major subtypes of sympatholytic antihypertensives?
A
- CNS
- autonomic ganglia
- post-ganglionic neurons
- block peripheral adrenergic receptors
6
Q
what class is hydrochlorothiazide?
A
thiazide diuretic
7
Q
hydrochlorothiazide pharmacodynamics
A
blocks reuptake of Cl and Na from tubular fluid after glomerular filtration
8
Q
how much will hydrochlorothiazide lower BP?
A
10-15mm
9
Q
HCTZ bioavailability
A
70%
10
Q
HCTZ excretion
A
urine, unchanged
11
Q
HCTZ half life
A
short (hours)
12
Q
HCTZ toxicity
A
- K and Mg depletion
- Na and Cl depletion
- metabolic alkalosis
- volume depletion
- worsen hyperuricemia
13
Q
HCTZ special considerations
A
- more side effects in geriatrics
- pregnancy class D
- less effective with low GFR
14
Q
HCTZ route
A
oral
15
Q
why might chlorthalidone be better than HCTZ?
A
- greater reduction of SBP
- better control of SBP at night
- longer half life (50 hours)
- 1.5-2x more potent per mg
16
Q
What class is chlorthalidone?
A
thiazide diuretic, same as HCTZ
17
Q
what class is lisinopril?
A
ACE inhibitor, subtype of RAA system inhibitors
18
Q
lisinopril indications
A
- hypertension/CHF
- preserve renal function
- preservation of LV function after MI
19
Q
lisinopril pharmacodynamics
A
- inhibits conversion of AT1 to AT2 by ACE
- diminishes vasoconstriction
- diminishes stimulation of aldosterone secretion
20
Q
lisinopril excretion
A
urine, unchanged
21
Q
lisinopril timing
A
- onset 1 hour
- peak 6 hrs
- duration 24 hrs
22
Q
lisinopril toxicity
A
- ortho hypotension
- caution impaired renal function
- caution renal artery stenosis
- caution diuretics
23
Q
lisinopril interactions
A
- NSAIDS may reduce ability to lower BP
24
Q
lisinopril special considerations
A
- may wan to discontinue diuretics before use
25
lisinopril route
oral
26
losartan class
ARB, RAA system inhibitor
27
losartan indications
- hypertension
| - CHF
28
losartan pharmacodynamics
block stimulation of AT1 receptors by angiotensin II, reduce vasoconstriction and production of aldosterone
29
losartan bioavailability
F 30%
30
losartan onset/timing
- onset 6 hrs
- extensive first pass effect
- active metabolite 40x more potent, much longer half life
31
losartan special considerations
- pregnancy
- caution with diuretics
- caution with renal stenosis, mitral or aortic stenosis
32
losartan route
oral
33
nitroprusside class
direct vasodilator
34
nitroprusside indications
- severe CHF
- severe pulmonary hypertension
- produce hypotension during surgery
35
nitroprusside pharmacodynamics
- direct on vascular smooth muscle of veins and arterioles
- metabolized to CN- and NO, activates guanylate cyclase, converts GTP and cCMP, leads to vasodilation, cGMP turned to GMP by PDE
36
nitroprusside route
IV only, continuous infusion
37
nitroprusside onset/timing
- minutes to onset
| - minutes to cessation
38
nitroprusside metabolism
CN- metabolite converted to SCN in liver and excreted in urine
39
nitroprusside toxicity
- excessive hypotension
- metabolic acidosis
- accumulation of CN- and thiocyanate
- headache
- decreased blood flow to brain
40
nitroprusside special considerations
monitor very closely to prevent accumulation of CN-
41
hydralazine class
direct vasodilator
42
hydralazine indications
- hypertension
| - CHF
43
hydralazine pharmacodynamics
- induces endothelium to produce NO, which then passes to the smooth muscle cells and induces production of cGMP
- minimal venodilating effect
44
contrast hydralazine and nitroprusside
- nitroprusside veno and vasodilates while hydralazine only minimally venodilates
45
hydralazine routes
oral, IM, IV
46
hydralazine metabolism
- metabolized extensively in GI mucosa and in liver
| - excreted as metabolites in urine
47
hydralazine F
40%
48
hydralazine onset vs route
- oral 30 min
- IV 10 min
- persists for 2-6 hours
49
hydralazine toxicity
```
more dangerous in patients with:
- renal disease
- prior stroke
- angina
can cause hyptotension, edema, drug-induced lupus
```
50
hydralazine special considerations
never use as chronic oral monotherapy for treatment of hypertension since edema and reflex tachycardia will result.
51
verapamil class
calcium entry blocker (CEB), vasodilator
52
verapamil indications
- hypertension
- angina
- arrhythmia
53
verapamil pharmacodynamics
- reduces BP by inhibiting influx of calcium through "slow channels" leading to peripheral arteriolar dilation
- negative inotropic effect
- reduces afterload (for angina) to decrease oxygen consumption
- inhibits spasm of coronary arteries
- blocks reentry paths through AV node in paroxysmal SVT
54
verapamil absorption speed
rapid
55
verapamil F
30%
56
verapamil clearance
liver and kidney
57
verapamil onset vs route
oral - 2hrs
| IV - 1-5mins
58
verapamil routes
oral, IV
59
verapamil half-life
6-12hrs
60
verapamil toxicity
- hypotension
- AV block
- worsening CHF
- bradycardia
61
verapamil interactions
- toxic effect on heart when given with b-blockers
62
verapamil special considerations
- reduce dose if someone has both hepatic and renal disease
63
nifedipine most closely resembles the actions of:
verapamil
64
methyldopa class
sympatholytic antihypertensive
65
methyldopa pharmacodynamics
- central a2 agonist
- also competitive inhibitor of L-DOPA decarboxylase which converts L-DOPA into dopamine which subsequently becomes norepinephrine and epinephrine
66
methyldopa indications
- hypertension
| - gestational hypertension
67
methyldopa F
50%
68
methyldopa half life
1-2 hours
69
methyldopa routes
oral, IV
70
reserpine class
sympatholytic antihypertensive
71
reserpine pharmacodynamics
irreversibly blocks vesicular monoamine transporter (VMAT) so presynaptic neurotransmitters can't be packaged into vesicles for release.
72
reserpine indications
- hypertension
| - psychotic symptoms
73
reserpine F
50%
74
reserpine metabolism
gut/liver
75
reserpine excretion
62% feces, 8% urine
76
reserpine half life
33 hours, with two phases, first one short, second one long
77
reserpine route
oral
78
what two drugs are similar to prazosin? what is their mechanism?
terazosin and doxazosin - a1 blockers that lower blood pressure. initially raise heart rate to meet homeostasis but then it adjusts.
