Antihypertensives Flashcards
(96 cards)
1
Q
Hydrochlorothiazide: class
A
Thiazide diuretic, reduces Na reabsorption in distal tubule
2
Q
Hydrocholorthiazide: indication
A
Antihypertensive, diuretic
3
Q
Lisinopril: class
A
ACE inhibitor
4
Q
Lisinopril: indication
A
Antihypertensive, CHF
5
Q
Captopril: class
A
ACE inhibitor
6
Q
Captopril: indication
A
Antihypertensive, CHF
7
Q
Enalapril: class
A
ACE Inhibitor
8
Q
Enalapril: indication
A
Antihypertensive, CHF
9
Q
Ramipril: class
A
ACE Inhibitor
10
Q
Ramipril: indication
A
Antihypertensive, CHF
11
Q
Losartan: class
A
Angiotensin-1 receptor blocker
12
Q
Losartan: indication
A
Antihypertensive, diuretic
13
Q
Nitroprusside: class
A
Venous and Arterial Vasodilator
14
Q
Nitroprusside: indication
A
Antihypertensive, CHF
15
Q
Hydralazine: class
A
Arterial vasodilator
16
Q
Hydralazine: indication
A
Antihypertensive, CHF
17
Q
Verapamil: class
A
Calcium entry blockers
18
Q
Verapamil: indication
A
Antihypertensive, antianginal, antiarrhythmic Class IV
19
Q
Nifedipine: class
A
Calcium entry blockers
20
Q
Nifedipine: indication
A
Antihypertensive, antianginal, antiarrhythmic
21
Q
Amlodipine: class
A
Calcium entry blockers
22
Q
Amlodipine: indication
A
Antihypertensive, antianginal, antiarrhythmic
23
Q
Diltiazem: class
A
Ca entry blocker
24
Q
Diltiazem: indication
A
Antihypertensive, antianginal, antiarrhythmic
25
Nicardipine: class
Ca entry blocker
26
Nicardipine: indication
Antihypertensive, antianginal, antiarrhythmic
27
Hydrochlorothiazide: PD
block reuptake of Cl and Na from tubular fluid after glomerular filtration; also appears to cause decrease in SVR via unclear mechanism; will lower BP by up to 10-15 mm in many patients; useful as monotherapy or in combinations; HCTZ most commonly used, but perhaps some slight edge to chlorthalidone (duration, efficacy)
28
Hydrochlorothiazide: PK
F ~70%, excreted unchanged in urine; short half-life (hours); HCTZ not available in IV formulation; onset 2 h, peak 5 h, duration 10 h
29
Hydrochlorothiazide: tox
allergy to sulfa antibiotics (?); cause K and Mg depletion; cause Na and Cl depletion, metabolic alkalosis; volume depletion; worsen hyperuricemia
30
Hydrochlorothiazide: interactions
additive effects with most other antihypertensives
31
Hydrochlorothiazide: special
more side effects in geriatric patients; Pregnancy Class D; much less effective in patients with reduced GFR
32
Hydrochlorothiazide: monitor
BP, weight, edema, K, Mg, BUN, creatinine
33
Lisinopril: PD
inhibits conversion of AT I to AT II by ACE; diminishes both vasocontriction and stimulation of aldosterone secretion by AT II
34
Lisinopril: PK
well absorbed; onset 1 h, peak 6 h, duration 24 h; once a day is fine; excreted primarily in urine as unchanged drug
35
Lisinopril: tox
orthostatic hypotension; use with caution in patients with impaired renal function, or renal artery stenosis; be careful in patients on diuretics, or those with aortic stenosis; angioedema, cough; acute renal failure
36
Lisinopril: interactinos
additive effects with most other antihypertensives; NSAIDs may reduce ability to lower BP; hyperkalemia with KCL, others
37
Lisinopril: special
often discontinue diuretics prior to beginning use to reduce hypotension; Category C/D in pregnancy, abnormal cartilage development
38
Lisinopril: monitor
BP, weight, edema, K, BUN, creatinine!!!!!
39
Why might Lisinopril be best option for preserving renal function?
Inhibits ATII, which causes constriction of efferent arterioles. Can damage glomeruli. But if you dilate the efferent, lowers pressure inside glomerulus, preserves fxn longer. Slows progression of renal failure in diabetics.
40
Losartan: PD
block stimulation of AT I receptor by angiotensin II, thereby reducing vasoconstriction and production of aldosterone
41
Losartan: PK
F ~30%; onset 6 h; extensive first pass effect; active metabolite is 40x more potent, much longer half-life
42
Losartan: tox
dizziness; orthostatic hypotension; worsening of renal failure
43
Losartan: interactions
additive effects with most other antihypertensives
44
Losartan: special
Pregnancy class C/D; use care in patients on diuretics, those with renal artery stenosis, those with mitral or aortic stenosis
45
Losartan: monitor
BP, weight, edema, lytes, BUN, creatinine!!!
46
Nitroprusside: PD
acts “directly” on vascular smooth muscle to cause dilatation of both veins and arterioles; metabolized to release CN- and NO, which activates guanylate cyclase, leads to production of cGMP from GTP, which then leads to vasodilation; cGMP then hydrolyzed to GMP by PDE
47
Nitroprusside: PK
only route is iv; rapid onset (minutes) and cessation (minutes), thereby allowing minute-by-minute titration; CN- metabolite is converted to SCN in liver, then excreted in urine; must be given by continuous infusion
48
Nitroprusside: tox
excessive hypotension; accumulation of CN- and thiocyanate; headache; decreased blood flow to brain
49
Nitroprusside: interactions
additive effects with most other antihypertensives
50
Nitroprusside: special
monitor patient VERYclosely—must be in ICU with arterial line; avoid high infusion rates or prolonged infusions, to prevent accumulation of CN-; use with caution in patients with increased intracranial pressure
51
Nitroprusside: monitor
BP, HR, metabolic acidosis; most often requires arterial line
52
Hydralazine: PD
“direct” acting vasodilator; seems to act by inducing endothelium to produce NO, which then passes to SM cells and induces production of cGMP, minimal venodilating effect
53
Hydralazine: PK
given po, im, iv; metabolized extensively in GI mucosa and in liver, eventually excreted as metabolites in urine; F ~40%; onset 30 after po dose, 10 min after iv dose; persist for 2-6 hours
54
Hydralazine: tox
more dangerous in patients with renal disease, prior stroke, angina; watch for hypotension, edema, occasionally drug-induced lupus
55
Hydralazine: interactions
additive effects with most other antihypertensives
56
Hydralazine: special
never use as chronic oral monotherapy for treatment of hypertension, since edema and reflex tachycardia will result; concern giving to patients with CAD
57
Hydralazine: monitor
BP, weight, edema, BUN, creatinine, symptoms of lupus or angina
58
Hydralazine: use in pregnancy
Lowers BP in 3rd tri. Used for short period of time, won't cause lupus.
59
Verapamil: PD
reduces BP by inhibiting influx of calcium through “slow channels”, thereby dilating peripheral arterioles; produces negative inotropic effect as well; for angina, reduces afterload, thus decreasing oxygen consumption; also, inhibits spasm of coronary arteries in vasospastic angina; blocks reentry paths through AV nodes in paroxysmal SVT
60
Verapamil: PK
absorbed rapidly, but F ~30%; also available in SR tablets; cleared by kidney and liver (produces active metabolites); onset 2 h po, 1-5 min iv; half-life 6-12 h; may be given po or iv
61
Verapamil: tox
hypotension, AV block, worsening of CHF, bradycardia
62
Verapamil: interactions
additive effects with most other antihypertensives; additive toxic effects on heart when given with beta-blockers
63
Verapamil: special
use reduced doses in patients with both renal and hepatic disease; short-acting nifedipine (and similar CEBs) can increase risk of MI (unclear why); Pregnancy C
64
Verapamil: monitor
BP, weight, edema
65
Nifedipine: same class as ?
same as Verapamil
66
Clonidine: PD
stimulates alpha-2 adrenoceptors in brainstem, thereby leading to down-regulation of sympathetic output
67
Clonidine: PK
Onset 1 h, duration 8 h, F~85%, also available as cutaneous patch
68
Clonidine: tox
withdraw gradually because of risk of rebound HTN; risk of bradycardia in sinus node disease; lethargy, fatigue, depression
69
Clonodine: interaction
additive effects with most other antihypertensives; additive sedation with other CNS drugs
70
Clonidine: special
Pregnancy class C; avoid in patients with renal insufficiency
71
Clonidine: monitor
follow BP and HR, fatigue
72
Methyldopa: class
a2 agonist (central action)
73
Methyldopa: indication
antihypertensive
74
Clonidine: class
a2 agonist (central action)
75
Clonidine: indication
antihypertensive
76
Trimethaphan: class
NN (ganglionic) blocker
77
Trimethaphan: indication
Antihypertensive
78
Reserpine: class
Blocks NE uptake into vesicles
79
Reserpine: indication
Antihypertensive
80
Reserpine: PD
binds to vesicles that contain NE or serotonin, preventing their uptake, and ultimately depleting the neuron of NE (or serotonin); this effect takes 2-3 weeks to develop, and including neurons and also the adrenal medulla
81
Reserpine: PK
good oral bioavailability, but biologic effects take 2-3 weeks to develop (via slow depletion of NE from vesicles)
82
Reserpine: tox
dizziness; orthostatic hypotension; depression
83
Reserpine: interaction
additive effects with most other antihypertensives
84
Reserpine: special
approved by the FDA in 1953!!! First antihypertensive drug approved, and first sympatholytic drug approved by the FDA (remember that in 1960’s, drugs included only reserpine, HCTZ, and hydralazine)
85
Reserpine: monitor
BP, sympathetic tone, depression!!!!
86
Reserpine: note
I include this drug to show that this mechanism does work, and for historical interest!! This drug is not used in the long-term management of HTN today in the US, but it is of great historical importance!!
87
Atenolol: class
B1 blocker
88
Atenolol: indication
Antihypertensive, antianginal, antiarrhythmic, anti-MI
89
Prazosin: class
A1 blocker
90
Prazosin: indication
Antihypertensive, Rx for BHP
91
Terazosin: class
A1 blocker
92
Terazosin: indication
Antihypertensive, Rx for BHP
93
Doxazosin: class
A1 blocker
94
Doxazosin: indication
Antihypertensive, Rx for BHP
95
Labetalol: class
A1 and B blocker
96
Labetalol: indication
Antihypertensive, pheochromocytoma, Hypertensive crisis, pre-eclampsia
