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Flashcards in Anti-HTN Deck (12)
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1
Q

hydrochlorothiazide

A

thiazide diuretic for anti-HTN

blocks reuptake of Cl and Na from tubular fluid after filtration; appears to cause a decrease in TPR via unclear mechanisms; lowers BP by 10-15mm in monotherapy, more in combinations; Chlorthalidone may eventually replace HCTZ b/c it may be more effective.

F~70%, excreted unchanged in urine (causes increase in frequency of urination); short half life (hours); only available as oral formulation; onset 2hr, peak 5h, duration 10h

may cause K and Mg depletion, Na and Cl depletion, metabolic alkalosis, volume depletion, worsen hyperuricemia

additive effects with other anti-HTN

more side effects with geriatric patients; pregnancy class D; less effective in patients with reduced GFR

12.5 or 25mg po every morning;

monitor BP, weight, edema, K, Mg, BUN, creatinine

2
Q

Lisinopril

A

ACE inhibitor for anti-HTN, treatment of CHF, preserving renal function, preserving LV function s/p MI, acute management of MI

inhibits conversion of AT1 to AT2 via ACE; attenuates AT2 induced vasoconstriction + aldosterone release

well absorbed, onset 1h, peak 6h, duration 24h; used once per day. excreted renal as unchanged drug

can cause orthostatic hypotension; caution in patients with impaired renal fxn or RAS (reduces GFR); careful use in patients on diuretics or with aortic stenosis; can cause angiodema in lips/throat/face (can be lethal); cough, acute renal failure

additive effects with other anti-HTN; nsaids may attenuate BP lowering effects; preserves K+, and can cause hyperkalemia if taken with KCl or others

D/C diuretics prior to beginning use to reduce hypotension; category C/D in pregnancy; can cause abnormal cartilage development

begin w/ 10mg per day, titrate upward to 40mg per day max

monitor BP, weight, edema, K, BUN, and creatinine (to assess renal fxn)

3
Q

Losartan

A

angiotensin-1 receptor blocker (ARB) for anti-HTN, preserving renal fxn, treatment of CHF

blocks stimulation of AT1R by AT2, reducing AT2 induced vasoconstriction + aldosterone release

F ~30%, onset 6h, extensive first pass; active metabolite is 40x more potent with longer half-life

can cause dizziness, orthostatic hypotension, worsening of renal failure

additive effects with other anti-HTN

pregnancy class C/D, use care in patients on diuretics or with RAS; caution with mitral or aortic stenosis

25-100mg per day for HTN

Monitor BP, weight, edema, electrolytes, BUN, creatinine

4
Q

Nitroprusside

A

vasodilator for acute anti-HTN, severe CHF, pulmonary HTN, and during surgery to produce controlled hypotension

metabolized to release CN- and NO; vascular smooth muscle dilatation in veins + arteries via activation of guanylate cyclase > increased cGMP > vasodilation > cGMP hydrolyzed to GMP by phosphodiesterase (PDE)

only administered via iv; rapid onset and cessation (allows minute to minute titration); CN- metabolite is converted to SCN in liver and excreted in urine

can cause excessive hypotension, accumulation of CN- and thiocyanate, headache, decreased blood flow to brain (syncope)

additive effect with other anti-HTN

only administered in ICU with arterial line; avoid high rate or prolonged infusion;

0.3-10mcg/kg/min IV infusion for HTN crisis

monitor BP, HR, metabolic acidosis

5
Q

Hydralazine

A

peripheral vasodilator for anti-HTN, treatment of CHF, vasodilator

“direct” acting vasodilator, acts by inducing endothelium to produce NO > increased cGMP; minimal venodilating effect

given po, im, or iv; metabolized extensively in GI mucosa and liver, excreted in urine as metabolites; F ~40%; onset 30m po, 10m iv; persists 2-6h

dangerous in patients with renal dz, prior stroke, angina; watch for hypotension, edema, drug-induced lupus

additive effects with other anti-HTN

never use as chronic oral mono therapy for HTN since it causes edema and reflex tachycardia; cautious use in patients with CAD

10-50mg po tid

monitor BP, weight, edema, BUN, creatinine, symptoms of lupus or angina

6
Q

Verapamil

A

calcium entry blocker for anti-HTN, anti-anginal, anti-arrythmic

reduces BP by inhibiting influx of calcium through “slow channels”, dilates peripheral arterioles; produces negative inotropic effect; reduces afterload (in angina) to lower oxygen consumption; inhibits spasm of coronary arteries in vasospastic angina; blocks reentry paths through AV nodes in paroxysmal SVT

absorbed rapidly, but F~30%; also available in SR tablets; cleared by liver and kidney (produces active metabolites); onset 2h po, 1-5m iv; half-life 6-12h, may be given po or iv

can cause hypotension, AV block, worsening of CHF, bradycardia

additive effects with other anti-HTN; additive toxic effects on heart when given with beta-blockers

reduce dose in patients with both renal and hepatic dz; short-acting nifedipine (other calcium entry blockers) can increase risk of MI for unclear reasons; pregnancy class C

80mg tid, or 240mg SR qd

monitor weight, edema, BP

7
Q

clonidine

A

CNS alpha-2 agonist for anti-HTN, adjunct to Rx of opioid withdrawal, migraine prophylaxis

stimulates a-2 AR in the brainstem leading to a down-regulation of sympathetic outflow

onset 1h, duration 8h, F~85%; also available as skin patch

withdraw gradually to avoid rebound HTN; risk of bradycardia in sinus node dz; causes lethargy, fatigue, depression

additive effects with other anti-HTN; additive sedation with other CNS drugs

Pregnancy C; avoid in patients with renal insufficiency

begin w/ 0.1mg po bid, up to 1.2mg per day; transdermal begin with 0.1mg per 24h, 7 day patch

monitor BP, HR, fatigue

8
Q

Trimethaphan

A

** this drug is not used in treatment of HTN; know mechanism only***

blocks ganglionic transmission for anti-HTN

blocks nicotinic transmission in both sympathetic and parasympathetic ganglia (all Nn receptors); produces vaso + veno dilation

useful only IV; produces BP fall w/in minutes; partly metabolized, partly excreted by kidneys

caution re sudden, severe drop in BP or HR; systemic reduction in all sympathetic or parasympathetic responses

additive effects w/ other anti-HTN

makes patients miserable, so only use during general anesthesia; tilt patients to help control BP

given by iv only, and only to treat HTN crisis, or for controlled hypotension during surgery

monitor minute to minute BP and HR changes

9
Q

Reserpine

A

not used in long-term management of HTN; only know mechanism

Rauwolfia alkaloid for anti-HTN

binds to vesicles that contain NE or serotonin, preventing uptake, and ultimately depleting the neuron of NE or serotonin; this effect takes 203 weeks to develop, and including neurons and also the adrenal medulla

good oral bioavailability, but biological effects take 2-3 weeks

causes dizziness, orthostatic hypertension, depression

additive effects with most other anti-HTN

approved by the FDA in 1953; first anti-HTN ever approved

for HTN, 0.1-0.2mg every day

monitor BP, sympathetic tone, depression

10
Q

Atenolol

A

B1-AR selective blocker for anti-HTN, antiarrhythmic, primary, secondary prevention of MI, anti-anginal

binds to b-AR with preferences for B1 over B2 (at higher doses, also binds to B2), leading to lower BP via several mechanisms (lower CO, less RAAS); less effective preventing strokes

available po or iv, variable oral F; onset 1-2h, duration 12-24h, given once daily, excreted renally

can cause excessive hypotension, bradycardia, heart block to worsen CHF (but it is indicated for mild/moderate CHF); worsens bronchospasm in asthmatics

additive effects with other anti-HTN, additive AV block with CEBs (calcium entry blockers)

may be useful in HTN patients with exertional angina, MI, a fib; do not withdraw abruptly, taper down slowly; may not be a first line drug any longer (not recommended for monotherapy)

for HTN, 25-100mg qd or bid

monitor BP, HR, exercise tolerance

11
Q

Prazosin

A

a1-AR blocker for anti-HTN, treatment of BPH, Raynaud’s, kidney stones

blocks a1-AR on arterioles and veins, inhibits NE mediated vaso and venoconstriction

available po or transdermal; variable oral F (60%), onset 2h, duration 12-24h, extensive liver metabolization

can cause excessive hypotension with syncope, especially orthostatic hypotension; diuretics

additive effects with most other anti-HTN especially diuretics

start gradually, at bedtime, to avoid syncope; male patients with BPH(?)

as mono therapy being at 1mg did, advance to 20mg per day divided did

monitor BP, weight, edema

12
Q

Labetalol

A

alpha & beta-AR blocker for anti-HTN, treatment of CHF

reduces BP by blocker NE receptors, thereby lowering BP by several mechanisms; patients differ in beta vs alpha blockade

excellent absorption but high first-pass effect, leading to F~25%; onset 1-2h after po, 2-5m iv; extensively metabolized in liver by IID6

avoid in patients with bradycardia, heart block, CHF, asthma, shock; use caution in patients with cardiomyopathy, pheochromocytoma; Pregnancy D

additive effects with most anti-HTN

use reduced doses in patients with impaired liver fxn; dizziness is most troubling early side effect, most often used for HTN crises (as with nitroprusside)

commonly given iv in small boluses of 20mg, followed by continuous infusion at 2mg/m; not usually given po for chronic treatment (80mg tid, or 240mgSR qd)

monitor BP and HR