Antihypertensives Flashcards
1
Q
diuretics in hypertension
A
- most popular anti-hypertensives
- hydrochlorothiazide, chlorthalidone
- increase in BP-> sodium accumulates in vascular smooth muscle and then exchanges for Ca which increase tone
- diuretics increase Na loss
- replace fluid-> no changes in BP
- replace salt-> increase BP
2
Q
use of diuretics in increase BP
A
- lower BP when used alone
- prevent false tolerance (increase BP which occurs with other anti-hypertensive drugs)
- prevent sodium accumulation
- good for elderly
- beta-blockers for young caucasian
3
Q
want to watch out for when using diuretics in increased BP
A
-beware of high blood lipids, increase glucose can block insulin release, potassium depletion due to high sodium in collecting duct and don’t give aspirin
4
Q
alpha-2 stimulants in HTN
A
alpha-2 adrenergic receptors
- mainly on nerve ends
- inhibits release of NT
- decrease sympathetic outflow from brainstem by acting on alpha-2 receptors
- decrease NE release heart and blood vessels
- baroreceptors still functional
5
Q
alpha-2 stimulant drugs
A
- alpha methyl DOPA
2. clonidine
6
Q
alpha methyl DOPA
A
- first on market
- irregular absorption
7
Q
clonidine
A
- good bioavailability but complex CNS effects
- also used in opiate withdrawal
8
Q
side effects of alpha-2 stimulants
A
- decrease mental acuity
- nightmares
- CNS depression
- dry mouth in 50%
- rebound increase BP on abrupt cessation of therapy
9
Q
vasodilators nin HTN
A
- hydralazine release NO to increase cyclic GMP and dilate arteries
- reflex tachycardia (desirable in pregnancy)
- some nausea, lupus in 15% (in slow acetylators)
- slow and fast acetylators
- contrast with alpha-blockers (which dilate arteries and veins, less postural hypotension)
10
Q
minoxidol in HTN
A
- dilates arteries (skin, sk. mm, heart, GI)
- use with beta-blocker, and diuretic
- opens ATP-sensitive potassium channels-> hyperpolization
- severe reflex tachycardia
- sodium retention (increase renin), also increase Na reabsorption in proximal tubule
- powerful, resistant in increase BP
- hair growth (hirsutism) (rogaine)
11
Q
ACE inhibitors
A
well tolerated
- captopril (8 hr duration)
- enalapril (24 hr duration)
12
Q
MOA of ACE inhibitors
A
- block formation of angiotensin II
- end product inhibition by analogs of 2aa fragment
- less angio II-> less vasoconstriction
- less aldosterone-> sodium loss
- block bradykinin metabolism-> vasodilation
13
Q
advantages in ACE inhibitors
A
- increase kidney blood flow: release PGE2, synergistic with diuretics
- good in elderly
- like beta-blockers, prevent 2nd heart attack
- no reflex tachycardia
- no CNS depression
- abrupt withdrawal no problem
14
Q
precautions with ACE inhibitors
A
- Chronic non-productive cough, ACE high in lungs
- Bad in pregnancy
- oligohydramnios (decrease amniotic fluid): fetal decrease in BP, and renal failure in 2nd/3rd trimester
- face/limb deformities in 1st trimester - prodrugs don’t work in patients with bad liver
- loss of taste with captopril
- severe allergic reactions 1st dose
15
Q
angiotensin II receptor blockers (ARB’s)
A
- competitive block of angiotensin II-1 receptor, little block of AT 2 receptor
- less cough, less angioedema
