101414 HTN pharm Flashcards
what is the JNC 8 recommendation for target BPs for pts over 60?
below 150 systolic and 90 diastolic (thought that higher BP was necessary for elderly to keep blood flow to vital organs)
anti hypertensive drugs classification
vasodilators
agents affecting adrenergic fxn
agents affecting renin angiotensin system
diuretics
effect of vasodilators
decreases peripheral arterial resistance, decreasing BP
baroreceptor activation can cause compensatory increase in sympathetic outflow. increases HR. reflex release of renin.
direct arterial vasodilators ex
hydralazine minoxidil diazoxide nitroprusside fenoldopam
how do you counteract the compensatory reflexes created by direct arterial vasodilators?
give concurrent beta blocker
hypertensive crisis is
BP over 180/120 mmHg
you will want to reduce the BP gradually
hypertensive urgency
elevated BP
no acute or progressing target-organ injury
hypertensive emergency
acute or progressing target organ damage (encephalopathy, intracrnial hemorrhage, acute left ventricular failure with pumonary edema, dissecting aortic aneurysm, unstable angina, eclampsia)
how should you approach hypertensive emergency?
treat quickly but not too quickly b/c if lower BP too fast, will get low perfusion to organs
MOA of nitric oxide donors
they form NO, which results in formation of cGMP, which activates protein kinase G to affect calcium and promote relaxation
what part of the vasculaure do nitric oxide donors work on?
primarily arterial but has venous component
ex of nitric oxide donor
nitroprusside
what is a side effect of nitroprusside
cyanide toxicity, so don’t want to use this for a long time
adverse effects of direct arterial vasodilators
sodium/water retention
tachycardia/angina
hydralazine-lupus like syndrome
minoxidil-hair growth
how do you prevent some of the side effects of direct arterial vasodilators?
use with diuretic (preferably thiazide) and beta blocker to reduce fluid retention and reflex tachycardia
effect of calcium ch blocker
decreases vascular tone to decrease BP
will see small increase in HR
ex of calcium channel blockers
nifedipine
diltiazem
verapamil
amlodipine
effects of dihydropyridines
baroreceptor mediated reflex tachycardia due to potent vasodilating effects
do NOT alter conduction through AV node
effects of non-dihydropyridines
decrease HR and slow AV node conduction
side effects of calcium ch blockers
flushing
headaches
negative ionotropic effect (greatest in verapamil)
constipation (greater in verapamil)
decreased AV conduction (greater in verapamil and diltiazem)
edema (greatest in nifedipine)
refractoriness (nifedipine)
vasoconstriction of arterioles in skin and viscera is mediated by which adrenergic receptor
alpha 1
vasodilation of skeletal muscle and liver arterioles is mediated by which adrenergic receptor
beta 2
bronchodilation is mediated by which adrenergic receptor
beta 2
increased renin secretion is mediated by which adrenergic receptor
alpha 1, beta 1
effect of alpha1/alpha2 combined blockers
decreases vascular tone
alpha 2 blocking- causes decreased venous tone
increases HR
effect of alpha1 blockers
decreases peripheral resistance
increases HR
ex of alpha 1 blockers
prazosin
alpha1 or alpha1/alpha2 blockers are more effective for anti-HTN?
alpha1 because of the lack of inhibition of alpha2 to inhibit NE release
what is the effect of alpha1 blockers on HR and renin release?
increase, but smaller increase than for alpha1/alpha2 blocker
don’t stimulate renin release
what is the first dose effect?
with alpha1 blockers-
the first dose–can get orthostatic hypotension. transient dizziness, palpitations, syncope within 1-3 hrs. reflex tachycardia.
how do you minimize the first dose effect?
use alpha1 blocker at bedtime
compare alpha1 blocker and mixed alpha1/beta blocker in terms of side effects
prazosin-orthostatic hypotension. headaches/dizziness.
labetalol/carvedilol-are alpha1 and beta1/beta2 blockers. mild orthostatic hypotension and headaches.
effect of beta blockers
decrease renin, decreasing peripheral resistance
decrease HR
ex of beta1 blockers
metoprolol
atenolol
where are beta2 receptors found
lungs
liver
pancreas
arteriolar smooth muscle
stimulation causes bronchodilation and vasodilation
mediate insulin secretion and glycogenolysis
why do beta blockers work better in young adults
because CO has a greater contribution to BP in younger adults
potential adverse effects of beta blockers
glucose intolerance, masked hypoglycemia
bradycardia, dizziness
bronchospasm
increased TGs and decreased HDL
CNS-depression, fatigue, sleep disturbance
reduced CO, exacerbation of heart failure
impotence
exercise intolerance
central alpha2 agonists’ effect
work on CNS to decrease sympathetic nervous sys
increases vagal tone
decreases vascular tone
decreases renin
DECREASES HR
ex of central alpha2 agonists
clonidine
guanabenz
alpha-methyldopa
adverse effects of central alpha2 agonists
sodium/water retention abrupt discontinuation may cause rebound HTN depression orthostatic hypotension dizziness
effects of neuronal and ganglionic blocking agents
decreases sympathetic nerv sys activity-decrease renin, decreases HR
ex of neuronal and ganglionic blockers
guanethidine
guanadrel
reserpine
trimethaphan
side effects of reserpine and guanethidine
sedation (reserpine) depression (reserpine) decreased CO sodium and water retention increased gastric acid secretion (reserpine) diarrhea bradycardia
use with diuretic (preferably thiazinde) to avoid fluid retention
effect of diuretics
decrease vascular volume, decreasing venous retruen and CO
cause compensatory increase in peripheral vascular resistance
side effects of diuretics
electrolyte disturbances hyperglycemia hypotension, orthostasis lipid abnormalities photosensitiity ototoxicity hyperuricemia, gout
aldosterone antagonists MOA
inhibit renal action of aldosterone (Na and water retention)
inhibit extrarenal action of aldosterone (fibrosis, inflammation)
ACE inhibitors, AT1 blockers, renin inhibitors effects
decrease vascular tone
decrease aldosterone to decrease venous return
what should yoo monitor with ACE inhibitors?
serum K and creatinine within 4 wks of initation or dose increase
adverse effects of ACE inhibitors
cough
angioedema
hyperkalemia
acute renal failure
AT1 receptor effects
vasoconstriction vascular proliferation aldosterone secretion cardiac myocyte proliferation increased sympath tone
AT2 receptor effects
vasodilation
antoproliferation
apoptosis
when do you see the maximal effect with losartan?
after 6 wks
note-renin angitensin system agents take time to see effects!
what are side effects for all renin angiotensin system inhibitors?
orthostatic hypotension
hyperkalemia
precautions for ACE inhibitors/ARB
can cause acute kidney failure in certain pts (bilateral renal artery stenosis)
pregnancy
what is a benefit of combo therapy?
diuretic decreases Na and will increase renin. so if you give an ARB, can counteract
can reduce BP further than with solo agents
what are some mixed vasodilators
nitroprusside ACE inhibitors and ARBs alpha adrenergic blockers alpha2 central agonists nesiritide ( no longer recommmended)
graded recommendations are used in JNC8 or 7?
8
race, CKD, and diabetic subgroups are addressed in JNC 8or 7?
8
what is recommended for the general population for treating HTN in JNC8
thiazide, CCB, ACEi, ARB
recommendation for black population in JNC8 in treating HTN?
CCB or thiazide
if goal of BP isn’t met after 1 month of treatment, according to JNC8, what should you do
increase dose of initial drug or
add second drug
what do African Am have increased risk of as side effect?
angioedema
what should be avoided in pregnancy?
ACEi and ARBs
in combo therapy, what should one of the agents be?
thiazide unless contraindicated
a diuretic (preferably thiazide)
in a hypertensive emergency, what is given?
sodium nitroprusside (adverse effect is cyanide toxicity) fenoldopam
esmolol, labetalol
