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Cardiovascular Unit > Hypertension Drugs > Flashcards

Hypertension Drugs Flashcards

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1
Q

what are the direct arterial vasodilators?

A

hydralazine, minoxidil, diazoxide, nitroprusside, fenoldopam

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2
Q

what mechanism do these drugs activate?

A

baroreceptor reflexes (due to potent reduction in perfusion pressure)

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3
Q

what is the effect of baroreceptor activation?

A

compensatory increase in sympathetic outflow, tachyphlaxis, reflex renin release

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4
Q

how can you counteract the reflex release of renin (d/t baroreceptor activation)

A

concurrent B-blocker administration

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5
Q

how does nitroprusside work?

A

G-cyclase converts GTP to cyclic GMP causing relaxation

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6
Q

what byproduct does nitroprusside produce?

A

cyanide. converted to thiocyanate in the liver, renal excretion.

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7
Q

adverse effects of direct arterial vasodilators?

A

sodium/water retention. tachycardia/angina

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8
Q

what specific side effect does hydralazine cause?

A

lupus-like syndrome

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9
Q

what specific side effect does minoxidil cause?

A

hair growth

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10
Q

with what other drug should direct arterial vasodilators be administered?

A

diuretic (thiazide) & B-blocker to reduce fluid retention and reflex tachy

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11
Q

what are the CCBs?

A

nifedipine, diltiazem, verapamil, amlodipine

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12
Q

what are the 2 CCB classes? which drugs are which?

A

dihydropyridines (nifedipine, amlodipine), non-dihydropyridines (verapamil, diltiazem)

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13
Q

what is the action of dihydropyridines?

A

baroreceptor-mediated reflex tachy d/t potent vasodilation. doesn’t alter AV node conduction

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14
Q

what is the action of non-dihydropyridines?

A

decrease HR, slow AV nodal conduction

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15
Q

adverse effects of all CCBs?

A

flushing, headaches

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16
Q

order of inotropic effects of CCBs?

A

verapamil > diltiazem > nefedipine

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17
Q

which CCB causes most constipation?

A

verapamil

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18
Q

which drug causes most edema?

A

nifedipine

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19
Q

which drug causes refractoriness?

A

nifedipine

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20
Q

which receptor causes increased contractility and HR?

A

beta 1

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21
Q

which receptor causes vasoconstriction in skin/viscera?

A

alpha 1

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22
Q

which receptor causes vasodilation in skeletal muscle/liver?

A

beta-2

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23
Q

which receptor causes bronchodilation?

A

beta-2

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24
Q

which receptor causes increased renin release?

A

beta 1, also alpha 1 somewhat

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25
what are the alpha 1&2 receptor blockers?
phenoxybenzamine, phentolamine
26
how do alpha receptor blockers work? what do they cause?
act on peripheral a receptors to inhibit smooth muscle catecholamine uptake in peripheral vasculature: vasodilation and BP lowering?
27
what are the a1 blockers?
prazosin, terazosin, doxazosin
28
what is the difference between a1&2 blockers and a1-selective blockers?
a1 have smaller increase in HR, don't stimulate renin release, doesn't block a2 so NE can inhibit its own release (neg feedback intact)
29
what side effect can happen with a1 blockers? how can you help this?
first dose effect: orthostatic hypOtension. transient dizziness, faintness, palpitations, syncope w/in 1-3 hrs of first dose. reflex tachy. take 1st dose at bedtime.
30
what are the B-blockers we know, and which receptors do they act on?
propranolol (B1&2), metoprolol (B1), atenolol (B1), labetalol (B1&2/a1)
31
where do B1 receptors act? effects?
heart, kidney. stimulation increases HR, contractility, renin release
32
where to B2 receptors act? effects?
lungs, liver, pancreas, arteriolar smooth muscle. bronchodliation and vasodilation. mediate insulin secretion and glycogenolysis.
33
generally, who do B blockers work best on?
young adults. in older adults, use in combination w diuretic
34
B1 selective blockers' use?
safer in patients w bronchospastic dz, peripheral arterial dz, diabetes. generally prefered.
35
potential adverse effects of B blockers?
glucose intolerance, masked hypoglycemia. bradycardia, dizziness. bronchospasm. increased trigs and decreased HDL. depression, fatigue, sleep disturbances. reduced CO, exacerbation of HF. impotence. exercise intolerance.
36
what are the central a2 agonists?
clonidine, guanabenz, a-methyldopa
37
effect of a2 agonists?
stimulate a2 receptors in brain: reduces sympathetic outflow from the brain's vasomotor center, increases vagal tone
38
AE of a2 agonists?
Na/H20 retention, rebound hypertension w abrupt discontinuation, depression, orthostatic hypotension + dizziness
39
specific AE of clonidine?
anticholinergic side effects
40
specific AE of methyldopa?
can cause hepatitis, hemolytic anemia (rare)
41
what are the neuronal & ganglionic blockers?
guanethidine, guanadrel, reserpine, trimethaphan
42
what are AE of reserpine and guanethidine?
sedation, depression and increased gastric acid secretion (reserpine) decreased CO, Na/H20 retention, diarrhea, bradycardia
43
how to use reserpine and guanethidine?
with diuretic (thiazide) to avoid fluid retention
44
what are the diuretics?
hydrocholorothiazide, furosemide, amiloride
45
how does BP drop w diuretics?
diuresis: reduced plasma and stroke vol decreases CO; causes compensatory increase in PVR
46
with chronic diuretic use, what happens to extracellular & plasma volume?
return to near pretreatment levels. PVR becomes lower than pretreatment values. results in chronic antiHTN effects.
47
potential AE of diuretics?
electrolyte disturbances (K esp, also Mg, Na, Ca); hyperglycemia, hypotension/orthostasis, ototoxicity, lipid abnormalities, photosensitivity, hyperuricemia & gout flare
48
aldosterone antagonist drugs? MOA?
spironolactone, eplerenone. inhibit renal (Na/H20 retention) and extra-renal (fibrosis, inflammation, etc) actions of aldosterone
49
what are the RAAS inhibitors?
aliskiren, losartan, captopril, enalapril, lisinopril
50
how do ACE inhibitors work? where is ACE located?
block ang I to ang II conversion. ACE is primarily in endothelial cells, but also BV (major site for ang II production)
51
what other important mediators do ACE inhibitors act on?
block bradykinin degradation: stimulate synthesis of other vasodilating substances like prostaglandin E2 and prostacyclin.
52
what helpful physical effect do ACE inhibitors have?
prevent or regress LVH
53
what do you have to monitor people on ACE inhibitors for?
serum K and SCr within 4 weeks of initiation or dose increase
54
what adverse effects do ACE inhibitors have?
cough (d/t bradykinin, 20%), angioedema, hyperkalemia (esp w CKD or DM), neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure
55
how are ARBs different from ACE inhibitors?
do not block bradykinin breakdown, so less cough.
56
adverse effects of ARBs?
orthostatic hypotension, renal insufficiency, hyperkalemia
57
role of AT1 vs AT2 receptors?
AT1: vasoconstriction, vasc proliferation, aldo secretion, cardiac myocyte proliferation, increased sympathetic tone. AT2: vasodilation, antiproliferation, apoptosis
58
how long do ARBs take to work?
1-2 months
59
what is the renin inhibitor? how does it work?
aliskiren. it inhibits the conversion of angiotensinogen to angiotensin 1. does not block bradykinin breakdown
60
aliskiren AE?
orthostatic hypotension, hyperkalemia
61
what are the 2 big ACE/ARB precautions?
acute kidney failure (if severe bilateral renal artery stenosis or severe stenosis in artery to solitary kidney), and pregancy
62
potential drug interactions with ACEs and ARBs?
meds that promote hyperkalemia, meds that have activity sensitive to changes in serum K, meds that can cause additive antihypertensive effects, and NSAIDs
63
what is some lifestyle modifications?
reduce BMI, DASH eating plan, reduce Na, increase exercise, reduce EtOH
64
new thing about JNC 8?
graded recommendations. address racial, CKD and diabetic subgroups.
65
JNC 7 vs 8 BP goals?
7 goal is <140/90 for all others
66
recommendations for general non-black population, including DM
JNC 7: first line is thiazide diuretics (no racial distinction) JNC 8 first line is thiazide, CCB, ACE-I, and ARBs
67
JNC8 black population recommendations for HTN?
CCB or Thiazide (grade B)
68
JNC8 DM patients recommendations for HTN?
thiazide, CCB, ACEi, ARB (grade B)
69
JNC8 CKD patients recommendations for HTN?
ACEi or ARB
70
JNC 8 treatment strategies (grade E)
if goal BP not met after 1 mo: increase dose or add a second (thiazide, CCB, ACEi, ARB) if goal BP not met after 2: add & titrate a third (thiazide, CCB, ACEi, ARB) but NOT ACE and ARB together
71
what strategy usually reduces LVH? what drugs do not?
aggressive BP control regresses LVH. but hydralazine and minoxidil do not!
72
what drugs may be better tolerated in the elderly (with isolated systolic HTN)
thiazide or CCB (not beta blockers)
73
what can you use during pregnancy? what can't you use?
methyldopa, beta-blockers, vasodilators (hydralazine). not ACEi or ARBs
74
what is resistant HTN?
failure to achieve BP goal on full doses of 3 drug regimen including a diuretic
75
what do you give for a hypertensive emergency?
sodium nitroprusside. fenoldopam. nitroglycerin. labetalol.
76
what do you give for eclampsia?
hydralazine

Cardiovascular Unit (16 decks)

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