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Cardiovascular Unit > Hypertension Drugs > Flashcards

Hypertension Drugs Flashcards

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
Q

what are the alpha 1&2 receptor blockers?

A

phenoxybenzamine, phentolamine

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26
Q

how do alpha receptor blockers work? what do they cause?

A

act on peripheral a receptors to inhibit smooth muscle catecholamine uptake in peripheral vasculature: vasodilation and BP lowering?

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27
Q

what are the a1 blockers?

A

prazosin, terazosin, doxazosin

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28
Q

what is the difference between a1&2 blockers and a1-selective blockers?

A

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)

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29
Q

what side effect can happen with a1 blockers? how can you help this?

A

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.

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30
Q

what are the B-blockers we know, and which receptors do they act on?

A

propranolol (B1&2), metoprolol (B1), atenolol (B1), labetalol (B1&2/a1)

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31
Q

where do B1 receptors act? effects?

A

heart, kidney. stimulation increases HR, contractility, renin release

32
Q

where to B2 receptors act? effects?

A

lungs, liver, pancreas, arteriolar smooth muscle. bronchodliation and vasodilation. mediate insulin secretion and glycogenolysis.

33
Q

generally, who do B blockers work best on?

A

young adults. in older adults, use in combination w diuretic

34
Q

B1 selective blockers’ use?

A

safer in patients w bronchospastic dz, peripheral arterial dz, diabetes. generally prefered.

35
Q

potential adverse effects of B blockers?

A

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
Q

what are the central a2 agonists?

A

clonidine, guanabenz, a-methyldopa

37
Q

effect of a2 agonists?

A

stimulate a2 receptors in brain: reduces sympathetic outflow from the brain’s vasomotor center, increases vagal tone

38
Q

AE of a2 agonists?

A

Na/H20 retention, rebound hypertension w abrupt discontinuation, depression, orthostatic hypotension + dizziness

39
Q

specific AE of clonidine?

A

anticholinergic side effects

40
Q

specific AE of methyldopa?

A

can cause hepatitis, hemolytic anemia (rare)

41
Q

what are the neuronal & ganglionic blockers?

A

guanethidine, guanadrel, reserpine, trimethaphan

42
Q

what are AE of reserpine and guanethidine?

A

sedation, depression and increased gastric acid secretion (reserpine)
decreased CO, Na/H20 retention, diarrhea, bradycardia

43
Q

how to use reserpine and guanethidine?

A

with diuretic (thiazide) to avoid fluid retention

44
Q

what are the diuretics?

A

hydrocholorothiazide, furosemide, amiloride

45
Q

how does BP drop w diuretics?

A

diuresis: reduced plasma and stroke vol decreases CO; causes compensatory increase in PVR

46
Q

with chronic diuretic use, what happens to extracellular & plasma volume?

A

return to near pretreatment levels. PVR becomes lower than pretreatment values. results in chronic antiHTN effects.

47
Q

potential AE of diuretics?

A

electrolyte disturbances (K esp, also Mg, Na, Ca); hyperglycemia, hypotension/orthostasis, ototoxicity, lipid abnormalities, photosensitivity, hyperuricemia & gout flare

48
Q

aldosterone antagonist drugs? MOA?

A

spironolactone, eplerenone. inhibit renal (Na/H20 retention) and extra-renal (fibrosis, inflammation, etc) actions of aldosterone

49
Q

what are the RAAS inhibitors?

A

aliskiren, losartan, captopril, enalapril, lisinopril

50
Q

how do ACE inhibitors work? where is ACE located?

A

block ang I to ang II conversion. ACE is primarily in endothelial cells, but also BV (major site for ang II production)

51
Q

what other important mediators do ACE inhibitors act on?

A

block bradykinin degradation: stimulate synthesis of other vasodilating substances like prostaglandin E2 and prostacyclin.

52
Q

what helpful physical effect do ACE inhibitors have?

A

prevent or regress LVH

53
Q

what do you have to monitor people on ACE inhibitors for?

A

serum K and SCr within 4 weeks of initiation or dose increase

54
Q

what adverse effects do ACE inhibitors have?

A

cough (d/t bradykinin, 20%), angioedema, hyperkalemia (esp w CKD or DM), neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure

55
Q

how are ARBs different from ACE inhibitors?

A

do not block bradykinin breakdown, so less cough.

56
Q

adverse effects of ARBs?

A

orthostatic hypotension, renal insufficiency, hyperkalemia

57
Q

role of AT1 vs AT2 receptors?

A

AT1: vasoconstriction, vasc proliferation, aldo secretion, cardiac myocyte proliferation, increased sympathetic tone. AT2: vasodilation, antiproliferation, apoptosis

58
Q

how long do ARBs take to work?

A

1-2 months

59
Q

what is the renin inhibitor? how does it work?

A

aliskiren. it inhibits the conversion of angiotensinogen to angiotensin 1. does not block bradykinin breakdown

60
Q

aliskiren AE?

A

orthostatic hypotension, hyperkalemia

61
Q

what are the 2 big ACE/ARB precautions?

A

acute kidney failure (if severe bilateral renal artery stenosis or severe stenosis in artery to solitary kidney), and pregancy

62
Q

potential drug interactions with ACEs and ARBs?

A

meds that promote hyperkalemia, meds that have activity sensitive to changes in serum K, meds that can cause additive antihypertensive effects, and NSAIDs

63
Q

what is some lifestyle modifications?

A

reduce BMI, DASH eating plan, reduce Na, increase exercise, reduce EtOH

64
Q

new thing about JNC 8?

A

graded recommendations. address racial, CKD and diabetic subgroups.

65
Q

JNC 7 vs 8 BP goals?

A

7 goal is <140/90 for all others

66
Q

recommendations for general non-black population, including DM

A

JNC 7: first line is thiazide diuretics (no racial distinction)
JNC 8 first line is thiazide, CCB, ACE-I, and ARBs

67
Q

JNC8 black population recommendations for HTN?

A

CCB or Thiazide (grade B)

68
Q

JNC8 DM patients recommendations for HTN?

A

thiazide, CCB, ACEi, ARB (grade B)

69
Q

JNC8 CKD patients recommendations for HTN?

A

ACEi or ARB

70
Q

JNC 8 treatment strategies (grade E)

A

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
Q

what strategy usually reduces LVH? what drugs do not?

A

aggressive BP control regresses LVH. but hydralazine and minoxidil do not!

72
Q

what drugs may be better tolerated in the elderly (with isolated systolic HTN)

A

thiazide or CCB (not beta blockers)

73
Q

what can you use during pregnancy? what can’t you use?

A

methyldopa, beta-blockers, vasodilators (hydralazine). not ACEi or ARBs

74
Q

what is resistant HTN?

A

failure to achieve BP goal on full doses of 3 drug regimen including a diuretic

75
Q

what do you give for a hypertensive emergency?

A

sodium nitroprusside. fenoldopam. nitroglycerin. labetalol.

76
Q

what do you give for eclampsia?

A

hydralazine

Cardiovascular Unit (16 decks)

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