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Cardiovascular > Hypertension Pharmacology > Flashcards

Hypertension Pharmacology Flashcards

1
Q

diuretics mechanism of action

A

reduction of extracellular volume and cardiac output

alteration of total body sodium is believed to cause decreased vascular resistance

decrease in plasma volume of 5% corresponds to effective treatment

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2
Q

distal convoluted tubule diuretics

A

thiazides such as hydrochlorothiazide, chlorthalidone, or metalazone

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3
Q

loop diuretics

A

furosemide, bumetanide, thacrynic acid

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4
Q

K+ sparing diuretics

A

spironolactone, epelrenone, triamterene, amiloride

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5
Q

mechanism of thiazide diuretics

A

inhibits the Na/Cl symporter in the distal convoluted tubule

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6
Q

side effects of distal convoluted tubule diuretics

A

impotence

fluid and electrolyte imbalances

impaired glucose tolerance

increased cholesterol

hyperkalemia

hyponatriemia,

hypercalcemia

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7
Q

mechanism of loop diuretics

A

furosemide, torsemide, bumetanide

inhibits the Na/K/2Cl symporter in the thick ascending limb of the loop of Henle

used for volume ovefrload, especially in chronic kidney disease patients

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8
Q

side-effects of loop diuretics

A

fluid and electrolyte imbalances

volume depletion

ototoxicity

hyperuricemia

hyperglycemia

increased LDL and triglycerides

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9
Q

mechanism of K+ sparing diuretics

A

triamterene, amiloride, spironolactone

triamterene and amiloride inhibit renal empithelial Na channels in the late distal tubule and collecting duct

spironolactone and eplerenone antagonize the mineralcorticoid receptor on epithelial cells in the late distal tubule and collecting duct

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10
Q

side effects of K+ sparing diuretics

A

amiloride and triamterene - hypokalemia, nausea

spironolactone - hyperkalemia, gynecomastia

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11
Q

using diuretics as treatment

A

proven efficacy and safety

often a first line treatment

avoid hypokalemia as the reduction in mortality from using diuretics is reduced if the diuretic causes the patient to have hypokalemia

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12
Q

types of sympatholytic drugs

A

centrally acting

alpha-adrenergic receptor antagonists

beta-receptor antagonists (blockers)

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13
Q

centrally acting sympatholytics

A

methyldopa, clonidine, guanabenz

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14
Q

mechanism of methyldopa

A

replaces norepinephrine in secretory vesicles of adrenergic neurons

although it is a potent vasoconstrictor, it acts centrally on the brain to inhibit central adrenergic outflow

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15
Q

mechanism of clonidine

A

stimulates the centrally located alpha2-receptor

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16
Q

side effects of centrally acting agents

A

methyldopa - sedation, dry mouth, decreased energy, depression, liver toxicity

clonidine, guanabenz, guanfacine - sedation/somnlocence, dry mouth, depression, bradycardia, withdrawal if high doses are stopped suddenly

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17
Q

alpha1-receptor blockers

A

prazosin, terazosin, doxazosin

blocks the alpha1-receptor

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18
Q

main effect of alpha-1 blockers

A

decreased peripheral vascular resistance

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19
Q

side effects of alpha1-receptor blockers

A

first dose phenomenon of orthostatic hypotension

water retention

possible CHF when given as monotherapy

usually used in conjunction with other agents for treatment of hypertension, primarily beta-blockers

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20
Q

beta-blocker mechanism of action

A

atenolol, metobrolol - selective beta1 blockers

propranolol, timolol - beta1 and beta2 blockers

beta1 blockade leads to slower heart rate and decreased contractility, which decreases renin release

beta2 blockade leads to bronchoconstriction, slight increase in peripheral vascular resistance (slight vasodilation)

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21
Q

side effects of beta-blockers

A

bradycardia, hyperkalemia, fatigue, cold extremities, and bronchospasm

may have adverse effect on lipid panel, and blunt symptoms of hypoglycemia

used preferably in patients with CAD, not for sole use in patietns with hypertension and heart failure

22
Q

labetolol and carvedilol

A

block beta receptors and some alpha-1 receptors

23
Q

drugs affecting the RAAS

A

ACE inhibitors - catopril, enalapril, lisinopril, quinapril, ramipril, benazepril, fosinopril

ARBs - losartan, candesartan, irbesartan, valsartan

24
Q

mechanism of action of ACE inhibitors

A

block the conversion of angiotensin I to the active angiotensin II by inhibiting ACE

25
Q

mechanism of action of ARBs

A

block the angiotensin II receptor type I

found in myocrdial tissue, brain, and kidney, smooth muscle cells, and adrenal glomerulosa cells

difference from ACE inhibitors is that it leads to decreased bradykinin

inhibits angiotensin less than ACE inhibitors as well

26
Q

effects of ACE inhibitors and ARBs

A

decreased intravascular volume

possible increase in cardiac output

decreased peripheral vascular resistance

27
Q

side effects of ACE inhibitors

A

cough, hyperkalemia, renal failure, fetal toxicity, angioedema

28
Q

side effects of ARBs

A

hyperkalemia

renal failure

fetal toxicity

rare angioedema and no cough

29
Q

ACE-I/ARB treatment population

A

hypertensive patients, particularly those with heart failure, diabets/proteinuria, or CAD/post MI

30
Q

effects of efferent arteriole constriction

A

increased glomerular capillary pressure

decreased peritubular capillary pressure

decreased nephrone plasma flow but increases GFR

31
Q

effects of efferent arteriole dilation

A

decreased glomerular capillary pressure

increased peritubular capillary pressure

increased nephron plasma flow

decreased GFR

32
Q

types of calcium channel blockers

A

phenylalkylamines

benzothiazepine

dihydropyridine

33
Q

CCB mechanism of action

A

block the L-type calcium channel preventing the influx of calcium

since contraction of the smooth muscle is dependent on calcium, less intracellular calcium results in less contraction

decreases peripheral vascular resistance

34
Q

dihydropyridine vs. non-dihydropyridine classes of CCBs

A

dihydropyridines - more peripheral effect

non-dihydropyridines - also affect the smooth muscles but have varying effects on the heart

35
Q

dihydropyridines

A

nifedipine, amlodipine, felodipine, nisoldipine, nitrendipine

large decrease in peripheral vascular resistance

some increase in cardiac output

metabolized by the CP-450 system

36
Q

side effects of dihydropyridines

A

heaches

flushing

dizziness

GERD

constipation

peripheral edema

37
Q

benzothiazepine

A

diltiazem

decreases cardiac output

decreases peripheral vascular resistance

metabolized by the CP-450 system

may inhibit the clearance of other drugs

38
Q

side effects of benzothiazepine

A

edema

headache

nausea

dizziness

constipation

diarrhea

bradycardia

39
Q

phenylalkylamines

A

verapamil

decreases cardiac output

decreases vascular resistance but not as much as diltiazem

metabolized by the CP-450 system

may inhibit clearance of other drugs

40
Q

target population of CCBs

A

safe in patients with diabetes, renal insufficiency, lipid problems, and asthma

use with caution in patietns with heart disease and conduction abnormalities

possibly synergistic with other agents, so it is a good add-on therapy

41
Q

peripheral vasodilators

A

hydralazine

minoxidil

sodium nitroprusside

42
Q

hydralazine mechanism of action

A

lowers blood pressure through relaxation of arteriolar smooth muscle

43
Q

minoxidil mechanism of action

A

activates a potassium channel in vascular smooth muscle, causing K+ efflux which hyperpolarizes and relaxes smooth muscle cells

44
Q

nitroprusside mechanism of action

A

metabolized by blood vessels to nitric oxide

nitric oxide activates guanyl cyclase which makes cGMP and vasodilates the blood vessels

45
Q

effects of peripheral vasodilators

A

increased intravascular volume

increased cardiac output

major decrease in peripheral vascular resistance

46
Q

side effects of hydralazine

A

headache

nausea

flushing

angina

edema/heart failure

drug induced lupus

47
Q

side effects of minoxidil

A

sodium and H2O retention

tachycardia/angina/heart failure

hypertrichosis

effusions

48
Q

side effects of nitroprusside

A

hypotension

cyanide and thicyanate toxicity

manifests as severe lactic acidosis

anorexia

fatigue

confusion

psychosis

49
Q

target population of peripheral vasodilators

A

used in patients with difficult to control blood pressure

often on multiple agents, which allows some control of the side effects of the vasodilators

50
Q

aliskiren

A

a direct renin inhibitor

can cause dizziness, hyperkalemia, and rash

should be used in people who have resistant hypertension or intolerant of other medication

51
Q

treating hypertensive emergencies

A

look for end organ damage - CNS, heart, kidneys, eyes

lower BP by about 20% from the mean arterial BP presentation to prevent ischemia

agents - nitroprusside, labetolol, hydralazine, enalaprilat, nicardipine

Cardiovascular (46 decks)

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