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Cardiovascular > Hypertension Pharmacology > Flashcards

Hypertension Pharmacology Flashcards

(51 cards)

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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

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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

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A

block beta receptors and some alpha-1 receptors

23
Q

drugs affecting the RAAS

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A

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

ARBs - losartan, candesartan, irbesartan, valsartan

24
Q

mechanism of action of ACE inhibitors

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A

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

25
mechanism of action of ARBs
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
effects of ACE inhibitors and ARBs
decreased intravascular volume possible increase in cardiac output decreased peripheral vascular resistance
27
side effects of ACE inhibitors
cough, hyperkalemia, renal failure, fetal toxicity, angioedema
28
side effects of ARBs
hyperkalemia renal failure fetal toxicity rare angioedema and no cough
29
ACE-I/ARB treatment population
hypertensive patients, particularly those with heart failure, diabets/proteinuria, or CAD/post MI
30
effects of efferent arteriole constriction
increased glomerular capillary pressure decreased peritubular capillary pressure decreased nephrone plasma flow but increases GFR
31
effects of efferent arteriole dilation
decreased glomerular capillary pressure increased peritubular capillary pressure increased nephron plasma flow decreased GFR
32
types of calcium channel blockers
phenylalkylamines benzothiazepine dihydropyridine
33
CCB mechanism of action
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
dihydropyridine vs. non-dihydropyridine classes of CCBs
dihydropyridines - more peripheral effect non-dihydropyridines - also affect the smooth muscles but have varying effects on the heart
35
dihydropyridines
nifedipine, amlodipine, felodipine, nisoldipine, nitrendipine large decrease in peripheral vascular resistance some increase in cardiac output metabolized by the CP-450 system
36
side effects of dihydropyridines
heaches flushing dizziness GERD constipation peripheral edema
37
benzothiazepine
diltiazem decreases cardiac output decreases peripheral vascular resistance metabolized by the CP-450 system may inhibit the clearance of other drugs
38
side effects of benzothiazepine
edema headache nausea dizziness constipation diarrhea bradycardia
39
phenylalkylamines
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
target population of CCBs
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
peripheral vasodilators
hydralazine minoxidil sodium nitroprusside
42
hydralazine mechanism of action
lowers blood pressure through relaxation of arteriolar smooth muscle
43
minoxidil mechanism of action
activates a potassium channel in vascular smooth muscle, causing K+ efflux which hyperpolarizes and relaxes smooth muscle cells
44
nitroprusside mechanism of action
metabolized by blood vessels to nitric oxide nitric oxide activates guanyl cyclase which makes cGMP and vasodilates the blood vessels
45
effects of peripheral vasodilators
increased intravascular volume increased cardiac output **major** decrease in peripheral vascular resistance
46
side effects of hydralazine
headache nausea flushing angina edema/heart failure drug induced lupus
47
side effects of minoxidil
sodium and H2O retention tachycardia/angina/heart failure hypertrichosis effusions
48
side effects of nitroprusside
hypotension cyanide and thicyanate toxicity manifests as severe lactic acidosis anorexia fatigue confusion psychosis
49
target population of peripheral vasodilators
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
aliskiren
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
treating hypertensive emergencies
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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