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Flashcards in Hypertension Pharmacology Deck (51)
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1

diuretics mechanism of action

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

2

distal convoluted tubule diuretics

thiazides such as hydrochlorothiazide, chlorthalidone, or metalazone

3

loop diuretics

furosemide, bumetanide, thacrynic acid

4

K+ sparing diuretics

spironolactone, epelrenone, triamterene, amiloride

5

mechanism of thiazide diuretics

inhibits the Na/Cl symporter in the distal convoluted tubule

6

side effects of distal convoluted tubule diuretics

impotence

fluid and electrolyte imbalances

impaired glucose tolerance

increased cholesterol

hyperkalemia

hyponatriemia,

hypercalcemia

7

mechanism of loop diuretics

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

8

side-effects of loop diuretics

fluid and electrolyte imbalances

volume depletion

ototoxicity

hyperuricemia

hyperglycemia

increased LDL and triglycerides

9

mechanism of K+ sparing diuretics

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

10

side effects of K+ sparing diuretics

amiloride and triamterene - hypokalemia, nausea

spironolactone - hyperkalemia, gynecomastia

11

using diuretics as treatment

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

 

12

types of sympatholytic drugs

centrally acting

alpha-adrenergic receptor antagonists

beta-receptor antagonists (blockers)

13

centrally acting sympatholytics

methyldopa, clonidine, guanabenz

14

mechanism of methyldopa

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

15

mechanism of clonidine

stimulates the centrally located alpha2-receptor

16

side effects of centrally acting agents

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

17

alpha1-receptor blockers

prazosin, terazosin, doxazosin

blocks the alpha1-receptor

18

main effect of alpha-1 blockers

decreased peripheral vascular resistance

19

side effects of alpha1-receptor blockers

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

20

beta-blocker mechanism of action

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)

21

side effects of beta-blockers

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

labetolol and carvedilol

block beta receptors and some alpha-1 receptors

23

drugs affecting the RAAS

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

ARBs - losartan, candesartan, irbesartan, valsartan

24

mechanism of action of ACE inhibitors

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