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Pharm Exam 2

Cardiovascular

QuestionAnswer
acebutolol partial beta agonist
isoprotenerol beta 1 and beta 2 agonist
dobutamine beta 1 agonist
albuterol beta 2 agonist (short acting)
salmeterol beta 2 agonist (long acting)
propranolol beta 1 and beta 2 antagonist
nadolol beta 1 and 2 antagonist
atenolol beta 1 antagonist
metoprolol beta 1 antagonist
hydrochlorothiazide, chlorthalidone thiazide diuretics, prevent Na+ reabsorption in distal tubule, hypokalemia
furosemide lasix, loop diuretic, prevents Na+ reabsorption in loop of Henle
ethacrynic acid loop diuretic, prevents Na+ reabsorption in loop of Henle
spirinolactone postassium sparing diuretic, antagonist at mineralocorticoid receptor, reduced expression of basolateral Na-K ATPase; not strong enough to be used alone
triamterine potassium sparing diuretic, blocks Na+ channels in collecting duct by preventing exchange at principal cells
amiloride potassium sparing diuretic, blocks Na+ channels in collecting duct by preventing exchange at principal cells
clonidine alpha 2 receptor agonist
reserpine catecholamine release inhibitor
prazosin alpha 1 antagonist
terazosin alpha 1 antagonist
hydralazine vasodilator, causes opening of K+ channels to hyperpolarize cell which decreases liklihood of Ca2+ channels opening
minoxidil, diazoxide vasodilators, open K+ channels and hyperpolarized cells which decreases risk of opening of Ca2+ channels
verapimil cardioselective CCB, relax vascular smooth muscle AND dec CO, dec AV nodal conduction, dec force of contraction
amlodipine long acting non-cardioselective CCB, safer
captopril ACEI
enalopril ACEI
losartan ARB
valsartan ARB
aliskerin renin inhibitor
ACEI block conversion of agn 1 to agn 2; inhibits metabolism of bradykinins (inflam mediators) so you get pro-inflam effects (angioedema, dry cough), hyperkalemia, never use in pregnancy
ARB antagonist at agn receptors, no effects on bradykinin metabolism (no cough, angioedema), never use in pregnancy
heparin IV anti-coag, stimulates antithrombin III system which regulates synthesis of clotting factors
warfarin prevents reactivation of vitamin K (cannot syn. clotting factors without vit K) - slower effect because wait for turnover of current clotting factors, never use in pregnancy
altepase t-PA activator drug
t-PA produces plasmin which destroys fibrin (breaks down clot)
streptokinase t-PA activator drug
aspirin anti-thrombotic, inhibits COX1 which reduce TXA2 synthesis (pro-clotting prostaglandin)
enoxaparin low molecular weight heparin
clopidogril anti-thrombotic, prevents ADP from bind to platelet, discourages platelet aggregation, more expensive than aspirin
abciximab GP2b/3a antibody (receptor blocker) that prevents platelet aggregation, platelet receptor antagonist to prevent physical contact between platelets
aspirin prophylaxis lowest dose 75-150 mg (baby aspirin is 81 mg); only to high risk people!! At time of MI, give 160 mg
APTT assess bleeding risk for patients on heparin
PT assess bleeding risk for patients on warfarin
anti-fibrinolytics prevents plasmin formation so clots cannot be broken down (opposite of t-PA)
vitamin K reverse effects of warfarin
protamine reverse effects of heparin
hemostatic aids facilitate natural hemostatic process; vasoconstrictors, clotting factors, collagen sheets
VLDL carrier of TGs
Niacin good for decreasing VLDLs (TG) by stimulating lipoprotein lipas, increased HDLs too
fibric acid derivatives decrease VLDL synthesis in the liver
gemfibrozil fibric acid derivative, decreases VLDL synthesis by breaking down VLDL
bile acid binding resins prevent bile acid reabsorption into the liver, body converts cholesterol to bile acid and takes it to SI so if we prevent reabsorption, body thinks it needs to make more bile acids and thus pulls more cholesterol out of the blood into cells; upreg recepto
colestipol bile acid binding resin
statins prevent cholesterol synthesis by inhibiting HMG CoA reductase so liver cells upregulate receptors because they don't synthesize it, brings more in from the blood
rhabdo side effect of statin, breakdown of skeletal smooth muscle, can plug up the glomerulus and cause kidney failiure, liver toxicity
ezetimibe aka zetia, prevents absorption of cholesterol from diet and reduced re-absorption of cholesterol secreted in bile, upregulates LDL receptors to lower LDL levels in blood
risk categories and LDL levels to start drugs low = 190, moderate = 160, moderate/high = 130, high = 100
vasodilators used to treat angina pectoris nitroglycerin, isososorbide dinitrate; CCBs
ideal vasodilator for angina dilation of veins, dilation of coronaries BUT dilating arterioloes DOES NOTHING!! (except shunt blood away from bigger arteries that need it)
digoxin Na/K ATPase inhibitor, increased contractility, bradycardia, slow AV nodal conduction
dobutamine beta 1 agonist
milrinone biryidine, increases cAMP and intracellular Ca2+ to increase contractility and vasodilate
ACEI for CHF relax vascular smooth muscle, dilate veins to decrease preload, reduce aldosterone secretion to lower BV (reduce preload) and prevent hypertrophy and remodeling
diuretics for CHF HCTZ, furosemide, spironolactone; good for decrease preload (prevent Na+ reabsorption), good for edema and preventing hypertrophy; often used in combo with ACEI
beta blockers for CHF metoprolol, carvedilol to decrease CO, decrease mortality, slow HR, prevent secretion of catecholamines
carvedilol beta and alpha 1 antagonist
vasodilators for CHF isososorbide dinitrate, hydralizine, BNP
BNP reduces preload and afterload, vasodilator for veins AND arteries, increases diuresis
Created by: RLeman
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