Exam 7 Pharmacology Part 1

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Can you name the Drugs for Exam 7 Pharmacology Part 1?

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Molecular ActionDrugDisease or Use
Inhibits the carboxylation of glutamate residues in Vitamin K-dependent clotting factorsVenous thromboembolic diseases, prevention of thromboembolism from atrial fibrillation, and others
Irreversible cyclo-oxygenase (1 and 2) inhibition; inhibition of platelet activationArterial thrombotic diseases, primary prevention of arterial thrombi
Accelerates inactivation of thrombin (factor IIa)Venous thromboembolism, cardiac vascular surgery, treatment of MI and unstable angina
(2) Block sodium channels in collecting ductPrevent hypokalemia during diuretic therapy
(2) Accelerates inactivation of factor XaVenous thromboembolism, cardiac vascular surgery, treatment of MI and unstable angina
(2) Cleave fibrin to resolve clotAcute myocardial infarction, acute ischemic stroke, acute pulmonary embolism, and others
Inhibits VLDL synthesis raising HDL - largest increase in HDL, small reduction in LDL, larger reduction in triglyceridesHypercholesterolemia (esp. with low HDL)
(2) Thrombin inhibitorsHigh risk angioplasty and HIT for 1, primary prevention of TE from Afib for other
Blocks intestinal transport of cholesterol, modest reduction in LDL, no change in HDLHypercholesterolemia
(2) Mineralocorticoid (aldosterone) receptor antagonistsPrevent hypokalemia during diuretic therapy, congestive heart failure, post-myocardial infarction prophylaxis against the development of congestive heart failure
(2) Blockers of GPIIb/IIIa receptor, inhibition of platelet aggregationPrevention of reocclusion after treatment of MI
Molecular ActionDrugDisease or Use
Increases osmolarity of extracellular fluid, washes out countercurrent multiplierRapid excretion of renal toxins and other toxins, cerebral edema, acute angle closure glaucoma
Inhibition of cyclic nucleotide phosphodiesterase; inhibition of platelet activationArterial thrombotic diseases (in combination)
(2) Inhibit sodium-chloride cotransport in distal tubule (elimination of Na+ and water), direct arterial vasodilation (reduced blood pressure)Primary drug for hypertension in most cases, mild congestive heart failure
(2) Activate PPAR-alpha --> inc. lipoprotein lipase activity, red. TG synthesis, increased β-oxidation of FAs, small red. in LDL, larger red. in TGs, mod. inc. in HDLHypercholesterolemia
(2) Antagonists of P2T purinergic receptor; inhibition of platelet aggregationPrevention of arterial thrombi, especially after treatment of MI
(2) Prevent binding of fibrinogen to thrombinThrombolytic therapy, heparin-induced thrombocytopenia
(2) Bind bile acids in intestine, modest reduction in LDL, little increase in HDLHypercholesterolemia (like fiber but better)
(6) Inhibit HMGCoA reductase, greatest reduction in LDL, little increase in HDLHypercholesterolemia
Monoclonal antibody directed against GPIIb/IIIa receptor, inhibition of platelet aggregationPrevention of reocclusion after treatment of MI
Inhibits NKCC2 cotransporter in thick ascending limb, stimulates NO/prostaglandin synthesis in veins, renal afferent arteriole, and to a lesser extent in other arteries. Dilates.Acute decompensated and chronic congestive heart failure, chronic renal insufficiency

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