Duke Med Exam 7 Drug List

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Mechanism and/or ActionDrugDisease or Use
Inhibits NKCC2 cotransporter in thick ascending limb, stimulates NO/prostaglandin synthesis in veins, renal afferent arteriole, and to a lesser extent in other arteries, dilation oAcute decompensated and chronic congestive heart failure, chronic renal insufficiency
Monoclonal antibody directed against GPIIb/IIIa receptor, inhibition of platelet aggregationPrevention of reocclusion after treatment of MI
Inhibits angiotensin-converting enzyme (ACE), arterial vasodilation, reverses cardiac and arterial remodeling, reduced aldosterone secretionHypertension (primary drug in cases of diabetes, post-MI, and chronic renal disease), post-MI prophylaxis against the development of congestive heart failure, systolic and diastolic congestive heart failure
Bind bile acids in intestine, modest reduction in LDL, little increase in HDLHypercholesterolemia
β1 antagonist/increases NO availability, reduces inotropy and chronotropy, vasodilation, anti-remodeling activityHypertension (esp. in persons who experience exercise intolerance or sexual dysfunction when treated with another beta blocker), diastolic congestive heart failure, stable angina
Activate PPARalpha leading to increased lipoprotein lipase activity, reduced triglyceride synthesis, increased β-oxidation of fatty acids, small reduction in LDL, larger reductionHypercholesterolemia
Thrombin inhibitorsHigh-risk angioplasty and haparin-induced thrombocytopenia, primary prevention of thromboembolism from atrial fibrillation
Antagonists of P2T purinergic receptor; inhibition of platelet aggregationPrevention of arterial thrombi, especially after treatment of MI
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
Block cardiac and vascular L-type calcium channels, stabilize inactivated state of those calcium channels, arterial vasodilation, reduce inotropy and chronotropy, reduce myocardialStable angina (as alternative to beta blocker esp. in persons with persistent asthma), diastolic congestive heart failure (as alternative to beta blocker esp. in persons with persistent asthma), supraventricular tachyarrhythmias
β1-selective antagonists, reduce inotropy and chronotropy, reduce myocardial oxygen demand, slow conduction and increase refractoriness in AV node, reverse cardiac and arterial reHypertension ( although being downgraded for this use), stable and unstable angina, diastolic congestive heart failure, supraventricular tachyarrythmias
Inhibits VLDL synthesis raising HDL - largest increase in HDL, small reduction in LDL, larger reduction in triglyceridesHypercholesterolemia (esp. with low HDL)
α1β antagonist, reduces inotropy and chronotropy, vasodilation, anti-oxidant, anti-apoptotic activityHypertension (esp. with hyperlipidemia or diabetes), systolic congestive heart failure, diastolic congestive heart failure, stable angina
Block potassium channels, varying effects on sodium and calcium channels, inhibit repolarization in the atria and ventriclesPrevent cardiac tachyarrythmias, terminate acute ventricular cardiac tachyarrythmias
Mineralocorticoid (aldosterone) receptor antagonistsPrevent hypokalemia during diuretic therapy, congestive heart failure, post-myocardial infarction prophylaxis against the development of congestive heart failure
Inhibits the carboxylation of glutamate residues in Vitamin K-dependent clotting factorsVenous thromboembolic diseases, prevention of thromboembolism from atrial fibrillation, and others
Source of NO + inhibitor of ROS production, dilation of veins more than arteries, anti-remodeling activityCongestive heart failure (African-Americans)
Irreversible cyclo-oxygenase (1 and 2) inhibition; inhibition of platelet activationArterial thrombotic diseases, primary prevention of arterial thrombi
Sources of NO in vascular smooth muscle, dilation of veins more than arteriesStable and unstable angina, acute decompensated congestive heart failure
Inhibits sodium-potassium ATPase resulting in greater delivery of calcium to the contractile apparatus of cardiomyocytes, increases activity in the vagus nerve, slows conduction anSystolic congestive heart failure, supraventricular arrythmias
Mechanism and/or ActionDrugDisease or Use
Blocks intestinal transport of cholesterol, modest reduction in LDL, no change in HDLHypercholesterolemia
Blocks the pacemaker channel in the SA node (HCN4), reduces heart rate without affecting inotropy or blood pressure, reduces myocardial oxygen demandStable angina
Cleave fibrin to resolve clotAcute myocardial infarction, acute ischemic stroke, acute pulmonary embolism, and others
Inhibition of cyclic nucleotide phosphodiesterase; inhibition of platelet activationArterial thrombotic diseases (in combination)
Blocks vascular L-type calcium channels, stabilizes inactivated state of those calcium channels, reduces myocardial oxygen demand, arterial vasodilationHypertension (usually as third drug or as second drug in isolated systolic hypertension), stable angina (as adjunct to nitrate + beta blocker), variant angina
Accelerates inactivation of thrombin (factor IIa)Venous thromboembolism, cardiac vascular surgery, treatment of MI and unstable angina
α1 receptor antagonist, vasodilationSecond-line hypertension (esp. in persons with high LDL and low HDL)
Increases cGMP in vascular smooth muscle, suppresses renin-angiotensin systemAcute decompensated congestive heart failure
Non-selective β receptor antagonist, blocks potassium channels, slows conduction in the AV node, increases the effective refractory period in the AV node, inhibits repolarization Prevent cardiac tachyarrhythmias
Blockers of GPIIb/IIIa receptor, inhibition of platelet aggregationPrevention of reocclusion after treatment of MI
Blocks late sodium channel, reduces inotropy without affecting heart rate or blood pressure, reduces myocardial oxygen demandStable angina
Increases osmolarity of extracellular fluid, washes out countercurrent multiplierRapid excretion of renal toxins and other toxins, cerebral edema, acute angle closure glaucoma
Block potassium channels, inhibit repolarization in the atria and ventriclesPrevent cardiac tachyarrhythmias
Accelerates inactivation of factor XaVenous thromboembolism, cardiac vascular surgery, treatment of MI and unstable angina
Blocks sodium channels, stabilizes inactivated state of sodium channels, slows conduction in the ventricles, increases the effective refractory period in the ventriclesTerminates acute ventricular tachyarrhythmias
AT1 receptor antagonist (ARB)Hypertension (primary drug in cases of diabetes, post-MI, and chronic renal disease), post-MI prophylaxis against the development of congestive heart failure, systolic and diastolic congestive heart failure
Activates A1 receptors in AV node, slows conduction in the AV node, increases the effective refractory period in the AV nodeTerminates acute supraventricular tachyarrythmias
Block sodium channels in collecting ductPrevent hypokalemia during diuretic therapy
Prevent binding of fibrinogen to thrombinThrombolytic therapy, heparin-induced thrombocytopenia
Inhibit HMGCoA reductase, greatest reduction in LDL, little increase in HDLHypercholesterolemia

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Created May 14, 2011ReportNominate
Tags:action, disease, drug, duke, exam, mechanism, med