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MOA of Cardiovascular Agents
Terms in this set (48)
Type III antiarrhythmic that prolongs the effective refractory period of atrial and ventricular tissue by blocking potassium conductance.
Long-acting dihydropyridine calcium-channel-blocking drug with potent arterial and coronary vasodilating properties.
Amlodipine Besylate; Benazepril Hydrochloride
Selective inhibitor of factor Xa. By inhibiting factor Xa, apixaban decreases thrombin generation and thrombus development.
Cardioselective β-adrenergic that decreases AV nodal conduction in supraventricular tachycardias and blockade of catecholamine-induced dysrhythmias.
Atorvastatin Calcium *Contraindicated in 1st Trimester
HMG-CoA reductase inhibitors competitively inhibit conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol synthesis. A compensatory increase in LDL receptors, which bind and remove circulating LDL-cholesterol, results. Production of LDL-cholesterol also can decrease because of decreased production of VLDL-cholesterol or increased VLDL; removal by LDL receptors.
Competitive ACE-I. It also reduces serum aldosterone, leading to decreased sodium retention, potentiates the vasodilator kallikrein-kinin system, and can alter prostanoid metabolism, inhibit the sympathetic nervous system, and inhibit the tissue renin-angiotensin system.
Selective α1- and nonselective β-adrenergic blocker that decreases AV nodal conduction in supraventricular tachycardias and blockade of catecholamine-induced dysrhythmia.
Increases sodium and chloride excretion by interfering with their reabsorption in the cortical-diluting segment of the nephron.
Stimulates presynaptic α2-adrenergic receptors and blocks postsynaptic α2-adrenergic receptors in the CNS by activating inhibitory neurons to decrease sympathetic outflow. Clonidine is not a complete agonist, so some of its effects might result from antagonist actions at presynaptic α-receptors. These actions reduce peripheral vascular resistance, renal vascular resistance, HR, and BP.
Antiplatelet agent that prevents platelet aggregation by direct inhibition of ADP binding to receptor sites, inhibiting subsequent activation of the glycoprotein IIb/IIIa complex. This action is irreversible; therefore, platelets exposed to clopidogrel are inhibited for their lifespans.
Cyanocobalamin (Vitamin B-12)
B12 is required for the synthesis of the amino acid methionine from homocysteine. A deficiency of B12 results in hyperhomocysteinemia and a decrease in methionine. Since methionine is required for DNA synthesis, B12 deficiency also results in decreased DNA synthesis, which presents clinically as macrocytic anemia when red blood cells are unable to extrude their nucleus.
Digitalis glycosides exert positive inotropic effects through improved availability of calcium to myocardial contractile elements, thereby increasing cardiac output in heart failure. Antiarrhythmic actions are caused primarily by an increase in AV nodal refractory period via increased vagal tone, sympathetic withdrawal, and direct mechanisms.
A calcium-channel-blocking drug that decreases HR, prolongs AV nodal conduction, and decreases arteriolar and coronary vascular tone. It also has negative inotropic properties.
A prodrug that is rapidly converted to its active metabolite, enalaprilat, a competitive ACEI. It reduces serum aldosterone, leading to decreased sodium retention, potentiates the vasodilator kallikrein-kinin system, and inhibits the sympathetic nervous system and tissue renin-angiotensin system. The net effect is reduction in total peripheral resistance and BP in hypertensive patients and reduction in elevated afterload in patients with heart failure.
Localizes at the brush border of the small intestine and inhibits the absorption of cholesterol, leading to a decrease in the delivery of intestinal cholesterol to the liver. This causes a reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood; this distinct mechanism is complementary to that of statins and of fenofibrate.
Fibric acid derivatives activate peroxisome proliferator-activated receptor α (PPARα), which increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity). The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.
Hydrochlorothiazide; Losartan Potassium
Lovastatin *Contraindicated in 1st Trimester
Nitroglycerin (sublingual & injectable)
Omega-3-Acid Ethyl Esters
Potassium Chloride (oral)
Pravastatin Sodium *Contraindicated in 1st Trimester
Rosuvastatin Calcium *Contraindicated in 1st Trimester
Simvastatin-*Contraindicated in 1st Trimester
Warfarin Sodium (Crystalline)-*Contraindicated in 1st Trimester
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