Pharmacology Mnemonics - Flash Cards

Name: Anistreplase/APSAC (Eminase)

Class: Antithrombotic Agent (Thrombolytic Agent)

Mechanism: Acylated plasminogen-streptokinase activator complex. Plasminogen active site is protected from inactivation. Poor thrombus specificity—catalyzes conversion of circulating & fibrin-bound plasminogen—results in a systemic lytic state.

Absorption: IV. Admin. w/large loading dose to overcome plasma antibodies.

Dist.: Metabolism.:

Excretion, t½: Longer t½ than streptokinase ® sustained fibrinolytic effect.

Toxicity/S.E.s: Hemorrhage. Allergic rxns—pruritis, flushing, urticaria. Higher incidence of allergic rxns. w/readministration. Pronounced hypotension (usu. transient). Delayed fever and arthralgia.

Utility: Treat acute MI (w/in 6 hr. of symptoms), massive PE, acute proximal vein thromboses, occlusion of dialysis access sites and indwelling catheters, occlusion of prosthetic heart valves.

Special Features: Best results in pts. that receive therapy < style=""> Pts. w/antibodies can develop therapeutic resistance.

Name: Streptokinase (Streptase)

Class: Antithrombotic Agent (Thrombolytic Agent)

Mechanism: Derived from b-hemolytic streptococci. Forms a complex w/plasminogen, exposing its active site. Poor thrombus specificity—catalyzes conversion of circulating and fibrin-bound plasminogen—results in a systemic lytic state.

Absorption: IV. Admin. w/large loading dose to overcome plasma antibodies.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Hemorrhage. Allergic rxns—pruritis, flushing, urticaria. Higher incidence of allergic rxns. w/readministration. Pronounced hypotension (usu. transient). Delayed fever and arthralgia.

Utility: Treat acute MI (w/in 6 hr. of symptoms), massive PE, acute proximal vein thromboses, occlusion of dialysis access sites and indwelling catheters, occlusion of prosthetic heart valves.

Special Features: Best results in pts. that receive therapy < style=""> Pts. w/antibodies can develop therapeutic resistance.

Name: Vitamin K₁ (Phytonadione)

Class: Anticoagulant Antagonist

Mechanism: Vit. K is necessary for g-carboxylation of thrombin, factors VII, IX, & X, and proteins C & S. The g-carboxylated residues are required for binding Ca²⁺, which is essential for their activity.

Absorption: Oral or SC preferred. IV admin. may cause shock or anaphylaxis.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: IV admin. may cause shock or anaphylaxis.

Utility: Reverse excessive bleeding due to warfarin—indicated for severe or continued bleeding if warfarin dosage adjustment is unsuccessful.

Special Features: Significant improvement in hemostasis may require as long as 24 hr. If immediate hemostasis is necessary, fresh frozen plasma should be infused.

Name: Warfarin (Coumadin)

Class: Antithrombotic Agent (Oral Anticoagulant)

Mechanism: Vitamin K antagonist ® ¯ g-carboxylation of thrombin, factors, VII, IX, & X, and proteins C & S ® inhib. of synth. of active coagulation factors. Does not alter organized clots.

Absorption: Oral.

Dist.: Almost completely bound (99%) to plasma proteins (mainly albumin).

Metabolism.: Microsomal enzymes in liver and kidneys.

Excretion, t½: Urine and stool.

Toxicity/S.E.s: Hemorrhage, hypersensitivity rxns., fetal toxicity. “Purple Toe” synd. (necrosis) assoc. w/protein C deficiency. During pregnancy, can cause birth defects and abortion. Many drug interactions.

Utility: Prevention of recurrent thrombotic events following acute Rx w/heparin. Valvular heart disease, prosthetic cardiac valves, AMI, atrial fibrillation.

Special Features: Max. effects require 2-7 days. Init. response may be procoagulant due to inhib. of protein C. Should have 6 day overlap w/heparin. Monitor PT.

Name: Antithrombin III (ATnativ)

Class: Antithrombotic Agent (Coagulation Inhibitor)

Mechanism: Prepared from pooled human plasma. Inhibits coagulation factors (thrombin, IXa, Xa, XIIa).

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Treat pts w/hereditary AT-III deficiency and neonates w/a family history of AT-III deficiency. Prophylaxis for deficient pts who are undergoing surgery or delivery at term.

Special Features:

Name: Protamine Sulfate

Class: Anticoagulant Antagonist

Mechanism: Binds tightly to heparin and rapidly reverses its effects. Also interacts w/platelets, fibrinogen, and other plasma proteins ® anticoagulant effect.

Absorption: IV infusion—slow rate.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Treat life-threatening hemorrhage 2° to heparin use.

Special Features: Use minimal effective dose.

Name: Enoxaparin (Lovenox)

Class: Antithrombotic Agent (Anticoagulant) (Low Molecular Weight Heparin)

Mechanism: Catalyzes complex formation btwn. plasma antithrombin III and various serine proteases of the coagulation pathway, including thrombin and activated factors IX, X, XI, & XII. Effect primarily due to thrombin inhib. Less effect on thrombin than heparin. Prevents further clot formation and thrombus propagation. Does not alter organized clots.

Absorp.: SC ® better bioavail. than heparin. Daily SC injxn has sim. efficacy to 2-3 injxns/d of heparin.

Dist.: Metabolism.: Hepatic.

Excretion, t½: Longer t½ than heparin. ¯ t½ w/pulm. embolism. ­ t½ w/hepatic cirrhosis or end-stage renal disease.

Toxicity/S.E.s: 1° = bleeding. Thrombocytopenia (bovine > porcine)—mild, severe (delayed onset; can occur w/heparin resistance ® thromboembolism & DIC). Long-term use ® osteoporosis. Non-teratogenic, but discontinue prior to delivery.

Utility: 1° prevention of DVT after hip replacement surgery.

Special Features: Primarily used for venous thromboses. Monitor PTT to achieve desired dose—1.5-2.5x normal PTT is therapeutic. ­ recurrence rate if PTT < style=""> Few drug interactions. Lower rate of bleeding than w/heparin.

Name: Heparin

Class: Antithrombotic Agent (Anticoagulant)

Mechanism: Catalyzes complex formation btwn. plasma antithrombin III and various serine proteases of the coagulation pathway, including thrombin and activated factors IX, X, XI, & XII. Effect primarily due to thrombin inhib. Prevents further clot formation and thrombus propagation. Does not alter organized clots.

Absorp.: IV, continuous IV®immed. onset. SC®1-2 hr onset w/variable bioavail.

Dist.: Metabolism.: Hepatic.

Excretion, t½: Rel. short t½. ¯ t½ w/pulm. embolism. ­ t½ w/hepatic cirrhosis or end-stage renal disease.

Toxicity/S.E.s: 1° = bleeding. Thrombocytopenia (bovine > porcine)—mild, severe (delayed onset; can occur w/heparin resistance ® thromboembolism & DIC). Long-term use ® osteoporosis. Non-teratogenic, but discontinue prior to delivery.

Utility: Symptomatic calf vein thrombi or thrombi extending above the popliteal vein, pulm. embolus, atrial fibrillation, valvular heart disease, CAD, adjunct to post-MI thrombolytic therapy. Use in general surgery for E on oral contraceptives.

Special Features: Primarily used for venous thromboses. Most widely used antithromb. agent. Monitor PTT to achieve desired dose—1.5-2.5x normal PTT is therapeutic. ­ recurrence rate if PTT < style=""> Few drug interactions.

Name: Abciximab (Reo-Pro)

Class: Antithrombotic Agent (Antiplatelet Agent)

Mechanism: Monoclonal antibody to GPIIb/IIIa. Interferes w/platelet-adhesive protein interactions.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Treat high risk angioplasty pts.

Special Features:

Name: Ticlopidine (Ticlid)

Class: Antithrombotic Agent (Antiplatelet Agent)

Mechanism: Unknown. Through some effect on platelet membranes, blocks ADP-induced aggregation. Interacts w/membrane glycoprotein IIb/IIIa.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Diarrhea, GI cramping, rash, ­ LDL & VLDL, leukopenia, agranulocytosis, pancytopenia.

Utility: Treat thromboses in patients unable to take aspirin. May be more effective than aspirin in 2° prevention of stroke in pts w/previous TIA.

Special Features: Several days required for effects to develop. Effects persist for several days after cessation of treatment. As effective in E as in G. Antithrombotic use is primarily for arterial thromboses.

Name: Dipyridamole (Persantine)

Class: Antithrombotic Agent (Antiplatelet Agent)

Mechanism: Inhib. PDE in platelets ® ­ cAMP ® inhib. of platelet activation.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Prevention of systemic embolism in pts. w/prosthetic heart valves. Admin. in combination w/warfarin.

Special Features: When used alone, ineffective for Rx of cerebral or CV thrombotic events. Not proven to be of additional benefit when admin. w/aspirin. Antithrombotic use is primarily for arterial thromboses.

Name: Acetylsalicylic Acid (Aspirin)

Class: Antithrombotic Agent (Antiplatelet Agent)

Mechanism: Irrevers. acetylation of cyclooxygenase ® ¯ platelet thromboxane synth.

Absorption: Oral ® rapid absorption.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: GI hemorrhage, hemorrhagic stroke. Use w/caution in pts on long-term oral anticoagulants. Hypersensitivity rxns—generalized urticaria, bronchial asthma, laryngeal edema, bronchoconstriction, hypotension, shock—may occur in 20-25% of pts w/asthma, nasal polyps, or chronic urticaria.

Utility: Acute MI, stable/unstable angina, 2° prevention in MI survivors. TIA. 2° prevention in nondisabling ischemic stroke. Prevention of saphenous vein bypass graft occlusion. Post-coronary angioplasty. 1° MI prophylaxis (325 mg/d) adjunctive to risk factor management. Headache.

Special Features: Low dose Rx optimal—75-325 mg/d. Antithrombotic use is primarily for arterial thromboses.

Name: Amyl Nitrate

Class: Antianginal Agent (Organonitrate)

Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® ­ cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O₂ demand. Inhib. of platelet fxn.

Absorption: Inhalation ® rapid onset.

Dist.:

Metabolism.: Hepatic inactivation via glutathione-organic nitrate reductase.

Excretion, t½: Renal. Short duration of action (3-5 min.).

Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP.

Utility: Treat angina. Not suitable for maintenance therapy.

Special Features:

Name: Isosorbide Dinitrate (Isordil)

Class: Antianginal Agent (Organonitrate)

Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® ­ cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O₂ demand. Inhib. of platelet fxn.

Absorption: Sublingual preferred ® complete absorption. Oral ® ­ 1^st pass Metabolism, low bioavail. Buccal/transdermal ® slow absorption.

Dist.:

Metabolism.: 80% converted to active Metabolismolite 5-ISMN before entering systemic circulation. Hepatic inactivation via glutathione-organic nitrate reductase.

Excretion, t½: Renal. 10 min. Short duration of action (20-30 min.).

Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP.

Utility: Treat angina. Subling. not suitable for maintenance therapy. Oral/buccal/transdermal for prophylaxis, but may ® tolerance

Special Features: 8+ hr. breaks necessary to avoid tolerance from slow absorp.

Name: Nitroglycerin (Nitro-Bid)

Class: Antianginal Agent (Organonitrate)

Mechanism: Converted to NO ® activation of cytosolic guanylate cyclase ® ­ cGMP ® activation of cGMP-dependent protein kinase ® smooth muscle relaxation ® vasodilation. Greater effect in veins & large arteries than in resistance vessels ® ¯¯ preload, ¯ afterload ® ¯ work ® ¯ O₂ demand. Inhib. of platelet fxn.

Absorption: Sublingual preferred. IV. Oral ® ­ 1^st pass Metabolism, low bioavail. Buccal/transdermal ® slow absorption.

Dist.:

Metabolism.: Hepatic (glutathione-organic nitrate reductase), extra-hepatic. Plasma clearance >> C.O.

Excretion, t½: Renal. 3 min. Short duration of action (20-30 min.).

Toxicity/S.E.s: Orthostatic hypotension, tachycardia, severe throbbing headache, dizziness, flushing, syncope. C/i w/elevated ICP.

Utility: Treat angina. Subling. not suitable for maintenance therapy. IV for severe recurrent unstable angina. Oral/buccal/transdermal for prophylaxis, but may ® tolerance.

Special Features: 8+ hr. breaks necessary to avoid tolerance from slow absorp.

Name: Probucol (Lorelco)

Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative)

Mechanism: Stim. LDL clearance by non-receptor pathways. May reduce risk of atherogenesis w/o altering serum cholesterol levels. May block oxidation of LDL. Moderate ¯ in cholesterol, LDL, & HDL. No effect on TG or VLDL.

Absorption:

Dist.: Stored in fat.

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Generally very well tolerated (2-6% incidence). Flatulence, n/v/d, abd. pain, headache, rash. C/i in monkeys (cardiac arrhythmias). Stored in fat. \ E advised to wait 6 mo. after last dose before becoming pregnant.

Utility: Treat hyperlipidemia IIA/IIB, but prob. not drug o’ first choice. May be useful for homozygous familial hypercholesterolemia (IIA). May cause regression of xanthomas.

Special Features: ¯ in LDL takes 1-3 mo., but some pts. don’t respond. Does not further reduce LDL when used w/lovastatin.

Name: Clofibrate (Atromid-S) mnemonic

Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative)

Mechanism: ­ catabolism of VLDL, in part 2° to ­ activity of lipoprotein lipase in adipose tissue. Moderate ¯ in TG & VLDL. Zero-mild ¯ in cholesterol. Zero-mild ­ in HDL. Mild ­ or ¯ in LDL.

Absorption:

Dist.:

Metabolism.: Glucuronide conjugation.

Excretion, t½: Renal excretion.

Toxicity/S.E.s: Generally well tolerated. Gallstones, nausea, diarrhea, abdominal discomfort. Displaces weakly acidic drugs (T3, T4, warfarin, phenytoin) from plasma proteins. Binds cholestyramine.

Utility: Treat severe hyperlipidemia IV refractory to gemfibrozil or niacin.

Special Features: Does not appear to decrease frequency of CHD-related incidents.

Name: Gemfibrozil (Lopid) mnemonic

Class: Blood Lipid-Lowering Agent (Fibric Acid Derivative)

Mechanism: ­ catabolism of VLDL, in part 2° to ­ activity of lipoprotein lipase in adipose tissue. Moderate ¯ in TG & VLDL. Mild ¯ in LDL and cholesterol. Moderate ­ in HDL.

Absorption:

Dist.:

Metabolism.: Glucuronide conjugation.

Excretion, t½: Renal excretion.

Toxicity/S.E.s: Generally well tolerated. GI distress, rash, musculoskeletal pain, blurred vision, anemia, leukopenia, gallstones. Adjust dose in pts. w/renal insufficiency.

Utility: DOC for hyperlipidemia III. Better tolerated than niacin for type IV, although less effective. Decreases frequency of CHD-related incidents.

Special Features:

Name: Nicotinic Acid (Niacin)

Class: Blood Lipid-Lowering Agent

Mechanism: Reduces synth. rate of VLDL. Inhib. lipolysis of TG in adipocytes. Large ¯ in TG. Moderate ¯ in cholesterol & VLDL. Mild ¯ in LDL. Zero-moderate ­ in HDL.

Absorption:

Dist.: Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Cutaneous flushing (92%), itching (49%), rashes (20%). Reduce w/aspirin pretreatment, admin. after meals, small init. dose gradually increased in size. Pruritis, dry skin, ­ pigmentation, hepatotoxicity, n/v, dyspepsia, peptic ulceration, ­ urinary frequency, dysuria, gout. High doses ® hepatic/pancreatic dysfxn. Coadmin. anti-hypertensives ® dizziness, syncope. Sustained-release preparations more commonly assoc. w/hepatotoxicity, dry eyes, ­ pigmentation, hyperglycemia.

Utility: Prob. DOC for hyperlipidemias IV and V. Very useful for III. Can be used for II. Synergy w/resins.

Name: Colestipol (Colestid)

Class: Blood Lipid-Lowering Agent (Resin)

Mechanism: Binds bile acids in intestine ® ­ defecation of bile acids, ­ conversion of cholesterol to bile acids, ¯ pool of hepatic cholesterol, ­ activity of apoB/E receptor, ­ LDL clearance, ¯ plasma cholesterol. Moderate ¯ in cholesterol & LDL. Mild ­ in HDL. Zero-moderate ­ in TG & VLDL.

Absorption: Oral. No absorption.

Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Flatulence, constipation, gas, n/v, steatorrhea. Supersaturation of cholesterol in bile ® gallstones, need for cholecystectomy. ¯ bile ® ¯ absorption of lipid-soluble drugs/vitamins. Binds acidic drugs. Weak stim. of VLDL synth. Do not use in pts. w/hyperTG w/o concurrent TG-lowering agent.

Utility: Treat hyperlipidemia IIA/IIB. Use alone or w/niacin, probucol, or HMG CoA reductase inhib.

Special Features: GI S.E.s reduced if taken immediately prior to meals. ½ dose + Metamucil™ ® ¯ constipation & bloating, but sim. efficacy.

Name: Cholestyramine (Cholybar)

Class: Blood Lipid-Lowering Agent (Resin)

Mechanism: Binds bile acids in intestine ® ­ defecation of bile acids, ­ conversion of cholesterol to bile acids, ¯ pool of hepatic cholesterol, ­ activity of apoB/E receptor, ­ LDL clearance, ¯ plasma cholesterol. Moderate ¯ in cholesterol & LDL. Mild ­ in HDL. Zero-moderate ­ in TG & VLDL.

Absorption: Oral. No absorption.

Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Up to 50% refuse to continue Rx. Flatulence, constipation, gas, n/v, steatorrhea. Supersaturation of cholesterol in bile ® gallstones, need for cholecystectomy. ¯ bile ® ¯ absorption of lipid-soluble drugs/vitamins. Binds acidic drugs. Weak stim. of VLDL synth. Do not use in pts. w/hyperTG w/o concurrent TG-lowering agent.

Utility: Treat hyperlipidemia IIA/IIB. Use alone or w/niacin, probucol, or HMG CoA reductase inhib.

Special Features: GI S.E.s reduced if taken immediately prior to meals. ½ dose + Metamucil™ ® ¯ constipation & bloating, but sim. efficacy.

Name: Simvastatin (Zocor)

Class: Blood Lipid-Lowering Agent (HMG CoA Reductase Inhibitor)

Mechanism: Inhib. of HMG CoA reductase ® ¯ cholesterol pool, ­ apoB/E receptor activity, ­ LDL clearance. Large reduction of cholesterol and LDL. Little/no ¯ in TGs, little/no ­ in HDL, no change in VLDL.

Absorption: Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Common mild GI disturbances. Reversible elevations of liver enzymes in 4-7% (if AST or ALT > 3x normal, discontinue). Possible muscle damage—much more likely w/concurrent cyclosporine, gemfibrozil, niacin, or erythromycin; or if pt has hepatic disease, a severe infxn, or renal insufficiency. Continued use w/myopathy may ® severe myositis, rhabdomyolysis, or acute renal failure. Can shorten sleep period by up to 18%. C/i in kids & preg. E.

Utility: Treat hyperlipidemia IIA/IIB refractory to diet and other drugs. May not be useful for pts. w/homozygous familial hypercholesterolemia.

Special Features: Most effective drug class for lowering LDL. Probably better tolerated than other cholesterol lowering drugs. Synergistic effects w/resins and niacin. If taken once/day, take at night (peak cholesterol synth. occurs between 12:00-3:00 a.m.).

Name: Pravastatin (Pravochol)

Class: Blood Lipid-Lowering Agent (HMG CoA Reductase Inhibitor)

Mechanism: Inhib. of HMG CoA reductase ® ¯ cholesterol pool, ­ apoB/E receptor activity, ­ LDL clearance. Large reduction of cholesterol and LDL. Little/no ¯ in TGs, little/no ­ in HDL, no change in VLDL.

Absorption: Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Common mild GI disturbances. Reversible elevations of liver enzymes in 4-7% (if AST or ALT > 3x normal, discontinue). Possible muscle damage—much more likely w/concurrent cyclosporine, gemfibrozil, niacin, or erythromycin; or if pt has hepatic disease, a severe infxn, or renal insufficiency. Continued use w/myopathy may ® severe myositis, rhabdomyolysis, or acute renal failure. C/i in kids & preg. E.

Utility: Treat pts. w/type IIA/IIB hyperlipidemia refractory to diet and other drugs. May not be useful for pts. w/homozygous familial hypercholesterolemia.

Special Features: Most effective drug class for lowering LDL. Probably better tolerated than other cholesterol lowering drugs. Synergistic effects w/resins and niacin. If taken once/day, take at night (peak cholesterol synth. occurs between 12:00-3:00 a.m.).

Name: Lovastatin (Mevacor)

Class: Blood Lipid-Lowering Agent (HMG CoA Reductase Inhibitor)

Mechanism: Inhib. of HMG CoA reductase ® ¯ cholesterol pool, ­ apoB/E receptor activity, ­ LDL clearance. Large reduction of cholesterol and LDL. Little/no ¯ in TGs, little/no ­ in HDL, no change in VLDL.

Absorption: Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Common mild GI disturbances. Reversible elevations of liver enzymes in 4-7% (if AST or ALT > 3x normal, discontinue). Possible muscle damage—much more likely w/concurrent cyclosporine, gemfibrozil, niacin, or erythromycin; or if pt has hepatic disease, a severe infxn, or renal insufficiency. Continued use w/myopathy may ® severe myositis, rhabdomyolysis, or acute renal failure. Can shorten sleep period by up to 18%. C/i in kids & preg. E.

Utility: Treat pts. w/type IIA/IIB hyperlipidemia refractory to diet and other drugs. May not be useful for pts. w/homozygous familial hypercholesterolemia.

Special Features: Most effective drug class for lowering LDL. Probably better tolerated than other cholesterol lowering drugs. Synergistic effects w/resins and niacin. If taken once/day, take at night (peak cholesterol synth. occurs between 12:00-3:00 a.m.).