Pharmacology Mnemonics

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Prednisone
2007-10-28 13:08:00
Name: Prednisone Class: Corticosteroid (Immunosuppressant) Mechanism: Inhib. of IL-1 & TNF synth/release from Mfs ® ¯ activation of T cells and Mfs, ¯ PMN fxn, ¯ T cell-dependent Ab production, ¯ complement activity, ¯ activity & release of kinins. Absorption: Oral Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Suppressed pituitary adrenal fxn, hypertension, weight gain, peptic ulcer, GI bleeding, euphoric personality changes, cataracts, hyperglycemia. Utility: Immunosuppression. Primarily employed to induce remission in patients w/acute lymphocytic leukemia, and for treatment of lymphomas. Treat hypercalcemia due to vit. D intox., sarcoidosis, or specific cancers (e.g., lymphoproliferative) (30-60 mg/d). Special Features:

OKT3 (Muromonab-CD3)
2007-10-28 13:08:00
Name: OKT3 (Muromonab-CD3) Class: Immunosuppressant Mechanism: Opsonizes T cells, modulates CD3 antigen recognition complex on T cells, blocks CTL killer function. Absorption: IV Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Chills, fever, thrombocytopenia, erythema, pruritis, hypersensitivity rxns, anti-OKT3 antibody production ( only given for 1-2 weeks). Utility: Prevent or reverse acute allograft rejection. Special Features: Murine monoclonal antibody against CD3 on T cells.
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Cyclosporine (Sandimmune)
2007-10-28 13:07:00
Name: Cyclosporine (Sandimmune) Class: Immunosuppressant Mechanism: Binds to calmodulin and a cytoplasmic cytophilin ® selective inhib. of transcription of IL-2 gene ® inhib. of IL-2 prod. & release from T4 cells, inhib. of proliferation of T8 cells, block of T4 activation of B cells. Absorption: Oral ® highly variable and incomplete absorption. Dist.: Large Vd. Binds in tissues. 60-70% contained in RBCs. Metabolism.: Extensive hepatic Metabolism involving cyt. P450 enzymes. 17 Metabolismolites known. Drug levels monitored by RIA or HPLC. Excretion, t½: Biliary excretion, minor renal excretion. Toxicity/S.E.s: Nephrotoxicity (main toxicity), hepatotoxicity, hirsutism, gingival hyperplasia, neurotoxicity, altered coagulability. But little (if any) bone marrow suppression. Drug interactions—rifampin & phenobarbital ® induction of hepatic Metabolism. Erythromycin ® inhib. of hepatic Metabolism. Ketoconazole & amphotericin ® ¯ clearance. Utility: Pr...
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Acetaminophen (Tylenol)
2007-10-26 23:14:00
Name: Acetaminophen (Tylenol) Class: Para-aminophenol (OTC) Mechanism: Weak inhib. of peripheral prostaglandin synth. More effective CNS cyclooxygenase inhib. ® antipyretic and analgesic properties. Absorption: Oral ® rapid & complete w/peak in 30-60 min. Not a weak acid. Dist.: Dist. throughout body fluids. Protein binding (20-50%) not significant. Metabolism.: No zero-order kinetics. Phase II conjug. w/glucuronic acid & sulfate. Phase I oxid. ® N-acetyl-benzoquinoneimine. Reacts w/sulfhydryl groups, but normally inactivated by glutathione (except in overdose). Excretion, t½: Majority excreted as conjug. Metabolismolites in urine. Not related to urine pH. 2 hr. Toxicity/S.E.s: Overdose ® depletion of hepatic glutathione ® rxn. w/sulfhydryl groups of hepatic proteins ® hepatic necrosis. Also renal tubular necrosis. Treatment w/N-acetylcysteine w/in 10 hr. of overdose can be life-saving. Utility: Analgesic and antipyretic efficacies comparable to aspi...

Phenacetin
2007-10-26 23:14:00
Name: Phenacetin Class: Para-aminophenol Mechanism: Converted to acetaminophen. Weak inhib. of peripheral prostaglandin synth. More effective CNS cyclooxygenase inhib. ® antipyretic and analgesic properties. Absorption: Oral ® rapid & complete. Not a weak acid. Dist.: Dist. throughout body fluids. Protein binding (20-50%) not significant. Metabolism.: No zero-order kinetics. Phase II conjug. w/glucuronic acid & sulfate. Phase I oxid. ® N-acetyl-benzoquinoneimine. Reacts w/sulfhydryl groups, but normally inactivated by glutathione (except in overdose). Excretion, t½: Majority excreted as conjug. Metabolismolites in urine. Not related to urine pH. Toxicity/S.E.s: Nephropathy assoc. w/chronic use. Overdose ® depletion of hepatic glutathione ® rxn. w/sulfhydryl groups of hepatic proteins ® hepatic necrosis. Also renal tubular necrosis. Treatment w/N-acetylcysteine w/in 10 hr. of overdose can be life-saving. Utility: Analgesic and antipyretic efficacies ...

Colchicine
2007-10-26 23:14:00
Name: Colchicine Class: Anti-Gout Agent Mechanism: Binds to tubulin ® inhib. of leukocyte migration & phagocytosis ®¯ inflamm. response. Absorption: Rapidly absorbed orally. Dist.: Metabolism.: Excretion, t½: Urine & feces. Toxicity/S.E.s: GI intolerance (n/v/d). Utility: Treat acute gout attacks. Use to prevent acute attacks while initiating allopurinol or probenecid therapy. Special Features: Not analgesic. No effect on uric acid production or excretion.

Allopurinol (Zyloprim)
2007-10-26 23:12:00
Name: Allo purinol (Zyloprim) Class: Anti-Gout Agent Mechanism: Inhibits xanthine oxidase ® ¯ production of uric acid. Absorption: Well absorbed orally. Dist.: Metabolism.: Metabolism. by xanthine oxidase to a longer acting active Metabolismolite. Excretion, t½: Toxicity/S.E.s: GI intolerance, skin rash. Drug Interactions: Inhib. Metabolism. of oral anticoagulants. Xanthine oxidase inactivates 6-mercaptopurine & azathioprine (cancer chemotherapeutic drugs). doses must be lowered when patient takes allopurinol. Utility: Treat chronic tophaceous gout, gout patients w/high excretion of uric acid, patients who cannot use probenecid or sulfinpyrazone, recurrent renal uric acid stones, renal impairment, grossly elevated serum acid concentrations (>13 mg/dL). Use also w/cancer chemotherapy to prevent urate nephropathy. Special Features:
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Sulfinpyrazone (Anturane)
2007-10-21 23:50:00
Name: Sulfinpyrazone (Anturane) Class: Anti-Gout Agent (Uricosuric Agent) Mechanism: Blocks proximal tubular reabsorption of uric acid. Absorption: Dist.: Metabolism.: Excretion, t½: Rapidly excreted by the kidneys. Toxicity/S.E.s: GI irritation (not severe). Skin rash. Rare aplastic anemia. Utility: Treat gout via increased urinary excretion of uric acid. Special Features: At low doses, sulfinpyrazone blocks proximal tubule secretionof uric acid.

Probenecid (Benemid)
2007-10-21 23:50:00
Name: Probenecid (Benemid) Class: Anti-Gout Agent (Uricosuric Agent) Mechanism: Blocks proximal tubular reabsorption of uric acid. Absorption: Dist.: Metabolism.: Excretion, t½: Reabsorbed by renal tubules & Metabolismolized slowly. Toxicity/S.E.s: GI irritation (not severe). Skin rash. Rare aplastic anemia. Utility: Treat gout via increased urinary excretion of uric acid. Blocks tubular secretion of penicillin; may be used to increase penicillin levels. Special Features: At low doses, probenecid blocks proximal tubule secretion of uric acid.
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Levamisole (Ergamisol)
2007-10-21 23:49:00
Name: Levamisole (Ergamisol) Class: Slow-Acting Antirheumatic Agent (Veterinary Anti-Helminthic Agent) Mechanism: Enhances cell-mediated immune responses (­ chemotaxis & phagocytosis of PMNs and Mfs, ­ T cell fxn). How these effects ameliorate RA is unknown. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: Rash (most common), leukopenia, agranulocytosis, thrombocytopenia, influenza-like illnesses, mouth ulcers, n/v. Utility: Treat rheumatoid arthritis (off-label use). Special Features:
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Sulfasalazine (Azulfidine)
2007-10-21 23:48:00
Name: Sulfasalazine (Azulfidine) Class: Sulfonamide (Slow-Acting Antirheumatic Agent) Mechanism: Comp. inhib. of PABA incorp. into dihydropteric acid ® inhib. of folic acid. Absorption: Poorly absorbed in GI tract. Distribution: GI tract Metabolism.: Hydrolyzed to active form by intest. bacteria. Excretion, t½: feces Toxicity/S.E.s: Interferes w/normal flora ® ¯ vit. K synth. Utility: Active in bowel lumen. Used prior to surgery to reduce microbe population. Treat inflammatory bowel disease, rheumatoid arthritis. Special Features: Broken down in intestines to liberate 5-aminosalicylate (anti-inflammatory).

Methotrexate (Rheumatrex)
2007-10-17 22:27:00
Name: Methotrexate (Rheumatrex) Class: Slow-Acting Antirheumatic Agent (AntiMetabolismolite) Mechanism: Inhib. dihydrofolate reductase ® inhib. of formation of tetrahydrofolic acid ® ¯ synth of purines, thymidylic acid, methionine, and serine ®¯ DNA/RNA/protein synth. ® eventual cell death. Absorption: Oral, IV, IM, IT. Dist.: No CNS unless administered IT. Metabolism.: Excretion, t½: Toxicity/S.E.s: Stomatitis, myelosuppression, erythema, rash, urticaria, alopecia, n/v/d. Long term use may ® hepatic fibrosis. High doses may ® crystalluria. Patient must be well hydrated and have alkaline urine to avoid renal toxicity. Also pulmonary toxicity in children. IT admin. ® subacute meningeal irritation, stiff neck, headache, fever; rarely seizures, encephalopathy, paraplegia. C/i w/pregnancy (teratogenic). Utility: Low doses useful in treating rheumatoid arthritis and severe psoriasis. Effective against acute lympho...

Hydroxychloroquine (Plaquenil)
2007-10-17 22:27:00
Name: Hydroxychloroquine (Plaquenil) Class: Slow-Acting Antirheumatic Agent (Anti-Malarial Agent) Mechanism: Unknown. Inhib. nucleic acid synth, stabilizes lysosomal membranes, traps free radicals. Absorption: Dist.: Metabolism.: Excretion, t½: Toxicity/S.E.s: GI upset, pruritis, headaches, visual disturbances, discoloration of nail beds and mucous membranes. Utility: Treat rheumatoid arthritis that has been unresponsive to NSAIDs. Also used to treat rheumatoid arthritis in conjunction w/an NSAID (allows use of lower dose of hydroxychloroquine). Special Features:

D-penicillamine (Cuprimine)
2007-10-17 22:26:00
Name: D-penicillamine (Cuprimine) Class: Slow-Acting Antirheumatic Agent Mechanism: Unknown. Suppresses/modifies immune system & interacts w/leukocyte membrane receptors. Also chelates heavy metals (e.g., Pb, Hg, As, Cu). Absorption: Oral. Dist.: 80% protein bound. Metabolism.: Excretion, t½: Urine. Toxicity/S.E.s: Mucocutaneous—pruritis, dermatitis. Renal—proteinuria,nephrotic synd. Hematologic—thrombocytopenia, aplastic anemia. Pulmonary—hemorrhagic pneumonitis. Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to NSAIDs or whose symptoms persist despite maximal tolerated doses of NSAIDs. Special Features:
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Ketorolac (Toradol)
2007-10-17 22:26:00
Name: Ketorolac (Toradol) Class: NSAID Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain). Absorption: Parenteral only. Dist.: Weak acid (pKa ~90% protein binding. Vd @ albumin Vd. Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.). Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, as...
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Gold (Auranofin, Aurothioglucose)
2007-10-17 22:26:00
Name: Gold (Auranofin, Aurothioglucose) Class: Slow-Acting Antirheumatic Agent Mechanism: Unknown. May involve alteration of macrophage fxn. Absorption: Auranofin—oral. Aurathioglucose—IM. Dist.: 95% protein bound. Metabolism.: Excretion, t½: 65% in urine, 35% feces. 5-6 days. Toxicity/S.E.s: Affects about 1/3 of patients. Mucocutaneous—pruritis & dermatitis. Renal—proteinuria, nephrotic synd., hematuria. Hematologic—eosinophilia, thrombocytopenia, aplastic anemia. Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to NSAIDs or whose symptoms persist despite maximal tolerated doses of NSAIDs. Special Features:

Diflunisal (Dolobid)
2007-10-17 22:25:00
Name: Diflunisal (Dolobid) Class: Salicylate. Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain). Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 2-3 hr. Dist.: Weak acid (pKa ~90% protein binding. Vd @ albumin Vd. No CNS. Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.). Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accumulation of orig. compound. t½ = 11-15 hr. Clearance decreased w/renal impairment & in the elderly. Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inh...

Piroxicam (Feldene)
2007-10-17 22:25:00
Name: Piroxicam (Feldene) Class: NSAID Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain). Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 3-5 hr. Dist.: Weak acid (pKa ~90% protein binding. Vd @ albumin Vd. Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.). Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accumulation of orig. compound. t½ = 30-86 hr. Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic renal failure...

Naproxen (Naprosyn)
2007-10-17 22:24:00
Name: Naproxen (Naprosyn) Class: NSAID Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain). Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 2-4 hr. Dist.: Weak acid (pKa ~90% protein binding. Vd @ albumin Vd. Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.). Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accumulation of orig. compound. t½ = 12-15 hr. Clearance decreased w/renal/hepatic impairment & in the elderly. Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of pl...

Flurbiprofen (Ansaid)
2007-10-17 13:21:00
Name: Flurbiprofen (Ansa id) Class: NSAID Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain). Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-5 hr. Dist.: Weak acid (pKa ~90% protein binding. Vd @ albumin Vd. Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.). Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. t½ = 5 hr. Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic renal failur...