Pharmacology Mnemonics - Flash Cards

Name: Liothyronine sodium (Cytomel)

Class: Thyroid Hormone

Mechanism: Sodium salt of T₃. T₃/T₄ synergize w/GH effects, increase BMR, potentiate catecholamine effects on heart, promote lipolysis, and decrease serum cholesterol.

Absorption: Oral ® 95% absorption.

Dist.: Poor placental transfer ® okay for pregnant E. Little in milk (use cautiously).

Metabolism.: Hepatic conjug. w/glucuronic & sulfuric acids.

Excretion, t½: Bile; some lost in stool due to enterohepatic circ. £ 2 d.

Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites ® marked increase of free levels.

Utility: Preferred in treatment of myxedema coma. Treat hypothyroidism and goiter (not due to iodine deficiency or hyperthyroidism).

Special Features: 50-75 mg/d. 4x the potency of levothyroxine sodium, but same efficacy.

Name: Levothyroxine sodium (Synthroid, Levothroid, Levoxine)

Class: Thyroid Hormone

Mechanism: Sodium salt of T₄. T₃/T₄ synergize w/GH effects, increase BMR, potentiate catecholamine effects on heart, promote lipolysis, and decrease serum cholesterol.

Absorption: Incomplete oral absorption—30-40% recovered in stool.

Dist.: Poor placental transfer ® okay for pregnant E. Little in milk (use cautiously).

Metabolism.: Hepatic conjug. w/glucuronic & sulfuric acids. Peripheral deiodination to T₃.

Excretion, t½: Bile; some lost in stool due to enterohepatic circ. 6-7 d.

Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites ® marked increase of free levels.

Utility: Treat hypothyroidism and goiter (not due to iodine deficiency or hyperthyroidism).

Special Features: 200-300 mg/d. 1/4 the potency of liothyronine sodium, but same efficacy.

Name: Thyroglobulin (Proloid)

Class: Thyroid Hormone

Mechanism: T₃/T₄ synergize w/GH effects, increase BMR, potentiate catecholamine effects on heart, promote lipolysis, and decrease serum cholesterol.

Absorption: Oral

Dist.: Poor placental transfer ® okay for pregnant E. Little in milk (use cautiously).

Metabolism.: T₄ & T₃ released by proteolysis after ingestion. Hepatic conjug. of T₄/T₃ w/glucuronic & sulfuric acids.

Excretion, t½: Bile; some lost in stool due to enterohepatic circulation.

Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites ® marked increase of free levels.

Utility: Treat hypothyroidism and goiter (not due to iodine deficiency or hyperthyroidism).

Name: Misoprostol (Cytotec)

Class: Gastric Protectant (Prostaglandin)

Mechanism: Analog of prostaglandin E₁. Inhib. secretion of HCl. Stimulates secretion of mucus & HCO₃ (cytoprotective).

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Diarrhea, nausea. Produces uterine contractions. \ c/i during pregnancy.

Utility: Only agent approved for prevention of gastric ulcers induced by NSAIDs. Less effective than H₂ antagonists for acute treatment of peptic ulcers.

Special Features:

Name: Bacillus Calumet-Guerin (BCG)

Class: Immunostimulant

Mechanism: Viable strain of Mycobaterium bovis. Enhances Mf activity, promotes Mf tumoricidal activity.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Treat bladder carcinoma and melanomas.

Special Features:

Name: Interferon g

Class: Immunostimulant

Mechanism: Binds to cell-surface receptors ® activation of NK cells and Mfs, promotion of conversion to TH₁ cells.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia; fatigue, malaise, anorexia, weight loss, alopecia, transient elevation of liver enzymes. High doses may ® transient & reversible nephrotoxicity.

Utility: Used to treat for chronic hepatitis B, virally induced tumors, recurrent varicella zoster, HSV keratitis, Kaposi’s sarcoma, hairy cell leukemia, cutaneous T cell lymphoma.

Special Features: Produced by memory TH₁ cells and NK cells. Interferon production is induced by dsRNA (poly I:C), ampligen (mismatched nucleotides), LPS.

Name: Interferon b

Class: Immunostimulant

Mechanism: Binds to cell-surface receptors ® inhib. of viral replication, inhib. of cell proliferation.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia; fatigue, malaise, anorexia, weight loss, alopecia, transient elevation of liver enzymes. High doses may ® transient & reversible nephrotoxicity.

Utility: Used to treat for chronic hepatitis B, virally induced tumors, recurrent varicella zoster, HSV keratitis, Kaposi’s sarcoma, hairy cell leukemia, cutaneous T cell lymphoma.

Special Features: Produced by fibroblasts. Interferon production is induced by dsRNA (poly I:C), ampligen (mismatched nucleotides), LPS.

Name: Interferon a

Class: Immunostimulant

Mechanism: Binds to cell-surface receptors ® inhib. of viral replication, inhib. of cell proliferation.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia; fatigue, malaise, anorexia, weight loss, alopecia, transient elevation of liver enzymes. High doses may ® transient & reversible nephrotoxicity.

Utility: IFN a2A is approved for mgt. of hairy cell leukemia. Also useful for chronic hepatitis B, virally induced tumors, recurrent varicella zoster, HSV keratitis, Kaposi’s sarcoma, cutaneous T cell lymphoma.

Special Features: Produced by mononuclear leukocytes. Interferon production is induced by dsRNA (poly I:C), ampligen (mismatched nucleotides), LPS.

Name: Erythropoietin (Epoetin Alfa, Epogen)

Class: Immunostimulant

Mechanism: Stim. division/differentiation of erythroid progenitors in bone marrow.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Usu. well-tolerated. Low incidence of hypertension, headache, seizures. Rare hypersensitivity rxns.

Utility: Treat anemia assoc. w/chronic renal failure, AZT therapy, cancer and chemotherapy. Supplemental iron eventually required in therapy.

Special Features: Manufactured by recombinant DNA technology. Identical to human erythropoietin.

Name: GM-CSF (Sargramostim)

Class: Immunostimulant

Mechanism: Stim. bone marrow production of precursors to PMNs, monocytes, platelets. Also activates PMNs, eosinophils, and monocytes.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Fever, dermatologic rxns, splenomegaly.

Utility: FDA-approved to increase myeloid recovery rate after bone marrow transplantation. Also used for hematological reconstitution after autologous bone marrow transplants and treatments w/bone marrow cytotoxic drugs.

Special Features: Greater severity of immunologic S.E.s than w/G-CSF.

Name: G-CSF (Filgrastim)

Class: Immunostimulant

Mechanism: Promotes growth & differentiation of granulocyte precursors.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Bone pain, fever, anti-CSF antibodies.

Utility: Restore hematopoiesis (FDA-approved to treat neutropenia), augment host defenses, esp. after cancer therapy.

Name: Antilymphocyte Globulin (ALG)

Class: Immunosuppressant

Mechanism: Polyclonal antibody to human lymphocytes (not selective to CD3) ® destruction and inactivation of lymphocytes.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Chills, fever, thrombocytopenia, erythema, pruritis, hypersensitivity rxns, anti-ALG antibody production (\ only given for 1-2 weeks).

Utility: Prevent or reverse acute allograft rejection.

Special Features:

Name: Cyclophosphamide (Cytoxan)

Class: Immunosuppressant (Alkylating Agent) (Cancer Chemotherapeutic Agent)

Mechanism: Activated via hepatic P450 Metabolismolism ® phosphoramide mustard. Phosphoramide mustard alkylates DNA ® cytotoxicity to dividing cells.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Bone marrow depression (esp. leukocytosis), hemorrhagic cystitis (may ® bladder fibrosis), n/v/d, alopecia, amenorrhea, testicular atrophy, sterility. Possible secondary malignancies years later.

Utility: Cancer chemotherapy, nephrotic syndrome, intractable rheumatoid arthritis.

Special Features: Therapeutic effect independent of level of P450 activity.

Name: Azathioprine (Imuran)

Class: Immunosuppressant (AntiMetabolismolite)

Mechanism: Converted to 6-mercaptopurine (thiol analog of hypoxanthine) ® inhib. of purine synth. ® cytotoxicity to dividing cells ® ¯ lymphocyte proliferation ® inhib. of cellular and humoral immunity.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Bone marrow depression (main toxicity), n/v/d, hepatotoxicity.

Utility: Primarily used in maintenance of remission in acute lymphoblastic leukemia.

Special Features:

Name: Methylprednisone

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: Parenteral

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 in treatment of lymphomas.

Special Features:

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:

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.

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: Prolong organ transplants (1° use). Suppress cell-med. diseases. Possible benefit w/early treatment of IDDM.

Special Features:

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 comparable to aspirin.

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 aspirin.

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.

Name: Allopurinol (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:

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 secretion
of uric acid.

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.

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:

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).

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:

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 lymphocytic leukemia, choriocarcinoma, Burkitt’s lymphoma, breast cancer, head/neck carcinomas. High doses are curative for osteogenic sarcoma and choriocarcinoma.

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:

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:

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 <5). ~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, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

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 <5). ~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. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

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 <5). ~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, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

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 <5). ~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 platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Flurbiprofen (Ansaid)

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 <5). ~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 failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Sulindac (Clinoril)

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. 1-2 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine, bile, feces. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. t½ = 8-16 hr. Decreased clearance w/hepatic impairment and 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 platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis, but less likely to cause kidney effects than other NSAIDs. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.