Pharmacology Mnemonics - Flash Cards

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

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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

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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.