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13 Cards in this Set
- Front
- Back
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What is the antiinflammatory MOA of NSAIDS?
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NSAIDS inhibit cyclooxygenase, the enzyme that synthesizes prostaglandins
Competes with PG at tissue receptor sites Inhibits release of lysosomal enzymes that destroy tissue inhibit neutrophil aggretation to inflamed tissue |
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What is the analgesic MOA?
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Inhibit synthesis of PG thereby decreasing sensitivity of peripheral px receptors
Prevent interference of PG with pathways that inhibit px signal transmission |
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What is the antipyretic MOA?
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Acts within CNS on heat regulating ctr in hypothalmus causing vasodilation of peripheral blood vessels and loss of body heat
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Are NSAIDS well or poorly absorbed?
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Very well
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How are NSAIDS eliminated and excreted?
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Eliminated by liver, excreted by kidneys
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What are the GI related A/E related to NSAID use?
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GI inflammation, bleeding, ulceration or perforation
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How would one treat the GI a/e of NSAIDS?
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Sucralfate
Histamine antagonists proton pump inhibitors |
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What are the renal a/e associated with NSAID use?
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decreased renal blood flow resulting in renal problems
Watch serum Cr, BUN. peripheral edema/wt gain |
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What are the hematologic a/e associated with NSAID use?
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impaired platelet aggregation
Aplastic anemia and agranulocytosis Thrombocytopenia |
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What are the CNS a/e associated with NSAID use?
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headaches
in elderly confusion, memory loss, psychosis, lgihtheadedness Tinnitus |
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What is Reye's syndrome?
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Vomiting and lethargy, seen more in young children
Fatty degeneration of liver and enecphalopathy also occurrs |
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Are NSAIDS recommended for use during pregnancy/lactation?
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No. Acetaminophen is the best agent for short term use in pregnancy.
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How is acetaminophen different from the MOA of NSAIDS?
a/e? od? |
It works by opposing impuleses peripherally (NSAIDs work centrally).
Has no effect on platelets or GI irritation OD-> hepatotoxicity |
