Pharmacology - NAIDS
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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 - 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 - What is the antipyretic MOA?
- Acts within CNS on heat regulating ctr in hypothalmus causing vasodilation of peripheral blood vessels and loss of body heat
- Are NSAIDS well or poorly absorbed?
- Very well
- How are NSAIDS eliminated and excreted?
- Eliminated by liver, excreted by kidneys
- What are the GI related A/E related to NSAID use?
- GI inflammation, bleeding, ulceration or perforation
- How would one treat the GI a/e of NSAIDS?
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Sucralfate
Histamine antagonists
proton pump inhibitors - 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 - What are the hematologic a/e associated with NSAID use?
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impaired platelet aggregation
Aplastic anemia and agranulocytosis
Thrombocytopenia - What are the CNS a/e associated with NSAID use?
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headaches
in elderly confusion, memory loss, psychosis, lgihtheadedness
Tinnitus - 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 - Are NSAIDS recommended for use during pregnancy/lactation?
- 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