Card Set Information

2011-04-18 13:32:36

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  1. Aspirin (acetylsalicylic acid: ASA)
    • Analgesic, anti-inflam, anti-pyretic, antithrombotic
    • Irrev inhibit COX thru acetylation (170:1 COX1:2)
    • Salicylic acid (metabolite) inhibits PG synth - majority of anti-inflam effects
    • SE: GI effects - nausea, vomiting, dyspepsia, heartburn, ulcers; bleeding; inhibition of uric acid secretion@renal tubule
    • Salicylicism: hyperthermia, hearing loss, tinnitus!
    • Low doses to block platelet aggregation, intermediate for antipyretic/analgesic, high dose for anti-inflamm
  2. Celecoxib
    • selective COX2, increased PG synth
    • analgesic, effective in hyperalgesia
    • TxA2 is produced by COX1 in platelets = does not inhibit platelet aggregation!
    • SE: risk dependes on duration of use; cardio SE, GI bleeding, ulceration, perforation
  3. Diclofenac
    • IM, rapid action
    • blocks arachidonate binding
    • analgesic, antipyretic, anti-inflamm
    • preferential COX2
    • SE: similar to others, hepatotoxicity
  4. Ibuprofen (advil, motrin, nuprin)
    • similar profile to ASA
    • SE: GI effects < ASA
  5. Indomethacin
    • More potent anti-inflam, same as ASA for analgesia, nonselective
    • PO, R, IV
    • For severe rheum arthritis, OA, acute gouty arthritis, ankylosing spondylitis
    • SE: similar to ASA but more severe
  6. Ketorolac
    • nonselective, comparable to morphine in analgesia w/less drowsiness, nausea, vomiting
    • PO, IV, opth, IM
    • SE: dosing restriction <5d due to incr. SE
  7. Naproxen (aleve, naprosyn)
    • nonselective
    • 1/2life 12-17h compared to ibuprofen (2h)
    • SE: GI effects less than ASA, indomethacin
  8. Sulindac
    • nonselective
    • OA, RA, ankylosing spondylitis, bursitis, acute gouty arthritis
    • w/celecoxib, only NSAID for regression of colorectal polyps w/familial adenomatous polyposis
    • GI: same for ASA
  9. Meloxicam
    • less selective for COX2 than celecoxib
    • SE: same as ASA
  10. acetaminophen
    • NOT NSAID! non-opioid analgesic
    • better for pts w/underlying renal disease
    • COX2 inhibitor, does not inhibit in periphery, no anti-inflamm!
    • SE: excess = hepatotoxicity, otherwise less than ASA
  11. Prostagladins in inflammation
    • PGI2: inhibits platelet aggregation, vasodilatation, vascular permeability (edema)
    • PGE2: pain, hyperalgesia, heat, vasodilatation, bronchoconstriction, synergistically act with other pro-inflammatory mediators (histamine, complement, LTB4)
    • TXA2: promotes platelet aggregation, vasoconstriction, bronchoconstriction.
  12. Drug interactions
  13. Displace other drugs from plasma protein binding sites:− Anti-coagulants (warfarin): Bleeding risk greatly increased − Phenytoin: (increased CNS toxicity, difficulty dosing) − Oral Hypoglycemics: (increased hypoglycemic risk) − Methotrexate: (increased toxicity)
    • Anti-Hypertensives (diuretics, beta blockers, ACE inhibitors): NSAIDs may blunt the anti-hypertensive effects and cause renal decompensation or renal failure in patients receiving these drugs
    • Methotrexate, digoxin, aminoglycosides, lithium: NSAIDs inhibit clearance
    • Probenecid: renal clearance of NSAIDs reduced by probenecid
    • Antacids: absorption of some NSAIDs inhibited by antacids
    • Aspirin: may lower levels of other NSAIDs, but side effects are additive
  14. Half life comparison
    • Short Half Life (< 6 hours): more rapid effect and clearance Aspirin (0.25-0.33 hrs), Diclofenac (1.1 ± 0.2 hrs), Ketoprofen (1.8 ± 0.4 hrs), Ibuprofen (2.1 ± 0.3 hrs), Indomethacin (4.6 ± 0.7 hrs)
    • Long Half Life (> 10 hours): slower onset of effect and slower clearance Naproxen (14 ± 2 hrs), Sulindac (14 ± 8hrs), Namebutone (26 ± 5 hrs), Piroxicam (57 ± 22 hrs) (also COX-2 Selective Inhibitors)
  15. Treatment of acetaminophen toxicity
  16. Discontinuation / Avoidance of NSAIDs
    • Take medication with meal
    • Pharmacologic − H2 Receptor Antagonists (high doses of ranitidine) − PPIs (omeprazole)
    • − Misoprostol (PGE 1 analog) which restores cytoprotective effects)
  17. NSAIDs in patients w/renal compromise
    • PGE2, PGI2 help vasodilate to maintain renal function
    • acute renal failure caused by decr. GFR