pharmacology test 4 NSAID

  1. inflammatory mediator
    vasodilator, increases permeability
  2. inflammatory mediator
    potent mediator of pain
  3. inflammatory mediator
    vasodilator, chemotactic
  4. inflammatory mediator
    increases permeability, chemotactic
  5. 4 main effects of chronic inflammation meidators
    • cell activation
    • PG-production
    • fibroblast
    • chemotaxis
    • proliferation
  6. what is stimulated by inflammation that causes leukocytes to slow and start rolling
  7. mediates sticking of the leukocytes to the endothelial wall
    • I-CAM
    • V-CAM
  8. leukocyte migration through the edothelial wall
  9. chemotaxis
    chemokines, leukotrienes, cytokines, f-MLP
  10. housekeeping enzyme
    maintains integrity of gastric mucosa
    maintains renal function
    COX 1
  11. inducible enzyme for inflammation
    COX 2
  12. inhibition of COX 1 results in what 3 things
    • gastric ulcer
    • renal failure
    • protection against acute MI
  13. inhibition of COX 2 results in what 3 things
    • antiinflammatory
    • antipyretic
    • analgesic action
  14. thromboxane (TxA2) causes
  15. prostacyclin (PGI2) causes
  16. Prostaglandins (PGD2, PGE2, PGF2) causes (3)
    • inflammation
    • fever
    • gastroprotection
  17. drug class that inhibits COX
  18. drug group that inhibits Phospholipase A2
  19. phospholipase A2 acts on the cell membrane and produces what
    arachidonic acid
  20. converts arachidonic acid to leukotrienes
  21. drug that inhibits lipoxygenase
  22. leukotriene responsible for chemotaxis
  23. drug to inhibit LTB4
  24. drug to inhibit LTD4 from receptor binding
  25. leukotriene binding causes what
  26. what converts arachidonic acid to prostaglandin H2
  27. where are thromboxanes produced from
  28. where are protacyclins produced from
  29. where are prostaglandins (PGD2, PGE2, PGF2) located
    blood stream
  30. why does low dose aspirin work on platelets and not endothelium
    platelets don't have DNA, it is for the life of the cell - 7 days
  31. how do NSAIDS induce asthma
    by inhibiting COX you shift the mechanism to the LOX side which is bronchoconstriction
  32. MOA of aspirin
    irreversible non-selective inhibitor of both COX - covalent
  33. absorption of aspirin
    • rapidly from stomach and small intestine
    • hydrolyzed to salicylic acid
  34. how does aspirin reduce fever
    inhibition of pyrogen-induced PG synthesis
  35. what is aspirin inhibiting that causes adverse GI effects
  36. drug to treat aspirin induced GI ulcer
    misoprostol (cytotec)
  37. doses of > 4g/day can cause what
  38. severe side effect of aspirin in children
    reye's syndrome
  39. aspirin and warfarin
    increased bleeding
  40. aspirin and glucocorticoids
    increased risk of gastric ulcer
  41. aspirin and alcohol
    increased risk of gastric ulcer
  42. aspirin and ibuprofen
    reduces platelet effect of aspirin
  43. sign of plain aspirin tablets gone bad
    odor of vinegar
  44. 2 differences of aspirin and other first generation NSAIDS
    • reversible inhibition of COX
    • does not protect against MI
  45. 4 nonacetylated salicylates (first generation NSAIDS)
    • choline salicylate (arthropan)
    • magnesium salicylate (magan)
    • sodium salicylate
    • salsalate (disalcid, mono-gesic)
  46. prodrug NSAID
    hydrolyzed in alkaline medium to release 2 molecules of salicylates
    salsalate (disalcid, mono-gesic)
  47. first generation NSAID
    propionic acid derivative
    ibuprofen (advil, motrin)
  48. drug of choice to promote closure of ductus arteriosus in preterm infants
  49. intravenous ibuprofen
  50. first generation NSAID not metabolized to salicylic acid
    T1/2 of 11-15h
    diflunical (dolobid)
  51. first generation NSAID for gouty arthritis
    indomethacin (indocin)
  52. first generation NSAID given post-surgery
    not to be taken longer than 5 days
    more peripheral
    ketorolac (Toradol)
  53. first generation NSAID with T 1/2 of 50h
    piroxicam (Feldene)
  54. first generation NSAID
    undergoes extensive enterohepatic circulation
    SE - steven johnson syndrome
    sulindac (clinoril)
  55. first generation NSAID
    approved for rheumatoid arthritis and osteoarthritis (not fever or inflammation)
    tolmetin (tolectin)
  56. first generation NSAID
    more cox 2 inhibition
    indicated for osteoarthritis
    meloxicam (mobic)
  57. 2 2nd generation NSAID
    • celecoxib (celebrex)
    • acetaminophen (tylenol)
  58. antidote for acetaminophen overdose and what does it mimic
    • acetylcysteine (mucomyst)
    • G-SH
  59. what metabolizes toxic metabolites of acetominphen to non-toxic
    G-SH (glutathione)
  60. how does alcohol stimulate acetominophen toxicity
    • increase toxic metabolites
    • inhibits G-SH
Card Set
pharmacology test 4 NSAID
pharmacology 4