pharm exam 3- eicosanoids

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pharm exam 3- eicosanoids
2013-03-23 18:34:36
aa emory

part 2
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  1. Eicosanoids are metabolites of __________ _______ that can be synthesized and released from nearly ___ cells to affect a broad range of biological.
    • arachadonic acid
    • all
  2. Autocoids are ________ which are biologically active compounds that are _______ synthesized and released.  they act _________. they have a short _____-_____ and duration of action.
    • eicosanoids
    • rapidly
    • locally
    • half-life
  3. biologically active eicosanoids include:
    PG, TX, LT
  4. Actions of Eicosanoids
    • inflammation
    • pain
    • fever
    • GI tract
    • bronchial smooth muscle
    • platelet aggregation
    • uterus
    • cardiovascular
    • others
  5. Indirect inhibitors of eicosanoids:
    • glucocorticoids
    • fx cox1/2, lipocortin, Hcz
  6. glucocorticoids prototypes
    hydrocortisone/cortisol, prednisone, decxamethasone
  7. glucocorticoids act by modifying gene expression.  T/F?
  8. glucocorticoids cellular actions:
    • upregulate lipocortin
    • down-regulate cox1/2
  9. glucocorticoids clinical uses
    • anti-inflammatory
    • replacement therapy
  10. glucocorticoids side fx
    long term= cushings syndrome
  11. NSAID prototypes
    • aspirin
    • Sulindac
    • Indomethacin
    • Ketorolac
    • Ibuprofen
    • Naproxem
  12. NSAID mechanism
    directly inhibit Cox-1 and Cox-2
  13. which NSAIDS are irreversible
    • aspirin
    • salycilates
  14. which NSAIDS are reversible
    • indomethacin
    • ibuprofen
    • acetaminophen
  15. reversibly binding NSAIDS are generally _______ acting.
  16. are reversible NSAIDS useful as blocker of clot formation?
    NO, only irreversible are
  17. Stephens johnson syndrome can occur with?
    acetic acids
  18. what are the NSAID Acetic Acids and Pyrroles?
    Indomethacin, Sulindac, Ketorolac
  19. What are the NSAID PROprinoic acids?
    IB, Naproxem
  20. are proprinoic acids reversible binders of cox1/2?
  21. Are NSAID propinoic acids useful in blocking clot formation?
  22. Acetaminophen  is believed to act by inhibiting _____, CNS specific.
    COX 1
  23. Acetaminophen fx:
    • weak inhibition of prostanoid synthesis
    • blocks prostanoid effects on T and pain in CNS
  24. Is Acetaminophen useful as an anti-inflammatory?
  25. Acetaminophen has the risk of __________, but not ________ or _________ like most NSAIDS.
    • hepatotoxicity
    • GI fx
    • blockade of plt aggregation
  26. What are the NSAID Selective COX-2 inhibitors?
    • rofecoxib (vioxx)
    • celecoxib (celebrex)
    • valdecoxib (bextra)
    • Etoricoxib (arcoxia)
  27. what is the cox 2 hypothesis?
    cox 2 more specific to inflammatory response
  28. what is the NSAID Selective COX-2 inhibitor mechanism of action?
    REVERSIBLE direct binding of Cox-2.  also binds cox 1 but is 30x more selective for cox 2
  29. What is the advantage of using NSAID Selective COX-2 inhibitors?
    REDUCED neg GI fx
  30. Celebrex is ____x more selective for Cox-2
  31. VIOXX is ____x more selective for Cox-2
  32. BEXTRA is ____x more selective for Cox-2
  33. ARCOXIA is ____x more selective for Cox-2
  34. Cox-2 selective inhibitors cause 2-3 fold increase in risk for
    heart attack
  35. which Cox-2 selective inhibitor is on market now?
  36. COX-2 is being studied to treat
    cancer and alzhiemers
  37. 5'-Lipoxygenase inhibitor prototypes
    Zileuton (Zyflo)
  38. 5'-Lipoxygenase inhibitor prototypes are useful in tx of astham and anaphylaxis.  Explain why:
    Leukotrienes are the most powerful constrictors of bronchial smooth muscle, and this inhibits the enzyme that makes leukotrienes.
  39. 5'-Lipoxygenase inhibitor use:
    long-term asthma management
  40. 5'-Lipoxygenase inhibitor prototypes side fx
    • gastric indigestion
    • short-acting-4x daily (compliance)
  41. the future of eicosanoid therapy is to target:
    individual receptors
  42. Receptor AGONIST prototypes:
    • Misoprostol (cytotec)
    • Dinoprstone/PGE2 (prostin E2)
    • Carboprost (Hemabate)
  43. Misoprostol is a ______ ________.  it's cellular action is mimic actions of _____.
    • receptor agonist
    • PGE2
  44. Clinical uses of Misoprostol (receptor agonist)
    • used w/ NSAID combo
    • prevents negative GI fx of NSAIDS
    • uterine stimulant
  45. side fx of Misoprostol (receptor agonist)
    • diarrhea
    • pregnancy
  46. DINOPROSTONE, CARBOPROST TROMETHAMINE, LATANOPROST mechanism, and cellular action. (receptor agonist)
    • FP receptor agonist, EP receptor agonist
    • mimics cellular action is PGE2, PGF2a
  47. DINOPROSTONE, CARBOPROST TROMETHAMINE, LATANOPROST clinical uses: (receptor agonist)
    • labor induction
    • refractory postpartum hemorrhage
    • induced abortion
    • anti-glaucomal EYE drop (xalatan)
    • diarrhea/ vomitting
    • uterine hypertonus
  49. (receptor agonist) EPOPROSTEROL/prostacyclin mechanism of action and cellular action:
    • IP2 receptor agonist
    • mimics action of PGI2
  50. (receptor agonist) EPOPROSTEROL/prostacyclin uses:
    serious pulmonary HTN
  51. (receptor agonist) EPOPROSTEROL/prostacyclin side fx:
    diarrhea, ^ HR, headache, nausea, flushing
  52. Leukotriene receptor ANTAGONISTS prototypes:
    • Monteleukast (singulair)
    • Zafirlukast (Accolate)
  53. Leukotriene receptor ANTAGONISTS mech of action and cell action
    • CLT1-R receptor antagonist
    • blocks actions of LTD4
  54. Leukotriene receptor ANTAGONISTS clinical uses and side fx:
    • chronic management of asthma
    • mild-GI, headahce, heartburn, allergic rx