BC #27 Eicosanoids.txt

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BC #27 Eicosanoids.txt
2011-02-09 18:55:45
BC Eicosanoids

BC #27 Eicosanoids
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  1. What cells produce prostanoids?
    All cells
  2. What cells produce leukotrienes?
    Lymphocytes and Macrophages
  3. What are the three important Prostanoids?
    • Prostaglandin (PG)
    • Prostacyclin (PGI)
    • Thromboxane (TX)
  4. What is the predominate Omega, 3 or 6, in the american diet?
    omega-6 >90%
  5. What is the number for a-linoleic acid?
    18:3, omega-3
  6. What is the number for linoleic acid?
    18:2, omega-6
  7. Out of the prostanoid derivatives EPA, DGLA and AA, which is the most inflammatory and prominent?
  8. Which is a stronger platelet inhibitor, PGI2 or PGI3?
  9. Which is a stronger platelet stimulator, TX2 or TX3?
  10. What are the cleaved products of Gs and Gq?
    • Gs= Adenylyl cyclase = cAMP
    • Gq= PLC = IP3 and DAG
  11. What is the four step process of prostaglandin and thromboxane production? (use AA)
    • 1) Ca activated PLA2, moves to membrane
    • 2) Release AA
    • 3) Production of PGH2 utilizing COX and peroxide (PGH Synthase rxn)
    • 4) Production of cell-specific prostanoid
  12. What is the RLE in prostanoid production?
  13. What is the process of forming leukotrienes?
    • 1) AA in lymphocyte or macrophage
    • 2) AA + 5-lipoxygenase
    • 3) 5-HPETE formed
    • 4) LT formed
  14. How does asprin induce asthma?
    • Asthma blocks COX
    • This shunts AA away from PG and TX production and into LT production
    • increased LT = more allregic/inflammation response
  15. Which is more common, COX-1 or COX-2?
    • COX-1: made in most cells
    • ***COX-2 is created during inflammation and immunity
  16. Which is more easily inhibited, COX-1 or COX-2 and why?
    COX-2 b/c of a larger area for inhibitor binding
  17. Where are the five common areas of COX-2 production?
    • Lung
    • Brain
    • Kidney
    • Endothelium
    • Bone
  18. What are the three keys to an NSAID?
    • 1) Anti-inflammation
    • 2) Analgesic
    • 3) Antipyretic
  19. Which does aspirin inhibit most, COX-1 or COX-2?
  20. What is the bleeding pathology of Aspirin?
    increased GI bleeding b/c of platelet inhibition (PGI3) and weak platelet stimulation (TX3)
  21. What is the positive and negative of celebrex?
    Positive: Blocks only COX-2 so it does not cause GI bleeding

    Negative: increased risk of heart attacks
  22. What is the effect of steroids (glucocorticoids) on PLA2?
  23. What is the affect of annexin-1 on PLA2?
  24. What prostanoids do Gs and Gq receive?
    • Gs: PGI2 = adenylyl cyclase and cAMP
    • Gq: TX2 = PLC = IP3 and DAG
  25. What prostaglandins do COX-1 and COX-2 help produce?
    • COX-1 = TX2 (platelets)
    • COX-2 = PGI2 (endothelium)
  26. How are prostanoids inactivated?
    At specific site of action
  27. How are prostanoids catabolized?
    • In lungs
    • Due to presence of 15-hydroxyprostaglandin dehydrogenase