Pathophys Test 2

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Author:
cgordon05
ID:
12583
Filename:
Pathophys Test 2
Updated:
2010-03-31 13:55:08
Tags:
PG LT TXA
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Description:
PG, LT, TXA
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  1. Be able to identify FA precursor for each series of PG, LT, or TXA. (p.16)
    Arachidonic acid and other 20-C PUFA give rise to eicosanoids.
  2. What FA would be precursor to TXA2? (p.18)
    • Arachidonic acidcyclooxygenase pathway
    • Catalyzes conversion of arachidonic acid to PGG2 --> PGH2 --> Thromboxane A2
  3. What effect would TXA2 have on platelet aggregation and vasoconstriction?
    • + platelet aggregation
    • + vasoconstriction
  4. Which cells synthesize and secrete TXA?
    Platelets
  5. What is the physiologic effect of PGI2?
    • Prostacyclin
    • Vasodilation
    • Inhibit platelet aggregation
  6. What cells synthesize PGI2 (prostacyclin)?
    Vascular endothelial cells
  7. How would steroids vs. ASA affect different pathways (cyclooxygenase and lipoxygenase) for generation of arachidonic acid metabolites? (p.18)
    • Steroids inhibit phospholipase, the enzyme that breaks down arachidonic acid to lipoxygenase and cyclooxygenase
    • Steroids stop arachidonic acid from being broken down to cyclooxygenase and lipoxygenase
    • ASA inhibits cyclooxygenase, which prevents formation of PGG2, but NOT lipoxygenase pathway, which leads to inflammation, vasoconstriction, bronchospasms, and increased permeability
  8. What is the mechanism by which these drugs affect inflammatory process?
    • Prostaglandins and leukotrienes mediate every step of acute inflammation
    • Glucocorticoids – strong inflammatory agents
    • o Function in part by inducing synthesis of protein that inhibits phospholipase A2
    • o If you inhibit this enzyme, you inhibit release of arachidonic acid
    • o In turn, both the end-products of lipoxygenase and cyclooxygenase are inhibited

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