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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.
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What FA would be precursor to TXA2? (p.18)
- Arachidonic acid – cyclooxygenase pathway
- Catalyzes conversion of arachidonic acid to PGG2 --> PGH2 --> Thromboxane A2
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What effect would TXA2 have on platelet aggregation and vasoconstriction?
- + platelet aggregation
- + vasoconstriction
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Which cells synthesize and secrete TXA?
Platelets
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What is the physiologic effect of PGI2?
- Prostacyclin
- Vasodilation
- Inhibit platelet aggregation
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What cells synthesize PGI2 (prostacyclin)?
Vascular endothelial cells
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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
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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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