PHYSL210A Lecture Notes - Lecture 6: Endothelium, Cyclooxygenase, Aspirin

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Lecture 5 recording 14: platelets and hemostasis: hemostasis, the prevention of blood loss. Factors which trigger vasoconstriction: an injury stimulates pain receptors that activate nerve endings that are directly affected by the cuts, causing vasoconstriction. Injury to blood vessel smooth muscle, causing vasoconstriction. Step 3: secondary hemostasis or blood clotting/coagulation (red thrombus) If the bleeding does not stop after the formation of the white thrombus, blood clotting enzymes are activated to form a stronger gel-like clot at the cut site. Once platelets are activated, they secrete the compounds: Prostacyclin (prostaglandin i2 or pgi2) inhibits platelet aggregation: nitric oxide (no) inhibits platelet adhesion, activation and aggregation, effects of arachidonic acid metabolites, the innate response of inflammation occurs within seconds of the initiation of injury. In the lipoxygenase pathway: arachidonic acid is converted to leukotrienes by the enzyme lipoxygenase, and these chemicals then initiate inflammatory responses of swelling.

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