Exam 1 Review:  Chapter 17:  Hemostasis I:  Platelets

hemorrhage - Any flow of blood from ruptured blood vessels; such bleeding may be internal or external.

hemostasis - The body processes by which the body controls the flow = hemorrhage of blood after vascular injury; it consists of four major events:  (1)  vascular constriction = vascular spasm, (2) platelet plug formation, (3) coagulation, i.e, fibrin formation, and (4) clot dissolution, i.e., fibrinolysis; each of the four processes is under complex regulatory control.

vascular constriction = vascular spasm - A sudden, brief tightening of the smooth muscle in a blood vessel; vascular spasms can temporarily reduce blood flow to tissues supplied by that vessel; a vascular spasm is the first response to significant hemorrhage and is more effective in smaller vessels; such vascular spasms are triggered by pain and by serotonin released from platelets; vascular spasms unrelated to hemostasis may cause pain and poor blood circulation

platelet plug - The collection of activated platelets which become trapped in a mesh of collagen fibers, which serve as the chemical trigger for activation, and form the first obstacle to further hemorrhage after a blood vessel becomes ruptured to any degree; for the smallest vascular injuries, the platelet plug may final event of hemostasis.

platelet adhesion = platelet aggregation - The process by which platelets adhere to the collagen of basement membrane beneath the endothelium at sites of vascular injury and, thus becoming activated, also stick to each other forming the platelet plug; aspirin, ibuprofen and related NSAIDs interfere with this process; this process is disrupted in disseminated intravascular coagulation (DIC) and in renal failure.

platelet release reaction - The release of a variety of regulatory substances from the alpha granules and dense bodies of activated platelets which contribute to the coagulation cascade which produces a blood clot.

Describe:

4. The three steps in platelet plug formation.

          (1)  platelets adhere to exposed collagen after any tear in vessel endothelium (assisted by von Willebrand factor)
          (2)  platelets activated by thrombin, breakdown and release various regulating and enhancing factors (serotonin, ADP, Thromboxane A₂)
          (3)  more platelets are attracted to the site and the platelet plug forms, a positive feedback situation until hemostasis occurs (limited by the platelet aggregation inhibitor, PGI₂ = prostacyclin)