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HEMOSTASIS

Hemostasis is the process of preventing the loss of blood when a blood vessel is injured. The platelets or thrombocytes, as discussed in the previous chapter, play an integral role in hemostasis when they are activated and begin clustering together or aggregating. In addition, vasoconstriction of the injured blood vessel decreases blood flow through the injured site such that a clot can form and not be dislodged. Vasoconstriction also decreases the amount of blood that could leak from the injured vessel. The final step in hemostasis is the formation of a permanent clot through activation of the multistep clotting mechanisms involving the formation of interwoven fibrin plugs which trap platelets and blood cells. Eventually scar formation and endothelialization will permanently repair the vessel and the clot will be reabsorbed.

Platelets play an early role in hemostasis. Platelets contain many receptors including ones for collagen, adenosine diphosphate (ADP), and von Willebrand factor. Platelets also contain two types of granules; one type contains substances that are secreted upon activation such as serotonin, ADP, and ATP which attract more platelets to aggregate. The second type of granule contains proteins such as clotting factors and platelet-derived growth factor which stimulate wound healing. When the vessel wall is injured, platelets adhere through von Willebrand factor which is present both in the plasma and in the vessel wall. Platelet collagen receptors also bind to the exposed collagen connective tissue surrounding the blood vessels in the damaged area. When the platelets contact collagen, they swell and become irregular and adhesive. They secrete ADP and other non-protein molecules from granules. These activate other platelets to adhere and secrete more activators. Serotonin and ADP are the primary mediators of platelet aggregation which can potentially be reversed at this stage. Enzymes in the cyclooxygenase pathway are activated to promote the formation of the prostaglandin thromboxane A2 (TXA2) from arachidonic acid, released from the membrane phospholipids. TXA2 and serotonin constrict the arterioles at the damaged site to decrease blood flow, thus helping to stabilize the platelets forming the clot. The combination of platelets secreting prostaglandin thromboxane A and injured epithelium’s decline in prostacyclin production, vasoconstriction and platelet aggregation is favored. Vasoconstriction and decreased blood flow is also important for decreasing the blood loss. The platelets have a life span of about 6 to 9 days, which explains why aspirin ingestion, which irreversibly inhibits the cyclooxygenase enzyme, COX1, and blocks the formation of thromboxane 2 A, is contraindicated for 2 weeks preceding surgery. Since the inhibition is irreversible, new platelets have to be released in order for normal clotting to occur. Ibuprofen and indomethacin only reversibly inhibit the COX1 enzyme.

The multistep clotting cascade progresses to the formation of monomer fibrin from the soluble plasma protein fibrinogen through the enzymatic action of thrombin (Figure 12-1). Fibrin forms dimers and ultimately cross linkages of fibrin strands are formed by activated factor XIII and calcium ...

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