Table of Contents
Definition of Platelet Aggregation
The process through which platelets respond to chemical signals in the blood, allowing them to adhere to each other and to collagen fibers in the blood to form the hemostatic plug that will become a blood clot at the conclusion of the coagulation cascade.
The formation of collagen and the conversion of fibrinogen (clotting factor I) to the enzyme fibrin together initiate a sequence of chemical conversions that alter platelet surface proteins as well as attract more platelets to the location of the injury.
As the coagulation cascade continues, platelets accumulate. The platelets change shape, developing threadlike extensions called pseudopods that allow them to extend like vines into the weave of collagen fibers.
The surface of the platelets continues to undergo chemical changes that attract fibrinogen and release arachidonic acid, which oxidizes to form prostaglandins, short-acting hormones that are key players in the immune system’s inflammation response. Prostaglandins further attract platelets to the site.
Converted clotting factors begin to weave fibers of protein among the fibers of fibrin, thrombin, and collagen, forming a netlike structure that entraps other cells flowing through the blood. When the clot reaches critical mass additional chemical reactions begin to shut down the coagulation cascade, bringing the clotting process to a halt.
The surface proteins of circulating platelets revert, and the platelets no longer adhere to each other. The reversion also activates mechanisms within the platelets that cause them to contract, pulling them tightly into the clot structure. Other proteins cause the clot to harden, cementing it in place.
Inflammation of the artery walls, such as occurs with coronary artery disease (CAD), attracts platelets in the same manner as do wounds, setting in motion the events of platelet aggregation in ways that are detrimental to health. Doctors often prescribe antiplatelet medications to slow platelet aggregation in people who have had heart attack or stroke, or who have CAD.
Most of these medications work by blocking the oxidation of arachidonic acid, which then inhibits prostaglandin formation. The most commonly used antiplatelet medication is aspirin. Platelet aggregation can also occur as a side effect of medications or a dysfunction of coagulation.
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