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High-Yield Terms
Hemostasis: refers to the process of blood clotting and then the subsequent dissolution of the clot following repair of the injured tissue
Intrinsic pathway: pathway of coagulation initiated in response to contact of blood with a negatively charged surface; primarily represents a pathophysiological reaction
Extrinsic pathway: pathway of coagulation initiated in response to release of tissue factor in response to vascular injury; represents the normal physiological pathway of coagulation
Platelets: also called thrombocytes; are small, disk-shaped nonnucleated fragments released from megakaryocytes involved in initiating hemostasis
Platelet glycoproteins: refers to several types of platelet surface receptors (eg, GPIIb-GPIIIa) involved in the processes of platelet activation and aggregation
Kallikrein: any of several serine proteases that cleave kininogens to form kinins; includes plasma and tissue kallikreins
Kinin: any of a group of vasoactive polypeptides (eg, bradykinin) formed by kallikrein-catalyzed cleavage of kininogens causing vasodilation and altering vascular permeability
Tenase complex: the complex of calcium ions and factors VIIIa, IXa, and X on the surface of activated platelets
Prothrombinase complex: a complex composed of platelet phospholipids, calcium ions, factors Va and Xa, and prothrombin
Thrombus: refers to the blood clot which is the final product of the blood coagulation
von Willebrand factor, vWF: a complex multimeric glycoprotein that is produced by and stored in the α-granules of platelets and found associated with subendothelial connective tissue.
Factor V Leiden: an inherited disorder of blood clotting resulting from a variant factor V that causes a hypercoagulability disorder
Partial thromboplastin time (PTT): assay for defects in activities of the intrinsic pathway of coagulation
Prothrombin time (PT): assay for defects in activities of the extrinsic pathway of coagulation
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The ability of the body to control the flow of blood following vascular injury is paramount to continued survival. The process of blood clotting and then the subsequent dissolution of the clot following repair of the injured tissue is termed hemostasis. Hemostasis proceeds through a series of 4 coordinated events required to respond to the loss of vascular integrity.
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The initial phase of the process is vascular constriction. This limits the flow of blood to the area of injury.
Activation of platelets is absolutely required for hemostasis to proceed. Platelets become activated by thrombin and aggregate at the site of injury, forming a temporary, loose platelet plug. Platelets clump by binding to collagen that becomes exposed following rupture of the endothelial lining of vessels. Upon activation, platelets release contents of their granules that are critical for the coagulation cascade. In addition to induced secretion, activated platelets change their shape to accommodate the formation of the plug.
To ensure stability of the initially loose platelet plug, a fibrin mesh (also called the clot) forms and entraps the plug. If the plug contains only platelets and fibrin, it is termed a white thrombus; if red blood cells are present, it is called a red thrombus.
Finally, the clot ...