Hemostasis and Coagulation

Primary Hemostasis. The delicate equilibrium between anticoagulation and coagulation is maintained by a complex system of counterbalanced blood proteins and cells (platelets). Many congenital and acquired disorders can push the system toward either bleeding or thrombosis. A number of tests can be used to evaluate the system and therapeutic modalities to correct these imbalances.
1. Platelets adhere to sites of endothelial disruption; undergo activation to recruit more platelets and amplify the platelet response; and then crosslink with fibrin, the end product of the plasma clotting factor cascade, to form a platelet plug (Fig. 16-1: Overview of platelet pathways for adherence, activation, stabilization, and physiologic inhibition).
2. To maintain hemostatic balance, platelets are naturally inhibited in their endothelial environment.
Secondary Hemostasis. Clotting factors in the plasma are activated at sites of endothelial injury and assemble in enzymatic complexes to activate thrombin.
1. The extrinsic pathway begins when endothelial disruption exposes tissue factor on underlying cell membranes, extrinsic to the circulation (Fig. 16-2: Summary of secondary hemostasis and the intrinsic, extrinsic, and common coagulation pathwaysA–E).
2. The intrinsic pathway involves thrombin that has several central functions (Fig. 16-2: Summary of secondary hemostasis and the intrinsic, extrinsic, and common coagulation pathwaysF–J).
  1. Clotting factors are primarily produced in the liver, except for VIII, which also is released by endothelial cells and is well maintained in liver disease.
  2. The plasma half-life of most clotting factors is around 1.5 to 3 days, but those of the factor VII (6 hours) and the cofactors V and VIII (8–12 hours) are much shorter.
3. Inhibition of Clotting Factors (Fig. 16-3: Depiction of the antithrombotic regulation of hemostasis).

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