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Factor VII

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Anatomy and Physiology I

Definition

Factor VII is a serine protease that plays a crucial role in the initiation of the extrinsic pathway of the blood coagulation cascade. It is an essential component in the process of hemostasis, the body's natural mechanism to stop bleeding and promote blood clot formation.

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5 Must Know Facts For Your Next Test

  1. Factor VII is synthesized in the liver and requires vitamin K for its proper activation and function.
  2. Activated factor VII (FVIIa) forms a complex with tissue factor, which then activates factor X, a key step in the initiation of the coagulation cascade.
  3. Factor VII deficiency is a rare inherited bleeding disorder that can lead to prolonged bleeding episodes and increased risk of hemorrhage.
  4. Recombinant activated factor VII (rFVIIa) is used as a hemostatic agent to treat bleeding disorders, such as hemophilia, and to control severe bleeding in trauma or surgical settings.
  5. Elevated levels of factor VII have been associated with an increased risk of thrombotic events, such as heart attacks and strokes, due to its role in promoting blood clot formation.

Review Questions

  • Explain the role of factor VII in the extrinsic pathway of the blood coagulation cascade.
    • Factor VII is a crucial component of the extrinsic pathway of blood coagulation. When tissue factor (TF) is exposed to the bloodstream, it binds to and activates factor VII, forming the TF-FVIIa complex. This complex then activates factor X, which is a key step in initiating the coagulation cascade and ultimately leading to the formation of a stable fibrin clot to stop bleeding.
  • Describe the relationship between factor VII, tissue factor, and the coagulation cascade.
    • The interaction between factor VII and tissue factor (TF) is a critical event in the initiation of the extrinsic pathway of the coagulation cascade. Tissue factor, a membrane-bound protein, is normally not exposed to the bloodstream. However, when tissue damage occurs, TF is exposed and binds to factor VII, activating it. The activated factor VII (FVIIa) then activates factor X, which in turn activates prothrombin to thrombin, leading to the formation of a fibrin clot. This cascade of enzymatic reactions involving various coagulation factors is essential for the body's hemostatic response to stop bleeding.
  • Analyze the clinical implications of factor VII deficiency and the use of recombinant activated factor VII (rFVIIa) in the treatment of bleeding disorders.
    • Factor VII deficiency is a rare inherited bleeding disorder that can lead to prolonged bleeding episodes and increased risk of hemorrhage. Individuals with factor VII deficiency lack the necessary factor VII to initiate the extrinsic pathway of the coagulation cascade, leading to impaired hemostasis. Recombinant activated factor VII (rFVIIa) has been developed as a hemostatic agent to treat such bleeding disorders, including hemophilia. When administered, rFVIIa can bypass the need for factor VII and directly activate factor X, thereby restoring the coagulation cascade and promoting the formation of a stable fibrin clot. The use of rFVIIa has been shown to be effective in controlling severe bleeding in trauma, surgical, and other clinical settings where rapid hemostasis is critical.

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