Hemostatic Disorders in Animals - Circulatory System - MSD Veterinary Manual

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• TF-bearing cells initiate hemostasis

• Hemostatic Disorders

• adequate number of functional platelets, an adequate concentration and activity of plasma coagulation and fibrinolytic proteins

• Citrated plasma samples are often used in veterinary medicine to determine fibrinogen concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), and d-dimer or fibrinogen degradation product (FDP) concentration

• a normally responsive blood vasculature

• organ capsules and the adventitia of blood vessel walls.

• expressed on fibroblasts and, on cellular activation, on vascular smooth muscle cells, monocytes, and neutrophils.

• The TF-bearing cells and platelet surfaces act as the main cellular surfaces for assembly of the procoagulant complexes.

• Any vessel injury leads to TF exposure. Factor VII binding to TF results in activation to Factor VIIa.

• cell-based, tissue factor (TF)/Factor VII–dependent model of hemostasis

• Factor VIIa bound to TF on the cell surface activates Factor IX to Factor IXa

• Factor X to Factor Xa

• Initially, the formed Factor Xa is limited to the TF-bearing cell, because Factor Xa that diffuses away from the cell is rapidly inhibited by TF pathway inhibitor (TFPI) or antithrombin.

• Together with formed Factor Va, Factor Xa is assembled into the prothrombinase complex on the surface of the TF-bearing cell.

• An initial small amount of thrombin close to the cell independent of the presence of platelets is generated and is responsible for activation of platelets, release of Factor V from the platelets, activation of Factor V, activation of Factor VIII and release of Factor VIII from von Willebrand factor, and activation of Factor XI.

• Platelets also are activated by other mechanisms, including vessel wall collagen and von Willebrand factor, leading to adhesion and aggregation at the injured site.