Pathophysiology

Once injured or activated by a toxic substance (e.g., bacterial toxins, placenta chemicals, snake venom, etc.), endothelial cells and monocytes respond by generating tissue factor on the cell surface. Generation of tissue factor-factor VIIa complexes leads to extrinsic pathway activation, excessive generation of thrombin and fibrin, generation of systemic microthrombi, and consumption of coagulation factors and platelets. In addition, inhibition of naturally occurring endothelium-linked anticoagulant pathways (e.g., antithrombin, protein C, and tissue factor pathway inhibitor) and fibrinolytic system (due to a rise in plasminogen activator inhibitor, PAI-1 concentrations) leads to a vast procoagulant state. While bleeding into the subcutaneous tissues, skin, and mucous membranes takes place, microvascular thrombosis exacerbates tissue ischemia 22

and organ damage.

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