Coagulation

As well as inflammation, there are abnormalities of both coagulation (clot formation) and fibrinolysis (break down of clot) as illustrated in Figure 7.2.

Increased coagulation driven by pro-inflammatory mediators, endothelial cell injury, tissue factor expression, and thrombin production

Figure 7.2 Abnormalities of coagulation and fibrinolysis

The many inflammatory mediators that are released promote coagulation. In addition, infectious agents can cause endothelial damage themselves, which also promotes coagulation. At each step in the cycle auto-amplification occurs, accelerating the coagulation abnormalities. Proinflammatory cytokines, such as interleukin 1A, interleukin 1B, and TNF, induce the expression of tissue factor (TF) on endothelial cells and monocytes initiating coagulation. TF is a key mediator between the immune system and coagulation and is the principle activator of coagulation causing large amounts of thrombin to be generated.

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