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The coagulation cascade can be divided into initiation and amplification phases (Figure 3). After vessel injury the TF:FVIIa complex activates both FX and FIX and together with FVa from activated platelets this leads to the generation of small amounts of thrombin. In this initial phase thrombin activates the cofactors FV and FVIII and also platelets. However, the TF:FVIIa complex is rapidly inhibited by TFPI in a FXa-dependent manner. Activated platelets play a key role in the amplification of the coagulation cascade because they provide a surface for the assembly of the tenase (FVIIIa:FIXa) and prothrombinase (FVa:FXa) complexes. Large amounts of thrombin  are generated and cleave fibrinogen to fibrin monomers that are crosslinked by FXIIIa.

Schematic representation of coagulation cascade, as described in previous text. The coagulation cascade divided into the extrinsic pathway, consisting of the FVIIa:TF complex and the intrinsic pathway, which follows a pathway of activation from FXII to FXIIa, then FX to FXa, then FXI to FXIa and FVIII to FVIIa. The two are activated by the FVIIa:TF complex. Both pathways go to the common pathway, which follows the activation pathway of FX to FXa and FV to FVa, then FII to FIIa, which, along with platelets, leads to fibrin clots.