The extrinsic and common coagulation pathways are essential for hemostasis. Formation of the fVIIa:tissue factor (TF) complex after vessel injury leads to activation of fX to fXa, which, together with its cofactor fVa, cleaves prothrombin to thrombin. Thrombin activates fV, fVIII, fXI, and fXIII, cleaves fibrinogen to fibrin, and activates platelets by cleavage of PARs. Direct thrombin inhibitors include bivalirudin, which is used in invasive cardiology, hirudin and argatraban, which are used to treat patients with heparin-induced thrombocytopenia and dabigatran, an orally available drug. Professional illustration by Marie Dauenheimer.

The extrinsic and common coagulation pathways are essential for hemostasis. Formation of the fVIIa:tissue factor (TF) complex after vessel injury leads to activation of fX to fXa, which, together with its cofactor fVa, cleaves prothrombin to thrombin. Thrombin activates fV, fVIII, fXI, and fXIII, cleaves fibrinogen to fibrin, and activates platelets by cleavage of PARs. Direct thrombin inhibitors include bivalirudin, which is used in invasive cardiology, hirudin and argatraban, which are used to treat patients with heparin-induced thrombocytopenia and dabigatran, an orally available drug. Professional illustration by Marie Dauenheimer.

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