FIGURE 2.

A summary of coagulation pathways. Coagulation occurs through contact activation (intrinsic), tissue factor (extrinsic), and common pathways when tissue damage occurs. The intrinsic pathway includes FVIII, FIX, FX, FX, FXI, and FXII. The extrinsic pathway contains coagulation factors FII, FVII, and FX. The common pathway also includes coagulation factors FI, FV, and FXIII. Each of these factors is activated by affecting the other factor. Anticoagulants are used to prevent blood clots in some diseases. Warfarin is one of these anticoagulants that inhibits FII, FIX, FX, protein‐S, and protein‐C. It can also block the conversion path of FVII to FVIIa. DOACs inhibit FXa. AT also blocks the conversion path of FII to FIIa and FX to FXa simultaneously. FIIa inhibitors include DTIs, DFXal, and LMWH. DTIs are inhibitors that inhibit the polymerization and stabilization pathway of FIa. UFH works to boost AT function. Aspirin inhibits the accumulation of active platelets next to each other. In addition to warfarin, TFPI can inhibit the conversion pathway of FVII to FVIIa. AT, antithrombin; DFXal, direct factor Xa inhibitors; DOACs, direct oral anticoagulants; DTIs, direct thrombin inhibitors; LMWH, low‐molecular‐weight heparin; RBC, red blood cells; TFPI, tissue factor pathway inhibitor; UFH, unfractionated heparin; WBC, white blood cells.