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The intrinsic pathway begins when blood contacts a negatively charged surface, activating Factor XII to XIIa. This process requires no tissue damage.

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Activated Factor XIIa converts Factor XI to XIa. This step requires calcium ions (Ca2+) as a cofactor.

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Factor XIa activates Factor IX to IXa, another calcium-dependent step in the cascade.

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Factor IXa combines with Factor VIIIa on phospholipid surfaces in the presence of calcium to form the 'tenase complex' which activates Factor X to Xa. This is a crucial bridge to the common pathway.

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The extrinsic pathway initiates when tissue damage exposes tissue factor (TF/Factor III) to the bloodstream.

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Tissue Factor combines with Factor VII, converting it to Factor VIIa. This process requires calcium ions.

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The TF-VIIa complex, in the presence of calcium and phospholipids, activates Factor X to Xa, leading to the common pathway.

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Factor Xa combines with Factor Va on phospholipid surfaces in the presence of calcium to form the prothrombinase complex.

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The prothrombinase complex converts prothrombin (Factor II) to thrombin (Factor IIa). This reaction requires calcium ions and phospholipid surfaces.

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Thrombin converts fibrinogen (Factor I) to fibrin monomers, which begin to form loose connections.

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Thrombin activates Factor XIII to XIIIa, which creates strong covalent bonds between fibrin molecules, forming a stable cross-linked fibrin clot.