(from the intrinsic system: contact activation) Factor XII becomes XIIa, which works to change factor XI into factor XIa. Then this (along with Ca2+) turns factor IX into factor IXa. This (along with phospholipids, factor VIIIa (from factor VIII), and Ca2+) turn factor X into factor Xa. (from the extrinsic system: tissue injury) Factor VII turns into factor VIIa. This and tissue factor released during tissue injury both assist in turning factor X into factor Xa. (From both systems) This is the beginning of the prothrombinase complex, from here factor Xa (with the help of Ca2+, factor Va (from factor V) and phospholipids (this is the end of the prothrombinase complex)) turns factor II (prothrombinase) into factor IIa (thrombin). Thrombin then assists in turning fibrinogen into fibrin (soluble) as well as turning soluble fibrin into insoluble fibrin by changing factor XIII into XIIIa which turns soluble fibrin into insoluble fibrin. When fibrinogen is turned into fibrin (soluble) fibrinopeptide A or B is released from fibrinogen. Fibrinogen is a peptide released from the amiuno end of fibrinogen by the action of thrombin to form fibrin during clotting of the blood. Thrombin can accelerate production of XIa, VIIa, and Va (positive feedback).

Factor VIIIa (from factor VIII), and Ca2+) turn factor X into factor Xa. Then factor XII becomes XIIa, which works to change factor XI into factor XIa. This is the beginning of the prothrombinase complex, from here factor Xa (with the help of Ca2+, factor Va (from factor V) and phospholipids (this is the end of the prothrombinase complex)) turns factor II (prothrombinase) into factor IIa (thrombin). Thrombin then turns plasminogen into plasmin (fibrin surface) as well as turns fibrin surface plasmin into fluid phase plasmin. Plasmin (fibrin surface) then turns fibrin into the fibrin-degredation products. Thrombin inhibits the production of XIa, VIIIa, and Va (negative feedback).

Initially plasminogen (fibrin surface) is assisted by t-PA (tissue plasminogen activator) to become plasmin (fibrin surface) which then changes insoluble fibrin into fibrin-degradation products. This is what causes fibrinolysis. The other pathway is plasminogen (fluid phase) which with the assistance of u-PA (urokinase-type plasminogen activator) to become plasmin (fluid phase). This does not appear to create fibrin-degradation products (?).

Plasmin (fluid surface) is assisted by t-PA to become plasminogen (fluid surface) in order to turn fibrin (insoluble) into fibrin-degradation products. this is what causes fibrinolysis. U-PA changes plasmin (fibrin surface) into plasminogen (fibrin surface). This does not effect fibrinolysis.