Plasma Coagulation Factors
Plasma factors form the basis of the coagulation cascade. Historically, they are designated by Roman numerals. Key representatives include:
- Factor I (Fibrinogen): A protein synthesized in the liver. Under the action of thrombin, it converts into insoluble fibrin, whose strands form the framework of the thrombus. It also participates in platelet aggregation.
- Factor II (Prothrombin): Produced in the liver with the participation of vitamin K. Converted by the prothrombinase complex into the active enzyme thrombin.
- Factor III (Tissue Thromboplastin): A cell membrane phospholipoprotein. Released upon tissue destruction and triggers the extrinsic coagulation pathway.
- Factor IV (Calcium Ions): Required at all stages of coagulation.
- Factor V (Proaccelerin, labile factor): A hepatic protein, precursor to accelerin (Va), which is necessary for prothrombinase formation.
- Factor VI: Removed from modern nomenclature.
- Factor VII (Proconvertin): A vitamin-K-dependent glycoprotein necessary for the formation of extrinsic prothrombinase and the activation of factor X.
- Factor VIII (Antihemophilic factor A): A glycoprotein required for the formation of intrinsic prothrombinase.
- Factor IX (Christmas factor, antihemophilic factor B): A glycoprotein. Interacting with other components, it participates in the activation of factor X.
- Factor X (Stuart–Prower factor): A glycoprotein participating in the formation of both extrinsic and intrinsic prothrombinase.
- Factor XI (Plasma thromboplastin antecedent / Rosenthal factor): A glycoprotein that, after interacting with factor XII, activates factor IX.
- Factor XII (Hageman factor): Initiates the intrinsic pathway of coagulation upon contact with damaged surfaces.
- Factor XIII (Fibrin-stabilizing factor): Stabilizes the formed fibrin mesh.
In addition to the numbered factors, there are Fletcher factor (plasma prekallikrein) and Fitzgerald factor (high-molecular-weight kininogen). Both are proteins involved in the activation of factors XI, XII, and the plasminogen system.
Platelet and Other Cellular Factors
Platelets contain substances necessary for blood clotting and wound healing, including various growth factors. A total of 12 platelet factors are known. The most significant are:
- Factor 3 (Platelet thromboplastin): A phospholipid of the blood platelet membrane. Released upon their destruction and plays a crucial role in initiating intrinsic prothrombinase formation.
- Factor 4 (Antiheparin factor): Responsible for binding and neutralizing heparin.
- Factor 5 (Platelet fibrinogen): Necessary for platelet aggregation. Under the influence of thrombin, it transforms into fibrin, strengthening the platelet plug.
- Factor 8 (Thrombasthenin): A specific complex of contractile proteins that provides clot retraction.
- Vasoconstriction factors: Vasoconstrictor factor (factor 9) and serotonin.
- Aggregation stimulators: Aggregation factor (factor 12) and ADP.
Upon platelet destruction or activation, thromboxane $A_2$ is also abundantly released—an extremely potent vasoconstrictor and aggregation stimulator.
Other cells are also involved in hemostasis. For example, erythrocytes and leukocytes contain coagulation factors, with erythrocytes serving as an important source of erythrocytic thromboplastin.
Tissue Factors and the Role of Vitamin K
Damaged body tissues supply their own substances regulating hemostasis to the bloodstream. These include highly active tissue thromboplastin and endothelial von Willebrand factor, which is absolutely essential for platelet adhesion to the vascular injury site. Tissues also contain antiheparin factor, platelet aggregation stimulators, fibrinolysis activators, and compounds structurally similar to plasma factors (V, VII, and X).
Vitamin K has immense clinical significance in the hemostatic system. Based on vitamin K dependence, factors are divided into two groups:
- Vitamin-K-dependent: factors II, VII, IX, and X.
- Vitamin-K-independent: all other factors.
Vitamin K deficiency leads to severe consequences: delayed blood clotting, increased bleeding tendency, and the development of subcutaneous and internal hemorrhages.