In the modern blood coagulation scheme, four phases are distinguished:
- Prothrombin formation (contact-kallikrein-kinikascade activation) – 5..7 minutes;
- Thrombin formation – 2..5 seconds;
- Fibrin formation – 2..5 seconds;
- Post-coagulation phase (formation of a hemostatically full clot) – 55..85 minutes.
A fraction of a second after damage to the vessel wall in the injury zone, a spasm of the vessels is observed, and a chain of platelet reactions develops, resulting in a platelet plug. First of all, platelets are activated by factors released from damaged tissue of the vessel, as well as by small amounts of thrombin, an enzyme that forms in response to damage.
Then platelets are bonded (aggregated) with each other and with fibrinogen contained in the blood plasma, and platelets adhere (adhesion) to the collagen fibers located in the vessel wall and the surface adhesive proteins of the endothelial cells. The process involves more and more platelets entering the damage zone. The first stage of adhesion and aggregation is reversible, but later these processes become irreversible.
Platelet aggregates are compacted, forming a plug that tightly closes the defect in small and medium vessels. Factors activating all blood cells and some coagulation factors in the blood are released from the adherent platelets, as a result of which a fibrin clot forms on the basis of a platelet plug.
Such a platelet-fibrin hemostatic plug can withstand high blood pressure after the restoration of blood flow in damaged medium-sized vessels. The mechanism of platelet adhesion to the vascular endothelium in areas with low and high blood flow rates is distinguished by a set of so-called adhesive receptors – proteins located on the cells of blood vessels.
|Factor:||Factor Name||Features and Functions|
|I||Fibrinogen||Protein-glycoprotein, which is produced by pairedimatic liver cells, is converted under the influence of thrombin into fibrin.|
|II||Prothrombin||Protein-glycoprotein, an inactive form of the enzyme thrombin, is synthesized in the liver with the participation of vitamin K.|
|III||Thromboplastin||Lipoprotein (a proteolytic enzyme) involved in local hemostasis, when in contact with plasma factors (VII and Ca), is able to activate factor X (the external pathway of prothrombinase formation). Simply put: turns prothrombin into thrombin.|
|IV||Calcium||Potentiates most coagulation factors – participates in the activation of prothrombinase and the formation of thrombin, is not consumed in the coagulation process.|
|V||Proaccelerin||Ac globulin, formed in the liver, is necessary for the formation of prothrombinase.|
|VI||Accelerin||Potentiates the conversion of prothrombin to thrombin.|
|VII||Proconvertin||It is synthesized in the liver with the participation of vitamin K, in an active form, along with factors III and IV, it activates factor X.|
|VIII||Antihemophilic Globulin A||A complex glycoprotein, the place of synthesis is not exactly established, activates the formation of thromboplastin.|
|IX||Antihemophilic Globulin B (Christmas Factor)||Beta globulin, formed in the liver, is involved in the formation of thrombin.|
|X||Thrombotropin (Stuart-Praer Factor)||Glycoprotein, produced in the liver, is involved in the formation of thrombin.|
|XI||Plasma Thromboplastin Precursor (Rosenthal Factor)||Glycoprotein activates factor X.|
|XII||Contact Activation Factor (Hageman Factor)||Activator of the coagulation trigger reaction and kinin system. Simply put, it starts and localizes thrombus formation.|
|XIII||Fibrin-stabilizing factor||Fibrinase, stabilizes fibrin in the presence of calcium, catalyzes the transamination of fibrin. Simply put, converts unstable fibrin to stable.|
|Fletcher Factor||Plasma prekallikrein activates factors VII, IX, converts kininogen to kinin.|
|Fitzgerald Factor||Kiinnogen, in active form (kinin) activates factor XI.|
|Von Willebrand factor||The component of factor VIII, produced in the endothelium, in the bloodstream, combining with the coagulation part, forms the polyocene factor VIII (antihemophilic globulin A).|
In the process of blood coagulation, special plasma proteins take part – the so-called coagulation factors, indicated by Roman numerals. These factors normally circulate in the blood in an inactive form. Damage to the vascular wall triggers a cascade chain of reactions in which coagulation factors become active.
First, the prothrombin activator is released, then, under its influence, prothrombin turns into thrombin. Thrombin, in turn, breaks down a large molecule of soluble globular fibrinogen protein into smaller fragments, which are then reunited into long strands of fibrin, an insoluble fibrillar protein.
Depending on the triggers, the external and internal blood coagulation pathways are distinguished. In both the external and internal pathways, blood coagulation factors are activated on the membranes of damaged cells, but in the first case, the triggering signal, the so-called tissue factor – thromboplastin – enters the blood from damaged tissues of the vessel.
Since it enters the blood from the outside, this coagulation pathway is called the external path. In the second case, the signal comes from activated platelets, and, since they are components of the blood, this coagulation pathway is called internal. This separation is rather arbitrary, since in the body both processes are closely interconnected. However, this separation greatly simplifies the interpretation of tests used to assess the state of the blood coagulation system.
The chain of transformations of inactive blood coagulation factors into active occurs with the obligatory participation of calcium ions, in particular, the conversion of prothrombin to thrombin. In addition to calcium and tissue factor, coagulation factors VII and X (plasma enzymes) are involved in the process.
The absence or decrease in the concentration of any of the necessary coagulation factors can cause prolonged and profuse blood loss.
Violations in the blood coagulation system can be both hereditary (hemophilia, thrombocytopathy), and acquired (thrombocytopenia). In people after 50-60 years, the content of fibrinogen in the blood increases, the number of activated platelets increases, a number of other changes occur, leading to an increase in blood coagulation and the risk of thrombosis.
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