The system of hemostasis or blood coagulation is a set of processes necessary to prevent and stop bleeding, as well as to maintain a normal liquid state of the blood. Normal blood flow ensures the delivery of oxygen and nutrients to tissues and organs.
Types of hemostasis
The blood clotting system has three main components:
- actual coagulation system - prevents and eliminates blood loss;
- anti-clotting system - prevents blood clots;
- fibrinolysis system - dissolves already formed blood clots.
All these three components must be in constant balance to prevent blockage of blood vessels by blood clots, or, conversely, high blood loss.
Hemostasis, that is, stopping bleeding, is of two types:
- platelet hemostasis - provided by adhesion (gluing) of platelets;
- coagulative hemostasis - provided by special plasma proteins - factors of the blood coagulation system.
Platelet hemostasis
This type of hemorrhage stop is included in the work first, even before the activation of the coagulation. If the vessel is damaged, its spasm is observed, that is, the narrowing of the lumen. Platelets are activated and adhere to the vascular wall, which is called adhesion. Then they stick together between themselves and fibrin threads. They are being aggregated. At first, this process is reversible, but after the formation of a large amount of fibrin, it becomes irreversible.
This type of hemostasis is effective for bleeding from vessels of small diameter: capillaries, arterioles, venules. For the final stop of bleeding from medium and large vessels, it is necessary to activate coagulation hemostasis, which is provided by blood clotting factors.
Coagulation hemostasis
This type of hemorrhage arrest, unlike platelet, is included in the work a little later, more time is needed to stop blood loss in this way. However, it is this hemostasis that is most effective for the final stop of bleeding.
Coagulation factors are produced in the liver and circulate in the blood in an inactive form. When the vessel wall is damaged, they are activated. First of all, prothrombin is activated, which then turns into thrombin. Thrombin splits large fibrinogen into smaller molecules, which at the next stage are combined again into a new substance - fibrin. First, soluble fibrin becomes insoluble and provides the final stop of bleeding.
Main components of coagulation hemostasis
As noted above, the main components of the coagulation type of hemorrhage are clotting factors. In total, they are distinguished by 12 pieces, each of which is indicated by a Roman numeral:
- I - fibrinogen;
- II - prothrombin;
- III - thromboplastin;
- IV - calcium ions;
- V - proaccelerin;
- VII - proconvertin;
- VIII - antihemophilic globulin A;
- IX - Christmas factor;
- X - Stuart-Prower factor (thrombotropin);
- XI - Rosenthal factor (precursor of plasma thromboplastin);
- XII - Hageman factor;
- XIII - fibrin stabilizing factor.
Earlier, factor VI (accelerin) was also present in the classification, but it was removed from the modern classification, since it is an active form of factor V.
In addition, one of the most important components of coagulation hemostasis is vitamin K. Some clotting factors and vitamin K are in direct relationship, because this vitamin is necessary for the synthesis of II, VII, IX and X factors.
Main types of factors
The 12 main components of coagulation hemostasis listed above are related to plasma coagulation factors. This means that these substances circulate in the free state in the blood plasma.
There are also substances that are located in platelets. They are called platelet clotting factors. Below is the main ones:
- PF-3 - platelet thromboplastin - a complex consisting of proteins and lipids, on the matrix of which the blood coagulation process takes place;
- PF-4 - antiheparin factor;
- PF-5 - provides adhesion of platelets to the vessel wall and with each other;
- PF-6 - needed to seal a blood clot;
- PF-10 - serotonin;
- PF-11 - consists of ATP and thromboxane.
The same compounds are open in other blood cells: erythrocytes and leukocytes. During blood transfusion (blood transfusion) with an incompatible group, these cells are massively destroyed and platelet coagulation factors in large quantities come out, which leads to the active formation of numerous blood clots. This condition is called disseminated intravascular coagulation syndrome (DIC).
Types of coagulation hemostasis
There are two mechanisms of coagulation: external and internal. Tissue factor is required to activate the external factor. These two mechanisms converge to produce clotting factor X, which is necessary for the formation of thrombin, which in turn converts fibrinogen to fibrin.
The cascade of these reactions is inhibited by antithrombin III, which is able to bind all factors except VIII. Also, the coagulation processes are affected by the protein C - protein S system, which inhibit the activity of factors V and VIII.
Phases of blood coagulation
Three consecutive phases must go through to completely stop bleeding.
The longestis the first phase. The greatest number of processes occurs at this stage.
To start this phase, an active prothrombinase complex must be formed, which, in turn, will make prothrombin active. Two types of this substance are formed: blood and tissue prothrombinase.
For the formation of the first, the activation of the Hageman factor is necessary, which occurs due to contact with the fibers of the damaged vascular wall. Factor XII also requires high molecular weight kininogen and kallikrein to function. They are not included in the main classification of blood coagulation factors, however, in some sources they are designated by the numbers XV and XIV, respectively. Further, the Hageman factor activates the XI Rosenthal factor. This leads to the activation of factors IX first, and then VIII. Antihemophilic globulin A is required for factor X to become active, after which it binds to calcium ions and factor V. Thus, blood prothrombinase is synthesized. All these reactions occur on the platelet thromboplastin (PF-3) matrix. This process is longer and takes up to 10 minutes.
The formation of tissue prothrombinase occurs more quickly and easily. First, tissue thromboplastin is activated, which appears in the blood after damage to the vascular wall. It combines with factor VII and calcium ions, thus activating Stuart-Prower factor X. The latter, in turn, interacts with tissue phospholipids and proaccelerin, which leads to the production of tissue prothrombinase. This mechanism is much faster - up to 10 seconds.
Second and third phases
The second phase begins with the conversion of prothrombin to active thrombin by the functioning of prothrombinase. This stage requires the action of such plasma coagulation factors as IV, V, X. The stage ends with the formation of thrombin and proceeds in a few seconds.
The third phase is the conversion of fibrinogen into insoluble fibrin. First, fibrin monomer is formed, which is provided by the action of thrombin. Further, it turns into a fibrin polymer, which is already an insoluble compound. This occurs under the influence of a fibrin-stabilizing factor. After the formation of a fibrin clot, blood cells are deposited on it, which leads to the formation of a blood clot.
After, under the influence of calcium ions and thrombostenin (a protein synthesized by platelets), the clot is retracted. During retraction, the thrombus loses up to half of its original size, as serum (plasma without fibrinogen) is squeezed out. This process takes several hours.
Fibrinolysis
So that the resulting thrombus does not completely clog the lumen of the vessel and does not stop the blood supply to the tissues corresponding to it, there is a system of fibrinolysis. It provides splitting of a fibrin clot. This process occurs at the same time as the thickening of the thrombus, but is much slower.
For the implementation of fibrinolysis, the action of a special substance is necessary -plasmin. It is formed in the blood from plasminogen, which is activated due to the presence of plasminogen activators. One such substance is urokinase. Initially, it is also in an inactive state, starting to function under the influence of adrenaline (a hormone secreted by the adrenal glands), lysokinases.
Plasmin decomposes fibrin into polypeptides, which leads to the dissolution of the blood clot. If the mechanisms of fibrinolysis are disturbed for any reason, the thrombus is replaced by connective tissue. It can suddenly break away from the vessel wall and cause a blockage somewhere else in the organ, which is called a thromboembolism.
Diagnosis of the state of hemostasis
If a person has a syndrome of increased bleeding (heavy bleeding during surgical interventions, nasal, uterine bleeding, causeless bruising), it is worth suspecting a pathology of blood clotting. To identify the cause of a coagulation disorder, it is advisable to take a general blood test, a coagulogram, which will display the state of coagulation hemostasis.
It is also advisable to determine the clotting factors, namely VIII and IX factors. Since a decrease in the concentration of these compounds most often leads to blood clotting disorders.
The main indicators characterizing the state of the blood coagulation system are:
- platelet count;
- bleeding time;
- clotting time;
- prothrombin time;
- prothrombin index;
- activated partial thromboplastin time (APTT);
- fibrinogen amount;
- activity of factors VIII and IX;
- vitamin K levels.
Pathology of hemostasis
The most common clotting factor deficiency disorder is hemophilia. This is a hereditary pathology transmitted along with the X chromosome. Mostly boys are ill, and girls can be carriers of the disease. This means that girls do not develop symptoms of the disease, but they can pass the hemophilia gene to their offspring.
With a deficiency of coagulation factor VIII, hemophilia A develops, with a decrease in the amount of IX - hemophilia B. The first variant is more severe and has a less favorable prognosis.
Clinically, hemophilia is manifested by increased blood loss after surgical interventions, cosmetic procedures, frequent nasal or uterine (in girls) bleeding. A characteristic feature of this pathology of hemostasis is the accumulation of blood in the joints (hemarthrosis), which is manifested by their soreness, swelling and redness.
Diagnosis and treatment of hemophilia
Diagnosis consists in determining the activity of factors (significantly reduced), conducting a coagulogram (prolongation of blood clotting time and APTT, increase in plasma recalcification time).
Hemophilia is treated with lifelong clotting factor replacement therapy (VIII and IX). Also recommended drugs that strengthen the vascular wall("Trental").
Thus, clotting factors play an important role in ensuring the normal functioning of the body. Their activity ensures the coordinated work of all internal organs due to the delivery of oxygen and essential nutrients to them.
