A hemostasis or blood coagulation system is a set of processes necessary to prevent and stop bleeding, as well as to maintain a normal liquid state of the blood. Thanks to the normal blood flow, oxygen and nutrients are delivered to tissues and organs.
Types of hemostasis
The blood coagulation system consists of three main components:
- the coagulation system itself - prevents and eliminates blood loss;
- anticoagulation system - prevents the formation of blood clots;
- fibrinolysis system - dissolves already formed blood clots.
All these three components must be in constant equilibrium in order to prevent clogging of blood vessels by blood clots, or, conversely, high blood loss.
Hemostasis, that is, stopping bleeding, can be of two types:
- platelet hemostasis - is provided by adhesion (gluing) of platelets;
- coagulation hemostasis - is provided by special plasma proteins - factors of the blood coagulation system.
Platelet hemostasis
This type of bleeding stop is included in the work first, even before coagulation activation. If the vessel is damaged, its spasm is observed, that is, a narrowing of the lumen. Platelets are activated and adhere to the vascular wall, which is called adhesion. Then they stick together with each other and fibrin threads. Their aggregation occurs. 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, activation of coagulation hemostasis, which is provided by coagulation factors, is necessary.
Coagulation hemostasis
This type of bleeding stop, in contrast to platelet count, is included in the work a little later, more time is needed to stop the 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. If the vessel wall is damaged, they are activated. First of all, prothrombin is activated, which then turns into thrombin. Thrombin, on the other hand, breaks down 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 a final stop to bleeding.
The main components of coagulation hemostasis
As already noted above, coagulation factors are the main components of the coagulation type of bleeding stop. In total, 12 pieces are distinguished, each of which is indicated by a Roman numeral:
- I - fibrinogen;
- II - prothrombin;
- III - thromboplastin;
- IV - calcium ions;
- V is proaccelerin;
- VII - proconvertin;
- VIII - antihemophilic globulin A;
- IX - Christmas factor;
- X - Stuart-Praer factor (thrombotropin);
- XI - Rosenthal factor (precursor of plasma thromboplastin);
- XII - Hageman factor;
- XIII - fibrin-stabilizing factor.
Previously, the VI factor (accelerin) was also present in the classification, but it was removed from the modern classification, since it is an active form of the V factor.
In addition, one of the most important components of coagulation hemostasis is vitamin K. Some coagulation factors and vitamin K are directly related, because this vitamin is necessary for the synthesis of factors II, VII, IX and X.
The main varieties of factors
The 12 main components of coagulation hemostasis listed above relate to plasma coagulation factors. This means that these substances circulate in a free state in blood plasma.
There are also substances that are located in platelets. They are called platelet coagulation factors. Below are 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 gluing of platelets to the vessel wall and with each other;
- PF-6 - necessary to seal a blood clot;
- PF-10 - serotonin;
- PF-11 - consists of ATP and thromboxane.
The same compounds are discovered in other blood cells: red blood cells and white blood cells. When blood transfusion (blood transfusion) with an incompatible group occurs, massive destruction of these cells occurs and platelet coagulation factors go out in large numbers, which leads to the active formation of numerous blood clots. This condition is called disseminated intravascular coagulation (DIC).
Types of coagulation hemostasis
There are two coagulation mechanisms: external and internal. To activate the external tissue factor is needed. These two mechanisms converge into one during the formation of the X coagulation factor necessary for the formation of thrombin, so that it, in turn, turns fibrinogen into fibrin.
The cascade of these reactions inhibits antithrombin III, which is able to bind all factors except VIII. The coagulation processes are also affected by the protein C system - protein S, which inhibit the activity of factors V and VIII.
Blood coagulation phases
To stop bleeding completely, three consecutive phases must pass.
The longest is the first phase. The greatest number of processes occurs at this stage.
To start this phase, an active prothrombinase complex must form, which, in turn, will make prothrombin active. Two types of this substance are formed: blood and tissue prothrombinases.
For the formation of the first, activation of the Hageman factor is necessary, which occurs due to contact with the fibers of the damaged vascular wall. Also, high molecular weight kininogen and kallikrein are necessary for the functioning of the XII factor. They are not included in the main classification of blood coagulation factors, however, in some sources their designation by numbers XV and XIV, respectively, is allowed. Further, the Hageman factor brings the Xenth Rosenthal factor into active state. This leads to the activation of first IX, and then VIII factors. Antihemophilic globulin A is necessary for the X factor to become active, after which it binds to calcium ions and the V factor. Thus, blood prothrombinase is synthesized. All these reactions occur on a platelet thromboplastin matrix (PF-3). This process is longer, its duration is 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 the VII factor and calcium ions, thus activating the X Stuart-Prauer factor. The latter, in turn, interacts with tissue phospholipids and proaccelerin, which leads to the production of tissue prothrbinase. 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 through the functioning of prothrombinase. For this stage, the action of such plasma coagulation factors as IV, V, X is necessary. The stage ends with the formation of thrombin and proceeds in a few seconds.
The third phase is the conversion of fibrinogen to insoluble fibrin. First, the fibrin monomer is formed, which is provided by the action of thrombin. Then 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 the fibrin clot, blood cells are deposited on it, which leads to the formation of a blood clot.
Then, under the influence of calcium ions and thrombostenin (a protein synthesized by a platelet), a clot retraction occurs. During retraction, the thrombus loses up to half its original size, as the blood serum is squeezed out (plasma without fibrinogen). This process takes several hours.
Fibrinolysis
So that the resulting blood clot 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 fibrinolysis system. It provides cleavage of the fibrin clot. This process occurs at the same time as the compaction of the thrombus, but it is much slower.
For the implementation of fibrinolysis, the action of a special substance, plasmin, is necessary. It is formed in the blood from plasminogen, which is activated due to the presence of plasminogen activators. One of these substances 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 a blood clot. If the mechanisms of fibrinolysis are disturbed for any reason, the thrombus is replaced by connective tissue. It can suddenly come off the vessel wall and cause a blockage somewhere in another organ, which is called thromboembolism.
Diagnosis of hemostasis
If a person has a syndrome of increased bleeding (severe bleeding during surgical interventions, nosebleeds, uterine bleeding, unreasonable appearance of bruises), it is worth suspecting a pathology of blood coagulation. To identify the causes of coagulation disorders, it is advisable to take a general blood test, a coagulogram that displays the state of coagulation hemostasis.
It is also advisable to determine coagulation factors, namely factor VIII and IX. Since a decrease in the concentration of precisely these compounds most often leads to blood coagulation disorders.
The main indicators characterizing the state of the blood coagulation system are:
- platelet count;
- bleeding time;
- coagulation time;
- prothrombin time;
- prothrombin index;
- activated partial thromboplastin time (APTT) ;
- the amount of fibrinogen;
- activity of factors VIII and IX;
- vitamin K.
Pathology of hemostasis
The most common disease that occurs with a deficiency of coagulation factors is hemophilia. This is a hereditary pathology transmitted along with the X chromosome. Mostly boys are sick, and girls can be carriers of the disease. This means that girls do not have symptoms of the disease, but they can pass the hemophilia gene on 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 proceeds more severely and has a less favorable prognosis.
Clinically, hemophilia is manifested by increased blood loss after surgery, cosmetic procedures, frequent nose or uterine bleeding (in girls). 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 (lengthening the time of blood coagulation and APTT, increasing the time of plasma recalcification).
Hemophilia treatment consists of lifelong replacement therapy with coagulation factors (VIII and IX). Also recommended drugs that strengthen the vascular wall ("Trental").
Thus, coagulation factors occupy an important place in ensuring the normal functioning of the body. Their activity ensures the coordinated work of all internal organs thanks to the delivery of oxygen and necessary nutrients to them.