The human body is a very complex and interesting device, consisting of several general biological systems. The platelet link of hemostasis is only part of the systems whose responsibilities include monitoring the vital components and structures of the body.
What is hemostasis
The term itself can be translated from Greek as a system that holds blood in place. First of all, it must be of a certain consistency, and the circulatory system is closed. If damage has occurred, then the blood should remain in a closed system and not leave its limits due to the ability to coagulate, which ensures the prevention of severe blood loss.
The system that stores blood in a liquid state is called hemostasis. When injuring the walls of blood vessels, the system will immediately begin to weaken and eliminate bleeding.
Main components
Vascular-platelet hemostasis is divided into four components:
- The endothelial layer is the inner lining of a person’s blood vessels that separates blood flow from deeper layers of the wall.
- Shaped blood elements - this includes platelet cells, red blood cells and white blood cells.
- Plasma components - which consist of an anticoagulant, fibrinolytic and coagulation system.
- Regulatory factors.
Bleeding mechanisms
The vascular-platelet link of hemostasis consists of three primary structures that work orderly and simultaneously.
They are divided into three types, according to the type of working conditions:
- Vascular-platelet (primary).
- Coagulation (secondary).
- Dissolution of a blood clot.
The main objective of this system is that, using the action of thrombin, a protein called fibrinogen is converted into liquid insoluble fibrin. Each blood clot in the body is a kind of combination of platelets with fibrin. They play a major role in the renewal of damaged blood vessel walls, and their growth factor helps in stimulating tissue regeneration.
Consists of several inseparable systems. Their stable functioning provides constant neurohumoral regulation. The micromechanisms of negative and positive communication within the system function flawlessly, which allows you to quickly create clots to prevent blood loss. And then just as quickly dissolve them as unnecessary.
Primary hemostasis
The ongoing collaboration of organic coatings for blood supply and platelets ensures the creation of amazing mechanisms.
Vascular-platelet hemostasis is the process of reducing or completely stopping blood loss in microcirculatory vessels, not exceeding 100 microns in the section. This is a combination of very complex functions performed at one time. The main task is to reduce or completely stop blood loss in the interval 2-3 minutes after the destruction of the capillaries.
There is an opinion that this mechanism is able to completely stop blood loss due to damage to large highways. And venous, arterial or arterial bleeding - only partially.
The reason is a different speed, as well as a difference in pressure, as a result of which in large blood circulation systems the formation of a platelet plug is simply impossible. After all, internal pressure is much greater than the permeability of the barrier itself. Because of this, although it slows down, it cannot be stopped without additional manipulations.
Platelet hemostasis begins to work literally in the first seconds after receiving damage. Subsequently, it is he who is responsible for the healing of the walls.
Work stages
Modern medicine distinguishes several main stages:
- Primary spasm - violation of the integrity of the coating and spasm leads to a reduction in the cells of the cells, which causes a reflex spasm.
- Adhesion - with the participation of electrostatic attraction, platelets are glued together using a special protein, which is often collagen. At this stage, the stopping of bleeding is provided with a kind of plug, consisting of blood clots.
- Secondary spasm - activation of platelets provokes thrombin in the sequence of metabolic reactions in the membranes of blood cells, due to which vasoactive components are released. This occurs due to the binding of platelet cells using special processes that form on the surface of the cells after they change shape from the usual oval to spherical. In this case, the bleeding stops completely.
- Aggregation - substances that are formed using a blood vessel with damage in combination with enhancing hormones cause gluing of collagen and platelets. The complete and correct passage of this process in the future ensures fast wound healing in the future.
- Clot retraction - due to the adhesion of cells, a temporary hemostatic tube forms, which blocks the defect and is a temporary replacement for a blood clot.
The stages of vascular platelet hemostasis are important for achieving a positive result, both individually and collectively. And violations in at least one, most likely, will lead to the fact that it will be almost impossible to slow down or stop the loss of blood.
How does bleeding stop
The primary role is played directly by the violation of the integrity of the walls. Indeed, precisely because of this, collagen is thrown into the bloodstream, formed as a result of exposure of subendothelial tissue structures.
Then platelet activation begins. This is due to the appearance of von Willebrand factor in the blood, which in turn is caused by a sharp jump in the amount of protein.
Being influenced by a certain number of factors, they begin to swell, become covered with numerous processes and close the area with damage.
The release of the contents occurs with the help of the resulting collagen.
The last stage occurs not without the help of such adrenal hormones as serotonin, adrenaline and norepinephrine, which, when they enter the bloodstream, cause spasm, due to which bleeding is systematically slowed.
Besides:
- platelet aggregation is significantly enhanced;
- a spasm of a blood vessel with damage occurs.
All processes involved in platelet hemostasis significantly reduce the amount of blood that is released from the wound, and also ensure the accumulation of hemostatic substances in the area of damage.
Then the newly formed plug gradually acquires a denser structure and is more firmly fixed in the damaged place. This is due to actomyosin-like proteins - thrombostenins, which make cells denser by squeezing it.
All together creates platelet hemostasis. In the damaged area, the formation of the coagulation link does not begin, but an unstable soft thrombus forms, which, if necessary, can completely stop the bleeding that has begun.
However, it is worth remembering that if the veins and arteries are damaged, this method will not bring the desired results, because the blood flow there is many times faster and under higher pressure.
Functional Process Disorders
Basically, any violation of platelet-vascular hemostasis is provoked by changes in the synthesis of any of the receptors located on the membrane plane.
The most commonly diagnosed diseases are:
- Bernard-Soulier Syndrome. This disorder is hereditary and manifests itself in hemorrhagic cell dystrophy. This is the case when the receptor, which is required to connect with von Willebrand factor, is not present on the membrane.
- Glanzman-Negli thrombasthenia. The protein that is needed for cell contact is not present on platelets. This does not allow to tighten the defect in a natural way.
- Osler's Syndrome. It is an inherited gene disease. It manifests itself in a decrease in adhesion due to a decrease in collagen content and the collapse of the vascular wall.
- Macrocytic thrombocytodystrophy. This pathology is transmitted exclusively by inheritance. The essence of the disease is the lack of interaction of the surfaces of blood cells. It is usually caused by the fact that there are no receptors for blood plasma glycoprotein.
- Glanzman's disease. It is a consequence of genetic disorders. The reason is the lack of fibrinogen receptors on the membrane. The development of changes is directly related to impaired platelet functionality.
In children, as a rule, the mechanisms of vascular-platelet hemostasis are impaired if the mother and child are incompatible with the platelet antigen. Also, the cause may be a girl’s systemic disease or splenectomy.
The clinical picture of the disease
The main symptoms are:
- Angiectasias are formed on the skin and mucous membrane, similar in nature to the hematoma after mechanical damage.
- Gastrointestinal bleeding.
- The appearance of a hematoma after a minor mechanical injury.
- A frequent manifestation of hematomas, which is caused by increased permeability of the walls of the vessels.
- Petechiae appear in damaged areas.
- If platelet hemostasis is impaired, then there is an increase or decrease in blood coagulation.
A few nuances
During the study, it is extremely important to remember several important nuances:
- Primary and secondary hemostasis are both interconnected and independent.
- The bottom line is the primary stop loss of blood or at least reduce it.
- Mostly mild bleeding stops within 3-5 minutes.
- Plasma and platelet hemostasis occurs with the help of platelets and von Willebrant factors.
- It is paramount in the elimination of any blood loss. But he cannot complete the bleeding from the vessels of the middle or large link.
Research methods
Basically, platelet hemostasis is assessed using the following methods:
- Cuff test - carried out to determine the degree of fragility of the capillaries. Method of implementation: with the help of medical intervention, venous pressure gradually increases, due to which a maximum of 10 petechiae appear on the forearm.
- Ivey method - used to estimate the time spent by the body on blood coagulation. Way of carrying out: the skin is pierced in the first third of a forearm. Ideally, it should curl in 5-8 minutes.
- Duke test - determines the rate of coagulation. Way of carrying out: the earlobe is pierced. The process should take no more than 2-4 minutes.
- Aggregation - used if necessary to evaluate the initial formation of a blood clot.
- Photoelectrocolorimetry using an aggregometer - used to determine the content of von Willebrand factor in plasma.
- The degree of retraction of a blood clot.
A reduced level of platelet count leads to pathologies of the functioning of the endothelium, which, in turn, increases the fragility of capillaries. At the same time, the adhesion and aggregation properties of the cells are violated, due to which the blood loss time increases and increases when integrity is violated.
The number of cells that exceeds the standard and their increased viscosity can trigger the appearance of diseases such as thrombocytosis, myocardial infarction, ischemia and obliterating diseases of the vessels of the hands or feet.
conclusions
Platelet hemostasis is one of the primary stages in stopping blood loss. For example, when injuring microvessels, this mechanism begins its work literally right away and continues until the complete loss of blood loss. Nevertheless, functional changes in his work provoke an imbalance, and lead to a variety of pathological conditions.
According to studies, the whole process as a whole takes no more than 4 minutes. Look at his symptoms, and even more so the methods of treatment are extremely ridiculous. Indeed, vascular-platelet hemostasis is not a disease, but a natural mechanism for protecting the body.