Platelet hemostasis: stages, symptoms, causes and consequences

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Platelet hemostasis: stages, symptoms, causes and consequences
Platelet hemostasis: stages, symptoms, causes and consequences

Video: Platelet hemostasis: stages, symptoms, causes and consequences

Video: Platelet hemostasis: stages, symptoms, causes and consequences
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The human body is a very complex and interesting device, consisting of several general biological systems. The platelet link of hemostasis is only a part of the systems whose duties include control over the vital components and structures of the body.

What is hemostasis

Question of medicine
Question of medicine

The term itself can be translated from Greek as a system that holds the blood in the right position. First of all, it must be of a certain consistency, and the circulatory system is closed. If damage occurs, then the blood must remain in a closed system and not leave its limits due to the ability to clot, which ensures the prevention of severe blood loss.

The system that keeps the blood in a liquid state is called hemostasis. If the walls of blood vessels are injured, the system will immediately begin to weaken and eliminate bleeding.

Main Components

Vascular-platelet hemostasis is divided into four components:

  1. The endothelial layer is the inner lining of human blood vessels,separates blood flow from the deeper layers of the wall.
  2. The formed blood cells - this includes platelets, red blood cells and white blood cells.
  3. Plasma components - which consist of an anticoagulant, fibrinolytic and coagulation system.
  4. Regulatory factors.

Mechanisms to eliminate bleeding

Shaped elements
Shaped elements

The vascular-platelet link of hemostasis consists of three primary structures that work in an orderly and simultaneously.

They are divided into three types, according to the type of working conditions:

  1. Vascular platelet (primary).
  2. Coagulation (minor).
  3. Clot dissolution.

The main task of this system is that with the help of thrombin, a protein called fibrinogen is converted into fibrin, which is insoluble in liquid. Each blood clot in the body is a kind of combination of platelets with fibrin. They play a major role in repairing damaged blood vessel walls, and their growth factor helps in stimulating tissue regeneration.

Consists of several inseparable systems. Their stable functioning ensures constant neurohumoral regulation. The negative and positive communication micro-mechanisms within the system function flawlessly, allowing for rapid clotting to prevent blood loss. And then just as quickly dissolve them as unnecessary.

Primary hemostasis

blood cells
blood cells

The ongoing collaboration of organic blood supply and platelet coatings provides amazing mechanisms.

Vascular-platelet hemostasis is the process of reducing or completely stopping blood loss in microcirculatory vessels, not exceeding 100 microns in section. This is a combination of very complex functions performed at the same time. The main task is to reduce or completely stop blood loss within 2-3 minutes after the destruction of the capillaries.

There is an opinion that this mechanism can completely stop blood loss in case of damage to large highways. And venous, arterial or arterial bleeding is only partly.

The reason is the difference in speed, as well as the difference in pressure, as a result of which the formation of a platelet plug is simply impossible in large bloodstream systems. After all, the internal pressure is much greater than the permeability of the barrier itself. Because of this, although it slows down the pace, it cannot be stopped without additional manipulations.

Platelet hemostasis begins to work literally in the first seconds after injury. Subsequently, it is he who is responsible for the healing of the walls.

Steps of work

Blood test
Blood test

Modern medicine distinguishes several main stages:

  1. Primary spasm - disruption of the coating and spasm leads to contraction of cell bodies, which causes reflex spasm.
  2. Adhesion - with the participation of electrostatic attraction, platelets are glued together using a special protein,which is often collagen. At this stage, the stoppage of bleeding is provided with a kind of cork, consisting of blood clots.
  3. Secondary spasm - activation of platelets provokes thrombin in a sequence of metabolic reactions in the membranes of blood cells, due to which vasoactive components are released. This is due to the binding of platelet cells with the help of 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.
  4. Aggregation – Substances produced by a damaged blood vessel, combined with enhancing hormones, cause collagen and platelets to stick together. Complete and correct passage of this process in the future guarantees rapid wound healing in the future.
  5. Clot retraction - due to sticky cells, a temporary hemostatic plug is formed, which covers the defect and is a temporary replacement for a thrombus.

The stages of vascular-platelet hemostasis are important to achieve 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 blood loss.

How does bleeding stop

Medicines for the patient
Medicines for the patient

The primary role is played directly by the violation of the integrity of the walls. After all, it is precisely as a result of this that collagen, formed as a result ofexposure 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 under the influence of 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 formed collagen.

human bleeding
human bleeding

The last step occurs not without the help of adrenal hormones such as serotonin, adrenaline and norepinephrine, which, when released into the bloodstream, cause a spasm, due to which bleeding is systematically slowed down.

Besides this:

  • platelet aggregation is greatly increased;
  • a spasm of a blood vessel with damage occurs.

All processes included 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 cork gradually acquires a denser structure and is stronger fixed in the damaged area. This is due to actomyosin-like proteins - thrombostenins, which make cells denser, squeezing it out.

All together creates platelet hemostasis itself. In the damaged area, the formation of a coagulation link does not begin, but an unstable soft thrombus is formed, which, if necessary, may well stop what has begun.bleeding.

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 disturbances

Basically, any violation of platelet-vascular hemostasis is provoked by changes in the synthesis of any of the receptors located on the plane of the membrane.

The most commonly diagnosed diseases are:

  1. Bernard-Soulier Syndrome. This disorder is hereditary and manifests itself in hemorrhagic dystrophy of cells. This is the case when the receptor required for binding to von Willebrand factor is not present on the membrane.
  2. Glantzman-Negley thrombasthenia. The protein required for cell contact is not present on platelets. This does not allow you to pull off the defect in a natural way.
  3. Osler Syndrome. It is an inherited genetic disorder. Manifested in a decrease in adhesion due to a decrease in the content of collagen and the collapse of the vascular wall.
  4. Macrocytic platelet dystrophy. This pathology is transmitted exclusively by inheritance. The essence of the disease is the lack of interaction between the surfaces of blood cells. Usually caused by lack of receptors for blood plasma glycoprotein.
  5. Glantzman's disease. It is the result of genetic disorders. The reason is the absence of fibrinogen receptors on the membrane. The development of changes is directly related to impaired platelet functionality.

Children tend to have mechanismsvascular-platelet hemostasis is impaired if the mother and child are incompatible in terms of platelet antigen. Also, the cause may be systemic diseases of the girl or splenectomy.

Clinical picture of the disease

Doctor's advice
Doctor's advice

The main symptoms are:

  • Angioectasias are formed on the skin and mucous membranes, similar in nature to a hematoma after mechanical damage.
  • Bleeding from the gastrointestinal tract.
  • The appearance of a hematoma after a minor mechanical injury.
  • Frequent manifestation of hematomas, which is caused by increased permeability of vessel walls.
  • Petechiae appear in damaged areas.
  • If platelet hemostasis is impaired, then there is an increase or decrease in blood clotting.

A few nuances

While studying, it is extremely important to remember a few important nuances:

  1. Primary and secondary hemostasis are both interconnected and independent.
  2. The bottom line is the primary stop of blood loss, or at least its reduction.
  3. Mostly light bleeding stops within 3-5 minutes.
  4. Plasma and platelet hemostasis occurs with the help of platelets and von Willebrant factors.
  5. Is paramount in the elimination of any blood loss. But he cannot complete bleeding from medium or large vessels.

Research methods

Basically, the assessment of platelet hemostasis is performed by suchmethods:

  1. Cuff test - performed to determine the degree of capillary fragility. 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.
  2. The Ivy method is used to estimate the time it takes the body to clot blood. Method of implementation: the skin is pierced in the first third of the forearm. Ideally, it should curl up in 5-8 minutes.
  3. Duke's test - determines the rate of clotting. Method of carrying out: the earlobe is pierced. The process should take no more than 2-4 minutes.
  4. Aggregation - used when it is necessary to evaluate the initial formation of a thrombus.
  5. Photoelectrocolorimetry using an aggregometer - used to determine the content of von Willebrand factor in plasma.
  6. Degree of clot retraction.

Reduced platelet count leads to abnormal endothelial functioning, which in turn increases capillary fragility. At the same time, the adhesion and aggregation properties of cells are violated, due to which the time of blood loss intensifies and increases when integrity is violated.

Excessive cell numbers and increased viscosity can cause diseases such as thrombocytosis, myocardial infarction, ischemia, and obliterative disease of the vessels of the arms or legs.

Conclusions

Platelet hemostasis is one of the primary steps in stopping blood loss. For example, when microvessels are injured, this mechanism starts its workliterally immediately and continues it until the complete cessation of blood loss. Nevertheless, functional changes in its work provoke an imbalance, and lead to a variety of pathological conditions.

According to research, the whole process takes no more than 4 minutes. Looking for symptoms in him, and even more so for the methods of his treatment, is extremely ridiculous. After all, vascular-platelet hemostasis is not a disease, but a natural defense mechanism of the body.

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