Blood coagulation mechanism: why does it happen? What determines blood clotting in the human body Blood clotting begins with the breakdown

Platelets (platelets) are produced in the red bone marrow. The content in 1 ml of blood is 300 thousand. The life span is 7-9 days.

Blood clotting on injury blood vessels takes place in 2 stages. First, platelets stick together and a temporary (unstable) thrombus is formed. Then, under the action of the thrombin enzyme, the fibrinogen protein dissolved in the blood turns into insoluble fibrin, the fibrin strands stick together, and a permanent thrombus is obtained.

Blood incoagulability can be caused by a lack of calcium, vitamin K (produced by the intestinal microflora), a hereditary disease (hemophilia).

With the "wrong" blood transfusion, the transfused erythrocytes carry foreign antigens, so they are devoured by local phagocytes. The massive destruction of red blood cells leads to blood clotting right in the vessels. (With a “correct” blood transfusion, transfused antibodies (agglutinins) turn out to be foreign particles, their destruction by local phagocytes does not lead to negative consequences.)

Tests

1. The essence of the blood coagulation process is
A) agglutination of erythrocytes
B) the transition of the soluble fibrinogen protein to the insoluble fibrin protein
C) an increase in the number of formed elements in 1 cm3 of blood
D) accumulation of leukocytes around foreign bodies and microorganisms

2. Involved in blood clotting
A) erythrocytes
B) lymphocytes
B) leukocytes
D) platelets

3. The essence of blood coagulation is
A) agglutination of erythrocytes
B) the conversion of fibrinogen to fibrin
B) the conversion of leukocytes into lymphocytes
D) adhesion of leukocytes

4. The number of platelets in the blood is determined in the patient before the operation in order to
A) describe the condition immune system
B) determine the oxygen content in the blood
C) identify the absence (or presence) inflammatory process in the body
D) determine the rate of blood clotting

5. The process of blood clotting begins with
A) increased blood pressure
B) destruction of platelets
B) accumulation in the vessel venous blood
D) the formation of a local focus of inflammation

6. One of the stages of thrombus formation in a blood vessel is
A) wound festering
B) hemoglobin synthesis
B) the formation of fibrin
D) an increase in the number of platelets

7. What is the basis of a thrombus?
A) an antibody
B) hemoglobin
B) cholesterol
D) fibrin

8. What is the name of non-nuclear blood cells, the destruction of which leads to blood clotting?
A) erythrocytes
B) platelets
B) lymphocytes
D) macrophages

9. What role do platelets play in human blood?
A) transport end products of metabolism
B) carry nutrients
B) participate in phagocytosis
D) participate in its coagulation

10. A thrombus that clogs the damaged area of the vessel is formed from a network of threads
A) fibrin
B) thrombin
B) fibrinogen
D) collapsing platelets

11. Which blood cells are characterized by the following features: flat, small, irregular shape nuclear-free formations that live for several days?
A) platelets
B) lymphocytes
B) erythrocytes
D) phagocytes

12. What does a blood clot mainly consist of?
A) prothrombin
B) thrombin
B) fibrin
D) fibrinogen

13. Choose the correct option describing the formation of a blood clot: under the action of X, Y dissolved in the blood turns into Z
A) X-thrombin Y-fibrinogen Z-fibrin
B) X-fibrin Y-thrombin Z-fibrinogen
C) X-fibrin Y-fibrinogen Z-thrombin
D) X-fibrinogen Y-thrombin Z-fibrin

The main fluid of the human body, blood, is characterized by a number of properties that are essential for the life of all organs and systems. One of these parameters is blood clotting, which characterizes the body's ability to prevent large blood losses when the integrity of blood vessels is violated by the formation of clots or blood clots.

How blood clotting occurs

The value of blood lies in its unique ability deliver nutrition and oxygen to all organs, ensure their interaction, evacuate waste slags and toxins from the body. Therefore, even a small loss of blood becomes a threat to health. The transition of blood from a liquid to a jelly-like state, that is, hemocoagulation, begins with a physicochemical change in the composition of the blood, namely, with the transformation of fibrinogen dissolved in plasma.

What substance is dominant in the formation of blood clots? Damage to blood vessels is a signal specifically for fibrinogen, which begins to transform, transforming into insoluble fibrin in the form of threads. These threads, intertwined, form a dense network, the cells of which hold back the formed elements of the blood, creating an insoluble plasma protein that forms a blood clot.

In the future, the wound closes, the clot thickens due to the intensive work of platelets, the edges of the wound tighten and the danger is neutralized. The clear, yellowish liquid released when a blood clot thickens is called serum.

To visualize this process more clearly, we can recall the method of obtaining cottage cheese: coagulation of the milk protein casein also contributes to the formation of whey. Over time, the wound resolves due to the gradual dissolution of fibrin clots in nearby tissues.

Thrombi or clots formed during this process are divided into 3 types:

A white blood clot formed from platelets and fibrin. Appears in lesions with high blood flow, mainly in the arteries. It is called so because there is a trace amount of erythrocytes in a blood clot.
Disseminated fibrin deposits form in very small vessels, capillaries.
Red thrombus. Clotted blood appears only in the absence of damage to the vascular wall, with slow blood flow.

What is involved in the mechanism of coagulation

The most important role in the mechanism of coagulation belongs to enzymes. This was first noticed in 1861, and they concluded that the process could not proceed in the absence of enzymes, namely, thrombin. Since coagulation is associated with the transition of fibrinogen dissolved in plasma into insoluble fibrin protein, this substance is the main one in coagulation processes.

Each of us has thrombin in a small amount in an inactive state. Its other name is prothrombin. It is synthesized by the liver, interacts with thromboplastin and calcium salts, turning into active thrombin. Calcium ions are present in the blood plasma, and thromboplastin is a product of the destruction of platelets and other cells.

To prevent the slowing down of the reaction or its failure, the presence of the most important enzymes and proteins in a certain concentration is necessary. For example, the well-known genetic disease hemophilia, in which a person is exhausted from bleeding and can lose a dangerous amount of blood due to a single scratch, is due to the fact that the blood globulin involved in the process does not cope with its task due to insufficient concentration.

The mechanism of blood clotting

Why does blood coagulate in damaged vessels?

The process of blood clotting is three phases that pass into each other:

The first phase is the formation of thromboplastin. It is he who receives the signal from the damaged vessels and starts the reaction. This is the most difficult stage due to the complex structure of thromboplastin.
Conversion of the inactive prothrombin enzyme to active thrombin.
Final phase. This stage ends the formation of a thrombus. Thrombin acts on fibrinogen with the participation of calcium ions, resulting in fibrin (an insoluble filamentous protein), which closes the wound. Calcium ions and thrombosthenin protein condense and fix the clot, resulting in thrombus retraction (reduction) by almost half in a few hours. Subsequently, the wound is replaced with connective tissue.

The cascade process of thrombus formation is quite complicated, since a huge number of various proteins and enzymes are involved in coagulation. These necessary cells involved in the process (proteins and enzymes) are blood coagulation factors, 35 of them are known, of which 22 are platelet and 13 are plasma.

Plasma factors are usually denoted by Roman numerals, and platelet factors by Arabic numerals. In the normal state, all these factors are present in the body in an inactive state, and in case of vascular damage, the process of their rapid activation starts, resulting in hemostasis, that is, bleeding stops.

Plasma factors are of a protein nature and are activated during vascular damage. They are divided into 2 groups:

Dependent on vitamin K and formed only in the liver;
Vitamin K independent.

Factors can also be found in leukocytes and erythrocytes, which determines the huge physiological role of these cells in blood coagulation.

Coagulation factors are present not only in the blood, but also in other tissues. The thromboplastin factor is found in large volumes in the cerebral cortex, placenta, and lungs.

Platelet factors perform the following tasks in the body:

Blood clotting norm over time

One of the main indicators of blood is a coagulogram - a study that determines the quality of coagulation. The doctor will always refer to this study if the patient has thrombosis, autoimmune disorders, varicose veins, unclear etiology acute and chronic bleeding. This analysis is also needed for necessary cases during surgery and during pregnancy.

The blood clot test is performed by drawing blood from a finger and measuring the time it takes for the bleeding to stop. The rate of coagulation is 3-4 minutes. After 6 minutes, it should already be a gelatinous clot. If blood is drawn from the capillaries, then a clot should form within 2 minutes.

Children have faster blood clotting than adults: blood stops after 1.2 minutes, and a blood clot forms after only 2.5-5 minutes.

Also in the study of blood, measurements are important:

Under what conditions is the equilibrium of two reverse systems maintained?

AT human body two systems work simultaneously to ensure coagulation processes: one organizes the early onset of thrombus formation in order to reduce blood loss to zero, while the other prevents this in every possible way and helps to maintain blood in the liquid phase. Often, with certain health disorders, pathological blood clotting occurs inside intact vessels, which is a great danger, far exceeding the danger from bleeding. For this reason, thrombosis of the vessels of the brain, pulmonary artery and other diseases occur.

It is important that both of these systems work correctly and be in a state of intravital equilibrium, in which the blood will clot only when the vessels are damaged, and remain liquid inside the undamaged ones.

Factors that cause blood to clot faster

Painful stimuli.
Nervous excitement, stress.
Intensive production of adrenaline by the adrenal glands.
Increased blood levels of vitamin K.
Salts of calcium.
Heat. It is known at what temperature blood coagulates in humans - at 42 degrees C.

Factors that prevent blood clotting

It is important, if you suspect poor blood clotting, to identify the causes of the situation, eliminating the risks of severe disorders.

The process of blood clotting is very important when it comes to healing wounds and small cuts. Blood coagulation is individual for each person and is determined by its physiological characteristics. During the flow of blood through the vessels of a person, its substance is liquid, but when a person is injured, changes occur in the consistency of the blood. This is manifested in the occurrence of a blood clot or blood clot. It plays the role of a kind of cork necessary to clog the wound. It is this thrombus that serves to stop the blood and its coagulation. Previously received damage is gradually eliminated and the wound heals. This is precisely what is explained by the course of the process of blood coagulation. healthy body it takes no more than five minutes to completely stop the blood and its subsequent coagulation.

However, there are cases in which there are violations of the course of the blood coagulation process. In particular, this applies to hemophilia. Such patients should be careful throughout their lives, because in their case fatal outcome can be caused by even a small cut. There were cases when severe bleeding occurred even without visible external mechanical damage and it was associated precisely with a violation of the blood coagulation process. This one is known enough rare disease, was in ancient times. In particular, representatives of the ruling dynasties suffered from violations of the blood coagulation process.

In addition, there are other violations of the blood coagulation process. Changes in the composition of the blood can be pathological in nature, and this is precisely what becomes a violation of the course of the process of its coagulation. In such cases, the so-called intravascular coagulation most often occurs. As a result, diseases that are more severe than hemophilia appear. This can be said about myocardial infarction or cerebral thrombosis. The prognosis of the course of such diseases can be extremely unpleasant.

blood clotting system

The blood coagulation system has certain functions, among which are the following:

The blood in the vessels is maintained in a liquid state.
Homeostasis is carried out, the consequence of which is the absence of large blood losses.

Homeostasis is a complex process, enzymatic type, the end result of which is the formation of a blood clot.

The blood coagulation system includes many components, it includes proteins, calcium ions, fragments of cell membranes, phospholipids. The components of the blood coagulation system are usually referred to as factors, which can be plasma, platelet and tissue factors. The first and last of these factors are most often indicated by Roman numerals, while platelet factors are indicated by Arabic numerals. The active factor is also usually denoted by the letter "a".

The bulk of the proteins of the blood coagulation system is characterized by enzymatic activity. The factors responsible for the course of the blood coagulation process are characterized by the ability to become catalysts for limited proteolysis reactions. They are called serine proteinases.

During the course of blood coagulation reactions, proteins act as a substrate, after which they become an enzyme. Among the proteins that take part in the process of blood coagulation, there are those that are not characterized by enzymatic activity, but accelerate the course of the enzymatic reaction. They are called paraenzymes.

The main mass of blood coagulation factors undergoes synthesis in an inactive form and has the form of paraenzymes. They are activated and their action is directed to the course of a direct reaction of blood coagulation. As a result, ferminogen turns into fibrin and it is he who forms the basis of the formed blood clot.

clotting time

There are several methods for determining the time of blood clotting, some of them can be noted.

The Morawitz method involves placing a drop of blood on a glass slide, after which a glass rod is passed through it in various directions. The period of blood clotting in this case can be called the period of time elapsed from the moment the blood was applied to the moment the fibrin threads appeared. Most often, this takes five minutes.
It is not difficult to carry out the Mas-Magro method. It involves applying petroleum jelly to a paraffin-coated glass, after which blood is dripped onto this glass from a pipette. From a drop of Vaseline, blood is also taken with a pipette, after which it is released back until a blood clot occurs. The time of blood clotting is carefully recorded.
The White-Little method involves placing blood into three silicone tubes. Each tube contains one milliliter of blood. After that, the blood in the tubes is heated to 37°C and the tubes are placed at an angle. It is customary to judge the end of the process after the blood in the test tubes stops moving. According to this method, the time of blood clotting is determined in six minutes.
With the Sukharev method, 30 milliliters of blood should be placed in the capillary tube. She is driven into middle part capillary, while the first drop is eliminated from it. Tilt the capillary every 30 seconds. The countdown stops as soon as the blood stops flowing. According to this method, the time of blood clotting is determined from two to five minutes.

The total number of such methods is about thirty. The clotting time set by them varies up to two to five minutes. The first three methods described above are considered to be the simplest. Sukharev's method is classified as unified, however, it does not give stable results. When conducting an analysis for the time of blood clotting, it is imperative to indicate which of the methods it was carried out with.

clotting factors

The conventional designation of the indicators under consideration in Roman numerals is accepted, they are special proteins of blood plasma that are involved in the process of its folding. They circulate in the blood stream, manifested in it in a passive form. With mechanical injury to the walls of blood vessels, a cascade chain of reactions is launched, while blood coagulation factors take an active form. The prothrombin activator is released in the very first place, while it causes the conversion of prothrombin to thrombin. With the help of thrombin, a large molecule of globular protein is split into smaller components, subsequently they are again combined into oblong filaments of fibrin, a fibrillar protein that cannot be split. Coagulation of one milliliter of blood involves the formation of thrombin, which is quite enough to coagulate the fibrinogen contained in three liters of blood. However, with full physiological conditions thrombin is generated only where the vascular wall is damaged.

Blood clotting pathways can be divided into internal and external, depending on the available launch scenarios. In both pathways of blood clotting, there is an activation of blood clotting factors on the membranes of damaged cells. With the external pathway of blood coagulation, the tissue thromboplastin activating factor is directed into the blood from vascular tissues that have previously been damaged. This path is called external, since it is directed from the outer space. During internal blood coagulation, a signal is received from previously activated platelets, this pathway is called internal, since they are considered the main blood factors. Taking into account the fact of the close relationship in the human body of these two processes of blood coagulation, the division can be considered rather arbitrary. However, it greatly simplifies the interpretation of tests performed to assess blood clotting.

Methods for conducting a blood test for coagulation are divided into four main groups:

General methods that can only give an approximate idea of the state of the coagulation cascade. A general assessment of the state of its individual stages is also given. When carrying out, it is possible to use special devices, as well as to issue a visual assessment.
Allowing you to specifically assess the lack of certain blood clotting factors. It implies the use of corrective coagulation tests, in which blood plasma is mixed with a similar substance in patients who already have a deficiency of certain blood clotting factors.
Conduct method quantification private components of the system by their individual activity, as well as by immunological markers.
Determination of the process of blood coagulation and fibrinolosis occurring in the depth of vessels by functional definition. Molecular markers of such activation are also taken into account. In the process of circulation, blood clotting factors, degranulation products, and platelets are determined. In addition, new antigenic markers of activation factors and their complexes are revealed, the metabolism of the marked components of the coagulating blood system is accelerated.

Thus, in order to determine blood coagulation, not only the methods given in laboratories are used. In addition to them, other types of research are carried out, such as radionuclide and immunological. In a large number of cases, the components that make up the system can be determined both immunologically and according to the principles of functional activity.

Blood clotting test

A blood test for clotting is called a coagulogram. To pass such an analysis, you must first determine the indications. Some diseases involve violations of blood clotting processes, it is these diseases that constitute the basis for conducting an analysis for blood clotting.

Among these diseases are:

autoimmune diseases;
malfunctions of the full functioning of the liver;
pathology of the development of the heart and blood vessels;
varicose veins;
diabetes mellitus;
acute form hemochromatosis.

In addition, a blood clotting test is necessary under certain conditions:

during pregnancy;
in periods after the operation or immediately before it;
when monitoring during treatment with anticoagulants;
if prolonged cardiac arrest is suspected.

The norms of the analysis for blood clotting can differ significantly from each other in different laboratories. The decisive word in such a situation always belongs to the attending physician. In addition, it should be understood that the norms for conducting the analysis can differ significantly in different trimesters of pregnancy.

There are eight norms for conducting a blood coagulation test:

Analysis of the blood itself for the period of coagulation. The norm of venous blood coagulation is ten minutes, for capillary blood the norm is two minutes. Low blood clotting is characterized by an increase in this parameter, its decrease indicates ultra-high clotting.
The so-called activated partial thromboplasty time. its normal value is from 25 to 35 seconds. An increase in the specified time interval indicates poor blood clotting, its decrease indicates hypercoagulability.
The prothrombin index is the time period that is read to determine the extrinsic pathway for blood clotting. Normally, it ranges from 80% to 120%. A lower value is a sign of hypercoagulability, while a high value indicates a violation of the blood's ability to clot.
Plasma protein - fibrinogen. The normal value of the indicator is from 5.9 to 11.7 µmol / l. It is possible to increase it in case of pregnancy, with heart attacks and burns. If the value of the indicator decreases, this indicates DIC or liver disease.
thrombin period. Evaluates the final stage of the folding process. The normal value of the indicator is from 11 to 18 seconds. Fibrinogen deficiency is accompanied by an increase in this indicator, while its decrease indicates an increased concentration of fibrinogen in the blood.
The normal value of the time of plasma recalcification in the blood is from one to two minutes.
The test for determining the tolerance of blood plasma to heparin is not used in all cases. normal value is a time from three to eleven minutes.
The normal value of the blood clot retraction parameter is from 44 to 65%

When conducting a blood test for clotting, within eight hours before it, you should not eat. Blood for analysis is taken from a vein, this is required to assess the state of venous blood. If you want to assess the coagulation of capillary blood, you should take blood from a finger.

Blood clotting disorders

Most often, blood clotting disorders are manifested in the appearance of bruises on the skin. They may occur unexpectedly or be the result of damage to the skin while playing or working. They may appear with minor mechanical damage. Especially if they are observed with repeated bleeding from the nose or as a result of injury to other parts of the body. In addition, bleeding from the gums increases significantly, wounds and cuts occur.

Causes of blood clotting disorders

Before defining the main causes of blood clotting disorders, it is necessary to define the concept of blood coagulation. It is generally accepted that blood coagulation during hemorrhage arrest is a complex combination of very complex processes of biochemical properties, which are caused by the action and joint action of forty physiologically active substances, which are plasma and platelet coagulation factors.

Violations of the blood coagulation process are directly related to the imbalance of the joint action of its coagulation factors, since only in the case of their joint action, the mechanism of natural formation of a blood clot is activated, after which the bleeding stops. Not less than an important factor, affecting the violation of blood coagulation processes, is the volume of platelets in the blood, which are synthesized by bone marrow cells.

Poor blood clotting may be associated with hereditary disorders. First of all, this can be said about hemophilia and von Willebrand disease. The latter disease is characterized by the absence of the corresponding factor in the composition of the blood, which causes a violation of blood clotting.

Very often, the cause of a blood clotting disorder is damage to the liver or a malfunction in its functioning. This can equally be attributed to infectious diseases, in particular hepatitis, and to diseases accompanied by the appearance of scars, such as cirrhosis of the liver.

Violation of blood clotting in diseases

In addition to hemophilia, von Willebrandt disease, and diseases associated with liver damage, bleeding disorders can be associated with other diseases. The reason may be in hereditary diseases, in which there is no fibrinogen in the human body, in particular in his blood. This in itself can cause a violation of the normal course of the blood coagulation process.

Certain diseases can cause reduced content in human blood platelets and their destruction in the spleen. The result will be an acute form of the pathogenesis of idiopathic thrombocytopenia, in which there are violations of normal blood clotting.

Blood coagulation - the transition from a liquid state to a jelly-like clot - is a biologically important protective reaction of the body that prevents blood loss.

At the site of injury to a small blood vessel, a blood clot is created - a blood clot, which is like a plug that clogs the vessel and stops further bleeding. With a decrease in the ability of blood to clot, even minor wounds can cause fatal bleeding.

The human blood released from the vessels begins to coagulate after 3-4 minutes, and after 5-6 minutes it completely turns into a gelatinous clot. If the inner lining (intima) of the blood vessels is damaged and if blood coagulation is increased, blood coagulation can also occur inside the blood vessels in the whole organism. In this case, a thrombus forms inside the vessel.

The basis of blood coagulation is a change in the physicochemical state of the protein contained in the plasma - fibrinogen. The latter passes from a soluble form to an insoluble one, turning into fibrin and forming a clot.

Fibrin falls out in the form of long thin threads, forming networks, in the loops of which formed elements are retained. If the blood released from the vessel is beaten with a panicle, then most of the resulting fibrin remains on the panicle. Fibrin well washed from erythrocytes has White color and fibrous structure.

Blood from which fibrin has been removed in this way is called defibrinated. It consists of formed elements and blood serum. Therefore, blood serum differs in its composition from plasma in the absence of fibrinogen.

Serum can be separated from a blood clot by leaving a test tube with clotted blood for a while. In this case, the blood clot in the test tube thickens, contracts, and a certain amount of serum is squeezed out of it.

Rice. 2. Scheme of blood coagulation.

Not only whole blood, but also plasma can coagulate. If the plasma is separated by centrifugation from the formed elements in the cold, which prevents blood clotting, and then the plasma is warmed to 20-35 °, then it will quickly clot.

A number of theories have been proposed to explain the mechanism of blood clotting. At present, the enzymatic theory of blood coagulation, the foundations of which were laid almost a century ago by A. Schmidt, enjoys general recognition.

According to this theory, the final stage of coagulation is the transition of fibrinogen dissolved in plasma into insoluble fibrin under the influence of the thrombin enzyme (Fig. 2, stage III).

There is no thrombin in the circulating blood. It is formed from a blood plasma protein - prothrombin, synthesized by the liver. The formation of thrombin requires the interaction of prothrombin with thromboplastin, which must occur in the presence of calcium ions (Fig. 2, stage II).

There is also no thromboplastin in the circulating blood. It is formed when platelets are destroyed (blood thromboplastin) or when tissues are damaged (tissue thromboplastin).

The formation of blood thromboplastin begins with the destruction of platelets and the interaction of the substances released during this process with the globulin present in the blood plasma - factor V (its other name is globulin-accelerator) and with another blood plasma globulin - the so-called antihemophilic globulin (its other name is thromboplastinogen), and also with another substance of the blood plasma - the so-called plasma component of thromboplastin (its other name is the Christmas factor). In addition, the formation of blood thromboplastin also requires the presence of calcium ions (see Fig. 2, stage I, left).

The formation of tissue thromboplastin occurs when substances released from destroyed tissue cells interact with the already mentioned blood plasma globulin - factor V, as well as with blood plasma globulin - factor VII (its other name is proconvertin) and also necessarily in the presence of calcium ions (Fig. 2 , stage I, right). After the occurrence of thromboplastin, the process of blood clotting quickly begins.

The above scheme is far from complete, since in reality much more different substances take part in the process of blood coagulation.

In the absence of the above-mentioned antihemophilic globulin in the blood, which takes part in the formation of thromboplastin, a disease occurs - hemophilia, characterized by a sharply reduced blood clotting. With hemophilia, even a small wound can lead to dangerous blood loss.

Developed chemical methods extraction of thrombin from plasma and obtaining it in large quantities (B. A. Kudryashov). This drug greatly accelerates blood clotting. So, oxalate blood, in which thrombin is not formed due to calcium precipitation, after the addition of thrombin, coagulates in a test tube for 2-3 seconds. If, when an organ is injured (for example, the liver, spleen, brain), bleeding cannot be stopped by ligation of the vessels, then applying gauze moistened with a thrombin solution to their surface quickly stops the bleeding.

After the transition of fibrinogen into fibrin, the resulting clot is compacted, contracted, in other words, it is retracted. This process is carried out under the influence of a substance called retractozyme, which is released during the breakdown of platelets. Experiments on rabbits have shown that with a sharp decrease in the number of platelets, blood coagulation can occur, but the clot does not thicken, and it remains loose, not providing good closure of the damaged blood vessel.

Blood clotting changes under the influence of the nervous system. Coagulation is accelerated by painful stimuli. An increase in blood clotting at the same time prevents blood loss. When the upper cervical sympathetic node is irritated, the blood coagulation time is shortened, and when it is removed, it is lengthened.

Blood coagulation can also change conditioned reflex. So, if any signal is repeatedly combined with pain irritation, then under the action of only one signal, which previously had no effect on blood coagulation, this process accelerates. One might think that when the nervous system is irritated, some substances are formed in the body that accelerate blood clotting. It is known, for example, that adrenaline, the release of which from the adrenal glands is stimulated nervous system and increases with painful stimuli and emotional states, increases blood clotting. At the same time, adrenaline constricts the arteries and arterioles and thereby also helps to reduce bleeding when blood vessels are injured. The adaptive significance of these facts is clear.

Row physical factors and chemical compounds inhibits blood clotting. In this regard, we should first of all note the effect of cold, which significantly slows down the process of blood coagulation.

Blood coagulation is also slowed down if the blood is placed in a glass vessel, the walls of which are coated with paraffin or silicone, after which they are not wetted by blood. In such a vessel, the blood can remain liquid for several hours. Under these conditions, the destruction of platelets and the release into the blood of the substances contained in them, which are involved in the formation of thrombin, are greatly hindered.

Blood clotting is prevented by oxalate and citrate salts. When sodium citrate is added to the blood, calcium ions are bound; ammonium oxalate causes calcium to precipitate. In both cases, the formation of thromboplastin and thrombin becomes impossible. Oxalates and citrates are used only to prevent blood clotting outside the body. They cannot be introduced into the body in large quantities, since the binding of calcium in the blood in the body causes severe impairment of vital activity.

Some substances, they are called anticoagulants, completely eliminate the possibility of blood clotting. These include heparin, which is secreted from lung and liver tissue, and hirudin, which is secreted from salivary glands leeches. Heparin interferes with the action of thrombin on fibrinogen, and also inhibits the activity of thromboplastin. Hirudin has a depressing effect on the third stage of the blood coagulation process, that is, it prevents the formation of fibrin.

There are also anticoagulants of the so-called indirect action. Without directly affecting the process of blood coagulation, they inhibit the formation of substances involved in this process. These include synthetic preparations - dicoumarin, pelentan, etc., blocking the synthesis of prothrombin and factor VII in the liver.

In the composition of serum proteins, another substance was found - fibrinolysin, which dissolves the formed fibrin. This substance is an enzyme found in the blood plasma in an inactive form. Its precursor, profibrinolysin, is activated by fibrinokinase found in many body tissues.

From all of the above, it follows that there are two systems in the blood at the same time: coagulation and anticoagulation. Normally, they are in a certain balance, which prevents the processes of intravascular blood coagulation. This balance is disturbed in certain diseases and injuries.

The value of the physiological anticoagulant system is shown in the experiments of B. A. Kudryashov. If a sufficient amount of thrombin is rapidly injected into an animal's vein, death occurs due to intravascular coagulation. If the same lethal dose thrombin is introduced into the body slowly, the animal does not die, but its blood largely loses its ability to clot.

This led to the conclusion that the introduction of thrombin causes the appearance of substances in the body that prevent blood clotting. The release of these substances is regulated by the nervous system. If one paw is denervated in a rat and thrombin is slowly injected into its vein, then the blood will clot only in the vessels of the denervated paw. It is believed that an increase in the level of thrombin in the vascular bed causes a reflex release by the vessel wall of substances that prevent coagulation. Transection of nerves, as well as exposure narcotic substances suppress this reflex.

1. The role of physiology in the dialectical materialistic understanding of the essence of life. Communication of physiology with other sciences.
2. The main stages in the development of physiology. Features of the modern period of development of physiology.
3. Analytical and systematic approaches to the study of body functions. The role of I.M. Sechenov and I.P. Pavlov in creating the materialistic foundations of physiology.
4. Basic forms of regulation of physiological functions (mechanical, humoral, nervous).
7. Modern ideas about the process of excitation. Local and spreading excitation. Action potential and its phases. The ratio of the phases of excitability to the phases of the action potential.
8. Laws of irritation of excitable tissues. The action of direct current on excitable tissues.
9. Physiological properties of skeletal muscle. Strength and muscle work.
11.Modern theory of muscle contraction and relaxation.
12. Functional characteristics of non-striated (smooth) muscles.
13. Distribution of excitation along non-myelinated and myelinated nerve fibers. Characteristics of their excitability and lability. Lability, parabiosis and its phases (N.E. Vvedensky).
14. The mechanism of the appearance of excitation in the receptors. Receptor and generator potentials.
15. Structure, classification and functional properties of synapses. Features of the transmission of excitation in the synapses of the central nervous system. Excitatory synapses and their mediator mechanisms, vpsp.
16. Functional properties of glandular cells.
17. The reflex principle of regulation (R. Descartes, Mr. Prohaska), its development in the works of I.M. Sechenov, I.P. Pavlova, p.K. Anokhin.
18. Basic principles and features of the spread of excitation in the central nervous system. General principles of the coordination activity of the central nervous system.
19. Inhibition in the central nervous system (IM Sechenov), its types and role. A modern idea of the mechanisms of central inhibition. Inhibitory synapses and their neurotransmitters. Ionic Mechanisms of TPSP.
21. See the role in the processes of regulation of the activity of the ode and vegetative functions of the body. Characteristics of spinal animals. Principles of the spinal cord. Clinically important spinal reflexes.
22. Medulla oblongata and bridge, their participation in the processes of self-regulation of functions.
23. Physiology of the midbrain, its reflex activity and participation in the processes of self-regulation of functions.
24. Decerebrate rigidity and the mechanism of its occurrence. The role of the midbrain and medulla oblongata in the regulation of muscle tone.
25. Static and statokinetic reflexes (r. Magnus). Self-regulatory mechanisms for maintaining body balance.
26. Physiology of the cerebellum, its influence on the motor and autonomic functions of the body.
27. Reticular formation of the brain stem. Descending and ascending influences of the reticular formation of the brain stem. Participation of the reticular formation in the formation of the integral activity of the organism.
28. Thalamus. Functional characteristics and features of the nuclear groups of the thalamus.
29. Hypothalamus. Characteristics of the main nuclear groups. Participation of the hypothalamus in the regulation of autonomic functions and in the formation of emotions and motivations.
30. Limbic system of the brain. Its role in the formation of biological motivations and emotions.
31. The role of the basal nuclei in the formation of muscle tone and complex motor acts.
32.Modern idea of the localization of functions in the cerebral cortex. Dynamic localization of functions.
35. Hormones of the pituitary gland, its functional connections with the hypothalamus and participation in the regulation of the activity of endocrine organs.
36. Hormones of the thyroid and parathyroid glands and their biological role.
37. Endocrine function of the pancreas and its role in the regulation of metabolism.
38. Physiology of the adrenal glands. The role of the hormones of the cortex and the adrenal medulla in the regulation of body functions.
39. Sex glands. Male and female sex hormones, their physiological role in the formation of sex and the regulation of reproductive processes. Endocrine function of the placenta.
40. Factors that shape sexual behavior. The role of biological and social factors in the formation of sexual behavior.
41. Physiology of the epiphysis. Physiology of the thymus.
42. The concept of the blood system. Properties and functions of blood. Basic physiological constants of blood and mechanisms of their maintenance.
43. Electrolyte composition of blood plasma. Osmotic pressure of blood plasma. A functional system that ensures the constancy of the osmotic pressure of the blood.
44. Functional system that maintains the constancy of blood acid
45. Blood plasma proteins, their characteristics and functional significance. Oncotic blood pressure and its role.
46. Characteristics of blood cells (erythrocytes, leukocytes, platelets) and their role in the body.
47. Types of hemoglobin and its compounds, their physiological significance.
48. Humoral and nervous regulation of erythro- and leukopoiesis.
49. The concept of hemostasis. The process of blood coagulation, its phases. Factors accelerating and slowing down blood coagulation.
50. Coagulation and anticoagulation systems of blood, as the main components of the functional system for maintaining the liquid state of the blood.
51. Blood types. Rh factor. Rules for blood transfusion.
53. Pressure in the pleural cavity, its origin and role in the mechanism of external respiration and changes in different phases of the respiratory cycle.
64. Food motivation. Physiological basis of hunger and satiety.
65. Digestion, its meaning. Functions of the digestive tract. Types of digestion depending on the origin and localization of hydrolysis.
66. Principles of regulation of the digestive system. The role of reflex, humoral and local mechanisms of regulation. Gastrointestinal hormones, their classification.
67. Digestion in the oral cavity: the composition and physiological role of saliva. Salivation and its regulation.
68. Self-regulation of the chewing act. Swallowing, its phases, self-regulation of this act. Functional features of the esophagus.
70. Types of contraction of the stomach. Neurohumoral regulation of stomach movements.
71. Exocrine activity of the pancreas. Composition and properties of pancreatic juice. Adaptive nature of pancreatic secretion to types of food and diets.
72. The role of the liver in digestion. Regulation of the formation of bile, its release into the duodenum.
73. Composition and properties of intestinal juice. Regulation of intestinal juice secretion.
74. Cavitary and membrane hydrolysis of nutrients in various parts of the small intestine. Motor activity of the small intestine and its regulation.
75. Features of digestion in the large intestine.
76. Absorption of substances in various parts of the digestive tract. Types and mechanisms of absorption of substances through biological membranes.
77. The concept of metabolism in the body. Processes of assimilation and dissimilation of substances. Plastic and energy role of nutrients.
78. Metabolism and specific synthesis of fats, carbohydrates, proteins in the body. Self-regulatory mechanism of nutrient metabolism.
79. The value of minerals, trace elements and vitamins in the body. Self-regulatory nature of ensuring water and mineral balance.
80. Basic exchange. Factors affecting the value of the main exchange. The value of determining the value of the main exchange for the clinic.
81. Energy balance of the body. Work exchange. Energy costs of the body in different types of labor.
82. Physiological nutritional norms depending on age, type of work and the state of the body. Features of nutrition in the conditions of the North.
84. Human body temperature and its daily fluctuations. The temperature of various parts of the skin and internal organs. Heat dissipation. Methods of heat transfer and their regulation.
87. Kidney. Formation of primary urine. Its quantity and composition. Filtration patterns.
88. Formation of final urine. Characterization of the process of reabsorption of various substances in the tubules and the nephron loop. The processes of secretion and excretion in the renal tubules.
89. Regulation of kidney activity. The role of nervous and humoral factors.
90. Composition, properties, volume of final urine. The process of urination, its regulation.
91. Excretory function of the skin, lungs and gastrointestinal tract.
92. Importance of blood circulation for the body. Blood circulation as a component of various functional systems that determine hemostasis.
96. Heterometric and homometric regulation of the activity of the heart. The law of the heart (E.H. Starling) and modern additions to it.
97. Hormonal regulation of the activity of the heart.
98. Characteristics of the influence of parasympathetic and sympathetic nerve fibers and their mediators on the activity of the heart. Reflexogenic fields and their significance in the regulation of the activity of the heart.
99. Basic laws of hemodynamics and their use to explain the movement of blood through the vessels. Functional structure of various departments of the vascular bed.
101. Linear and volumetric velocity of blood in various parts of the bloodstream and factors that cause them.
102. Arterial and venous pulse, their origin. Analysis of sphygmogram and phlebogram.
104. Lymphatic system. Lymph formation, its mechanisms. Functions of the lymph and features of the regulation of lymph formation and lymph outflow.
2) Intraorganic plexuses of postcapillaries and small, valved, lymphatic vessels;
3) Extraorgan draining lymphatic vessels flowing into the main lymphatic trunks, interrupted on their way by lymph nodes;
4) The main lymphatic ducts - the thoracic and right lymphatic, flowing into the large veins of the neck.
105. Functional features of the structure, function and regulation of the vessels of the lungs, heart and other organs.
106. Reflex regulation of vascular tone. Vasomotor center, its efferent influences. Afferent influences on the vasomotor center. Humoral influences on the vascular center.
107. Teachings of I.P. Pavlov about analyzers. Receptor department of analyzers. Classification, functional properties and features of receptors. Functional lability (p. G. Sinyakin).
109. Characteristics of the visual analyzer. receptor apparatus. Photochemical processes in the retina under the action of light.
110. Color perception (M.V. Lomonosov, Mr. Helmholtz, I.P. Lazarev). The main forms of color vision impairment. The modern concept of color perception.
111. Physiological mechanisms of eye accommodation. Adaptation of the visual analyzer, its mechanisms. The role of efferent influences.
112. Conductive and cortical sections of the visual analyzer. Formation of a visual image. The role of the right and left hemispheres in visual perception.
114. Features of the conductive and cortical sections of the auditory analyzer. Theories of sound perception (Helmholtz, Bekesy).
116. Motor analyzer, its role in the perception and evaluation of the position of the body in space and the formation of movements.
117. Tactile analyzer. Classification of tactile receptors, features of their structure and function.
119. Physiological characteristics of the olfactory analyzer. Classification of odors, the mechanism of their perception.
120. Physiological characteristics of the taste analyzer. The mechanism of generation of receptor potential under the action of taste stimuli of different modality.
121. The role of the interoceptive analyzer in maintaining the constancy of the internal environment of the body, its structure. Classification of interoreceptors, features of their functioning.
122. Congenital forms of behavior (unconditional reflexes and instincts), their classification and significance for adaptive activity.
124. The phenomenon of inhibition in higher nervous activity. Types of braking. The modern idea of the mechanisms of inhibition.
125. Analytical and synthetic activity of the cerebral cortex. Dynamic stereotype, its physiological essence, significance for learning and acquiring labor skills.
126. The architecture of a holistic behavioral act from the point of view of the theory of the functional system p.K. Anokhin.
128. Teaching of p.K. Anokhin about functional systems and self-regulation of functions. Nodal mechanisms of a functional system.
129. Motivation. Classification of motivations, mechanisms of their occurrence. Needs.
130. Memory. memory mechanisms. Theories of memory.
131. Teachings of I.P. Pavlov about the types of higher nervous activity, their classification and characteristics. The teachings of I.P. Pavlov about I and II signal systems.
132. Physiological mechanisms of sleep. Sleep phases. sleep theories.
133. Features of perception in humans. Attention. The significance of the works of I.P. Pavlov and A.A. Ukhtomsky to understand the physiological mechanisms of attention. Physiological correlates of attention.
137. Thinking. Consciousness. Physiological approaches to the study of the thinking process. Components :

vascular wall (endothelium);

blood cells (platelets, leukocytes, erythrocytes);

plasma enzyme systems (blood coagulation system, fibrinolysis system, clecrein-kinin system);

regulatory mechanisms.

Functions of the hemostasis system:

Maintaining blood in the vascular bed in a liquid state.

Stop bleeding.

Mediation of interprotein and intercellular interactions.

Opsonic - cleaning the bloodstream from the products of phagocytosis of a non-bacterial nature.

Reparative - healing of injuries and restoration of the integrity and viability of blood vessels and tissues. There are two mechanism of hemostasis:

vascular-platelet (microcircular);

coagulation (blood clotting).

A full-fledged hemostatic function of the body is possible under the condition of close interaction of these two mechanisms.

Vascular-platelet mechanism of hemostasis provides a stop of bleeding in the smallest vessels, where there is a low blood pressure and a small lumen of the vessels. Stop bleeding can occur due to:

vascular contractions;

the formation of a platelet plug;

combinations of both.

The vascular-platelet mechanism ensures the stoppage of bleeding due to the ability of the endothelium to synthesize and release biologically active substances into the blood that change the lumen of the vessels, as well as the adhesive-aggregation function of platelets. The change in the lumen of the vessels occurs due to the contraction of the smooth muscle elements of the walls of the vessels, both in a reflex and humoral way. Platelets have the ability to adhere (the ability to stick to a foreign surface) and aggregation (the ability to stick together with each other). This contributes to the formation of a platelet plug and starts the process of blood clotting.

Stopping bleeding due to the vascular-platelet mechanism of hemostasis is carried out as follows: in case of injury, vasospasm occurs due to reflex contraction (short-term primary spasm) and the action of biologically active substances on the vascular wall (serotonin, adrenaline, norepinephrine), which are released from platelets and damaged tissue . This spasm is secondary and more prolonged. In parallel, the formation of a platelet plug occurs, which closes the lumen of the damaged vessel. Its formation is based on the ability of platelets to adhesion and aggregation. Platelets are easily destroyed and biologically isolated active substances and platelet factors. They contribute to vasospasm and start the process of blood clotting, which results in the formation of insoluble protein fibrin. Fibrin threads braid platelets, and a fibrin-platelet structure is formed - a platelet plug. A special protein, thrombostein, is secreted from platelets, under the influence of which the platelet plug is reduced and a platelet thrombus is formed. The thrombus firmly closes the lumen of the vessel, and the bleeding stops.

Coagulation mechanism of hemostasis Provides stoppage of bleeding large vessels(vessels muscular type). Stopping bleeding is carried out due to blood clotting - hemocoagulation. The process of blood coagulation consists in the transition of the soluble plasma protein fibrinogen into the insoluble protein fibrin. Blood from a liquid state passes into a gelatinous state, a clot is formed, which closes the lumen of the vessel. The clot consists of fibrin and settled blood cells - erythrocytes. A clot attached to the vessel wall is called a thrombus, it undergoes further retraction (contraction) and fibrinolysis (dissolution). Blood clotting factors are involved in blood clotting. They are found in blood plasma, formed elements, tissues.

blood clotting is a complex enzymatic, chain (cascade), matrix process, the essence of which is the transition of the soluble fibrinogen protein to the insoluble fibrin protein. The process is called cascade, since during the course of coagulation there is a sequential chain activation of blood coagulation factors. The process is matrix, since the activation of hemocoagulation factors occurs on the matrix. The matrix is the phospholipids of the membranes of destroyed platelets and fragments of tissue cells.
The process of blood clotting occurs in three phases.
Essencefirst phase consists in the activation of the X-factor of blood coagulation and the formation of prothrombinase. Prothrombinase is a complex complex consisting of active plasma X-factor, active plasma V-factor and third platelet factor. The activation of the X factor occurs in two ways. The division is based on the source of the matrices on which the cascade of enzymatic processes takes place. With an external activation mechanism, the source of matrices is tissue thromboplastin (phospholipid fragments of cell membranes of damaged tissues), with an internal one - exposed collagen fibers, phospholipid fragments of cell membranes of blood cells.
Essencesecond phase - the formation of the active proteolytic enzyme thrombin from the inactive precursor of prothrombin under the influence of prothrombinase. This phase requires Ca ions.
Essencethird phase - the transition of soluble plasma protein fibrinogen into insoluble fibrin. This phase is carried out three 3 stages.
1. Proteolytic. Thrombin has esterase activity and cleaves fibrinogen to form fibrin monomers. The catalyst for this stage are Ca ions, II and IX prothrombin factors.
2. Physico-chemical, or polymerization stage. It is based on a spontaneous self-assembly process leading to the aggregation of fibrin monomers, which proceeds according to the “side-to-side” or “end-to-end” principle. Self-assembly is carried out by forming longitudinal and transverse bonds between fibrin monomers with the formation of a fibrin polymer (fibrin-S). Fibrin-S fibers are easily lysed not only under the influence of plasmin, but also complex compounds that do not have fibrinolytic activity.
3. Enzymatic. Fibrin is stabilized in the presence of active plasma factor XIII. Fibrin-S becomes fibrin-I (insoluble fibrin). Fibrin-I attaches to the vascular wall, forms a network where blood cells (erythrocytes) become entangled and a red blood clot forms, which closes the lumen of the damaged vessel. In the future, retraction of the blood clot is observed - the fibrin filaments are reduced, the clot thickens, decreases in size, serum rich in the thrombin enzyme is squeezed out of it. Under the influence of thrombin, fibrinogen again turns into fibrin, due to this, the thrombus increases in size, which helps to better stop bleeding. The process of thrombus retraction is facilitated by thrombosthenin, a contractive protein of platelets, and plasma fibrinogen. Over time, the thrombus undergoes fibrinolysis (or dissolution). The acceleration of blood clotting is called hypercoagulation, and the slowdown is called hypocoagulation.