MODERN EDUCATION AND DEVELOPMENT
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MODERN CONCEPTS OF BLOOD COAGULATION MECHANISMS
Daminov F.A.– DSc, Ass.Professor, head of the department of clinical
laboratory diagnosis with the course of clinical laboratory diagnostics of PGD;
Djabbarova N.R.- assistant of the department of clinical laboratory diagnosis
with the course of clinical laboratory diagnostics of PGD;
Xasanova D.V.- cadet of the department of clinical laboratory diagnosis with
the course of clinical laboratory diagnostics of PGD;
Samarkand state medical university
Samarkand, Uzbekistan
The study of blood coagulation mechanisms and their regulation is impossible
without the use of laboratory tests. To date, virtually all factors involved in blood
coagulation are known. Their primary, secondary and tertiary structures have been
discovered. Genes responsible for the formation of these factors have been discovered
and deciphered. At the same time, in everyday practice, the study of haemocoagulation
in the human div is carried out using laboratory methods, which are not always
perfect.
Keywords: blood coagulation, haemocoagulation, DIC, thrombosis,
fibrinogen;
The process of intravascular blood coagulation, or haemocoagulation, occurs
constantly throughout human life. At the same time, its intensity varies. Violations of
the intensity of intravascular coagulation lead to the development of such pathological
manifestations as haemorrhages, thromboses and DIC, which is sometimes called
thrombo-haemorrhagic syndrome.
Haemocoagulation within the vascular bed is carried out by the interaction of
the procoagulant system, which forms fibrin, platelets, which often initiate clotting
processes, and the fibrinolysis system, which regulates the size of the forming blood
clot. Activated platelets and membranes of damaged cells participate in the formation
of specific complexes consisting mainly of proteins - procoagulants, which provide the
MODERN EDUCATION AND DEVELOPMENT
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phenomenon of blood coagulation itself. Modern ideas about the mechanism of
functioning of the platelet component of haemocoagulation can be presented as
follows.
Normal platelets are disc-shaped and move in the circulating blood in isolation
from each other without interacting with the vascular endothelium. When the vascular
wall is damaged, platelets with the help of Willebrand factor adhere to subendothelial
structures - collagen fibres, myofibrils, myocytes. In this case, they acquire a spherical
shape. This stage is denoted by the term ‘platelet adhesion’. After 30-60 seconds,
adhered platelets release into the environment ADP, serotonin, adrenaline, fibrinogen,
platelet factor 4 and a number of other biologically active substances.
There is a stimulation of platelet aggregation, which means their adhesion to
each other. In this case, the release of biologically active substances from platelets
increases. This phenomenon is referred to as the ‘release reaction’. As a result, there is
a rapid formation of a loose platelet plug, which provides primary haemostasis, but is
unstable and can be destroyed. In this regard, this phase is usually called reversible
platelet aggregation.
Due to the avalanche-like increase in the concentration of aggregates, the
reversible phase of platelet aggregation turns into irreversible. Thrombin, formed as a
result of activation of plasma clotting factors, plays a significant role in this. Platelets
themselves contribute to the activation of factor CP, the formation of active factor X
and the appearance of tissue factor. When platelet membranes are destroyed, conditions
are created for the unification of platelet aggregates and compaction of the resulting
clot. This phenomenon is called blood clot retraction. Simultaneously with platelets in
the process of haemocoagulation participate procoagulants - a group of proteins and
calcium ions, which in the process of their interaction lead to the formation of fibrin.
It is fibrin that is the basis of both haemostatic and thrombotic phenomena.
Procoagulants are designated by Roman numerals: I - Fibrinogen, II -
Prothrombin, III - Tissue factor, IV - Calcium ions, V-VI - Proaccelerin-Accelerin, VII
- Proconvertin, VIII - Antihaemophilic globulin, IX - Christmas factor, X - Stuart
factor, XI - Plasma thromboplastin precursor, XII - Hageman factor, XIII - Fibrin-
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stabilising factor. It is now generally accepted to use the numerical designation of
factors other than tissue factor and calcium ions, sometimes fibrinogen and
prothrombin. In addition to these factors, prekallikrein, also known as Fletcher factor,
and a high molecular weight kininogen, called Fitzgerald factor, are involved in the
process of fibrin formation. It is assumed that the process of fibrin formation consists
of the sequential interaction of all factors with each other.
At the same time, some of them - proenzymes are converted into active
enzymes, and some serve only to ensure the interaction of the enzyme and substrate.
For a long time, the theory of the presence of two pathways of activation of plasma
haemostasis and fibrin formation prevailed. The internal pathway of fibrin formation
assumed the initial activation of factor XII, which with the participation of
prekallikrein and high molecular weight kininogen activates factor XI, then factors IX
and VIII are activated and include active factor X in the process.
The external pathway began with the formation of a complex of factor VIIa
and tissue factor, which activated factor X. This was followed by the formation of
prothrombinase (factor Xa + factor Va), the transition of prothrombin to thrombin and
the formation of fibrin clot. Further studies showed that the leading role in the initiation
of blood coagulation belongs to the tissue factor and the external pathway of fibrin
formation.
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