Physiology of haemostasis system
Hemostasis system
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Hemostasis is very important for our life,
because if we are live our hemostatic system is
very strong. They are includes in a case of
trauma, cutting the vessels etc. Hemostasis is
the physiologic system, which support the
blood in the fluid condition and prevent
bloodless. Hemostasis system vital necessary
and functionally connect with the
cardiovascular, breathing, endocrine and other
systems.
The components of hemostasis
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The components of hemostasis are wall of the vessels,
blood cells – platelets, erythrocytes, leucocytes,
enzymes and nonenzymes components of plasma –
clotting and anticlotting substances, fibrinolysis
components of hemostasis. There are 2 kinds of
hemostasis. They are vessel-platelets (primary) and
coagulative (secondary) hemostasis. Primary
hemostasis activity begin the first after the destroyed
of vessels. Secondary hemostasis starts after that in
case the primary hemostasis do not stopped the
bloodless.
Vessel-platelets hemostasis (or primary
hemostasis include in clotting first of all after the
destroyed the safe of vessel wall.)
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Properties and function of platelets
Quantity of platelets is 180-320 G/L. Diameter of platelets is
1-4 micrometers, thickness – 0,5-0,75 micrometers. They are
the little peace of megacariocytes cytoplasm (from one
megacariocytes may develop few hundred of platelets).
Platelets circulated in blood from 5 to 11 days and than
destroyed in liver, lungs, spleen by the cells of macrophagal
system.
Function of platelets are:
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1. hemostatic function – platelets produce substances, which
are secure the hemostasis. 2. Angiotrophic function – provide
trophic of endotheliocytes of vessel wall, support structure and
functions of microvessels. These function is realize by
adgesion of platelets to endotheliocytes and injection the
enzymes into the endotheliocytes. For one day near 35 G/L
platelets do this function. 3. Transport function – transfer the
enzymes, ADP, serotonin and other. 4. Phagocytosis function –
the contain of platelets help to kill viruses and antigens bodies.
5. Regeneratory function – platelets have the growth factor,
which help to grow the endothelial and muscles cells which
are present in the vessel wall.
Stages of vessel-platelets hemostasis
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1. Shorting spasm of the vessels – vascular spasm duration to 1
minute is caused by catecholamins and other enzymes.
Diameter of vessels decrease on ½-⅓. Mechanism of it
development determine by secretion of serotonin and
thromboxan A2 from platelets and epinephrine from ending of
sympathetic nerves.
2. Adgesion of platelets – activation of platelets and stick it to
the place of defect in vessel wall.
3. Reverse aggregation of platelets – the thromb which are
formed may make way for plasma.
4. Unreverse aggregation of platelets – the thromb which are
formed can not may make way for plasma.
5. Retraction of platelets plug – decrease the size of plug, pack
down the plug.
Investigation of vessel-platelets hemostasis
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1. Calculation of the platelets quantity 180-320
G/L.
2. Determination of duration of capillary
bleeding after Duke’s method – to 3 minute in
norm.
3. Sample of fragility of capillars – to 10
petechias in norm in a round with diameter 5
santimetres.
Coagulative (secondary) hemostasis.
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Characteristics of clotting factors
There are 12 clotting factors:
I – fibrinogen; II – prothrombine; III –
thromboplastin of tissue; IV – ions of calcium; V –
proaccelerin; VII – proconvertin; VIII –
antihemophylic factor A; IX – Christmas factor or
antihemofilic factor B; X – Stuart-Prower factor or
prothrombinase; XI – plasma thromboplastin
antecedent; XII – Hageman factor; XIII – fibrin
stabilizing factor.
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Some of them are enzymes – II, VII, IX, X, XI,
XII,XIII; other are not – I, III, IV, V, VIII. The
vitamin K is necessary for the functional
activity of II, VII, IX, X factors.
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External mechanism of the first stage (3 factors from the injure
tissues go to plasma and interactions with VII factor, the last is
activated. VII active factor and IV factors form the complex
1a: III + VII active + IV, which is activated X factor.)
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Inner mechanism of the first stage (Factor 3 of
platelets – platelets thromboplastine – influence on
XII factor. Active XII factor + XI is complex 1.
Active XI factor activated IX factor. Active IX factor
+ VIII factor + IV factor is complex 2. Complex 1a
and 2 are activate X factor. Factor X active + V + IV
formed complex 3 or thrombinasa complex.)
Course of the second and third stages (The second
stage – formation of thrombin from prothrombin. The
third stage is formation of fibrin from fibrinogen. The
last stage has 3 period; formation of fibrinmonomers; formation of fibrin S (solubilis);
formation of fibrin I (insolubilis). Calcium is
necessary for all stages.)
Regulation of the clotting mechanisms
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Increase of clotting names hypercoagulation, decrease
– hypocoagulation. Hypercoagulation may be in a
stress cases. It depends on epinephrine, which
concentration increased in the cases of stress.
Epinephrine increase from the vessels walls factors
from which produced prothrombinasa. In cases of big
concentration epinephrine should activate XII factor
in a bloodstream. It divides fats and fat acids, which
have
prothrombinase
activity.
After
the
hypercoagulation stage may be secondary
hypocoagulation.
Coagulogram
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Time of clotting by Ly-Wait – 5-10 minutes;
time of plasma recalcification – 60-120
seconds; thrombotest – IV, V, VI degree;
thromboplastin time – 12-15 seconds;
thromboplastin index – 80-105 %;
concentration of fibrinogen – 2-4 g/L;
tolerancy of plasma to heparin – 6-11 minutes;
heparin time – 50-60 seconds; fibrinolysis –
15-20 %.
Anticoagulative mechanisms. Fibrinolysis.
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The tendency of blood to clot is balanced by a
number of limiting reactions that tend to
prevent clotting inside the blood vessels and to
break down any clots that do form.
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The primary anticoagulants are
antithrombin III (It is the most important
anticoagulant in the blood); heparin (This substance
was originally found in the liver, by large basophilic
cells (mast cells) in tissues of various organs. Heparin
reduces the ability of the blood to clot by blocking the
change of prothrombin to thrombin. It can also be
used to aid in reducing clots in cases in which internal
clotting has already occurred. Heparin form complex
with antithrombin-III. Activate nonenzyme
fibrinolysis.);
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alpha-2-macroglobulin, alpha-1-antitripsin, protein C (Alpha2-macroglobulin is a similar to antithrombin-heparin cofactor
in that it combines with the proteolytic coagulation factors. Its
activity is not accelerated by heparin. Its function is mainly to
act as a binding agent for the coagulation factors and prevent
their proteolytic action until they can be destroyed in various
ways. It a faint inhibitor of thrombin, connect with plasmin.
Alpha-1-antitripsin inhibits thrombin activity, IXa, XIa, XIIa
factors, plasmin and kallilrein. Protein C inhibits VIIIa, Va
factors. It activity depend of thrombin and vitamin K
concentration.
Functionation of secondary anticlotting
substances
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Primary anticoagulants are produce and
present all time in plasma and secondary
anticoagulants form in a case of blood clotting.
They are antithrombin-I or fibrin and products
of fibrinolysis or products of fibrinogen
degradation. Fibrin is sorbs and inactivates
thrombin and Xa factor. Products of
fibrinolysis inactivate ending stage of clotting,
IXa factor, platelets' agregation.
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