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BLOODSVSTEMS.

fi
• Blood is a fluid which circulate between heart ,
arteries . Veins
by capillaries .


According to Lange ;
Periferal blood

}
-

Organs of hematopoiesis R
P
-

'
O '
O -
'

organs of hemolysis
neuro humoral
Regulatory apparatus
- .


osmotic
pressure ; (7. B ATM )
• Functions ; The which
pressure
-

① . Homeostatic forces the water to


pass through
membrane
② .
Informative →
Transport of macromolecules . the
semipermeable
concentrated solution
③ Transport to the .

⑨ Respiration Depends the


-

. . on

③ .

special trophic number rather than the


type
of
⑥ .

Excitatory particle -

⑦ Defensive Regulates movement of


-
-

water beta cell and intercellular fluid .

• Blood → Plasma
this in
plasma
Osmolarity

erythrocytes Tenuoustest
o
• ,

Platelets The number of osmdes


per
. -

liter of solution ( plasma )

Blood 't
*
plasma so to 60 •
Tonicity ;
-

* Water -

924 .
-

osmolarity of a solution due

Potions Ft
* to the
plasma
-
.
.

*
tarots -
40 to 457 .

(
solutions ;

¥¥¥-

Isotonic

osmolarity
enwehiophaghmaa
- the same

enromboastes o g as .

4.5 S x told 5-9 xroa IN 400×091't '

g.so f q

§£
-
-

DE
-

I § j

Hypertonic } Hypotonic

Hematocrit → The
percentage of blood Volume o
g
-
Greater osmolarity is

that made In osmolarity


inypernytopoign }
is of cells lesser
up
.

↳ Depends on ;
O EE
h
O

#
, ,

r . Sese ( Higher in men ) These solutions are used for

2. Age ( Higher in newborns ) the transfusion of various drugs .


Quantity of blood is determined by , § When there is a difference
" "
Binds to
Using dyes such Evan's Blue →
plasma proteins in osmotic pressure , water
-

as .

Injecting albumin labeled as radioactive iodine to the compartment that


serum
goes
-

of
has a higher concentration
Total blood volume The Volume X too

=
-
plasma solutes .

In
hypper tonic → cell shrink
)
- .

( ooo -
ht
-
In
hypotonic → cell swelling .

Ohcotic Pressure I ⑧ Bpcarbonatebuffer.rs
.
Consits of weak carbonic acid and Na Hoz .

Functions with in order to maintain


created respiratory

part of osmotic system


pressure
-

pcos at 40 mmHg .

Only by blood The colloid


, plasma proteins .

↳ creation of HOI in
plasma .

due to colloids
osmotic pressure the plasma
is known colic ③ Phosphate buffer → Present with mono
hydrogen phosphate or Az
as On
pressure
.
.
g

Important homeostasis component


- -

for a) Viscosity ;
Responsible the 054 of the
-
.

buffering Blood viscosity is measurement of


capacity
-

. a

resistance of blood to flow .

of functional system maintaining osmotic


pressure
-

Determined by ,
formed elements

① .
0 . A - R 3
Y macromolecular
components .

-
P Osmotic
.
= 7,3 atm . -
Anemia leads to decrease blood ,

viscosity level lead to heart faliure .

② Peri feral → in tissues in central receptors


3 Osmo
- .
.


Normal level is 37°C → 3×503 to 4×63 Ps .

③ Structures of the
hypothalamus limbic system
.

,
y
reticular formation .
§ Blood rheology ;

Influenced by ,

④ Drink food behaviour , changes activity of organs The intrinsic


properties
y
i
.
the . .

of excretion
) water content in tissue / Volume of @ .
Features of their own movement

circulating blood of blood flow Interaction between themselves


g Speed .
3 .

} with the walls of the vessels .

③ . Feedback .

Depends on the rheological properties ;


a) Maintaining pH i . Periferal resistance
3
load
PH is stable Hydrogen Pon concentration in the heart
mainlining of

an the .

body fluids both embrace


Mulay } intracellularly .

2 .
The effectiveness of trans
cap
:

beta blood and


Eg ; -

vary exchange ,

D. pit of the ECF → F. 40 tissue .

2.) of arterial blood → 7.42


pH
3) pH of Venous blood → 7.36

4) .
Intracellular
pH → 7 - 20

§ Blood buffers •

① .
→ Hemoglobin accept At as it has histidine .


Deoxygenated hemoglobin has a higher tendency
Ht
to
accept

of Affinity to Ht Pons ;

At tissue level where CO2 is


haemoglobin

more
,
g
Ht H203
accepts as
many cop
is
present
as .

if

Hzcoz remains ionized as Ht and ttcog so heamoglobin
can accept Ht .

• At the level of lungs where Oz is more haemoglobin releases

released Ht
Ht Y combines with Oz .
The will bind
again with
Haj to

form Hzcog → H2O t CO2


=
↳ removed by ,
CONT
lungs
.


.
Plasma –55% - 60% in which 92% is water, 7% is protein – 58 %
albumins
37% globulins 7 fibrinogen
1> Regulatory and clotting factors 1 % - non protein –
• Nitrogen free – organic – glucose , neutrals fats, and organic
acids such as citrate, lactate, pyruvate etc.
• Inorganic- Electrolytes – Main contributors of osmotic pressure,
and hence participate in regulation of water and salts level in
body. Ex- Na, k, Ca, Mg, p04, cl, hco3, so4 ,
• Nitrogen containing- To nitrogen-containing plasma components
include the breakdown products of proteins and nucleic acids:
urea, uric acid, creatine, creatinine, as well as amino acids
absorbed in the gastrointestinal tract.
• The nitrogen contained in these compounds is called residual (it
is determined after the precipitation of proteins).
• Normally, the concentration of residual nitrogen in plasma in
adults ranges from 20 to 40 mg%. Half of this amount is urea -
10-20 mg% all plasma components can be divided into
functional, i.e. involved in the performance of blood functions,
and non- functional, i.e. non-specific, simply tolerated by her.
• The first include proteins and electrolytes.
• To the second:
1) nutrients (proteins, fats, carbohydrates), vitamins (all known),
trace
elements (the most important Fe, Cu, Co, I);

2) intermediate exchange products (organic acids);

3) hormones and enzymes (over 50);

4) the final metabolic products to be excreted (toxins - CO 2 , urea, uric acid, creatine,
creatinine, etc.).

• The simplest of them is an isotonic NaCl solution. More physiological are


solutions with a salt composition corresponding to that in plasma,

• Ringer (contains NaCl, KCl, CaCl 2 , NaHCO 3(to give a buffer capacity)),
• Ringer-Locke (differs from the first solution by the presence of a nutrient -
glucose and oxygen saturation), Tyrode (in addition to the components included
in the previous solution, contains MgCl 2 and NaH 2 PO 4 ).

• However, with massive blood loss, the introduction of these solutions is


useless, since they are rapidly excreted from the body.

• In this regard, colloidal blood substitutes containing proteins or polysaccharides


(gelatinol, hemodesis, reopoliglukin, etc.) have been developed .

• However, these solutions, like saline, cannot replace red blood cells - carriers of O 2
and CO 2.

• For this purpose, hemoglobin solutions and fluorocarbon emulsions are used. In the
years 70-89, a plasma substitute was created in Russia with gas transportation
properties and a multifunctional effect - perfluorane.

Plasma proteins perform a number of


important functions:
1. Transport - participate in the transfer of many factors due to the ability to form
complexes.
2. Protective: a) ensure the preservation of bcc in the vascular bed when it is
damaged (proteins of the coagulation system, fibrinolysis); b) participate in the
immune processes of the body.
3. Create colloid-osmotic (oncotic) blood pressure and regulate the osmotic
pressure, because they can bind low molecular weight compounds.
4. Buffer - participate in maintaining a constant pH of the blood.

5. Trophic - provide amino acids with vital organs (brain, heart, etc.) during
fasting or inadequate protein nutrition.

In 3 l of plasma, contained on average in an adult, there are approximately


200 g of protein. It is captured by the cells of the reticulo-endothelial system
and is split there. The resulting amino acids enter the bloodstream and are
used when necessary.

6. Affect the rheological properties of blood.

7. Prevent the sedimentation of red blood cells,


because create the same negative charge on their shell (“z” - potential).

8. Regulate the state of aggregation of blood - contribute to the preservation


of its liquid state, since some of them are anticoagulants.

9. Creator connections (for example, nerve growth factors, erythropoietins).

TOP BTV SAC

• Suspension and colloid properties of the blood cellular elements-


Suspension ( size of suspended particles is more than 100nm)

• Plasma – colloid ( size of dissolved particle less than 100nm)


• Suspension and colloid properties can be estimated by ESR
• ESR is a type of blood test which is a non specific measure for
inflammation
Esr measures the rate at which erythrocytes coagulates or
settledown in 1 hr

ESR is governed by – Pro sedimentation factor – the factors


that causes coagulation , large proteins that is globulin( raised
during infection ) fibrinogen( occurs in pregnancy more)
Negative charge around erythrocytes zeta potential – Factor
resisting sedimentation

Clusters or stacks of rbc is called rouleaux which enhance esr


In females- 5-12 mm/h In males 4-10mm/h
Hemolysis- The breakdown or destruction of rbc and release of Hb
into the blood stream . life span (120) days . removed from
circulation by spleen.
Types of hemolysis-
Extrinsic- Antibodies against RBC Intrinsic – Problems within RBC
Physical – osmotic ( hypotonic) Mechanical ( due to pressure)
Thermal ( due to heat)
Chemical – Due to drugs
Biological – Poison or blood transfusion
STRUCTURE
Form – biconcave discs having a mean diameter of about 7.8
micrometers and a thickness at the thickest point of 2.5 micrometers
and in the center of 1 micrometer or less Contains hemaglobin , no
nucleus and circular biconcave (the surface to volume ratio is
greater )all which enables increase capacity and transport of o2
Life span -120 days
Content- 4.5- 5 * 10^12/L
FUNCTION
1) respiratory – transport of oxygen from the lungs to the tissues and
carbon dioxide from the tissues to the lungs;
2) buffer – red blood cells are responsible for most of the buffering
power of whole blood because hemoglobin is an excellent acid-base
buffer (as is true of most proteins);
3) hemostatic – participation in hemostasis (the stopping of a flow
of blood), because: 1) erythrocytes contain factors of clotting; 2)
porous surface of erythrocytes catalyses clotting; 3) form of
erythrocytes convenient for attachment of fibrin fibers. From the
other side, erythrocytes participate in the maintenance of the fluid
state of blood, because contain heparin and other anticoagulants
(having the effect of retarding or inhibiting the coagulation of the
blood);
4) trophic – transport of nutrients;
5) regulatory – transport of hormones, enzymes (cholinesterase,
carbonic anhydrase , phosphatase), vitamins (В1, В2, В6, ascorbic
acid), other biologicaly active substances;
6) defensive – absorption of toxic substances;
7) determine blood types – their membrane contain a great number
of antigens;
8) influence on rheological properties of blood – the viscosity of
blood depends from the erythrocytes number;
9) provide the relative constancy of plasma composition – when an
excess of salts, proteins and fats erythrocytes absorb them; when
lack of them – give back to plasma;
10) regulate erythropoiesis – contain factors which provide this
processes when enter bone marrow at destruction of erythrocytes;
11) informational – provide interaction of cells, because
Leukocytes- 4-9 *10^9
Structurally they can be classified based on Granulations
Granulocytes- Eosinophil, basophil , Neutrophil Agranulocytes-
Monocytes ,
• Memory
• Monocytes- 6% - 3 days Immune surveillance
• Eosinophil – 8-12 days Defence against parasites -3%
• Basophils- A few hours to few days-
• Inflammatory response Leukocyte formula-% of WBC *total wbc count / 100
Leucocytosis- increase in wbc formation

• Physiological cause-
1. After heavy exercise

2. After a meal

3. After mental effort or emotional pain

4. Develops quickly but short term

5. The number of leucocytes increases insignificantly Leucocyte formula doesn’t


change

6. Reactive cause

7. Due to inflammation or infectious disease

8. Develops slowly but long term

9. The no. of leukocytes increase significantly

10. Leucocyte formula changes

11. Leucopenia – decrease in wbc count

12. Oppression of leucopoesis or destruction of wbc


PLATELETS – 250-400 *10^9

• structure small, granulated bodies. They lack nuclei and are 2- 4 um in diameter

• Function – Ability to aggregate at vascular injury

• Life span – 5 to 12 days

• Thrombopoesis – the process of generation of thrombocyte from megakaryocytes


cytoplasm of bone marrow, abt 60- 75% is present in circulatory system and rest
in spleen

• Regulation – colony stimulating factors control production of megakaryocytes and


thrombopoetin is important for maturation of thrombocytes

• there are thrombopoietin receptors on platelets.

Consequently, when the number of platelets is low, less is bound and more is
available to stimulate production of platelets.

Conversely, when the number of platelets is high, more is bound and less is
available, producing a form of feedback control of platelet production. The amino
terminal portion of the thrombopoietin molecule has the platelet-stimulating activity,
whereas the carboxyl terminal portion contains many carbohydrate residues and is
concerned with the bioavailability of the molecule.

When the platelet count is low, clot retraction is deficient and there is poor
constriction of ruptured vessels. The resulting clinical syndrome (thrombocytopenic
purpura) is characterized by easy bruisability and multiple subcutaneous
hemorrhages
Blood grouping must be considered for blood transfusion, organ and tissue
transplantation. It matters in forensic science.

• A blood group is understood to be its immuno-genetic characteristics, due to


specific antigens ( agglutinogens ), which form in the early period of embryonic
development and do not change throughout life.

• By their chemical nature, agglutinogens are glycolipids, glycoproteins or


lipoproteins.

• They are located in the membranes of red blood cells, white blood cells, platelets,
cells of all tissues, as well as in blood plasma and biological fluids.

• In erythrocytes alone, more than 500 agglutinogens are currently discovered. 140
of them are combined into 20 systems, the rest are common or individual. In
general, the antigenic "pattern" of each person is unique (with the exception of
identical twins).

• Therefore, there are as many blood types as there are people on earth. This means
that a person can be recognized by a blood stain in the same way as by
fingerprints.

• Specific plasma antibodies that are part of the gamma globulin fraction,
agglutinins, can react with agglutinogens.

• Their molecules, with 2 binding sites, form a “bridge” between two red blood
cells during the antigen-antibody reaction.

• As a result, gluing of the latter occurs - agglutination.


The blood of different people has different antigenic and immune properties. When
blood transfusions from one person to another were first attempted, the transfusions
were successful only in some instances. Often complications of transfusions
occurred that led to death. Blood types (groups) were discovered in 1900
by the Austrian immunologist K. Landsteiner. Blood types immuno-genetic
properties of the blood. They are inherent. There are antibodies in the plasma and
antigens on surfaces of red cells. Antibodies another name is agglutinins (α and β)
can react with antigens. The result is agglutination. Antibody + antigen →
agglutination.
• Agglutination is the process of clumping of red blood cell.

• For this reason, it is easy for blood from a donor to be mismatched with that of a recipient.

• Recipient is a person that receives something (a recipient of the blood). Donor someone who
gives a part of their body or some of their blood to be used by doctors to help a person who is
ill.

• Blood type is determined by antigens. The number of combinations of antigens is more than the
number of people in the world. Each man has the individual set of antigens.

• Each man has the individual blood type. The number of blood types is equal to the number of
people. Two particular groups of antigens are more likely than the others to cause blood
transfusion reactions:

1. O-A-B system

2. Rh system.

• O-A-B blood groups: two antigens (A and B) occur on surfaces of red blood cells.

• Another name of these antigens is agglutinogens because they often cause the blood cell
agglutination. People may have neither of them, one, or both simultaneously.

• Depending on the presence or absence of the A and B agglutinogens there are 4 O-AB blood
types:

1. When neither A nor B agglutinogen is present, the blood group is type O. Group O contains
and agglutinins in plasma.

2. When only type A agglutinogen is present, the blood is type A. Group A contains A
agglutinogens and agglutinins.

3. When only type B agglutinogen is present, the blood is type B. Group B contains B
agglutinogens and agglutinins.

4. When both A and B agglutinogens are present, the blood is type AB. Group AB contains both
A and B agglutinogens but no agglutinins.
BOMBAY BLOOD -Respective of being O as a universal donor all ABO has H antigen .
recently it was discovered some people did not have the H antigen, and hence made
antibodies against it.

Along with the O-A-B blood group system, the Rh system is important in the transfusion of blood.
Rh factor.

• These types are designated C, D, E, c, d, and e.

• A person who has the C antigen does not have the c antigen, but the person missing the C
antigen always has the c antigen.

• The same is true for the D-d and E-e antigens. Because of the manner of inheritance of these
factors each person has one of each of the three pairs.

• The type D antigen is widely prevalent in the population and considerably more antigenic
than the other Rh antigens: a person who has type D antigen is Rh positive and a person who
does not have type D antigen is Rh negative. About 85% of all white people are Rh positive
and 15%, Rh negative. In American blacks, the percentage of Rh positives is about 95,
whereas in African blacks, it is virtually 100%.

• Either Rh positive or Rh negative people do not have antibodies against Rh antigen.

• Anti-rhesus antibody may develop only in Rh negative persons in two situations when Rh
antigen enters their blood.

1. The first case is mismatched blood transfusion of Rh-positive blood to the Rh-negative
recipient.

In this case the foreign Rh antigen (D-antigen) enters the organism. In response to
this antigen the antibody formation process is initiated. This is a slow process; the
maximal antibodies concentration is reached in 2–4 months after the transfusion,
when most of the transfused cells have already finished their life. But since then
the antibody concentration may remain at a rather high level for a long time, at
least for a few years. So, while the first mismatched blood transfusion of
Rhpositive blood to the Rh-negative person does not have visible consequences
(it causes the initiation of anti-Rh antibodies formation), the second and any other
repeated similar transfusion do result in the immediate agglutination of Rh-
positive donor red cells. In case of repeated transfusion of Rh-positive blood to
such a person who is already immunized against the Rh antigen by mismatched
transfusion in the past, the transfusion reaction
can be as severe as a transfusion reaction caused by mismatched types
of blood of ABO system.

2. Another case is a pregnancy of Rh-negative mother with Rh-positive fetus.

During pregnancy normally mother is not exposed to the Rh antigen of a fetus


since the mother’s blood is separated from the fetus blood by the placenta.

At the time of birth, however, a certain amount of the newborn baby’s blood
may enter the mother’s circulation, and the mother’s immune system may
begin to produce antibodies against the Rh antigen.

It does not always occur since the amount of infant’s red blood cells that enter
mother’s circulation may be minimal. But if the woman starts to produce
antibodies against the Rh factor and their level remains high for at least a few
years, in the second and subsequent pregnancies these antibodies could cross
the placenta and cause agglutination and hemolysis of the Rh- positive red
blood cells of the fetus. Therefore, the second and other next babies could be
born with a condition called erythroblastosis fetalis, or hemolytic disease of
the newborn.

• Rh null – they do not have any Rh antigen and hence the blood group is also
called golden blood

Leukocyte blood groups.

• Like the RBC the leukocytes also have antigens on them. Their importance come
in transplantation
Classification of leukocytic antigen are based on 3 groups

1. Common Leukocytic Antigen or antigen of main locus

2. Granulocytic antigen

3. Lymphocytic antigen
1. The HLA system belongs to antigen of main locus and has 4 sublocus system A,B,C,D Out of
which A and B are more concentrated HLA compatibility is used in allograft HLA
compatibility is also analysed in pregnant women inorder to prevent miscarriage

28.

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I – FOOOLISH - FIBRINOGEN
Fibrinolysis
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Some
coagulation factors Ig
synthesis -
(Prothrombin ] Cfibrinogen → fibrin ) ( production of fibrin)
g. Surface
glycoprotein Adhesion
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Aggregation General of blood
Mechanism clotting
.

3
steps
-

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① Trauma to blood Vessels


2
Stages
.

of hemostasis
Prothombrin activator

① Primary / Vascular Thrombocytesy .

⑧ .
Catalyzed conversion of ,

TT Pronthombrin → Thrombin

activates

999 eregate to form


loss of
Constricts to stop "
"

blood
platelet plug
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↳ vascular spasm Is The
phase has 3 stages ;
phase of platelet adhesion
.

a .

b.
phase of platelet aggregation .

c .

Newly arriving platelet -

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a vessel is damaged or injured .

⑨ Coagulation phase
Begins 309 after injury
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-
or more .

-
Converts fibrinogen → fibrin ( insoluble) .

③ . Retraction
Formation of
platelet plug / White thrombus
-
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charism
Antiehromboplastin Heparin

Basically 2
types ; f)
antithrombin
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coagulation)
located in blood
Pro Promote
coagulants
.

1 .
-

Coagulants ¥E secondary →
fibrinolysis
Anti Inhibit
coagulation

2 -
.
.
.

ANTI COGULANTS

Blood balance between the two


coagulation depends on one

coagulants .

§ Blood coagulation pathway ;

① .
Intrinsic

⑨ Extrinsic ( Due to tissue trauma )


③ .
Common .

overview
;
-

Intrinsic Pathway →

Extrinsic
pathway →
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pathway ;

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a -
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D Intrinsic
pathway ; Trauma to blood cells .

I
xI→x Same as extrinsic

µ pathway µ
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XI

EE
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fast ca
et

II →
⑥ ix

LClotretraction.LI
• After formation ,
the clot starts contracting .
A straw colored fluid called
serum oozes out of the clot -

Responsible proteins are


a

,

i . Actin

2. Myosin
3 .
Thrombosthenin
Regulation of hemocoagulation

The following changes in the rate of blood coagulation are distinguished: increase - hypercoagulemia
and decrease - hypocoagulemia.

Activation of the sympathetic part of the autonomic nervous system (stress, pain, emotions,
physical activity) leads to the development of hypercoagulemia.

This was first established by W. Cannon at the beginning of the 20th century. The physiological
significance of hypercoagulemiaconsists in the fact that it provides a more rapid formation of a
blood clot if necessary. So, with massive blood loss, wounds and injuries with damage to large blood
vessels, blood coagulates in just 20- 40 seconds instead of 5-10 minutes.

This defensive reaction has developed during evolution. Acceleration of blood coagulation is achieved
by shortening the longest phase of the process - the formation of prothrombinase.

Hypercoagulemia is due to the effects of norepinephrine and adrenaline.

The value of adrenaline:

1. It releases thromboplastin from the walls of blood vessels, which contributes to the rapid formation
of tissue prothrombinase in the bloodstream.
2. Activates the XII factor, which causes the formation of blood prothrombinase.
3. Increases the activity of tissue lipases, which leads to the entry into the blood of lipolysis products -
fatty acids that contribute to the formation of thromboplastin.

4. Enhances the “recoil effect” from blood cells, especially from red blood cells, phospholipids, on the
matrix of which blood prothrombinase is formed.
Activation of the parasympathetic part of the autonomic nervous
system (vagus nerve irritation, intravenous administration of acetylcholine) also causes
hypercoagulemia, because promotes the release of thromboplastin from the walls of blood vessels,
and also stimulates thrombocytopoiesis (A.A. Markosyan).
The cortex of the cerebral hemispheres has the same effect on hemocoagulation- through the
autonomic nervous system and endocrine glands that produce vasoactive hormones.

A change in the lumen of the vessels is accompanied by the release of thromboplastin from their
walls along with anticoagulants and fibrinolysis activators.

Thus, the main effectors in the regulation of blood coagulation are vessels. But it also matters the
activity of the kidneys and the gastrointestinal tract, which remove an excess of procoagulants.
Therefore, in the process of evolution, only one defensive reaction of the hemostasis system has
been fixed - hypercoagulemia, aimed at emergency stopping of bleeding. Hypocoagulemia is always
secondary, i.e. due to the expenditure of coagulation factors during primary hypercoagulemia.

Hemostasis( haima , Greek - blood, stasis , Greek -


stationary state) is a complex biological process that ensures
the stopping of bleeding when a vessel is damaged.
The value of hemostasis.
1. Protective - the resulting thrombus ( thrombos , Greek - a
blood clot) seals the vessel, which preserves the integrity of
the vascular bed and the volume of circulating blood.
2. Restores the liquid state of the blood and the patency of the
vessel.
3. Stimulates the intensity of reparative processes in the
vessel wall.
4. Regulates transcapillary metabolism.

The hemostatic system consists of 4 links.


1. Humoral - plasma coagulation factors.
2. Elementary cell - hemocyte coagulation factors.
3. Tissue - coagulation factors of tissues and the tissues
themselves in which they are synthesized.
4. Regulatory - neurohumoral mechanisms that regulate blood
coagulation and anticoagulation.