Physiology of Blood

1. Physiology of Blood

2. Blood in the system of body fluids

4. Blood content
 liquid portion or plasma (52-64%)
 cells or formed elements (36-48%):
erythrocytes (red blood cells),
leucocytes (white blood corpuscles),
and thrombocytes (blood platelets).
 Definite volumetric correlation
between the plasma and formed
elements is haematocrit (36-48%)

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6. Blood plasma composition 90 to 92 % water
 8 to 10 % dry matter, mainly proteins and
salts.
 The total protein content is 7 to 8 %; albumins
(about 4.5 per cent), globulins (2 to 3 %), and
fibrinogen (0.2-0.4 %).
 non-protein nitrogenous compounds (amino
acids and polypeptides), and products of
protein decomposition (urea, uric acid, creatine,
creatinine).
 nitrogen-free organic substances are glucose
4.4-6.6 mmol/1,neutral fats and lipoids.
 Mineral substances - 0.9 %. (Na+, K+, Ca2+
cations and Cl-, HPO42-, and HCO3- anions).

7. Functions of plasma proteins
 Create oncotic pressure
 Buffer system
 Create blood viscosity
 Partake in blood coagulation
 Partake in humoral immunity
 Transport function
 Nutritive function

8. Parameters of blood homeostasis
 Viscosity (5,0)
 pH (7,4 for arterial, 7,35 for
venous)
 Osmotic pressure (7,6 atm)
 Glucose content (3,3-5,5 mmol/l)
 Protein content (65-85 gr/l)
 Ionic content

10. Erythrocytes in
blood capillaries
Erythrocytes in blood tube

11. Sickle cell disease

13. Mature neutrophil

14. eosinophil

15. basophil

17. Phases of haemostasis
 Vascular platelet haemostasis
 Coagulation haemostasis
 Fibrinolysis

18. Stages of vascular platelet
haemostasis
 1. Reflex spasm of the damaged
vessels (serotonin, adrenaline,
noradrenalin).
 2. Platelet adhesion to the site of
trauma due the fact that a negative
electric charge of the vessel at the
site of damage is altered to a
positive one. Usually takes 3-10
sec.

19.  3. The reversed platelet
aggregation begins nearly
simultaneously with adhesion. The
'extrinsic' ADP released from the
damaged vessel and the 'intrinsic'
ADP released from the platelets and
erythrocytes are the main
stimulators of this process. A loose
platelet plug is formed through
which blood plasma leaks.

20.  4. In the irreversible platelet aggregation a
platelet clot becomes impermeable to blood.
 This is due to the action of thrombin that
causes destruction of the platelet
membrane('viscous metamorphosis' of
platelets).
 All the platelet factors and the new amounts of
ADP are released to increase the size of a
platelet thrombus.
 The release of the platelet factor 3 gives rise to
the production of platelet prothrombinase
switching on the mechanism of coagulation
haemostasis.
 A small number of fibrin filaments is formed on
platelet aggregations whose mesh work retains
erythrocytes and leucocytes.

21.  5. Retraction of a platelet thrombus
implies its thickening and fixation at
the site of damage at the expense
of thrombosthenin contraction.

22. Coagulation haemostasis
Phase I. Formation of prothrombinase.
 The extrinsic (tissue) and intrinsic (blood)
mechanisms are distinguished in this
process.
 The extrinsic mechanism is triggered by
tissue thromboplastin which is released
from the damaged vessel and surrounding
tissues. Tissue prothrombinase takes 5-10
sec for its formation.
 In the intrinsic mechanism thromboplastin
and other factors are transported by blood
proper. Blood prothrombinase is formed in
5-10 min.

23. Phase II. Thrombin formation
 this process takes 2-5 sec.
 This rate can be explained by the
fact that prothrombinase adsorbs
prothrombin and converts it into
thrombin on its surface.
 This process proceeds in the
presence of factors V, X and Ca2+.

24. Phase III. Fibrinogen is converted into
fibrin.
 This process has three stages.
 In the first stage soluble fibrin monomer
is formed from fibrinogen under the
action of thrombin.
 In the second stage fibrin monomers are
polymerized under the action of Ca2+
ions with the formation of fibrin polymer
(soluble fibrin S).
 The third stage involves formation of the
final or insoluble fibrin

25. FIBRINOLYSIS
 Fibrin breakdown is effected by the
proteolytic enzyme plasmin
 it is present in the plasma as
proenzyme plasminogen.
 Blood and tissue activators are
required for the conversion of
plasminogen into plasmin.

26. The fluidity of blood is preserved due to
 (1) smooth surface of vascular endothelium
hinders blood clotting; this prevents activation
of Hageman factor and platelet aggregation;
 (2) the vessel walls and formed elements have
negative charges due to which blood cells are
pushed away from the vascular walls;
 (3) vessel walls are covered with a thin layer of
soluble fibrin that adsorbs active coagulation
factors, especially thrombin;
 (4) blood coagulation is prevented due to a
high rate of blood flow so that the coagulation
factors cannot be accumulated in one place;
 (5) natural anticoagulants maintain blood
fluidity.

28. BLOOD GROUPS
 In 1901 K. Landsteiner and in 1903
J. Jansky found that erythrocytes
glue together when the blood of
different persons is mixed up.
 In 1930 K. Landsteiner was
awarded a Nobel Prize for discovery
of the blood groups.

29.  More than 200 various agglutinogens
have been discovered in human
erythrocytes
 140 of which are united into 20 systems
(groups), while the rest are either
common or individual.
 This determines the remarkable unique
nature of antigens, so every man has his
own blood group.
 These agglutinogen systems are
distinguished from the ABO system in
that they have no natural agglutinins in
plasma similar to α and β -agglutinins.

30. Antigens on erythrocyte membrane

31. ANTIGENES STRUCTURE
B antigen A antigenH antigen (O blood group)

33. Ig G STRUCTURE

34. Ig M STRUCTURE

35. Anti А(α) & anti В(β) antibodies are Ig M, which have 10 cites to
bind antigenes
 Only in АВО system they are
ready antibodies Anti А(α) &
anti В(β)
 There are no antigens on
erythrocytes to the
antibodies present in blood!

36. ANTIBODIES FORMATION
 No antibodies in newborns.
 They are formed during the first 3-
4 months. Their max concentration
is reached to 13-14 years.
 Why are they formed?

37. Hypothesis on the mechanisms of antibodies
formation
 Antibodies are formed to the
antigens of food or bacteria
present in the intestines.
 There are bacteria in the
intestines with the same
antigens (А or В) as
erythrocytes

38. If there is just B antigen in the tested blood, this must be В(III)
group
A or B or both
antigens present
B antigen
present
no A antigen

39. If there is just A antigen in the tested blood, this must be A(II)
group
A or B or both
antigens present
A antigen
present
no B antigen

40. If there are both A & B antigens in the tested blood, this
must be АВ (IV) group
A or B or both
antigens present
A antigen
present
B antigen
present

41. If there are no antigens in the tested blood, this must be
O (I) group
antigens A & B are
both absent
no B antigen
no A antigen

42. A or B or both
antigens present
no B antigen no A antigen
Which blood group is this?

43. In blood transfusion АВО & Rh systems are
taken into account because:
 These antigens are most widely
spread;
 They have the greatest
agglutinating capacity;
 There are ready antibodies in
АВО system & first transfusion
of incompatible blood would
cause haemotransfusion.

44. Consequences of blood clotting in the vessels:
 Capillaries are blocked with
erythrocyte clots;
 Kidney filter is damaged;
 Haemoglobin in blood plasma
increases blood viscosity, BP
increases, heart rate increases
 Toxins released cause fever,
sweating

45. Rh system

Blood which erythrocytes have D antigen is called
rhesus-positive Rh+ (85% of all the
population).
 The rest 15% don’t have this antigen and their
blood is called rhesus negative Rh-.

46. Rh system
 Antibodies to Rh-factor arte not inborn,
they can be formed after Rh(+) blood is
transfused to Rh(-) recepient.
 These antibodies are IgG, incomplete
antibodies, so they can penetrate blood-
tissue barriers.

47. Ig G STRUCTURE

48. Rhesus conflicts.
 In blood transfusion: first blood
transfusion of Rh(+) blood to Rh(-)
recipient would cause only antibodies
formation. There is no agglutination until
antibodies are formed.
 Second transfusion of the Rh(+) blood
would cause agglutination because
antibodies (аnti D aglutinins) were
already formed.

49. Rhesus conflicts.
 In pregnancy : if mother is Rh(+) &
fetus is Rh(-) .
 Develops during second pregnancy.
Mother’s antibodies can pass haemato-
placentar barrier & cause erythrocytes
agglutination in fetus.