2 курс / Нормальная физиология / Учебное_пособие_по_физиологии_крови_Авдеева_Е_В_,_Репалова_Н_В_

38. WRITE THE MISSING WORD!

THE INCREASED QUANTITY OF LEUKOCYTES IS CALLED [___].

39. WRITE THE MISSING WORDS!

THE ACETIC ACID [___] THE MEMBRANES OF [___].

40. FIND THE CORRECT ANSWER!

WHICH OF THE FOLLOWING DOES NOT DESCRIBE BASOPHILS?

1.nucleus usually has two lobes

2.cytoplasm exhibits distinctive red-stained granules

3.produce chemical substances that are involved in the inflammatory and allergic responses

4.the percentage range is 1% and less

41. WRITE THE MISSING WORD!

THE ABILITY OF THE HUMAN BODY TO RESIST ALMOST ALL TYPES OF ORGANISMS OR TOXINS THAT TEND TO DAMAGE THE TISSUES AND ORGANS IS CALLED [___] IMMUNITY.

42. FIND THE CORRECT ANSWER!

MONOCYTE-MACROPHAGE SYSTEM IS LOCATED IN:

1.all tissues

2.only in lymph nodes

3.only in bone marrow

4.only in spleen

43. FIND THE CORRECT ANSWER!

‘E’ IN THE FORMULA OF LEUKOCYTE CALCULATION MEANS THE

1.total number of the leukocytes in 1 liter of blood

2.total number of leukocytes within 25 big squares

3.dilution

4.volume of fluid under one small square

5.number of small squares in 25 big squares.

44. WRITE THE MISSING WORD!

WHITE BLOOD CELLS WHICH FORM ANTIBODIES ARE CALLED [___].

45. FIND THE CORRECT ANSWER!

THE TYPE OF IMMUNITY WHICH COME INTO PLAY IMMEDIATELY OR WITHIN HOURS OF AN ANTIGEN'S APPEARANCE IN THE BODY IS CALLED

1.innate immunity

2.acquired immunity

3.humoral immunity

4.T-cell immunity

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46. FIND THE CORRECT ANSWER!

THE TYPE OF IMMUNITY WHICH OBTAINED FROM THE DEVELOPMENT OF ANTIBODIES IN RESPONSE TO EXPOSURE TO AN ANTIGEN IS CALLED

1.innate immunity

2.acquired immunity

3.humoral immunity

4.T-cell immunity

47. WRITE THE MISSING WORDS!

ACQUIRED IMMUNITY CAN BE ACTIVE[___] OR [___].

48. FIND THE CORRECT ANSWER!

LIMPHOCYTES CAN NORMALLY CIRCULATE AN AVERAGE OF [___] BEFORE BEING DESTROYED

1.120 days

2.2-4 weeks

3.4-5 days

4.10-20 hours

5.several years

49. FIND THE CORRECT ANSWER!

MINIMUM OSMOTIC RESISTANCE OF NORMAL ERYTHROCYTES IS

1.0.42-0.48% of NaCl

2.0.30-0.32% of NaCl

3.0.1-0.2% of NaCl

4.2-3% of cytric acid

5.0.40-0.42% of KCl

50. FIND THE CORRECT ANSWER!

MAXIMUM OSMOTIC RESISTANCE OF NORMAL ERYTHROCYTES IS

1.0.42-0.48% of NaCl

2.0.30-0.32% of NaCl

3.0.1-0.2% of NaCl

4.2-3% of cytric acid

5.0.40-0.42% of KCl

PLASMA PROTEINS INCLUDE:

1.albumins

2.fibrinogen

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3.mast cells

4.globulins

5.monocyte

52. FIND SEVERAL CORRECT ANSWERS!

FUNCTIONS OF T-LYMPHOCYTES ARE:

1.imune memory

2.ativiruses immunity

3.atitissue immunity

4.regulation of phagocytosis

5.hemostasis

53. FIND THE CORRECT ANSWER!

A NEUTROPHIL CAN USUALLY PHAGOCYTIZE:

1.3 to 20 bacteria

2.20 to 30 bacteria

3.3 to 10 bacteria

4.more than 100 bacteria

FOREIGN PROTEINS WHICH INVADE THE BODY CAUSING AN IMMUNE RESPONSE ARE CALLED [___] ANTIGENS.

THE PERCENTAGE RANGE FOR NEUTROPHILS IS:

1.2-4%

2.70-80%

3.20-30%

4.50-70%

5.3-5%

THE PERCENTAGE RANGE FOR MONOCYTES IS:

1.2-4%

2.20-30%

3.3-8%

4.10-15%

5.70-85%

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OBLIGATORY TASKS

It is compulsory to carry out the tasks for self-preparation

1.Write down the formula for calculation of leukocytes and explain the meaning of each element.

2.Determine the quantity of leukocytes in blood, if there are 3 leukocytes in one small square of a count camera.

3.During calculation of the leukocytes in man's blood there were found 27 leukocytes in 25 big square of a count camera. Calculate the leukocytes in the blood patient. Compare the result with the norm. Make a conclusion.

4.During the determination of the erythrocyte sedimentation rate were obtained following data: ESR = 25 mm/h. Compare the result with the norm. Make a conclusion.

5.The result of the investigation osmotic resistance of erythrocytes was follow:

minimum osmotic resistance is 0,45%, maximum osmotic resistance is 0,35%. Compare the result with the norm. Make a conclusion.

6.As a result of starvation in humans decreased blood levels of albumin and globulins. Appearance of the patient has changed dramatically: increased volume of extremities, the skin is smooth. Explain the mechanism of this phenomenon.

7.In a patient with a diagnosis of allergic rhinitis, a general blood test showed an increase of eosinophils in 2 times. Explain why there has been an increase in the number of eosinophils in the blood.

8.In test tubes containing different solutions, is added a drop of blood , what happens to the red blood cell (hemolysis, wrinkling ,swelling or remain unchanged) to the following solutions:

a.NaCl 0.3%

b.NaCl 0.9%

c.glucose 5.5% (blood isotonic)

d.glucose 0.9%

e.NaCl 30%

f.Proteins 8%

9.How is known the osmotic pressure of blood plasma relatively constant. How can we explain the persistence of the osmotic pressure at various modes of drinking: a) excessive drinking, eg a few glasses of water or tea;

b) xerophagy (water restriction).

10.Fridentals experiment shows that in blood are buffer systems and the

alkaline reserve is considerably greater than the acid. Explain what the predominance of alkaline compound in the blood.

11.Draw a schematic capillary. Show the hydrostatic and oncotic pressure in the arterial and venous end. Explain the role of oncotic pressure in the exchange

of water between blood and tissue fluid.

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RECOMMENDED LITERATURE

1.Guyton, A.C. Textbook of medical physiology / A.C. Guyton, J.E. Hall. – 11 th ed. - Philadelphia: Elsevier Saunder. – 2006. – Ch. 30, 33, 34.

2.Ganong, W.F. Review of medical physiology / W.F. Ganong. – 22 th ed. - New York : Lange Medical Books / McGraw-Hill. - 2005. – Section VI, Ch. 27.

3.Lecture material.

4.Avdeyeva, E.V. Supplement for laboratory classes in normal physiology (for

students of medical, stomatological and pharmaceutical faculties) / E.V. Avdeyeva., L.I. Khokhlova. - Kursk, 2004. - P. 7-8.

5. Zavyalov, A.V. Methodical handbook in normal physiology. Tasks for selfcontrol: physiology of blood system, cardiovascular physiology / A.V. Zavyalov, E.V. Avdeyeva, L.I. Khokhlova. – Kursk, 2000.

SUPPLEMENTARY LITERATURE

1.Gutnik, K.B. Physiology for “lazy” students / K.B. Gutnik, V. Kobrin, D. Nash.

– M. : Логосфера, 2009. – 200 p.

2.Widmaier, E.Vander’s human physiology. The mechanisms of body function. / E. Widmaier, H. Raff, K. Strang. – Boston : Mc. Graw-Hill, Higher Education, 2008. – 770 p.

HEMOSTASIS AND BLOOD COAGULATION. BLOOD GROUPS.

TRANSFUSION

TOPIC MOTIVATION

Hemostasis is an evolutionary formed defense reaction of an organism, evident in bleeding, which prevents damaging of the vessel wall. Hemostasis system is the totality of blood and vessel components that provides quick prevention of bleedings when required. Study of hemostasis nature, finding out its components and separate sections provides us with an important knowledge to correct abnormalities in case they occur.

PURPOSE OF SELF-PREPARATION

After learning this material, the student has to know: the mechanisms of hemostasis and hemocoagulation processes, coagulation and anticoagulation systems of the blood and organism, neuro-humoral regulation mechanisms of the coagulation process, notion of blood groups system and blood transfusion rules. The student should also know the methods of determining blood groups and be able to conduct blood coagulation tests.

PLAN OF THE TOPIC STUDY

1.Hemostasis.

a)Stages of hemostasis.

b)Characteristic and biological significance of hemostasis.

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2.Physical and chemical characteristics of platelets.

3.Vascular platelet hemostasis.

4.Mechanism of blood coagulation.

a)Formation of prothrombin activator.

b)Formation of thrombin.

c)Formation of fibrin fibers.

5.Clot retraction.

6.Fibrinolysis.

7.Anticoagulation mechanisms, anticoagulants.

8.Regulation of blood clotting.

9.Blood coagulation tests.

a)Bleeding time test.

b)Clotting time test.

c)Prothrombin time test.

10.Blood groups.

a)Major O-A-B blood types.

b)Methods of determining blood groups.

11.Rh blood types.

12.Rh immune response.

13.Main principles of blood transfusion.

a)Direct agglutination.

b)Reverse agglutination.

THE QUESTIONS YOU SHOULD PAY ATTENTION TO

1. Platelets (or thrombocytes).

Platelets are a component of blood whose function (along with the coagulation factors) is to stop bleeding by clumping and clotting blood vessel injuries.

Thrombocytes are formed in the bone marrow from cells called megakaryocytes (fig. 33).

Fig. 33. Formation of platelets.

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They have no nucleus, but can secrete a variety of substances: ATP, ADP, serotonin, pyrophosphate, adrenalin, calcium, low-molecular proteins, Willebrant factor, fibrinogen, enzymes. In their cytoplasm are such active factors as actin and myosin molecules, which are contractile proteins similar to those found in muscle cells, and still another contractile protein, thrombosthenin, that can cause the platelets to contract; residuals of both the endoplasmic reticulum and the Golgi apparatus that synthesize various enzymes and especially store large quantities of calcium ions; mitochondria and enzyme systems that are capable of forming adenosine triphosphate (ATP) and adenosine diphosphate (ADP); enzyme systems that synthesize prostaglandins, which are local hormones that cause many vascular and other local tissue reactions; an important protein called fibrin-stabilizing factor, and a growth factor that causes vascular endothelial cells, vascular smooth muscle cells, and fibroblasts to multiply and grow, thus causing cellular growth that eventually helps repair damaged vascular walls. The cell membrane of the platelets is also important. On its surface is a coat of glycoproteins that repulses adherence to normal endothelium and yet causes adherence to injured areas of the vessel wall, especially to injured endothelial cells and even more so to any exposed collagen from deep within the vessel wall. In addition, the platelet membrane contains large amounts of phospholipids that activate multiple stages in the blood-clotting process.

Platelets are normal concentration in the blood is about 250000 per cubic millimeter. The decrease of thrombocytes amount is called thrombocytopenia, the increase is thrombocytosis.

They remain functional for about 7-10 days (after which they are removed from the blood by macrophages in the spleen and the liver). Platelets play an important role in hemostasis (preventing blood loss).

2. Hemostasis.

It is prevention of blood loss from a broken vessel.

Hemostasis system is the system, which provides maintenance of the blood fluidity and stoppage of bleeding after injure of blood vessels (fig. 34).

Fig. 34. Major components of hemostasis.

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2.1.Functions of haemostasis system.

1.Provides maintenance of the blood fluidity.

2.Stops the blood when a vessel wall is damaged.

2.2.Structure of haemostasis system.

1.Blood vessels walls.

2.Formed blood elements.

3.Biochemical systems of blood plasma:

system of blood coagulation;

anticoagulative system;

fibrinolytic system;

calicrein-kinine system.

2.3.Mechanisms of haemostasis.

I. Vascular-platelet (primary, microcirculatory).

Provides stoppage of bleeding in vessels of the microcirculatory system with the diameter less than 100 mkm. A vessel wall and thrombocytes take part in this mechanism. Results in white clot, which consists of thrombocytes.

II. Coagulatory (secondary, macrocirculatory).

It is the continuation of vessel-thrombocytory and it is based on it. Provides stoppage of bleeding in vessels with a diameter more than 100 mkm. Results in red clot, which consists of fibrin and the formed blood elements.

I. Vascular-platelet haemostasis.

Vascular-platelet haemostasis is performed in several stages:

1.spasm of damaged vessels;

2.adhesion of thrombocytes;

3.reversible platelets aggregation;

4.irreversible platelets aggregation;

5.retraction of platelet plug.

1.Spasm of damaged vessels.

There are two types of vessel spasm:

Primary. It has a reflex origin. It appears in first seconds of a damage with the help of the sympathetic nervous system.

Secondary. It is due to release of biologically active substances in the damage spot (serotonin, epinephrine, thromboxan). It appears in few seconds after a damage.

Spasm of vessels develops fast enough and disappears in few seconds and bleeding continues.

The nervous reflexes are initiated by pain nerve impulses or other sensory impulses that originate from the traumatized vessel or nearby tissues. However, even more vasoconstriction probably results from the local myogenic contraction of the blood vessels initiated by direct damage to the vascular wall (fig. 35). And, for the

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smaller vessels, the platelets are responsible for much of the vasoconstriction by releasing a vasoconstrictor substance, thromboxane A2. The more severely a vessel is traumatized, the greater the degree of vascular spasm.

Fig. 35. Spasm of damaged vessels.

2. Adhesion of thrombocytes.

There are 2 stages of adhesion:

Precontact stage. It is associated with the changes in a shape of thrombocytes. They take the spheroid shape with 3 to 10 processes.

Contact stage. It is associated with the attachment of thrombocytes to the endothelium of blood vessels. Thrombocyte can interact with a vessel wall directly and also with the help of special protein – Willebrant factor (fig. 36).

Fig. 36. Adhesion of thrombocytes.

Adhesion occurs easier with the help of two factors:

Negative charge of a vessel at the site of a damage is changed to positive. Negatively charged platelets adhere to it.

Slow down of the blood movement in microcirculatory vessels.

3.Reversible platelets aggregation – is the aggregation of thrombocytes in the damage spot and conglutination of them one to another (fig. 37).

The reasons of aggregation are aggregants. Aggregants can have

thrombocytory origin (those that are released by thrombocytes) and not-

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thrombocytory (those that are released by other cells or are formed in plasma). The main aggregants are:

1)ADP;

2)Thromboxan A2 and arachidonic acid;

3)Biogenic amines (adrenalin, serotonin);

4)Factor of thrombocytes aggregation;

5)Thrombin;

6)Thrombospondin.

Reversible aggregation begins simultaneously with adhesion. ADP released from the damaged vessels (“extrinsic”), from platelets. Platelet plug is formed and through this plug, blood plasma can penetrate.

Fig. 37. Reversible platelets aggregation.

4. Irreversible platelets aggregation.

Aggregation with the damage of thrombocytes and it cannot be stopped (fig.38). The reason of it is thrombin. A platelet plug, under the influence of thrombin becomes impermeable to blood. Thrombin causes destruction of platelet membrane and content of platelets are released into blood. The formation of bridges between thrombocytes, which are formed with plasma proteins. These proteins are aggregation co-factors of plasma. Fibrinogen, albumins, agrexons A and B.

Fig. 38. Irreversible platelets aggregation.

5. Retraction of platelet plug – packing, retraction of thrombus in consequence of which it loses extra water and become hard. The contraction of thrombus is performed with the help of protein thrombostenin.

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