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Ministry of public health of ukraine

Bukovinian state medical university


on the cathedral meeting of the

Department of patient care and higher nurse education


minute № ____

Head of department

Associate professor Plesh I.A.

Methodical guidelines

for 3rd – year students of the medical faculty

Module 2

The main duties and professional skills of nurse

at the surgical department

Semantic module 1

Haemostasis. Blood transfusion.

Resuscitation in surgical patients.


Bleeding and blood loss

Subject: Nursing practice

3rd-year students of Medical faculty

Speciality: "General medicine" – 7.110101

7.110104 – "Pediatrics"

Duration - 1 hour

Methodical guidelines composed by:

Professor R.I. Sydorchuk

Assoc. professor O.Y. Khomko

Assistant R.P. Knut

Chernivtsi – 2008

AIM: To acquaint students with the general attributes of a bleeding and a hemorrhage. To acquaint students with bases of transfusiology: techniques of definition of blood groups and a rhesus of an accessory. Realization individual, a rhesus and biological compatibility, ways of preparation, conservation and reservation of hemotransfusion agents. To acquaint with modern indications and contraindications to a hemotransfusion, rules and engineering of transfusion therapy, preparation of system for a hemotransfusion. And also, to acquaint students with possible reactions and complications at a hemotransfusion, its components, preparations, blood substitutes, their prophylaxis, treatment, filling of the medical documentation.

^ PROFESSIONAL MOTIVATION: The bleeding - one of the most drama situations in medicine and consequently takes a special place in surgery. It arises both at mechanical damages and at many surgical diseases. The loss of blood causes in an organism of change and frames threat for life of the patient. Delayed recognition and overdue representation both the first medical, and the surgical aid may result in unforeseen consequences. In this case, infusional-transfusion therapy takes the important place, concerns to its outstanding achievements and there is no alternative replacement at treatment serious blood loss and many other acute and chronic diseases, in particular a hematological structure. Any of mistakes at definition as groups of a blood, and may result a rhesus of the factor in serious consequences for life of patients and victims. The opportunity of restoration of a hemorrhage has considerably expanded a range of surgical interventions not only by granting the help by the patient with massive hemorrhages, and also at performance of difficult surgical interventions. The special discipline - clinical transfusiology which surveys different aspects of a hemotransfusion, its components, and blood substitutes for today is generated. The transfusion to the patient of a blood of its components and preparations may be carried out only under the consent of the patient. He should know, than refusal of application of hemotransfusion agents threatens him, at the same time he should be informed, what complications and consequences of such treatment may be. So modern international conventions on human rights and laws of Ukraine.


Bleeding and coagulation

Bleeding is an effusion of blood out of blood channel into tissues and cavities of the organism (abdominal, thoracic, cranial, into joints,etc.) or into the surroundings (out).

The cause of bleeding is a disturbance of vascular vessel safety due to one or another agent: trauma, arrosion of vessel in various diseases and purulent processes, increase of blood pressure in a vessel, sharp decrease of atmospheric pressure. Vessel wall permeability for blood may be not only due to the damage of vessel, but also change of blood chemism, toxic effect, disturbance of vitamins balance in the organism, etc.

Haemophilia, scarlet fever, sepsis, scurvy, etc. are the examples of diseases, causing bleeding due to a change of blood chemism. The diseases may by accompanied by bleedings due to the disturbance of vascular wall permeability caused by toxins anchavitaminosis. 86

Diffuse impregnation wilh blood of any tissue (subcutaneous fat, brain tissue, etc.) is called haemorrage; accumulation of blood, by tissues -haematoma.

According to the anatomical regions bleedings can be distinguished: arterial, venous, capilary, parenchymatous.

Due to the cause they can be a) bleeding of mechanical nature i.e. damage of the vessel is due to mechanical cause; b) bleeding of neuro-trophic nature i.e. vessel permeability is due to trophic disturbances of its wall (sepsis, scarlet fever, scurvy, etc.). Taking into consideration clinical manifestations bleedings are divided into a) external; b) internal; c) conceated.

In arterial external bleeding blood of bright red colour effuses by pulsatile spurt. Such bleeding quikly results in acute anaemia. The following symptoms characterize acute anaemia: persisting paleness, trembling and small pulse, progressing decrease of blood pressure, dizziness, nausea, vomiting, syncope.

External venous bleeding is characterized by slow effusion of dark blood.

Injury of large veins of neck is dangerous due to a possibility of development of air embolism of brain vessels and cardiac pressure in these veins during breathing in.

General symptoms are the same for all types of bleeding, including inner bleedings in various cavities. They are observed in heavy loss of blood and consist of appearance of acute anaemia (paleness, dizziness, syncope, trembling small pulse, progressing decrease of blood pressure).

The local symptoms are various. In bleeding into cranial cavity symptoms of brain compressing develop; bleeding into pleural cavity (haemothorax) is accompanied by compression of the lung from damaged side. It bleeds to a dyspnoe. Limitation of respiratory excursions of thoracic cavity, dullness on percussion, weakness of vocal fremitus, weakness of respiratory sounds in the place of blood accumulation are noticed. In exploratory puncture of thoracic cavity presence of blood in pleural cavity is noted. Haemoperitoneum results from subcutaneous ruptures of parenchymatous organs (spleen, liver, etc.), rupture of uterine tube, or ectopic pregnancy, injury of abdominal organs, etc. and manifests symptoms of peritoneum irritation (pains, tension of abdominal muscles, nausea, vomiting, etc.) and loss of resonauce in sloping parts of abdominal cavity, determined by percussion.

Early secondary bleedings are due to thrombus prolapse. Quite often it heppens due to improvement of the patient's general condition, increase of blood pressure or due to stoppage of vascular spasm during bleeding.

Late secondary bleedings most often result from the development of wound infection, leading to thrombus fusion and arrosion of blood vessel.

Brochoscopy, thoracoscopy, esophagoscopy, gastroscopy, duodenoscopy, rectoromanoscopy, colonoscopy, laparoscopy, cystoscopy are widely used in diagnostics of interna) bleeding.

Bleedings are dangerous, first of all, due to development of acute anaemia and exsanguination of brain (syndrome of acute blood loss).

The patient may die due to the disturbance of function of vitally important centers. A sharp decrease of maximum blood pressure to 80 mm Hg or decrease of haemoglobin content by 1/3 of the initial values in acute blood loss in considered to be extremely dangerous for life, because compensatory processes have no time to develop and prevent brain anaemia. In slow (during several weeks) loss of blood an organism adapts to chronic anaemia and may function for a long time, even if haemoglobin level is very low.

In internal bleeding, blood being effused into closed cavity, may compress a vitally important organ (brain, heart, lung, etc.) violate its function and become dangerous for the patient's life.

An organism responds to any bleeding with reaction, directed to adaptation to the decrease of circulating blood volume. The mechanism 88 of adaptation is intricate and includes the following: 1) spasm of vessels; 2) increase of heart activity and respiration: 3) increase of circulating blood volume due to blood brought into the blood channel from the depot and tissue fluid (autohaemodilution).

Biochemical characteristics of blood, the condition of its coagulating system, in particular, are of great importance. In normal blood coagulation, even in extensive wounds, bleeding may stop due to the blood coagulation and thrombosing of damaged vessels.


Techniques of temporary haemostasis include application of a pressure bandage, elevated position of an extremity, maximum flexion of an extremity in joint region and compression of vessels in that area, compression with fingers, applying a tourniquet and also applying a clamp on a bleeding vessel in the wound.

After applying a tourniquet the blood circulation in the extremity is

completely controlled which may lead to gangrene. The tourniquet should be loosen every 2 hours. The time of applying a tourniquet should be written down on a note which is pushed in under a tourniquet (on the patient's emergency medical tag).

All techniques of final haemostasis can be devided into 4 groups: 1) mechanical; 2) thermal; 3) chemical and 4) biological.

Mechanical techniques of haemostasis include ligating a vessel in the wound or at a distance, under - running a bleeding vessel, a pressure bandage and packing.

Thermal methods of haemostasis are based on the property of low temperatures cause spasm of vessels, and high ones - coagulate proteins and increase blood coagulation.

Chemical methods of haemostasis include application of vasoconstrictors and preparations increasing blood coagulation.

Biological methods of coagulation:

1)packing the bleeding wound with the patient's own tissues (omentum, muscle, subcutaneous fat, fascia);

2) transfusion of small quantities of blood, fresh plasma, serum, thrombocytes, fibrinogen, etc., injection of protrombin complex - concentrate of coagulating factors II-VII-IX-X, antihemophilic globulin A;

3) injection of vitamins;

4) intramuscular injection of human or animal serum;

5) local application of blood derivatives (thrombin, haemostatic sponge, isogenic fibrinous film, biological antiseptic pack, etc.).

^ Haemostatic system

The haemostatic system is a complex of countervailing pressures, one toward coagulation and blood clotting and the other toward anticoagulation and maintenance of blood fluidity. Blood and fabrics enter into system of haemocoagulation, which produse, use and allocate from organism substances, necessary for the given process.

It is useful to consider the events of normal haemostasis in three phases. The first phase includes the immediate control mechanisms related to the vascular response and the formation of a platelet plug at the site of vessel injury. The second phase includes the long-term control mechanisms involved in the coagulation cascade. The opposing mechanisms directed toward maintaining blood fluidity and clot destruction may be considered as components of the third phase. There is considerable overlap and interaction among these three phases.

Several humoral agents act to stimulate the clotting system to stop haemorrahe. Tromboxane causes constriction of smooth muscle and is active early after vessel injury. Tromboxane is synthesized through prostaglandin metabolism, is released primarily by platelets at the site of disruption of the endothelial surface, and induces platelet aggregation. Agents such as epinephrine and norepinephrine cause vasoconstriction 90 of larger vessels and induce platelet aggregation. Arteries are much more efficient than veins in vasoconstricting and sealing when injured. As is frequently mentioned, partial transection is more likely to lead to significant blood loss than complete transection because partial transection prevents complete vasoconstriction.

The relative composition of a thrombus is dictated largery by local blood flow conditions. In areas of sluggish blood flow where fluid shear stress is low or werw eddies of the flow permit long residence of blood elements near abnormal surfaces, activation of clotting factors leads to a buildup of procoagulants and ultimately to formation of a plasma clot, the so-called red trombus. This is a clot composed of red cells trapped in fibrin strands. It predominates in peripheral veins and other areas of low flow. In the regions were blood flow is brisk, and the fluid shear stress is greater, as in the peripheral arteries, the so-called white thrombus is more common. The white trombus is characteristic of arteries and other high flow areas.

The vessel-thrombocyte reaction provides haemostasis only in small vessels with low blood pressure. Haemostasis begins in large vessels, but thrombocytic thrombus do not maintain high pressure and are washed away. In such vessels haemostasis can be achieved by formation (education)of a fibrin thrombus, which is stronger. The formation of the fibrin thrombus is accomplished in three phases.

Phase I. The most complex and the congest phase is formation of prothrombinase. In this process we distinguish external and internal (blood) system. The external way is started fabric thromboplastin, which is allocated from walls of the damaged vessel and environmental fibers. The push for formation fabric prothrombinase is served by damage of walls of vessels with allocation from them in blood fabric thromboplastin, representing splinters of the cell membranes.

The formation of fabric prothrombinase is the starting mechanism for the subsequent reactions. Fabric of prothrombinase results in 9i formation of small quantities of thrombin which are sufficient for aggregation of platelets.

Blood prolhrombinase is formed much slower. As a rule, in the place of injury of vessels a small amount of erythrocytes collapses.

Phase 2. The appearance prothrombinase marks the beginning of the second phase of blood clothing formation of thrombin. In comparison with the first phase this process proceeds seconds instantly - for 2 - 5c. Such speed is caused by that prothrombinase adsorbs a prothrombase and on the surface transforms it in thrombin. This process proceeds at participation of the factors V and X.

Phase 3. Transformation of fibrinogen to fibrin. This process proceeds in three stages. During 1st stage under influence of thrombin is formed fibrin-mono from fibrinogen. During 2-nd stage under influence of ions Na2 + comes polymerisation of fibrin-mono and the fibrin-polymer (soluble fibrin "S" is formed). And the 3-d stage at participation of the factor XIII and fibrinase of fabrics, platelet and RBC is formed final or insoluble fibrin. Fibrinase forms strong peptid connection between the next molecules of fibrin-polymer, that cements fibers, increases its mechanical durability and stability to fibrinolysis. The formation of fibrin it is formation of a blood thrombus.


After formation of a fibrin clot last phase including two processes - retraction and begining of fibrinolysis. Retraction provides condensation and fastening of a thrombus in the damaged vessel. It is carried out only sufficient amount of platelet and use the contracting protein fibers of thrombostenin. At the reduction it compresses a clot to 25-50% of initial volume, that fixes it in a vessel more reliably retraction comes to an end during 2-3 after formation of a clot.

Simultaneously with retraction, but with smaller speed fibrinolysis starts. The main function of fibrinolysis - restoration of the lumen of the vessel, stoppered by a clot. 92

The splitting of fibrin is carried out by proteolytic enzyme plasmin, with which is in plasma as proenzyme plasminogen. For its transformation in plasmin the activators contained in blood and fabrics are required. Thus, the system of fibrinolysis, has the internal and external mechanism of activation. The internal mechanism is carried out by enzymes of blood, and external fabric activators.

^ Anticoagulation mechanisms

Circulating blood has necessary for curtailing, but remains liquid. Preservation of a liquid condition of blood - main function of coagulation system. Blood represents the protective adaptation included at damage of vessels.

The liquid condition of blood is kept by numerous mechanisms:

1) clotting of blood is interfered by a smooth surface endothelium of vessels, that prevents activation of the Hageman factor and aggregation of trombocytes;

2) walls of vessels are covered with a thin layer of soluble fibrin adsorbing the active factors of clotting thrombin;

3) clotting is prevented by hight rate of blood circulation, that does not allow the factors of haemocoagulation to achieve the necessary concentration in one place;

4) liquid condition of blood is supported by natural anticoagulation substance.

Development of hypercoagulation that is activation of sympathetic part of vegetative nervous system and stress reactions is caused by epinephrine and norepinephrine. Epinephrine releases thromboplastin, from the walls of vessels, which quickly turns prothrombinase in blood. Under the influence of epinephrine natural anticoagulants and activators of fibrinolisis are also released from the walls of the vessels, but the action of more powerful thromboplastin is determining. At present vessels are considered the main factor in regulation of curtailing blood. The second factor of hypercoagulation is activation by epinephrine Hageman factor, which is a basis of formation of blood prothrombinase. Hypercoagulaemia is achieved at the expense of the factor of blood clothing, therefore after cancellation of irritant on the organism it is replaced by secondary hypocoagulaemia. The development hypercoagulaemia prepares the organism for faster formation of a clot in danger of trauma or other damages. Thus, during evolution in the system of haemocoagulation only protective adaptation reaction - hypercoagulaemia, directed on an urgent stop of the bleeding was generated.

Platelets are important components of the haemostatic system. When platelets encounter exposes collagen, they aggregate and adhere to nonendothelial surfaces. Following the aggregation and adherence serotonin and thromboxane are released, that aid is vessel contraction. In addition there is productive of substances that further accelerate platelet adherence, including epinefrine, adenosine diphosphate, and thromboxane. This acceleration reaction recruits other platelets, thus forming a plug in the areas of damaged blood vessels. Thrombosthenin is a contractile protein within platelets that causes platelet contraction and reinforces the clot. Furthermore, platelets release platelet factor III, a thrombogenic phospholipid that promotes coagulation, and thrombin, which contributes to local platelet aggregation and adherence.

The coagulation system is made up of a system of enzymes that circulate in the inactivated precursor form and are activated by a proteolytic cascade. The activation requires several cofactors, of which calcium is probably the most important. The fibrin clot is formed through initiation of one of the two pathways. The intrinsic and extrinsic pathways. The intrinsic pathway is a cascade that begins with factor XII. This factor is then activated to XIIA; similary factor XI becomes XIA, factor IX becomes IXA. and factor VIII becomes VIIIA. Then factors V and X, thrombin is activated. The extrinsic pathway begins 94 with factor VII and then activates factors X and V once again to form thrombin from prothrombin. After thrombin has split fibrinogen to form a soluble fibrin monomer, the monomer binds to form insoluble fibrin. Factor XIII forms a firmer chemical bond and thus a stronger clot by acting on fibrin. The cascade of proteolysis that makes up the coagulation system amplifies the system's response because each enzyme tends to activate a more powerful enzyme; thus an initial small stimulus causes a large reaction.

The fibrinolytic system is important in opposing the tendency toward blood coagulation and maintaining the fluid characteristics of blood in the intravascular space. The main product of the fibrinolytic pathway is plasmin, also called fibrinolysin. Plasmin, a strong proteolytic enzyme, reduces fibrin to soluble fragments. Plasmin is formed from plasminogen, another circulating precursor; a variety of plasminogen activators stimulate this formation. Tissue plasminogen activator and other activators that are found in a variety of secretions are effective in stimulating plasmynogen to be lysed to form plasmin. The liver is important in clearing the blood stream of activated metabolites of both fibrinolysis and coagulation. Therefore liver dysfunction from any cause may push the coagulation system in one direction or the other.

Plasmin acts not only on fibrin but also on fibrinogen and factors II, V, VIII, and, as some data suggest, on factors IX and XI. This powerful serine protease effectively metabolizes a number of other proteins including growth hormone, insulin, and adrenocorticotropic hormone (ACTH). Futhermore, it activates factor XII, and when activated through factor XII, plasmin can trigger the complement, kinin, and coagulation system.

The coagulation system is involved in the kinin complement systems. The effect of high molecular weight kininogen is to activate factor XII. Fragments of factor XIIA, generated by plasmin, stimulate the change of prekallikrein to kalikrein. This change sets off the conversion of 95 kininogen to kinin and also activates complemets C1, C2, and C5. These complements may also replace factor D in the alternative complement pathway. ,

A variety of circulating antiproteases block the proteolytic enzymes of the complement, kininogen. coagulation pathways. Antithrombin III is a powerful ingibitor of the coagulation system. Deficiencies in antithrombin III are associated with significant thrombotic disorders. Other important antiproteases include alpha-macroglobulin, alpha-antitrypsin, and alpha-plasma inhibitor.

  1. ^

    Objectives for Students’ Independent Studies

You should prepare for the practical class using the existing textbooks and lectures. Special attention should be paid to the following:

Theme 1. Bleeding and a hemorrhage. Methods of a temporary and final control of a bleeding.

  1. Concept about a bleeding and blood loss.

  2. Classification of bleedings (on the mechanism, the attitude to medium, term of occurrence, clinical course).

  3. Local attributes of an external bleeding.

  4. General attributes of a hemorrhage and an anemia.

  5. Basic attributes of an internal bleeding.

  6. Degrees of an acute hemorrhage.

  7. Techniques of determination of blood loss volume.

  8. That such Algover index?

  9. What mechanism of an independent control of bleeding?

  10. Main principles of treatment of bleedings.

  11. Methods of a temporary control of bleeding (pressing of vessels in a wound, a compressing bandage, a flexion of an extremity, pressing of vessels on an extent, a dense tamponade of a wound, an applying a tourniquet, garrot, a clamp on a vessel).

  12. Methods of a final control of a bleeding (mechanical, physical, chemical, biological).

  13. The vascular seam. Concept about a transplantation and an alloplasty.

  14. Complications of bleedings: a loss of consciousness, a collapse, a hemorrhagic shock, clinical attributes, the first medical service.

Theme 2. Doctrine about a blood. Tests at a hemotransfusion.

  1. Blood group systems.

  2. Antigens AB0.

  3. Antibodies of system AB0.

  4. Methods of determination of blood groups of system AB0.

  5. Agglutinogenes revealating by direct reaction.

  6. Revealing агглютининов by an indirect way.

  7. Blood cross-match.

  8. Methods of blood grouping in AB0.

  9. Causes and prevention of mistakes at blood-grouping.

  10. Blood-groups of rh-system.

  11. Methods of determination of the rh-factor.

  12. Preparation of system for blood transfusion.

I.Tests and Assignments for Self – assessment

Multiple Choices.

Choose the correct answer/statement:

  1. Indications for blood transfusion are:

    1. an allergic status of the patient;

    2. a shock;

    3. presence of hepato-kidney insufficiency;

    4. a loss of consciousness;

    5. presence of avitaminosis at the patient;

  2. Optimum temperature for keeping of conserved blood:

    1. from 0 up to +2С;

    2. from +4 up to +6С;

    3. from +8 up to +10С;

    4. -1С;

    5. -2С.

  3. Point out the main differential diagnostic sign between acute and chronic blood loss.

    1. speed of arterial pressure decrease;

    2. indices of red blood;

    3. hematocrit index;

    4. size of a "shock" index;

    5. volume index of circulating blood.

  4. Define the correctly signed blood group A(II) according to agglutinogen-agglutinin system.

    1. А;

    2. 0;

    3. В;

    4. АВо;

Real-life situations to be solved:

  1. Patient М., 27 years old, blood group 0(I). She is in medical establishment concerning late miscarriage, posthemorrhagic anemia, septicemia. Is carried out scraping of cavity uterine. The blood transfusion of group B(III) is wrongly began. After introduction 100 ml of blood at the patient the pains in back, shiver have appeared. The transfusion is stopped. In 15 minutes the state shortly has worsened: adynamia, acute pallor, acrocyanosis, down-pour sweat, shiver. Pulse 96 per minute, weak filling, arterial pressure of 75/40 mm of a hg. What hemotransfusional complication was developed at the patient?

  2. Patient G., 34 years old, was operated concerning broken tubal pregnancy. In postoperative period the transfusion one group of blood was carried out. During one from injections at the patient the pains in muscles have appeared a headache. Temperature of a body 37,7С. what kind of hemotransfusional complication was developed at the patient?

II.Answers to the Self-Assessment:

    1. B;

    2. B;

    3. A;

    4. A;

    5. Hemotransfusional shock, II level.

    6. Pyrogenous reaction, not serious level.


Essential reading:

  1. Gostishchev V.K. General surgery /The manual. – M.: GEOTAR-MED, 2003. – 220p.

  2. ^

    Lectures prof. B.I. Dmitriev from Odessa State Medical University.

  3. Surgery: Text-book for English medium medical students / S.I. Shevchenko, O.A. Tonkoglas, I.M. Lodyana, R.S. Shevchenko. – Kharkiv: KSMU, 2001. – 344p.

  4. Kushnir R. Ya. General surgery /Lectures.- Ternopil, Ukrmedknyha, 2005.- 308 p.

  5. Butyrsky A. General surgery /The manual.- Simpheropol: publishers CGMU, 2004.- 478 p.

Further reading:

  1. Oxford handbook of clinical surgery / Edited by G.R. Mc Latchie, D.J. Leaper, 2002.- 930 p.

  2. Polskaya L.V. Nursing procedures in therapeutic practice.- Simpheropol, Universum, 2004.- 192 p.

  3. Clinical Nursing Skills and Techniques: basic, intermediate and advanced. The C.V. Mosby Company, 1986.- 1296 p.


IV.Students’ Practical Activities:

Theme 1. Bleeding and a hemorrhage. Methods of a temporary and final control of a bleeding.

    • Work 1. To determine a kind of external bleeding.

    • Work 2. Selection of kind of temporary method control of bleeding.

      Theme 2. Doctrine about a blood. Tests at a hemotransfusion.

    • Work 3. Determination of the blood groups with the help of standart serum.

    • Work 4. Determination of the Rh- factor with the help of antirhesus serum.

    • Work 5. Realization of tests before a hemotransfusion.

V.Seminar Discussion Of Theoretical Questions And Practical Work:

VI.The initial level of knowledge and skills is checked by the decision of situational problems (tasks) from each theme, answers to tests such as "Step", constructive questions etc.

Students must know:

  • To estimate the data of the general blood test.

  • To estimate results of the anamnesis, given objective inspection.

  • To estimate a degree of gravity of a bleeding.

  • To know signs of an acute and chronic bleeding.

  • Definition individual and rhesuses - compatibilities.

  • The choice of a hemotransfusion agent for transfusion therapy.

  • Rules of filling of the documentation after a hemotransfusion.

Students should be able to:

  1. To estimate given digital research of a rectum at a gastrointestinal bleeding.

  2. To define of blood groups and a rhesus - accessory.

  3. To diagnose the basic complications after transfusion therapy.

  4. To give the first help during complications at hemotransfusional therapy.

  5. To prepare equipment for realization of definition of blood groups by standard serums and monoclonal antibodies.

  6. To carry out definition of blood groups with the help of standard serums and monoclonal antibodies.

  7. To prepare equipment for realization of definition of a Rh factor and to determine a Rh factor of a blood. To determine individual and rhesus - compatibility of a blood.

  8. To choose of a hemotransfusion agent for transfusion therapy.


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Ministry of public health of ukraine Bukovinian state medical university iconMinistry of public health of ukraine bukovinian state medical university

Ministry of public health of ukraine Bukovinian state medical university iconMinistry of public health of ukraine bukovinian state medical university

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Ministry of public health of ukraine Bukovinian state medical university iconMinistry of public health of ukraine bukovinian state medical university

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Ministry of public health of ukraine Bukovinian state medical university iconMinistry of public health of ukraine bukovinian state medical university

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