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MINISTRY OF HEALTH CARE OF UKRAINE NATIONAL MEDICAL UNIVERSITY AFTER DANYLO HALYTSKY “Confermed” on the methodical discussion at the department of pathologic physiology Chief of the department Professor Regeda M.S. __________________________ (signature) “ ” _____________________ 2008 MANUAL for the students’ self-training in preparation to practical (seminar) lesson Study discipline Modul # Thematical module # Pathological physiology Topic of the lesson CONCEPT OF IMMUNE SYSTEM, IMMUNOPATHOLOGY. ALLERGY Year of study Faculties Medical Lviv 2008 1 CONCEPT OF IMMUNE SYSTEM, IMMUNOPATHOLOGY. ALLERGY I. ACTUALITY OF THE THEME Immunity refers to protection against infections, and the immune system is the collection of cells and molecules that are responsible for defending us against the countless pathogenic microbes in our environment. Deficiencies in immune defenses result in an increased susceptibility to infections, which can be life-threatening if the deficits are not corrected. On the other hand, the immune system is itself capable of causing great harm and is the root cause of some of the most vexing and intractable diseases of the modern world. Thus, diseases of immunity range from those caused by "too little" to those caused by "too much or inappropriate" immune activity. II. STUDY AIM 1. To know: kinds of allergens and antibodies, classification, stages of allergic reactions. Mechanisms of their development, ways of diagnostics and hyposensitization, properties of the development of some sicknesses, interconnection between allergy and immunity, inflammation, heredity. 2. To know experimentally reproduce anaphylaxis. 3. To be able to recognize tissue basophiles in smear in the stage of degranulation. 4. To be able to recognize the symptoms of anaphylactic shock. III. EDUCATIONAL AIM 1. To create an idea of intensive increase of the influence of environmental factors as potential allergens and of polyvalent sensitization of population. 2. To develop sense of professional responsibility for timely and righteous help during anaphylactic reactions. 3. To form sympathetic relation to sufferings of experimental animals. To develop idea of patient’s sufferings in the same situations. IV. THE CONTENT OF THE TOPIC 2 Structurally-logical scheme of the theme’s content ALLERGIC REACTIONS Types of reactions Of the immediate type Of the delayed type Stimulating Cytotoxic Hypersensitivity of delayed type Endogenous allergens Immunocomplex Exogenous allergens Anaphylactic Etiology Pathogenesis: Production and release of biologically active substances B. Final consequences Necrosis Death Mediators of delayed type Increase of vessel tonus, dilation, increase of permeability Spasm of smooth musculature A. Primary violations Cell death 3. Pathophysiological logical stage Violation of blood vessels permeability Mediators of immediate type Activation of T-killers and other subpopulations of lymphocytes Violation of structure and function of organs and tissues 3 Inflammation Activation of SMF Deactivation of biologically active substances; inhibition of immunocytes T-lymphocytes sensitization, connection with antigen Violation of coagulation and anticoagulation blood systems 2. Pathochemical stage Genesis of antibodies, creation of antigen-antibody complexes Irritation of nervous receptors, pain, itching 1. Immunological stage Shock Type Immediate (type I) hypersensitivity Prototype Disorder Anaphylaxis, allergies, bronchial asthma (atopic forms) Immune Mechanisms Production of IgE antibody →immediate release of vasoactive amines and other mediators from mast cells; recruitment of inflammatory cells (late-phase reaction) Antibody-mediated Autoimmune hemolytic anemia; Production of IgG, IgM →binds to antigen on target (type II) Goodpasture syndrome cell or tissue →phagocytosis or lysis of target cell hypersensitivity by activated complement or Fc receptors; recruitment of leukocytes Immune complexSystemic lupus erythematosus; Deposition of antigen-antibody complexes mediated (type III) some forms of glomerulonephritis; →complement activation →recruitment of hypersensitivity serum sickness; Arthus reaction leukocytes by complement products and Fc receptors →release of enzymes and other toxic molecules T-cell-mediated (type Contact dermatitis; multiple Activated T lymphocytes →(i) release of cytokines IV) hypersensitivity sclerosis; type I diabetes; transplant and macrophage activation; (ii) T-cell-mediated rejection; tuberculosis cytotoxicity Table1. Mechanisms of Immunologically Mediated Diseases Pathologic Lesions Vascular dilation, edema, smooth muscle contraction, mucus production, inflammation Disease Systemic lupus erythematosus Clinicopathologic Manifestations Nephritis, skin lesions, arthritis, others Nephritis Antigen Involved Nuclear antigens Poststreptococcal glomerulonephritis Polyarteritis nodosa Reactive arthritis Serum sickness Streptococcal cell wall antigen(s); may be "planted" in glomerular basement membrane Hepatitis B virus antigen Bacterial antigens (Yersinia) Various proteins, such as foreign serum protein (horse anti-thymocyte globulin) Arthus reaction (experimental) Various foreign proteins Table 2. Examples of Immune Complex-Mediated Diseases 4 Phagocytosis and lysis of cells; inflammation; in some diseases, functional derangements without cell or tissue injury Inflammation, necrotizing vasculitis (fibrinoid necrosis) Perivascular cellular infiltrates, edema, cell destruction, granuloma formation Systemic vasculitis Acute arthritis Arthritis, vasculitis, nephritis Cutaneous vasculitis Disease Autoimmune hemolytic anemia Autoimmune thrombocytopenic purpura Pemphigus vulgaris Target Antigen Erythrocyte membrane proteins (Rh blood group antigens, I antigen) Platelet membrane proteins (gpllb:Illa integrin) Mechanisms of Disease Opsonization and phagocytosis of erythrocytes Opsonization and phagocytosis of platelets Proteins in intercellular junctions of epidermal Antibody-mediated activation of proteases, cells (epidermal cadherin) disruption of intercellular adhesions Vasculitis caused by ANCA Neutrophil granule proteins, presumably released Neutrophil degranulation and inflammation from activated neutrophils Goodpasture syndrome Noncollagenous protein in basement membranes Complement- and Fc receptor-mediated of kidney glomeruli and lung alveoli inflammation Acute rheumatic fever Streptococcal cell wall antigen; antibody cross- Inflammation, macrophage activation reacts with myocardial antigen Myasthenia gravis Acetylcholine receptor Antibody inhibits acetylcholine binding, down-modulates receptors Graves disease TSH receptor Antibody-mediated stimulation of TSH (hyperthyroidism) receptors Insulin-resistant diabetes Insulin receptor Antibody inhibits binding of insulin Pernicious anemia Intrinsic factor of gastric parietal cells Neutralization of intrinsic factor, decreased absorption of vitamin B12 Table 3. Examples of Antibody-Mediated Diseases (Type II Hypersensitivity) 5 Clinicopathologic Manifestations Hemolysis, anemia Bleeding Skin vesicles (bullae) Vasculitis Nephritis, lung hemorrhage Myocarditis, arthritis Muscle weakness, paralysis Hyperthyroidism Hyperglycemia, ketoacidosis Abnormal erythropoiesis, anemia Disease Type 1 diabetes mellitus Multiple sclerosis Rheumatoid arthritis Peripheral neuropathy; GuillainBarré syndrome? Inflammatory bowel disease (Crohn's disease) Contact dermatitis Specificity of Pathogenic T cells Antigens of pancreatic islet βcells (insulin, glutamic acid decarboxylase, others) Protein antigens in CNS myelin (myelin basic protein, proteolipid protein) Unknown antigen in joint synovium (type II collagen?); role of antibodies? Protein antigens of peripheral nerve myelin Unknown antigen; may be derived from intestinal microbes Environmental chemicals, e.g., poison ivy (pentadecylcatechol) Table 4 Examples of T-Cell-Mediated (Type IV) Hypersensitivity 6 Clinicopathologic Manifestations Insulitis (chronic inflammation in islets), destruction of βcells; diabetes Demyelination in CNS with perivascular inflammation; paralysis, ocular lesions Chronic arthritis with inflammation, destruction of articular cartilage and bone Neuritis, paralysis Chronic inflammation of ileum and colon, often with granulomas; fibrosis, stricture Dermatitis, with itching; usually short-lived, may be chronic with persistent exposure Immediate (Type I) Hypersensitivity Also called allergic reactions, or allergiesInduced by environmental antigens (allergens) that stimulate strong TH2 responses and IgE production in genetically susceptible individualsIgE coats mast cells by binding to Fcε receptors; re-exposure to the allergen leads to cross-linking of the IgE and FcεRI, activation of mast cells, and release of mediators.Principal mediators are histamine, proteases and other granule contents; prostaglandins and leukotrienes; cytokines.Mediators are responsible for the immediate vascular and smooth muscle reactions and the late-phase reaction (inflammation).The clinical manifestations may be local or systemic, and range from mildly annoying rhinitis to fatal anaphylaxis. Pathogenesis of Diseases Caused by Antibodies and Immune Complexes Antibodies can coat (opsonize) cells, with or without complement proteins, and target these cells for phagocytosis by phagocytes (macrophages), which express receptors for the Fc tails of lgG and for complement proteins. The result is depletion of the opsonized cells.Antibodies and immune complexes may deposit in tissues or blood vessels, and elicit an acute inflammatory reaction by activating complement, with release of breakdown products, or by engaging Fc receptors of leukocytes. The inflammatory reaction causes tissue injury.Antibodies can bind to cell surface receptors or essential molecules, and cause functional derangements (either inhibition or unregulated activation) without cell injury. Mechanisms of T-Cell-Mediated Hypersensitivity Reactions Delayed-type hypersensitivity (DTH): CD4+ T cells are activated by exposure to a protein antigen and differentiate into TH1 effector cells. Subsequent exposure to the antigen results in the secretion of cytokines. IFN-γ activates macrophages to produce substances that cause tissue damage and promote fibrosis, and TNF promotes inflammation.T-cell-mediated cytotoxicity: CD8+ cytotoxic T lymphocytes (CTLs) specific for an antigen recognize cells expressing the target antigen and kill these cells. CD8+ T cells also secrete IFN-γ. 7 V. PLAN AND ORGANIZATIONAL STRUCTURE OF THE TOPIC # Main stages of the topic. Its function and Methods of Facilities content control and study I. PREPARATORY STAGE 1. Organization of the topic See item actuality of the theme 2. Setting of the educational aim See item educational aim 3. Control of the knowledge and skills entry 1. Individual Tables level: oral Slides questioning 2. Writing theoretical Control questions questioning 3. Test Test of the 2nd control level II. MAIN STAGE 1. Forming professional knowledge and skills 1. To be able to reproduce in experiment the reaction of tissue basophiles degranulation. 2. To be able to reproduce in experiment anaphylactic shock on guinea-pig. Experimental practicum Experimental practicum III. CONCLUDING STAGE 1. Control and correction of the level of professional knowledge and skills 2. Making conclusion of the lesson 3. Home task. Educational literature on the topic: main and additional Control after correct formulation of the results and conclusions of practical work Solution of situation tasks Estimation of the students work 1 1 20 Orientation chart; 50 supports; set of surgical equipment; sensitized rat; microscope; smears; sensitized guinea-pig; solution of horse serum; syringes; slides; tables. Protocols of the experiment 10 Situation tasks of the 2nd level 3 Orientation chart of the independent work 8 Time in minutes 2 VI. MATERIALS OF THE PROVIDING OF THE TOPIC VI.1. MATERIALS OF CONTROL AFTER THE PREPARATORY STAGE OF THE LESSON Questions for individual oral and wring theoretical questioning 1. Definition of the concept “allergy”. Allergy and immunity. 2. Kinds of allergens. Meaning of hereditary factors in development of allergy. 3. Principles of allergic reactions classification (after Cumbs and Jell). 4. Stages of allergic reactions development. 5. Anaphylactic reactions: experimental models, immunological mechanisms of their development, role of tissue basophiles, basic clinical symptoms (hives, Kwinke sweliing, polinosis, atopic bronchial asthma, anaphylactic shock). 6. Active and passive anaphylaxis. 7. Pathogenesis of anaphylactic shock. 8. Cytotoxic reactions: mechanisms of cytolysis, main clinical forms (haemolytic disease of the newborns). 9. Immunocmpex reactions: mechanism of the development of local and general injuries, main clinical forms (serum disease). 10. Hypersensitivity reactions of delayed type: mechanism of development, role of lymphokines, main clinical forms (tuberculin reaction, contact dermatitis, inflectionalallergic bronchial asthma, autoimmune diseases, graft versus hot disease, Layel Syndrome). 11. Autoallergic reactions: principles and mechanisms of development. 12. Basic principles of prevention, treatment and diagnostics of allergic diseases. Hyposensitization after Bezredko. 13. Notion about immunodeficiency. Examples of these diseases. MULTIPLE-CHOICE QUESTIONS 1. A 19-YEAR-OLD FEMALE WITH MULTIPLE EPISODES OF SEXUALLY TRANSMITTED DISEASES PRESENTS TO THE EMERGENCY ROOM BLEEDING PER VAGINA. HER LAST PERIOD WAS 13 WEEKS AGO. SHE IS KNOWN TO BE RH -VE. ECTOPIC PREGNANCY IS DIAGNOSED AND SHE UNDERGOES EMERGENCY SURGERY. THIS MOTHER IS AT RISK OF DEVELOPING: A. Type II Hypersensitivity, following sensitization from a possible Rh+ve fetus (now aborted) B. Transfusion reaction now, from spillover of fetal blood into the maternal circulation C. Serum sickness from spillover of fetal blood into the maternal circulation D. A delayed type (Type IV) hypersensitivity reaction to fetal red blood cells 2. ANTIGEN PRESENTING CELLS DISPLAY ANTIGEN FRAGMENTS IN ASSOCIATION WITH CLASS II MHC MOLECULES. WHICH ONE OF THE FOLLOWING CELLS DOES NOT FUNCTION AS AN ANTIGEN PRESENTING CELL? A. B cells B. Dendritic cells C. Neutrophils D. Macrophages 3. WHICH ONE OF THE FOLLOWING CELLS IS NOT AN ANTIGEN PRESENTING CELL? A. Neutrophil B. B cell C. Macrophage D. Dendritic cell 4. A POSITIVE MANTOUX SKIN REACTION INVOLVES THE INTERACTION OF: A. Antigen, complement, and lymphokines B. Antigen-antibody complexes, complement, and neutrophils C. Memory T cells, cytokines, and macrophages D. IgE antibody, antigen, and mast cells E. Antigen, macrophages, and complement 9 5. ALL OF THE FOLLOWING MAY SERVE AS OPSONINS FOR PHAGOCYTOSIS EXCEPT A. C5a B. C3b C. CRP D. IgG 6. THE MAJOR IMMUNOGLOBULIN CLASS IN NORMAL ADULT HUMAN SERUM IS A. IgA B. IgG C. IgM D. IgE E. IgD 7. WHICH ONE OF THE FOLLOWING IS NOT CLASSIFIED AS A REACTIVE OXYGEN INTERMEDIATE? A. nitric oxide B. superoxide C. hydrogen peroxide D. hydroxyl radical 8. THE PREDOMINANT ANTIBODY FOUND IN A PRIMARY IMMUNE RESPONSE IS A. IgA B. IgG C. IgM D. IgE E. IgD 9. HELMINTHS ARE DESTROYED BY THE ACTION OF ENZYMES RELEASED BY WHICH ONE OF THE FOLLOWING CELL TYPES? A. eosinophils B. natural killer cells C. macrophages D. neutrophils 10. WHICH IMMUNOGLOBULIN CLASS IS FOUND ON THE SURFACE OF MAST CELLS? A. IgA B. IgG C. IgM D. IgE E. IgD 11. ACTIVATION OF COMPLEMENT GENERATES PROTEOLYTIC FRAGMENTS AND ACTIVATED PROTEINS THAT FACILITATE A. opsonin mediated phagocytosis B. mast cell degranulation C. osmotic lysis of cells D. all of the above 12. WHICH IMMUNOGLOBULIN CLASS IS A MAJOR COMPONENT OF MUCOSAL SECRETIONS? A. IgA B. IgG C. IgM D. IgE E. IgD 13. WHICH IMMUNOGLOBULIN CLASS CROSSES THE PLACENTA? A. IgG B. IgE C. IgM D. IgA E. IgD 14. WHICH IMMUNOGLOBULIN CLASS IS EXPRESSED ON IMMATURE B CELLS? A. IgG 10 B. C. D. E. IgE IgM IgA IgD 15. ALL THE FOLLOWING ARE BIOLOGICAL FUNCTIONS ATTRIBUTED TO TNF EXCEPT A. induction of chemoattractant secretion by endothelial cells B. induction of adhesion molecules on endothelial cells C. activation of neutrophils and monocytes D. impairment of macrophage cytotoxicity E. induction of IL-1 and IL-6 secretion by macrophages 16. WHICH IMMUNOGLOBULIN CLASS CAN CROSS THE PLACENTA? A. IgA B. IgG C. IgM D. IgE E. IgD 17. WHICH OF THE FOLLOWING CELLS ARE IMPORTANT IN AN INNATE IMMUNE RESPONSE TO EXTRACELLULAR BACTERIA? A. T lymphocytes B. B lymphocytes C. Neutrophils D. Eosinophils E. Mast cells 18. WHICH ONE OF THE FOLLOWING DOES KILL VIRALLY INFECTED CELLS? A. Th1 cells B. Th2 cells C. Both Th1 and Th2 cells D. CTL E. All of the above 19. WHICH ONE OF THE FOLLOWING DOES SECRETE CYTOKINES REQUIRED FOR ACTIVATION OF MACROPHAGES? A. Th1 cells B. Th2 cells C. Both Th1 and Th2 cells D. CTL E. All of the above 20. WHICH ONE OF THE FOLLOWING MAY DIFFERENTIATE INTO MEMORY CELLS? A. Th1 cells B. Th2 cells C. Both Th1 and Th2 cells D. CTL E. All of the above 21. MAST CELL DERIVED HISTAMINE INDUCES VASODILATATION. WHICH OF THE FOLLOWING INFLAMMATORY MEDIATORS INDUCE DEGRANULATION OF MAST CELLS AND HISTAMINE RELEASE? A. Crosslinking of IgE bound to mast cell FcεR B. Binding of complement fragment C3a C. Binding of complement fragment C5a D. All of the above E. Only a and c 22. SELECTIN/LIGAND INTERACTION MEDIATES LEUKOCYTE ROLLING ON INFLAMED ENDOTHELIUM. WHICH OF THE FOLLOWING SELECTINS ARE INDUCED ON ENDOTHELIAL CELLS DURING THE INFLAMMATORY RESPONSE? A. P-selectin B. E-selectin C. L-selectin 11 D. E. All of the above Only a and b 23. WHICH OF THE FOLLOWING DOES NOT PLAY A ROLE IN HOST DEFENSE TO MYCOBACTERIUM TUBERCULOSIS? A. reactive oxygen intermediates B. interferon gamma C. tumor necrosis factor D. lysosomal enzymes E. nitric oxide 24. WHICH ONE OF THE FOLLOWING IS THE MOST POTENT AND EFFECTIVE ANTIGENPRESENTING CELL (APC)? A. Monocytes-macrophages B. Mast cells C. T lymphocytes D. B lymphocytes E. Dendritic-Langerhans cells 25. EOSINOPHILS ARE ASSOCIATED WITH THE DEFENSE AGAINST INFECTIONS CAUSED BY A. Virus B. Intracellular bacteria C. Extracellular bacteria D. Invasive parasites E. Mycoplasma 26. DURING AN IMMUNE RESPONSE, ANTIBODIES ARE MADE AGAINST DIFFERENT STRUCTURES (USUALLY PROTEINS) ON AN INFECTIOUS AGENT. THESE STRUCTURES ARE REFERRED TO AS A. Adjuvants B. Allotypes C. Isotypes D. Epitopes E. Alleles 27. WHICH ONE OF THE FOLLOWING COMPLEMENT COMPONENTS ENHANCES PHAGOCYTOSIS OF BACTERIA BY OPSONIZATION? A. C1 B. Factor B C. C3b D. C5a E. C5b6789 28. WHICH ONE OF THE FOLLOWING COMPLEMENT COMPONENTS MEDIATES CYTOLYSIS? A. C1 B. Factor B C. C3b D. C5a E. C5b6789 29. WHICH ONE OF THE FOLLOWING COMPLEMENT COMPONENTS IS A CHEMOATTRACTANT FOR NEUTROPHILS? A. C1 B. Factor B C. C3b D. C5a E. C5b6789 30. WHICH ONE OF THE FOLLOWING COMPLEMENT COMPONENTS BINDS TO ANTIBODY TO ACTIVATE THE CLASSICAL PATHWAY? A. C1 B. Factor B C. C3b D. C5a E. C5b6789 12 31. DIRECT KILLING OF CELLS INFECTED WITH VIRUS IS USUALLY ACCOMPLISHED BY A. CD8-positive T cells B. CD4-positive T helper 1 cells C. CD4-positive T helper 2 cells D. plasma cells E. CD19-positive B cells 32. MYCOBACTERIUM TUBERCULOSIS RESULTS IN AN INTRACELLULAR BACTERIAL INFECTION THAT PROVOKES WHICH ONE OF THE FOLLOWING IMMUNE RESPONSES? A. Natural killer cytotoxic response B. CD8-positive cytotoxic T cell response C. T helper 1 delayed type hypersensitivity response D. Complement mediated lysis of infected cell E. Eosinophilia 33. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH GOODPASTURE’S SYNDROME? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 34. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH SERUM SICKNESS? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 35. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH A TUBERCULIN REACTION? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 36. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH POISON IVY? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 37. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH AN ANAPHYLACTIC REACTION AFTER A BEE STING? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 38. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH HEMOLYTIC DISEASE OF THE NEWBORN? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 39. WHICH HYPERSENSITIVITY REACTION IS ASSOCIATED WITH POSTSTREPTOCOCCAL GLOMERULONEPHRITIS? A. Type I: immediate B. Type II: cytotoxic C. Type III: immune complex D. Type IV: cell mediated 40. A PATIENT WITH RECURRENT INFECTIONS WITH YEAST AND THE INCAPACITY TO CONTROL VIRAL INFECTIONS MAY INDICATE A DEFICIENCY IN A. Cellular immunity 13 B. C. D. E. Complement Granulocytes Humoral immunity Eosinophils 41. WHICH CYTOKINE PROMOTES VARIOUS BIOLOGIC ACTIONS ASSOCIATED WITH INFLAMMATION? A. IFN- ) B. IL-2 (interleukin 2) C. IL-4 (interleukin 4) D. TNF-(tumor necrosis factor) E. TGF-(transforming growth factor) 42. WHICH CYTOKINE FUNCTIONS AS A PROMOTOR OF T HELPER 2 (TH2) DEVELOPMENT AND IGE SYNTHESIS? A. IFN- (interferon ) B. IL-2 (interleukin 2) C. IL-4 (interleukin 4) D. TNF- (tumour necrosis factor ) E. TGF-(transforming growth factor) 43. WHICH CYTOKINE FUNCTIONS AS AN ACTIVATOR OF MACROPHAGES AND NATURAL KILLER (NK) CELLS? A. IFN- ) B. IL-2 (interleukin 2) C. IL-4 (interleukin 4) D. TNF- (tumour necrosis factor ) E. TGF- (transforming growth factor ) 14 # 1. 2. VI.2. MATERIALS OF METHODICAL PROVIDING OF THE MAIN STAGE OF THE LESSON Orientation chart fro forming practical knowledge and skills Task Indications to the task To reproduce model of anaphylactic reaction on tissue basophiles of a sensitized rat. Get a rat sensitized with In a tail vein inject 0.5 ml of horse serum 3 times in a day. antigen – horse serum. After 12-15 min get the animal dead with the help of ether. Prepare emulsion of tissue Insert 5 ml of hemocel in the abdominal cavity, make basophiles. massage, dissect the abdominal cavity, collect liquid. Conduct the reaction of tissue On the glass, preliminary painted with neutral red, mix a drop basophiles with antigen. of liquid and allergen. Cover with a covering glass. Incubate for 10 min in thermostat in temperatute of 37Co. Preparing of control Analogically mix drops of the liquid and a dog serum. Incubate for 10 min in thermostat in temperatute of 37Co. Observe under microscope Observe under big magnification, using emersion oil. tissue basophiles degranulation. Fix and form the results of the Draw and describe shortly the changes, which are observed. experiment. Make Write down in a protocol the results received. conclusions. To reproduce model of anaphylactic reaction on guinea-pig. Get a guinea-pig sensitized Insert 0.1 ml of dissolved horse serum in proportion 1:10 with antigen – horse serum. under the abdomen skin (intraabdominaly). 14 days after that fix the guinea-pig: may one student fix guinea-pig in his hands; the other must pull the rear leg a little aside, shave the fur over femoral vein, and cut the skin with fascia (square 0.5 cm2) after that insert 1 ml of horse serum in the vein. Pay attention to general behaviour, position, huddling of fur, Monitor after the animal coughing, involuntary defecation, urination, rhythm of during development of breathing, yawning movements of the jaws, twitching of nose anaphylactic shock. wings, cramps. With the help of stop-watch indicate and write the time of every symptom’s beginning. When the breathing is stopped and corneal reflexes (touch the cornea with a piece of cotton) are ceased the death is established. Dissection is performed on the mean line of the thoracic and Conduct dissection of the abdominal cavities. animal Press the trachea and separate the lung-heart complex; put it Assess the symptoms of Auer- on a watches’ glass. The lungs are overfilled with the air; and Luis-Bezredko therefore when pressing the lungs the air goes out of them. Increased peristaltic movements, the blood is of dark-red colour and liquid. Examine intestines, blood in Describe manifestations of anaphylactic shock development magisterial vessels and dissection of the animal after its death. Draw and shortly describe the picture observed. Write down in a protocol the results received. Fix and form the results of the 15 experiment. Make conclusions. VI.3. MATERIALS OF CONTROL FOR THE CONCLUDING STAGE OF THE LESSON 1. PROTOCOL 2. SITUATION TASKS OF THE 2ND LEVEL #1. A rabbit previously sensitized with a serum, received intravenous dose of allergen. Anaphylactic shock began emerging 1 min after that injection. After 5 min the animal has died. What became the main reason of the death? #2. In a teenager of 14 years old, who addressed to an allergologist, the symptoms of choking and severe coughing with excretion of small amount of viscous mucilaginous expectorating fluid were observed. The boy has fallen ill half-year after gaining aquarium and starting feeding fishes with dry food. In examination of the boy a sharp increase of IgE has been found. Basophiles and mast cells’ degranulation reaction were positive. What the positive reaction to dry food certifies about? Which type of pathological reaction dose this disease belong to? VI.4. MATERIALS OF METHODICAL PROVIDING FOR STUDENTS’ INDEPENDENT WORK ORIENTATION CHART FRO ORGANIZATION OF STUDENTS’ INDEPENDENT WORK WITH EDUCATIONAL LITERATURE # Task Indications to the task 1 Describe the properties of Instruction to task. development of hives 2 Describe the properties of development of Kwinke swelling Take into consideration the reaction of blood circulation violations 3 Polinosis: describe Etiology andpathogenesis. Describe the mechanism of development serum disease. Methods of allergic diseases diagnostics. Basic principles of treatment of allergic reactions Schematically: count all possible plants-allergens. 4 5 6 Take into consideration the properties of flowing after the 1st and 2nd types of allergic reactions. Give in the form of structural-logical scheme. Specific hyposensitization (after Bezredko), and unspecific; indicate antihistamine and hormonal medicines. 16 VII. REFERENCE Educational: A. Main 1) Pathological physiology. After redaction of A.I. Bereznyakova. Charkiv: Zoloti storinky. 2003 2) Pathological physiology. After redaction of M.N. Zayka, Yu.V.Byts. Kyiv: Vyshcha shkola, 1995. B. Additional 3) Pathological physiology. After redaction of A.D. Ado, V.V. Novytsky, Tomsk: Un-ta. 1994 4) Pathological physiology. The course of lectures. After redaction of P.F. Letvitsky, M.:Medicina.1995 5) Agadganyan N.A. Organism and gas environment. M., 1972 6) Big medical encyclopedia 7) Kolchinskaya A.Z. Oxygen, physical state, working ability. K.: Naukova dumka. 17