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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
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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
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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.
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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.
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