Metod. pharm f-ty 1st semester book 2017 Module 1

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
Pathophysiology MODULE 1
GENERAL PATHOLOGY
Training-methodical manual
for class and out-of-class work for pharmaceutical faculty students
Prepared by:
Gerasymchuk M. R.
Cherkasova V. V.
Zaiats L. M.

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
Department of Pathophysiology
GENERAL NOSOLOGY.
TYPICAL PATHOLOGICAL PROCESSES
(Pharmaceutical faculty)
Training-methodical manual
for class and out-of-class work of students
Student ________________group of pharmaceutical faculty
(name and surname)
Prepared by:
Gerasymchuk M. R.
Cherkasova V. V.
Zaiats L. M.
3

«The general nosology. Typical pathological processes»
Training-methodical manual for class and out-of-class work for
pharmaceutical students / M.R. Gerasymchuk, V.V. Cherkasova, L.M.
Zaiats // IFNMU. Department of pathological physiology. – 2017. – 48 p.
Discussed and approved by the profile commission of medical & biological
disciplines meeting of Ivano-Frankivsk National Medical University.
Protocol № ___ from «___» _________ 2017 year
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Calendar plan of practical classes
of pathological physiology for the students of the II course in the III semester
THEME OF PRACTICAL STUDIES DATES Hours
1. Subject and tasks of pathological physiology. Nosology.
Pathogenic effect of ionizing radiation on the body.
08.09.2017 2
2. Allergy. 15.09.2017 2
3. Pathophysiology of tissue growth. Tumors, etiology,
pathogenesis.
22.09.2017 2
4. Inflammation. 29.09.2017 2
5. Pathophysiology of the basic metabolism. Starvation.
Carbohydrate metabolism pathology.
06.10.2017 2
6. Pathology of fat metabolism. Etiology and pathogenesis of
atherosclerosis.
13.10.2017 2
The final module control: 4
7. Module 1. Practical part 08.12.2017
8. Module 1. Theoretical part 15.12.2017
Total hours 16
Calendar plan of lectures
№ THEME OF LECTURE DATES Hours
1. Pathophysiology of immune reactivity. Allergy. 12.09.17 2
2. Cell damage. 26.09.17 2
3. Pathophysiology of tissue growth. Tumors 10.10.17 2
4. Pathophysiology of peripheral circulation and microcirculation. 24.10.17 2
5. Inflammation: classification, etiology, pathogenesis. 07.11.17 2
6. Violation of protein and carbohydrate metabolism. Diabetes. 21.11.17 2
7. Violation of lipid metabolism. 05.12.17 2
Total hours 14
The ESTIMATION FOR THE MODULE is defined as a sum of marks of current
educational activity (in points), which is proposed during the evaluation of theoretical
knowledges and practical skills. Maximal amount of points, which a student can collect -
200 points during of every module study, including for current educational activity – 120
points (together the semantic modules are 110 points, individual work is 12 points), on
results final module control are 80 points.
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Control of theoretical and
practical preparation
0 – 4 points – completely prepared homework;
0 – 10 points – oral answer;
0 – 4 points – test control during class.
Minimum – 0 points; positive – 9; maximum – 18 points
Topic № 1. Subject and tasks of pathological physiology. Nosology.
Pathogenic effect of ionizing radiation on the body.
1. Actuality of the theme. Pathological physiology is science, that studies
the functional changes at a sick man and animals. It studies the most general
conformities to the law of origin, development, consequences of illness. By
experiment we may reproduced and study on animals the separate models of
illnesses, violation of organs and systems for cognition of basic conformities to
the law of development of illnesses of man. Consequently, the experiment is the
basic method of pathophysiology.
Knowledge of theoretical and clinical aspects of diverse kinds pathogenic
action of radial energy necessary doctors for organization and realizing of
prophylaxis methods, and also cure of professional diseases.
2. Length of the employment – 1 hour 30 min.
3. Aim:
To know such terms as the "modelling", "experiment”, external and
internal causes of disease.
To be able:
a) The modelling of various forms of pathologic processes, protective and
adaptive reactions of humans. Experimental therapy as an important method of
studying and introducing the new ways of treatment;
b) analyze the role of environmental factors in disease occurrence;
etiological factor initiates the pathologic process and then disappears, so the
pathogenesis develops without etiological factor (trauma, radiation).
c) Explain pathogenesis of ionizing radiation.
To perform practical work:
1. Main features and purpose of experiment in pathophysiology. Correlation
of method of clinical supervision with the pathophysiological experiment
2. To analyse the “vicious circle” in the pathogenesis. Causes and
consequences constantly change their places.
3. To study common laws of occurrence and development of conditions
caused by effect of x-ray energy, changes of atmospheric pressure, infrared and
ultraviolet rays, thermal factors on organism.
4. Basic level.
The name of the previous
and future disciplines
The receiving of the skills
1. histology Relations between pathophysiology and other
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2. biochemistry
3. physiology
4. pharmacokinetic
scientific disciplines. Ionizing radiation. Main
characteristics. Physical and chemical
ionizing radiation interchange in organism.
5. Control questions of the theme:
1. Term definition – what is pathophysiology? Why is pathophysiology
important?
2. History of pathophysiology development. Significance of scientific
works of K. Bernar, R. Virchow, U. Kongeim, I. I. Mechnikov, G. Selie and
other famous investigators. The origin of pathological physiology as a scientific
discipline. Formation and development of pathological physiology in Ukraine.
Scientific schools of pathophysiologists, the main directions of their activity.
3. The connect between the pathophysiology and other disciplines.
4. General pathophysiology, special or systemic and clinical
pathophysiology.
5. Methods of pathological physiology. An experiment as the main method
of pathophysiology, its significance for solving fundamental problems of
medicine.
6. Disease as a biological, medical and social problem. The abstract and the
concrete in the concept “disease”. Unity of the destructive and protective in
disease. Principles of disease classification, classification of WHO. The main
laws of a disease course. The main directions in the development of doctrine of
disease: humoral (Hippocrates), cellular (R. Virchow). Their development in the
modern stage.
7. Definition of the concept “pathogenesis”. The destructive and adaptive
phenomena of pathogenesis. Manifestations of injury at different levels: a
molecular, cellular, tissue, organ, organism one.
8. Protective reactions of adaptation. Adaptation, compensation.
Mechanisms of immediate and long-term adaptation. The role of nervous and
humoral factors in their realization.
9. The cause-effect relations in pathogenesis. Variants of direct cause-
effect relations. “Circulars vicious”. The main link of pathogenesis. Role of the
local and general in pathogenesis.
10. Pathogenic effect of ionizing radiation. Types of ionizing radiation.
Radiosensitivity of tissues.
11. Mechanisms of direct and indirect radiation damage of biological
structures. Water radiolysis. Radiotoxins. Manifestations of radiation damages
on molecular, cellular, tissue, organ and system levels.
12. Pathogenesis of radiation sickness, its main forms and syndromes. Early
and late effects of large and small doses of ionizing radiation. Natural
mechanisms of antiradiation protection. Pathophysiological bases of
radioprotection.
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6. Independent audience work of student.
Protocol № 1 Date_____________________
Experimental work 1. Acquaintance with the methods of fixing of
laboratory animals and technique of injections. Using dressing forceps a rat
is taken, imposing them on the skin of cervical area. Holding dressing forceps in
a right hand, by free fingers of left hand the tail of animal is fixed. Straps are
imposed with loops at first on back, and then on front extremities and fix a rat in
position on the back. Acquaint with the technique of hypodermic,
intramuscular, intravenous injections. The animals are release from straps begin
front and than back extremities and take off dressing forceps.
Conclusion: _________________________________________________
Experimental work 2. Determining the amount of hemoglobin. Solution
of hydrochloric acid pours in a test-tube of hemometr to the number 2 on the
scale. Then collects 0.02 ml blood in capillary and outpour it in a test tube.
Mixture leaves for 5 minutes. After distilled water pour full in the test-tube until
the color of liquid in a test tube will be evened with the color of standard
solution. Calculate the amount of hemoglobin in mmol/l. Formula of
calculation: B • 0,6206, where
B – is an amount of hemoglobin in g%; 0,6206 – is a coefficient of count in
unit of SI.
Conclusion: _________________________________________________
Experimental work 3. To learn on sliding seats and sketch changes
from the side of peripheral blood and marrow of guinea-pigs with acute
and chronic radiation illness.
Conclusion: _________________________________________________
7. Practice Examination.
Practice examination type 1. Choose the correct answer:
Test 1. Which scientist emphasized senescence of connective tissue cells
cytoplasm?
A. Bogomolets
B. Mechnikov
C. Dilman
D. Frolkis
E. Berdichev
Test 2. The preventive radioprotector was given to a worker of a
nuclear power station. What mechanism from the below mentioned is
considered to be the main mechanism of radioprotection?
A. Increasing of respiration
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B. Inhibition of free radicals formation
C. Activation of oxidation reactions
D. Prevention of tissue’s hypoxia
E. Increasing of tissue blood supply
Test 3. A worker of radiological department was exposed to radiation
once as result of violation of the rules of safety appliances.
Ulcerogangrenous stomatitis developed in him in 8 days. Patient’s blood
test showed: RBC – 3.2 x 1012
/L, reticulocytes – 0.01 %, Hb – 60 g/L, WBC
– 2.3 x 109
/L, and platelets – 50 x 109
/L. Which period of radiation sickness
are described changes typical for?
A. Period of primary reactions
B. Period of manifestation
C. Latent period
D. Pretended well-being period
E. Outcomes
Test 4. A 39-years-old patient has been suffering from gastric ulcer for
last 4 years. Pain in epigastric region, heartburn, nausea, and constipation
appear mainly in autumn and spring. Name this condition.
A. Remission
B. Acute period
C. Complication
D. Pathologic condition
E. Relapse
Test 5. A man took electric wire with high tension by both hands. He
died momentary in result of:
A. Intracerebral bleeding
B. Respiratory standstill
C. Cardiac fibrillation
D. Burns
E. Tearing extremities off
Practice examination type 3
I. Give the description of each form of radiation disease (1 – acute, 2 –
chronic):
Indicator 1/2 Indicator 1/2
A
The disturbance of
hemopoiesis and blood
system (lymphopenia,
thrombocytopenia)
F Hemorrhagic syndrome
G
Sexual dysfunction
B Anemia H Spasm paralytic syndrome
C
Immune reactivity
decrease
J
Shock
D
Dysfunction of the
alimentary tract, vomiting,
anorexia, diarrhea
K
Asthenia
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E Necrotic tonsillitis L Trophic disorders
Give answer to the questions of the real-life task:
TASKS
1.
What direction of electricity through the human body is the most
dangerous?
A Head C Heart
B Kidney D Liver
2.
When the man is less sensitive to the electric current?
A Under narcosis C Hypoxia
B Tiredness D Alcohol intoxication
3.
The most resistant to electric current are all the below mentioned
except:
A External epidermal layer D Muscles
B Tendons and bones E Blood
C Nerves F Cerebrospinal fluid
II. For each statement choose T (true) or F (false) in the list provided.
№ Statement T F
1
The first period of acute radiation disease (ARD) with
duration from several hours to 1-2 days is characterized by
excitation, headache, instability of the vegetative functions,
lability of the arterial pressure and pulse
2
Latent period (one week) is accompanied by leukopenia
(progressing of lymphocytopenia, development of
granulocytopenia).
3
The third period is characterized by progressing leukopenia,
anemia. Hemorrhagic syndrome develops. Decrease of
immunologic reactivity.
4
Outcome of the ARD are multiple inflammatory processes
(necrotic angina, pneumonia, frontitis and others).
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th
ed./Kumar, Abbas, Fauto.–2015.–Ch.9.–P.426–432.
2. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simf. – 2011. – P. 12–85.
3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P.
10–12, 16–21, 24–34.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc.
– 2010. – P. 3–13, 15–24, 1280–1283.
Additional:
5. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– New York,
Milwaukee. – 2009. – P. 2–10.
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6. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for
medical students and practitioners. Ed. by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 9–29.
7. General and clinical pathophysiology. Workbook for medical students and practitioners. – Odessa. –
2001. – P. 11–12.
Topic 2. Allergy
1. Actuality of the theme. The immediate-type allergy is often met in
practical activity of physicians of various specialties. That is because of the
great environmental pollution by industrial products, chemical matters, and
allergens of vegetable animal, bacterial, fungus origin and also due to a wide
use of various drugs. That type of allergy can develop suddenly. The severity of
their proceeding is various – from slight reactions to anaphylactic shock
dangerous for one’s life. Preventing and treatment of the allergy reactions is
based on knowledge about their development mechanisms.
2. Duration of the class – 1 h 30 min.
3. Aim:
To know that allergy is a complex of breaches, appearing in our organism
by the humoral immunological reactions. Both inflammation and allergy is a
protective response on the exo- and endogenous factor.
To be able: to analyze the pathogenesis of allergy by A.D. Ado.
To perform practical work: to analyze the mechanisms of
immunologically mediated disorders by Coombs and Gell (1968)
4. Basic level.
The name of the previous and
future disciplines
1. histology
2. biochemistry
3. physiology
4. immunology
5. pharmacognosy
Structure and function of organs and
vessels. Immunity and its mechanisms.
Antigens and antibodies, their structure
and function. Sensitizing.
5. The advices for students.
Classification of allergic reactions by Coombs and Gell (1968)
№ Type Prototype disorder Immune mechanism
1. Anaphylactic
type
Anaphylaxia, some forms of
bronchial asthma
Formation of IgE
(cytotropic) antibody →
release of vasoactive
amines and other
mediators from basophils
and mast cells.
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2. Cytotoxic
type
Autoimmune hemolytic
anemia, erythroblastosis
fetalis, cytotoxic reactions
the action of large doses of
Bogomglets’s ACS
(antireticular cytotoxic
serum)
Formation of IgG, IgM →
binds to antigen on target
cell surface →
phagocytosis of target cell
or lysis by C8,9
3. Immune
complex
disease
Arthus reaction serum
sickness, systemic lupus
erythematosus, certain
forms of acute
glomerulonephritis
Ag + Ab →activated Co
→ attracted complexes
neutrophils → release of
lysosomal enzymes
4. Cell –
mediated
(delayer) hy-
persensitivity
Tuberculosis, contact
dermatitis, transplant
rejection
Sensitized thymus-derived
T-lymphocytes → release
of lymphokins and T-cell-
mediated cytotoxicity.
5. By Roight
Stimulating
allergic
reactions.
Via BAS,
hormones,
mediators
Collagen diseases,
connective tissue diseases,
rheumatoid arthritis and
other.
The cells, containing Ag,
begin to function
intensively under the
influence of Ab. Than cells
are secreted hormones or
mediators.
1.Allergy. Definition of the concept and general characteristics of allergy.
2.Allergy and immunity. Etiology of allergy, kinds of exo- and endogenous
allergens. The significance of hereditary and acquired factors in the
development of allergy.
3.Principles of classification of allergic reactions. General characteristics of
allergic reactions by Coombs and Gell. Stages of the pathogenesis of allergic
reactions.
4.Anaphylactic reactions: experimental models, main clinical forms.
Immune mechanisms of anaphylactic reactions, the role of mast cells in their
development. Active and passive anaphylaxis, pathogenesis of anaphylactic
shock.
5.Cytotoxic reactions: experimental modeling, main clinical forms.
Mechanisms of antibody-mediated diseases. Mechanisms of cytolysis.
Examples of diseases, cytotoxic: autoimmune hemolytic anemia, acute
rheumatic fever, Goodpasture syndrome, transfusion reaction, autoimmune
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thrombocytopenic purpura; non-cytotoxic: Graves’ disease (hyperthyroidism),
myasthenia gravis, insulin-resistant diabetes, pernicious anemia.
6.Immune complex-mediated reactions, experimental modeling,
pathogenesis, clinical forms. Factors determining the pathogenesis of immune
complexes. Immune complex damages, their local and general manifestations.
Examples of diseases: Systemic lupus erythematosus, rheumatoid arthritis,
post-streptococcal glomerulonephritis, serum sickness, Arthus reaction,
Sjögren syndrome.
7.Reactions of hypersensitivity of a delayed type: experimental modeling,
main clinical forms. Features of immune mechanisms. The role of lymphokines.
8.Autoallergic diseases. Causes and mechanisms of their development. The
role of an autoallergic component in the pathogenesis of diseases.
9.Pseudoallergic reactions. The main principles of prophylaxis and treatment
of allergic reactions. Desensitization.
10.The experimental modeling of pathology of the immune system.
11.Pathophysiological bases of transplantation of organs and tissues. Immune
tolerance, its types. Methods of experimental modeling of immune tolerance.
12.Mechanisms of development of immune tolerance and their disorders. The
main principles of immune stimulation and immune suppression.
13.Immune interrelations in system “mother-fetus”.
14.“Graft versus host” reaction, conditions of its development, acute and
chronic forms.
15.A stimulative and inhibitory variant of reactions (Vth type of allergic
reactions). Graves disease (hyperthyroidism), myasthenia gravis, and insulin-
resistant diabetes.
7. Students’ practical activities.
Protocol № 2 Date_____________________
Experimental work 1. Anaphylactic shock in a guinea pig. Watching a
movie by the results of experiment and analysis of observed results.
Reproduction: 0.5 ml of horse serum was injected into a peritoneal cavity
of a guinea pig two weeks before the main experiment. In a day of experiment
guinea pig is fixed on a desk, then researcher cutes skin along medial line of the
neck, and separates jugular vein. After this, he injects 2.0 ml of the horse serum
into the jugular vein and students observe anaphylactic shock manifestation.
After animal death researcher separates cardiac-pulmonary complex. Pay
attention to the character of damage in the lungs. It is necessary to answer on
questions at prepare of protocol in part «Discussion».
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1) What type of allergy is it? Explain. 2) What is the mechanism of animal
sensitization? 3) What is the role of biologically active substances in
anaphylactic shock manifestation? 4) What was the reason for animal death?
Explain why. 5) Is it possible to cause an anaphylactic shock by repeat injection
of horse serum if an experiment could be unsuccessful? Explain.
Through 1.5- 2 min. mark the first symptoms of shock: scratching of snout,
standing of wool, an anxiety of animal, cough, cyanosis of a snout. A next
symptom is departing of excrement and urine. Cramps, at first tonic (a guinea
pig falls on a side, quotation marks pronate, muscles are tense), and then clonic
(shallow cramps of extremities), liquid breathing, with large pauses.
Death comes in default of breathing and work of the heart is stored.
Determination of degree of shock:
- I stage (+) - characterized by standing of wool;
- II stage (++) is standing of wool, cough, scratching of snout;
- III stage (+++) --standing of wool, cough, scratching of snout, departing
of excrement and urine, cramp;
- IV stage (++++) -- standing of wool, cough, scratching of snout, departing
of excrement and urine, death.
It is convenient to analyze the dynamics of anaphylactic-type of allergy
using, as an illustration, the experimental parenteral injection of a heteroserum
to a healthy animal (twice with the two-week interval).
Conclusion: _________________________________________________
____________________________________________________________________
____________________________________________________________________
____________________________________________________________________
Experimental work 2. To learn displays and analyze the mechanism of
development of hypersensitiveness of delayed type into a rat.
For the receipt of hypersensitiveness of slow type animal, three days prior
to experience sensitize (introduction to the pillow of paw tuberculin Freund's
adjuvant in an amount 100 MCL. 3 times with an interval in two weeks. Before
24 hours to experiment enter intraperitoneally) anaphylaxis-provoking dose of
tuberculin (0.3 ml). On session for a rat under anesthesia open an abdominal
region, look after the displays of allergic reaction from the side peritoneum and
prepare strokes-imprints. Strokes dye after Romanovsky's stain. The dried
upstroke is fixed three minutes in the glass with a methyl alcohol, and then dyes
Romanovsky's stain during 20-25 min. The morphological displays of
hypersensitiveness of slow type study under the immersion increase of
microscope. In the strokes-imprints of experimental animals find plenty of
lymphocytes and monocytes. Comparison the strokes of animals of controls
paint out also.
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The results of experience describe and sketch. To explain displays and
mechanism of development of hypersensitiveness of slow type into a rat on the
basis of findings facts.
Conclusion: _________________________________________________
____________________________________________________________________
____________________________________________________________________
Practice examination type 1 Choose the correct answer:
Test 1. A woman has been applying a new cosmetic preparation for a
week that resulted in eye-lid inflammation accompanied by hyperemia,
infiltration and painfulness. What type of allergic reaction was developed?
A. III
B. V
C. II
D. I
E. ІV
Test 2. On the 8th day since the patient was inoculated with antitetanic
serum because of dirty wound of his foot he has developed rising
temperature up to 380
С, pains in the joints, rash and itch. The blood tests
revealed leukopenia and thrombocytopenia. Allergic reaction of what type
has developed in this case?
A. Immune complex
B. Cytotoxic
C. Delayed type of hypersensitivity
D. Stimulating
E. Anaphylactic
Test 3. A 27- year-old woman has dropped penicillin containing eye
drops. In few minutes there appeared feeling of itching, burning of the
skin, lips and eyelids edema, whistling cough, decreasing of blood pressure
(BP). What antibodies take part in the development of this allergic
reaction?
A. IgA and IgM
B. IgM and IgG
C. IgM and IgD
D. IgE and IgG
E. IgG and IgD
Test 4. A child was born with cleft palate. Examination revealed aorta
defects and reduced number of T-lymphocytes in blood. What
immunodeficiency syndrome is it?
A. Wiskott-Aldrich
B. Chediak-Higashi
C. Louis-Bar
D. Swiss-type
E. DiGeorge
Test 5. A 50 year old man who was referred to the hospital for
treatment of cervical lymphadenitis underwent test for induvidual
sensitivity to penicillin. 30 seconds after he went hot all over, AP dropped
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down to 0 mm Hg that led to cardiac arrest. Resuscitation was
unsuccessful. Autopsy results: acute venous plethora of internal organs;
histological examination of skin (from the site of injection) revealed
degranulation of mast cells (tissue basophils). Degranulation was also
revealed in myocardium and lungs. What type of hypersensitivity reaction
is it?
A. Anaphylactic
B. Complement-mediated cytotoxic
C. Delayed-type hypersensitivity
D. Immunecomplex-mediated
E. -
Practice examination type 2. Give answers to the questions of the real-
life task:
Task 1. The 46 year old man, a soloist of the theatre, addressed to a doctor
with the complaints on frequent attacks of cold, headache, edema of the face,
fever. Disease became acute after going outside. He was treated because acute
respiratory disease. For the last time medical therapy did not help and even
forced headache, cold. Doctor suspected allergy.
1. What is your opinion? Explain it.
2. If this is allergy what is its type?
3. Explain mechanisms of found disorders.
4. What do you recommend to the patient?
Answer for the task 1: _________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Task 2. Equal sizes skin allotransplant was engrafted to two groups of
rabbits. A herewith leucocytes suspension taken from rabbits-donors of
allotransplant was infected intravenously to one group rabbit 2 weeks before
transplantation.
In what group of rabbits rejection of skin transplants will occur first? Why?
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
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Task 3. The 36 year old worker was hospitalized to dermatological
department of clinic. He complains on rash skin hands and itch. The rash
appeared two months ago. An application skin test with nickel sulphate was
positive. A test on of macrophages migration inhibition with nickel is positive
too.
1. What one does testify allergy nature of the disease?
2. Is there any base to recognize this disease as a delayed allergy?
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Signature___________________
Literature:
international ed./ V.Kumar, A.K.Abbas, J.C.Aster –
2015. – Chapter 6. – P. 186–200, 211–231, 237–263.
2. Robbins Basic Pathology 9th
edition./ Kumar, Abbas, Fauto. – 2013. – Chapter 4. – P. 99–158
3. General and clinical pathophysiology. Ed/ by prof. A.V. Kubyskin. Simf.–2011.– P. 233–257.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne Publ. – 2010. – P. 87–100.
Additional:
– 2010. – P. 222–241.
Milwaukee. – 2009. – P. 410–424.
medical students and practitioners. Ed. by prof. Zaporozan,OSMU. – Odesa. –2005.– P.96–104.
4. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins),
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapters 10– P. 168 – 177.
5. Silbernagl S. Color Atlas of Pathophysiology / S.Silbernagl, F.Lang // Thieme. NY. – 2000. – P. 52–59.
Topic 3: Pathophysiology of tissue growth. Tumors, etiology, pathogenesis.
1. Actuality of the theme. By the prognoses of worldwide health
protection organization morbidity and death rate from oncologic diseases in the
whole world will grow in 2 times for period from 1999 year for 2020: from 10
to the 20 million new cases and from 6 to the 12 million registered deaths.
Taking into account that in the developed countries there is a tendency to
deceleration of growth of morbidity and death rate from malignant tumors (due
to the prophylaxis and due to the improvement of early diagnostics and
treatment), clearly, that a basic increase will be at developing countries
(countries of former USSR). That is why doctors have to expect serious increase
of morbidity and death rate from oncological pathology.
2. Length of the employment – 1h 30 min.
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3. Aim: To form for students a concept about basic conformities to the law
and biological features of tumor growth, modern looks to etiology and
pathogenesis of tumors with the purpose of understanding of basic principles of
prophylaxis and treatment of oncological diseases.
To know:
1. To know determination of conceptions "hypertrophy", "hyperplasia",
"regeneration", "atrophy", "dystrophy", "tumor".
2. To know the features of innocent and malignant tumors growth.
3. To describe principal reasons of tumor growth.
4. To be able to explain the mechanisms of transformation of normal cell in
a tumor one.
5. To know general principles of patients treatment with malignant tumors.
To be able:
- to explain intercommunication between a tumor and organism;
- to explain pathogenesis of basic displays from the side of organism at
tumor growth;
- to explain the mechanisms of antitumor defense in an organism.
4. Basic level.
The name of the previous and
future disciplines
1. histology
2. biochemistry
3. physiology
4. microbiology
5. oncology
6. pharmacognosia
Structure of cell
Mechanisms of cell division
Principles of metabolism (albumen,
carbohydrate, fatty)
Imagination about DNA- and RNA-
contained viruses
Heyflik’s limit - it the maximal amount of cell divisions, which is
genetically programmed. It is different for every cells type. For fibroblasts, for
example, it is divisions.
Pasteur’s negative effect - is disintegration of carbohydrates to pyruvate
and transformation of it on lactic acid in aerobic conditions.
7 warning signs of cancer
C change in bowel or bladder habit
A a sore that doesn’t heal
U unusual bleeding or discharge
T thickening or lump
 I indigestion
O obvious change in wart or mole
N nagging cough or hoarseness
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1. Determination of concept is a “tumor”. Biological features of tumor
growth.
2. Tumor atypia, its kinds and description.
3. To explain essence of biochemical, physical and chemical,
morphological and functional cataplasia.
4. Etiology of tumors. Classification of carcinogenic factors.
5. A role of physical factors is in the origin of tumors. Radiation
carcinogenesis.
6. A role of chemical factors is in the origin of tumor growth. Exogenous
and endogenous carcinogens. Chemical carcinogenesis.
7. A role of viruses is in the origin of tumors. Viral carcinogenesis.
8. Basic methods of experimental design of tumors.
9. Mechanism of transformation of healthy cell in a tumor, essence of
mutational and to epigenomic carcinogenesis.
10. Mechanisms of invasive growth and metastasis of tumors.
11. Changes are in an organism at a tumor process.
7. Students’ practical activities
Protocol № 3 Date_____________________
Experimental work 1. Acquaintance with trasplanted tumor strains
(movie)
1. Ascitec Erlih's carcinoma in mouse. Initial tumor is spontaneous
cancer of mammalian gland. Strain exists from 1905. Percentage of positive
transplantion is 100. Latent period is 4-6 days. Lifetime animal with tumor is 7-
16 days. In intraperitoneal tumor transplantion ascite develops, for this they
inject into abdominal cavity 0.2 ml of ascitic liquid, which contains much tumor
cells. In intracutaneus introduction of this liquid tumor develops too.
2. Krocker's sarcoma in mouse. Initial tumor is sarcoma, which is
received in a result of malignisation of transplanted carcinoma of mammalian
gland. Strain exists from 1914. Histological type of tumor is
polymorphocellular sarcoma. Percentage of positive transplantation is 100.
Lifetime is 30 days.
Conclusion: __________________________________________________________
Experimental work 2. Demonstrate of macropreparation of
experimental tumors.
19

Conclusion: __________________________________________________________
Test 1. It is established that tumor tissue receives in 20-25 times less of
glucose that intact tissue in equal glucose amount. What metabolic
changings lead to such event?
A. Aerobic glycolysis enhancement
B. Oxydation improvement
C. Normal interaction of these processes
D. Tissue respiration improvement
E. Decreasing of anaerobic glycolysis
Test 2. An alcoholic woman has born a girl with mental and physical
developmental lag. Doctors diagnosed the girl with fetal alcohol syndrome.
What effect is the cause of the girl's state?
A. Malignization
B. Carcinogenic
C. Mechanic
D. Teratogenic
E. Mutagenic
Test 3. A patient who has been abusing tobacco smoking for a long
time has got cough accompanied by excretion of viscous mucus; weakness
after minor physical stress, pale skin. The patient has also lost 12,0 kg of
body weight. Endoscopic examination of biopsy material his illness was
diagnosed as squamous cell carcinoma. Name a pathological process that
preceded formation of the tumor:
A. Necrosis
B. Hyperplasia
C. Hypoplasia
D. Sclerosis
E. Metaplasia
Test 4. They got nitrogenous nitrite to experimental animals. A tumor
was developed in 80% of animals. What was the group of cancerogens?
A. Nitrosamines
B. Polycyclic carbohydrates
C. Aminoasosubstances
D. Simple chemical substances
E. Hormones
Test 5. After Chernobyl disaster morbidity of tumors has been
increasing. What action of the radiation has been appearing?
A. Cytostatics
B. Thermal
C. Mutagenic
D. Oncogenic
E. Immunostimulative
20

Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. Man, 65 years old, who were smoking during 35, signs the
decrease of appetite, weight loss, dry cough, shortness of breath, decrease of
capacity during last few months. At an inspection: anemia, leucocytes -
10,5x109
/l, methamielocytes-3%, stab neutrophiles -9%, segmentonuclear
neutrophiles-61%, lymphocytes-17%, monocytes -10%, ESR - 21 mm/hour.
The orbed darkening in the area of right bronchial tube with the diameter of
2sm was discovered at X-ray examination.
1) What kind of pathology was diagnosed at patient?
2) Possible etiologic factors of this pathology.
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Task 2. Man, 49 years old, was on a clinical account concerning ulcerous
illness of stomach during 25 years. Tumor formation of small curvature of
stomach was founded at the duty fibrogastroscopy review. Cancer of stomach
was diagnosed after cytological examination.
1) Tumor, definition.
2) What is the mechanism of this tumor development?
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Signature___________________
Literature
Basic:
int. ed. / V.Kumar, A.K.Abbas, J.C.Aster – 2015. –
Ch. 7. – P. 265–338.
edition./ Kumar, Abbas, Fauto. – 2013. – Ch. 5. – P. 161–213.
4. Symeonova N.K. Pathophysiology /N.K. Symeonova//Kyiv, AUS medicine Publ.–2010.–P. 142–160.
5. Copstead Lee-Ellen C.Pathophysiology /Lee-EllenC.Copstead,J.L.Banasic //Elsevier–2010.–P.128–159.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Ch. 5 – P. 64 – 83.
Additional:
1. Pathophysiology, Concepts of Altered Health States/C.Mattson Porth, G.Matfin.– NY–2009.–P.156–
197.
ed./ Kumar, Abbas, Fauto. –2007.–Ch.6.–P.174–
224.
medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 105–114.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F.Lang // Thieme. NY – 2000. – P. 14–17.
21

Topic 4: Inflammation.
1. The actuality of the theme. Inflammation is the reaction of
vascularized tissue to local injury. The causes of inflammation are many and
varied. Inflammation commonly results because of an immune response to
infectious microorganisms. Other causes of inflammation are trauma, surgery,
caustic chemicals, extremes of heat and cold and ischemic damage to body
tissues. Inflammatory conditions are named by adding the suffix -itis to the
affected organ or system. For example, appendicitis refers to inflammation of
the appendix, pericarditis to inflammation of the pericardium, and neuritis to
inflammation of a nerve. More descriptive expressions of the inflammatory
process might indicate whether the process was acute or chronic and what type
of exudate was formed (e.g., acute fibrinous pericarditis).
2. Duration of the class – 1h 30 min.
3. Aim:
To know: 1. Definition of the notion "inflammation". 2. Causes of the
inflammation. 3. The role of mediators in inflammation development. 4. The
meaning of the organism reactivity in inflammation development. 5. The
general manifestation of inflammatory reaction. 6. Clinical symptoms of the
inflammation. 7. Causes and mechanisms of the vascular permeability disorder
in inflammation. 8. Methods of the vascular permeability study in the area of
inflammation. 9. A common concept is about phagocytes (macrophages and
polymorphous leukocytes).
To be able:
- to describe the processes of alteration, exudation, and proliferation;
- to give a description of mediators of inflammation and explain their role
in the pathogenesis of inflammation;
- to reproduce inflammation in an experiment.
To perform practical work: to analyse the pathogenesis of inflammation:
disorders and after effect.
4. Basic level.
1. Histology
2. biochemistry
3. physiology
4. pharmacognosy
5. internal medicine
Functional parts of the bloodstream. Conception
about the microcirculation. Mechanisms of
regulation of blood circulation in capillaries and
venules. A conception of the role of connecting
tissue cells, their structure, main functions. The
22

6. surgery concept is about the products of an arachidonic
acid cascade, the kallikrein-kinin system of
blood, complement system.
1.Definition of the concept “inflammation”. Etiology of inflammation.
Classification of the inflammatory agents.
2.Stages of inflammation. Local symptoms of inflammation in the
experiment (Cels, Galen). Classification of inflammation.
3.Primary and secondary alteration. Causes and mechanisms of secondary
alteration.
4.Role of lysosomal enzymes, free radicals, peroxides and system of
complement in tissue injury.
5.Biochemical and physicochemical disorders in focus of inflammation.
6.Local acidosis, hyperosmia, hyperoncia.
7.Mediators of inflammation. Their classification. Role of cytokines in the
pathogenesis of inflammation.
8.Products of tissue basophile degranulation.
9.Derivates of arachidonic acid: prostaglandins, leukotrienes, thromboxanes.
10.Kallikrein-kinin system.
11.Complement activation in the development of the inflammatory process.
12.Exudation. Mechanisms of exudation. Causes and mechanisms of increase
in permeability of a vascular wall. Early and late stages of increase in
permeability. Kinds of exudates.
13.Emigration. Leukocyte emigration stages. Mechanisms of margination of
leukocytes. Exogenous and endogenous chemotaxis. Phagocytosis.
14.Phagocytosis. Stages. Mechanisms of absorption, elimination and
overcooking of microorganisms by phagocytes. O2-dependent and O2-
independent killing. Disorders: Chediak-Higashi syndrome, chronic
granulomatous disease, myeloperoxidase deficiency.
15.Proliferation. Mechanisms of proliferation and its regulation. The concept
of growth factors. Role of protein kinase C and tyrosine protein kinases in
activation of proliferative processes. Mechanisms of sclerosis.
16.General symptoms of inflammation: fever, leukocytosis, “acute phase
response in inflammation”.
17.Relation of local and general disorders at inflammation. Role of reactivity
in development of inflammation, the significance of immune reactions at an
inflammatory process. Inflammation and allergy.
18.Biochemical and physical and chemical changes are in the place of
inflammation. Reasons for development of acidosis in the inflammative tissues.
23

19. Influence of nervous and hormonal factors during inflammation. The
significance of inflammation for an organism.
20. Principles of anti-inflammatory therapy.
Protocol № 4 Date_____________________
Experimental work 1. To look after phagocytosis of bird's erythrocytes
in peritoneum exudate of a rat. With the purpose of recreation of aseptic
inflammation for days of the experiment, a rat enters intraperitoneal sterile beef-
extract [meat infusion] broth. At the beginning of employment in an abdominal
region enter 5 ml suspension of bird's erythrocytes (not more than 1 ml on the
50g masses). Through 25 min by pipette collect exudate. Then prepare strokes
and painted after Pappengeymom. Method of coloring - on a stroke inflicts the
counted up amount of drops of paint of May-Grunwald and rocks (swinging
lightly) during 3 min. (fixing). Add the same amount of the distilled water, mix
up a waggle and abandon on 1-2 min. (coloring). A smear is united and, not
washing water, on a stroke inflicts the Romanovskyy smear (a 1 drop is on 1 ml
of the distilled water) on 6 min. Wash off a smear by water, a stroke is dried out
by filtration paper. Cellular composition of exudate is studied under the
immersion increase of microscope and painted the phenomenon of phagocytosis
in a protocol.
Conclusion: _________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Experimental work 2. Microscope investigation of exudates.
The object of work: to acquaint the students with the methodic of determination
of the subtitles of amylolytic enzymes of pus.
Summary; to determine the enzymic special features of pus the serum of pus is prepared. For this purpose the pus
exudate is centrifuged, the upper layer is aspirated, and diluted with the physiological solution in 10 times.
1. Serous-purulent exudate got from the abdominal cavity of guinea-pig 3 hours after injection 1 ml of a suspension of
Staphylococcus culture. (There are more segmental and stable neutrophils, lymphocytes, monocytes, cells of mesothelium specimen.
There are visible cocci accumulations. It is observed microbes engulfed by neutrophils and monocytes. There is fragment of blood
cells and mesothelium).
2. Serous-purulent exudate got from the abdominal cavity of guinea-pig 24 hours after injection of 1 ml suspension of
Staphylococcus culture. In comparison with the previous specimen, here is observed many monocytes. Apart from them engulfed
remains of diverse cells (cultural phagocytosis), many destroyed cells (purulent bodies).
3. Purulent exudate has taken in the patients. It is observed a large number of destroyed leucocytes and cultural elements in
vision sight – compact shapeless mass, in which difficult to distinguish the structural tissues elements.
To draw and to note morphological peculiarities of exudates. Write down the experiment results and protocol of experiment
according to a scheme.
Questions for discussion.
1. What is it purulent bogy? 2. What does origin have the enzymes in
inflammatory exudate? 3. What is the mechanism of leucocytes destroying in
inflammation area?
24

The amylolytic adaptability of the pus is determined by the following way:
prepare several tests - tubes (8) with the main solution of pus serum. Pour 1 ml
of the physiologic solution into each test - tube except the first one.
Pour 1 ml of pus serum into the first test - tube. Pour 1 ml of pus serum
into the second one and mix it with 1ml of the physiologic solution; pour 1 ml
of a mixture from the second test - tube into the third one, from the third one
into the fourth one and so on to the end. Pour 1 ml of the mixture out of the 8th
test - tube. In such a way we get a number of dilutions of the serum of the pus
1:10, 1:20, and 1:40 and so on. Add to each dilution 5 ml of starch 1:1000 and
put the test - tube rack into the thermostat for 30 min. The stark is decomposed
under the influence of the amylolytic enzymes passing the stages of the
formation of erythro - and achrodextrins. Lughole’s iodine solution is an
indicator of stark decomposition. The latter acts with not decomposed stark -a
blue staining, with erythrodextrin - a red one and with achrodextrin - a yellow
staining.
For example, if a red staining is obtained in the 6th test-tube it means that the enzyme titer is 1.320 as 1 ml of
serum in the dilution 1: 320 decomposes 5 ml of stark in the dilution 1:1000 for 30 min before erythrodextrins.
1:1 0 1:20 1:40 1:80 1:160 1:320 1:640 1:1280
Conclusion: __________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Properties Serous exudate Transudate
Specific gravity
Albumen in %
Mucus in %
Capability to coagulation
A common amount of
cells is in 1 mm3
25

рН
Osmotic pressure
Experimental work 3. Vessels reactions to inflammation of mesentery
in a frog (Kongaim's experiment). Fix the frog on the board with the backup.
Make the side cut of the abdominal skin. Open the abdominal cavity, stretch out
intestine, strain out the mesentery above an opening in the board and fix the
intestine with the pins. Look over the microscope development of the vessel
reactions for the inflammation (change of the vessels diameter, change of the
blood flow speed, margination of leucocytes, thrombosis). Differentiate up
stages. Drawdown there. Write down the experiment results and protocol of
experiment according to a scheme.
Questions for discussion:
1. Enumerate the stages of the microcirculatory disorders in the area of the
inflammation.
2. What is the main in the development of arterial hyperemia?
3. What processes promote the slowing down of blood flow and
development of the venous hyperemia?
4. Which stages of the leucocytes migration did you see?
Conclusion: _________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Practical work 1. Watching movies “Inflammation”. Distinguish all
stages of inflammation and explain according to movie main pathogenic links.
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Practical work 2.Watching movie “Inflammation and Immune
response”. Notice in protocol main etiological factors of inflammation, explain
pathogenesis of immune response, general symptoms and comlications.
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Practice examination type 1: Choose the correct answer:
Test 1. Aspirin has antiinflammatory effect due to inhibition of the
cyclooxygenase activity. Level of what biological active acids will decrease?
A. Biogenic amines
B. Catecholamines
C. Prostaglandins
D. Leucotriens
E. Iodinethyronyns
26

Test 2. Necrosis focus appeared in the area of hyperemia and skin
edema in few hours after burn. What mechanism strengthens destructive
events in the inflammation area?
A. Proliferation of fibroblasts
B. Secondary alteration
C. Primary alteration
D. Emigration of lymphocytes
E. Diapedesis of erythrocytes
Test 3. At the laboratory experiment the leukocyte culture was mixed
with staphylococci. Neutrophile leukocytes engulfed and digested bacterial
cells. This processes are termed:
A. Facilitated diffusion
B. Diffusion
C. Osmosis
D. Phagocytosis
E. Pinocytosis
Test 4. A 16-year-old boy was performed an appendectomy. He has
been hospitalized for right lower quadrant abdominal pain within 18
hours. The surgical specimen is edematous and erythematous. Infiltration
by what of the following cells is the most typical for the process occur here?
A. Basophils
B. Monocytes
C. Limphocytes
D. Eosinophils
E. Neutrophils
Test 5. Inflammatory processes cause synthesis of protein of acute
phase in an organism. What substances stimulate their synthesis?
A. Interleukin-1
B. Angiotensin
C. Interferons
D. Immunoglobulins
E. Biogenic amines
Practice examination type 2. Give answer to the questions of the real-
life task
Task 1. In the result of burn of a shoulder an inflammation developed with
sharply expressed pain. 1. Why did the pain appear? 2. Enumerate other
possible displays of inflammatory reaction 3. What is their pathogenesis?
Answer for the task 1___________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Task 2. A patient addressed to doctor with complains about the pain and
noise in the left ear, lowering of hearing. During the examination of the
tympanic membrane, the dense net of dilated vessels is revealed. The upper part
of the tympanic membrane is dark red, the lower ones are brighter.
27

1. What pathological process did develop in the ear? 2. Why do different
parts of the tympanic membrane have a different color? 3. What is the
mechanism of the found vessel disturbances?
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Task 3. From pleural cavity of the patient doctor got exudate of such
composition: protein 58 g/l, leukocytes – 6200/mcl, prevail neutrophils, much
wholes and destroyed cells, рН 6.6.
1. What exudate did doctor get in the patient? 2. Explain mechanism of
exudate formation in pleural cavity. 3. What is the origin of found cells? 4.
What is the positive and negative role of exudate in inflammation?
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Signature___________________
Literature:
Basic:
international edition / V.Kumar, A.K.Abbas,
J.C.Aster – 2015. – Chapter 3. – P. 93–110.
edition./ Kumar, Abbas, Fauto. – 2013. – Chapter 2. – P. 53–73.
120–131.
Additional:
– 2010. – P. 197–203.
Milwaukee. – 2009. – P. 377–400.
medical students and practitioners. Ed. by prof.Zaporozan, OSMU. – Odesa. – 2005.– P. 68–77.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Chapter 9 – P. 150 – 161.
Topic 5: Pathophysiology of the basic metabolism. Starvation.
Carbohydrate metabolism pathology.
1. Actuality of the theme. For data of the WHO, more than half of
population of globe chronically is undernourished. Therefore starvation is the
28

social problem is considered not only as medical, but also as asocial problem.
This pathological process accompanies with a number of diseases, mainly of
digestive system. There is protein-calorie insufficiency more often.
The changes of metabolism for starvation are carried out nervous,
endocrine and peripheral mechanisms of regulation. Due to such regulation
there is a redistribution of nutritious substances for maintenance of functions of
the vital bodies (heart, brain) and preservation of life on long time.
Diabetes mellitus is a disease resulting from absolute or relative insulin
insufficiency and accompanying by disturbance of metabolism mainly,
carbohydrate one. The main manifestation of diabetes mellitus is
hyperglycemia, sometimes reaching 25 mrnol/1, glucosuria with glucose in
urine up to 555-666 mmol/1 (100-200 g/day), polyuria (to 10-12 I of urine per
day), polyphagia and polydipsia. It is also characterized by the increased level
of lactic acid (lactocydemia) — over 0.8 mmpl/1 (N — 0,033-0,078 mmol/1);
lipemia — 50-100 g/1 (N — 3,5-8 g/1), sometimes ketonemia (by
determination of acetone) with the increased level of ketone bodies to 5200
mcmol/1 (N < 517 mcmol/I).
2. Length of the employment – 1h 30min.
3. Aim: To know principal reasons, mechanisms of starvation development
and metabolic disturbance in it. Learn reasons and mechanisms of development
of basic types hypo- and hyperglycemia. To study etiology, pathogenesis,
mechanism of development of basic displays of diabetes mellitus, its pathogenic
treatment.
To know: the disturbance of energy metabolism, the disturbance of basal
metabolism, the disturbances of protein metabolism, the disturbance of
transamination and oxidative desamination, the disturbance of decarboxilation.
To be able: to analyse of the pathogenesis of the starvation and Diabetis
Mellitus.
To perform practical work: to analyse the pathogenesis of the
medicinal starvation (fasting). to analyse the pathogenesis of type 2 diabetes
mellitus. Genetic predisposition and environmental influences converge to
cause insulin resistance. Compensatory β-cell hyperplasia can maintain
normoglycemia, but eventually β-cell secretory dysfunction sets in, leading to
impaired glucose tolerance and eventually frank diabetes. Rare instances of
primary β-cell failure can directly lead to type 2 diabetes without a state of
insulin resistance.
4. Basic level.
The name of the
previous and future
disciplines
29

1. Histology
2. biochemistry
3. physiology
4. endocrynology
5. pharmacognozia
6. pharmacotherapy
Significance of proteins, fats, carbohydrates, water,
vitamins for normal ability to live of an organism.
Mechanisms of neuro-humoral regulation of
metabolism and energy. Indexes of metabolism and
energy exchange in an organism. Value of meal
components (albumens, lipids, carbohydrates,
vitamins and other) for the normal vital functions of
organism. Mechanisms of the neurohumoral
regulation of metabolism and energy exchange.
Role of carbohydrates in an organism.
Interconnection of carbohydrate, lipid and protein
metabolism. Neurohumoral regulation of
carbohydrate metabolism. Scheme of normal
glycogen metabolism in the liver and skeletal
muscles. Neuroendocrine regulation of
carbohydrate metabolism.
Table 1. Etiologic Classification of Diabetes Mellitus
Type Subtypes Etiology of Glucose Intolerance
I. Type 1* (Beta cell destruction usually
leading to absolute insulin
deficiency)
A. Immune-mediated
B. Idiopathic
Autoimmune destruction of beta
cells
Unknown
II. Type 2* (May range from predominantly
insulin resistance with relative
insulin deficiency to a
predominantly secretory defect with
insulin resistance)
III. Other
Specific Types
A. Genetic defects of beta cell
function, e.g., chromosome 7,
glucokinase
B. Genetic defects in insulin action,
e.g., leprechaunism, Rabson-
Mendenhall syndrome
C. Diseases of the exocrine
pancreas, e.g., pancreatitis,
neoplasms, cystic fibrosis
D. Endocrine disorders, e.g.,
acromegaly, Cushing’s syndrome
E. Drug or chemical-induced, e.g.,
Vacor, glucocorticoids, thiazide
diuretics, α-Interferon
Regulates insulin secretion due to
defect in glucokinase generation
Pediatric syndromes that have
mutations in insulin receptors
Loss or destruction of insulin-
producing beta cells
Diabetogenic effects of excess
hormone levels
Toxic destruction of beta cells
Insulin resistance
Impaired insulin secretion
Production of islet cell antibodies
Beta cell injury followed by
30

F. Infections, e.g., congenital
rubella, cytomegalovirus
G. Uncommon forms of immune-
mediated diabetes, e.g., “stiff man
syndrome”
H. Other genetic syndromes
sometimes associated with diabetes,
e.g., Down syndrome, Klinefelter’s
syndrome, Turner’s syndrome
autoimmune response
Autoimmune disorder of central
nervous system with immune-
mediated beta cell destruction
Disorders of glucose tolerance
related to defects associated with
chromosomal abnormalities
IV. Gestational
diabetes
mellitus
(GDM)
(Any degree of glucose intolerance
with onset or first recognition
during pregnancy)
Combination of insulin resistance
and impaired insulin secretion
Table 2. Actions of Insulin and Glucagon on Glucose, Fat, and Protein
Metabolism
Insulin Glucagon
Glucose
Glucose transport
Glycogen synthesis
Gluconeogenesis
Increases glucose transport into
skeletal muscle and adipose
tissue
Increases glycogen synthesis
Decreases gluconeogenesis
Promotes glycogen breakdown
Increases gluconeogenesis
Fats
Triglyceride
synthesis
Triglyceride
transport into
adipose tissue
Activation of adipose
cell lipase
Increases triglyceride synthesis
Increases fatty acid transport
into adipose cells
Inhibits adipose cell lipase
Activates lipoprotein lipase in
capillary walls
Enhances lipolysis in adipose
tissue, liberating fatty
acids and glycerol for use in
gluconeogenesis
Activates adipose cell lipase
Proteins
Amino acid transport
Protein synthesis
Protein breakdown
Increases active transport of
amino acids into cells
Increases protein synthesis by
increasing transcription of
messenger RNA and
accelerating protein synthesis
by ribosomal RNA
Decreases protein breakdown
by enhancing the use of glucose
and fatty acids as fuel
Increases transport of amino
acids into hepatic cells
Increases breakdown of
proteins into amino acids for
use in gluconeogenesis
Increases conversion of amino
acids into glucose precursors
1. What is the basic metabolism? The main stages of energy metabolism.
Basal metabolism. Disorders of energy metabolism.
2. Alimentary starvation, determination. Reasons of starvation.
3. Pathophysiological description of complete starvation periods.
Contribution of V.Pashutin to development of studies about starvation.
31

4. Protein-calorie deficiency. Reasons. Mechanisms of basic
manifestations development.
5. Starvation at children. Reasons of origin. Features of development.
6. What is respiratory coefficient (RC)? What is it equal at norm? How RC
changes at the all 3 periods of complete starvation with water?
7. Kwashiorkor. Reasons of development. Description.
8. Factors which influence on resistance of an organism to starvation.
Conception about starvation diet.
9. Etiology and pathogenesis of rachitis. Hypervitaminosis D at children.
Principles of prophylaxis and therapy of rachitis.
10. Disorders of carbohydrate metabolism. Disorders of absorption of
carbohydrates, process of synthesis, accumulation and decomposition of
glycogen, transport of carbohydrates into cells.
11. Disorders of nervous and hormonal regulation of carbohydrate
metabolism.
12. Hypoglycemia, causes and mechanisms. Hypoglycemic coma.
13. Hyperglycemia, causes and mechanisms. Hyperglycemic coma.
14. Glucosuria, causes and mechanisms.
15. Describe the main cause of pancreas alterations.
16. Diabetes mellitus. Classification of WHO. Causes and mechanisms of
development of insulin-dependent and insulin-independent diabetes mellitus.
Role of heredity in their occurrence.
17. Note the Classification of Diabetes and Glucose Intolerance
Conditions.Causes of extrapancreatic insufficiency of insulin, mechanisms of
resistance to insulin.
18. Disorders of carbohydrate and other kinds of metabolism at diabetes
mellitus.
19. Identify the acute complication of diabetes mellitus; describe the
features of each.Pathogenesis of the main complications of diabetes mellitus:
macro- and microangiopathies, neuropathies.
20. Experimental models of diabetes mellitus. Principles of pathogenetic
treatment of diabetes mellitus.
Protocol № 12 Date_____________________
Experimental work 1. Read results of blood and urine tests and reveal
period of starvation.
Blood glucose – 3.3-5.5 mmol/l
General protein - 65-85 g/l
Albumin - 61+0.70 %
Globulin - 38+0.79 %
Residual nitrogen - 14-28
mmol/l
32

General lipids – 4.0-7.0 g/l
Cholesterol – 5.0+0.3 mmol/l
Ketonic bodies - up to 5.2
mmol/l (2-10 mg %)
pH of blood – 7.35-7.45
pO2 - 100+10 mm Hg
p CO2 - 40+5 mm Hg
Shift of buffer bases (SBB) –
2.4+2.3 mmol/l
General bilirubin – 8.5-20.5
mmol/l
Na+
- 130-170 mmol/l
K+
- 4-6 mmol/l
Ca++
- 2.27-2.75 mmol/l
Phosphates – 1.1 mmol/l
Osmotic pressure of plasma and
cell - 310+5 mmol/l
Urine:
pH – 5.5-6.5
Diuresis – 0.8-1.6 l
Urea - 20-35 g/day
A. General Protein in
blood
49,8 g/l B. General Protein
in blood
36 g/l
Level of glucose in blood 2,8 mmol/l Level of glucose in
blood
2,1 mmol/l
Residual nitrogen 34,0
mmol/l
Residual nitrogen 61 mmol/l
C. General Protein in
blood
40 g/l Ketonic bodies 550
mkmol/l
Level of glucose in blood 3,2 mmol/l General lipids 10 g/l
Residual nitrogen 45 mmol/l
Ketonic bodies 250
mkmol/l
pH of blood 7,3
Conclusion:
__________________________________________________________
Practical work 1. Video observation: „Child dies every six minutes in
Horn of Africa”, “Anorexia problems”. Notice in protocol main etiological
factors of starvation and its periods, explain pathogenesis of general symptoms
and comlications.
Practical work 2. Video observation: „Express-methods of
determination of glucoses concentrations in blood”, “Diabetes and
associated complications”, “Glucose metabolism”. Notice in protocol main
33

etiological factors of diabetes mellitus, explain pathogenesis of general
symptoms and comlications.
Test 1. A 4 y.o. child with signs of durative proteine starvation was
admitted to the hospital. The signs were as follows: growth inhibition,
anemia, edema, mental deficiency. Choose a cause of edema development:
A. Reduced synthesis of hemoglobin
B. Reduced synthesis of albumins
C. Reduced synthesis of lipoproteins
D. Reduced synthesis of globulins
E. Reduced synthesis of glycoproteins
Test 2. When measuring power inputs of a man by the method of
indirect calorimetry the following results were obtained: 1000 ml oxygen
consumption and 800 ml carbon dioxide liberation per minute. The man
under examination has the following respiratory coefficient:
A. 1,0
B. 0,9
C. 0,8
D. 1,25
E. 0,84
Test 3. Patient with diabetes mellitus experienced loss of consciousness
and convulsions after injection of insulin. What is the result of
biochemical blood analysis for concentration of the sugar?
A. 10,0 mmol/L
B. 3,3 mmol/L
C. 5,5 mmol/L
D. 1,5 mmol/L
E. 8,0 mmol/L
Test 4. A patient was delivered to the hospital by an emergency team.
Objectively: grave condition, unconscious, adynamia. Cutaneous surfaces
are dry, eyes are sunken, face is cyanotic. There is tachycardia and smell
of acetone from the mouth. Analysis results: blood glucose - 20,1
micromole/l (standard is 3,3-5,5 micromole/l), urine glucose - 3,5%
(standard is - 0). What is the most probable diagnosis?
A. Acute alcoholic intoxication
B. Anaphylactic shock
C. Hyperglycemic coma
D. Acute heart failure
E. Hypoglycemic coma
34

Test 5. The patient with diabetes mellitus has been delivered in
hospital in the state of unconsciousness. Arterial pressure is low. The
patient has acidosis. Point substances, which accumulation in the blood
results in these manifestations:
A. Ketone bodies
B. Monosaccharides
C. Cholesterol esters
D. High fatty acids
E. Amino acids
Practice examination type 2 (Examples of the questions):
1. What is the difference between starvation, fasting and cachexia?
Starvation is ________________________________________________
Fasting is ___________________________________________________
Cachexia is__________________________________________________
2. What is the basic difference between marasmus and kwashiorkor? 3.
During a period of fasting, from which source does the body obtain glucose?
4. How long does this supply last? 5. When this supply is exhausted, why
doesn't the body become hypoglycaemic? 6. What are the substrates for
gluconeogenesis?
Answers for the task: __________________________________________________
Practice examination type 3 Give answer to the questions of the real-
life task:
Task 1. The examined has the following results of glucose-tolerance test:
level of sugar in blood fasting is 7,0 mmol/l, in 1 hour after reception of
glucose it equals to 8,8 mmol/l, in 2 hours after reception of glucose – 7,2
mmol/l. 1. What do these results testify about? 2. Draw the curve of change of
sugar level in blood of the healthy person within two hours after sugar load. 3.
What is the difference in test result in healthy person and this patient? 4. What
practical significance has the test with glucose load, how is it called?
Answers for the task 1: _________________________________________________
Task 2. Diabetes mellitus is developed after removal of pancreas in dog.
Would the diabetes mellitus is developed, if we instead of pancreas removal:
35

1. Tie up its output duct? 2.Introduce alloxan? 3.Introduce parathormone?
Task 3. The weight loss of a 45% of rats body is marked at the 7th days
from the beginning of complete starvation with water. A respiratory coefficient
is 0,8. At some animals there are areas of skin necrosis. What is the period of
starvation?
1)What is the type of starvation at a patient? What is the period of
starvation? Characteristic of this period of starvation.
Signature___________________
Literature:
Basic:
edition./ Kumar, Abbas, Fauto. – 2013. – Chapter
6. – P. 228, 232–233, Chapter 19. – P. 739–751.
2. General and clinical pathophysiology. Ed. by prof. A.V. Kubyskin. Simf. – 2011. – P. 281–321.
174–187, 200–223.
Additional:
– 2010. – P. 942–987.
Milwaukee. – 2009. – P. 998–1007, 1047–1075.
3. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide
for medical students and practitioners. Ed. by prof. Zaporozan, OSMU. –Odesa.–2005.– P.123–144.
4. Essentials of Pathophysiology: Concepts of Altered Health States, Trade paperback (2003) / Carol
Mattson Porth, Kathryn J. Gaspard. – Chapters 29, 32 – P. 517 – 521, 524–527, 560 – 578.
Topic 6: Pathology of fat metabolism.
Etiology and pathogenesis of atherosclerosis
1. Actuality of the theme. Atherosclerosis – exceptionally widespread
disease. On data WHO, mortalitis of the patients in the age 35-44 years for
damages of heart and vessels connected with atherosclerosis, increased lately
by 60%. The knowledge of the reasons and mechanisms of atherosclerosis
36

development is necessary for the doctors of various profession for prophylaxis
and treatment of this disease. According to modern notions, main etiological
factors of atherosclerosis is dyslipoproteinemia and increased permeability
arterial wall for lipoproteins. The primary prophylaxis foresee realization of
such methods, as organization of rational nutrition, early preventing obesity,
increase of physical activity, revealing and treatment arterial hypertension and
diabetes mellitus, fighting with smoking and abusing by alcohol.
2. Length of the employment – 1 h 30 min.
3. Aim:
To know: there are following disturbances of lipide metabolism:
1. Hyperlipemia (essential, genotypic, retention, transport types)
2. Atherosclerosis, arteriosclerosis
3. Obesity
4. Fatty infiltration and dystrophy (liver and oth. organs), fatty
degeneration.
To be able: to analyse of the pathogenesis of the atherosclerosis.
Arteriosclerosis is a chronic disease of the arterial system characterized by
abnormal thickening and hardening of the vessel walls. Smooth muscle cells
and collagen fibers migrate into the tunica intima causing it to stiffen and
thicken; this decreases the artery's ability to change lumen size.
I stage is deposition of lipids → irritation of the histiocytes →
proliferation of the histiocytes.
II stage is xanthomatosis → histiocytes → capture of lipids —> irritation
of fibroblasts → thickening of the subendothelium, deformation of the elastic
tissue → consolidation of the connective fibers.
III stage - patches, nutrient material is received by histiocytes with
difficulty, necrosis.
IV stage is atheromatosis, formation of ulcers, which can perforate
thrombi are formed.
To perform practical work: to analyse the sequence of cellular
interactions in atherosclerosis.
4. Basic level.
1. Histology
2. biochemistry
3. physiology
4. internal medicine
5. pharmacotherapy
Lipids and lipoproteins of blood plasma.
Transport of lipids. Intermediate metabolism
of fat. Sources cholesterol of blood plasma
and it metabolism. Anatomic-physiological
features of vessels.
37

Table 1. Hyperlipoproteinemia Classification accepted by WHO.
Type
Chylo
mic-
rons
VL
DH
LD
L
Cho
lest
erol
Tri
gly
ceri
des
Lipopro-
tein
disorders
Hereditar
y origin
Acqua-
red
I- hyper-
chylomic-
ronemia
↑
Nor
m
Nor
m
Nor
m
↑↑
Chylomic
-ron
Excess
Deficiency
lipoprotein
lipase
Systemic
lupus
erythoma
tosus
(SLE)
II a
hyper – β –
lipoprote
inemia
_____
__
Nor
m
↑↑ ↑↑
Nor
m
LDL
Excess
Family
hyperchole
sterinemia
(deficienc
y receptors
to LDL)
Hypothy
roidism
II b
hyper – β –
lipoprote-
inemia
_____
__
↑ ↑ ↑ ↑
LDL and
VLDL
excess
Combine
familial
hypercholi
steri-
nemia
Nephri-
tic
syndrome
III
familial
dis–β–
lipoprote
inemia
_____
__
Floating
-β-
lipoprotei
n
↑ ↑
Chylomic
ron
remnant
and IDL
excess
Family
hyperlipop
rotein
emia the
IIId
type
Obesity
IV
hyperpre –
β–lipoprote
inemia
_____
___
↑
Nor
m
Nor
m
(↑)
↑
VLDL
excess
Combine
family
hyperlipid
emia
Diabe-
tes
mellitus
V
Combina-
tion of
hyperpre –
β– lipo
proteinmia
↑ ↑ Nor
m
Nor
m
(↑)
↑↑
Chylomic
ron and
VLDL
excess
Family
hypertrigly
cerides
Alcohol
intoxi-
cation
38

& hyperchy
lomicrone
mia
Legend: ↑ - increase Ch – chylomicrons, LDL – low density lipoproteides,
VLDL – very low density lipoproteides, IDL – intermediate density lipoproteins.
1. Disorders of fat metabolism. Disorders of digestion and lipid
absorption.
2. Disorders of lipid transport in blood. Hyper-, hypo- and
dyslipoproteinemias. Modified lipoproteins.
3. Disorders of nervous and humoral regulation of lipid metabolism.
4. Atherosclerosis: of concept, role of risk factors.
5. Main links of pathogenesis of atherosclerosis.
6. Reasons of hyper-β-lipoproteinemia.
7. Reasons of multiplying permeability of vascular wall are for
lipoproteins.
8. Protective role of α-lipoproteins and reasons of hypo-α-
lipoproteinemia.
9. Basic directions of prophylaxis of atherosclerosis.
10. Inherited violations of lipidic metabolism.
11. Disorders of lipid accumulation. Primary and secondary obesity.
Experimental models and pathogenesis of obesity.
12. Distinguish between hypertrophic and hyperplastic obesity.
13. Hyperketonemia: causes, mechanisms, consequences.
14. Disorders of intermediate exchange of lipids in cells. Mechanisms of
fatty dystrophy.
Protocol № 13 Date_____________________
Practical work 1. Video observation: “Obesity”, “Obesity and chronic
diseases”. Notice in protocol main etiological factors of obesity, explain
pathogenesis of general symptoms and comlications.
Conclusion: __________________________________________________________
____________________________________________________________________
39

____________________________________________________________________
____________________________________________________________________
____________________________________________________________________
Practical work 2. Calculate your own body mass index (BMI):
Conclusion:
__________________________________________________________
____________________________________________________________________
____________________________________________________________________
____________________________________________________________________
Practice examination type 1. Give correct answers to the tests:
Test 1. Apoprotein - is:
А. Protein cellular receptors to lipoprotein of blood plasma
В. Variant of “modificated” lipoproteids
С. Lipoproteins of blood plasma without albuminous part
D. Albuminous component of blood plasma lipoproteins
Е. Anomal proteins with characteristics of lipoproteins
Test 2. A 70 year old man is ill with vascular atherosclerosis of lower
extremities and coronary heart disease. Examination revealed disturbance
of lipid blood composition. The main factor of atherosclerosis
pathogenesis is the excess of the following lipoproteins:
A. Low-density lipoproteins
B. Intermediate density
lipoproteins
C. Cholesterol
D. High-density lipoproteins
E. Chylomicrons
Test 3. The quantity of plasma albumens changed in a man which
executed a physical work in the conditions of high temperature. How did
quantity of plasma albumins change?
A. Absolute hypoproteinemia
B. Paraproteinemia
C. Dysproteinemia
D. Absolute hyperproteinemia
E. Relative hyperproteinemia
Test 4. Increased amount of free fat acids is observed in the blood of
the patients with diabetes mellitus. It can be caused by:
A. Activation of the ketone bodies utilization
B. Activation of the synthesis of the apolipoproteins
C. Increased activity of triglyceridelipase adipocytes
D. Storage of palmitatoil-CoA
E. Decreased activity of phosphatidylcholine-cholesterol-acyltransferase
blood plasma
Test 5. Man, 70 years, suffers from atherosclerosis of lower
extremities vessels and ischemic heart disease. Violation of lipid
40

composition of blood was founded during examination. What lipoprotein
is the main link in atherosclerosis pathogenesis?
A. Low density
B. Cholesterol
C. High density
D. Intermediate density
E. Chilomicrons
Practice examination type 2. Give answers for questions of the real-life
tasks:
Task 1. Patient, 60 years, suffers from atherosclerosis of the vessels of
the lower extremities, ischemic heart disease. At the investigation
hyperlipidemia was founded.
1. What class of lipoproteins of blood plasma will be increased?
2. What classes of lipoproteins do you know? Characteristic.
3. Рrinciples of pharmacocorrection.
Task 2. Patient has encephalitis. After the disease she suffers from
increasing of appetite (polyphagia), increasing of body weight. Obesity
developed. 1. What is the type of obesity? 2. What are the reasons of its
development? 3. Classification of the obesity according to pathogenesis?
Practice examination type 3: What is true (T). What is false (F)?
№ Statement Т F
A. Cholesterol is a product which is difficult to metabolize.
B.
The subendothelium of the vessels is a bradytrophism of
tissue.
C.
Cholesterol is formed in the liver from fats, carbohydrates,
proteins.
D.
Cholesterol is a hydrophobic substance, its connection with
protein (and with lipids) is necessary for the transformation
into the hydrophilic state.
E. A lot of cholesterol is contained in B-lipoproteins (70–75 %).
41

F. B-lipoproteins are increased in the body of elderly persons.
G.
Hypodynamia and hypoxia predispose to atherosclerosis
because of the decreased oxydation of lipids and promote
accumulation of cholesterol in subendothelium.
H. Hyperlipemia is associated with atherosclerosis and obesity.
L. Obesity may occur without atherosclerosis.
Signature___________________
Literature:
Basic:
ed./Kumar, Abbas, Fauto.–2013.–Ch.7.–P. 302–307.
3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publ. – 2010.–P.223–234.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. –
2010. – P. 362–367, 825, 974–975.
Milwaukee. – 2009. – P. 982–998, 479–489.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease8th
ed./Kumar, Abbas, Fauto.–2007.–Ch.10.–P.343–353.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapt. 15, 29 – P. 254–260, 521 – 524.
medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 145–153.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart. New York. –
2000. – P. 26–27, 236–239, 244–249.
42

MODULE 1
“The general nosology. Pathogenic effect of factors of external and internal
environment”.
1. Pathophysiology as an educational discipline. History of development of
pathophysiology.
2. Basic concepts: health, illness (WHO), pathological reaction, pathological process,
pathological status, typical pathological processes.
3. Methods of pathological physiology. Experiment. Kinds of experiment. The basic
stages of realization of experimental researches.
4. Etiology and pathogenesis of pathological processes. Causes in pathology. The role of
causes and conditions in origin of diseases.
5. Causes and consequences in pathogenesis of diseases. Specific and non-specific
mechanisms of disease development.
6. Influence of environmental factors on organism. The mechanical, physical, chemical
and biological factors. Social conditions and their role in etiology and pathogenesis of
diseases. Social illnesses.
7. Definition of pathogenesis. Damaging and compensation phenomena in pathogenesis
(by the example of hemorrhage). Local and general changes in pathogenesis (by the example
of inflammation, fever, shock). The formation of vicious circles in pathogenesis of diseases
(by the example of shock, kidney edema and molecular mechanisms of damage of a cell).
8. The role of heredity in pathology. General mechanisms of origin of hereditary illnesses.
9. Concept of constitution, its role in pathology. The basic classifications of constitution
types. The modern approaches to the definition of constitution. The role of sex and age in
pathology.
10. Reactivity and resistance: definition, types, mechanisms. Dependence of reactivity on
age, sex, heredity.
11. Immune protection: humoral and cellular mechanisms. Kinds of impairment. Immune
deficiency.
12. Nonspecific protection, its cellular and humoral mechanisms. Mechnikov’s doctrine
on phagocytosis. Changes in phagocytosis: reasons, mechanisms, consequences.
13. Specific immunity, its humoral and cellular mechanisms. Classes of
immunoglobulins, their functional properties.
14. Primary immune deficiency: classification, reasons and mechanisms of
development. Pathogenesis of basic clinical signs at B- and Т-lymphocyte deficiency.
43

15. Secondary immune deficiency: reasons and mechanisms of development. AIDS:
etiology, pathogenesis.
16. Immune deficiency status, the way of its correction. Reaction "graft-versus-host".
17. Autoimmune status: its mechanisms and symptomatology (by the example of
hemolytic anemia, diabetes, etc.)
18. Allergy. Etiology of allergy. Types of allergic reactions, phases of their development.
19. Anaphylactic shock, its experimental modeling and pathogenesis. The role of
Sakharov’s works. Active and passive anaphylaxis. Desensitization.
20. Anaphylaxic type of allergic reactions (Ig-E mediated), their pathogenesis and
clinical forms.
21. Cytotoxic specific type of allergic reactions, their pathogenesis and clinical forms.
Mechanism of cellular injury. Posttransfusion shock. Cytotoxic specific reactions in
experiment and clinic; significance of Bogomolets’ works.
22. Allergic reactions caused by free immune complexes. Their pathogenesis and clinical
forms.
23. Cell-mediated allergic reactions: the basic clinical forms, characteristics of stages. The
role of lymphokines.
24. “Graft versus host” reaction, conditions of its development, acute and chronic forms.
The main principles of immune stimulation and immune suppression.
25. “Host versus graft” reaction, conditions of its development, acute and chronic forms.
The main principles of immune stimulation and immune suppression.
«Typical pathological processes»
1. Active and passive hyperemia. Etiology and pathogenesis. Consequences of changes
in microcirculation.
2. Etiology and pathogenesis of ischemia, consequences. Factors influencing the
development of ischemia. Mechanisms of cell damage in ischemia. Stasis.
3. Etiology and pathogenesis of thrombosis. Humoral and cellular factors of thrombosis
(endothelium, thrombocytes). Causes and mechanisms of adhesion and aggregation.
4. Hemorrhage. Changes in blood clotting and fibrinolysis. Disseminated intravascular
coagulation (DIC) syndrome.
5. Embolism, kinds of embolus, their classification, embolism of systemic and
pulmonary circulation. Consequences.
6. Concept of inflammation. The basic processes in inflammation. Primary and
secondary alteration: reasons and mechanisms. Types of inflammation and their
characteristics.
7. Biochemical changes in the focus of inflammation. Biologically active substances of
inflammation, their origin and mechanism of action.
8. Changes of microcirculation and drainage of tissue in the focus of inflammation, their
mechanism.
9. Exudation, its reasons and consequences. Pathogenesis of permeability changes of a
vessel wall in inflammation. Influence of BAS (biological active substances) upon
inflammation and hormonal factors.
10. Phases, mechanism and significance of leukocyte emigration. The role of leukocytes
in development of local and general signs of inflammation. Phagocytosis.
11. Proliferation as a component of inflammation. Concept of growth factors and
mechanisms of their action. Influence of hormonal factors on inflammation.
44

12. Significance of inflammation. A dialectic approach to estimation of compensating and
damaging phenomena in the mechanism of inflammatory reaction.
13. Problem of "general" and "local" in pathology. Interrelation of general and local
changes in an inflammatory process.
14. Definition of the concept "tumor". The basic laws of neoplasm growth. Tumor
development.
15. Theories of carcinogenesis. The role of oncogens and immune system.
16. Methods of experimental modeling of tumors: transplantation, induction, ex-
plantation. Factors of carcinogenesis. The role of immune system in origin and development
of tumors.
17. Etyology of tumors. The role of physical and chemical factors in origin of malignant
tumors. Classification and characteristics of basic groups of chemical cancerogens.
18. Clinical manifestations of cancer. Mechanisms of invasive growth and metastasis of
malignant tumors.
19. The influence of organism on different tumors (role of immune, genetic and hormonal
factors).
20. Molecular mechanisms of cell damage. The role of lipid peroxidation, proteolysis and
calcium ions in damage processes. Mechanisms of protection and adaptation of cells to the
action of pathogenic agents.
21. Changes in production and transformation of energy in cells.
22. Damage of cells. Mechanisms of damage of cellular structures: membranes,
mitochondria, lysosomes.
23. Ionic changes in cells: mechanisms of development and consequences.
“Typical disorders of metabolism”.
1. Changes in carbohydrate metabolism. Hyper- and hypoglycemia. Reasons and
mechanisms of their origin. Hyper- and hypoglycemic coma.
2. Diabetes. Pathogenesis of insulin insufficiency. Diabetes of 1 and 2 types. The role of
genetic factors in their origin. Experimental models of insulin deficiency.
3. Pathogenesis of diabetes. All kinds of metabolic derangements.
4. Changes in organs and systems at diabetes. Mechanism of development of basic clinical
signs and complications at diabetes. Types of comas at diabetes.
5. Pathology of fatty exchange. Ketonemia, its etiology and consequences. Adiposity, its
types.
6. Changes in calcium and phosphate homeostasis. Hypo- and hyperfunction of
parathyroid glands. Hypo- and hypercalcemia: reasons and mechanisms of their
development.
7. Pathology of protein exchange. Function of the liver at pathology of protein exchange.
Azotemia, its consequences. Positive and negative nitrogen balance.
8. Acidosis. Classification, reasons of development, compensation reaction and
pathological changes in organism, parameters of acid-base balance, principles of correction.
9. Alkalosis. Classification, reasons of development, compensation reaction and
pathological changes in organism, parameters of acid-base balance, principles of correction.
10. Disturbances of salt and water homeostasis. Different forms of water deficiency and
water excess. Na and K ion imbalance: reasons and mechanisms of development, basic
clinical manifestations.
45

11. Isosmotic excess. Mechanisms of liquid delay in organism. Edemas, their types and
pathogenesis.
12. Water excess: reasons, pathogenesis and consequences.
13. Isosmotic loss: reasons, pathogenesis, consequences.
14. Water and salt deficiency: reasons, pathogenesis, consequences.
15. Edemas. Etiology and pathogenesis of their different forms. The role of hormonal
control of salt and water.
16. Toxic, allergic and traumatic edemas, their pathogenesis.
17. Fever. Etiology and pathogenesis, types. Primary and secondary pyrogens, their origin
and mechanism of action. Thermal balance in various stages of fever.
18. Functional and metabolic changes in organism at various stages of fever.
19. Difference between fever and hyperthermia. A dialectic approach to estimation of
feverish reaction significance.
20.Starvation, its types. Complete starvation, its stages. Mechanism of hungry
edema.
21.Starvation as a social problem. Qualitative starvation and its consequences.
Protein deficiency.
22.Hypoxia, its kinds. Etiology and pathogenesis of separate kinds of hypoxia.
The role of etiological factors in the development of hypoxia.
23.Functional and biochemical adaptation at hypoxia.
24.Pathophysiology of cell damage at hypoxia and the way of their protection.
25.Compensation and pathological changes in organs and systems at hypoxia.
Notes
46

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