Metod. med 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 medical faculty students
Prepared by:
Gerasymchuk M. R.
Cherkasova V. V.
Zaiats L. M.
Ivano-Frankivsk, 2017

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«The general nosology. Typical pathological processes»
Training-methodical manual for class and out-of-class work for
medical students / M.R. Gerasymchuk, V.V. Cherkasova, L.M. Zaiats //
IFNMU. Department of pathological physiology. – 2017. – 92 p. Discussed
and approved on 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 STUDIES
of pathological physiology for the students of the III course in the V semester
THEME OF PRACTICAL STUDIES DATES
1. The object, and tasks of pathophysiology. Methods of
pathophysiological investigations. Basic steps in pathological
physiology development.
04.09–08.09
2. General nosology. The doctrine of etiology and pathogenesis.
Pathogenic effect of ionizing radiation on the body.
11.09–15.09
3. The role of heredity and constitution in pathology. 18.09–22.09
4. Pathology of reactivity. Violation of immunological reactivity. 25.09–29.09
5. Hypersensitivity reactions of immediate and delayed type. 02.10–06.10
6. Cell pathophysiology. 09.10–13.10
7. Typical disorders of peripheral blood flow and microcirculation. 16.10–20.10
8. Inflammation: phlogogenic factors, pathogenesis of alteration,
mediators. Kongeim’s experiment.
23.10–27.10
9. Inflammation: pathogenesis of exudation and proliferation. 30.10–03.11
10. Disorders of thermal metabolism. Fever. 06.11–10.11
11. Tumors. 13.11–17.11
12. Starvation.Hypoxia. 20.11–24.11
13. Disorders of carbohydrate metabolism. Diabetes mellitus. 27.11–01.12
14. Disorders of lipid metabolism. Medical and social problems of obesity. 04.12–08.12
15. Disorders of water-electrolyte metabolism and microelements
metabolism.
11.12–15.12
16. Module 1 (practical part) 18.12–22.12
17. Module 2 (theoretical part) 25.12–29.12
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 module topics are 120 points), on results final module control are 80 points.
Control of theoretical and
practical preparation
0 – 2 points – completely prepared homework;
0 – 5 points – oral answer;
0 – 1 points – test control during class.
Minimum – 0 points; positive – 4; maximum – 8 points

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Topic № 1. The object, and tasks of pathophysiology. Methods of
pathophysiological investigations. Basic steps in pathological physiology
development. General nosology. Teaching about etiology and pathogenesis.
Pathogenic effect of radiation and electric current.
1. The The 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 reproduce and study on animals the separate models of
illnesses, violation of organs and systems for the cognition of basic conformities
to the law of development of illnesses of man. Consequently, the experiment is
the basic method of pathophysiology. 2. Duration of the class – 1 hour 30 min.
3. Aim:
To know such terms as the «modelling», «experiment».
To be able:
a) The modeling of various forms of pathologic processes, protective and
adaptive reactions of humans;
b) Experimental therapy as an important method of studying and introducing
the new ways of treatment;
c) Clinical studying of various diseases with functional, biochemical,
immunological and other tests due to pathophysiology groundation therapy.
To perform practical work:
1. Main features and purpose of experiment in pathophysiology. Correlation
of method of clinical supervision with the pathophysiological experiment.
2. Possible experiment on a human? Mental and ethical aspects of
pathophysiological experiment.
3. Causes and consequences constantly change their places. The cause
(etiological factors) causes the pathologic reactions (process) and then these
reactions return to the first agent (etiological factor) and intensify it.
4. To analyse the “vicious circle” in the pathogenesis. Causes and
consequences constantly change their places.
4. Basic level.
The name of the previous and future disciplines The receiving of the skills
1. histology
2. biochemistry
3. physiology
4. internal medicine
5. reanimatology
6. radiology
Ionizing radiation. Main
characteristics. Physical and chemical
ionizing radiation interchange in
organism. Gas composition of air and
partial pressure of oxygen. Functional
units structure of respiratory system,
blood, blood circulation system.
5. Control questions of the theme:
1. Term definition – what is pathophysiology? Explain role in medicine.

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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. General
pathophysiology, special or systemic and clinical pathophysiology.
4. Methods of pathological physiology. An experiment as the main method
of pathophysiology, its significance for solving fundamental problems of
medicine.
5. Name the methods and the aims of pathophysiology. Gist of experimental
method. Modeling pathological processes and diseases on animals: possibilities
and limitations. Significance of comparative-evolutional method for
development of pathophysiology.
6. Rules of work with laboratory animals. Types of experiment. General
principles of planning the experimental investigations, count, statistic processing
and analysis of the results.
7. Definition a notion “experiment”, peculiarities, significance and lacks of
acute experiment, peculiarities of chronic experiment. Experimental therapy.
8. General doctrine of disease. The basic concepts of general nosology.
Norm, health, disease (definition of WHO). A pathological process. A
pathological condition, pathological reaction.
9. 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.
10.Stages of disease development. Remission, relapse, complication.
Variants of disease outcome: complete and incomplete recovery.
11.Terminal conditions: pre-agony, agony, clinical death.
Pathophysiological bases of reanimation.
12. The main directions in the development of doctrine of disease: humoral
(Hippocrates), cellular (R. Virchow). Their development in the modern stage.
13. Definition of the concept “etiology”. Problem of causality in pathology.
The role of causes and conditions in occurrence of diseases. The main directions
in the development of doctrine of etiology: monocausalism, conditionalism,
constitutionalism, psychosomatic conception, etc.
14.Modern concepts of causality in pathology. Classification of etiological
factors. External and internal etiological factors. The concept of risk factors.
“Diseases of civilization”. Ecological, genetic, accumulative and ontogenetic
conceptions of occurrence of human diseases. Etiotropic principles of prevention
and treatment.

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15.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.
16. Protective reactions of adaptation. Adaptation, compensation.
Mechanisms of immediate and long-term adaptation. The role of nervous and
humoral factors in their realization. “Compensatory-adaptative reactions”, types
of compensatory-adaptative reactions, role of compensatory-adaptative reactions
in convalescence mechanisms.
17. 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.
18. Concept of localization and generalization of pathological processes.
Ways of their distribution. Specific and nonspecific mechanisms of pathogenesis.
Pathogenetic principles of disease treatment.
19.Pathogenic effect of ionizing radiation. Types of ionizing radiation.
Radiosensitivity of tissues. Mechanisms of direct and indirect radiation damage
of biological structures. Water radiolysis. Radiotoxins.
20.Manifestations of radiation damages on molecular, cellular, tissue, organ
and system levels.
21.Pathogenesis of radiation sickness, its main forms and syndromes. Early
and late effects of large and small doses of ionizing radiation.
22.Natural mechanisms of antiradiation protection. Pathophysiological bases
of radioprotection.
23.Influence of low atmosphere pressure upon organism, man activity in
condition of low atmosphere pressure, mechanisms of low atmosphere pressure
action, manifestations.
24.Influence of high atmosphere pressure upon organism, man activity in
condition of high atmosphere pressure, mechanism of high atmosphere pressure
action, manifestations of saturation and desaturation, hyperbaric oxygenation
use in medicine.
25.Pathogenic influence of electric current.
6. Independent audience work of student.
Protocol № 1 Date_____________________
Experimental work 1. Determining the amount of haemoglobin. Solution
of hydrochloric acid pours in a test-tube of hemometer 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 haemoglobin in mmol/l. Formula of

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calculation: B • 0,6206, where B – is an amount of haemoglobin in g%; 0,6206 –
is a coefficient of count in unit of SI.
Conclusion:____________________________________________________________
Experimental work 2. Determining the amount of erythrocytes. In a test-
tube pour 4 ml of a 3% solution of chloride of sodium. By a capillary pipette
collect 0,02 ml blood and produce it on the bottom of test tube. The contents is
carefully mixed. Then drop of liquids by pipette place under preliminary
grinding (rubbing) in integumentary (covered) small glass of account chamber.
Count up erythrocytes in 5 large (that in 80 small) squares of net of Goryaeva
and calculate their amount in 1 litr of blood after a formula:
lТ
ААА
/
100
10
100
10
80
2004000 128


where: A – is an amount of red corpuscles
in 5 large squares; 4000 – the volume of small square makes 1/4000 mm3; 200 –
is dilution of blood; 80 – is an amount of the counted up small squares; 108 is a
multiplier for the count of amount of red corpuscles in unit of SI; T – 1012.
Conclusion:____________________________________________________________
Experimental work 3. Count of amount of leucocytes. In a test-tube pour
0,4 ml of a 3% solution of vinegar acid. By a capillary pipette collect 0,02 ml
blood and outpour it on the bottom of test-tube. Mixture is mixed, and then fills
the chamber of Goryaeva. Count up the amount of leucocytes in 100 large
squares of net. Expect the amount of leucocytes in 1 l of blood.
lG
АА
Х /
20
10
11600
204000 6



 , where: A – is an amount of leucocytes in 100
large squares; 1600 – is an amount of the calculated small squares;
4000
1
it is a
volume of small square in mm3; 20 – is a degree dilution of blood; 106 – is a
multiplier for the count of amount of leucocytes in unit of SI; G – giga - 109.
Conclusion:____________________________________________________________
8. 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 people, living in endemic centre, has recovered the three-day
malaria. In one and a half year after moving in the other places occured
malaria once again. What the most probable form of this disease?
A. Superinfection
B. Reinfection
C. The Relapse
D. Persistent infection
E. Secondary infection
Test 3. Which one of the methods is the most important at
pathophysiology?
A. Epidemiological
B. Anatomical
C. Clinical
D. Experimental
Test 4. Through day after irradiation (the dose 3,5 Gr.) beside damaged
in shelters: erythrocytes-4,7 1012
/l, hemoglobin-9,0 mmol/l, leukocytes-11
109
/l, thrombocytes-270 109
/l. In daub shelters: basophils-1%, eosinophils-
3%, neutrophils-81%, lymphocytes-11%, monocytes-4%. For what period
sharp radiation sickness typical specified shifts?
A. The Primary reaction
B. The Peak disease
C. The Rumpled welfare
D. Reconstruction
E. Terminations
Test 5. Sudden death during dehermitizing of aircraft at height 19000 m
is rose owing to:
A. Carbonic acid deficit
B. Organism desaturation
C. Gas embolism
D. Oxygen deficit
Е. Height meteorism
Test 6. A 49-year-old man was suffering 12 years ago from rheumatic
myocarditis, endocarditis, and insufficiency of mitral valve. Examinations
showed the absence of inflammatory process, sufficient minute blood
volume. What is it?
A. Pathological reaction
B. Pathological process
C. Typical pathological process
D. Compensatory reaction
E. Pathological condition
Test 7. 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 8. Gasping respiration appears in a patient with severe lung
pathology. What terminal condition is this characteristic for?
A. Agony B. Pre-agony

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C. Clinical death
D. Biological death
E. Terminal pause
Test 9. Respiratory standstill developed in a man as a result of action of
electric current from town mains for 0.1 seconds with position of electrodes
“right hand – head”. Indicate the most probable reason for this
complication.
A. Paralysis of inspiration center
B. Emotional stress
C. Paralysis of respiratory muscles
D. Reflex respiratory standstill (pain shock)
E. Total paralysis of respiratory center
Practice examination type 2 Give answer to the questions of the real-life
tasks:
Task 1. Experimentator should study mechanismas of dyspnea in case of
disorders of blood circulation in the lungs. Which main periods of
pathophysiological experiment he should make?
1 3
2 4
Task 2. In dog under anesthesia, was destroied cusp of mitral valve and in
this ways reproduce cardiac insufficiency. Which method of disease modeling
used?
______________________________________________________________________
Task 3. As a result of damage one of atomic electric station blocks arose
emissions of ionizing rays products. In zone of raised radiation activity found
oneself three men. Approximately they got on 250-300 Rad. They immediately
delivered in clinic.
1. What consequences do follow to wait in victim?
2. What periods pick out in development of radial sick?
3. What researches you should make for clearing up of lesion degree?
4. How would be differ state irradiated being received 50R? 500R? 6000R?
Answerfor the task: ____________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Practice examination type 3
I. Give the description of each form of radiation disease (1 – acute, 2 –
chronic):

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Indicator 1/2 Indicator 1/2
A
The disturbance of hemo-
poiesis 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
E Necrotic tonsillitis L Trophic disorders
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
The outcome of the ARD is multiple inflammatory processes
(necrotic angina, pneumonia, frontitis and others).
III. 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
Signature___________________

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Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./Kumar, Abbas, Fauto.–2015.–Ch.9.–P.426–432.
2. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simferopol. – 2011. – P. 17–85.
3. Pathophysiology, N.K. Symeonova. Kyiv, AUS medicine Publishing. – 2010. – P. 24–34.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. –
2010. – P. 3–13, 1280–1283.
Additional:
1. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– New York,
Milwaukee. – 2009. – P. 2–10.
2. J.B.Walter I.C.Talbot General pathology. Seventh edition. – 1996. – P. 1–17.
Topic 2: Role of heredity, constitution and aging changes in pathology.
1. The actuality of the theme. Genetic and congenital defects are important
at all levels of healthcare because they affect all age groups and can involve
almost any of the body tissues and organs. Congenital defects, sometimes called
birth defects, develop during prenatal life and usually are apparent at birth or
shortly thereafter.
About 2000 different hereditary diseases are known now. 4 % of new-born
suffer from these or other genetically conditioned defects. Heredity pathology
plays an important role in development of such hereditary conditioned diseases,
as atherosclerosis, essential hypertension, rheumatism, diabetes mellitus, and
gout.
2. Duration of the class – 1 h 30 min.
3. Aim:
To know the role of hereditary factors and constitution in the development
of diseases and pathological processes.
To be able: to analyze the pathogenesis of chromosomal diseases,
phenylketonuria.
To perform practical work: Characterize fragile X-associated mental
retardation syndrome produces a unique combination of phenotypic features that
affect the central nervous system, the testes, and the cranial skeleton.
4. Basic level.
The name of the previous and
future disciplines
The receiving of the skills
1. histology
2. biochemistry
3. physiology
4. pediatrics
Encoding of hereditary information.
Legitimacy and types of hereditary signs
transmission in generations.
Cytological genetic base.
1.Heredity as a cause and condition of disease development. Relation of the
hereditary and acquired in pathogenesis. Hereditary and congenital diseases.
Gene- and phenocopies. Classification of hereditary diseases.

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2.Mutations. Principles of their classification. Causes of mutations.
Mutagenic factors of a physical, chemical and biological origin.
3.Mendelian disorders: diseases caused by single-gene defects:
• autosomal dominant (Huntington disease, neurofibromatosis type 1,
Marfan syndrome, Familial hypercholesterolemia (LDL receptor deficiency),
acute intermittent porphyria);
• autosomal recessive (Cystic fibrosis, sickle cell anemia, phenylketonuria,
Tay-Sachs disease (hexosaminidase A deficiency));
• X-linked (Fragile X syndrome, hypophosphatemic rickets, Duchenne
muscular dystrophy, Lesch-Nyhan syndrome, Glucose-6-phosphate
dehydrogenase deficiency, Hemophilia A and B, red-green color blindness,
Menke’s disease).
4.Monogenic hereditary diseases. Antigen associative diseases.
4a. Diseases caused by mutations in genes encoding structural proteins:
Marfan Syndrome, Ehlers-Danlos Syndromes
4b. Diseases Caused by Mutations in Genes Encoding Receptor Proteins or
Channels: Familial Hypercholesterolemia, Cystic Fibrosis;
4c. Diseases Caused by Mutations in Genes Encoding Enzyme Proteins:
phenylketonuria, Galactosemia; Lysosomal Storage Diseases: Tay-Sachs Disease
(GM2 Gangliosidosis: Deficiency in Hexosaminidase β Subunit), Niemann-Pick
Disease Types A, B and C, Gaucher Disease, Mucopolysaccharidoses; Glycogen
Storage Diseases (Glycogenoses): von Gierke disease, Pompe disease, McArdle
disease;
4d. Mitochondrial diseases: Leber hereditary optic neuropathy, MELAS:
mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes),
myoclonic epilepsy with ragged red muscle fibers).
4e. Diseases caused by alterations of imprinted regions: Prader-Willi and
Angelman Syndromes.
5.Systems of anti mutational protection. Mechanisms of DNA reparation.
The role of disorders of reparative systems and “immune control” in an
occurrence of hereditary pathology.
6.Chromosomal diseases. Mechanisms of occurrence of the genome and
chromosomal mutations. Polyploidy, aneuploidy, deletion, duplication,
inversion, translocation.
6a. Cytogenetic disorders involving autosomes: trisomy 21 (Down
Syndrome), 22q11.2 deletion syndrome, trisomy 18 (Edwards syndrome),
trisomy 13 (Patau syndrome);
6b. Cytogenetic disorders involving sex chromosomes: Klinefelter
syndrome, Turner syndrome, “Super-woman” syndrome.
7.Congenital anomalies: polydactyly, cleft lip, cleft palate. Etiology.
Pathogenesis. Perinatal infections (TORCH Toxoplasma (T), rubella virus (R),

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cytomegalovirus (C), herpesvirus (H), and any of a number of other (O)
microbes such as Treponema pallidum).
8.Methods of investigation, prophylaxis, and treatment of hereditary
diseases. Ways of correction of genetic defects. Outlooks of gene engineering.
9.Constitution, its role in pathology. Classification of constitutional types by
Hippocrates, Sigot, Kretchmer, I. P. Pavlov, A. A. Bogomolets. The concept of
diatheses.
6. Students’ practical activities.
Protocol № 2 Date_____________________
Experimental work 1. There is research of sexual chromatin (Bara's
bodies) in the epithelium cells of mucous layer of mouth. The impression
smear (touch smear) prepares from the mucous layer of mouth. The drop of a 1%
solution of acetoorcein on the smear. The drop is covered integumentary glass so
that paint evenly spread on the stroke and air under glass must be absent. A
surplus of paint is taken off by a filtration paper. Study preparation under the
small increase of microscope (lens×20, eyepiece×10). Find the accumulation of
cells and study it under immersion increase (lens×90, eyepiece×10). Interphase
nuclei are counted and mark how many they have contained the Bara's bodies.
Count up 100 cells. For an analysis, it is necessary to take away unharmed cells
with a round or oval nucleus. Sexual chromatin is placed under a nuclear
membrane, has a semilunar or triangle shape. For women – 28% all nuclei of
cells of epitheliums contain sexual chromatin, and for men - 0-1%.
Conclusion:____________________________________________________________
Experimental work 2. To define content of phenylpyruvic acid in urine.
For the exposure of phenylpyruvic acid in urine use the test-paper of type
“Biofan”, which are imbued by buffer solution of chlorous iron. The end of test-
paper is put into urine and through 30 sec. the results. A test is considered
positive if the test-paper becomes a green color.
Conclusion:____________________________________________________________
Test 1. Which of the following characteristics are most typical of
multifactorial inheritance?
A. Sex predilection
B. Mitochondrial inheritance
C. Recurrence risks reflect the
number of affected relatives

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D. Major cause of miscarriages E. Maternally derived
Test 2. In which variant of karyotype in the nucleus of somatic cells only
one Bar’s body can be found?
A. 47 XX, 15+
B. 45 XO
C. 45 XY
D.47 XY, 21+
E. 48 XXXY
Test 3. At examining of a patient-doctor stressed attention to her low
growth, wide shieldlike, insufficient physical and sexual development.
External genitalia formed on a feminine type, internal was underdeveloped.
Barr body in cells of mouth mucous membrane was not determined. For
what disease is it typical?
A. Klinefelter’s syndrome
B. Turner’s syndrome
C. Х-trisomy syndrome
D. Down’s illness
Е. Pathau’s syndrome
Test 4. Which of the following is most likely in an untreated child with
phenylketonuria (PKU)?
A. Elevated tyrosine
B. Increased skin pigmentation
C. Normal phenylalanine
hydroxylase levels
D. Elevated alanine
E. Decreased skin pigmentation
Test 5. The boy was born by woman 45 years with fission of the upper
lip ("cleft lip" and "cleft palate"). Significant breaches are discovered.
Under additional examination on the part of nervous, cardiovascular
systems and visions. At study, Karyotype is diagnosed trisomy on 13
chromosomes. What syndrome exists beside boy?
A. Klinefelter
B. Edwards
C. Turner
D. Patau
E. Down
Practice examination type 2. Give answers to the questions of the
picture and real-life task:
A young woman is referred for genetic counseling. She has a 3-year-old boy
with developmental delay and small joint hyperextensibility. The pediatrician has
diagnosed fragile X-associated mental retardation. She is currently pregnant with
her second child at 14 weeks of gestation. The family history is unremarkable.
1. What is the genetic mutation responsible for fragile X-associated mental
retardation? How does it cause the clinical syndrome of developmental delay,
joint hyperextensibility, large testes, and facial abnormalities?
2. Which parent is the probable carrier of the genetic mutation? Explain
why this parent and the grandparents are phenotypically unaffected.
3. What is the likelihood that the unborn child will be affected?
Answer for the task: ____________________________________________
______________________________________________________________________
______________________________________________________________________

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______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Picture. Inpute in the empty spaces apropriate sypmtoms or fitures.

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For each statement write T (true) or F (false) in the blank provided
№ Statement T F
1 Hypertension is a multifactorial disease.
2 Fat intake is a risk factor for many diseases.
3
A multifactorial trait is expressed when multiple genes and
environmental influences blend together.
4
In Down’s syndrome, the pathology is manifested
independently of an environment.
5
It is easy to distinguish between the effects of shared
environmental factors and the effects of common pool genes.
6 Psychiatric disorders do not manifest familial patterns.
7 Relative risk is a ratio between incidence and individuals.
8
Early type II diabetes may develop when an individual’s diet
changes to heavy carbohydrate consumption.
9
Finding and understanding environmental factors that affect
penetrance of specific genes is important if chronic familial
diseases are to be prevented.
10
A variation in the phenotype for different genotypes caused by
the environmental factors is a threshold liability trait.
11
The frequency of genetic disease in the population depends on
phenotypes.
12
Risk factors, when removed or eliminated, delay or prevent
disease.
13 A proband is the individual beginning the pedigree.
14
The recurrence risk is less when more than one sibling is
affected.
15
The existence of a particular risk factor indicates an individual
will develop a specific disease.
16
The expression of a disease may require both an inherited
defect and environmental exposure.
17
Multifactorial diseases can change substantially from one
population to another because gene frequencies and
environments differ.
18 Dizygotic twins are identical.
19
Recurrence risk is higher if the disease is more severe in the
proband.
20
The prevalence rate is the number of individuals affected by a
disease.
21
The incidence rate is the number of persons who have died
from the disease.

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Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th international ed./ V.Kumar, A.K.Abbas, J.C.Aster –
2015. – Chapters 5, 10. – P. 137-182, 451–480.
2. Robbins and Cotran Pathologic Basis of Disease 9thed./ Kumar, Abbas, Fauto. – 2013.–Ch6.–P. 215–268.
3. General and clinical pathophysiology. Ed. by prof. A.V. Kubyskin. Simferopol. – 2011. – P. 86–104.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C.Copstead, J.L.Banasic//Else.Inc.–2010.–P.86–127.
5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins),
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapters 3-4– P. 36 – 62.
6. Symeonova N.K. Pathophysiology. – N.K. Symeonova. Kyiv, AUS M-ne Publishing. – 2010. – P. 44–65.
7. Pathophysiology, Concepts of Altered Health States, C.M.Porth, G. Matfin.– NY,M. –2009.–P.133–156.
Additional:
8. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for
medical students and practitioners. Edited by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 49–60.
9. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.St. NY. – 2000. – P. 2–9.
10. J.B.Walter I.C.Talbot General pathology. Seventh edition. – 1996. – P. 59–87.
Topic 3. Pathology of reactivity. Disorders of immune reactivity. AIDS.
1. The actuality of the theme. Reactivity is the characteristic of the
organism to react in a certain way on the influence of the environment. It is the
same as growing up, feeding, and metabolism.
Any pathological process in one or another degree changes the reactivity of
the organism and in the time the changing reactivity which exceeds physiological
of the organism can become a main development of the disease.
2. Duration of the class – 1h 30min.
3. Aim: to know types of reactivity.
To be able: to analyze the specific and non-specific reactivity.
To perform practical work: Resistance. Types. Interaction with reactivity.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
4. immunology
Structure of the blood-brain barrier and others
hystohaematic barriers.
Physiological reactivity indexes.
Structure of central nervous system, eye, thyroid
gland, internal ear, and testis.
5. The advice for students . Properties of Human Immunoglobulins
Class
Ig
Content
in blood
serum
mg/L
% of
total
Ig
level
Mole-
cular
mass
kD
Fixatio
n of
comple-
ment
Trans-
ference
hrough
the
placent
Function
IgG
gen.
8-16 80 150 ++ +
Secondary immune response,
protection from bacteria and
viruses displays antiviral,IgG1 65 150 ++ +

18
1.Definition of the concept of reactivity. Reactivity as a condition of disease
development. Types of reactivity.
2.Dependence of reactivity on sex, age, heredity, condition of immune,
nervous and endocrine systems. Influence of environment on the reactivity of
organism. Manifestations of reactivity on a molecular, cellular, tissue, organ,
system level and on the level of the whole organism.
3.Reactivity by Bogomolets. Explain term “physiological system of
connecting tissue” and name elements of this system by Bogomoletz. What is a
role of this system in the maintenance of organisms’ homeostasis?
4.The theory of Hans’a Seley of diseases of adaptation.
5.Reactivity and biological barriers.
6.Definition of the concept of resistance. Passive and active resistance. The
connection of resistance with reactivity.
IgG2 23 150 + + antitoxin, and antibacterial
properties; only Ig that
crosses the placenta;
responsible for protection of
newborn; activates
complement and binds to
macrophages
IgG3 8 150 +++ +
IgG4 4 150 - +
IgM 0.5-2 6 900 +++ - Primary immune response
Forms the natural antibodies
such as those for ABO blood
antigens; prominent in early
immune responses; activates
complement
IgA
plasm.
1.4-1.9 13 160 - - Predominant Ig in
bodysecretions,
such as saliva,
nasal and
respiratory
secretions, and
breast milk;
protects mucous
membranes
IgA
secr.
2-5 380 - -
Mucous
membrane
protection
IgD 0-0.4 0-1 180 - -
Membrane receptors found
on B lymphocytes; needed
for maturation of B cells
IgE
14-450
ng/ml
0.002 190 - -
Reagines, protection from
parasites.
Binds to mast cells and
basophils; involved in
parasitic infections, allergic
and hypersensitivity
reactions.

19
7.Mechanisms of nonspecific resistance. Biological barriers, their
classification, significance for a resistance of organism.
8.Humoral factors of nonspecific resistance of an organism to infectious
agents (lysozyme, C-reactive protein, interferons).
9.Complement system and its disorders.
10.Phagocytosis, its mechanisms. Disorders of phagocytosis: causes,
mechanisms, consequences. Chediak-Higashi syndrome.
11.Mechanisms of the normal immune response of a humoral and cellular
type, their disorders. Role of lymphocytes, macrophages, eosinophils,
neutrophils. Major Histocompatibility Complex Molecules: The peptide display
system of adaptive immunity.
12.Immunologic tolerance: central and peripheral.
13.Immunodeficiency, a definition of the concept, classification (WHO).
Bruton’s X-linked agammaglobulinemia, Common variable immunodeficiency,
Ig A deficiency, X-linked hyper-IgM Syndrome, DiGeorge’s syndrome, Severe
Combined Immunodeficiency, agammaglobulinemia (Swiss type), Wiscott-
Aldrich syndrome.
14.Pathogenesis of the main clinical manifestations of isolated and combined
disorders of functions of T- and B-lymphocytes. Causes, mechanisms of
development and types of initial immunodeficiencies. The role of physical,
chemical and biological factors in the development of secondary
immunodeficiencies (clinical examples).
15. Pathophysiological characteristics of the acquired immunodeficiency
syndrome (AIDS).
Protocol № 3 Date_____________________
Experimental work 1. To learn the violations of barriers function and
adaptations of an organism in the conditions of a convulsive attack. A test it
is carried out on two mise or young rats. On employment 1% solution of trypan
blue subcutaneously in animals, from a calculation 2 ml on 100 gr of mass. In 30
min 0,3 ml enter intraperitoneal camphorated oil to one of the animals. This
animal is placed under a glass hubcap and mark time of offensive of cramps,
their character and time of death. Animals are killed and studied organs, a
substance of brain and liquid eye.
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________

20
Experimental work 2. An action of decreased atmospheric pressure
upon organism of a rat (experiment). Place animal under a glass bell. Acquaint
with a condition of the animal before experiment beginning (behavior, skin
color, breathing rate, a reaction to sound irritant). By the medium of pump
gradually diminish pressure under the bell. Observe change of animal condition.
Clock each supervision. After the beginning of first cramps in animal gradually
let air in and observes renewal of organism functions. Write down the
experiment results in the table and protocol of experiment according to the
scheme:
Animal
Beginning
of
experiment
Behavior
Breath
rate
Color of
visible
cutaneous
covering
Time of
offensive of
cramps
1.Adult
2.New
born
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Test 1. The deficient content of immunoglobulins was revealed in a
patient. What cells of immune system produce immunoglobulins?
A. Plasma cells
B. T-killers
C. B-lymphocytes
D. T-helpers
E. NK-killers
Test 2. The gene coding for HLA antigen is present on:
A. 6 q
B. 6 p
C. 16 p
D. 16 q
E. 21 p
Test 3. The complement component with opsonin activity is:
А. C1
В. С3а
C. C3b
D. С5а
Test 4. Various cells of the oral mucous membrane and antimicrobial
substances synthesized by these cells play an important part in the local
immunity of the oral cavity. Specify the key factors for the local immunity:
A. Eosinophils
B. B-lymphocytes

21
C. IgG
D. Macrophages
E. Secretory IgA
Test 5. Which cytokine promotes the proliferation of T and B
lymphocytes?
A. IFN-γ (interferon γ)
B. IL-2 (interleukin 2)
C. IL-4 (interleukin 4)
D. TNF-α (tumor necrosis factor α)
E.TGF-β (transforming growth
factor β)
Test 6. The immunoblot detected gp120 protein in the blood serum. This
protein is typical for the following disease:
A. Virus B hepatitis
B. HIV-infection
C. Tuberculosis
D. Syphilis
E. Poliomyelitis
Test 7. Blood analysis of a patient showed signs of HIV infection
(human immunodeficiency virus). Which cells does HIV-virus primarily?
A. Specialized nervous cells (neurons)
B. Mast cells
C. Cells that contain receptor IgM (B-lymphocytes)
D. Proliferating cells (stem hematoplastic cells)
E. Cells that contain receptor T4 (T-helpers)
Test 8. A pregnant woman was detected to have IgM to rubella virus.
An obstetriciangynecologist recommended therapeutic abortion due to the
high risk of teratogenic affection of the fetus. Detection of IgM was of great
importance as it is these specific immunoglobulins that:
A. Indicate recent infection
B. Penetrate placental barrier
C. Have the largest molecular weight
D. Are associated with anaphylactic reactions
E. Are the main factor of antiviral protection
Test 9. A 5-year-old child is diagnosed with Bruton syndrome (X-linked
agammaglobulinemia) that manifests itself in severe clinical course of
bacterial infections and absence of B lymphocytes and plasma cells. What
changes of immunoglobulin content can be observed in blood serum of the
child with immunodeficiency?
A. Increased IgA, IgM
B. Decreased IgA, IgM
C. Decreased IgD, IgE
D. Increased IgD, IgE
E. No changes
Test 10. A 13-year-old boy presents with eczematous rashes on his shins
and torso. Anamnesis states cases of otitis, pneumonia, and furuncles in the
patient. Blood test: platelets - 70 · 109
/l, low activity of T helper and T

22
suppressor cells, low IgM, with normal IgA and IgG. What immunodeficient
disease does this boy have?
A. DiGeorge syndrome
B. Louis-Bar syndrome (Ataxiatelangiectasia)
C. Severe combined immunodeficiency (Swiss type)
D. Wiskott-Aldrich syndrome
E. Chediak-Higashi syndrome
Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. An 18-year-old man presents with complaints of fever, facial pain,
and nasal congestion consistent with a diagnosis of acute sinusitis. His medical
history is notable for multiple sinus infections, two episodes of pneumonia, and
chronic diarrhea, all suggestive of primary immunodeficiency syndrome.
Workup establishes a diagnosis of common variable immunodeficiency.
1.What are the common infectious manifestations of common variable
immunodeficiency? 2. What are the underlying immunologic abnormalities
responsible for these infectious manifestations? 3. What other diseases is
this patient at increased risk for? 4. What treatment is indicated?
Answerfor the task 1: ___________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Task 2. The patient was hospitalized with complaints on cough, rise of
temperature up to 38-39 C, weakness, and headache. Illness was related to
super cooling. Pneumonia was diagnosed after clinical research.
1. What was a direct cause of the disease? 2. What role in disease beginning
did cooling play? 3. What reactivity mechanisms did lead to organism resistance
reduce? 4. What are your recommendations for organism resistance rising to
catarrhal diseases?
Answer for the task 2: ___________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th international edition./ V.Kumar, A.K.Abbas,

23
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. Simferopol. – 2011. – P. 209–233.
4. Pathophysiology, Concepts of Altered Health States, C.M.Porth, G.Matfin.– NY. – 2009. – P. 400–427.
5. Symeonova N.K. Pathophysiology. – N.K. Symeonova. Kyiv, AUS M-ne Publ. – 2010. – P. 65–84.
2010. – P. 203–221, 263–286.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Ch.7-8, 10. – P. 121 – 149, 178–189.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – 2007. – Chapter 5.
– P. 108–118, 152–165.
2. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.. NY. – 2000. – P. 42–47.
medical students and practitioners. Ed. by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 42–48.
Topic 4. Immediate types of hypersensitivity reactions.
1. The 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.
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)
2. 4. Basic level.
The name of the previous and future
disciplines
1. Histology
2. Biochemistry
3. Physiology
4. Immunology
5. Anaestesiology
Structure and function of organs and vessels.
Immunity and its mechanisms. Antigens and
antibodies, their structure and function.
Sensitizing.
5. The advice for students .
Classificaton 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

24
amines and other mediators from
basophils and mast cells.
2. Cytotoxic type Autoimmune hemolytic
anemia, erythroblastosis feta-
lis, cytotoxic reactions the
action of large doses ofBogo-
mglets’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 neutrophills
→ release of lysosomal enzymes
4. Cell – mediated
(delayer)
hypersensivity
Tuberculosis, contact
dermatitis, transplant
rejection
Sensitized thymus-derived
T-lymphocytes → release of
lymphokines 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 Cumbs and Gell. Stages of 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 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 pathogenesis of immune
complexes. Immune complex damages, their local and general manifestations.
Examples of diseases: Systemic lupus erythematosus, rheumatoid arthritis,

25
poststreptococcal glomerulonephritis, serum sickness, Arthus reaction, Sjögren
syndrome.
Protocol № 4 Date_____________________
Experimental work. 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».
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: ____________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________

26
Test 1. Anaphylactic shock developed in a patient with botulism after
second injection of antitoxic antibotulinus serum mixture. What is the main
mechanism of anaphylaxis?
A. Interaction of T-lymphocytes with mediators
B. Interaction of antigen with IgM
C. Interaction of macrophages with antigens
D. Interaction of antigen with IgE
E. Interaction of T-lymphocytes with tissue basophils
Test 2. In the 1960s, it was quickly ascertained that Peace Corpus
workers sent to schistosome-endemic areas were exposed to massive initial
doses of cercariae before any protective immunity existed. In these
individuals, IgG antibodies developed in response to the developing worms,
and when the adults began their prodigious release of eggs into the
circulation, the patients suffered acute and potentially life-threatening
symptoms of fever, edema, arthralgia, and rush. Which of the following is
another condition that arises by a similar immunologic mechanism?
A. Atopic allergy
B. Arthus reaction
C. Goodpasture syndrome
D. Tuberculin reaction
E. Transfusion reaction
Test 3. Catarrhal inflammation of bulbar conjunctiva and nose mucous
membrane develop in patient every year in spring and early summer, when
trees and flowers are in blossom. Production of specific antibodies to pollen
underlies this syndrome. What cells activate and develop exocytosis in this
syndrome?
A. Neutrophils
B. Macrophages
C. Lymphocytes
D. Mast cells
E. Throbocytes
Test 4. It is known that bronchial asthma develops by mechanism of
immediate hypersensitivity, which includes 3 sequential stages:
A. Immunological, pathochemical, pathophisiological
B. Pathochemical, pathophisiological, immunological
C. Pathochemical, immunological, pathophisiological
D. Pathophisiological, immunological, pathochemical
E. Pathophisiological, pathochemical, immunological
Test 5. Man with the caries is subjected to constant sensitization by
streptococcus antigen. What disease can appear due to this etiological
factor?
A. Glomerulonephritis
B. Pancreatitis
C. Myocarditis
D. Pulpits
E. Periodontitis

Test 6. A child with diphtheria 10 days after injection of antitoxic
antidiphtherial serum has developed skin rash, accompanied by severe itch,
rising temperature up to 380C and joints pain. What is the cause of these
symptoms?
A. Delayed type of hypersensitivity
B. Anaphylactic reaction
C. Contact allergy
D. Atopia
E. Serum sickness
Practice examination type 2. Give answer to the questions of the real-life
task: 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?
Answerfor the task______________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Practice examination type 3. Put number of these illustrations (1 to 6) in
the correct order as to how anaphylaxis develops with brief explanation of
each step.

28
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./Kumar, Abbas, Fauto.–2013.– Ch.4.–P.109–117.
2. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simfer. – 2011. – P. 233–257.
2010. – P. 222–241.
Milwaukee. – 2009. – P. 410–424.
5. Symeonova N.K. Pathophysiology. – N.K. Symeonova. Kyiv, AUS medicine Publ. – 2010.–P.87–100.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8thed./Kumar, Abbas, Fauto. –2007.–Ch.7.–P.119–152.
medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 96–104.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 10. – P. 168 – 177.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart. New York. –
2000. – P. 52–59.
Topic 5: Reactions of hypersensitivity of a delayed type.
Autoimune diseases. Transplantology.
1. The actuality of the theme. The human immune network is a
multifaceted defense system that has evolved to protect against invading
microorganisms, prevent the proliferation of cancer cells, and mediate the
healing of damaged tissue. Under normal conditions, the immune response deters
or prevents disease. However, occasionally the inadequate, inappropriate, or
misdirected activation of the immune system can lead to debilitating or life-
threatening illnesses, typified by allergic or hypersensitivity reactions,
transplantation immunopathology, autoimmune disorders, and
immunodeficiency states. Preventing and treatment of the allergy reactions is
based on knowledge about their development mechanisms.
3. Aim:
To know that allergy is a complex of breaches, appearing in our organism by
the cellular immunological reactions. Both inflammation and allergy is protective
response on the exo- and endogenous factor.
To be able:
1) determine the leading link of the cellular immune reactions pathogenesis
and cause-effect relations of separate pathogenetic mechanisms;
2) draw a conclusion about the character of pathological changes during
cellular immune reactions in organism and possible mechanisms of their
development on the ground of functional and biochemical investigation data.
To perform practical work: to analyse the mechanisms of cellular
immunologycally mediated disorders by Coombs and Gell (1968) and explain
stimulating allergic reactions by Roight.

29
By Roight – stimulating allergic reactions. Via BAS, hormones, mediators
the cells, containing Ag, begin to function intensively under the influence of Ab.
Than cells are secreted hormones or mediators. Ex. Collagen diseases,
connective tissue diseases, rheumatoid arthritis and other.
4. Basic level.
The name of the previous
and future disciplines
1. histology
2. biochemistry
3. physiology
4. immunology
Structure and function of organs and vessels. Influence
of BAS on vessel wall. Cellular Immunity and its
mechanisms. Antigens and antibodies, their structure and
function.
1. Reactions of hypersensitivity of a delayed type: experimental modeling,
main clinical forms. Features of immune mechanisms. The role of lymphokines.
2. Autoallergic diseases. Causes and mechanisms of their development. The
role of autoallergic component in pathogenesis of diseases.
3. Pseudoallergic reactions.
4. The main principles of prophylaxis and treatment of allergic reactions.
Desensibilization.
5. The experimental modeling of pathology of the immune system.
6. Pathophysiological bases of transplantation of organs and tissues.
7. Immune tolerance, its types. Methods of experimental modeling of
immune tolerance.
8. Mechanisms of development of immune tolerance and their disorders.
9. Immune interrelations in system “mother-fetus”.
10.“Graft versus host” reaction, conditions of its development, acute and
chronic forms.
11.“Host versus graft” reaction, conditions of its development, acute and
chronic forms.
12.The main principles of immune stimulation and immune suppression.
13.V types of allergic reactions.
Protocol № 5 Date_____________________
Experiment 1. 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

30
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.
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: ____________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Test 1. Allergic diagnostic tests are used for the diagnosis of many
infectious diseases (tuberculosis, brucelosis, tularemia etc). Diagnosis is
confirmed if papula and redness appear in the place of the allergen
injection. Antigens interaction reaction is conditioned by:
A. IgE and lymphokines
B. IgM and macrophages
C. T-lymphocytes and
lymphokines
D. IgE and T-lymphocytes
E. IgM and tissue basophiles
Test 2. Thyrotoxicosis was diagnosed in a patient. Antithyroid
antibodies were found in his blood. Which type of allergic reaction is
observed at development of this disease?
A. Immune complex-mediated
B. Stimulating
C. Anaphylactic
D. Cytotoxic
E. Delayed type hypersensitivity
Test 3. 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. Complement mediated lysis of infected cell
D. T helper 1 delayed type hypersensitivity response
E. Eosinophilia
Test 4. Hyperergic inflammation form of upper respiratory tract
(larynx, trachea, bronchi) develops at a 6-year-old child. Threat of the
respiratory impairment develops and then necessity of using anti-

31
inflammatory hormones occurs. Which hormone has anti-inflammatory
property?
A. Cortisol
B. Adrenaline
C. Growth hormone
D. Testosterone
E. Insulin
Test 5. An alloimmune disorder is:
A. Graft rejection
B. Insulin-dependent diabetes
C. Myxedema
D. All of the above are correct
E. None of the above is correct.
life tasks:
Task 1. 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?
Answerfor the task 1_____________________________________________________
______________________________________________________________________________________
__________________________________________________________________________
Task 2. Skin allotransplant 6 dm2 was engrafted to of rats. Rejection
occurred during first 14 days. 30 days after rejection of allotransplant the same
donor’s skin were engrafted to same animals. What will be life duration of
transplants after repeated engrafting? Explain, why?
__________________________________________________________________________
__________________________________________________________________________
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?
__________________________________________________________________________
__________________________________________________________________________
Practice examination type 3: Rebus riddle. Solve the riddle to learn a
characteristic of a skin disorder.

32
__________________________________________________________________________
__________________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./Kumar, Abbas, Fauto.–2013.–Ch.4.–P.122–139.
2. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simf. – 2011. – P. 233–249.
3. Symeonova N.K. Pathophysiology. – N.K. Symeonova. Kyiv, AUS medicine Publ. – 2010.–P.95-100.
2010. – P. 222–241.
Milwaukee. – 2009. – P. 416–424.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease8thed./Kumar, Abbas, Fauto.–2007–Ch.7.–P.119–131.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapters 10– P. 168 – 172.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. NY. – 2000. – P. 52–55.
Topic 6. Cell injury. General mechanisms of cell damage.
1. The actuality of the theme. Cellular injury can be caused by any factor
that disrupts cellular structures or deprives the cell of oxygen and nutrients
required for survival. The injury may be reversible (sublethal) or irreversible
(lethal) and is classified broadly as chemical, hypoxia (lack of sufficient
oxygen), free radical, or infectious. Cellular injuries from various causes have
different clinical and pathophysiologic manifestations.

33
Cellular death is confirmed by structural changes seen when cells are stained
and examined under a microscope. No biochemical indicators of cellular death
are universally applicable because we still do not know precisely what
biochemical functions must be compromised before a cell dies.2. Duration of
the class – 1h 30min.
3. Aim: to know the cell responses to injury and the major types of cellular
necrosis.
To be able: to analyze the main molecular mechanism of cell membrane
damage, cellular adaptations occurring in atrophy, hypertrophy, hyperplasia,
dysplasia, metaplasia and two pathways of apoptosis.
To perform practical work: describe the cell responses on injury and
mechanisms of apoptosis.
4. Basic level.
1. histology
2. biochemistry
3. physiology
4. pathomorphology
5. surgery
Types and sources of radial energy. Properties of ionizing rays.
Use of X-rays and radioactive elements in popular equipment
and medicine. Main measures safety due to deal with X rays
and radioactive particles. Ecological catastrophes with
radioactive environment pollution. Blood cells and methods of
their count. A bioelectrical activity of central nervous system
and its registration. Fluid mosaic model of the plasma
membrane. Cell populations and cycle landmarks. Lipid
peroxidation. Erythrocytes in hypertonic, isotonic, and
hypotonic solutions.
1. The advice for students.
Structural-functional organization of a cell:
The nucleus contains genetic material of a cell.
The membrane provides the integrity of cell structures.
Lysosomes contain a wide spectrum of hydrolytic enzymes.
Mitochondria provide energy needs of a cell by synthesis of ATP.
Ribosomes carry out protein synthesis.
The endoplasmic reticulum is a membranous structure containing
ribosomes and detoxic enzymes.
Golgi complex accumulates and distributes proteins necessary for
construction of various structural elements of a cell.
Homeostasis is the concept of a dynamic steady state, turnover of bodily
substances that maintain physiologic parameters within narrow limits. Stressors
cause reactions that alter this dynamic steady state or homeostasis. Deviations
from normal values, or homeostasis, cause disease.
Necrosis is local cell death and involves the process of cellular self-digestion
known as autodigestion or autolysis. As necrosis progresses, most organelles are
disrupted and karyolysis, nuclear dissolution from the action of hydrolytic

34
enzymes, becomes evident. There are four major types of necrosis: coagulative,
liquefactive, caseous, and fat. Gangrenous necrosis is not a distinctive type of
cell death but refers to large areas of tissue death.
The two pathways of apoptosis differ in their induction and regulation, and
both culminate in the activation of "executioner" caspases. The induction of
apoptosis is dependent on a balance between pro- and anti-apoptotic signals and
intracellular proteins. The figure shows the pathways that induce apoptotic cell
death, and the anti-apoptotic proteins that inhibit mitochondrial leakiness and
cytochrome c-dependent caspase activation and thus function as regulators of
mitochondrial apoptosis.
1. Cellular injury. Characteristics of the concept of “injury”. Principles of
classification of cell injuries.
2. Pathology of signalization. Pathology of signal reception. Disorders of
secondary messеngers.
3. Damage to an executive apparatus of a cell. Pathochemical consequences
of damage to a cellular nucleus. Proteins of thermal shock, antioncogenes,
immediate genes of pre-early reaction.
4. Mechanisms and manifestations of damage to subcellular structures:
plasmatic membrane, mitochondria, endoplasmatic reticulum, lysosomes,
microtubules and microfilaments, nucleus and cytoplasm.
5. Cellular adaptation to stress. Hypertrophy, hyperplasia, atrophy,
metaplasia. Cellular and subcellular regeneration.
6. Molecular mechanisms of cell injury. The role of lipid mechanisms in the
pathogenesis of alteration: lipid peroxidation, activation of membrane
phospholipids and free fatty acids. Ischemia-reperfusion injury ischemia-
reperfusion injury.
7. Causes, mechanisms, and consequences of intracellular calcium
concentration increase.
8. Role of electrolyte-osmotic mechanisms in cell injury. Causes,
mechanisms, and consequences of disorders of electrolyte transport system in
cells.
9. Causes and development of intracellular acidosis in cell injury.
10.Mechanisms of protection and adaptation of cell. Protective and
compensative reactions for the renovation of intracellular homeostasis.
11. Antioxidant mechanisms of cells.
12. Mechanisms of apoptosis. The mitochondrial (intrinsic) pathway of
apoptosis, the death receptor (extrinsic) pathway of apoptosis, activation, and
function of caspases. Autophagy.
13. Necrosis: coagulative, liquefactive, gangrenous, gangrenous, caseous,
fat, fibrinoid.
14. Principles of prevention and pathogenetic therapy of cell injury.

35
7. Students’ practical activities
Protocol № 6 Date_____________________
Experiment work. To learn the damage of tissues basophile in rat under
effect with adrenalin. In the abdominal region of rat enter 5 ml of hemocoel. An
animal is killed by ether; good massage a stomach, dissect the abdominal region
and collect a liquid in the test-tube. To the got liquid add 0.1% alcoholic solution
of neutral red (from the calculation of 0.2 ml paint on 1 ml liquids). Carefully
mix and make strokes in which study the initial state of tissue basophile (lens
90, eyepiece10). A liquid which remained is poured out for 1 ml in 2 test
tubes: in the first (control) add 0.2 ml of physiological solution, in the second –
0.2 ml (20 μkg) adrenalin.
Conclusion:____________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
Practice examination type 1: Choose the correct answer:
Test 1. Activation of universal membrane structure injuring mechanism
occurs during reperfusion syndrome. This mechanism is referred to as:
A. Beta-oxidation of lipids
B. Oxidation of cytochromes
C. Microsomal oxidation
D. Knoop-Lienen cycle
E. Peroxidation of lipids
Test 2. Which ions accumulation in the cytoplasm of muscular cells
accounts for stable constriction of myofibrils?
A. Calcium
B. Sodium
C. Potassium
D. Magnesium
E. Hydrogen
Test 3. Which of the following cellular injury is reversible?
A. Hyaline deposits in Liver
B. Dystrophic calcification in
tissue
C. Coagulative necrosis
D. Cloudy swelling
E. All of the above
Test 4. In the process of metabolism in the human organism, the active
forms of oxygen are formed, including superoxide anion radical. With the
aid of which ferments this anion is inactivated?
A. Glucose reductase
B. Glucose peroxidase
C. Super oxide dimutase
D. Catalase
E. Peroxidase
Test 5. Apoptosis is inhibited by:

A. bcl-2
B. p53
С. ras
D. c-myc
E. p21
task. The nurse in the Emergency Department is caring for a client who has
acute heart failure. The physician is writing orders for pharmacological
management, including diuretics. Which laboratory value is most important for
the nurse to check before administering medications to treat heart failure?
A. Platelet count.
B. Potassium.
C. Calcium.
D. White blood cell count.
Answerfor the task:_____________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./ Kumar, Abbas, Fauto. – 2013. –Ch.1.–P.1–28.
2. General and clinical pathophysiology / Ed. by A.V. Kubyshkin – V: NK Publ. – 2011. – P. 134–165.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc,
4th ed. – 2010. – P. 30–84.
4. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– NY,
Milwaukee. – 2009. – P. 99–109.
5. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Copyright В. –
Lippincott Williams & Wilkins – 2008. – Chapter 1. – P. 3–35.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8th ed./Kumar, Abbas, Fauto.–2007.–Chap.1–P. 1–30
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Сhapters 1-2. – P. 1–14, 28–35.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. NY. – 2000. – P. 2–13.
Topic 7: Pathophysiology of the micro- and macrocirculation.
1. The actuality of the theme. Blood vessels function in the delivery of
oxygen and nutrients to the tissues and in the removal of waste products from the
tissues. Unlike disorders of the respiratory system or central circulation that
cause hypoxia and impair oxygenation of tissues throughout the body, the effects
of blood vessel disease usually are limited to local tissues supplied by a
particular vessel or group of vessels.
Disturbances in blood flow can result from pathologic changes in the vessel
wall (i.e., atherosclerosis, vasculitides), acute vessel obstruction caused by
thrombus or embolus, vasospasm (i.e., Raynaud’s phenomenon), abnormal
vessel dilation (i.e., arterial aneurysms or varicose veins), or compression of

37
blood vessels by extravascular forces (i.e., tumors, edema, or firm surfaces such
as those associated with pressure ulcers).
2. Duration of the class – 1 hour 30 min.
3. Aim:
To know the basic factors of clot formation as the Virchow’s triad:
1. Injury to a vessel’s wall (by mechanic factors, electric current, chemical,
biological factors). These abnormalities also accompany atherosclerosis,
hypertension, and allergic process.
2. Disturbance of the balance between coagulation and fibrinolytic systems.
3. Slowing of blood flow and its abnormalities. It explains why thrombosis
of veins occurs 5 times more often than one of the arteries.
To be able: to study typical disorders of microcirculation, their significance,
and possible consequences.
To perform practical work: to analyze the pathogenesis of sludge
formation.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
4. surgery
Structure of vascular stream. Vessels, which form the
microcirculation stream. Structure and functions of
endothelial cells, basal membrane. Two types of nitric
oxide (NO) synthesis in endothelium and macrophages.
The coagulation cascade. The- central roles of thrombin in
hemostasis and cellular activation. The central roles of
thrombin in hemostasis and cellular activation.
Dynamics of Transcapillar Fluid Exchange (by Starling and Gayton)
Active powers
Arterial end of
capillary
mm Hg
Equilibrium point
mm Hg
Venous end of
capillary
mm Hg
Pressing out
Capillary hydrostatic
pressure
30.0 17.0 10.0
Attractive tissue pressure 5.3 5.3 5.3
Interstitial oncotic pressure 6.0 6.0 6.0
Total 41.3 28.3 21.3
Retentive
Oncotic pressure of plasma 28.0 28.0 28.0
Resulting In tissue 13.3 In tissue 0.3 In vessel 6.7
1.Definition of the concept of arterial hyperemia, etiology, and pathogenesis,
classification. External symptoms of arterial hyperemia.
2.Changes in tissues caused by arterial hyperemia, their significance, and
possible consequences.

38
3.Etiology and pathogenesis of venous hyperemia (congestion), etiology and
pathogenesis, external symptoms of venous hyperemia.
4.Changes in tissues caused by venous hyperemia, their significance, and
possible consequences.
5.Definition of the concept of ischemia. Etiology, pathogenesis of ischemia.
Changes in tissues at ischemia, their significance. Consequences and outcomes
of ischemia. External symptoms of ischemia.
6.The concept of reperfusion syndrome, ischemic toxicosis.
7.Definition of stasis. Etiology. Pathogenesis. Capillary (true) stasis.
8.Thrombosis as a reason for peripheral circulation disorder. Etiology and
pathogenesis.
9.Embolism as a reason for local circulation disorder. Stages and mechanisms
of embolism, types of emboli. The role of reflex mechanisms in the development
of common disorders caused by an embolism.
10. Embolism of systemic and pulmonary circulation; embolism of the portal
vein.
11. Typical disorders of microcirculation. Intravascular disorders of
microcirculation: changes of fluidity and rheological properties of blood.
12. Hemoconcentration, disturbances of suspension stability, aggregation and
agglutination of erythrocytes, sludge-phenomenon.
13. The role of aggregation of thrombocytes and disseminated intravascular
coagulation in development of microcirculation disorders (DIC-syndrome).
14. Disorders of tone, mechanical safety, and permeability of microvessels.
15. Extracellular disorders of microcirculation. Accumulation of
physiologically active substances, ions, edematous fluid in perivascular space.
16. Mesenchymal dystrophy. Capillarotrophic insufficiency.
17. Typical disorders of lymphodynamics: mechanical, dynamical and
resorption insufficiency of lymph circulation.
Protocol № 7 Date_____________________
Experimental work 1. Venous hyperemia and venous stasis of the hand
(experiment). Measure up the arterial pressure. Fill the cuff with air so that
pressure in it becomes equal to diastolic pressure. Thus arterial blood float will
supply active, and venous outflow will decrease. Venous hyperemia will arise. 2
min after it is necessary to pay attention to visible symptoms and complaints due
caused by venous hyperemia. Then increase pressure in the cuff up to average
mean between systolic and diastolic. Venous stasis will arise. Arterial blood
inflow preserves but venous outflow stops. Ask the examined person about his
complaints, study skin color, skin temperature and sensitiveness, the condition of

39
superficial veins. Let the air out from the cuff. Note the results of examining in
the table and do protocol by a standard scheme.
Indexes Venous hyperemia Venous stasis
Complaints of the examined
Skin colour
Skin temperature
Skin sensitiveness
Condition of superficial veins
Conclusion: __________________________________________________________
Experimental work 2. Ischemic stasis and reactive arterial hyperemia of
the hand (experiment). To put a cuff, connected to sphygmomanometer on the
medial third of shoulder. Measure up the arterial pressure. To fill the cuff with
air so that pressure is 10 points higher than systolic pressure. Thus arterial and
venous blood flow stops. Ischemic stasis develops. Ask the examined person
about his complaints, study skin color, skin temperature and sensitiveness, the
condition of superficial veins. Let the air out from the cuff and observe arising
from reactive hyperemia. Note the results of examining in the table and do
protocol by a standard scheme.
Indexes Ischemic stasis Reactive hyperemia
Complaints of the inspected
Skin color
Skin temperature
Skin sensitiveness
Note the results of examining in the table and does protocol by standard
scheme explaining mechanism of every sign arise.
Conclusion: __________________________________________________________
Experimental work 3. Fatty embolism of the frog's tongues vessels
(experiment). Anesthetize the frog. Fix it on the board with the back down. Cut
its chest and open the heart. Put a cotton ball moistened with the solution of
Ringer on the heart. Take out the frog's tongue and straighten it upon the opening
in the board, watch the circulation of the vessels under the microscope. Carefully
inject 0,5-1,0 ml of fat emulsion into the ventricle of the heart. Continue to

40
observe the circulation in the vessels of the tongue. Draw the picture you
observed under the microscope. An answer to questions in a discussion:
1. What kind of typical disorders of regional blood circulation is it? 2. What
kind of embolism can be concerned the process which appeared during the
experiment? 3. Can fatty embolism of the brain appear when big tubular bones
are broken?
Conclusion: __________________________________________________________
8. Practice Examination
Test 1. Upper neck node of a sympathetic trunk was removed from the
rabbit on an experiment. Reddening and increased temperature of the skin
of the head are observed. What form of peripheral circulation of the blood
developed in the rabbit?
A. Venous hyperemia
B. Stasis
C. Neuroparalytic arterial
hyperemia
D. Metabolic arterial hyperemia
E. Neurotonic arterial hyperemia
Test 2. A 54-year-old man was admitted to the hospital with complaints
of pain in the right subcostal region, vomiting with blood. Objectively:
enlarged liver, varicose veins in the stomach and esophagus. Dysfunction of
what vessel is likely to be?
A. Vena hepatica
B. Vena cava superior
C. Vena cava inferior
D. Vena porta
E. Aorta abdominalis
Test 3. What are the mechanisms of aggregate formation?
A. Vascular wall damage.
B. Blood flow impairment.
C. Changes in protein composition of blood.
D. Quantitative and qualitative corpuscles.
E. All the above-mentioned factors.
Test 4. What does the term “sludge” mean?
A. Penetration of foreign bodies into the blood and their accumulation in it.
B. Formation of a large quantity of immunocomplexes in blood.
C. Accumulation and aggregation of blood cells in the microcirculatory bad.
D. An extreme degree of corpuscle aggregation.
E. Septicemia.
Test 5. After fast surgical removing of coronary artery occlusion in a
patient with ischemic heart disease, secondary injury of myocardium
develop (reperfusion syndrome) characterized by necrobiotic changes in the
focus of previous ischemia. This complication results from:

41
A. Excessive accumulation of calcium ions
B. Deficiency of potassium ions
C. Deficiency of adenosine triphosphate
D. Accumulation of hydrogen ions
E. Deficiency of creatine phosphate
Test 6. A patient has acute pain in his chest, dyspnea, tachycardia,
cyanosis, and decreased BP. Pulmonary infarction was diagnosed in this
patient. Which factor is the most common cause of pulmonary infarction?
A. Congestion in the pulmonary circulation
B. Embolism by thrombus from veins of lower extremities
C. Increase in number of platelets
D. Activation of fibrinolytic system
E. Pneumothorax
Practice examination type 2. Give answers for the real-life tasks (yes/no)
Task 1. Pick out microcirculatory vessels:
Indication y/n Indication y/n
A Large arteries. E Venules.
B Small arteries. F Arteriovenular
anastomoses (shunts).
C Arterioles. G Veins.
D Capillaries. H Aorta
Task 2. Which are the regulating mechanisms of microcirculatory vessels:
A Reflex. C Hemitic.
B Humoral. D Genetic.
Task 3. What is true (T), what is false (F) in the following:
Questions T F
A Intravascular blood clotting (IVBC) can be generalized
(disseminated) and local
B The process of a platelet plug formation could be divided into
two stages: the cellular stage and the plasma stage of
coagulation
C The stage of adherence, aggregation, and agglutination of
platelets and other blood cells is caused by the activating effect
of various aggregation stimulators (thrombin, factor of platelets
aggregation, serotonin, prostaglandins, thromboxane A2 and
others)
D The second stage is characterized with the formation of active
thrombin, which catalyzes transformation of fibrinogen into
fibrin with the formation of a clot
Practice examinationtype 3

42
Task 1. What is true (T), what is false (F) in the folowing functional
changes for arterial hyperemia
Questions T F
A Speeding up of blood flow in microcirculation bed
B Intensifying of metabolism and organ functioning
C Dilatation of small arteries, arterioles, capillaries
D Increasing the number of functioning vessels
E Hypoxia
Task 2. Match the correct answer what is physiological (a) and what is
pathologic (b) arterial hyperemia
Indication a/b Indication a/b
A Infectious rash F Heat hyperemia
B Ultraviolet erythema G Systemic lupus
erythematosus
C Hyperemia of the brain in
mental activity
H Hyperemia of the brain in
meningitis
D Hyperemia of pancreatic
gland and stomach in
digestion
J Hyperemia of skeletal
muscles in hard physical
work
E Typhoid fever K Inflammatory hyperemia
Task 1. Plaster bandage was imposed on the patient with the right humeral
bone fracture. Next day the soft-tissue swelling appeared, extremity became
cyanotic, the temperature of the injured hand skin decreased.
1. What violation of circulation of blood arose up? 2. Explain the
mechanisms of development of the soft-tissue swelling. 3. What is the
mechanism of skin cyanosis?
Answersfor the task 1. _________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 2. Alpinists slowly rose on the slope of a mountain during 6 hours.
With every step, getting up was given all heavier. A general weakness,
palpitation, shortness of breath, syncope, head pain, a decrease in appetite,
meteorism ware marked.
1. What was the direct reason for these disorders at alpinists? 2. How is this
symptom-complex named? 3. Explain the mechanism of violations development.
4. At what height were alpinists on approximately? 5. What value has
tachycardia and tachypnoea in this situation, what are the mechanisms of their
development?

43
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 3. Patient V. was in a surgical clinic with thrombophlebitis of right
lower extremity. After a careless movement the expressed shortness of breath,
pain in a thorax, cyanosis arose up.
1) Are these violations resulted by thrombophlebitis of lower extremity? In
what cases are such consequences of thrombophlebitis possible? What did arise
up at the patient? Is localization of complications at this patient casual? Explain.
2) Is development of complications of thrombophlebitis possible from the side
of other organs - brain, kidney, spleen?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th ed/ Kumar, Abbas, Fauto. –2013.–Ch 3.–P.75–97.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C.Copstead, J.L.Banasic // Elsev.–2010.–P.347–371.
5. Pathophysiology, Concepts of Altered Health States, C.Mattson Porth,G.Matfin.–NY.–2009.–P.462–474.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8th ed./Kumar, Abbas, Fauto. –2007.–Ch.4.–P. 81–100.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapters 15. – P. 263 – 272, 178–189.
Topic 8: Inflammation: phlogogenic factors, pathogenesis of alteration,
local and general sings. Kongeim’s experiment.
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

44
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. 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.
To be able:
- to describe the processes of alteration, exudation and proliferation;
- to give description of mediators of inflammation and explain their role in
pathogenesis of inflammation;
- to reproduce inflammation in an experiment.
To perform practical work: to analyse of the pathogenesis of
inflammation: disorders and after effect.
1. Basic level.
1. Histology
2. biochemistry
3. physiology
5. surgery
Functional parts of bloodstream. Conception about the
microcirculation. Mechanisms of regulation of blood
circulation in capillaries and venules. Conception about
the role of connecting tissue cells, their structure, main
functions. Conceptis about the products ofarachidonic
acid cascade, kalikrein-kinin system of blood,
complement system
5. The advice for students . Inflammation hallmarks
Systemic Local
Leukocytosis  redness (rubor)
 heat (calor)
 pain (dolor)
 swelling (tumor)
 loss of function
(functio laesa)
Leukopenia (in inflammation of viral origin)
Fever
Change of protein composition of blood: acute phase α-
protein (acute inflammation) and -globulins (chronic
inflammation)
Change of ferment composition of blood: increase of
transaminase, hyaluronidase, trombokinase activity
Increase of erythrocyte sedimentation
Change of hormone content:
 catecholamins
 corticosteroids

45
Immune system alterations and allergization of organism:
 antibody titre
 appearance of sensibilizing lymphocytes in blood
 development of allergic reactions
1.Definition of the concept “inflammation”. Etiology of inflammation.
Classification of the inflammatory agents.
2.Stages of inflammation. Cardinal symptoms of inflammation in
experiment (Cels, Galen). Classification of inflammation.
3.Acute inflammation. Primary and secondary alteration. Causes and
mechanisms of secondary alteration.
4.Mediators of inflammation. Their classification. Role of cytokines in
pathogenesis of inflammation.
5.Role of lysosomal enzymes, free radicals, peroxides and system of
complement in tissue injury.
6.Complement activation in the development of inflammatory process. Its
disorders.
7.Products of tissue basophile degranulation.
8.Derivates of arachidonic acid: prostaglandins, leukotrienes, thromboxanes.
9.Kallikrein-kinin system.
10.Biochemical and physicochemical disorders in focus of inflammation.
Local acidosis, hyperosmia, hyperoncia.
11.Methods of study of vascular permeability are in the hearth of
inflammation.
12.Cellular events: leukocyte recruitment and activation. Endothelial and
leukocyte adhesion molecules.
Protocol № 8 Date_____________________
Experimental work. The change of the vessels permeability for
anaphylaxis-like inflammation (experiment). It is necessary to inject trypan
blue under the back skin of the rat in the quantity of 1-2 ml. 20 minutes after
causing the inflammation on the rear extremity using the method mentioned
above. After some time examine the skin color change of the animal and also
compare the color of injured and opposite extremities. Analyse the mechanism of
the permeability change. Write down the experiment results and protocol of
experiment according to a scheme. For a discussion of the results, it is necessary
to give an answer to questions.
1. Enumerate local signs of inflammation.
2. What do biological active substances appear in the area of inflammation?

46
3. How and why the permeability of the vessels in the area of the
inflammation does change?
4. What changes in the metabolism to promote the development of the
inflammation signs?
5. What meaning does inflammation have for an organism?
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Test 1. Blood plasma of a healthy man contains several dozens of
proteins. During an illness new proteins can originate, namely the protein of
"acute phase". Select such protein from the listed below:
A. G immunoglobulin
B. Prothrombin
C. C-reactive protein
D. Fibrinogen
E. A immunoglobulin
Test 2. Which one of the following enzymes is the major component of
granulocytes producing antibacterial activity during acute inflammation?
A. Myeloperoxidase
B. Acid hydrolase
С. Protease
D. Lysozyme
Test 3. Humoral mediators of inflammation include:
А. Histamine
В. Interleukine
С. Prostaglandin Е2
D. Serotonin
Е. Bradykinin
Test 4. The first cells which migrate in area of inflammation are:
A. Neutrophiles
B. Lymphocytes
C. Monocytes
D. Eosinophiles
E. Basophiles
Test 5. Necrosis focus was observed in the area of hyperemia and skin
edema in a few hours after burn. What mechanism strengthens destructive
effects in the inflammation area?
A. Proliferation of fibroblasts
B. Diapedesis of erythrocytes
C. Primary alteration
D. Secondary alteration
E. Emigration of lymphocytes
Test 6. Prostaglandins (PGs) have effects on a variety of tissues. The
different prostaglandins may have different effects. Which of the following
is not correct statement?
A. The human arteriolar smooth muscle is relaxed by PgE2 and PgI2 where as
TxA2 and PgF2α cause vasoconstriction.
B. PgE2 has marked oxytocic action while PgF2α has tocolytic action.

47
С. PgE1 and PgI2 inhibit platelet aggregation where as TxA2 facilitate
aggregation.
D. PgE2 is a bronchodilator whereas PgF1α is a bronchoconstrictor.
Practice examination type 2. Give answers of the real-life tasks:
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?
Answersfor 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.
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?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./ Kumar, Abbas, Fauto. –2013.–Ch.2.–P.29–53.
4. Copstead Lee-Ellen C. Pathophysiology / Lee-E.C.Copstead, J.L.Banasic // Elsevier– 2010. – P.197–199.
5. Pathophysiology, Concepts of Altered Health States/C.Mattson Porth,G.Matfin.– NY.–2009.–P.377–390.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8thed./ Kumar, Abbas, Fauto.–2007.–Ch.2.–P.31–53.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapters 9. – P. 150 – 156.
Topic 9: Inflammation. Pathogenesis of exudation and proliferation
1. The actuality of the theme. Processes of exudation and emigration of
leukocytes, and also phagocytosis is main moments in the development of

48
inflammatory reaction. They determine the biological essence of inflammation
and value of it as the evolutional produced standard reaction of organism on
damage. Ability to estimate character of exudation, it cellular composition,
physical and chemical properties, their value in the mechanism of development,
motion and investigation of inflammatory process helps a doctor not only to
decide a question about etiology of this process, degree of his expressed but also
correctly to make tactic of treatment, forecast it possible consequences.
3. Aim: Able to expose essence of processes of exudation and emigration of
leucocytes and phagocytosis, their mechanisms and place in development of
inflammation, to estimate their biological value, determine character of exudates,
his property. Able to use this information with the purpose of establishment of
etiology, choice of tactic of treatment and prognostication of investigation of
inflammatory process.
To know:
- kinds, structure and function of leukocytes;
- a common concept is about phagocytes (macrophages and polymorphous
leucocytes);
- phagocytosis as biological phenomenon;
To be able:
- to explain the mechanisms of the separate stages of phagocytosis;
- to describe kinds and reasons for violations of phagocytosis;
- to estimate the biological value of phagocytosis at inflammation;
Task is to independent extracurricular work:
Mechanisms of development of vascular reaction are in the сirculatory bed
of inflammation. Mechanisms of liquid motion through vascular membranes.
Kinds, structure and functions of leukocytes. A common concept is about
phagocytes (macrophages and polymorphous leukocytes). Phagocytosis as
biological phenomenon, it mechanisms. A common concept about biological
theory of inflammation of Mechnykov.
To perform practical work: to analyse of the pathogenesis of
inflammation: disorders and after effect.
4. Basic level.
1. histology
2. biochemistry
3. physiology
5. surgery
6. traumatology
Meaning of mechanical, physical, chemical, biological
and mental factors in etiology of inflammation. Physical
and chemical indexes of metabolism in tissues. Structure
of the microcirculatory stream. Main data about allergy
and immunity. Meaning of an organism reactivity in
pathology.

49
1.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.
2.Emigration. Leukocyte emigration stages. Mechanisms of margination of
leukocytes. Exogenous and endogenous chemotaxins. Role of adhesion
molecules. Leukocyte adhesion deficiency.
3.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.
4.Proliferation. Mechanisms of proliferation and its regulation. Concept of
growth factors. Role of protein kinase C and tyrosine protein kinases in
activation of proliferative processes. Mechanisms of sclerosis.
5.General symptoms of inflammation: fever, leukocytosis, “acute phase
response in inflammation”.
6.Relation of local and general disorders at inflammation. Role of reactivity
in development of inflammation, significance of immune reactions at
inflammatory process. Inflammation and allergy.
7.Biochemical and physical and chemical changes are in the hearth of
inflammation. Reasons of development of acidosis in the inflammative tissues.
8. Influence of nervous and hormonal factors during inflammation.
Significance of inflammation for organism.
9. Principles of anti-inflammatory therapy.
Protocol № 9 Date_____________________
Experimental work 1. 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

50
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?
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.
1:10 1:20 1:40 1:80 1:160 1:320 1:640 1:1280
Conclusion: ____________________________________________________________
______________________________________________________________________

51
PROPERTIES SEROUS EXUDATE TRANSUDATE
Specific gravity
Albumen in %
Mucus in %
Capability to
coagulation
A common amount of
cells is in 1 mm3
рН
Osmotic pressure
Experimental work 2. Vessels reactions to inflammation of mesentery
in a frog (Kongaim's experiment). Fix the frog on the board with the backup.
Make the sidecut 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: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
8. Practice Examination
Test 1. In inflammation, vasodilatation (vascular permeability)
means :
A. Capillary
B. Venules
C. Arterioles
D. Arteriolo-venular
anastomoses
E. None
Test 2. To the molecules of intercellular adhesion belong:
A. Leukotrienes
B. Interleukin-1, 6, TNF
C. Selektines, integrines
D. IgA, IgE, IgM
E. Lysosomal enzymes

Test 3. Proliferation - is… :
A. Destruction of cells
B. Damage of cells
C. Exit of cells into the area of
inflammation
D. Reproduction of cells
E. Accumulation of exudate
Test 4. During the second component of inflammation takes place:
A. Exit of water, albumens and blood cells into the area of inflammation
B. Damage of cells
C. Release of BAS
D. Reproduction of cells
E. Emigration of leukocytes
Test 5. Exudate of next composition: albumen 4%(in a norm to 1,5%), a
lot of cells, neutrophiles prevail – was got from a pleural cavity at a patient.
Name the type of exudate.
A. Purulent
B. Hemorrhagic
S. Serous
D. Fibrinous
E. Catarrhal
Test 6. A patient with infectious mononucleosis had been taking
glucocorticoids for two weeks. He was brought into remission, but he fell ill
with acute attack of chronic tonsillitis. What action of glucocorticoids
caused this complication?
A. Antitoxic
B. Antiinflammatory
C. Antishock
D. Antiallergic
E. Immunosuppressive
task: From pleural cavity of the patient doctor got exudate of such composition:
protein 58 g/l, leucocytes – 6200/mcl, prevail neutrophiles, 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.
Answersfor the task: ____________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th international edition / V.Kumar, A.K.Abbas,
J.C.Aster – 2015. – Chapter 3. – P. 93–110.
2. Robbins Basic Pathology 9th edition./ Kumar, Abbas, Fauto. – 2013. – Chapter 2. – P. 53–73.
3. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simferopol. – 2011. – P. 196–209.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne Publ. – 2010. – P. 125–131.
5. Copstead Lee-Ellen C. Pathophysiology / Lee-E.C. Copstead, J.L.Banasic //Elsevier–2010. – P. 198–203.

53
Additional:
1. Pathophysiology, Concepts of Altered Health States/C.Mattson Porth,G.Matfin.– NY.–2009.–P.390–400.
2. Robbins and Cotran Pathologic Basis of Disease 8th ed./Kumar,Abbas,Fauto. –2007. – Ch.2–3.–P. 53–78.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 9 – P. 154 – 155, 157–161.
Topic 10: Disorders of thermal metabolism. Fever.
1. The actuality of the theme. In all hospitals it is obligatory is carried
outpatients’ thermometry. In the case history, there is a temperature list where is
the morning and evening temperature, as well as the diagram of its changes.
According to type of the curve, they define the fever type. It has diagnostic
significance because a lot of infectious diseases are accompanied by fever with
typical temperature curve. Fever has mainly protective role. Only in the persons
with serious disorders of cardiovascular, nervous and other systems and in
children the high temperature (above 39 °C) can be dangerous. The doctor must
evaluate the fever significance in the patient and will plan the treatment.
3. Aim:
To khow, that fever is a typical pathological process, the main signs of
which are changes in thermoregulation and increase of body temperature.
To be able: to analyze the pathogenetic stages of a fever.
To perform practical work: Mechanisms acting IL-1β
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
4. pediatrics
6. surgery
Thermoregulatory mechanisms. Biochemical and
physical-chemical indexes of metabolism in tissues.
Specific types of fever
Body temperature can be:
1) 36.6оC (97.88 F)- normal,
2) 37-38оC (98.6 – 100.4 F) - subfebrile,
3) 38-39оC (100.4 – 102.2 F) - febrile,
4) 39-41оC (102.2 – 105.8 F) - pyretic,
5) Over 41оC (more than 105.8 F) - hyperpyretic
Formulas for conversion of both Celsius to
Fahrenheit and Fahrenheit to Celsius are as follows:
(X°C × 9/5) + 32 =Y°F;
(X°F – 32) × 5/9 =Y°C;

54
Performance of the various types of fever
a) Fever continues; b) Fever continues to abrupt onset and remission; c) Fever remittent; d)
intermittent fever; e) undulant fever; f) Relapsing fever
TABLE 1 Heat Gain and Heat Loss ResponsesUsedin
Regulationof Body Temperature
Heat Gain Heat Loss
Body Response
Mechanism of
Action
Body Response
Mechanism of
Action
Vasoconstriction of
the superficial blood
vessels
Confines blood flow
to the inner core of the
body, with the skin and
subcutaneous tissues
acting as insulation to
prevent loss of core
heat
Dilatation of the
superficial blood
vessels
Delivers blood
containing core
heat to the
periphery where it
is dissipated
through radiation,
conduction, and
convection
Contraction of the
pilomotor muscles that
surround the hairs on
the skin
Reduces the heat loss
surface of the skin
Sweating Increases heat
loss through
evaporation
Assumption of the
huddle position with
the extremities held
close to the body
Reduces the area for
heat loss
Shivering Increases heat
production by the
muscles
Increased production
of epinephrine
Increases the heat
production associated
with metabolism
Increased production
of thyroid hormone
Is a long-term
mechanism that
increases metabolism
and heat production
1. Definition of the concept and general characteristics of fever. Development
of feverish reaction in phylo- and ontogenesis.
2. Etiology of fever. Principles of classification of pyrogens.
3. Chemical nature of pyrogenic substances.
4. Formation of pyrogens in infectious process, aseptic injury of tissues and
immune reactions.
5. The concept of primary and secondary pyrogens. Role of interleukins in the
pathogenesis of fever. Role of prostaglandins in thermoregulation.
6. Stages of fever. Types of fever.
7. Role of nervous, endocrine and immune systems in the development of
fever.

55
8. Changes in metabolism and physiological functions in fever.
9. Protective significance and pathological manifestations of fever.
10. Pathophysiological principles of antipyretic therapy. The concept of
pyrotherapy.
11. The main differences between fever, exogenous hyperthermia and other
kinds of hyperthermia.
Protocol № 10 Date_____________________
Experimental work. Experimental fever in a rabbit. Before the experiment, it is
necessary to check rabbit’s rectal temperature and temperature of ear skin, determine the
respiratory rate. Then inject pyrogenal (0,5 mg/kg) in the rabbit's angular ear vein. Every 15
minutes check body’s temperature in the rectum and ear skin and also determine the
respiratory rate. The results put down on the table. Show these changes in the rectal
temperature, the temperature of the ear skin, and the respiratory rate graphically. Do protocol
of experiment according to a scheme, for discussion answer for control question.
Time
Rectal temperature
(C)
Skin temperature (C) Breathing rate
1. What stages of fever did you observe? 2. Explain mechanism and significance of skin
temperature changes. 3. Why did the breathing rate change? 4. What parts of the nervous
system to take part in the thermoregulation? 5. What cells are the main producers of the
interleukin-1?
Conclusion:____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Test 1. Inclination of the set point of thermoregulation to higher level
due to action of IL-1 is in a patient. What is the name of this typical
pathological process?
A. Hypothermia
B. Hyperthermia
C. Fever
D. Inflammation
E. Hypoxia
Test 2. Fever in a patient develops in following succession of stages:
A. Incrementi; fastigii; decrementi
B. Incrementy; decrementy; fastigii
C. Fastigii; decrementi; incrementi
D. Fastigii; incrementi; decrementi
E. Decrementi; fastigii; incrementi

56
Test 3. After blood trasfusion patient complaints feeling of heat, rigor,
increase of body temperature to +400
C. Its known the cause of elevation
temperature is secretion of endogenous pyrogens. Which cells produce
endopyrogens?
A. Erythrocytes
B. Platelets
C. Endotheliocytes
D. B-lymphocytes
E. Macrophages
Test 4. A 50-year-old patient with typhoid fever was treated with
Levomycetin, the next day his condition became worse, temperature rises to
39,60
С. What caused worsening?
A. Secondary infection addition
B. Reinfection
C. The effect of endotoxin agent
D. Allergic reaction
E. Irresponsiveness of an agent to the levomycetin
Test 5. A patient in winter fall down into ice-hole froze and falls ill. The
temperature increased up to 39.70
С and ranged from 39.00
C tо 39.80
С.
Name the type of temperature curve of this patient.
A. Febris recurrens
B. Febris intermittens
C. Febris continua
D. Febris remittens
E. Febris hectica
Practice examination type 2. Give answer for the real-life task:
Tasks. The patient had a headache. Then temperature increased up to
37.6˚C. In the evening the patient felt the strong heat. The temperature
increased up to 40.2 ˚C. The doctor diagnosed influenza. 1. Explain a reason
for the fever. 2. Trace the stage of fever in stages. 3. Explain the mechanism
of temperature increase. 4. How can you explain the chill? 5. Do you
consider that body temperature of the patients would be reduced?
Answers for the task:
____________________________________________________
___________________________________________________________________
___
___________________________________________________________________
___
___________________________________________________________________
___
Signature___________________
Literature:
Basic:
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publ.–2010.–P. 131–
142.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier
Inc. – 2010. – P. 202–203.
4. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.– New
York, Milwaukee. – 2009. – P. 214–231.

57
Additional:
2003 / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 9 – P. 161 – 166.
2. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. NY – 2000. – P.
20–25.
Topic 11: Tumor growth.
1. The actuality of the theme. Malignant tumors take second place as
the reasons of death of population after cardio-vascular diseases from data of
WHO. Factors which cause development of tumors are widespread on a
production, in an environment, way of life. In Ukraine after an accident on
the Chornobyl nuclear plant amount of oncological diseases grew
considerably, in particular thyroid gland, system of blood. The experimental
study of this typical pathological process will allow specialists to learn the
biological features of tumor growth, reason and mechanisms of development
of tumors, intercommunication of tumor and organism.
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: reasons and mechanisms of origin and development of tumors;
features of tumor tissue; classification and description of carcinogenic
factors; methods of experimental design of tumors; stages of carcinogenesis.
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 defence in an
organism.
4. Basic level.
1. histology
2. biochemistry
3. physiology
4. oncology
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 the type of every cell. For
fibroblasts, for example, it is divisions.
Pasteur’s negative effect - is a disintegration of carbohydrates to

58
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 a nagging coughs or hoarseness
1. A general characteristic of basic types of tissue growth violations
(hypoplasia, hyperplasia, aplasia, atrophy).
2. Definition of "tumor" and "tumor process", general laws of tumor
growth. Stages of tumors development.
3. Molecular genetic bases of unlimited growth and potential immortality
of tumor cells. What is Heyflik’s limit (barrier)?
4. To explain the essence of biochemical, physical and chemical,
morphological and functional cataplasia.
Anaplasia: signs of structural, functional, physical and chemical,
biochemical, antigen anaplasia.
5. Characteristic of expansive and infiltrative (invasive) growth of tumors.
6. Principles of tumors classification, experimental study of etiology and
pathogenesis of tumors: methods of induction, transplantation, explantation.
7. Etiology of tumors, physical, chemical and biological carcinogenic
factors, properties of carcinogenic factors which determine their carcinogenic
action.
8. Risk factors (genetic/chromosome defects and anomalies of a
constitution) and condition of appearance and development of tumors.
9. Physical carcinogenic factors, the role of ionizing rays and ultraviolet
rays.
10. Chemical carcinogens, their classification, exo- and endogenous
carcinogens chemical carcinogens, features of the chemical structure of
substances which determine their carcinogenicity, cancerogenesis and
syncancirogenesis.
11. Biological carcinogenic factors: phyto (cycadin), mycotic (aflatoxin),
viruses.
12. Classification of oncogenic viruses, viral cancerogenesis, experimental
proves of the viral origin of tumors.
13. Pathogenesis of tumor growth, pathogenesis of its stages (blast
transformation, promotion, and progression), immortalization and damage of
cellular mechanisms of division as basic events of blast transformation

59
14. Mutational and epigenome mechanisms of malignant transformation.
15. Violation of the system of genes which provide a cellular division, a
concept of proto-oncogenes, oncogenes (cellular, viral), genes-suppressors of
cellular division, methods of transformation of proto-oncogene into an
oncogene, types of оncoproteins.
16. Role of apoptosis in the pathogenesis of tumor, a concept about
inductors and suppressors of apoptosis.
17. Mechanisms of deviation of the transformed cells from an apoptosis.
18. Stage of progression, its mechanisms.
19. Co-existing of tumor and organism, an influence of tumor on an
organism, mechanisms of cancer cachexy, mechanisms of natural
antioncological defense, immune and no immune mechanisms of resistance,
mechanisms of deviation of tumors from immune supervision,
pathophysiological bases of prophylaxis and treatment of tumors.
Protocol № 11 Date_____________________
Experimental work 1. Acquaintance with transplanted tumor strains
1. Ascitic Ehrlich's carcinoma in a mouse. An initial tumor is
spontaneous cancer of mammalian gland. Strain exists from 1905. Percentage
of positive transplantation is 100. The latent period is 4-6 days. Lifetime
animal with a tumor is 7-16 days. In intraperitoneal tumor transplantation,
ascites develops, for this, they inject into abdominal cavity 0.2 ml of ascitic
liquid, which contains much tumor cells. In an intracutaneus introduction of
this liquid tumor develops too.
2. Krocker's sarcoma in the mouse. An initial tumor is a sarcoma,
which is received as a result of malignisation of transplanted carcinoma of a
mammalian gland. Strain exists from 1914. Histological type of tumor is a
polymorphocellular sarcoma. Percentage of positive transplantation is 100.
Lifetime is 30 days.
3. Sarcoma М-1 in rats. An initial tumor is a sarcoma, which is getting
in the rat by the carcinogenic substance 3,4-benzopyrene in Shabad's
laboratory in 1943. Histological tumor type is a polymorphocellular sarcoma.
Percentage of positive transplantation is 98-100. The latent period is 6-7
days. Lifetime animal with a tumor is 25-35 days.
4. Braun-Piers’ carcinoma in rabbits. An initial tumor is a
spontaneous tumor in rabbit, to which brought syphilitic material into the
scrotum (in 1916). 4 year after scrotum skin inflammation tumor developed.
Histological type is an epithelial multicellular medullar unstructured

60
tumor. Percentage of positive transplantation is 90-95. The tumor is
characterized by intensive growth and inclination to central necrosis, very
quickly metastasizing. The primary tumor sometimes resolves, but animal
perishes from metastases in inner organs.
To protocol of experiment according to a scheme. In part of protocol
“Experiments results and their discussion,” it is necessary to draw changes
and give confirmation of main peculiarities neoplastic growth (unlimited and
unregulated growth, aplasia).
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Experimental work 2. Demonstrate of macropreparation of
experimental tumors.
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practical work 1. Watching movies “Pathways to Cancer”, “Journey
In to Nanothehcnology of Cancer”. Notice in protocol main etiological
factors of cancer; explain pathogenesis of general symptoms and
comlications.
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practice examination type 1. Give correct answers to the tests:
Test 1. After Chornobyl catastrophe morbidity of tumors has been
increasing. What action of the radiation has been appearing?
A. Cytostatics
B. Thermal
C. Mutagenic
D. Oncogenic
E. Immunostimulatory
Test 2. A patient who has been abusing tobacco smoking for a long time
has got a 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 the
formation of the tumor:
A. Hypoplasia
B. Hyperplasia
C. Metaplasia
D. Sclerosis
E. Necrosis
Test 3. A patient with lung cancer has been smoking 30 cigarettes per
day for 20 years. What is the group of carcinogens in tobacco smog?
A. Polycyclic carbohydrates
B. Aminoasosubstances
C. Nitrosamines
D. Amines

61
E. Heterocyclic carbohydrates
Test 4. Adult somatic cells, as compared to fetal cells have a very limited
capacity to multiply. It can be explained by:
A. Adult cells have CDK inhibitors which cause cell cycle arrest.
B. Fetal cells have CDK promoters which facilitate cell division.
С Telomeres at the end of chromosomes in adults prevent them from
multiplying indefinitely.
D. In fetal cells, the protease, which normally degrades CDK, is absent.
Test 5. Most common malignancy in AIDS:
A. B-cell lymphoma
B. Kaposi's sarcoma
С. Leukemias
D. Burkitt’s Lymphoma
Test 6. An example of a tumor suppressor gene is:
A. myс
В. fos
С. ras .
D. Rb
Test 7. It is established that tumor tissue receives 20-25 times less of
glucose that intact tissue in equal glucose amount. What metabolic changing
lead to such event?
A. Aerobic glycolysis enhancement
B. Oxidation improvement
C. Normal interaction of these processes
D. Tissue respiration improvement
E. Decreasing of anaerobic glycolysis
Practice examination type 2. Give answers for questions of the real-life
tasks. The 54 years old woman was hospitalized in a regional oncological clinic
for investigation. At examination doctor revealed the tumor of dense
consistency, knobby, painless, and soldered with surround tissue. Axillar
lymphatic nodes were increased. On the base of clinical and histological
researche cancer of mammalian gland was diagnosed. At operation gland,
region lymphatic nodes, and ovaries were removed. 1. Why doctor did do
conclusion, that this is malignant tumor? 2. Why in the patient were increased
axillar lymphatic nodes? What purpose their remove with? 3. Why ovaries are
removed in the patient?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
task:
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: anaemia, leucocytes – 10.5x109/l,

62
methamielocytes-3%, stabs 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. What kind of pathology was diagnosed at
patient? 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. Tumoral formation of small curvature of
stomach was founded at the duty fibrogastroscopy review. Cancer of stomach
was diagnosed after cytological examination. Tumor, definition. What is the
mechanism of this tumor development?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th int. ed. / V.Kumar, A.K.Abbas, J.C.Aster – 2015. –
Ch. 7. – P. 265–338.
2. Robbins Basic Pathology 9th 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.
2. Robbins and Cotran Pathologic Basis of Disease 8th ed./ Kumar, Abbas, Fauto. –2007.–Ch.6.–P.174–224.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. NY – 2000. – P. 14–17.
Topic 12: Starvation. Hypoxia
1. The actuality of the theme. For data of the WHO, more than half of
population of globe chronically is undernourished. Therefore starvation is the
social problem is considered not only as medical but also as a social problem.
This pathological process accompanies a number of diseases, mainly of the
digestive system. There is protein-calorie insufficiency more often.

63
The study of hypoxia takes an important place in pathophysiology, so as
accompanies almost all illnesses of man. A division of hypoxia is on hypoxic,
respiratory, and circulatory and the mixed is represented by the wide of diseases
which arises up at. A lot of types of professional activity are also related to the
development of hypoxia. The study of the pathogenesis of hypoxia, protective-
adaptive mechanisms, and pathological changes are important for the choice of
pathogenetic therapy of the hypoxic states. Professional selection of high-
resistant to hypoxia people, and also adaptation to an oxygen insufficiency
become a relevant problem in medicine.
2. Duration of the class – 1h 30min.
3. Aim: To know principal reasons, mechanisms of starvation development
and metabolic disturbance in it.
To know the disturbance of energy metabolism, the disturbance of basal
metabolism, the disturbances of protein metabolism, the disturbance of
transamination and oxidative deamination, the disturbance of decarboxylation
and mechanisms of hypoxia disorders.
To be able: to analyze the pathogenesis of the starvation and analyze of the
two stages of hypoxia-compensation and decompensation specific and non-
specific reactivity and types of hypoxia (hypoxic, respiratory, haemic,
circulatory, tissue and combined).
To perform practical work: to analyze the pathogenesis of the medicinal
starvation (fasting) and explain the causes of oxygen deficiency.
4. Basic level.
1. Histology
2. Biochemistry
3. Physiology
4. Internal medicine
5. Diethology
6. Intensive care
7. Surgery
8. Sports medicine
The 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 an organism. Mechanisms of the neurohumoral
regulation of metabolism and energy exchange.
Indexes of respiratory function blood. Construction of
hemoglobin. The mechanism of oxygen transport by
hemoglobin. Enzymes of the respiratory chain. The
mechanisms of transport of electrons on a respiratory chain.
5. The advice for students .
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
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

64
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
Systems of oxygen supply of organism: system of external respiration -
blood system - circulatory system - microcirculatory vessels - tissues and cells.
Oxygen cascades of an organism:
• Atmospheric air – pO2 - 160 mm Hg.
• Alveoli - pO2 - 100 mm Hg (13.6 kPa).
• Arterial blood - pO2 - 85-95 mm Hg (13.3 kPa).
• Mixed venous blood - pO2 - 40-50 mm Hg (5.3 – 6.7 kPa).
• Tissues - pO2 - 5-20 mm Hg (0.7 – 2.7 kPa).
• Hemoglobin (Hb) is a protein with a molecular weight of 64800 Dalton.
It consists of four subunits containing Fe++. Each of four molecules of
Fe++ binds one molecule of O2 (1 Mol Hb binds 4 Mol O2 or 1g Hb can
attach 1.38 ml O2).
Hypoxia – is a typical pathologic process, developing as a result of
insufficient tissue supply by oxygen or its disturbing use.
The types of hypoxia. As to the mechanisms of development, there are
hypoxic, respiratory, haemic, circulatory, tissue and combined hypoxia.
1. What is the basic metabolism? The main stages of energy metabolism.
Basal metabolism. Disorders of energy metabolism.
2. Alimentary starvation, determination. Reasons for starvation.
3. Pathophysiological description of complete starvation periods.
Contribution of V.Pashutin to development of studies about starvation.
4. What is respiratory coefficient (RC)? What is it equal at norm? How RC
changes at the I, II and III period of complete starvation with water?
5. Protein-calorie deficiency. Reasons. Mechanisms of basic manifestations
development.
6. Starvation at children. Kwashiorkor. Alimentary marasmus. Reasons for
origin. Features of development.
7. Anorexia nervosa and bulimia. Reasons for development. Pathogenesis.
8. Factors which influence on resistance of an organism to starvation. A
conception of starvation diet.
9. Hypoxia. Definition of the concept. Principle of classification of hypoxic

65
conditions.
10.Mechanisms of development of hypoxia: reduction of delivery of oxygen
and disorders of its utilization by cells.
11.Etiology and pathogenesis of the basic types of hypoxia: hypoxic,
respiratory, circulatory, hemic, tissue. Mixed forms of hypoxia.
12.Clinical manifestations and mechanisms of cyanide and CO poisoning,
methemoglobinemia.
13.Parameters of gas structure of arterial and venous blood at various types
of oxygen starvation. Emergent and long-time adaptive reactions of the
organism in hypoxia.
14.Mechanisms of hypoxic damage of cells. Pathogenesis of hypoxic
necrobiosis.
15.Oxygen therapy. Iso- and hyperbaric oxygenation. Resistance of
individual organs and tissues to hypoxia.
16.Toxic effect of oxygen. Hyperoxia and free-radical reactions. Hyperoxia
as a cause of hypoxia.
Protocol № 12 Date_____________________
Experimental work 1. Read results of blood and urine tests and reveal
a 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
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
Level of glucose in blood 2,8 mmol/l
Residual nitrogen 34,0 mmol/l

66
B.General Protein in blood 40 g/l
Residual nitrogen 45 mmol/l
Ketonic bodies 250 mkmol/l
pH of blood 7,3
C.General Protein in blood 36 g/l
Residual nitrogen 61 mmol/l
Ketonic bodies 550 mkmol/l
General lipids 10 g/l
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Experimental work 2. To recreate of hemic hypoxia by poisoning
smoky gas. Mixture serves as a source of smoky gas from equal parts of
sulphuric and formic acids, which is placed on the bottom of desiccator. Acids
cover a grate, place on a rat and close desiccator by the lid, during 25-30 min.
watch on the state an animal (shortness of breath, cramps, death). At a section
pay attention to the color of blood and internal organs (raspberry blood), as a
result of the formation of carboxyhemoglobin).
Conclusion: ________________________________________________________
Experimental work 3. An express-method of determination of
carboxyhemoglobin in blood. On the smear glass inflicts the drop of blood of
intact rat and alongside drop blood rat which poisoning smoky gas. B every drop
of blood adds a 2% solution of sulphuric copper on a 1 drop, mixed them. After 1
minute the drop of blood of experimental rat acquires a rich redder raspberry
color, and normal blood is greyish brown.
Conclusion: ________________________________________________________
Test 1. There is only one source of water for the body at absolute
starvation - a process of organic compounds oxidation. Which of the
following substances in these conditions is the main source of endogenous
water?

A. Fats
B. Proteins
C. Carbohydrates
D.Glycoproteins
E. Lipoproteins
Test 2. Negative nitrogen balance, hypoproteinemia, violation of water-
salt metabolism combined with the normal function of digestive system was
founded at the vegetarians. Name the reason for this state.
A. Monotonous protein diet
B. Monotonous carbohydrate diet
C. Lack of unsaturated fatty acids
D. Deficiency of phospholipids
in the food
E. Lack of vitamin E in the food
Test 3. At 10th
day of medical starvation the patient suffers from
excitation, deep, noisy breathing, blood pressure dropped to 90/60 mmHg,
oliguria, urine with a smell of acetone. Name the reason for this state.
A. Ketosis
B. Non-gas alkalosis
C. Hyperglycemia
D. Hypoglycemia
E. Gas acidosis
Test 4. Esophagus stenosis developed in a patient after a chemical burn.
Severe weight loss arose. In the blood: erythrocyte.-3.0х1012
/l, Hb-106 g/l,
whole protein - 57g/l. What type of starvation developed in a patient?
A. Absolute
B. Albumen
C. Water
D. Incomplete
E. Complete
Test 5. During a total (with water) alimentary starvation the generalized
edema has developed. Which of the pathogenic factors is dominant in this
case?
A. Reduced osmotic pressure of blood plasma
B. Reduced hydrostatic pressure of interstitial fluid
C. Reduced oncotic pressure of blood plasma
D. Increased oncotic pressure of interstitial fluid
E. Increased osmotic pressure of interstitial fluid
Test 6. A 65-year-old patient suffers from aortic valve stenosis. She has
symptoms of heart failure such as dyspnea, cyanosis, and edema that
appeared after viral infection. She was admitted to the therapeutic
department. Which type of hypoxia is in the patient?
A. Hypoxic
B. Hemic
C. Circulatory
D. Respiratory
E. Tissue
Test 7. A 70-year-old patient underwent medical treatment for ischemic
heart disease, heart failure in a cardiological department. Which type of
hypoxia was in the patient?
A. Circulatory
B. Hemic
C. Respiratory
D. Tissue

68
E. Mixed
Test 8. A 13-year-old girl undergoes treatment for iron-deficiency
anemia in a hematological department. Which type of hypoxia does this
patient have?
A. Circulatory
B. Hemic
C. Tissue
D. Respiratory
E. Mixed
Test 9. A 56-year-old woman suffers from thyrotoxicosis for a long time.
Which type of hypoxia can develop in this patient?
A. Tissue
B. Hemic
C. Circulatory
D. Respiratory
E. Mixed
Test 10. Group of tourists ascended to the altitude of 4200 m. Three
alpinists complained of a headache, pain in their ears and frontal sinuses,
somnolence, considerable muscular weakness, irritability during the ascent.
The possible reason for the appearance of these symptoms was:
A. Gas saturation in blood
B. Hyperbaric oxygenation
C. Caisson disease
D. Altitude sickness
E. Altitude decompression
Practice examination type 2. Give answers for questions of the real-life
tasks:
Task 1. In one of the members of the high-mountainous expedition, the
erose increasing and deepening of breath has occurred which was replaced by a
sudden oppression it and loss of consciousness.
1. Explain the mechanism of increasing and deepening of breath for want of
rising on height. 2. Why was stimulation of breath replaced it by oppression? 3.
How the acid-base balance in the climber was changed which has suffered? 4.
What for him is better - inhalation of pure oxygen or carbogen?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 2. In the patient, who was on the surgical table under narcosis, the
sharp oppression of breath has occurred. The pulse has become rare and weak,
appeared cyanosis. The emergency measures accepted by the anaesthesiologist
liquidated these disorders. 1. What can be connected the oppression of breath
with? 2. How, in your opinion, the contents of oxygen and carbonic acid in
arterial of blood were changed in the patient? 3. Explain appearance of the
cyanosis. 4. How are you evaluating changes of the pulse in this case?
______________________________________________________________________

69
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practice examination type 3. Give answer to the questions below:
1. What is the difference between starvation, fasting and cachexia?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
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?
Glycerol: which is released _____________________________________?
Amino acids: from the so-called _________________________________
Lactate:_____________________________________________________
Give answer to the questions of the real-life tasks:
Task 1. After chemical burn in the patient was developed esophageal
stenosis, that hindered reception of food. After that occurred cachexia – a weight
of the body decreased on 16 %. Data assay of blood: erythrocytes – 3.1*1012/l,
leucocytes – 5.2*109/l, hemoglobin – 113 g/l, a concentration of glucose – 3.7
mmol/l, contents of protein – 57 g/l.
1. What kind of starvation in the patient? 2. Possible consequences of
hypoproteinemia. How to normalize the contents of protein in blood? 3. How do
you explain decrease of form elements and hemoglobin in blood? 4. How is the
level of sugar in blood in starvation person supported? 5. How will be changed a
resistance of an organism to an action of the infectious agents?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________

70
______________________________________________________________________
Task 2. The weight loss of a 45% of rat’s 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? What is the type of starvation in a patient? What is the period of
starvation? Characteristic of this period of starvation.
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th international edition / V.Kumar, A.K.Abbas,
J.C.Aster – 2015. – Chapters 2, 3, 9, 12, 28. – P. 39, 50–51, 70-71, 432–449, 529, 1263–1267.
2. Robbins Basic Pathology 9th ed./ Kumar, Abbas, Fauto. – 2013. – Chs. 1,7,22 – P.17, 293–306, 814–816.
3. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha
Publishers – 2011. – P. 121–134, 281–293.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, M-ne Publishing. – 2010. – P. 160–187.
5. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc,
4th edition. – 2010. – P. 529–530, 969–987.
Additional:
Milwaukee. – 2009. – P. 998–1007.
3. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), 2003
/ Carol Mattson Porth, Kathryn J. Gaspard. – Chapter 19, 29 – P. 351–356, 517 – 521, 524–527.
2000. – P. 26–27, 122–131.
Topic 13: Disorders of carbohydrate metabolism. Diabetes mellitus.
1. The actuality of the theme. 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).

71
3. Aim: Learn reasons and mechanisms of development of basic type’s
hypo- and hyperglycemia. To study etiology, pathogenesis, mechanism of
development of basic displays of diabetes mellitus, its pathogenic treatment.
To khow the pathology of carbohydrate metabolism, the main cause of
pancreas alteration: Hereditary predisposition, emotional overstrain, trauma,
tumor, an inflammatory process under influence infection/ viruses, autoimmune
conflict, hypoxia, overeating.
To be able: to analyze the pathogenesis of the Diabetes Mellitus.
To perform practical work: to analyze 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.
4. Basic level.
1. histology
2. biochemistry
3. physiology
5. endocrinology
6. surgery
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. Etiologic Classification of Diabetes Mellitus
Type Subtypes Etiologyof 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., chromosome7,
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
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

72
D. Endocrine disorders, e.g.,
acromegaly, Cushing’s syndrome
E. Drug or chemical-induced, e.g.,
Vacor, glucocorticoids, thiazide
diuretics, α-Interferon
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
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
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
1.Disorders of carbohydrate metabolism. Disorders of absorption of
carbohydrates, a process of synthesis, accumulation, and decomposition of
glycogen, transport of carbohydrates into cells.
2.Disorders of nervous & hormonal regulation of carbohydrate metabolism.
3.Hypoglycemia, causes, and mechanisms. Hypoglycemic coma.
4.Hyperglycemia, causes, and mechanisms. Hyperglycemic coma.
5.Glucosuria, causes, and mechanisms.
6.Describe the main cause of pancreas alterations.
7.Diabetes mellitus. Classification of WHO. Causes and mechanisms of
development of insulin-dependent and insulin-independent diabetes mellitus.
Role of heredity in their occurrence.
8.Note the Classification of Diabetes and Glucose Intolerance Conditions.
Causes of extrapancreatic insufficiency of insulin, mechanisms of resistance to
insulin.
9.Identify the acute complication of diabetes mellitus; describe the features of
each.Pathogenesis of the main complications of diabetes mellitus: macro- and
microangiopathies, neuropathies.
10.Experimental models of diabetes mellitus. Principles of pathogenetic
treatment of diabetes mellitus.
11.Glycogen storage diseases (glycogenosis). Etiology, pathogenesis. Von
Gierke disease, type I. Pompe disease, type II. McArdle syndrome, type V.
12.Disorders of carbohydrate metabolism: galactosemia, fructosemia.

73
Protocol № 13 Date_____________________
Experimental work 1. Determination of glucose concentration in a
condition of insulin intoxication to model experimental hypoglycemia for a
rabbit. Students work as brigades. The first brigade carries out the test on a
determination of glucose in the control samples; the other one carries out the test
in experimental samples: before and after insulin introduction.
Insulin is entered into the rabbit which was not fed by 24 hours in an amount
10 ME on the 1 kg of weight under the skin of the back.
The first test is carried out in 15 minutes after insulin introduction, then in 30
min., in 1 hour, in 1.5 hours.
Blood for the test in an amount 0.1 ml is taken from an ear regional vein.
After taking the blood the 10-15 ml of 30% glucose solution is entered into
the rabbit throw the ear regional vein or through the mouth with the purpose to
remove of insulin hypoglycemia. COURSE OF ANALYSIS:
1.Fill in two test tubes with 1 ml of a decinormal solution of caustic soda and
5 ml of 0.45% solution of sulfuric zinc.
2.Add to one of the test tubes 0.1 ml of blood; wash a pipette solution from a
test tube 2-3 times. The second test tube remains the control.
3.Put both test tubes in a water bath for 3 min.
4.Filter the maintenance of test tube through the sterile cotton wool in a glass.
5.Wash test tubes twice by 3 ml of the distilled water which is poured on a
filter. At the end of filtration, the filter is levitated on an edge of the bailer. Wait
while all liquid will flow from it. Take away the filter from the bailer and shake
off the drops of liquid which remained in the bailer in a glass.
6.Add to the filtrate 2 ml K3[Fe(CN)6] 1: 200.
7.Boil in a water bath for 15 min.
8.Cool glasses and add to every 2 ml of a mixture of salts.
9.Add to each glass 2 ml of 3 % to the solution of СН3СООН.
10.Add 2-3 drops of 1 % to the solution of starch.
11.Titrate the maintenance of glasses by hyposulphite 1:200 to discoloring.
12.Find the maintenance of glucose at the table by the amounts of
hyposulphite which we used for titration.
13.Find the maintenance of glucose in the control tube at the table by the
amounts of hyposulphite which we used for titration.
14.Find a difference in the maintenance of glucose in an experimental test
tube, take away an error, and determine the maintenance of glucose in blood in
mg %. For the translation of the got result in mmol/l (international unit) use the
coefficient – 0.05.

74
An initial maintenance of glucose in the blood before the introduction of
insulin is____8.8_______mmol/l,
after the introduction of insulin :
in 15 min. - __ 6.8______mmol/l,
in 30 min. - _____4.2____ mmol/l;
in 90 min. - _____4.0_ mmol/l
in 120 min.- _____4.8____ mmol/l
Conclusion:____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Experimental work 2. Investigation of ketone bodies in urine in the
patients with diabetes mellitus. To 3 ml of urine add 1.5 ml of 10 % NaОН.
Filter the solution. Add 2 ml of 0.1 N solution of iodine into filtrate. In presence
of ketone bodies in urine in some seconds there is turbidity. Reaction is positive
in presence of 0.05 g of ketone bodies in 1 l of urine. 1. What is the name of the
appearance of ketone bodies in urine? 2. Explain the mechanism of this disorder.
Conclusion:____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practical work. Video observation: “Express-methods of determination
of glucoses concentrations in blood”, “Diabetes and associated
complications”, “Glucose metabolism”. Notice in protocol main etiological
factors of diabetes mellitus; explain pathogenesis of general symptoms and
comlications.
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Test 1. A patient suffers from neurodermatitis for a long time, use
prednisolone. During examination increase of glucose in blood was found.
What link of carbohydrate metabolism influence prednisolone?
A. Increase of suction of glucose in an intestine
B. Activation of gluconeogenesis
C. Decrease of synthesis of glycogen
D. Activating of breaking up of insulin
E. Activating of gluconeogenesis

75
Test 2. A 19-years-old patient has suffered from diabetes mellitus since
he was 8. He took cure irregularly. He was admitted to the hospital in
connection with diabetes ketoacidosis development. What kind of
respiration is the most possible in this condition?
A. Chane-Stocks respiration
B. Biot’s respiration
C. Kussmaul respiration
D. Inspiratory breathlessness
E. Expiratory breathlessness
Test 3. On the empty stomach in the patient’s blood glucose level was
5.65 mmol/L, in an hour after usage of sugar it was 8.55 mmol/L, in 2 hours
– 4.95 mmol/L. Such indicators are typical for:
A. Patient with non-insulin dependent diabetes mellitus
B. Patient with insulin-dependent diabetes mellitus
C. Patient with thyrotoxicosis
D. Patient with hidden diabetes mellitus
E. Healthy person
Test 4. Diabetes mellitus causes ketosis as a result of activated oxidation
of fatty acids. What may disorders of acid-base equilibrium be caused by
excessive accumulation of ketone bodies in blood?
A. Respiratory acidosis
B. Metabolic alkalosis
C. Any changes wouldn't happen
D. Metabolic acidosis
E. Respiratory alkalosis
Test 5. A patient is ill with diabetes mellitus that is accompanied by
hyperglycemia over 7.2 mmol/l on an empty stomach. The level of what
blood plasma protein allows estimating the glycemia rate retrospectively (4-
8 weeks before examination)?
A. C-reactive protein
B. Glycated hemoglobin
C. Fibrinogen
D. Albumin
E. Ceruloplasmin
Test 6. Is hyperuricemia seen in?
A. McCardle's disease
B. Pompes' disease
С. von Gierke's disease
D. Tauri's disease
Test 7. A child with point mutation presents with an absence of glucose
6-phosphatase, hypoglycemia, and hepatomegaly. What pathology are these
signs characteristic of?
A. Von Gierke’s disease (Glycogen storage disease type I)
B. Cori’s disease (Glycogen storage disease type III)
C. Addison’s disease (Primary adrenal insufficiency)
D. Parkinson’s disease
E. McArdle’s disease (Glycogen storage disease type V)

76
Test 8. A characteristic sign of glycogenosis is muscle pain during
physical work. Blood examination usually reveals hypoglycemia. This
pathology is caused by congenital deficiency of the following enzyme:
A. Glucose6-phosphate dehydrogenase
B. Lysosomalglycosidase
C. α-amylase
D. γ-amylase
E. Glycogen phosphorylase
life task:
Task 1. The examined has the following results of the 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 a test result in a healthy person and this patient? 4. What
practical significance has the test with glucose load, how is it called?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 2. Diabetes mellitus is developed after removal of pancreas in dog.
Would the diabetes mellitus is developed, if we instead of pancreas removal:
1. Tie up its output duct? 2. Introduce alloxan? 3. Introduce parathormone?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 3. The experimental models of diabetes mellitus are received by the
way of pancreas removal, introduction of allocsan, somatotropic hormone, and
glucagon. 1. In what cases does absolute insulin insufficiency is occured in what
– relative? 2. Explain the mechanism of insulin insufficiency in each case. 3.
What other hormones we can use for modeling of diabetes?
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practice examination type 3 – Algorithm for skills passing “Analyses of
the glucose-tolerance test indexes at the patients with diabetes mellitus”
1. Name the reasons for the GTT. Standard answer:
______________________________________________________________________
______________________________________________________________________

77
2. Name the main stages of the GTT. Standard answer:
______________________________________________________________________
______________________________________________________________________
3. Appraise the results of GTT in this patient in accordance with the
diagnostic criterias of diabetes mellitus and other categories of
hyperglycaemia.
Standard answer:
Conclusion
Concentration of
glucose in the capillary
blood on an empty
stomach
Concentration of
glucose in capillary
blood after 2 hours after
the glucose loading
Diabetes mellitus More than _____ mmol/l
More than or equal to
________mmol/L
Disordered glucose
tolerance
Less than _____ mmol/l __________ mmol/l
Disordered blood
glucose
______ mmol/l Less than ____ mmol/l
Signature___________________
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9th edition./ Kumar, Abbas, Fauto. – 2013. – Chapter 6.
– P. 228, 232–233, Chapter 19. – P. 739–751.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-E.C. Copstead, J.L.Banasic//Elsevier– 2010. – P. 942–968.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publ.–2010.– P. 200–223.
5. Pathophysiology, Concepts of Altered Health State s/ C.M.Porth, G.Matfin.– NY.– 2009.– P.1047–1075.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease8thed./Kumar, Abbas, Fauto.–2007.–Ch.20.–P.775–787.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 32 – P. 560 – 578.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // T. NY– 2000. – P. 244–243.
Topic 14: Disorders of lipid metabolism.
Medical and social problems of obesity.
1. The actuality of the theme. Obesity is an increase in body fat mass and
a metabolic disorder that has increased significantly over the past two decades.
Obesity is an energy imbalance, with energy intake exceeding energy
expenditure, and is defined as a body mass index (BMI) greater than 30.
It is a major cause of morbidity, death, and high healthcare cost in the
United States and worldwide. Obesity is also a risk factor for hypertension,

78
stroke, hepatobiliary disease (gallstones and nonalcoholic steatohepatitis),
osteoarthritis, and sleep apnea. Obesity is increasing in children and obese
children tend to become obese adults.
3. Aim:
To know: there are following disturbances of lipide metabolism: 1.
Hyperlipemia (essential, genotypic, retention, transport types). 2. Obesity. 3.
Fatty infiltration and dystrophy (liver and oth. organs), fatty degeneration.
To be able: to analyse of the pathogenesis of the obesity.
To perform practical work: to analyse the sequence of cellular interactions
in obesity.
4. Basic level.
future disciplines
1. Histology
2. Biochemistry
3. Physiology
4. Internal medicine
5. Cardiology
Lipids and lipoproteins of blood plasma.Transport
of lipids. Intermediate metabolism of fat. Sources
cholesterol in blood plasma and its metabolism.
Anatomic-physiological features of vessels.
1. Fat is a source of reserve energy, its supplies are 10%.
2. Fat is a source of endogenous metabolic water.
3. Fat participates in heat production and saving one as it conducts heat poorly.
4. Cholesterol participates in: construction of the cellular membrane and
consequently in its permeability; being the dielectric it provides the conduction
of impulses in the definite direction (without myelin coat may be “chaos” in
n.s.); the corticosteroids, sex hormones, bile acids, vit.D are formed from
cholesterol.
The main objective of studying lipid metabolism is to reveal as early as
possible hyperlipidemia as a risk factor for cardiovascular disease (one of the
leading causes of death).
Table. Hyperlipoproteinemia Classification accepted by WHO.
Type
Chylomic
-rons
VLD
H
LDL
Chole
sterol
Trigl
yceri
des
Lipoprote-
in
disorders
Hereditary
origin
Acquared
I-
hyperchylo-
micronemia
↑
Nor
m
Nor
m
Nor
m
↑↑
Chylomic-
ron
Excess
Deficiency
lipoproteinli-
pase
Systemic
lupus
erythomato-
sus (SLE)
II a
hyper – β –
lipoproteine-
mia
_______
Nor
m
↑↑ ↑↑
Nor
m
LDL
Excess
Family
hypercholes-
terinemia
(deficiency
receptors to
Hypothy-
roidism

79
LDL)
II b
hyper – β –
lipoproteine-
mia
_______ ↑ ↑ ↑ ↑
LDL and
VLDL
excess
Combine
familial
hypercholis-
terinemia
Nephritic
syndrome
III
familial dis–
β–
lipoproteine-
mia
_______
Floating -β-
lipoprotein
↑ ↑
Chylomicro
n remnant
and IDL
excess
Family
hyperlipopro-
tein emia the
IIId type
Obesity
IV
hyperpre –β–
lipoproteine-
mia
________ ↑
Nor
m
Nor
m (↑ )
↑
VLDL
excess
Combine
family
hyperlipide-
mia
Diabetes
mellitus
V
combination
of hyperpre –
β–
lipoproteine-
mia and
hyperchylo-
micronemia
↑ ↑
Nor
m
Nor
m (↑)
↑↑
Chylomicro
n and VLDL
excess
Family
hypertrigly-
cerides
Alcohol
intoxication
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.Reasons for hyper-β-lipoproteinemia.
5.Reasons of multiplying permeability of vascular wall are for lipoproteins.
6.Protective role of α-lipoproteins and reasons of hypo-α-lipoproteinemia.
7.Basic directions for prophylaxis of atherosclerosis.
8.Inherited violations of lipidic metabolism.
9.Disorders of lipid accumulation. Primary and secondary obesity.
Experimental models and pathogenesis of obesity.
10.Distinguish between hypertrophic and hyperplastic obesity.
11.Complications and associated diseases of obesity. Pickwickian syndrome,
nonalcoholic fatty liver disease, cholelithiasis, osteoarthritis.
12.Prader-Willi syndrome. Etiology, pathogenesis.
13.Hyperketonemia: causes, mechanisms, consequences.
14.Disorders of intermediate exchange of lipids in cells. Mechanisms of fatty
dystrophy.

80
15.Genetic deficiencies of sphingolipid catabolism: Tay-Sachs, Gaucher
disease, Niemann-Pick disease, Farby disease. I-Cell disease.
Protocol № 14 Date_____________________
Practical work 1. Video observation: “Obesity”, “Obesity and chronic
diseases”. Notice in protocol main etiological factors of obesity; explain the
pathogenesis of general symptoms and complications.
Conclusion: ___________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practical work 2. Calculate your own body mass index (BMI):
Conclusion: ___________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
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. Cholesterol content in blood serum of a 12-year-old boy is 25
mmol/l. Anamnesis states hereditary familial hypercholesterolemia caused
by synthesis disruption of receptor-related proteins for:
A. Chylomicrons
B. High-density lipoproteins
C. Low-density lipoproteins
D. Very low-density lipoproteins
E. Middle-density lipoproteins
Test 3. The quantity of plasma albumins changed in a man which
executed a physical work in the conditions of high temperature. How did
quantity of plasma albumins change?
A. Relative hyperproteinemia
B. Paraproteinemia
C. Dysproteinemia
D. Absolute hyperproteinemia
E. Absolute hypoproteinemia

Test 4. Increase of free lipid acids in patients with diabetes mellitus
blood was observed. What is the reason of this state?
A. Activating of apolipoproteins of А-1, А-2, А-4 synthesis
B. Accumulation of palmytin –Co-A in cytosolum
C. Increase of adipocytes trigliceridlipase activity
D. Decline of phosphatidilcholin – cholesterin acetyltransferase activity in
the blood
E. Activating of keton bodies utilization
Test 5. Cholesterol stones may develop in:
A. Estrogen therapy
B. Type-IV hyperlipidemia
C. Pregnancy
D. Diabetes mellitus
E. All of the above
task. 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 of
the hydrophilic state.
E. A lot of cholesterol is contained in B-lipoproteins (70–75 %).
F. B-lipoproteins are increased in the body of elderly persons.
G.
Hypodynamia and hypoxia predispose to atherosclerosis
because of the decreased oxidation of lipids and promote
accumulation of cholesterol in subendothelium.
H. Hyperlipemia is associated with atherosclerosis and obesity.
L. Obesity may occur without atherosclerosis.
Signature_________________________

82
Literature:
Basic:
1. Robbins and Cotran Pathologic Basis of Disease 9thed./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.
2010. – P. 362–367, 825, 974–975.
Milwaukee. – 2009. – P. 982–998, 479–489.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease8thed./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.
2000. – P. 26–27, 236–239, 244–249.
Topic 15: Pathology of water-electrolyte and microelements metabolism.
1. The actuality of the theme. The state of dehydration can arise in the
person in time stay on place with hot climate owing to excessive of sweating and
hyperventilation. However water deficiency is more often is observed for various
pathological states - strong diarrhea, vomiting, complicated swallowing (tumour,
atresia of the esophagus), extensive burns, significant blood loss, diseases of
brain, which are accompanied by absence of thirst sensation, in the heavy
patients and weakened children. This state especially is dangerous for children
first two years life in connection with disorder of neuroendocrine regulation of
water-electrolytes metabolism. Dehydration in them quite often leads to death.
3. Aim:
To know: Disorders of water balance, explain the mechanisms of their
development. To modulate different pathogenetic forms of edema, to be able to
explain the mechanisms of their development.
To be able: to analyze the pathogenesis of the edema (typical pathologic
process, which is characterized by the increased amount of water in the
extracellular space).
To perform practical work: To analyze of the classification of the
disorders of fluid homeostasis.
4. Basic level.
future disciplines

83
1. histology
2. biochemistry
3. physiology
4. intensive care
5. surgery
Metabolism of water between blood and tissues after
Starling. Contents of electrolytes in blood plasma in a
norm. Mechanisms of regulation water-salt metabolism.
Buffer systems of the organism. Mechanisms of
regulation of acid-base balance.
Amount and composition of liquid in different sectors of organism
Sector
Volume,
l(70kg)
Na+
meq/l
K+
meq/l
Cl-
meq/l
HCO3
-
meq/l
PO4
3-
meq/l
Intravascular 3 142 4.5 104 24 2
Intercellular 11-12 145 4.4 117 27 2.3
Intracellular 27 12 150 4 12 40
Transcellular 1 - - - - -
Gastric juice
2-2.5 per
day
60 7 100 0 -
Pancreatic
juice
1.5-2 per
day
130 7 60 100 -
Sweat
0.2 per
day
45 5 58 0 -
Clinical manifestation of excess and deficit states of major electrolytes.
Electrolyte Excess Deficit
Sodium
Hypernatremia > 147 mEq/L
Cellular shrinking may cause central
nervous system irritability,
tachycardia, dry and flushed skin,
hypertension, thirst, elevated
temperature, weight loss, oliguria,
anuria.
Hyponatrenia < 135 mEq/L
cellular swelling, may cause cerebral
edema, polyuria, headache, stupor,
coma, peripheral edema, an absence
of thirst, decreased body temperature,
rapid pulse, hypo-tension, nausea,
vomiting.
Potassium
Hyperkalemia > 5.5 mEq/L
Depressed conductivity in heart,
muscle cramping, parasthesias,
nausea, diarrhea, associated with
metabolic acidosis.
Hypokalemia < 3.5 mEq/L
Cardiac irritability, dysrhythmias,
vomiting, paralytic ileus, thirst,
associated with metabolic alkalosis,
inability to concentrate the urine.
Calcium
Hypercalcemia >12 mg/dl
Decreased neuromuscular excita-
bility, muscle weakness, central
nervous system depression, stuporto
coma, increased risk of bone
fracture,vomiting, kidney stones
Hypocalcemia <8.5mg/dl
Increased neuromuscular excitability,
skeletal muscle cramps, tetany,
laryngospasm, asphyxiation, death.
Phosphate
Hyperphosphatemia >4.5mg/dl
See hypocalcemia
Hypophosphatemia<2mg/dl
Anorexia, muscle weakness, tremors,
seizers, coma, anemia, bleeding,
leukocytes alteration.

84
Magnesium
Hypermagnesemia >2,5mEq/L
Skeletal muscle depression, muscle
weakness, hypotension, bradycardia,
respiratory depression.
Hypomagnesemia <1.5mEq/L
Hypocalcemia and hypokaliemia,
neuromuscular irritability, tetany,
convulsions, tachycardia, hyper-
tension.
Measurement Units
Laboratory measurements of electrolytes in body fluids are expressed as a
concentration or amount of solute in a given volume of fluid, such as milligrams
per deciliter (mg/dL), milliequivalents per liter (mEq/L), or millimoles per liter
(mmol/L).
The use of milligrams (mg) per deciliter expresses the weight of the solute
in one-tenth of a liter (dL). The concentration of electrolytes, such as calcium,
phosphate, and magnesium, is often expressed in mg/dL.
The milliequivalent is used to express the charge equivalency for a given
weight of an electrolyte: 1 mEq of sodium has the same number of charges as 1
mEq of chloride, regardless of molecular weight. The number of milliequivalents
of an electrolyte in a liter of solution can be derived from the following equation:
mEq = (mg/100 mL x 10 x valence) / atomic weight
The Systeme Internationale (SI) units express electrolyte concentration in
millimoles per liter (mmol/L). A millimole is one-thousandth of a mole, or the
molecular weight of a substance expressed in milligrams. The number of
millimoles of an electrolyte in a liter of solution can be calculated using the
following equation: mmol/L = (mEq/L) / valence
1.The relative size of the body fluid compartments expressed as a percentage
of total body water.
2.Describe the balance concept.
3.What is a positive balance of water metabolism?
4.What is negative water balance?
5.What are the consequences of fluid imbalance?
6.How is electrolyte imbalance characterized?
7.What is the mechanism of edemas? Classification of edema, types (cardiac,
kidney, pulmonary).
8.Several principal pathogenic factors of edema.
9.A quantity of sodium in blood plasma in a norm.
10.The quantity of potassium in blood plasma in a norm.
11.The quantity of phosphorus in blood plasma in a norm.
12.The quantity of calcium in blood plasma in a norm.

85
Protocol № 15 Date_____________________
Object of work: to show a formation of frog back arms edema at the passing
through the vascular net of a solution of lactic acid; to show the development of
lungs edema at a white rat after the intraperitoneal introduction of adrenalin.
Experimental work № 1. Prepare preparation of back arms of a frog.
Dissect an abdominal region by the longitudinal slit, extract internals.
Place ligature under an aorta, incise an aorta, insert into a glass cannula and
fix it by ligature. The upperparts of the trunk are chopped off. Fill a cannula with
Ringer’s solution for cool-blooded animals and unite it with the apparatus which
consists of two Marriott’s tubes connected with a T-joint by rubber tubing with
pressed-on clamps.
Fill one burette by solution of Ringer
and another one by lactic acid solution
painted by methylene-blue.
At first pass Ringer’s solution through
the preparation of arms vessels and count
up the amount of drops.
Close the clamp of burette with
Ringer’s solution and open the clamp of
burette with a lactic acid solution. Count
up a number of drops.
Pass a few times by turns Ringer’s
solution and lactic acid solution.
Look after development of frog back
arms edema.
№ Amount of drops of Ringer’s
solution
Number of a lactic acid solution
drops
1
2
3
4
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Experimental work 2. Account of an amount and structure of a liquid
for introduction to the patient for want of dehydration
Example. Data of an inspection of a patient: weight of body - 70 kg,
hematocrit – 0.50 l/l, contents sodium in serum of blood - 132 mmol/l (average

86
norm - 142, oscillation - 135-145), contents calcium – 3.8 mmol/l (norm - 5,
oscillation – 3.9-5.8).
Conclusions: 1. Inthe patient hypoosmolar dehydration with deficiency of
potassium. 2. It is necessary for the patient to fill water, sodium, and potassium.
Stages of account
1. Determination deficiency of water
1.1. Determination a degree of dehydration (percent of loss extracellular
of a liquid):
1.2. Determination of quantity extracellular liquid in the patient:
1.3. Determination of quantity extracellular liquid before disease:
1.4. It is necessary to enter quantity lost liquid, to the patient:
15.7 – 14.,0 = 1,7 l
2. Determination deficiency of sodium
2.1. Determination deficiency of sodium in 1 l extracellular liquid:
142 - 132 = 10 mmol/l
2.2. Determination deficiency of sodium in all extracellular liquid:
10 х 14 = 140 mmol
2.3. Determination percentage concentration of solution NaCl for
transfusion. We prepare such solution, that 1 ml it contained 1 mmol NaCl, and 1
l - accordingly 1 mol NaCl (that is 58.5 g of dry substance). It - approximately
5.8 % solution.
3. Determination deficiency of potassium
3.1. Determination deficiency of potassium in the 1 l extracellular liquid:
5.0 – 3.8 = 1.2 mmol/l
3.2. Determination deficiency of potassium in the all extracellular liquid:
1.2 х 14 = 16.8 mmol
3.3. Determination percentage concentration of a solution КСl for
transfusion. We prepare a solution from an account, that in 1 ml it was 1 mmol
КСl. Then 1 l will contain 1 mol КСl, that is 75.5 g (approximately 7.5 % a
solution).
The answer: ___________________________________________________
The deficiency of a liquid and electrolites can be also calculated under the
formulas Mc Criston and Miller:

87
1.
2. Dе = 0,2 х M х (En – Ee)
The denotations in the formulas: DH2O - deficiency of extracelular water
(l); DE - deficiency of electrolytes in extracelular water (mmol); Нсn - average
value hematocrit in norm (0.45 l/l); Нс - significance hematocrit in the patient;
En - average concentration electrolyte in serum blood in norm (mmol/l); EE -
Concentration of electrolyte in whey of blood of the patient (mmol/l); М -
Weight of a body of the patient; 0.2 - Volume of extracelular liquid (20%)
Conclusion: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Test 1. A hypertensive glucose solution was introduced into a patient. It
will intensify water movement:
A. From the intercellular liquid to the cells
B. From the cells to the intercellular liquid
C. From the intercellular liquid to the capillaries
D. From the capillaries to the intercellular liquid
E. There will be no changes of water movement
Test 2. Periodic renal colics attacks are observed in the woman with
primary hyperparathyroidism. Ultrasound examination revealed small
stones in the kidneys. What is the cause of the formation of the stones?
A. Hypercholesterinemia
B. Hyperkalemia
C. Hypercalcemia
D. Hyperphosphatemia
E. Hyperuricemia
Test 3. A patient was stung by a bee. Examination revealed that his left
hand was hot, pink, and edematic; there was a big red blister on the site of
the sting. What is the leading mechanism of edema development?
A. Increased vessel permeability
B. Reduced vessel filling
C. Injury of vessels caused by the
sting
D. Drop of oncotic pressure in tissue
E. Drop of osmotic pressure in tissue
Test 4. A patient ill with enteritis accompanied by massive diarrhea has
low water rate in the extracellular space, high water rate inside the cells and
low blood osmolarity. What is such disturbance of water-electrolytic
metabolism called?
A. Hypo-osmolar hypohydration
B. Hyperosmolar hypohydration
C. Osmolar hypohydration
D. Hypo-osmolar hyperhydration

88
E. Hyperosmolar hyperhydration
Test 5. Edema was modeling to the white rat by the injection of
adrenalin. What pathogenetic mechanism of edema development?
A. Oncotic
B. Hydrodynamic
C. Membranogenic
D. Lymphogenic
E. Colloid-osmotic
Test 6. A 50-year-old patient complains of thirst, drinking a lot of water,
marked polyuria. Blood glucose is 4.8mmol/L, urine glucose, and acetone
bodies are absent, urine is colorless, specific gravity is 1,002-1,004. What is
the cause of polyuria?
A. Hypothyroidism
B. Thyrotoxicosis
C. Aldosteronism
D. Insulin insufficiency
E. Vasopressin insufficiency
Test 7. A 2-year-old child experienced convulsions because of lowering
calcium ions concentration in the blood plasma. A function of what structure
is decreased?
A. Pineal gland
B. Thymus
C. Hypophysis
D. Adrenal cortex
E. Parathyroid glands
task: A 70-year-old female was brought to an urgent care facility complaining of
severe muscle weakness and a 3-week history of diarrhea. The on-site clinical
laboratory provided electrolyte test results as follows: Na+ = 142 mEq/L; K+ =
2.1 mEq/L; Cl- = 94 mEq/L; CO2
+ = 30 mEq/L.
1. What are electrolyte levels abnormal? 2. Is there a medical emergency? 3.
If so, what is it and what should be done?
______________________________________________________________________
______________________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology. Ed. by prof. A.V.Kubyskin. Simf.–2011. – P. 333–243, 348–360.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publ.–2010.– P. 252–266.
2010. – P. 592–614.
Milwaukee. – 2009. – P. 761–805.
5. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Copyright В. –
Lippincott Williams & Wilkins – 2008. – Chr 19. – P. 563–578.
Additional:
medical students and practitioners. Ed. by prof. Zaporozan,OSMU. – Odesa. – 2005.– P. 154–163.
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 6 – P. 84 – 108.
3. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // NY. – 2000. – P. 122–131.

89
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.
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.

90
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.
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.

91
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.
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 metabolyc changes in organism at various stages of fever.
19. Difference between fever and hyperthermia. A dialectic approach to estimation of
feverish reaction significance.

92
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.

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

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