Metod. recommendation practicum stomat f-ty 2nd-semester book 2018 Module 1

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
MODULE 1
GENERAL PATHOLOGY
Training-methodical manual for class and out-of-class work for
STOMATOLOGICAL FACULTY STUDENTS
Prepared by:
Gerasymchuk M. R.
CherkasovaV. V.
Zaiats L. M
Ivano-Frankivsk, 2018

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

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«The general nosology. Typical pathological processes»
Training-methodical manual for class and out-of-class work for
stomatological students / M.R. Gerasymchuk, V.V. Cherkasova, L.M. Zaiats
// IFNMU. Department of pathophysiology. – 2018. – 98 p. Discussed and
approved by profile commission of medical&biological disciplines meeting
of Ivano-Frankivsk National Medical University.
Protocol № __ from «__» ________________ 2018 year

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CALENDAR PLAN OF PRACTICAL CLASSES
Theme of lessons Dates Hours
1. Subject and tasks of pathophysiology. Methods of pathophysiological
investigations. Main periods of pathophysiology development.
15.01 2
2. The general studying about disease, etiology, and pathogenesis. Pathogenic
effect of ionizing radiation.
22.01 2
3. General pathophysiology of the cell. 29.01 2
4. Role of heredity and constitution in pathology. 05.02 2
5. Practical skills for the chapter “The general nosology. Pathogenic effects of
factors of the external environment. Role of internal factors in pathology”.
12.05 2
6. Disorders of peripheral blood flow and microcirculation. 09.02 2
7. Inflammation: flogogenic factors, pathogenesis of alteration, mediators; local
and general sings; Kongeims’ experiment. Pathogenesis of exudation and
proliferation.
26.02 2
8. Fever. 05.03 2
9. Pathology of reactivity. Disorders of immune reactivity. 12.03 2
10. Allergy. 19.03 2
11. Starvation. Hypoxia. 26.03 2
12. Tumors. 02.04 2
13. Practical skills for chapter “Typical pathological processes”. 09.04 2
14. Disorders of water-electrolyte metabolism and metabolism of microelements. 16.04 2
15. Disorders of acid-base balance. 23.04 2
16. Disorders of carbohydrate metabolism. Diabetes mellitus. 30.04 2
17. Disorders of lipid metabolism: dyslipoproteinemias; obesity. Medical problems
related to obesity.
07.05 2
18. Practical skills for chapter “Typical disorders of metabolism”. 14.05 2
19. Module 1 (practical control) 21.05 2
20. Module 2 (theoretical control) 28.05 2
Total hours 40
CALENDAR PLAN OF LECTURES
№ Theme of lecture Dates Hours
1. General pathophysiology of the cell. 25.01.18 2
2. Typical disorders of peripheral circulation and microcirculation. 08.02.18 2
3. Inflammation. Principles of classification, kinds, typical sings. Mediators
of inflammation.
22.02.18 2
4. Fever 12.03.18 2
5.
Pathology of reactivity. Disorders of immune system activity. Immunity
insufficiency. Allergy. Immune reactions as way of tissue damage or
dysfunction. Autoimmune diseases.
22.03.18 2
6. Hypoxia. 26.03.18 2
7.
Tumors. Principles of classification, kinds, typical features of tissue
growth. Etiology and pathogenesis of tissue growth.
05.04.18 2
8. Pathophysiology of acid-base balance and water-electrolyte metabolism. 19.04.18 2
9. Disorders of the carbohydrate metabolism. Diabetes mellitus. 23.04.18 2
10. Pathophysiology of the blood system. Anemias. 03.05.18 2
Total hours 20

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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 knowledge and practical skills. Maximal amount of points, which a student
can collect – 200 points during of every module study, including for current
educational activity – 120 points (together the semantic modules are 108 points,
individual work is 12 points), on results final module control are 80 points.
Control of theoretical and practical preparation
0 – 2 points – completely prepared homework; 0 – 3 points – oral answer;
0 – 1 points – test control during class.
Minimum – 0 points; minimum positive – 3; maximum – 6 points
Practical lessons are structured and provide a comprehensive assessment scores in all
learning activities (learning tasks) that students perform during practical classes:
«0» points – student just present in the class, but not fulfilled the task for self-knowledge
control, refuses to answer in the polling (quiz), does not participate in the discussion of
practical work and demonstration material, did not answer for the question of the final test
control. A student has not prepared homework.
«1» point – the student completed the task for self-knowledge, but can not explain the
solution of control tasks, do not know main part of the program material, does not participate
in the discussion of practical tasks, not solved the 50% of the final test control tasks. A
student has not prepared homework.
«2» points – student completed the task for self-knowledge control, but in the explanation
assumes inaccuracies; in the polling – knows the main program material, but not remember
its details; uses incorrect definitions or terminology, but make a sequences in the learned
material; has difficulties in solving practical problems and making conclusions, solved 51-
60% of the final test control tasks. A student has not prepared homework properly.
«3» points – student is prepared to the lesson, knows the program material, intelligently
and good present it, able to explain the main idea of practical tasks, correctly analyzes of
displayed material, competently and logical makes conclusions, solved 61-70% of the final
test control tasks. The student has prepared homework properly.
«4» points – student is prepared for class, knows the program material, intelligently and
logical explains it, is able to explain the practical tasks, correctly analyzes of displayed
material, competently and logical makes conclusions, solved 71-80% of the final test control
tasks. The student has prepared homework properly.
«5» points – student mastered the program material thoroughly, consistently, competently
and logical makes explanations, tightly linking theory with practice, to cope with the reasons
of practical work, demonstration material, able to analyze and make appropriate conclusions,
solved 81 – 90% of the final test control tasks. The student has prepared homework properly.
«6» points – student deeply learned program material, thoroughly, consistently,
competently and logical teaching, closely linking theory with practice, has no difficulties in
the response to changed tasks, easily cope with the reasons of practical work, demonstration
material, able to analyze and make the appropriate conclusions, solved 91 – 100% final test
control tasks. The student has prepared homework properly.

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Topic № 1. Subject and tasks of pathophysiology.
Methods of pathophysiological investigations.
Main periods of pathophysiology development.
1. The actuality of the theme. Pathological physiology is science that
studies the functional changes in a sick man and animals. It studies the most
general conformities to the law of origin, development, consequences of illness.
By experiment, we may be reproduced 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 analyse modelling 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 basic therapy.
To perform practical work:
1. Main features and purpose of an experiment in pathophysiology. 2.
Correlation of method of clinical supervision with the pathophysiological
experiment. 3. Possible experiment on a man? 4. Mental and ethical aspects of
the pathophysiological experiment.
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
Relations between
pathophysiology and other
scientific disciplines
5. Control questions of the theme:
1. Term definition – what is pathophysiology? Why is pathophysiology
important?
2. History of pathophysiology development. The significance of scientific
works of K. Bernard, 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 connection between the pathophysiology and other disciplines.
4. General pathophysiology, special or systemic and clinical
pathophysiology.

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5. Methods of pathological physiology. An experiment as the main method
of pathophysiology, its significance for solving fundamental problems of
medicine.
6. Name the methods and the aims of pathophysiology. The gist of the
experimental method.
7. Modeling pathological processes and diseases on animals: possibilities
and limitations. The significance of comparative-evolutional method for
development of pathophysiology.
8. Rules of work with laboratory animals. Types of an experiment. General
principles of planning the experimental investigations, count, statistic processing
and analysis of the results.
9. Definition a notion “experiment”, peculiarities, significance and lacks of
acute experiment, peculiarities of chronic experiment
10.Experimental therapy.
6. Task for independent extracurricular work.
Protocol № 1 Date_____________________
Experimental work. Acquaintance with the methods of fixing of
laboratory animals and technique of injections.
A. Using dressing forceps a rat is taken, imposing them on the skin of
cervical area. Holding dressing forceps in a right hand, by free fingers of left
hand the tail of animal is fixed. Straps are imposed with loops at first on the
back, and then on front extremities and fix a rat in position on the back. Acquaint
with the technique of hypodermic, intramuscular, intravenous injections. The
animals are released from straps begin front and then back extremities and take
off dressing forceps.
B. The rat is placed under a glass hubcap. The common being and conduct
of animal are studied, a reaction to a sound irritant (patter by pincers on a
hubcap), corneal reflex. Count up breathing frequency during 10 sec., multiply a
result on 6 and get data after 1 minute. The piece of cotton wool is moistening by
ether and places him under a hubcap. Watch after the development of anesthesia
at a rat, the phases of his development are marked. In the moment of the
offensive of narcotic sleep take out an animal from under a hubcap and study the
common being, the presence of reflexes, breathing frequency is counted up. The
animal can be fixed at this time. After an awakening animal is released, again
count up breathing frequency and check up renewal of reflexes. The results of
experience are written down in a protocol.
Conclusion:________________________________________________________
Practical work. Watching documental movies about methods of
experimental research

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Conclusion:________________________________________________________
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. Which one of the methods is the most important in
pathophysiology?
A. Epidemiological
B. Anatomical
C. Clinical
D. Experimental
Practice examination type 2. Give answer to the questions of the real-life
task: Experimentator should study mechanisms of dyspnea in case of disorders
of blood circulation in the lungs. Which main periods of a pathophysiological
experiment he should make?
1 3
2 4
Signature___________________
Literature:
1. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simferopol. – 2011. – P. 12–17.
2. 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. 9–11.
3. Pathophysiology, N.K. Symeonova. Kyiv, AUS medicine Publishing. – 2010. – P. 10–12.
4. Lee-Ellen C. Copstead. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc.
– 2010. – P. 15–24.
Topic 2: The general studying about disease, etiology, and pathogenesis.
Pathogenic effect of ionizing radiation.
1. The actuality of the theme. In everyday practical activity doctor always
takes into account of illness nature and peculiarities of its course. This is
important for planning of prophylactic arrangements, diagnosis rising, and
selection of drugs. In illness are distinguished two processes: а) damage property
illness; b) physiological measure against illness, which is complex of protective
compensatory-adaptation reactions. Knowledge of theoretical and clinical
aspects of the diverse kind’s pathogenic action of radial energy necessary doctors
for an organization and realizing of prophylaxis methods, and also cures of
professional diseases.
2. Duration of the class – 1 h 30 min.
3. Aim: to know external and internal causes of disease.

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To be able:
1) analyze the role of environmental factors in disease occurrence;
2) persistence of the causal agent, which causes the disease, is delayed in an
organism (healthy bacilli-carrier);
3) carry out independently the simplest experimental investigations on
animals;
4) explain the pathogenesis of ionizing radiation
To perform practical work: 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. To nalyse the “vicious circle” in the pathogenesis. Causes and
consequences constantly change their places.
A. Basic level.
The name of the previous
and future disciplines
The receiving of the skills
1. histology
2. biochemistry
3. physiology
5. radiology
Gas composition of air and partial pressure of
oxygen. Functional units structure of respiratory system,
blood, blood circulation system. Physical and chemical
indexes of gases interchange in organism. Neurohumoral
regulation of breathing and blood circulation.
A. Control questions of the theme:
1. General doctrine of disease. The basic concepts of general nosology.
Norm, health, disease (definition of WHO). A pathological process. A
pathological condition, pathological reaction.
2. 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.
3. Stages of disease development. Remission, relapse, complication. Variants
of disease outcome: complete and incomplete recovery. The main directions in
the development of doctrine of disease: humoral (Hippocrates), cellular (R.
Virchow). Their development in the modern stage.
4. 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, essence of Freudism etc.
5. Modern concepts of causality in pathology. Classification of etiological
factors. External and internal etiological factors.
6. 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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7. Notion “compensatory-adaptative reactions”, types of compensatory-
adaptative reactions, role of compensatory-adaptative reactions in convalescence
mechanisms.
8. 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.
9. The cause-effect relations in pathogenesis. Variants of direct cause-effect
relations. “Circulus vicious”. The main link of pathogenesis. Role of the local
and general in pathogenesis.
10. Concept of localization and generalization of pathological processes.
Ways of their distribution. Specific and nonspecific mechanisms of pathogenesis.
Pathogenetic principles of disease treatment.
11.Pathogenic effect of ionizing radiation. Types of ionizing radiation.
Radiosensitivity of tissues.
12.Mechanisms of direct and indirect radiation damage of biological
structures. Water radiolysis. Radiotoxins.
13.Manifestations of radiation damages on molecular, cellular, tissue, organ
and system levels.
14.Pathogenesis of radiation sickness, its main forms and syndromes. Early
and late effects of large and small doses of ionizing radiation.
15.Natural mechanisms of antiradiation protection. Pathophysiological bases
of radioprotection.
16.Influence of low and high atmosphere pressure upon organism,
mechanisms of manifestations of saturation and desaturation, hyperbaric
oxygenation use in medicine.
17.Pathogenic influence of electric current.
A. Students’ practical activities
Protocol № 2 Date_____________________
Experimental work 1. Determining the number 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 content 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 the
Goryaev’ net and calculate their amount in 1 litre of blood after a formula:
lТ
ААА
/
100
10
100
10
80
2004000 128


where:
A – is a numberof 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

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the counted up small squares; 108 is a multiplier for the count of amount of red
corpuscles in unit of SI; T – 1012.
Experimental work 2. Count of a number of leukocytes.
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. A mixture
is mixed, and then fills the chamber of Goryaev’. Count up the number of
leukocytes in 100 large squares of the net. Expect the number of leukocytes in 1
L of blood.
lG
АА
Х /
20
10
11600
204000 6



 , where “A” – is a number of leukocytes in 100
large squares; 1600 – is a number 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 leukocytes in unit of SI; G – giga – 109.
A. Practice Examination.
Practice examination type 1 Choose the correct answer:
Test 1. A 12-year-old boy came home from school and started
complaining of a headache, sickness, chill, periodical muscle pain, appetite
loss, and flabbiness. What period of illness are these symptoms typical for?
A. High point of illness
B. Incubative
C. Prodromal
D. End of illness
E. Latent
Test 2. A 49-year-old man was suffering 12 years ago from rheumatic
myocarditis, endocarditis, and insufficiency of the 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 3. A 39-years-old patient has been suffering from gastric ulcer for
last 4 years. Pain in the epigastric region, heartburn, nausea, and
constipation appear mainly in autumn and spring. Name this condition.
A. Remission B. Acute period

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C. Complication
D. Pathologic condition
E. Relapse
Test 4. Through 8 days after irradiation beside damaged developed
erosive-ulcerous stomatitis. In blood: erythrocytes-3.2*1012/l, hemoglobin-
100 g/l, leukocytes-1.2*109
/l, thrombocytes-90*109
/l. For what period sharp
radiation sickness, bone-marrow form, typical described change?
A. Prodromal
B. Dromal (initial response)
C. Imaginary well-being
D. Clinically expressed signs
E. Outcome of disease
Test 5. A man took electric wire with high tension by both hands. He
died momentarily with the result of:
A. Intracerebral bleeding
B. Respiratory standstill
C. Cardiac fibrillation
D. Burns
E. Tearing extremities off
Practice examination type 2
I. Give the description of each form of radiation disease (1 – acute, 2 –
chronic):
Indicator 1/2 Indicator 1/2
A
The disturbance of
hemopoiesis and blood
system (lymphopenia,
thrombocytopenia)
F Hemorrhagic syndrome
G Sexual dysfunction
B Anemia H Spasm paralytic syndrome
C Immune reactivity decrease J Shock
D
Dysfunction of the
alimentary tract, vomiting,
anorexia, diarrhea
K Asthenia
E Necrotic tonsillitis L Trophic disorders
Give answer to the questions of the real-life task:
TASKS
1.
What direction of electricity through the human body is the most
dangerous?
A Head C Heart
B Kidney D Liver
2.
When is the man less sensitive to the electric current?
A Under narcosis C Hypoxia
B Tiredness D Alcohol intoxication
3.
The most resistant to electric current is all the below mentioned
except:
A External epidermal layer D Muscles

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B Tendons and bones E Blood
C Nerves F Cerebrospinal fluid
II. For each statement choose T (true) or F (false) in the list provided.
№ Statement T F
1
The first period of acute radiation disease (ARD) with duration
from several hours to 1-2 days is characterized by excitation,
headache, instability of the vegetative functions, lability of the
arterial pressure and pulse
2
Latent period (one week) is accompanied by leukopenia
(progressing of lymphocytopenia, development of
granulocytopenia).
3
The third period is characterized by progressing leukopenia,
anemia. Hemorrhagic syndrome develops. Decrease of
immunologic reactivity.
4
The outcome of the ARD is multiple inflammatory processes
(necrotic angina, pneumonia, frontitis and others).
Signature___________________
Literature:
Basic:
1. Robbins & 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.
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. 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. 10–29.
Topic 3. 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.
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.

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3. Aim: to know the cell responses to injury and the major types of cellular
necrosis.
To be able: to analyze nalysen 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.
5. 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 conceptof 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 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

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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.
7. Students’ practical activities
Protocol № 3 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

17
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:____________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
__________________________________________________________________________
8. Practice Examination.
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.

18
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
medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 30–41.
3. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), 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 // Th. NY. – 2000. – P. 2–13.
Topic 4. The role of heredity and constitution 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. Spina bifida and cleft lip, for example, are apparent at birth,
but other malformations, such as kidney and heart defects, may be present at birth
but may not become apparent until they begin to produce symptoms. Not all
genetic disorders are congenital, and many are not apparent until later in life.
About 2000 different hereditary diseases are known now. 4 % of new-born
suffer from these or other genetically conditioned defects. This testifies
importance of ability to participate in exposure methods of hereditary diseases,
study ways of their prophylaxis and treatment principles. 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.

19
To be able: to analyze the pathogenesis of chromosomal diseases,
phenylketonuria.
A task is to independent extracurricular work:
1. Structure and function of genotype. 2. Types of inheritance. 3. Mutation,
of concept, mutagenic factors. 4. What the induced and spontaneous mutation? 5.
Mutations of genes as a reason of the inherited illnesses. 6. Methods of research
of heredity in a man. 7. A role of the genetic monitoring in the prophylaxis of the
inherited pathology.
4. Basic level.
The name of the previous and future
disciplines
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.
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;

20
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),
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 № 4 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%.

21
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: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Practice examination type 1. Choose the correct answer:
Test 1. An 8-month-old child has a non-closed palate, a number of eye
defects, microcephaly, a disorder of the cardiovascular system. Cytogenetic
analysis revealed 47 chromosomes with an additional 13th chromosome.
What diagnosis can be made on the basis of clinical observations and
cytogenetic examinations?
A. Down's syndrome
B. Edwards' syndrome
C. Patau's syndrome
D. Cat cry syndrome
E. Klinefelter's syndrome
Test 2. In which variant of karyotype in the nucleus of somatic cells only
one Barr’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. Excessive hairiness of auricles (hypertrichosis) is determined by
a gene which is localized in Y-chromosome. Father has this feature. What is
the probability of the fact that the boy will be born with such anomaly?
A. 0%
B. 75%
C. 25%
D. 35%
E. 100%
Test 5. A 28-year-old woman consulted a doctor about sterility.
Examination revealed underdeveloped ovaries and uterus, irregular

22
menstrual cycle. Study of sex chromatin revealed 2 Barr's bodies in most
somatic cells. What chromosome disease is the most probable in this case?
A. Turner's syndrome
B. Patau's syndrome
C. Edwards' syndrome
D. Tripl-X syndrome
E. Klinefelter's syndrome
Test 6. 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 7. 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
Test 8. A child with a history of frequent angine and pharyngitis has
been diagnosed with lymphadenopathy and splenomegaly. His appearance is
characterised by pastosity and paleness, muscular tissue is poorly developed.
Lymphocytosis is present. What kind of diathesis is it?
A. Lymphohypoplastic diathesis
B. Exudative diathesis
C. Gouty diathesis
D. Asthenic diathesis
E. Hemorrhagic diathesis
Practice examination type 2. Give answers to the questions of the real-
life task: Woman is heterozygous on phenylketonuria gene, and her husband is
homozygous on normal alleles of this gene.
1. What is probability in this family of giving birth to a child sick with
phenylketonuria? 2. Define probability of phenylketonuria display, if husband is
heterozygous on given gene.
Answersfor the task: __________________________________________________
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.

23
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.
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 & Cotran Pathologic Basis of Disease 9thed./Kumar, Abbas, Fauto.–2013.–Ch.6.–P.215–268.
3. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simf. – 2011. – P. 86–104.
4. Symeonova N.K. Pathophysiology. – N.K. Symeonova. Kyiv, AUS M-ne Publ. – 2010. – P.44–65.
medical students and practitioners. Edited by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 49–60.

24
6. 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.
Additional:
1. Copstead Lee-Ellen C., Jacquelyn L. Banasic. Pathophysiology // Elsevier Inc. – 2010. – P. 86–127.
Milwaukee. – 2009. – P. 133–156.
3. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // New York. – 2000. – P. 2–9.
4. J.B.Walter I.C.Talbot General Pathology. Seventh edition. – 1996. – P. 59–87.
Topic № 5.
Practical skills for chapter “The general nosology. Pathogenic effects of
factors of external environment. Role of internal factors in pathology”.
Control questions:
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 researchers.
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. 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.
9. Mutations. Principles of their classification. Causes of mutations.
Mutagenic factors of a physical, chemical and biological origin.
10.Autosomal dominant Mendelian disorders caused by single-gene defects:
Huntington disease, neurofibromatosis type 1, Marfan syndrome, Familial
hypercholesterolemia (LDL receptor deficiency), acute intermittent porphyria;
11.Autosomal recessive Mendelian disorders: Cystic fibrosis, sickle cell
anemia, phenylketonuria, Tay-Sachs disease (hexosaminidase A deficiency);

25
12.X-linked disorders: 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.
13.Diseases caused by mutations in genes encoding structural proteins: Marfan
syndrome, Ehlers-Danlos Syndromes.
14.Diseases Caused by Mutations in Genes Encoding Receptor Proteins or
Channels: Familial Hypercholesterolemia, Cystic Fibrosis;
15.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;
16.Mitochondrial diseases: Leber hereditary optic neuropathy, MELAS:
mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes),
myoclonic epilepsy with ragged red muscle fibers).
17.Diseases caused by alterations of imprinted regions: Prader-Willi and
Angelman Syndromes.
18.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.
19.Chromosomal diseases. Mechanisms of occurrence of the genome and
chromosomal mutations. Polyploidy, aneuploidy, deletion, duplication, inversion,
translocation.
20.Cytogenetic disorders involving autosomes: trisomy 21 (Down Syndrome),
22q11.2 deletion syndrome, trisomy 18 (Edwards syndrome), trisomy 13 (Patau
syndrome);
21.Cytogenetic disorders involving sex chromosomes: Klinefelter syndrome,
Turner syndrome, “Super-woman” syndrome.
22.Congenital anomalies: polydactyly, cleft lip, cleft palate. Etiology.
Pathogenesis. Perinatal infections (TORCH Toxoplasma (T), rubella virus (R),
cytomegalovirus (C), herpesvirus (H), and any of a number of other (O) microbes
such as Treponema pallidum).
23.Methods of investigation, prophylaxis, and treatment of hereditary diseases.
Ways of correction of genetic defects. Outlooks of gene engineering.
24.Constitution, its role in pathology. Classification of constitutional types by
Hippocrates, Sigot, Kretchmer, I. P. Pavlov, A. A. Bogomolets. The concept of
diatheses.
25.Cellular injury. Characteristics of the concept of “injury”. Principles of
classification of cell injuries.

26
26.Pathology of signalization. Pathology of signal reception. Disorders of
secondary messеngers.
27.Mechanisms and manifestations of damage to subcellular structures:
plasmatic membrane, mitochondria, endoplasmatic reticulum, lysosomes,
microtubules and microfilaments, nucleus and cytoplasm.
28.Cellular adaptation to stress. Hypertrophy, hyperplasia, atrophy, metaplasia.
Cellular and subcellular regeneration.
29.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.
30.Causes, mechanisms, and consequences of intracellular calcium
concentration increase.
31.Role of electrolyte-osmotic mechanisms in cell injury. Causes, mechanisms,
and consequences of disorders of electrolyte transport system in cells.
32.Causes and development of intracellular acidosis in cell injury.
33. Antioxidant mechanisms of cells.
34. Mechanisms of apoptosis. The mitochondrial (intrinsic) pathway of
apoptosis, the death receptor (extrinsic) pathway of apoptosis, activation, and
function of caspases. Autophagy.
35.Necrosis: coagulative, liquefactive, gangrenous, gangrenous, caseous, fat,
fibrinoid.
Topic 6. Disorders of peripheral blood flow and microcirculation.
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 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:

27
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.
The name of the previous and
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.
1. 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.
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.

28
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 № 6 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
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

29
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
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

30
experiment? 3. Can fatty embolism of the brain appear when big tubular bones
are broken?
Conclusion: __________________________________________________________
Practice examination type 1. Choose the correct answer:
Test 1. What does the term “sludge” mean?
A. Penetration of foreign bodies into the blood and their accumulation in it.
B. Formation of a lot 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 2. Ganglion sympathectomy was performed to a patient who suffers
from obliterative endarteritis and caused the development of arterial
hyperemia. What is kind?
A. Work
B. Reactive
C. Neurotonic
D. Neuroparalytic
Е. Metabolic
Test 3. What is the basic factor of clot formation (the Virchow's triad)?
A. Endothelial injury (phlebitis, atherosclerosis, mechanical injury)
B. Disbalance between coagulation and fibrinolytic systems
C. Slowing down of the blood flow
D. All of the above are correct
Test 4. High level of arterial blood pressure is observed in a patient with
renal disease accompanied by ischemia of renal parenchyma. What is the
leading factor of increase in arterial blood pressure in this patient?
A. Excess of angiotensin II
B. Excess of antidiuretic hormone
C. Augmentation of cardiac output
D. Increase in tonus of sympathetic nervous system
E. Hypercatecholaminemia
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:
A. Accumulation of hydrogen ions
B. Deficiency of potassium ions
C. Deficiency of adenosine triphosphate
D. Excessive accumulation of calcium ions
E. Deficiency of creatine phosphate

31
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
tasks:
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?
Answersfor the task 2.: _________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
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.

32
2) Is development of complications of thrombophlebitis possible from the side
of other organs - brain, kidney, spleen?
Answersfor the task 3. _________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Task 1. 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 by the formation of active
thrombin, which catalyzes transformation of fibrinogen into
fibrin with the formation of a clot
Task 2. What is true (T), what is false (F) in the following 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 3. 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
J Hyperemia of skeletal
muscles in hard physical

33
digestion work
E Typhoid fever K Inflammatory hyperemia
Signature___________________
Literature:
Basic:
1. Robbins & Cotran Pathologic Basis of Disease 9th ed/ Kumar, Abbas, Fauto. –2013.–Ch 3.–P.75–97.
4. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins),
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. Ch. 15. – P. 263 – 272, 178–189.
medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 60–67.
Additional:
1. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. –
2010. – P. 347–371.
2. Robbins&Cotran Pathologic Basis of Disease 8thed./Kumar, Abbas, Fauto. –2007.–Ch.4.–P. 81–100.
Milwaukee. – 2009. – P. 462–474.
Topic 7. Inflammation: flogogenic factors, pathogenesis of alteration,
mediators; local and general sings; Kongeims’ experiment.
Pathogenesis of exudation and proliferation.
The actuality of the theme. Inflammation is the reaction of vascularized
tissue to local injury. The causes of inflammation are many and varied.
Inflammation commonly results because of an immune response to infectious
microorganisms. Other causes of inflammation are trauma, surgery, caustic
chemicals, extremes of heat and cold and ischemic damage to body tissues.
Inflammatory conditions are named by adding the suffix -itis to the affected
organ or system. For example, appendicitis refers to inflammation of the
appendix, pericarditis to inflammation of the pericardium, and neuritis to
inflammation of a nerve. More descriptive expressions of the inflammatory
process might indicate whether the process was acute or chronic and what type of
exudate was formed (e.g., acute fibrinous pericarditis).
Processes of exudation and emigration of leukocytes, and also phagocytosis
is main moments in the development of 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.

34
2. Duration of the class – 1h 30 min.
3. Aim:
To know 1. Definition of the notion "inflammation". 2. Causes of the
inflammation. 3. The role of mediators in inflammation development. 4. The
meaning of the organism reactivity in inflammation development. 5. The general
manifestation of inflammatory reaction. 6. Clinical symptoms of the
inflammation. 7. Causes and mechanisms of the vascular permeability disorder in
inflammation. 8. Methods of the vascular permeability study in the area of
inflammation. 9. A common concept is about phagocytes (macrophages and
polymorphous leukocytes).
To be able:
- to describe the processes of alteration, exudation, and proliferation;
- to give a description of mediators of inflammation and explain their role in
the pathogenesis of inflammation;
- to reproduce inflammation in an experiment.
- to explain the mechanisms of the separate stages of phagocytosis;
- to describe kinds and reasons for violations of phagocytosis
To perform practical work: to analyze the pathogenesis of inflammation:
disorders and after effect.
4. Basic level.
1. Histology
2. biochemistry
3. physiology
4. pharmacognosy
6. surgery
Functional parts of the bloodstream. Conception
about the microcirculation. Mechanisms of
regulation of blood circulation in capillaries and
venules. A conception of the role of connecting
tissue cells, their structure, main functions. The
concept is about the products of an arachidonic
acid cascade, the kallikrein-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

35
Increase of erythrocyte sedimentation
Change of hormone content:
 catecholamins
 corticosteroids
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. Local symptoms of inflammation in the experiment
(Cels, Galen). Classification of inflammation.
3.Primary and secondary alteration. Causes and mechanisms of secondary
alteration.
4.Role of lysosomal enzymes, free radicals, peroxides and system of
complement in tissue injury.
5.Biochemical and physicochemical disorders in focus of inflammation.
6.Local acidosis, hyperosmia, hyperoncia.
7.Mediators of inflammation. Their classification. Role of cytokines in the
pathogenesis of inflammation.
8.Products of tissue basophile degranulation.
9.Derivates of arachidonic acid: prostaglandins, leukotrienes, thromboxanes.
10.Kallikrein-kinin system.
11.Complement activation in the development of the inflammatory process.
12.Exudation. Mechanisms of exudation. Causes and mechanisms of increase
in permeability of a vascular wall. Early and late stages of increase in
permeability. Kinds of exudates.
13.Emigration. Leukocyte emigration stages. Mechanisms of margination of
leukocytes. Exogenous and endogenous chemotaxis. Phagocytosis.
14.Phagocytosis. Stages. Mechanisms of absorption, elimination and
overcooking of microorganisms by phagocytes. O2-dependent and O2-
independent killing. Disorders: Chediak-Higashi syndrome, chronic
granulomatous disease, myeloperoxidase deficiency.
15.Proliferation. Mechanisms of proliferation and its regulation. The concept
of growth factors. Role of protein kinase C and tyrosine protein kinases in
activation of proliferative processes. Mechanisms of sclerosis.

36
16.General symptoms of inflammation: fever, leukocytosis, “acute phase
response in inflammation”.
17.Relation of local and general disorders at inflammation. Role of reactivity
in development of inflammation, the significance of immune reactions at an
inflammatory process. Inflammation and allergy.
18.Biochemical and physical and chemical changes are in the place of
inflammation. Reasons for development of acidosis in the inflammative tissues.
19. Influence of nervous and hormonal factors during inflammation. The
significance of inflammation for an organism.
20. Principles of anti-inflammatory therapy.
Protocol № 7 Date_____________________
Experimental work 1. 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: ____________________________________________________________
______________________________________________________________________
______________________________________________________________________
______________________________________________________________________
Experimental work 2. Microscope investigation of exudates.
The object of work: to acquaint the students with the methodic of
determination of the subtitles of amylolytic enzymes of pus.
Summary; to determine the enzymic special features of pus the serum of
pus is prepared. For this purpose the pus exudate is centrifuged, the upper layer is
aspirated, and diluted with the physiological solution in 10 times.
1. Serous-purulent exudate got from the abdominal cavity of guinea-pig 3
hours after injection 1 ml of a suspension of Staphylococcus culture. (There are

37
more segmental and stable neutrophils, lymphocytes, monocytes, cells of
mesothelium specimen. There are visible cocci accumulations. It is observed
microbes engulfed by neutrophils and monocytes. There is fragment of blood
cells and mesothelium).
2. Serous-purulent exudate got from the abdominal cavity of guinea-pig 24
hours after injection of 1 ml suspension of Staphylococcus culture. In comparison
with the previous specimen, here is observed many monocytes. Apart from them
engulfed remains of diverse cells (cultural phagocytosis), many destroyed cells
(purulent bodies).
3. Purulent exudate has taken in the patients. It is observed a large number
of destroyed leucocytes and cultural elements in vision sight – compact shapeless
mass, in which difficult to distinguish the structural tissues elements.
To draw and to note morphological peculiarities of exudates. Write down
the experiment results and protocol of experiment according to a scheme.
Questions for discussion.
1. What is it purulent bogy? 2. What does origin have the enzymes in
inflammatory exudate? 3. What is the mechanism of leucocytes destroying in
inflammation area?
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.
1:1 0 1:20 1:40 1:80 1:160 1:320 1:640 1:1280
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

38
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.
Conclusion: ______________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
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
Conclusion: _________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Experimental work 3. To look after phagocytosis of bird's erythrocytes
in peritoneum exudate of a rat. With the purpose of recreation of aseptic
inflammation for days of the experiment, a rat enters intraperitoneal sterile beef-
extract [meat infusion] broth. At the beginning of employment in an abdominal
region enter 5 ml suspension of bird's erythrocytes (not more than 1 ml on the
50g masses). Through 25 min by pipette collect exudate. Then prepare strokes
and painted after Pappengeymom. Method of coloring - on a stroke inflicts the
counted up amount of drops of paint of May-Grunwald and rocks (swinging
lightly) during 3 min. (fixing). Add the same amount of the distilled water, mix
up a waggle and abandon on 1-2 min. (coloring). A smear is united and, not
washing water, on a stroke inflicts the Romanovskyy smear (a 1 drop is on 1 ml
of the distilled water) on 6 min. Wash off a smear by water, a stroke is dried out
by filtration paper. Cellular composition of exudate is studied under the
immersion increase of microscope and painted the phenomenon of phagocytosis
in a protocol.
Conclusion: _______________________________________________

39
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Practical work 1. Watching movies “Inflammation”. Distinguish all stages
of inflammation and explain according to movie main pathogenetic links.
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Practical work 2.Watching movie “Inflammation and Immune response”.
Notice in protocol main etiological factors of inflammation; explain pathogenesis
of immune response, general symptoms and comlications.
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Test 1. Necrosis focus appeared in the area of hyperemia and skin edema
in few hours after burning. What mechanism strengthens destructive events
in the inflammation area?
A. Proliferation of fibroblasts
B. Secondary alteration
C. Primary alteration
D. Emigration of lymphocytes
E. Diapedesis of erythrocytes
Test 2. Aspirin has an antiinflammatory effect due to inhibition of the
cyclooxygenase activity. Level of what biological active acids will decrease?
A. Biogenic amines
B. Catecholamines
C. Prostaglandins
D. Leucotriens
E. Iodinethyronyns
Test 3. Among the humoral mediators of the inflammation, the most
meaning is:
А. Hageman's factor
В. Bradykinin
С. α2– globulin
D. Complement system
E. Prekallikrein
Test 4. A 16-year-old boy has performed an appendectomy. He has
been hospitalized for right lower quadrant abdominal pain within 18
hours. The surgical specimen is edematous and erythematous. Infiltration
by what of the following cells is the most typical for the process occurs
here?
A. Basophils
B. Monocytes
C. Limphocytes
D. Eosinophils
E. Neutrophils
Test 5. To the molecules of intercellular adhesion belong:
A. Leukotrienes
B. Interleukin-1, 6, TNF
C. Selektins, integrins
D. IgA, IgE, IgM

40
E. Lysosomal enzymes
Test 6. At the laboratory experiment, the leukocyte culture was mixed
with staphylococci. Neutrophile leukocytes engulfed and digested bacterial
cells. This process is called:
A. Facilitated diffusion
B. Diffusion
C. Osmosis
D. Phagocytosis
E. Pinocytosis
Test 7. Exudation - is:
A. Damage to cells
B. An exit of liquid and components of blood plasma dissolved in it from
the vessels into the area of inflammation
C. Regeneration of cells
D. Transition of liquid from the tissues into the vessels
E. Reproduction of cells
Test 8. Exudate of next composition: albumen 4% (in a norm to
1,5%), a lot of cells, neutrophils 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 9. Proliferation - is…:
A. Destruction of cells
B. Damage to cells
C. Exit of cells into the area of
inflammation
D. Reproduction of cells
E. Accumulation of exudate
Test 10. A patient with infectious mononucleosis had been taking
glucocorticoids for two weeks. He was brought into remission, but he fell ill
with an acute attack of chronic tonsillitis. What action of glucocorticoids
caused this complication?
A. Antitoxic
B. Antiinflammatory
C. Antishock
D. Antiallergic
E. Immunosuppressive
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: ________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________

41
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?
Answersfor the task 2: ________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Task 3. From pleural cavity of the patient doctor got exudate of such
composition: protein 58 g/l, leukocytes – 6200/mcl, prevail neutrophils, much
wholes and destroyed cells, рН 6.6.
1. What exudate did doctor get in the patient? 2. Explain mechanism of
exudate formation in pleural cavity. 3. What is the origin of found cells? 4. What
is the positive and negative role of exudate in inflammation?
Answerfor the task 3___________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
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.
4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, M-ne Publishing. – 2010. – P. 120–131.
Additional:
1. Copstead Lee-Ellen C., Banasic Jacquelyn L. Pathophysiology // Elsevier Inc. – 2010. – P. 197–203.
2. Pathophysiology, Concepts of Altered Health States, C. M. Porth, G. Matfin.– NY – 2009. – P. 377–400.
medical students and practitioners. Ed. by prof.Zaporozan, OSMU. – Odesa. – 2005.– P. 68–77.
4. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins),
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Chapter 9 – P. 150 – 161.
Topic 8. 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

42
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.
2. Duration of the class – 1h 30 min.
3. Aim:
To know, 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;
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

43
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.
8. Changes in metabolism and physiological functions in fever.
9. Protective significance and pathological manifestations of fever.

44
10. Pathophysiological principles of antipyretic therapy. The concept of
pyrotherapy.
11. The main differences between fever, exogenous hyperthermia and other
kinds of hyperthermia.
Protocol № 8 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

45
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
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?
Answersfor the task: __________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
Signature___________________
Literature:
Basic:
General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simf. – 2011. – P. 257–280.
Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, Medicine Publ.–2010.–P. 131–142.
Copstead Lee-Ellen C., Banasic Jacquelyn L. Pathophysiology // Elsevier Inc. – 2010. – P. 202–203.
Pathophysiology, Concepts of Altered Health States, C. Mattson Porth, Glenn Matfin.– NY – 2009. – P. 214–231.
Additional:
Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), 2003 / Carol
Mattson Porth, Kathryn J. Gaspard. Chapter 9 – P. 161 – 166.
Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // NY – 2000. – P. 20–25.

46
Topic 9. Pathology of reactivity.
Disorders of immune reactivity.
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,
antitoxin, and antibacterial
properties; only Ig that
crosses the placenta;
responsible for protection of
newborn; activates
complement and binds to
macrophages
IgG1 65 150 ++ +
IgG2 23 150 + +
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
IgA
secr.
2-5 380 - -
Mucous
membrane

47
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.
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
protection respiratory
secretions, and
breast milk;
protects mucous
membranes
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.

Metod. recommendation practicum stomat f-ty 2nd-semester book 2018 Module 1

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