Kursk State Medical University

Department of Pathophysiology

TEACHING INSTRUCTIONS FOR FOREIGN STUDENTS

IN THE PATHOPHYSIOLOGICAL PRACTICAL SESSIONS

The Head of the

Pathophysiology Department,
professor L. Severyanova

Kursk – 2003
УДК: 616-092=111(072) Печатается по решению
ББК: 52.5я7Англ. редакционно-издательского
совета КГМУ

Severyanova L.A., Lyashev Y.D., Antopolskaya E.V. Teaching

instructions in Pathophysiology for the students of Medical faculty. – Kursk:
KGMU, 2003. – 40 р.

Authors: professor L.A. Severyanova

professor Y.D. Lyashev
associate professor E.V. Antopolskaya

These instructions contain the basic information for the students and
teachers on organization of theoretical preparing for practical sessions and the
description of experimental works. The plans of each topic and the questions for
self-assessment help students to study necessary material.

ISBN: 5-7487-0695-4 ББК: 52.5я7Англ.

© Коллектив авторов, КГМУ, 2003

 THE BASIC METHODS OF THE WORK WITH ANIMALS

1. Animal fixation has great meaning for successful implementation of

experiments. The different methods of fixation are used for each animal species.
Rabbits are fixed with arms, binding to operating table or placement in
special boxes. Boxes with special openings are used for head fixation. Guinea pigs,
white rats and mice are fixed with hands (for injections), bound to table. Frogs are
fixed with sticking to a special table, with arms or are unmoved by means of spinal
cord destruction after previous decapitation or without one.
Dog fixation. It should fix dogs standing in special mount (partial fixation)
or lying on operating table depending on research. Sometimes it’s required to fix
additionally the one part of the body (head, extremity, tail). In these cases we use
the fixation with hands or additional binding to mouth. In some experiments we
use myorelaxants for the full unmoving of dogs without narcosis (curare 1 ml of
1% solution per 11 kg b.w. or its substitutes: dithillin, diplacin and etc).
Narcosis. All of narcosis types are used for anaesthesia in surgeries and full
unmoving: inhalator, injective (intravenous, intramuscular, intraperitoneal,
subcutaneous) or combined and mixed. Morphine-ether, morphine-hexenal,
hexenal anesthesia are the most frequently used for dogs. Morphine is injected
subcutaneously
30-40 min before surgery in dose of 0,5 -0,75 ml of 1% solution on 1 kg b.w. Dog
is bound to surgical mount after vomiting and sleeping and given to inhale with
ether through the mask. 10% solution of hexenal in dose 40-50 mg/kg is injected
intraperitoneally in morphine - hexenal anaesthesia 40-50 min after morphine
injection. Narcosis lasts during 3-4 hours. Intravenous hexenal injection in dose of
30 mg/kg provides narcosis during 15 min without premedication. Narcosis
prolongation is provided with additional hexenal injections. Hexenal narcosis is
achieved in rabbits with the injection intravenously of 5% solution in dose 30-40
mg/kg.
Ether narcosis is given to rabbits with ether inhalation through the mask.
Guinea pigs, rats, mice and cats are put under glass cowl and put cotton
wool lump moistened with ether for providing of ether narcosis in them. Animal is
fixed to laboratory table after fall asleep and narcosis is continued with ether
inhalation through special mask.
Uretan narcosis is achieved with the subcutaneous injection of10% solution
in dose: to guinea pig -1,5 g/kg, to rat - 1g/kg, to mouse - 15 mg on 10 g b.w.
Frog. The cotton wool lump moistened with ether is put on frog belly for
some minutes and it is enough to provide for ether anaesthesia. 10% uretan is
injected in subcutaneous lymphatic bag in dose 1,5-2 ml (0,2 g for frog). The frog
is placed within 10-15 min. in 10% solution of alcohol for providing of alcohol
anaesthesia and narcosis prolongs within 20 min.

TOPIC: “THE CONCEPT OF “DISEASE”. DYING AND REANIMATION”

I. The aim of individual work. As the result of individual work a student
must know:
 - short history of the development of notions about “disease”;
- definition and essence of basic notions and terms of pathology;
- general periods of typical disease development and basic forms of atypical
disease development;
II. Items for self-assessment.
1. The modern definition of “disease” and its basis.
2. The essence of the notion of “pathological process” and its relations to
“disease” phenomenon.
3. The essence of the notion “pathological state” and its interconnection with
the notions of “pathological process” and “disease”.
4. The types of symptoms and their characteristics.
5. The essence of the notions of “syndrome” and “symptom complex”.
6. The periods of typical disease development and their characteristics.
7. The forms of atypical disease development and their characteristics.
8. The factors, which determine the origin of different forms of atypical
disease development.
9. The principles of disease classification.
10. The characteristics of terminal states.
11. The stages of nervous system functions depression.
12. The peculiarities of the changes of heart activity.
13. The mechanism of respiration changes development in dying.
14. The compensatory mechanisms of nervous and cardiovascular system in
dying.
15. Hypoxia and metabolic acidosis as the most important mechanisms of
dying process.
16. The role of Russian scientists in reanimation science development.
17. The basic principles of modern reanimatology.
18. The methods of respiration and heart activity resuming and their
pathophysiological basis.
19. The pathophysiological approach to psychoneurological functions
resuming in reanimation.
20. The stages of postreanimation period and their characteristics.
21. Postreanimation disease and its pathogenesis.

Practical Part. Experiment description.

“The reanimation of rat after experimental asphyxia”.
1. Place a rat under a cap and put down the cotton wool moistened with the
ether.
2. When the rat is asleep, inject 1% hexenal solution intraperitoneally in the
dose of 10 mg per 100 g of body weight.
3. Put the narcotized rat on the laboratory desk.
4. Reveal the trachea by means of the middle cutting of the neck tissue and
introduce the ligature after it.
5. Cut the trachea between the second and the third cartillages.
6. Introduce a glass tube into the cutting and fix it using ligature.
 7. Reproduce asphyxia, closing the tube.
8. Watch the asphyxia stages development.
9. Fill the table with the data obtained.

Duration of respiratory pathways

closing. The time of reanimation beginning.
Character and volume of reanimation Results of reanimation measures.
measures.
1) Till the expiratory breathlessness а) At once after restoration respiratory
termination. tract passability.
2) Till the ceasing of terminal respiration. b) The restoration of respiratory tract
3) 1 min after the terminal respiration passability.
ceasin. c) The restoration of respiratory tract
4) 3 min after the terminal respiration passability, artificial lung ventilation
ceasing. through the special tube and indirect heart
massage.
d) The restoration of respiratory tract
passability and rhythmical thorax
squeezing.
10. Explain the mechanisms, which provide the effective reanimation in
dependence on the time of reanimation beginning.
11. Make a conclusion. Write down a protocol.

TOPIC: “GENERAL ETIOLOGY”

I. The purpose of individual work. As the result of individual work a student
must know:
- modern definition of “etiology”;
- classification of the causes of disease;
- crucial mechanisms of social factors action as promoting disease origin.
II. Items for self-assessment.
1. Definition of “etiology”.
2. Meaning of the cause and conditions in the disease origin.
3. Modern understanding of the role of “external” and “internal” causes in
disease origin.
4. The classification of disease causes.
5. Mechanism of the action of “indifferent” factor.
6. Role of social factors in the origin and the prevention of disease.
7. Modern understanding of polyetiologency in the pathology.
8. Essence of monocausalism, constitutionalism, conditionalism and their
estimation.

Practical Part. Experiment description.

“The dependence of injury severity on extraordinary irritant strength”.
1. Remove the frog head and put the frog on the left palm with belly down
and with cranial end to yourself. Introduce the pointed end of scissors into
esophagus and make longitudinal dissection along paravertebral lines and remove
the vertebrae. Put the frog on laboratory table, straighten the esophagus and wash
properly it with physiological solution (0,9% sodium chloride solution).
2. Spot the time of the movement of cork lump from the glottis to cardia.
Then act successively on mucosa with 10 %, 50% and 96% ethanol and spot the
time of cork movement after each action of new concentration.
3. Explain the experimental results depending on the mechanisms of ethanol
action on biological structures.
4. Present the experimental data in table. Write down the resume.

TOPIC: “GENERAL PATHOGENESIS”

I. The purpose of individual work. As the result of individual work a student
is to know:
- modern definition of “pathogenesis”;
- role of a etiological factor in the pathogenesis;
- role of the morphological and functional changes in the pathogenesis;
- character of the primary injury and role of its location in the pathogenesis;
- essence of the basic link of the pathogenesis, causal - effect relations and
the meaning of “vircious circle” in the pathogenesis;
- general pathogenic mechanisms and their interaction in disease
development;
- mechanisms of recovery and restoration of impaired functions of the
organism.
II. Items for self-assessment.
1. Role of etiological factor in pathogenesis.
2. Role of the location and character of primary injury in pathogenesis.
3. The “basic link” and the guiding factors of pathogenesis.
4. Causal - effect relations and the “vircious circle” of pathogenesis.
5. Role of the nervous system in the pathogenesis of diseases.
6. Essence of cortical - visceral theory in pathology.
7. Humoral mechanisms of pathogenesis.
8. Hormonal mechanisms of pathogenesis.
9. Essence of Selye’s stress theory.
10. Interrelations of nervous and hormonal mechanisms in pathogenesis.
11. Role of immune mechanisms in pathogenesis.
12. Role of connective tissue in pathogenesis.
13. Interrelations of destructive and defensive-adaptive reactions in
pathogenesis.
14. Interaction of local and general changes in pathogenesis.
15. Interconnection of morphological and functional changes in
pathogenesis.
16. Notion of “functional diseases”.
17. Recovery and its mechanisms.
18. Mechanisms of the restoration of impaired functions.

Practical Part. Experiment № 1. Description.

 “The influence of narcosis on the development of oxygen deprivation in mice”.
1. Inject subcutanuously 1% hexenal solution to 2 mice of the same weight
in accordance with the table:
Mice weight Solution volume Mice weight Solution volume
15 g 0,16 ml 21 g 0,28 ml
16 g 0,18 ml 22 g 0,30 ml
17 g 0,19 ml 23 g 0,33 ml
18 g 0,21 ml 24 g 0,36 ml
19 g 0,23 ml 25 g 0,38 ml
20 g 0,25 ml 26 g 0,40 ml

2. 12-15 min later (2 narcotized mice and 2 control ones) are placed into
separate retorts (100 ml volume). The retorts are closed hermetically. Watch the
mice till their death.
3. Explain the results. You should remember about the influence of nervous
system on the general state of organism and pathological process development.
4. Write down experiment resume.

Experiment № 2. Description.
“The influence of environment temperature on the development
of oxygen deprivation in mice”.
1. Pick out 9 mice with the same weight.
2. Place these mice in separate retorts. Close the retorts hermetically.
3. Place these retorts likewise: 3 of them - into warm water (T=38-40 C), 3
of them - into cold water or snow (T=0), and the last ones should remain in normal
temperature condition.
4. Watch the mice till their death.
5. Explain gained results. Write down the resume.

TOPIC: “REACTIVITY AND RESISTANCE OF HUMAN ORGANISM”

I. The purpose of individual work. As the result of individual work a student
must know:
- definitions of “reactivity” and “resistance”;
- interconnection between reactivity and resistance;
- peculiarities of the principal aspects of human organism reactivity and
resistance;
- mechanisms of principal external and internal factors influence on
organism reactivity;
- main ways and principles of the change of organism reactivity.
II. Items for self-assessment.
1. The definitions of “reactivity” and “resistance”.
2. The classification of reactivity.
3. The aspects of the group and individual reactivity and resistance.
4. The interconnection between the reactivity and the resistance of organism.
5. The cell mechanisms of reactivity and resistance.
6. The essence and peculiarities of the specific reactivity resistance.
 7. The peculiarities of the reactivity and resistance of female organism.
8. The peculiarities of the reactivity and resistance of newborns and infants.
9. The peculiarities of the reactivity and resistance of children from 2 to 10-
12 years.
10. Physiological peculiarities of the reactivity and resistance in juvenile
age.
11. Physiological mechanisms of the reactivity and resistance decrease in old
age.
12. The essence and the manifestations of the physiological reactivity.
13. The conditions of formation and the peculiarities of the of pathological
reactivity manifestation.
14. The essence of the specific and non-specific reactivity and resistance.
15. The essence and the peculiarities of passive and active resistance.
16. The influence of constitution and the type of highest nerve activity and
the morbidity of human beings.
17. The mechanisms of the influence of protective inhibition and excitation
in CNS on the reactivity and the resistance of human organism.
18. Mechanisms of the influence of endocrine system on reactivity and
resistance.
19. Mechanisms of the influence of external factors on reactivity and
resistance.
20. Means of the directed change of specific and non-specific reactivity and
the resistance of organism.

Practical Part. Experiment № 1. Description.

“The influence of narcosis on the result of electroshock in mice”.
1. Take 2 mice. Inject 1% hexenal solution to one of them subcutaneously in
accordance with the table from teaching instruction to “Pathogenesis”.
2. In 12-15 min (when mice are asleep) both mice should be placed into a
device for electroshock.
3. Give electroshock to both mice during 3 sec, then 6, 9, 12 sec as long as
both mice die.
4. Find the connection between the mice resistance to electroshock and the
changes of reactivity under the influence of narcosis.

Experiment № 2. Description.
1. Place a mouse into a retort in a refrigerator for 50 min.
2. Place overcooled and control mice in a device for electroshock.
3. Give electroshock to both mice in the same way as in the previous
experiment.
4. Explain mechanisms of the reactivity change to electroshock after
cooling.

INDIVIDUAL WORK
 TOPIC: “SIGNIFICANCE OF THE EXTERNAL ENVIRONMENT
IN THE ORIGIN OF DISEASE”
Items for self-assessment.
1. Pathogenetic physical factors: mechanical ones, kinetoses, acoustic
waves.
2. Pathogenetic action of thermal factors: general and local effects of heat
and cold.
3. Effects of radiant energy.
4. X-rays as pathogenetic factor.
5. Radiation sickness; the forms of the disease, the mechanisms of ionising
radiation action (free radicals formation, metabolic disorders etc).
6. Local and general effects of electric current.
7. Pathogenic action of chemical factors.
8. Effects of altered atmospheric pressure.
9. Biological factors: microbes, parasites.

TOPIC: “THE MECHANISM OF ACUTE AND CHRONIC ALCOHOL.

ACTION ON THE HUMAN ORGANISM”
I. The purpose of individual work. As the result of individual work a student
must know:
- the modern notions of the mechanisms of the acute and chronic alcohol
action on the human organism;
- the mechanisms of steady pathological attraction to ethanol.
II. Items for self-assessment.
1. Endogenous ethanol formation and the main metabolism ways of
endogenous and exogenous ethanol. The meaning of ethanol and its metabolites in
healthy organism.
2. Basic phases of acute ethanol action and their dependence dosage.
3. Basic mechanisms (theories) explaining ethanol and acetaldehyde effect
in organism.
4. The toxic acute ethanol action on the cell membranes.
5. Acute molecular (metabolic) effects of ethanol in single injection.
6. Acute effects of ethanol on the CNS neurotransmitters.
7. The mechanism of the excitation, inhibition and narcotic phases in acute
alcohol action.
8. Alcoholism, its stages.
9. The mechanism of psychic dependence on alcohol, the essence of “opiate
hypotheses”. “Vicious circle” formation.
10. The definition of tolerance to alcohol, the mechanisms of its formation.
11. Abstinence syndrome in alcoholism, the mechanisms of its formation.
12. “Vicious circle” of the physical alcohol dependence formation.
13. The molecular mechanisms of tolerance to ethanol formation.
14. The toxic ethanol action on membrane in chronic alcohol consumption.
15. Imbalance of neurotransmitters systems in chronic alcohol action.
 16. Manifestations of abstinence syndrome and the mechanisms of their
development.
17. The mechanisms of cardiomyocytes injury in ethanol action.
18. Toxic - allergic heart damage in alcoholism, basic syndromes.
19. The peculiarities of liver pathology, digestive tract injury, pathologic
changes of the nervous system and in blood. The alcoholic microangiopathy
development.
20. Ethanol influence on heredity. Alcoholic fetus syndrome.
21. The principles of the correction of ethanol influence on organism.

Practical Part. Experiment description.

“The development of acute alcohol effects in rats”.
1. Take two rats. Weight them. Inject intraperitoneally 25% ethanol solution
to both of them: to one of them – in dose 1,5 g per 1 kg of body weight, and to
another one – in dose 4,5 g per 1 kg of body weight. Set both rats into the glass
boxes.
2. Observe for the development of the consequential stages of acute alcohol
effect (excitation, inhibition, narcosis). pay attention to the character of rat’s
movements and the dependence on the duration of these stages on the dose.
3. Explain the mechanisms of the development of the different stages in
acute alcohol consumption. Write down the protocol.

TOPIC: “PATHOPHYSIOLOGY OF PERIPHERAL CIRCULATION AND

MICROCIRCULATION. THROMBOSIS AND EMBOLISM”
I. The purpose of individual work. As the result of individual work a student
must know:
- the causes of origin and the mechanisms of the development of the
different forms of peripheral circulation and microcirculation disorders;
- the basic manifestations and consequences of ischemia, arterial and venous
hyperemia, their development;
- origin, causes and the mechanisms of thrombosis and embolism
development;
- pathophysiological principles of the prevention and therapy of thrombosis
and embolism.
II. Items for self-assessment.
1. Basic forms of peripheral circulation disorders.
2. Origin, causes and the mechanisms of the development of
microcirculation changes in arterial hyperemia.
3. Mechanisms of development and the peculiarities of microcirculation
changes in arterial hyperemia.
4. Consequences of arterial hyperemia and possibilities of its using in clinic.
5. Origin causes and the mechanisms of venous hyperemia development.
6. Character of microcirculation changes in venous hyperemia.
 7. Consequences of venous hyperemia and the mechanisms of its
development.
8. Stasis, its types, the mechanism of development.
9. Origin, causes and the mechanisms of ischemia development.
10. Character of microcirculation changes in ischemia.
11. Meaning of collateral circulation in ischemia.
12. Etiology and pathogenesis of thrombosis.
13. Peculiarities of the mechanisms of arterial and venous thrombi
formation.
14. Outcomes of arterial and venous thromboses.
15. Embolism and its types.
16. Causes and the mechanisms of embolism development.
17. Peculiarities of embolism development in greater and lesser circulation.
18. Embolism consequences.
19. Infarction and its types.
20. Causes and mechanisms of infarction development.
21. Meaning of collateral circulation in the development and overcomes of
thrombosis, embolism and infarction.

Practical Part. Experiment description.

“Visible manifestations of arterial hyperemia in rabbits”.
1. Use 3 rabbits in experiments. Rub one ear with cotton wool lump
moistened with ether. Compare the ears of these rabbits with control one.
2. Draw the attention to the character and the degree of the expression of
observed circulation changes of rabbit’s ears.
3. Explain the mechanisms of arterial hyperemia clinical manifestations
development. Write down the protocol. Draw the experimental results with colour
pencils in copybooks.

TOPIC: “FEVER”
I. The purpose of individual work. As the result of individual work a student
must know:
- definition of fever;
- etiology, pathogenesis and biological essence of fever;
- mechanism and peculiarities of fever, developing in different diseases.
II. Items for self-assessment.
1. Etiology of fever. Infectious and non-infectious fevers.
2. Modern definition of fever.
3. Pyrogens and their classification.
4. Fever pathogenesis.
5. Correlation of heat production and heat loss.
6. Role of nervous mechanisms in fever development.
7.Fever influence on vitally-important functions of organism.
8. Pathogenic peculiarities of fever in different diseases.
9. Fever influence on infectious and non-infectious disease development.
 10. Biological essence of fever.
11. Comparative characteristics of fever and overheating (hyperthermia) of
an organism.
12. Physician’s tactic in temperature rise in “fever” patients and in the cases
of the overheating of organism.
13. Pathophysiological basis of using artificial fever in medicine.

Practical Part. Experiment № 1. Description.

“Fever development in dependence on functional state
of nervous system in an animal”.
1. Take the body temperature of 2 rabbits using the mercurial termometer.
2. Give to one rabbit intravenously hexenal solution. Another rabbit is a
control one.
3. Inject intravenously 1 unit/kg b.w. of pyrogenal to control and
experimental rabbits. Then determine body temperature every 20 minutes in both
rabbits.
4. Present the received results in the form of temperature curves.
5. Compare the temperature changes in both rabbits. Make conclusions.
6. Write down the experimental protocol.

Experiment № 2. Description.
“The result of overheating depending on the level
of thermoregulation mechanism development”.
1. Take the rabbit and frog body temperature measure the heart rhythm (HR)
and the frequency of respiration (FR) in the rabbit.
2. Place the rabbit in the thermostat (T=40C) for 20 minutes, watch
behavioral changes, coloration and position of ears, FR. place the frog into the
water
(T=38-40 C) for 20 minutes.
3. Take the rabbit out of thermostat and sport the same parameters
immediately, them repeat this procedure twice after 15 and 30 minutes.
4. Take the frog out of the water and make the conclusion about it’s state.
5. Fill obtained results in the table. Compare them; explain the result of
overheating in animals depending on the level of the development of
thermoregulation mechanism in them.

TOPIC: “INFLAMMATION”
I. The purpose of individual work. As the result of individual work students
must know:
- modern definition and classification of inflammation;
- main processes of inflammation and the mechanisms of their development;
- principal clinical signs of inflammation and the mechanisms of their origin;
- principles of pathogenic therapy.
II. Items for self-assessment.
 1. The essence of nutritive, vascular, physical - chemical biochemical and
biological theories of inflammation.
2. Modern definition of inflammation and its basis.
3. Classification of inflammation.
4. Mechanisms of alterative changes in the focus of inflammation.
5. Local signs of inflammation and the mechanisms of their development.
6. Peculiarities of metabolic changes at the place of inflammation.
7. Physical - chemical changes in the focus-point of inflammation and the
mechanisms of their development.
8. Mechanisms of circulation and microcirculation changes in inflammatory
focus.
9. Mechanisms of the development of exudation and its importance in
inflammation.
10. Role of neural and hormonal mechanisms in inflammation development.
11. Role of biological active substances in inflammation development.
12. The mechanisms of leukocytes immigration in inflammation focus-point.
13. Mechanisms of proliferative changes in inflammation focus - point.
14. General changes in the organism in inflammation focus-point.
15. Interconnection between local and general changes in inflammation
development.
16. Defensive-adaptive and alterative reactions in inflammation.
17. Mechanisms of the barrier function of inflammation reaction.
18. Pathogenetic therapy of inflammation.

Practical Part. Experiment № 1. Description.

“The vascular reaction in the inflammation of frog intestine mesenterium”.
1. The spinal cord of a frog should be destroyed by probe without vascular
system injuries.
2. After placing of unmoved frog on laboratory desk you should make
incision on the right side of the body and fix intestine loop with needles without
mesenterium vessels injures.
3. Place the preparation for microscopic examination and study blood flow
in arterioles, capillaries, venuli. Pay attention to speed and character of blood
flow, to number of and the width of capillaries, to the beginning of the margination
of leukocytes with low magnification and watch leukocytes emigration using high
magnification.
4. Explain the mechanisms of vascular reaction development and leukocytes
emigration.
5. Draw the stages of vascular disturbances, margination and emigration of
leukocytes, describe the mechanisms of development of these phenomena and
make necessary conclusions.

Experiment № 2. Description.
“Phagocytosis of bird erythrocytes in guinea pig peritoneum”.
 1. Prepare microscope for examination. Find the groups of erythrocytes and
leukocytes under small magnification in the smear. Put the drop on examination
using immerssion system. Note, the bird erythrocytes have nuclei, but guinea pig
phagocytes are mono- and polynuclear cells. Find all phagocytosis stages and
watch the sequence of erythrocyte structure changes in the process of
phagocytosis.
2. Point out the character of interaction between erythrocytes and
phagocytes, explain mechanisms and give the assessment of the biological essence
of everything you have watched.
3. Draw the stages of phagocytosis in colour pencils, write down the analysis
and conclusions.

TOPIC: “ALLERGY”
I. The purpose of individual work. As the result of individual work a student
must know:
- the principal notions and terms of allergology;
- principles of the classification of allergic reactions;
- general mechanisms of the origin and the development of the main stages
of allergic reactions;
- mechanism of the development of clinical signs of allergic reactions;
- principles of prevention and pathogenic therapy of allergic reactions.
II. Items for self-assessment.
1. History of the development of science about allergy and modern
definition of “allergy”.
2. Principles of the classification of allergic reactions.
3. Mechanisms of the development of the allergic reactions of immediate
type.
4. Mechanisms of the development of the allergic reactions of delayed type.
5. Comparative characteristics of the mechanisms of the development of
allergic reactions of immediate and delayed types.
6. Mechanisms of development and peculiarities of active and passive
sensitization.
7. Mechanisms of development and stages of anaphylactic shock.
8. Peculiarities of the development of anaphylaxis shock in animals and
humans.
9. Mechanism of specific and non-specific hyposensitization.
10. Reasons of origin and mechanisms of serum disease development.
11. Mechanisms of endogenous allergens formation and autoallergy
development.
12. Mechanisms of transplantat lesion reactions.
13. Mechanisms of drug allergy development.
14. Role of nervous and endocrine systems in allergy development.
15. Pathophysiological basis of allergy prophylaxis and treatment.

Practical Part. Experiment № 1. Description.

 “The reaction of mast-cells to anaphylactogen”.
1. Prepare the microscope for examination. Take a control smear (action of
non - specific antigen) put it and find a group of mast-cells under low
magnification, then put a drop of immersion oil and settle the objective “90”. Pay
attention to the cell sizes and forms comparing nucleus and cytoplasm. Pay
attention the density of granulas in cytoplasm and to the character of colouring.
2. Make the same operations with experimental smear (action of
anaphylactogen).
3. Explain the mechanisms of degranulation and the changes of cell
colouring. Give the assessment of biological essence of the observed process.
4. Draw the experimental results in colour pencils and make necessary
conclsions.
Experiment № 2. Description.
“Allergoid edema in rats”.
1. Inject intraperitoneally to rat a dimedrol solution in dose: 2,5 mg/100 g
b.w. After 15 minutes inject intraperitoneally a 20% polyglucin solution in dose of
0,5 ml/100 g b.w. to two rats.
2. 40 minutes after pay attention to edema development (on the muzzle, on
extremities) in experimental rat.
3. Explain the mechanisms of edema development in rat after polyglucin
injection.
4. Write down the protocol, explain the results and make conclusions.

TOPIC: “THE CHANGE OF GENERAL BLOOD VOLUME.

POLYCYTHEMIAS. ANEMIAS”
I. The purpose of individual work. As the result of individual work a student
must know:
- types of the changes of erythrocytes count per blood volume unit;
- causes and mechanisms of these changes, their classification;
- compensatory-adaptive mechanisms of the changes of erythrocytes count
blood volume unit;
- mechanism of the changes of peripheral blood composition in anemias and
polycythemias.
II. Items for self-assessment.
1. Classification of general blood volume changes.
2. Causes and mechanisms of hypervolemias origin.
3. Causes and mechanisms of hypovolemias origin.
4. Definition and classification of polycythemias.
5. Comparative characteristics of the different types of polycythemias.
6. Definition of anemia.
7. The main principles of anemias classification.
8. Anemia types according to the different principles of classification.
9. Mechanisms of development and blood changes in hereditary hemolytic
anemias.
 10. Etiology, pathogenesis and blood changes in acquired hemolytic
anemias.
11. Etiology, pathogenesis and blood changes in posthemorragic anemias.
12. Etiology, pathogenesis and blood picture in B-(foliac)-acid deficiency
anemia (pernicious anemia).
13. Etiology, pathogenesis and blood changes in iron-deficiency anemia.
14. Pathogenesis and blood changes in infection-toxic anemia.
15. Regenerative and degenerative changes of erythrocytes in anemias.
16. Basic compensatory - adaptive mechanisms anemias.

Practical part. Experiment № 1.

“The examination of the peripheral blood of an animal with experimental anemia”.
1. The determination of erythrocyte count in the peripheral blood of healthy
rabbit on photoelectrocalorimeter (FEC).
2. The determination of erythrocytes count in the peripheral blood of rabbit
with experimental anemia on FEC.
3. The determination of hemoglobin content of the peripheral blood of a
healthy rabbit and one with experimental anemia with using of Saly’s hemometer.
4. Count colour index using formula: CI= HB/ 2x N, N is two first figures of
erythrocyte number.
5. Microscopic examination of peripheral blood pap-smear, colour in
Romanovsky-Gimza: Watch red blood cells under high magnification. Pay
attention to cells size, shape and colouring character and immature red cells
presence. Pick out degenerative and regenerative characteristics of erythrocytes.
6. Microscopic examination of peripheral blood pap-smear, colored in
brilliant - cresil – blau. Look for the erythrocytes with basophilic reticular
substance using immersion system. Match these cells with mature ones and paint
them. Sport the proportion of mature erythrocytes and reticulocytes and calculate
percentage.
7. Compare the peripheral blood indices of healthy rabbit and with
experimental anemia. Spot the types of qualitative changes of erythrocytes.
Estimate the degree of their expression and establish their interconnection with
quantitative changes of erythrocytes. Estimate the degree of their expression and
establish their interconnection with quantitative indices of rabbit experimental
anemia.
8. Establish the types of experimental anemia. Classify according to colored
index, erythropoiesis type, and the regenerative capability of bone marrow. Explain
the mechanism of the development of anemia in rabbit.

Task № 2. Write conclusion on blood analysis.

1. Spot the quantitative and qualitative changes of erythrocytes and
hemoglobin. Determine the character of the changes in coloured index,
reticulocytes count, hemopoiesis type, cell size.
2. Make up the protocol. Explain the mechanisms of the anemia
development.
 TOPIC: “LEUKOCYTOSES. LEUKOPENIAS”
I. The purpose of individual work. As the result of individual work student is
to know:
- classification and basic mechanisms of leukocytosis development;
- qualitative changes of leukocytes in leukocytoses;
- types and mechanisms of the development of leukemoid reactions;
- causes and mechanisms of the development of leukopenias.
II. Items for self-assessment.
1. Definition of leukocytosis and the principles of leukocytosis
classification.
2. Leukocytosis types in different classifications.
3. Causes and mechanisms of the development of physiological
leukocytoses.
4. Qualitative changes of leukocytes in leukocytoses.
5. Role of hormonal mechanisms in leukocytoses development.
6. Character of sympathetic - adrenal influence on leukopoiesis.
7. Character of cholinergic influence on leukopoiesis.
8. Role of leukopoietins and cellular mechanisms in leukocytoses
development.
9. Causes and mechanisms of the development of neutrophilia.
10. Causes and mechanisms of the development of eosinophilia, basophilia,
monocytosis, lymphocytosis.
11. Mechanisms of leukocytosis development in acute infectious diseases.
12. Definition and classification of leukemoid reactions.
13. Basic hematological manifestations of leukemoid reactions.
14. Definition and classification of leukopenias.
15. Causes and mechanisms of the development of leukopenias.
Practical part. Task № 1. Write conclusion on blood analysis.
1. Characterize the leukocytosis or leukopenia in accordance with main
classifications. Determine the disease, which can manifest the same changes of
“white blood”.
2. Write down the protocol. Explain the mechanisms of development of
disclosed pathology.

TOPIC: “LEUKEMIAS”
I. The purpose of individual work. As the result of individual work a student
has to know:
- modern notions about the etiology and pathogenesis of leukemias;
- classification of leukemias;
- composition of peripheral blood in the different types of leukemias;
- mechanisms of the organism’s activity disorder in leukemias.
II. Items for self-assessment.
1. Definition and classification of leukemias.
2. Causes and conditions of leukemias origin.
 3. Modern notion of leukemias pathogenesis.
4. Role of the genetic change of cell in leukemias development.
5. Meaning of neuroendocrine regulation insufficiency in leukemias
development.
6. Theories of the insufficiency of immune system in leukemias.
7. Mechanisms of tumor progression development and its basic signs in
leukemias.
8. Blood composition in myeloleukemias, the hematological differences
between acute and chronic myeloleukemias.
9. Blood composition in polycythemia vera.
10. Blood composition in leukemia - reticulosis.
11. Mechanisms of anemia and hemorrhage diathesis development in
leukemias.
12. Causes of the hypersegmentation of leukocyte nuclei in leukemias.

Practical part. Task № 1.

Write down conclusion in blood analysis in leukemias patient.
1. Characterize the red and white blood change in accordance with usual
classifications. Establish the type of leukemias in accordance with classifications.
2. Write down the protocol. Explain the mechanisms of anemia and
hemorrhage diathesis development in leukemias.

Task № 2. “The microscopic examination of peripheral blood pap-swear of

leukemias patients. One of them in patient with myeloleukemias and
the other one
in patient with lympholeukemias.
1. Pay attention to the correlation of red and white blood cells. Establish the
presence or absence of blast cells, intermediary forms and mature of segment
nuclei neutrophils, spot the change of proportion of eosinophils, basophils and
neutrophils, atypical cell structures (polymorphism, asynchronism of the
development of nuclei and cytoplasm, micro- and anisocytosis, unusual cell
inclusions).
2. Draw the received data.

TOPIC: “PATHOPHYSIOLOGY OF HEMOSTASIS”

I. The purpose of individual work. As the result of individual work a student
is to know:
- causes of origin and the mechanisms of the development of the different
forms of hemorrhagic, thrombophilic and thrombophilic - hemorrhagic syndromes.
- classification of hemostasis disorders;
- mechanisms of hemostasis disorders in concrete diseases and the principles
of the correction of hemostasis disorders.
II. Items for self-assessment.
1. Modern notions about factors participating in the regulation of
aggregative blood condition.
 2. Modern notions about hemostasis mechanisms.
3. Modern notions about the mechanisms of the activation and inhibition of
anticoagulation blood system.
4. Classification of hemostasis disorders.
5. Mechanisms of the development of hereditary coagulopathias.
6. Causes of origin and the mechanisms of the development of acquired
coagulopathias.
7. Mechanisms of hemostasis disorders in hereditary angiopathias.
8. Causes of origin and the mechanisms of the development of acquired
angiopathias.
9. Classification and the causes of thrombocytopathias origin.
10. Mechanisms of the development of megakaryocytic and
amegakaryocytic thrombocytopenias.
11. Mechanisms of the hemostasis disorder in thrombopenias and proper
thrombopathies.
12. Origin, causes and the general mechanisms of the development of
thrombophilic diatheses.
13. Peculiarities of the development of venous and arterial thromboses.
14. Origin causes and the mechanisms of the development of disseminated
intravascular blood coagulation (DIBC).
15. Pathogenesis of hemorrhagic syndrome in DIBC.
16. Pathophysiological basis of the treatment principles of hemostasis
disorders.

Practical part. Experiment description.

“The heparin influence on blood coagulation”
1. Spot the coagulation time of the rabbit’s blood using electrocoagulograph.
(Take 1 ml of blood from the marginal ear vein of a rabbit).
2. Inject 200-500 units of heparin intravenously to the same rabbit. 3-5 min
after injection take the equal volume of blood.
3. Spot the coagulation time in the same manner.
4. Explain received results. Write down the protocol.
The scheme of blood analysis.
1.       Decrease of RBС and hemoglobin content or hemoglobin content only
anemia:
- colour index: decrease hypochromic
normal normochromic
increase hyperchromic
- capability to regeneration: RC count is decreased hypogenerative
N reticulocytes (RC) RC count is normal regenerative
count is 0,2-1,2% RC count is increased
hyperregenerative
- type of erythropoiesis: presence of megaloblasts, megalocytes
megaloblastic
absence of megaloblasts, megalocytes
normoblastic
-           according to pathogenesis:
-           posthemorrhagic: I stage – without changes
II stage – normochromic, normoblastic, regenerative
III stage – hypochromic, normoblastic,
hyperregenerative
-           B12 – foliac deficiency – hyperchromic, megaloblastic, hypogenerative
-           Iron – deficiency – hypochromic, normoblastic, regenerative or
hyperregenerative
-           hemolytic – hyperchromic, normochromic, hypochromic, normoblastic,
regenerative or hyperregenerative. Appearance of abnormal RBС, for example,
microspherocytosis.
2.       Increase of RBС count erythrocytosis. Erythrocytosis classifications
are not used in analyses.
3.       Increase of WBC count leucocytosis.
- according to number of WBC: from 9109/l to 15109/l – moderate
from 15 109/l to 30109/l – middle
expressed
from 30109/l and more – excessive.
-           according to the prevalent type of WBC: basophilia
eosinophilia
neutrophilia
lymphcytosis
monocytosis
-           in neutrophilia – type of nuclear shift: increase of band – nuclear
neutrophils hyporegenerative left nuclear shift
-         increase of juvenilles regenerative left nuclear
shift
-         presence of myelocytes, myeloblasts
hyperregenerative left nuclear shift
-         sum of immature neutrophils is more than segment
– nuclear neutrophils.
4. Decrease of WBC count leukopenia.
-       according to inhibited portion of leukocytes: neutrophilic
lymphocytic, mixed.
5. Increase of coagulation time and (or) bleeding time hemorrhagic
diathesis.
-   Retraction is incomplete for 24 hours thrombocytopathy.
Thrombocytopathy is divided on two forms:
- true thrombocytopathy – number of platelets is increased or
normal.
- thrombocytopenia number of platelets is decreased.
- Retraction is complete and bleeding time is increased
angiopathy.
1. Red blood cells.
 Erythrocyte count: 2,8x1012/l
Hemoglobin content: 84g/l
Colour index: 0,9
Reticulocyte count: 0,1%
Special remarks:
anisocytosis: expressed
poikilocytosis: expressed
2. White blood cells:
Leukocyte count: 82,5x 109/l

lymphoc monoc
neutrophils
bas ytes ytes
o- eosinop mye pro- myeloc metamyelo band segmen
phi hils lo- myeloc ytes cytes - ted-
ls blas ytes nucl nuclear
ts ear

0% 8% 62% 4% 0% 0% 2% 12% 10% 2%

Special remarks:
3. Hemostasis condition:
Thrombocyte count: 112x109/l
Blood clotting time: 14 min.
Blood bleeding time: 4 min.
Retraction of blood clot: incomplete
4. Erythrocyte sedimentation rate (ESR): 19 mm
_____________________________________________________________________________________
1. Red blood cells.
Erythrocyte count: 3,8x1012/l
Hemoglobin content: 68g/l
Colour index: 0,5
Reticulocyte count: 4,6%
Special remarks:
anisocytosis: expressed
poikilocytosis: expressed
2. White blood cells:
Leukocyte count: 18,0x 109/l

lymph mon
neutrophils o- o-
bas
eosin cytes cytes
o-
o- myel promyeloc myel metamyeloc band- segment
phil
phils o- ytes o- ytes nucle ed-
s
blast cytes ar nuclear
s

8% 2% 0% 0% 0% 1% 12% 53% 20% 4%

Special remarks:
 3. Hemostasis condition:
Thrombocyte count: 420x109/l
Blood clotting time: 30 min.
Blood bleeding time: 2 min.
Retraction of blood clot: complete
4. Erythrocyte sedimentation rate (ESR): 6 mm
__________________________________________________________________
__
1. Red blood cells.
Erythrocyte count: 1,44x1012/l
Hemoglobin content: 66g/l
Colour index: 1,4
Reticulocyte count: 0,4%
Special remarks:
anisocytosis: expressed
poikilocytosis: expressed
megalocytes, megaloblasts.
2. White blood cells:
Leukocyte count: 2,8x 109/l

lym-
monoc
neutrophils phocy
ytes
tes
basop eosinop
mye promy myeloc metamyelo band segmen
hils hils
lo- elo- ytes cytes - ted-
blas cytes nucl nuclear
ts ear

0% 5% 0% 0% 0% 0% 6% 53% 32% 4%
Special remarks:
3. Hemostasis condition:
Thrombocyte count: 120x109/l
Blood clotting time: 10 min.
Blood bleeding time: 2 min.
Retraction of blood clot: complete
4. Erythrocyte sedimentation rate (ESR): 6 mm

TOPIC: “PATHOPHYSIOLOGY OF KIDNEYS”

I. The purpose of individual work. As the result of individual work a student
is to know:
- the causes and the mechanisms of the development of uropoiesis disorders;
- main types of diuresis disorders ;
- qualitative urine changes.
II. Items for self-assessment.
1. Basic causes and the types of the disorders of urine formation and urine
output;
 2. Causes and the mechanisms of the disorder of glomerular filtration and
renal tubular reabsorbtion.
3. Renal tubular secretion and the mechanisms of its disorders.
4. Basic types of disorders quantitative of urine and their characteristics.
5. Causes and the mechanisms of the development of olyguria, anuria,
polyuria, nocturia, micturia.
6. Basic types of the qualitative changes of urine.
7. Causes and the mechanisms of the proteinuria, glucosuria, hematuria,
cylindruria.
8. Forms of renal failure and their manifestations.
9. Uremia, the pathogenesis of uremic manifestations.
10. Principles of the treatment of renal failure patients.

Practical part. Experiment description.

“The diuresis change in different action on organism”.
1. Make sure that the measuring test-tube is dry and you should place the
narrow part of funnel in test-tube on 1 cm.
2. Use 2 frogs. Inject 3 ml of distilled water in back lymphatic cavity to one
of them and 3 ml of distilled water, 0,2 ml of pituitary extract to other. Place both
frogs in the funnels.
3. 45-60 min later massage the belly of both frogs and then place frogs in the
pot. Measure the volume of urine.
4. Compare the amount of urine eliminated by both of frogs. Explain
received results.
5. Write down the protocol of experiment.

TOPIC: “DISORDER OF WATER METABOLISM”

I. The purpose of individual work. As the result of individual work a student
must know:
- classification of water metabolism disorders, etiology and pathogenesis of
their basic forms;
- mechanism of water metabolism disorders in concrete diseases.
II. Items for self-assessment.
1. Basic mechanisms of dehydration development.
2. Etiology and pathogenesis of dehydration in primary water metabolism
disorder.
3. Etiology and pathogenesis of dehydration in primary electrolytes
metabolism disorder.
4. Edemas, the principles of classification.
5. Types of edemas according to their etiology and pathogenesis.
6. Basic pathogenic mechanisms of edemas development.
7. Meaning of neuroendocrine mechanisms in edema development.
8. Meaning of microcirculation factors (hydrostatic, membranic, lymphatic)
in edema development.
 9. Role of tissue factors (hydrophility of interstitial colloids, osmotic and
oncotic pressure in tissue fluid) in edema development.
10. Meaning of blood factors in edema development.
11. Pathogenesis of the main types of edemas (cardiac, renal, inflammatory).
12. Main mechanisms of the injury action of edemas.
13. Defensive - adaptive role of edemas.

Practical part. Experiment № 1. Description.

“The influence of tissue osmotic pressure on edema development”.
1. Pick out two frogs. Inject 3 ml of the 3% solution of sodium chloride to
one of them, and the same volume of physiological solution to other one.
2. Place both frogs in glasses and measure their weight together withthe
glass. Pour out water and measure the frog weight second time.
3. Explain the mechanisms of weight changes in both of frogs.
4. Write down protocol of the experiment. Make up a conclusion.

Experiment № 2. Description.
“The influence of pH on edema development”.
1. Take three Petri’s plates. Pour the distilled water in one of them, the 0,1 N
solution of sodium chloride in the other one, and 0,01 N solution of sodium
chloride in the third one.
2. Place the pieces of dry gelatinose in each plate for 1 hour.
3. Compare the degree of gelatinose swelling in all plates.
4. Explain the gained results. Write down the protocol.

TOPIC: “PATHPHYSIOLOGY OF EXTERNAL RESPIRATION”

I. The purpose of individual work. As the result of individual work a student
must know:
- the causes and mechanisms of the development and biological meaning of
different types of external respiration disorders;
- the mechanisms of development of compensatory reactions in different
types of external respiration disorders.
II. Items for self-assessment.
1. The causes and the mechanisms of the development of external respiration
disorder under the influence of environmental factors.
2. The mechanisms of external respiration disorder in the functional
disturbances of organism organs and systems.
3. Definition of breathlessness and characteristics of its distinct types.
4. The causes, mechanisms of the development and the peculiarities of the
interchange of gases in hyperpnoe, pneumonic breathlessness, inspiratory
breathlessness, expiratory breathlessness, stenotic one.
5. Role of nasal cavity in the origin of the disorders of external respiration
and gases exchange.
6. Mechanisms of the development and the biological meaning of cough and
sneezing.
 7. The causes and mechanisms of the development of respiration disorders in
asphyxia.
8. Terminal respiration, its types and the mechanism of development.
9. Mechanisms of compensation of external respiration disorders.

Practical part. Experiment № 1. Description.

“The change of respiration in the stenosis of respiratory tract in rabbit.”
1. Put a rabbit on special table on the back. Put the resin cuff on the chest
and connect with Marrey’s capsule by resin tube. Regulate the pneumogramm on
kimograph.
2. Press the rabbit larynx or trachea till the appearance of the respiration
change in constant respiration registration.
3. Pay attention to the frequency and depth of respiration.
4. Explain the mechanisms of the change of the respiration.
5. Write down the protocol.

Experiment № 2. Description.
“The influence of the chemical irritation of the upper part of the respiratory tract
on the rhythm and depth of the respiration in rabbit.”
1. Carry out the actions in the manner like as in exp. N1.
2. Pay attention to the respiration changes after ammonium solution
inspiration. Inject 7-9 drops of 1% dicainum solution in the both nostrils and repeat
again the investigation 10-15 min later.
3. Explain the mechanisms of respiration changes.
4. Paint the pneumogramms in worksheet. Write down the protocol of
experiment.

TOPIC: “HYPOXIAS. THE ACID-BASE IMBALANCE”

I. The purpose of individual work. As the result of individual work a student
must know:
- the causes and the mechanisms of the development of acid-base balance
disorders;
- the mechanisms of the disorders of distinct organs and systems functions in
acidosis and alkalosis;
- the mechanisms of the development of compensatory reactions in acid -
base imbalance;
- the causes and the mechanisms of the development of hypoxias, the
character of changes of metabolism and organism vital activity in hypoxias.
II. Items for self-assessment.
1. Acid-base balance disorders, their classification.
2. The causes and the mechanisms of gas and metabolic acidosis and
alkalosis.
3. Changes of blood buffer systems in acidosis and alkalosis.
4. Changes of the function of organs and systems in acidosis and alkalosis.
5. Types of hypoxias and their characteristics.
 6. Respiratory compensatory-adaptive mechanisms in hypoxias.
7. Hemodynamics, blood and tissues compensatory-adaptive mechanisms in
hypoxias.
8. Changes of arterial-venous difference in oxygen in the distinct types of
hypoxias.

Practical Part. Experiment description.

“Experimental asphyxia”.
1. Give the ether anaesthesia to the rat. Then inject intraperitioneally
hexenal solution in dose of 100,0 mg per 100 g b.w. Cut the skin at the neck.
Reveal the trachea and place the ligature under trachea. Regulate the
pneumogramm registration.
2. Produce the gradual pressing of trachea in constant respiration
registration.
3. Pay attention to gradually developed respiration disturbances. Explain the
mechanisms of clinical asphyxia manifestations. Write down the protocol.
The indices characterizing acid-base balance (ABB). The following
indices are used in practice:
1. actual pH - factual magnitude of negative logarithm of proton
concentration in blood On the one hand this index characterizes the interconnection
of acids and bases in investigated blood, but on other hand it is integral index,
which shows the degree of compensation and injuring factor action, directed on
the change of medium acidity, and which is changed in defensive organism
possibilities increase. Normal indices of pH=7,4 (7,35-7,45).
2. pCO2 partial pressure of carbon dioxide in blood. It characterizes the
respiratory component of the mechanisms of acid-base homeostasis and the
functional state of respiratory system. This index can show the development of
compensatory reactions in ABB changes as well as the disturbances of respiratory
system. Normal indices pCO2=4,7-6,0 kPa.
3. BB - the buffer bases of blood. It characterizes the displacement of all
blood buffer systems and the state of the metabolic component of acid-base
homeostasis BB -44-52 mmol/l in healthy men.
4. BE - base excess; it characterizes the shift of acids and bases in
comparison with proper magnitudes for this blood. In norm BB is +-2,5 mmol/1.
Negative BE means indicate of the excess of metabolic acids or deficiency of bases
in organism and the necessity to use the acid drugs for disorder correction.
5. SB - standart bicarbonate. It’s bicarbonate concentration, which is
determined in standart conditions (pCO2=40 Hg mm, HbO =100%, t=38C). As two
previous indices it reflects the state of metabolic components of the mechanisms of
acid-base homeostasis too. The changes of this index are always the sign of ABB
disorder. In respiratory insufficiency its shifts are the signs of metabolic
compensation. Normal SB indices are 24-28 mmol/l.
The actual pH is used for the estimation of ABB shifts as well as the degree
of its compensation: The decrease of this index is the sign of acidosis development
and its increase is the sign of alkalosis one. The shifts in the limits 7,35-7,45 are
compensatory, however, there are the expressed changes of buffer systems reserves
and the heightening of physiologic mechanisms activity in this state. The shifts in
limits
7,30-7,48 reflect the subcompensatory forms of ABB disorders.
More expressed pH shifts are the sign of the decompensatory forms of
acidosis and alkalosis.
The respiratory acidosis and alkaloses are determined in blood pCO 2. Non-
gas acidosis and alkaloses are determined in BB, BE, SB changes.
For characteristics of ABB disorders it’s necessary to testify the process
phase, besides the name, which is determined after analysis of cause and primary
mechanism of disorder. In acute phase the buffer system react, but there are no the
responsible reactions of physiologic mechanisms and compensatory shifts. In
chronic processes there are stable ABB disorders with the different degree of
compensation expression stipulated with the activity of lungs and kidneys. The
detail analysis of clinical dynamics is necessary for the exact diagnosis or patient
state.

TOPIC: “PATHOPHYSIOLOGY OF DIGESTION”

I. The purpose of individual work. As the result of individual work a student
must know:
- causes of digestion system functions disorders;
- main manifestations of digestion disorders;
- origin causes and the mechanisms of the development of the disturbances
in the functions of the separate parts of digestive tract;
- etiology and pathogenesis of the peptic ulcer of duodenum and stomach.
II. Items for self-assessment.
1. Basic causes of digestion disorders.
2. Common signs of digestion disorders and the mechanisms of their
development.
3. Causes of the disorder of chewing and main mechanisms of digestion
disorder in throat.
4. Causes of hypersalivation and hyposalivation and the mechanisms of
digestion disorder of them.
5. Etiology and the pathogenesis of cavities and paradontosis.
6. Characteristics of pathological gastric secretion types.
7. Causes of hyposecretion and hypersecretion in stomach and the
mechanisms of digestion disturbances development.
8. Causes of disorder and the mechanisms of the development of digestion
disturbances.
9. Causes of the disorder of external pancreatic secretion and the
mechanisms of the development of digestion disturbances.
10. Causes of the disorder of intestine functions and the mechanisms of the
development of digestion disturbances.
11. Causes and the mechanisms of the development of intestinal
autointoxication.
 12. Ulcerous disease of stomach and duodenum. Definition. Theories of
development.
13. Modern notions about etiology and pathogenesis of peptic ulcer.
14. Digestion disorders in secretion and cholecystopancreosimin failures.
15. Consequences of the different parts of digestion tract removing.

TOPIC: “PATHOPHYSIOLOGY OF LIVER”

I. The purpose of individual work. As the result of individual work a student
must know:
- clinical manifestations of liver pathology and the mechanisms of their
development;
- the principal mechanisms of hepatocyte injury.
II. Items for self-assessment.
1. Etiology of liver diseases.
2. Immune mechanisms of liver pathology development.
3. Mechanisms of primary necrobiosis and the secondary cytolysis of
hepatocytes in liver pathology.
4. Intracellular cholestasis as the mechanism of hepatocyte injury.
5. Mechanism of the disturbances in carbohydrate, lipid and protein
metabolism in the liver pathology.
6. Role of nervous mechanisms in the development of fatty liver.
7. Etiology, pathogenesis and manifestations of the different types of
jaundice.
8. Pathogenesis of the nervous and endocrine disorders in liver pathology.
9. Pathogenesis of the disturbances in the functions of cardio-vascular,
respiratory, digestive systems in liver pathology.
10. Pathogenesis of hemopoiesis disorders and blood coagulation in liver
failure.
11. Pathogenesis of ascitis development in cirrhoses.
12. Pathogenesis of cholestones formation in the cholestone disease.

Practical part. Experiment description.

“The influence of the bile on the blood coagulation”.
1. Put the drops of bile on the subject glass. The following degrees of bile
are used: 1:2, 1:5, 1:10. Add to each of bile drops one drop of blood (taken from
marginal ear vein of a rabbit).
2. Pay attention to blood coagulation time in different specimens. Explain
the received results. Write down the protocol.

TOPIC: “ARRHYTHMIAS”
I. The purpose of individual work. As the result of individual work a student
is to know:
- general causes of origin and the classification of heart rhythm disorder.
- the principal mechanisms of different arrhythmias development (the main
theories).
 - electrocardiographic manifestations and the mechanisms of their formation
in the different types of arrhythmias.
II. Items for self-assessment.
1. General causes of heart rhythm disorders.
2. The causes and mechanisms of the development of sinus tachycardia and
sinus bradycardia.
3. The causes and the mechanisms of the development of sinus node disease
and respiratory arrhythmia.
4. The causes and the mechanisms of the development of premature beats
and of the paroxismal tachycardia.
5. The mechanisms of electrocardiographic manifestations in the distinct
types of premature beats (atrial, atrioventricular, ventricular, interpolated).
6. Atrial flatter and atrial fibrillation. The causes and the mechanisms of
their development.
7. The causes and the mechanisms of the development of ventricular
fibrillation.
8. Disturbances in myocardium conductivity. The major kinds.
9. Electrocardiographic characteristics of the distinct types of cardiac blocks.
10. The causes and the mechanisms of the development of the paradoxal
pulse and of the intermitent one.

Practical part. Experiment description.

“Reflex changes of heart rhythm in rabbit.”
1. Fix the rabbit to laboratory table on the back.
2. Put on electrocardiographic needle electrodes and switch on an
electrocardiograph. Write down the initial ECG.
3. During electrocardiogram registration bring to the rabbit’s nose,
moistened by ammonia chloride. Pay attention to the speed of the development of
heart rhythm disorders and their duration after stopping of irritation action.
4. Define the character of heart rhythm disorders and the consequence of
their development. Explain the mechanisms of their arising.
5. Write down the protocol. Explain the mechanisms of data obtained.

Analysis of patient’s ECG. Write the conclusion.

The scheme of ECG analysis.
1. Define the rhythm of heart activity according to the arrangement of ECG-
waves and intervals. Establish the heart pacemaker. calculate heart rate and
regularity of heart beats. and direction.
2. Measure the R-R interval duration, compare the duration of distinct R-R
intervals and average duration. In regular rhythm the deviations of distinct R-R
intervals are not more than 10% of average duration.
3. Characterize QRS-complex and its waves.
4. Analyze S-T interval condition.
Describe the data obtained. Write down the resume and the possible
diagnosis.
 The order of ECG analysis.
1.       P-wave is before QRST-complex-> sinus rhythm.
2.       The intervals R-R are equal -> rhythm is correct, R-R are unequal ->
rhythm is incorrect.
3.       Frequency of heart rhythm -> HR=60/R-R(mm)x0,02.
4.       Conclusion.
Atrial premature beats: - form of P-wave is incorrect; -compensatory pause
is incomplete.
Ventricle premature beats: - Form of QRST-complex is changed; - QRST-
complex is wide; - compensatory pause is complete; - P-wave is absent.
Right ventricle premature beats: - wide R-jag is in V5 and V6; - deep S or
QS is in V1 and V2.
Left ventricle premature beats: - wide R-jag is in V1 and V2; - deep and wide
S is in V5 and V6.
Paroxismal tachycardia: - HR is 160-250 per 1 min; - HR is correct; -
QRST-complex is deformed.
Atrial flatter: P-wave is absent; - F-waves are appeared.
Ventricle fibrillation: - QRST-complexes are absent; - the waves of different
and altitude are appeared.
Atrial-ventricle block: the first degree: - increase of P-Q interval more than
0,2 sec; the second degree: - progressive increase of P-Q interval, absence of 7th-8th
ventricular complex; the third stage - increase of P-Q interval, absence of 2nd-3rd
ventricular complex; complete block – frequency of P-waves is 70, frequency of
QRST is 30-40.

TOPIC: “CORONARY BLOOD FLOW INSUFFICIENCY”

1. The purpose of individual work. As the result of individual work a student
has to know:
- causes of coronary blood flow failure;
- risk factors in the development of atherosclerosis that is the main cause of
coronary heart disease;
- basic forms of coronary heart disease and the mechanisms of their
development.
II. Items for self-assessment.
1. The definition of “coronary blood flow failure” and its clinic forms.
2. General causes of coronary blood flow failure.
3. Risk factors of atherosclerosis development and coronary heart disease.
4. The causes and the mechanisms of the development of the stable angina
pectoris.
5. The mechanisms of the development of the angina pectoris forms at the
rest condition.
6. The mechanisms of the development of myocardial infarction.
7. The mechanisms of the reversible and irreversible cardiomyocytes injury.
8. The mechanisms of the development of microcirculation disturbances in
cardiogenic shock.
 9. Immune disorders in myocardial infarction and their role in postinfarction
syndrome development.

Practical part. Experiment description.

“Reproduction of pituitrin myocardium ishemia in rabbit”.
1. Fix the rabbit on its back to special table. Put on the needle electrodes,
and turn on the electrocardiograph.
2. Inject intravenously (slowly) the pituitrin in dose 0,5 unit/kg in the
volume 2 ml. Record ECG without a break during 1,5-2 min.
3. Pay attention to the changes of heart rhythm and heart rate , the duration
of P-Q interval, the position of ST segment, the voltage of T-wave. Explain the
received results.
4. Write down the protocol.

Analysis of a patient’s ECG tracing.

TOPIC: “DISORDERS OF VASCULAR TONE”

I. The purpose of individual work. As result of individual work a student has
to know:
- definition of the essential (primary) hypertension and the secondary
(symptomatic) hypertension;
- etiology and pathogenesis of essential hypertension and the principal forms
of the secondary ones;
- the causes and the mechanisms of the development of the acute and chronic
forms of hypotensions;
II. Items for self-assessment.
1. The definitions of “the essential hypertension” and “the secondary
hypertension”.
2. The causes and the predisposing factors of the essential hypertension.
3. The major pathogenetic mechanisms of the essential hypertension
development.
4. The main mechanisms of catecholamine including into the essential
hypertension pathogenesis.
5. Sodium role in hypertension development.
6. The role of renal mechanisms in the essential hypertension development.
7. Peculiarities of the pathogenesis of high- and low-renin forms of essential
hypertension.
8. The principal forms of chronic hypotension and the mechanisms of their
development.
9. The causes and the pathogenesis of distinct shocks.
10. The causes and the development of collapse and fainting.

Practical part. Analysis of patient’s ECG tracing.

 TOPIC: “HEART FAILURE. DISORDERS OF GENERAL
CIRCULATION”
I. The purpose of individual work. As the result of individual work a student
has to know:
- main cardiac and extracardiac reserves of circulation and the mechanisms
of their involvement;
- the stages of the compensatory heart hypertrophy development and the
mechanisms of cardiosclerosis formation in hypertrophy;
- the causes and the mechanisms of heart failure and their classification;
- the mechanisms of the development of the heart failure;
- pathogenesis of main manifestations in the heart failure;
- etiology and pathogenesis of the vascular form of general circulation
failure;
- etiology and pathogenesis of pericardiac form of general circulation
failure.
II. Items for self-assessment.
1. Heart failure and the causes of its development.
2. Cardiac mechanisms (reserves), opposed to cardiac failure development.
3. Reserves of the heart stroke and minute blood volume.
4. Stages of compensatory heart hypertrophy and the mechanisms of their
development.
5. The mechanisms of the progressive cardiosclerosis development in
hypertrophied myocardium.
6. General mechanisms of heart failure development.
7. The major mechanisms of cardiomyocytes injury in heart failure.
8. The mechanisms of the disturbances in the heart activity in sodium,
potassium and calcium metabolism disorders.
9. The main compensatory reactions arising during cardiac failure
development.
10. The main causes and the mechanisms of the development of the
pericardiac form of general circulation failure.
11. The basic causes and the mechanisms of the development of the vascular
form of general circulation failure.
12. The mechanisms of the development of hemodynamics disorder in
accordance with the theory of the insufficiency of cardiac output.
13. Peculiarities of hemodynamics disorders in the different types of heart
valves defect.

Practical part. Analysis of patient’s ECG sample.

TOPIC: “GENERAL PATHOPHYSIOLOGY OF ENDOCRINAL

DISORDERS. PATHOPHYSIOLOGY OF PITUITARY GLAND AND
GONADS”
I. The purpose of individual work. As the result of individual work a student
has to know:
 - the general causes and the conditions of the endocrinopathias development;
- classifications of endocrinopathias.
- the general mechanisms of the disorders of endocrine glands functions.
II. Items for self-assessment.
1. The basic causes and the conditions of endocrinal pathology origin.
2. The principal types of the disorders of endocrinal glands.
3. The main causes of the extragladular changes of endocrine activity.
4. The basic causes of the functional disorders of hypothalamus - pituitary
gland complex.
5. The main hormone capacities.
6. The basic methods of endocrinal pathology reproduction.
7. Pituitary hormones and their biological action.
8. The causes and the mechanisms of the development of hypophyseal
cachexia (Simmonds’ disease).
9. Origin causes and the mechanisms of development and the clinical signs
of somatotropin (growth hormone) hyperproduction and hypoproduction.
10. Clinical signs of the disorder of thyrotropin secretion.
11. The disorders caused by hypophysectomy.
12. The causes and the mechanisms of the development of the gonads
activity.
13. The causes, mechanisms of the development and male and female hypo-
and hypergonadism.
14. The causes and the mechanism of the development of menstrual cycle
disorders.
15. The causes, the mechanisms of development and manifestations of the
premature puberty.

Practical part. Description of experiment.

“The influence of gonadotropins on the spermatogenesis in a frog male”.
1. Insert carefully the tip of pippete into cloaka and take off the drop of fluid.
Put the fluid on the slide and look at cloaka content under low magnification in
dark field.
2. Take in syringe 1,5 - 2,0 ml urine taken from pregnant woman. Make the
skin incision along the middle line of the back below the head. Inject of urine in
the subcutaneous space in the caudal direction. Put the frog in ban with water.
3. Repeat experiment 30-45 min after injection of urine. Pay attention to the
number of sperm cells and to their motility.
4. Explain received results. Write down the protocol.

TOPIC: “PATHOPHYSIOLOGY OF ADRENAL GLANDS AND THYMUS”

I. The purpose of individual work. As the result of individual work a student
has to know:
- the causes and the mechanisms of the development of the adrenal gland
pathology;
 - the mechanisms of the disorders of metabolism and organism function in
different forms of the hyperfunction and hypofunction of adrenals;
- the causes and mechanisms of the development of thymus functions
disorders.
II. Items for self-assessment.
1. The major kinds of hypercortisolism. difference between pituitary-
dependent and pituitary-independent Cushing’s syndromes.
2. Changes of the functions of organs and systems in hypercortisolism.
3. Pathogenesis and clinical manifestations of the primary and secondary
aldosteronism.
4. The types of adrenogenital syndromes and the mechanisms of their
clinical manifestations development.
5. The pathogenesis of syndromes, arising as the result of the adrenal
medulla hypofunction.
6. The causes and the mechanisms of the development of the acute adrenal
insufficiency and its clinical manifestations.
7. The causes and the mechanisms of metabolic changes, organs and systems
functions in the chronic total failure of renal glands.
8. Role of adrenal glands in adaptive reactions formation.
9. The mechanisms of the function disorders after thymusectomy and in the
thymus aplasia.
Practical part. Experiment description.
“The change of epinephrine content of animal blood in stress”.
1. Narcotize a rat with ether. Inject intraperitoneally or intramuscular by
hexenal solution in proportion - 0,2 ml of 5% hexenal solution per 100 g body
weight. Fix the rat to laboratory desk and inject 2,0 ml of 3% sodium citrate.
2. Insert 0,5 ml 3% sodium citrate solution into 3 probes. The first test-tube
is used as control. Insert two drops of blood into the second one. Fix the electrodes
to the back extremities and produce electric shock for 3 sec. After this cut off the
nail tip and insert two blood drops into the third test-tube. The second and third
test-tubes are put on in the bushes, then are equilibrated with water and are
centrifuged at 3000g for 2- 3 min. Above - sedimental fluid is transfered into test -
tubes N4 and N5 from N2 and N3 respectively. Add one drop of 10% solution of
FeCl3 and one drop of
10% NaOH solution into 1, 4, 5 test - tubes.
3. Assess the solution colour and sediment amount in test-tubes, that
depends on epinephrine concentration.
4. Explain received data. Write down the protocol.

TOPIC: “PATHOPHYSIOLOGY OF PANCREAS

AND CARBOHYDRATE METABOLISM”
I. The purpose of individual work. As the result of individual work a student
must know:
- the causes and mechanisms of diabetes mellitus development;
- the causes and the mechanisms of hypoglycemia states;
 - the mechanism of the metabolism disorders and the organism’s functions in
diabetes mellitus.
II. Items for self-assessment.
1. The causes and the mechanisms of the disorders of carbohydrates
absorption.
2. The disorders of synthesis and destruction glycogen, glycogenoses.
3. Disorders of carbohydrates metabolism.
4. Diabetes mellitus, the definition and the forms of diabetes mellitus.
5. The causes of the pancreatic and extrapancreatic form of diabetes
mellitus.
6. The basic signs of diabetes mellitus.
7. The mechanisms of the disorders of carbohydrate, protein, lipid and water
metabolism in diabetes mellitus.
8. The mechanisms of hyperglycemia, glycosuria, polyuria, polydypsia,
hyperketonemia and ketonuria in diabetes mellitus.
9. The disorders of the functions of cardiac-vascular system, liver and
immune system and the decrease of organism resistance in diabetes mellitus, their
manifestations.
10. The peculiarities of metabolism disorders in total diabetes mellitus.
11. The causes and the mechanisms of the hypoglycemia development.

Practical part. Experiment description.

“Insulin hypoglycemia in mice”.
1. Inject subcutaneously (on the back) insulin in dose of 0,4 - 0,6 - 0,8 units
to mice. Place them under glass cap.
2. Observe the mice behavior, pay attention to motor activity. In
hypoglycemia shock development pay attention to the sequence of disturbances:
seizures, decerebral rigidity, breathing changes.
3. Explain the mechanism of the origin of insulin hypoglycemia signs.
4. Write down the protocol.

TOPIC: “PATHOPHYSIOLOGY OF THYROID

AND PARATHYROID GLANDS”
I. The purpose of individual work. As the result of individual work a student
has to know:
- the causes and the mechanisms of the development of the thyroid gland
hyperfunction and hypofunction;
- the mechanisms of the development of metabolism disorders and organism
function in hypo- and hyperthyroidism;
- etiology and pathogenesis of endemic goitre;
- the causes and the mechanisms of the hypo- and hyperfunction of the
parathyroid glands development;
- the mechanisms of the metabolism and distinct functions disorders in hypo-
and hyperparathyroidism.
II. Items for self-assessment.
 1. The causes and the origin mechanisms of hyperthyroidism.
2. Pathogenesis of the main signs of hyperthyroidism.
3. The mechanisms of the metabolic disturbances in the hyperthyroidism.
4. The pathogenesis of nervous system function disorders in
hyperthyroidism.
5. The mechanisms of the cardio-vascular disorders in hyperthyroidism.
6. The pathogenesis of adrenal disorders in hyperthyroidism.
7. The causes and the mechanisms of hypothyroidism.
8. Mechanisms of the development of protein, water, basic and carbohydrate
metabolisms in hypothyroidism.
9. The pathogenesis of nervous system disorders in hypothyroidism.
10. Pathogenesis of the cardiac - vascular disorders in hypothyroidism.
11. The pathogenesis of immune disorders in hypothyroidism.
12. The mechanisms of the cretinism and mixedema development.
13. The etiology and pathogenesis of the endemic goitre.
14. The of thyreocalcitonism in pathology.
15. The causes of hypo- and hyperfunction of the parathyroid glands.
16. The pathogenesis of metabolism and organism functions disorders in
hypo- and hyperfunction of parathyroid glands.
17. The pathogenesis of neuro-muscular excitability change in the
hypofunction of parathyroid glands.

Practical part. Experiment description.

“The sensitivity of animals with hyper- and hypothyroidism
to high external temperature action”.
1. Use 3 guinea pigs in experiment: a) control one; b) guinea pig with
hyperthyroidism (received thyreoidin in dose 0,1 g / 100 g b.w. for 5 days); c)
hypothyroidism one (received metyluracyl in dose 0,03 g / 100 g b.w. for 5 days).
2. Analyze the initial animal state. Mind the motor activity, image,
respiration rate.
3. Spot the animal reaction to the high external temperature. Place animal in
termostat at 50 C for 10-15 min and observe for their behavior. Then take off
animal from termostat and assess the degree of hyperthermia at each animal and
also the behavior changes, respiratory rate, colour of skin and mucosas.
4. Explain differences in the sensitivity of the animals in hyperthyroidism
and hypothyroidism to high external temperature.
5. Make a conclusion. Write down the protocol.

TOPIC: “GENERAL PATHOPHYSIOLOGY OF NERVOUS SYSTEM.

SENSORY AND MOTOR DISORDERS”
I. The purpose of individual work. As the result of individual work a student
has to know:
- the causes and the mechanisms of the nervous system functions disorders;
- the mechanisms of the development of the motor and sensory disorders in
nervous system pathology;
 II. Items for self-assessment.
1. Mechanisms of nervous system disorders.
2. The essence of conditions serving as a basis of the pathological reactivity
of nervous system.
3. Signs of the pathological reactivity of nervous system.
4. Essence and the mechanisms of the development of “pathological
dominanta.”
5. Peculiarities of “pathological parabiosis” and the mechanisms of its
development.
6. Essence and the mechanisms of the development of “ill punctum”.
7. Types of pathological reflexes and the mechanisms of their development.
8. The consequences of the upper motor neurons lesion.
9. The consequences of the lower motor neurons lesion.
10. Causes and the mechanisms of the development of different types of
ataxias.
11. Causes and the mechanisms of the development of hyperkinesias.
12. Types of the disturbances of simple sensitivity.
13. Mechanisms of the development of the dissociated disorders of
sensitivity.
14. Mechanisms of the complex sensitive disorders.
15. The major kinds of pathological pain, the mechanisms of their
development.
16. The mechanisms of the reffered pain development.
17.Character of motor and sensory disturbances in one-half spinal cord
dissection.
18. Removal of the Primary Motor Cortex.
19. Effects of lesions in the motor cortex or corticospinal pathway. The
Babinski sign.
20. Athetosis, ballism, chorea.

Practical part. Experiment description.

“Ataxia as the result of afferent impulsation”.
1. Watch the loosely moved rabbit and pay attention to synchronisn and
symmetry of the movements of its back extremities.
2. Fix the rabbit to laboratory desk. Remove the hair on the side - back of
thigh and rub the skin by spiritus. Inject subcutaneously and intramuscular 20-30
ml of 0,5% of novocain solution at this site.
3. Compare the movements and the muscular tone of the rabbit’s extremities
20-30 min after injection.
4. Explain the received results. Remember that novocain blocks the afferent
impulsation. Write down the report.

TOPIC: “PATHOPHYSIOLOGY OF THE HIGHEST NERVOUS

ACTIVITY”
 I. The purpose of individual work. As the result of individual work a student
has to know:
- the etiology and pathogenesis of the general disturbances in the highest
nervous activity;
- the main manifestations of the highest nervous activity and the mechanisms
of their development;
- common features of the highest nervous activity disorders in traumatic
injury to the cerebral cortex.
II. Items for self-assessment.
1. Common manifestations of the cerebral cortex activity in traumatic
injuries.
2. Consequence of hemisphere cortex removing.
3. Consequences of cerebral cortex removing in both hemispheres.
4. The mechanisms of the restoration and compensation of the disturbed
functions of the cerebral cortex.
5. The essence of the “lack of information” theory of neurosis origin.
6. The essence of the “biological” theory of neurosis origin.
7. The theory of “adaptive energy deficiency” of neurosis origin.
8 Main principles and the methods of receiving of experimental neuroses.
9. Factors which promote the neurosis development.
10. The meaning of the highest nervous activity type in neurosis
development.
11. The main pathophysiological changes in neuroses. The mechanism of the
development of phasic manifestations in neuroses.
12. Principles of the prophylaxis and therapy of neuroses.

Practical part. Experiment description.

“The influence of sound irritant on an animal organism
in dependence on functional state of the CNS”.
1. Take 8-10 mice, mark them with the ink and put them into the special
cage with reaction. Divide the groups the animals according to their behavior in
response to irritant sound into (i) the calm animals and (ii) the excitable ones.
2. Inject subcutaneously 0,2 ml of 10% coffein solution to the animals of the
1st group to increase their excitability. Inject s/c 0,2 ml 3% solution of Na 2Br to
animals of the 2nd group to decrease their high excitability.
3. Put the animals again into the cage with bells 15-20 min, watch the animal
reaction to the sound.
4. Explain the character of the behavior reactions of mice to the action of
irritant sound. Clear up the character of functional state of the nervous system after
the drug injections. Explain the change of mice response to the sound irritant after
the drug correction of CNS state.
5. Write down the protocol of experiments. Present the received results in
the table.
 TOPIC: “PATHOPHYSIOLOGY OF AUTONOMIC NERVOUS SYSTEM
AND THE NEUROGENIC DYSTROPHIES”
I. The purpose of individual work. As the result of individual work a student
has to know:
- etiology and pathogenesis of the autonomic nervous system dysfunctions;
- etiology and pathogenesis of neurogenic dystrophies;
- the common clinical manifestations of autonomic nervous system injury
and the neurogenic dystrophies.
II. Items for self-assessment.
1. The definition of tissue and cell trophism.
2. The modern notions about the nervous trophic influences.
3. The causes and the mechanisms of the neurogenic dystrophies
development.
4. The peculiarities of centrogenic dystrophies development.
5. The tissue disturbances characterising neurogenic dystrophies.
6. Structural - functional peculiarities of parasympathetic and sympathetic
subdivisions of the nervous system.
7. Interrelations between the sympathetic and parasympathetic subdivisions
of CNS.
8. The changes, originating in a human organism as the result of autonomic
nervous centers injury.
9. The pathogenesis of denervation hypersensitivity.
10. The consequences of the peripheral vegetative nerve injury in humans
(the syndromes of increased nerve fibers irritation and of the denervation).
 Content

THE BASIC METHODS OF THE WORK WITH 3

ANIMALS………………….
THE CONCEPT OF “DISEASE”. DYING AND 3
REANIMATION…………….
GENERAL 5
ETIOLOGY………………………………………………………….
GENERAL 6
PATHOGENESIS…………………………………………………...
REACTIVITY AND RESISTANCE OF HUMAN 7
ORGANISM……………….
SIGNIFICANCE OF THE EXTERNAL ENVIRONMENT
IN THE ORIGIN OF
DISEASE…………………………………………………. 8
THE MECHANISM OF ACUTE AND CHRONIC ALCOHOL.
ACTION ON THE HUMAN
ORGANISM……………………………………… 9
PATHOPHYSIOLOGY OF PERIPHERAL CIRCULATION
AND MICROCIRCULATION. THROMBOSIS AND 1
EMBOLISM…………... 0
FEVER………………………………………………………………………… 1
… 1
INFLAMMATION…………………………………………………………… 1
…. 2
ALLERGY…………………………………………………………………… 1
….. 3
THE CHANGE OF GENERAL BLOOD VOLUME.
POLYCYTHEMIAS. ANEMIAS…………………………………………. 1
…….. 5
LEUKOCYTOSES. 1
LEUKOPENIAS…………………………………………… 6
LEUKEMIAS…………………………………………………………………. 1
…. 7
PATHOPHYSIOLOGY OF 1
HEMOSTASIS…………………………………….. 8
PATHOPHYSIOLOGY OF 2
KIDNEYS…………………………………………. 1
DISORDER OF WATER 2
METABOLISM……………………………………… 2
PATHOPHYSIOLOGY OF EXTERNAL 2
RESPIRATION…………………….. 3
HYPOXIAS. THE ACID-BASE 2
IMBALANCE………………………………… 4
PATHOPHYSIOLOGY OF 2
DIGESTION………………………………………. 6
PATHOPHYSIOLOGY OF 2
LIVER……………………………………………... 7
ARRHYTHMIAS………………………………………………………………. 2
.. 7
CORONARY BLOOD FLOW 2
INSUFFICIENCY……………………………… 9
DISORDERS OF VASCULAR 3
TONE………………………………………….. 0
HEART FAILURE. DISORDERS OF GENERAL 3
CIRCULATION…………… 0
GENERAL PATHOPHYSIOLOGY OF ENDOCRINAL DISORDERS.
PATHOPHYSIOLOGY OF PITUITARY GLAND AND GONADS……. 3
…….. 1
PATHOPHYSIOLOGY OF ADRENAL GLANDS AND THYMUS……. 3
…….. 2
PATHOPHYSIOLOGY OF PANCREAS AND CARBOHYDRATE
METABOLISM………………………………………………………………… 3
.. 3
PATHOPHYSIOLOGY OF THYROID AND PARATHYROID 3
GLANDS…… 4
GENERAL PATHOPHYSIOLOGY OF NERVOUS SYSTEM.
SENSORY AND MOTOR 3
DISORDERS……………………………………….. 5
PATHOPHYSIOLOGY OF THE HIGHEST NERVOUS
ACTIVITY…………………………………………………………………… 3
….. 6
PATHOPHYSIOLOGY OF AUTONOMIC NERVOUS SYSTEM
AND THE NEUROGENIC 3
DYSTROPHIES…………………………………… 7
Издательство Курского государственного медицинского университета
305041, г. Курск, ул. К. Маркса, 3.

Лицензия ЛР № 020862 от 30.04.99 г.

Тираж 100 экз.

Отпечатано в типографии КГМУ.

305041, г. Курск, ул. К. Маркса, 3.

Заказ № 763