Metod.stomat.f-ty 1st semester book Module 2

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
MODULE 2
PATHOPHYSIOLOGY OF ORGANS AND
SYSTEMS
Training-methodical manual
for class and out-of-class work for students of stomatological faculty
Prepared by:
Gerasymchuk M. R.
Cherkasova V. V.
Zaiats L. M.

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
Pathophysiology
MODULE 2
PATHOPHYSIOLOGY OF ORGANS AND
SYSTEMS
Training-methodical manual
for class and out-of-class work for students of stomatological faculty
Student ________________group of stomatological faculty
(name and surname)
Prepared by:
Gerasymchuk M. R.
Cherkasova V. V.
Zaiyats L. M.
3

Ivano-Frankivsk, 2017
«PATHOPHYSIOLOGY OF ORGANS AND SYSTEMS»
Training-methodical manual for class and out-of-class work for
students of stomatological faculty / M.R. Gerasymchuk, V.V. Cherkasova,
L.M. Zaiats // IFNMU. Department of pathological physiology. – 2017. –
110 p. Discussed and approved on profile commission of
medical&biological disciplines meeting of Ivano-Frankivsk National
Medical University.
Protocol № ____ from «___» ________ 2017 year
4

Calendar plan of practical classes
of pathological physiology for the students of the III course in the V semester
THEME OF PRACTICAL STUDIES DATES Hours
1. Violation of blood system. Erythrocytosis. Anemias. Posthemorrhagic anemia. 06.09.2017 2
2. Hemolytic anemias and anemias with disorders of erythropoiesis. 13.09.2017 2
3. Leukocytosis and leukopenias. 16.09.2017 2
4. Diseases of the hemopoietic system. Leukemias. 20.09.2017 2
5. Violation of hemostasis. 27.09.2017 2
6. Practical skills for chapter “Pathophysiology of blood” 30.09.2017 2
7. Cardiac arrhythmias. 04.10.2017 2
8. Insufficiency of circulation of blood. Heart failure. 11.10.2017 2
9. Insufficiency of coronary blood circulation. Ischemic heart disease. 14.10.2017 2
10. Disorders of vascular tone. 18.10.2017 2
11. Pathophysiology of the external respiration. Respiratory failure. 25.10.2017 2
12.
Practical skills for chapter “Pathophysiology circulatory system and
respiration”.
28.10.2017 2
13.
Violation of digestion in an oral cavity. Disorders of salivation. Caries.
Periodontitis.
01.11.2017 2
14. Violation of digestion in a stomach. Etiology. Pathogenesis of ulcer disease. 08.11.2017 2
15.
Violation of digestion in an intestine. Acute pancreatitis. Intestinal
obstruction.
11.11.2017 2
16. Pathophysiology of the liver. Liver insufficiency. 15.11.2017 2
17. Pathophysiology of kidneys. Renal failure. 18.11.2017 2
18. Practical skills for chapter “Pathology of digestion, liver, and kidneys” 22.11.2017 2
19. Pathophysiology of the hypothalamic-pituitary system and adrenal glands. 25.11.2017 2
20. Pathophysiology of thyroid and parathyroid glands. 29.11.2017 2
21.
Violation of sensory, sensory, motor and trophic function of the nervous
system.
02.12.2017 2
22. Pathophysiology of integrative nervous activity. Experimental neuroses. 06.12.2017 2
23. Pathophysiology of extremal conditions. 09.12.2017 2
24. Module 2. Practical part 13.12.2017 2
25. Module 2. Theoretical part 16.12.2017 2
Total hours 50
Calendar plan of lectures
THEME OF LECTURE DATES Hours
1.
Leukocytosis and leukopenias. Diseases of the hemopoietic system.
Leukemia’s.
09.09.17 2
2.
Pathophysiology of blood circulation. Heart failure. Insufficiency of coronary
blood circulation. Ischaemic heart disease. Disorders of vascular tone.
23.09.17 2
3. Pathophysiology of digestion and liver. 07.10.17 2
4. Pathophysiology of kidneys. Renal failure. 21.10.17 2
5. Pathophysiology of the regulatory systems. 04.11.17 2
Total hours 10
5

The ESTIMATION FOR THE MODULE is defined as a sum of marks
of current educational activity (in points), which is proposed during the
evaluation of theoretical knowledges and practical skills. Maximal amount of
points, which a student can collect - 200 points during of every module study,
including for current educational activity – 120 points (together the practical
skills are 115 points, individual work is 5 points), on results final module
control are 80 points.
Control of theoretical and
practical preparation
0 – 2 points – completely prepared homework;
0 – 2 points – oral answer;
0 – 1 points – test control during class.
Minimum – 0 points; positive – 3; maximum – 5
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
answerfor the question of the final test control.
"2" 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.
"3" 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 51-70% of the final test
control tasks.
"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 71-90% of the final test control tasks.
"5" 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.
6

Topic 1: Violation of blood system. Erythrocytosis. Anemias.
Posthemorrhagic anemia.
1. Actuality of the theme. The system of blood is the internal environment
of organism. The normal state of blood, its cellular composition, is in close
interrelation with activity of different organs and systems (by the nervous
system, marrow, liver, kidneys, spleen, and endocrine glands). That is why
violations from the side of blood can arise up in connection with changes in
these organs or as a result of direct influence on blood of different pathological
factors.
2. Length of the employment – 1h 30 min.
3. Aim: Form for students the picture of reasons, mechanisms and
consequences of violations of general volume of blood at different pathological
processes. Able to estimate the quantitative changes of RBC, haemoglobin and
color index, indexes of physiology regeneration of marrow, degenerative
changes of RBC at posthemorrhagic anaemia.
To khow:
- determination of concept is “anaemia” and principles of classification;
- etiology and pathogenesis of acute and chronic posthemorrhagic anaemia;
- etiology, pathogenesis and displays of violation of general volume of
blood;
- method of determination of haemoglobin, color index, amount of RBC in
peripheral bloo.
To be able:
- to describe the picture of blood at acute and chronic posthemorrhagic
anaemia in its different stages;
- to estimate, using got in an experiment given, quantitative changes of
RBC, haemoglobin and color index, indexes of physiology regeneration of
marrow, degenerative changes of RBC at posthemorrhagic anaemia.
Task for independent extracurricular work.
1. Able to analyse the value of volume, will make and basic functions of
blood for support of normal vital functions.
2. Methods of determining the amount of haemoglobin, RBC in blood, color
index.
3. Erytropoiesis in a norm, nomenclature and morphology of red blood.
4. Normal indexes of line of RBC: table of contents of RBC, haemoglobin,
color index, amount of reticulocyte.
To perform practical work: to analyse of the normal content of blood
average:
4. Basic level.
7

The name of the previous and
future disciplines
The receiving of the skills
1. Histology
2. Biochemistry
3. Pphysiology
4. Internal medicine
5. Haemathology
6. Surgical stomatology
Scheme of erythropoiesis.
Quantitative parameters of red blood.
Technique of erythrocytes account.
Technique of determination of the hemoglobin
content.
Technique of determination of a colour index.
5. The advices for student
Normal content of erythrocytes (red blood cells - RBC) and hemoglobin in blood:
Erythrocytes: M — 4.0-5.0·1012
/l; F — 3.9-4.7·1012
/l; Newborn: 5-6·1012
/l
Hemoglobin (Hb): M - 135-160 g/l; F - 120-140 g/l;
Mean corpuscular hemoglobin (MCH) = [Hb] / RBC count: 0.85-1.15
Reticulocytes: 2-10 % (of total erythrocyte number)
Erythrocytes sedimentation rate (ESR): M - 2-10 mm/h; F - 2-15mm/h
Hematocrit: Adults: M - 40-48%; F - 36-42%; Newborn: 45-54%
Size of erythrocyte- 7-8 µm
Life span of erythrocyte - 120 days
Maturation of erythrocyte - 3 days
Total amount of erythrocytes in blood of adults - 25·1012
/l
Destroyed and formed daily up to 1% of total amount of erythrocytes (210 billion).
Iron in blood 8.53-28.06 µmol/l
Ferritin, serum in men 96±7.63 µg/l, in women 45.5±4.58 µg/l.
5.2. Practical part: Manual Cell
Counting (by microscope)
Neubauer counting chamber from above with
cover slip. Notice the two counting grids which are
recognized as crosses.
Schematic representation of the Neubauer counting
chamber's counting grid: blue = area of the leukocyte count
red = areas of the erythrocyte and platelet counts
Since blood cells are counted per unit volume (per
liter), it is vital that the volume of blood, in which the
cells are counted, corresponds to a known quantity. This
makes the Neubauer
counting chamber a
useful method. A
special objective slide
on which two 3 x 3
mm long counting
grids were engraved
comprises the Neubauer counting chamber.
8

The counting grid is composed of 9 big squares, measuring 1 x 1 mm . From these
squares, the central square contains 25 medium sized squares each measuring 0.2 x 0.2
mm. These are further divided into 16 small squares each measuring 0.05 x 0.05 mm. The
large central square is also called the erythrocyte grid. The squares highlighted in red
correspond to 80 small squares, that are used to establish the erythrocyte and platelet
counts. The large squares marked in blue are used to establish the leukocyte count.
During the chamber count, all cells that lie on the left and the lower border or that just
touch it are counted. None of the cells on the upper and the right border or those that just
touch it will be counted. This procedure is also known as the L-form rule
Filled circles = count; Empty circles = do not count
Schematic representation of a medium-sized square (0.2 x 0.2 mm) of the Neubauer
counting chamber's erythrocyte grid.
Schematic representation of the
Neubauer counting chamber side view blue
= chamber depth
On both sides of the counting grid, an edge
can be found. A cover slip is placed on top of it. If the cover slip is properly placed, a
distance of 0.1 mm (chamber depth) will exist between the counting grid and the cover
slip. The volume that is over the squares of the counting net corresponds to 0.1µl in a large
square (1mm x 1mm x 0.1 mm = 0.1mm3
= 0.1µl) and to 0.00025µl in a small square
(0.05 mm x 0.05 mm x 0.1 mm = 0.00025mm3
= 0.00025µl).
Photographic representation of the
Neubauer counting chamber side view,
Notice the short distance of 0.1 mm between
object slide and the cover slip.
Manual Reticulocyte Counting
Reticulocytes are stained without fixation (supravital staining) with either new
methylene blue or brilliant cresyl blue and applied to an ordinary glass slide. A special
eyepiece is used which reduces the field of vision to a small square for counting. Around
1000 erythrocytes (500 in each of the two films) are counted, and the reticulocytes which
are recognizable due to their reticular markings are counted. The number of reticulocytes
per erythrocytes is expressed as a percent. The lower the number of reticulocytes, the more
inaccurate the value. When 1000 erythrocytes are counted, a coefficient of variation of
±10% is achieved for a reticulocyte percentage of 1-2% (= normal range).
6. Control questions of the theme:
1. The types of changes of general volume of blood.
2. To give determination of “hypovolemia”, its kinds and examples.
3. To give determination of “hypervolemia”, its kinds and examples.
4. Determination of concept is “anaemia”.
5. Classifications of anaemias.
6. Etiology of acute posthemorrhagic anaemia.
7. To give description of phases of compensation of organism on acute
hemorrhage.
9

8. A picture of peripheral blood is in the bone-cerebral phase of
compensation after hemorrhage.
9. Etiology and pathogenesis of chronic posthemorrhagic anaemia.
7. Students’ practical activities
Protocol № 1 Date_____________________
Experimental work 1. Define amount of haemoglobin for a rabbit with
acute posthemorrhagic anemia in blood. In a test tube from hemometer
collect solution of salt acid to the number 2 on the scale.
Collect 0,02 ml of blood into capillary, wipe the tag of capillary by cotton
wool and out blood into the test tube with salt acid. A liquid is mixed and give
to stand 5 min. Then refill the distilled water and mixed by a glass stick until the
color of liquid in a test tube will be equal with the color of standard solution of
hemometer. Formula of calculation: Hb = A×0,6206, where “A” is an amount of
haemoglobin in g%; 0,6206 is a coefficient of count in unit of SI. For example:
A = 10 g%, then 10 • 0,6206 = 6,2 mmol/l.
Conclusion: ___________________________________________________________
_________________________________________________________________________
________________________________________________________________
Experimental work 2. Count up the amount of RBC for a rabbit. In a
test-tube pour 4 ml of a 3% solution of chloride of sodium. By a capillary
pipette collect 0,02 ml blood and produce it on the bottom of test tube. The
contents is carefully mixed. Then drop of liquids by pipette place under
preliminary grinding (rubbing) in integumentary (covered) small glass of
account chamber. Count up erythrocytes in 5 large (that in 80 small) squares of
net of Goryaeva and calculate their amount in 1 litre of blood after a formula:
lТ
ААА
/
100
10
100
10
80
2004000 128
=•=•
••
where A – is an amount of RBC in 5 large
squares; 4000 – the volume of small square makes 1/4000 mm3
; 200 – is
dilution of blood; 80 – is an amount of the counted up small squares; 108
is a
multiplier for the count of amount of RBC in unit of SI; T – 1012
.
Conclusion: ___________________________________________________________
_________________________________________________________________________
________________________________________________________________
Experimental work 3. To define the coloured index.
Formula of calculation: Er
Нв
CI
•
=
2
Unit of Hb is mmol/l, Er is T/l.
10

For example: Hb of experience - 6,2 mmol/l, RBC of experience - 3 x
1012
/l. Then 1
32
2,6
≈
•
=CI
Conclusion: ___________________________________________________________
_________________________________________________________________________
________________________________________________________________
Experimental work 4. Analysis of hemograms:
1. Analyse and estimate quantity of each indicator of red blood
(erythrocytes, hemoglobin, CI): norm, more, less.
2. Select the type of anemia according to colour index: normochromic,
hyperchromic, hypochromic.
3. Give the examples of diseases in wich this anemia occurs.
Hemogram 1
Eryth-
rocytes
Hemo-
glo-
bin
CI ESR
Leu-
kocy-
tes
Baso-
phils
Eosi-
no-
phils
Neutrophils
Lym-
pho-
cytes
Mo-
no-
cy-
tes
meta-
myelо-
cytes
stab-
nucle-
onic
segmen-
tonucle-
onic
·1012
/l g/l mm/h ·109
/l % % % % % % %
2,9 58 0,62 9 6 1 2 - 5 56 31 5
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 2
Eryth-
rocytes
He-
mo-
glo-
bin
CI ESR
Leu-
kocy-
tes
Ba-
so-
phils
Eosi-
no-
phils
Neutrophils
Lym-
pho-
cytes
Mo-
no-
cy-
tes
meta-
myelо-
cytes
stab-
nucle-
onic
segmen-
tonucle-
onic
·1012
/l g/l mm/h ·109
/l % % % % % % %
3,25 100 0,92 7 7 1 3 1 4 55 31 5
Conclusion: ________________________________________________________
___________________________________________________________________
7. Practice Examination.
Practice examination type 1: Choose the correct answer:
Test 1. A 32-year-old patient was admitted to the hospital with gross
bloodloss due to auto accident trauma. Ps – 110 Bpm, RR - 22 pm, BP-
100/60mm Hg. What changes in the blood will occur in an hour after the
bloodloss?
A. Hypovolemia
B. Hypoproteinemia
C. Hypochromia of erythrocytes
D. Leukopenia
E. Erythropenia
11

Test 2. Examination of a 43 y.o. anephric patient revealed anemia
symptoms. What is the cause of these symptoms?
A. Folic acid deficit
B. Reduced synthesis of erythropoietins
C. Vitamin B12 deficit
D. Enhanced destruction of erythrocytes
E. Iron deficit
Test 3. A patient's blood was analyzed and the decreased erythrocyte’s
sedimentation rate (ESR) was discovered. What disease from the listed
below is accompanied with decreased ESR?
A. Myocardial infarction
B. Hepatitis
C. Splenomegaly
D. Polycytemia
E. Vitamin B deficiency
Test 4. Patient 54 year-old, 5th day after surgical operation. Blood
count: Erythrocytes 3,6*1012
/l, Hemoglobin 95 g/l, Erythrocyte’s
hemoglobin content (color index) 0,78; Leukocytes 16*109
/l, Platelets
450*109
/l Blood picture: anizocytosis, poikilocytosis, reticulocytes - 3,8%.
What anemia does this patient have?
A. Chronic posthemorragic
anemia
B. Acquired hemolytic anemia
C. Acute posthemorragic anemia
D. Anemia from iron deficiency
E. Hypoplastic anemia
Test 5. A 30-year-old patient’s blood test revealed the following:
erythrocyte count is 6 · 1012
/l, hemoglobin is 10,55mmol/l. Vaquez’s disease
was diagnosed. Name the leading part of pathogenesis:
A. Iron-deficiency
B. B12-deficiency
C. Hypoxia
D. Neoplastic erythroid
hyperplasia
E. Acidosis
Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. Victim is delivered in receiving branch of hospital by the casual
transport through 8 minutes after traffic incident. Complains on pain in stomach
with irradiation into the right shoulder. The skin is pale, is covered with cold
sweat. Arterial pressure - 95/70 mm Hg, pulse – 102 beats for 1 minute, breath -
28 for 1 minute. The blood was taken immediately on analysis an amount of
erythrocytes - 4,2×1012
/l, hemoglobin content - 122 g/l.
1. Analyse these data. What parameters deviate from norm? 2. What it is
possible to think about in this case? 3. How does it explained painless of skin?
What does it mean this reaction? 4. How do you evaluate the increase of rate
pulse and breath?
Answer for the task 1: ___________________________________________________
12

Task 2. Amount of erythrocytes of the patient 3,5·1012
/l, contain of Hb - 86
g/l. 1. What is this state name? 2. Define colour index. 3. What does it testifie
about?
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed. by A.V.Kubyshkin–Vinn:NovaKnuhaPubl–2011.–P.361–381.
1. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010.–
P. 290–308, 319–320.
2. Pathophysiology, Concepts of Altered Health States/ C.M.Porth, G.Matfin.–NY,M.–2009.–P.278–285.
3. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene,
Norman D. Harris // IL 60030-7820, 3rd
ed, USA. – 2008. – Chapters 11. – P. 705–712.
4. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th
edition. Copyright В. – Lippincott Williams &
Wilkins – 2008. – Chapters 12. – P. 354–357, 363–365, 368–382.
5. Robbins and Cotran Pathologic Basis of Disease 8th
ed./Kumar,Abbas,Fauto 2007. –Ch.12.– P. 422–424.
Additional:
1. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback
(2003) / Carol Mattson Porth, Kathryn J Gaspard. – Chapter 13. – P. 216–221.
Silbernagl S. Color Atlas of Pathophysiology /S.Silbernagl, F.Lang//Thieme.Stuttt.NY.–2000.–P.28–33.
Topic 2: Hemolytic anaemias and anaemias with disorders of
erythropoesis.
1. Actuality of the theme. Anemia is a haematological symptom of various
diseases (illnesses of gastro-intestainal pathway, kydneys, infectious and
helmintosis, malignant tumors, inherited and purchased diseases of children,
different intoxications). Except this, anemia can take primary character, coming
forward as an independent haematological disease. Thus, the pathophysiological
mechanisms of development of the anaemic states are difficult enough and
various. Knowledge of basic haematological displays of anemias, reasons and
mechanisms of their development in every case enables a doctor not only in
good time to diagnose but also map out measures of prophylaxis and rational
pathogenetic therapy of this type of pathology. The qualitative features of
erythrocytes of peripheral blood and bone marrow allow to determine a kind of
anemia, to make submission about regenerative ability of bone marrow and to
inspect efficiency of treatment. For example, erythrocytes with the distinctive
morphological characteristics are peculiar for iron-deficiency anemia
13

(hypochromic erythrocytes), B12 (folic)-deficiency anemia (megaloblastes and
megalocytes), sickle-cell anemia (sickle-shape erythrocytes), thalassemia (target
like erythrocytes), Minkovskyi-Shoffar’s anemia (microspherocytes). The
increase of amount reticulocytes in peripheral blood testifies for good
compensator possibility of bone marrow.
3. Aim: To form for the students of concept about etiology and
pathogenesis of hemolytic and megaloblastic anemias, ability to characterize
their basic haematological displays, estimate the high-quality changes of RBC
and haemoglobin as index of tension of compensate mechanisms or pathological
changes.
To khow:
- principal reasons of origin and pathogenesis of hemolytic anemias and
anemias are as a result of violation of erythropoiesis;
- a role of industrial and domestic factors is in the origin of anemias;
- basic clinical and haematological syndromes are at B12- and folic acid
deficit anemia;
- a mechanism of origin of icterus is at hemolytic anemias.
To be able:
- to describe basic haematological indexes at hemolytic and megaloblastic
anemias;
- to explain principles of experimental design of hemolytic and
megaloblastic anemias;
- on the basis of information of experiment able to estimate the quantitative
and high-quality changes of RBC and haemoglobin as index of tension of
compensate mechanisms or pathological changes at hemolytic or megaloblastic
anemias.
A task is to independent extracurricular work:
1. To know erythropoiesis in a norm, morphology of cells of red blood.
2. Functions of RBC, structure and functions of haemoglobin.
3. Able to explain a biosynthesis gem; value of iron for a synthesis gem.
4. To know the exchange of iron, vitamin of B12 and folic acid in organism.
5. To know the normal indexes of number of RBC, amount of haemoglobin,
color index, amount of reticulocytes for the grown man.
6. Able to prepare and paint the samples of blood.
7. To define the number of RBC, concentration of haemoglobin, color index
and amount of reticulocytes in blood.
To perform practical work: to analyse of the pathogenesis of the
hemolytic anemias
4. Basic level.
14

future disciplines
1. histology
2. biochemistry
3. physiology
4. haemathology
5. stomatology
Scheme of erythropoiesis
Regulation of erythropoiesis
Form and size of erythrocytes
Structure of haemoglobin
5. The advices for student
In hereditary hemolytic anemia, hemolysis is caused by reduction of
osmotic and mechanical resistance of erythrocytes.
In hereditary membranopathy (microspherocytic hemolytic anemia or
disease of Minkovsky-Shoffar) genetic deficiency in the membrane of
erythrocytes of Ca2+
-dependent ATP-phase and phospholipids results in
increased permeability of the membrane.
In hereditary fermentopathy, for example, glucose-6-
phosphatedehydrogenasodeficient (G-6-PhDG) anemia, acute intravascular
hemolysis of erythrocytes is caused by damage of the cellular membranes by
peroxide as the erythrocytes with deficiency G-6-PGDG have reduced contents
of the restored glutation (oxidant).
Intracellular hemolysis of erythrocytes in hereditary hemoglobinopathy is
connected with synthesis of abnormal or not peculiar to the given age
hemoglobin.
In the norm the fetal erythrocytes contain mainly fetal hemoglobin HbF
and their synthesis begins after the 8th
week of the embrional life; newborn’s
erythrocytes have 70-90% of HbF and 10-30% of HbA1; by the end of the first
year of life and in adult, erythrocytes contain 96-98% HbA1, 3%HbA2and 1-2%
of HbF.
In sickle cell anemia HbS is formed (in β-chain of globin glutamic acid is
substituted for valin) which in its restored condition falls out in crystals and
causes erythrocyte deformity (sickle cells); hypoxia contributes to
intensification of hemolysis of such erythrocytes.
The red cell membrane cytoskeleton and the effect of alterations in the
cytoskeleton proteins on red cell shape. With mutations that affect the integrity
of the membrane cytoskeleton, the normal biconcave erythrocyte loses
membrane fragments. To accommodate the loss of surface area, the cell adopts
a spherical shape. Such spherocytic cells are less deformable than normal and
are therefore trapped in the splenic cords, where they are phagocytosed by
macrophages.
1. Etiology of the purchased hemolitic anemias, their kinds.
15

2. To explain the mechanism of hemolysis at the purchased hemolytic
anemias.
3. To give description of picture of peripheral blood at the purchased
hemolytic anemia.
4. To name the types of the inherited hemolytic anemias.
5. To explain pathogenesis hereditary spherocytosis (Minkowsky-Shauffard
disease), picture of blood at this pathology.
6. To explain pathogenesis of glucose 6-phosphate dehydrogenase deficit
anemia.
7. To name kinds, explain pathogenesis, picture of peripheral blood at
inherited hemoglobinopathy.
8. To explain pathogenesis of sickle cell anemia, picture of peripheral
blood.
9. To name kinds, make examples of anemias as a result of violation of
erythropoiesis.
10. Etiology, pathogenesis, picture of blood of asiderotic (iron-deficiency)
anemia.
11. Kinds and etiology of B12-folic acid deficit anemias.
12. Etiology, pathogenesis of pernicious (Addison-Birmer’s) anemia.
13. To give description of picture of peripheral blood at pernicious anemia.
Protocol № 2 Date_____________________
Experimental work 1. To learn the picture of blood for a rabbit with
experimental hemolytic anemia. Within a week three times (with a two-day
interval) a 3% solution of phenylhydrazine is entered hypodermic a rabbit (dose
of 0,6 ml per 1 kg of mass).
Cut off wool on ear of rabbit, a skin is wiped an alcohol, dry out ether and
prick a regional vein. The drop of blood inflict on the edge of subject glass,
stretch on all it surface by the polished subject glass, leaned to the drop under
the corner of 45°.
On the stroke dried up on air inflict the counted up amount of drops of paint
of May-gryunval'da and paint during 3 min. (fixing). Then inflict the same
amount of drops of the distilled water, mix up a waggle (colouring). A paint is
united and, not washing water, a stroke is inundated the divorced paint of
Romanovsky (1 drop on 1 ml distill water) on 6 min. Wash off a paint by water,
dry out a stroke and study under a immersion increase.
Conclusion: ________________________________________________________
___________________________________________________________________
16

Experimental work 2. To learn the picture of peripheral blood for an
animal with megaloblastic anemia. Daily, during 5 days, intraperitoneum is
entered an animal water solution of saponin, from the calculation of 5 mg per 1
kg of mass.
On lesson the skin of ear of animal is wiped an alcohol and do an incision.
Prepare the thin stroke of blood, and after drying out dye after Pappengeym. A
stroke is ready to consider under a immersion increase.
To sketch the picture of blood at hemolytic and megaloblastic anemias.
Conclusion: ________________________________________________________
___________________________________________________________________
Experimental work 3. Analysis of hemograms.
1. Analyse and estimate quantity of each indicator of red blood
(erythrocytes, hemoglobin, CI): norm, more, less.
2. Select the type of anemia according to colour index: normochromic,
hyperchromic, hypochromic.
3. Give the examples of diseases in wich this anemia occurs.
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 1
Eryth-
rocytes
He-
mo-
glo-
bin
CI ESR
Leu-
kocy-
tes
Ba-
so-
phils
Eosi-
no-
phils
Neutrophils
Lym-
pho-
cytes
Mo-
no-
cy-
tes
meta-
myelо-
cytes
stab-
nucle-
onic
segmen-
tonucle-
onic
·1012
/l g/l mm/h ·109
/l % % % % % % %
2,79 110 0,63 8 5 1 4 - 2 59 28 6
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 2
Eryth-
rocytes
He-
mo-
glo-
bin
CI ESR
Leu-
kocy-
tes
Ba-
so-
phils
Eosi-
no-
phils
Neutrophils
Lym-
pho-
cytes
Mo-
no-
cy-
tes
meta-
myelо-
cytes
stab-
nucle-
onic
segmen-
tonucle-
onic
·1012
/l g/l mm/h ·109
/l % % % % % % %
3,27 142 1,42 5 7 1 5 1 6 53 30 4
Conclusion: ________________________________________________________
___________________________________________________________________
___________________________________________________________
Test 1. Along with normal hemoglobin types there can be pathological
ones in the organism of an adult. Name one of them:
A. HbF B. HbA1 C. HbA2
17

D. HbS E. HbO2
Test 2. A 25 year old Palestinian woman complains of weakness,
dizziness, dyspnea. In anamnesis: periodically exacerbating anemia. In
blood: Hb - 60g/l, erythrocytes - 2,5*1012
/l, reticulocytes - 35‰, anisocytosis
and poikilocytosis of erythrocytes, a lot of target cells and
polychromatophils. What type of anemia is it?
A. Sickle-cell anemia
B. Addison-Biermer disease
C. Glucose 6-phosphate dehydrogenase-deficient anemia
D. Minkowsky-Shauffard disease
E. Thalassemia
Test 3. A 34 year old woman was diagnosed with hereditary
microspherocytic hemolytic anemia (Minkowsky-Shauffard disease). What
mechanism caused haemolysis of erythrocytes?
A. Autoimmune disorder
B. Bone marrow hypoploasia
C. Enzymopathy
D. Membranopathy
E. Hemoglobinopathy
Test 4. A 56 year old patient came to a hospital with complaints about
general weakness, tongue pain and burning, sensation of limb numbness. In
the past he underwent resection of forestomach. In blood: Hb-80 g/l;
erythrocytes - 2,0*1012
/l; colour index - 1,2, leukocytes - 3,5*109
/l. What
anemia type is it?
A. B12-folate deficient
B. Hemolytic
C. Aplastic
D. Iron-deficient
E. Posthemorrhagic
Test 5. 2 years ago a patient underwent resection of pyloric part of
stomach. He complains of weakness, periodical dark shadows beneath his
eyes, dyspnea. In blood: Hb - 70g/l, erythrocytes - 3,0*1012
/l, colour index -
0,7. What changes of erythrocytes in blood smears are the most typical for
this condition?
A. Megalocytes
B. Ovalocytes
C. Schizocytes
D. Macrocytes
E. Microcytes
Test 6. A 20 year old patient complains of general weakness, dizziness,
quick fatigability. Blood analysis results: Hb - 80g/l. Microscopical
examination results: erythrocytes are of modified form. This condition
might be caused by:
A. Obturative jaundice
B. Sickle-cell anemia
C. Hepatocellular jaundice
D. Acute intermittent porphyria
E. Addison's disease
Practice examination type 2. Give answers to the questions of the real-
life tasks:
18

Task 1. In a patient with anemia there is following picture of blood: an
amount of erythrocytes - 1,4·1012
/l, haemoglobin content - 62g/l; aniso- and
poikilocytes megaloblastes, megalocytes in smear. 1. What type of anemia such
changes are characterized for? 2. Why does it develop? 3. Why in this case is
sharply expressed erythropenia? 4. Give the morphological characteristic to
megaloblastes and megalocytes. 5. Calculate colour index.
Task 2. The blood of patient with anemia is characterized by parameters:
amount of erythrocytes – 3,5·1012
/l, haemoglobin content - 50g/l; in blood smear
– annulocytes, poikilocytes, microcytes. 1. For what kind of anemia these
parameters are characterized? 2. Calculate colour indexand determine, to what
group (according to colour index) this anemia concern. 3. Why erythrocytes are
acquired of rings form.
Answer for the task 2: __________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed.by A.V.Kubyshkin–Vinn:NovaKnuhaPubl–2011.–P.381– 409.
2. Copstead L-E.C.Pathophysiology/L-E.C.Copstead, J.L.Banasik // ElsevierInc 4th
ed.–2010.– P. 310–329.
Wilkins – 2008. – Chapters 12. – P. 363–365, 368–382.
edition, USA. – 2008. – Ch. 11. – P. 712–724.
ed/ Kumar, Abbas, Fauto 2007.–Ch.12.–P. 422–441.
Additional:
7. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback
(2003) / Carol Mattson Porth, Kathryn J Gaspard. – Chapter 13. – P. 221–230.
8. SilbernaglS. Color Atlas of Pathophysiology/S.Silbernagl,F.Lang//Thieme.Stuttg. NY.– 2000.–P.34–41.
Topic 3. Leukocytosis and leukopenias.
1. Actuality of the theme. Leucocytosis are considered as a reaction
hematopoietic system due to action of physiological and pathological irritations.
Leucocytosis is a pathological symptom of many diseases. In a basis of
leucocytosis lay pathophysiological mechanisms connected with proliferation,
maturation going out of leucocytes and their flow into vessels and
redestribution.
19

Leucopenia may depend upon oppressive influence of some toxines on the
maturation and outflow of leucocytes from the bone-marrow. Often these
phenomenas are observed during the infectious diseases. They have significanse
for the differential diagnostic. If for the disease is characterised leucocytosis, the
availability of leucopenia testifies on depression of hemopoietic system.
3. Aim:
To know: types of the left nuclear deviation.
To be able: to analyse of the quantitative and qualitative changes of
leucocytes in blood.
quantitative and qualitative changes of leucocytes in blood. The increase of
leucocyte quantity is called leucocytosis, and the decrease-leucopenia. The
norm is 4-9G/l or 4-9*109
/l. The quantitative changes are increased quantity of
immature forms in blood and degeneration of leucocytes.
Task for independent extracurricular work.
1. To know leucopoesis in a norm, morphology of white blood cells.
2. Methods of determining the amount of white blood cells in the blood.
3. Anatomy and functions of primary and secondary hematopoietic organs.
4. Basic level.
The name of the previous
and future disciplines
1. histology
2. biochemistry
3. physiology
4. stomatology
Scheme of leucopoesis.
Leucocytes formula of blood.
Function of leucocytes.
Methods of counting of leucocytes maintenance in blood.
5. The advices for students.
Leucocytosis. Leucocytosis –is the increase of total leucocyte quantity in
blood – over 9G/l (9/109
/l).
Leucopenia. Leucopenia –is the decrease of total leucocyte number in
blood –below 4G/l (4*109
).
Manual leukocyte differential
To manually classify leukocytes, a blood film is stained with May-Gruenwald-
Giemsa. The different types of leukocytes from the film are counted under a
microscope. Since the leukocytes are not evenly distributed in the film and the
same cell may not be counted more than once, the preparation should be
systematically screened.
20

Pull film Push film
Rümke table % = percentage
of a type of leukocyte to the total
number shaded dark red =
percentage of identified leukocytes
(Table modified from the CD-
ROM "Das interaktive Handbuch
der Hämatologie")
At least 100 leukocytes should
be counted and classified. Ideally, 2
x 100 cells (in two blood films)
should be counted. It is nearly
impossible to count more than 100
leukocytes in severe leukopenias. On the other hand, in the case of very high leukocyte
counts, 400 leukocytes should be counted. Percentages achieved in this way are converted
to absolute values via the leukocyte count (e.g. 20% lymphocytes with a leukocyte count
of 6.0 x 109
/L corresponds to an absolute lymphocyte count of 0.2 x 6.0 = 1.2 x 109
/L).
Precision must be discussed again. Since leukocytes such as eosinophils
and basophils only constitute a small part of the total number of leukocytes, the
accuracy of their counts is rather small when only 100 leukocytes are counted.
This is especially important when the leukocyte count is very high (e.g. 1
eosinophil per 100 leukocytes in a leukocyte count of 60.0 x 109
/L already
corresponds to 60.0 x 107/L). To what degree the leukocyte differential values
can vary, independent of the number of differentiated cells, can be determined
from the Rümke table (see below).
If the actual percentage of a patient's basophils are 5%, for example, the
value found by counting 100 leukocytes may be between 2 and 11%. Only by
counting 10,000 cells (performed accurately only by automated counters), has
the obtained value a precision of ±10%. If the percentage of a cell type is 50% a
precision of ±10% is achieved with 500 counted leukocytes.
1. What is leukocytosis? Classification of the leukocytosis.
2. Etiology of the leukocytosis.
3. The mechanisms of leucocytosis.
4. Blood picture under the leukocytosis.
21

5. What is leukopenia? Classification of the leukopenia.
6. Etiology of the leukopenia.
7. The mechanisms of leucopenia.
8. What is aleukia, agranulocytosis?
9. Blood picture under the leukopenia.
10. Leucocyte degeneration in blood.
11. Hereditary WBC abnormalities.
Protocol № 3 Date_____________________
Experimental work 1. Count up a leucocytic formula (leucogram) at an
abscess. To prepare the stroke of blood, taken from the vein of ear of rabbit and
to paint it after Pappengeym. See the stroke under a immersion increase. The
stroke of blood is mentally divided into four fields, conducting the lines which
are perpendicular one to one through the center of stroke. Count up in every
field 25 leucocytes, moving a stroke on the broken line. Count up separate types
of leucocytes using a meter.
Formula: LG
А
L
АА
/
20
/10
20
10
11600
204000 96
=•=•
•
••
,
А – amount of leucocytes in 100 big squares; 1600 – amount of small squares; 4000
1
-
a volume of small square is in microliter; 20 - is a degree of breeding of blood; 106
- is a
multiplier for the count of amount of leucocytes in CI units; G - giga = 109
Conclusion:__________________________________________________________
Experimental work 2. Define the index of nuclear change.
The index of nuclear change of neutrophiles is determined after a formula:
S
BYМ
%
%%% ++
where
M – mielocytes B – band [stab] neutrophiles
Y – young neutrophiles S – segmented [polynuclear] neutrophiles.
Index of nuclear exchange in norm 0,6-0,8
Conclusion:__________________________________________________________
____________________________________________________________________
22

Test 1. A 16-year-old boy was performed an appendectomy. He has
been hospitalized for right lower quadrant abdominal pain within 18
hours. The surgical specimen is edematous and erythematous. Infiltration
by what of the following cells is the most typical for the process occuring
here?
A. Basophils
B. Eosinophils
C. Monocytes
D. Neutrophils
E. Limphocytes
Test 2. A patient operated on complicated appendicitis has the
following changes of blood count: erythrocytes - 4,0.1012
/l, Нb - 120 g/l,
color index - 0,9, leukocytes – 18,109
/l, basophils - 0, eosinophils - 0,
myelocytes - 0, juvenile - 0, stab neutrophils - 20, segmentonuclear
neutrophils - 53, lymphocytes - 21, monocytes - 5. How is such nuclear shift
of leukocytic formula called?
A. Hyperregenerative
B. Regeneratively-degenerative
C. Regenerative left shift
D. Degenerative left shift
E. Right shift
Test 3. A 3-year-old child has eaten some strawberries. Soon he developed
a rash and itching. What was found in the child’s leukogram?
A. Monocytosis
B. Lymphocytosis
C. Eosinophilia
D. Hypolymphemia
E. Neutrophilic
leukocytosis
Test 4. Lazy leucocyte syndrome is because of:
A. Disorder of phagocytosis
B. Cellular immunodeficiency
C. Combined immunodeficiency
D. Disorder of complement
Test 5. A 5 year old child is ill with measles. Blood analysis revealed
increase of total number of leukocytes up to 13*109
/l. Leukogram:
basophils - 0, eosinophils - 1, myelocytes - 0, juvenile neutrophils - 0, band
neutrophils - 2, segmented neutrophils - 41, lymphocytes - 26, monocytes -
30. Name this phenomenon:
A. Lymphocytosis
B. Agranulocytosis
C. Eosinopenia
D. Monocytosis
E. Neutropenia
Test 6. A 26 year old man is in the torpid shock phase as a result of a
car accident. In blood: 3,2*109
/l. What is the leading mechanism of
leukopenia development?
A. Redistribution of leukocytes in bloodstream
B. Leikopoiesis inhibition
C. Lysis of leukocytes in the blood-forming organs
D. Intensified elimination of leukocytes from the organism
E. Disturbed going out of mature leukocytes from the marrow into the
blood
23

Practice examination type 2 Give answer to the questions of the real-
life tasks:
Amount of
leucocytes
Baso
-
phile
s
Eosino
-philes
Neutrophiles
Lym-
phocyte
s
Mono
-cytesMyelo-
cytes
Meta-
myelo-
cytes
Stab-
nucleo
-nic
Segmen
-tonuc-
leonic
Task1 12,0·109
/l 1 % 2 % - 1 % 15 % 57 % 20 % 4 %
Task 2 58,3·109
/l 1 % 3 % Single 3 % 38 % 48 % 4 % 3 %
Task 3 1,35·109
/l 0,5
%
1,5 % - - 4 % 17 % 65 % 12 %
Task 4 11,4·109
/l 2 % 16 % - - 1 % 55 % 24 % 2 %
Task 5 2,0·109
/l 1 % 2 % - 1 % 15 % 57 % 20 % 4 %
Answer for the tasks: ___________________________________________________
_____________________________________________________________________
_____________________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/ Ed. by A.V.Kubyshkin – V:NK P. – 2011. – P.286–287,322–333.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne P. – 2010. – P. 266–322.
Norman D. Harris // London, 3rd
ed, USA. – 2008. – Ch 11. – P. 725–726.
ed/Kumar, Abbas .– 2007.– Ch 12.– P.441–468
Additional:
1. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. – P. 242–262.
2. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – NY. – 2009. – P. 278–
323.
Wilkins – 2008. – Chapter 12. – P. 357–359, 363, 366–367, 382–387.
4. 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. 179–191.
5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003)
/ Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 11. – P. 191-205.
Topic 4: Diseases of the hemopoietic system. Leukemia’s.
1. Actuality of the theme. Steady growth of number of leucosis among the
population of many countries of the world and high lethality demand steadfast
attention to the given pathology. Preventive measures have the large
significance in struggle with leucosis. Therefore it is important for the future
doctor to acquire existing submissions about etiology of leucosis (chemical
cancerogens, ionizing radiation, virus infection). Each form of leucosis differs
by characteristic shifts of cytostructure of peripheral blood and bone marrow.
On these features differential diagnostics of leucosis is constructed. It is
24

necessary to mark that the therapy of leucosis mainly pathogenetic. The
deepening of our submissions about separate chains of pathogenesis will
promote perfecting of purposeful treatment.
3. Aim:
To know: leukemia –is a disease of tumor nature, originating from blood
cells with initial affection of the bone marrow.
To be able: to analyse of the pathogenesis and blood data under acute and
chronic leukemia.
leukemia. Oncogenic viruses, ionizing radiation and chemical substances cause
mutation of genes or epigenomic disturbance of regulation of multiplication and
maturation of hematopoietic cells of the II-nd and III-rd levels. Leukemia
viruses can cause such chromosomal translocation that result in transmission of
the oncogenes, localized in chromosomes, to the part of genome where they can
be activated
4. Basic level.
1. histology
2. biochemistry
3. physiology
4. oncology
5. surgical
stomatology
Scheme of hematopoisis.
Morphological features of leucocytes.
Leucocytic formula of blood.
Function of leucocytes.
1. Determination and general definition of leucosis. Classification of
leucosis is after motion and morphological signs.
2. Modern theories of origin of leucosis: role of viruses, ionizing radiation,
chemical matters, inherited anomalies. Tumor nature of leucosis. Basic displays
of tumor progression.
3. Features of hemopoiesis, picture of peripheral blood, leucogram at an
acute myeloleucosis [myeloleukemia].
4. Features of hemopoiesis, picture of blood at chronic myeloleucosis.
5. Picture of blood, leukogram at an acute lympholeucosis [lymphatic
leukemia].
6. Picture of blood, leukogram at a chronic lympholeucosis.
7. A mechanism of development of anemia at acute and chronic leucosis.
8. Violation of reactivity of organism is at leucosis.
9. A role of the inherited anomalies is in development of leucosis.
6. Independent audience work of student
25

Protocol № 4 Date_____________________
Experimental work 1. Learn the picture of peripheral blood and
marrow at the different types of leucosis. Use the strokes of blood of patients
with acute and chronic myeloleukemia, acute and chronic lymphatic leukemia.
Study strokes under a immersion increase and draw the picture of blood. Count
up a leukogram, index of nuclear change at every type of leucosis, using the
method of before unit
Conclusion:___________________________________________________________
Experimental work 2. Counting of leucocytic formula in smear of blood
sick on leucosis.
a) Acute lymphoblastic leucosis
b) Acute myeloblastic leucosis
c) Chronic myelocytic leucosis
d) Chronic lymphocytic leucosis
Study smear in immersial microscope objective. For determination of
leucocytic formula is necessary to calculate 100 leucocytes. Counting should be
done in four various parts of smear, moving subject glass so that the fields of
sight were on sufficient distance from either and other. For it also necessary pay
attention to the form, sizes of cells, colour, granularity in protoplazma, form and
colour of a nucleus. Put the results of counting in the table:
Baso-
philes
Eosino-
philes
Neutrophiles
Lympho-
blasts
Limpho-
cytes
Mono-
cytes
Mye
lob-
lasts
Promy
elo-
cytes
Myelo-
cytes
Meta
mye-
locytes
Stab
nuc-
leonic
Segmen
Tonuc
lenic
Practice examination type 1. Choose correct answer of the tests:
Test 1. A patient with acute myeloblast leucosis has developed liver and
spleen enlargement, anemia, myeloblasts in peripheral blood. What
principal sign allows to differ myeloblast leukosis from chronic one?
A. Leukemic gap
B. Pancytopenia
C. Anemia
D. Blast cells in peripheral blood
E. Thrombocytopenia
Test 2. A 23 y.o. patient complains of weakness, temperature rise up to
38-400
C. Objectively: liver and spleen are enlarged. Hemogram: Hb- 100
g/l, erythrocytes - 2,9*1012
/l, leukocytes - 4,4*109
/l, thrombocytes – 48*109
/l,
26

segmentonuclear neutrophils - 17%, lymphocytes - 15%, blast cells - 68%.
All cytochemical reactions are negative. Make a hematological conclusion:
A. Acute erythromyelosis
B. Acute myeloblastic leukosis
C. Chronic myeloleukosis
D. Undifferentiated leukosis
E. Acute lymphoblastic leukosis
Test 3. Increase in Alkaline phosphatase is seen in :
A. Chronic mieloleucosis (CML)
B. Leukemoid reaction
С. Eosinophilia
D. Malaria
Test 4. Mongolism is characteristically associated with:
A. Acute lymphoblastic
leukaemia
B. Chronic lymphatic leukaemia
C. Chronic myeloid leukaemia
D. Acute myeloid leukaemia
E. Erythroleukaemia
Test 5. Philadelphia chromosome (Phi) is commonly associated with :
A. Chronic lymphatic leukemia
B. Leukemoid reaction
C. Acute monocytic leukemia
D. None of the above
Practice examination type 2. Give answer for the questions of the real-
life tasks:
Task 1.
Total
amount of
leucocytes
Baso-
philes
Eosino-
philes
Neutrophiles
Lympho-
blasts
Lympho-
cytes
Mono-
cytesMyelo-
blasts
Meta-
mye-
locytes
Stab
Seg-
mental
100,0*109
/l 1% 2% 0% 0% 4% 7% 2% 80% 4%
60*109
/l 0% 3% - 1% 3% 6% 43% 39% 5%
22*109
/l 2% 2% - - 5% 38% 9% 42% 4%
48,5*109
/l 1% 1% 0% 1% 3% 21% 36% 34% 3%
1. Indicate, what parameters mentioned deviate from norm. What the
essence of this deviation - decrease, increase, appearance of the unusual forms?
2. What form of leucosis this leukogram is characterized for?
Answer for the task 1:___________________________________________________
Task 2.
Total
amount of
leucocytes
Baso-
philes
Eosi-
nophi-
les
Neutrophiles
Lym-
pho-
cytes
Mono-
cytes
Myelo-
blasts
Promiel
ocytes
Myelo-
cytes
Meta-
myelo-
cytes
Stab
Seg-
mental
75,0*109
/l 1% 1 % 78% 2% - - 3% 3% 10% 2%
54*109
/l - 1% 18% 0% 1% 3% 5% 50% 16% 6%
39*109
/l 1% 2% 9% - 2% 5% 7% 41% 20% 13%
250*109
/l 2% 4 % 11 % 6 % 10 % 14 % 13 % 21 % 18 % 1 %
27

1. Indicate, what from above mentioned parameters deviate from norm. In what
the essence of this deviation – decrease, increase, appearance of the unusual
forms consists? 2. What form of leucosis this leukogram is characterized for?
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/ Ed. by A.V.Kubyshkin – V: NK Publ. – 2011. – P. 286–287,
322–333.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // K, M-ne Publ. – 2010. – P. 266–322.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. –
2010. – P. 242–262.
4. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice /
Russell J. Greene, Norman D. Harris // London, 3rd
ed, USA. – 2008. – Ch 11. – P. 725–726.
Additional:
1. Pathophysiology, Concepts of Altered Health States/C.Porth, G.Matfin. – NY– 2009.–
P.278–323.
edition. Copyright В. –
Lippincott Williams & Wilkins – 2008. – Chapter 12. – P. 357–359, 363, 366–367, 382–387.
3. Robbins & Cotran Pathologic Basis of Disease 8th
ed./ Kumar, Abbas, Fauto.–2007.–Ch.12.–
P.441–468.
4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for
medical students and practitioners. Ed. by prof. Zaporozan, OSMU. – O. – 2005.– P. 179–191.
5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins),
Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 11. – P. 191-205.
Topic 5. Violation of hemostasis.
1. Actuality of the theme. One of major functions of blood there is support
of its liquid state into vessels and coagulates of blood at violation of integrity of
vascular wall. The liquid state of blood is saved due to balance between
coagulative and anticoagulative, fibrinolytic and kallikrein-kinin systems.
Violation in the system of hemostasis can take place in three directions: 1)
decline of coagulative ability of blood and origin of hemorragic diathesis; 2)
increase of coagulative ability of blood and origin of thromboses; 3) origin of
thrombohemorragic syndrome, which shows up increase of thrombosis and
hemorrhagic diathesis both.
2. Length of the employment – 1 h 30 min.
28

3. Aim: To form for students the modern knowledge of reasons and
mechanisms of violation thrombocyte-vascular and coagulative hemostasis, to
design these processes in an experiment on animals with the purpose of
cognition of reasons and terms of their origin, mechanisms of development,
consequences and value of these processes in pathology of man.
To khow:
- etiologic factors which predetermine violation of producing blood clots;
- basic phases of process of producing blood clots;
- reasons and mechanisms of origin of hemorrhagic diathesis;
- reasons and mechanisms of violation thrombocyte-vascular hemostasis;
- etiology and pathogenesis of disseminated intravascular clotting [DIC];
- inherited violations of blood clotting.
To be able:
- to explain the mechanisms of interrelation of basic factors of coagulative
and anticoagulative systems in the process of clotting;
- to reproduce violation of blood clotting in an experiment;
- to calculate prothrombin time [PT] and prothrombin index;
- to count up the amount of platelets in peripheral blood.
Modern presentations about coagulative and anticoagulative system of blood.
Mechanisms of the physiology blood clotting. Thrombosis as local violation of
circulation of blood.Stages of blood clotting.
To perform practical work: to analyse of the pathogenesis of the platelet
adhesion and aggregation.
4. Basic level.
The name of the previous and future
disciplines
1. histology
2. biochemistry
3. physiology
4. internal medicine
5. haematology
Vesseles-thrombocytous and plasmatic factors,
which participate in coagulation of blood.
Stage of blood coagulation.
Significance ancoagulative and fibrinolytic
systems of blood.
1. What is hemostasis pathology. Classification of hemostasis pathology.
2. Normal hemostasis.
3. The classical coagulation cascade.
4. Virchow's triad in thrombosis.
5. Decreasing of blood coagulation ability.
6. Thrombocytopenia and thrombocytopathy.
7. Increasing of blood coagulation ability.
29

8. Generalized disseminated intravascular blood coagulation (DIC-
syndrome).
9. Hereditary disorders of coagulation.
6. Independent audience work of student
Protocol № 5 Date_____________________
Experimental work 1. Define prothrombin time [PT] for a dog with the
cirrhosis of liver. In advance oily solution of carbon tetrachloride is entered a
dog from the calculation of 4 ml per 1 kg of mass. Before lesson for a dog take
4,5 ml of blood, add 0,5 ml of a 0,1% solution of oxalic sodium and spin, take
the plasma. In test tube pour 0,2 ml of plasma, warm up on an water bath at
38°N, add 0,2 ml warmed to a 38°N mixture from equal parts of thromboplastin
and 0,5% solution of calcium chloride. Carefully mix up a glass stick,
continuing to hold in a water bath. Calculate time from adding mixture to the
first signs of coagulation of plasma (in seconds).
Calculate the prothrombin indexes after formula: B
А
Х
•
=
100
, where A – time
of coagulation of control plasma (seconds); B – time of coagulation of
experimental plasma (seconds). A normal index of is equal 70-100%.
Conclusion
Experimental work 2. Count up the amount of thrombocytes for a
rabbit with radiation illness. Three days prior to lesson an animal is exposed
to the X-rays.
On the area of regional vein ears inflict a few drops of a 14% solution of
magnesium sulphate, prick a vein; carefully mix up blood a glass stick with
magnesia in correlation 2:10.
From the got mixture prepare a stroke, dye it after Pappengeym (to repaint
for the best visibility of trombocytes). A count is conducted under a immersion
increase in the narrowed eyeshot. Count up the amount of trombocytes on 1000
RBC.
Formula of calculation: 1000
АН
Х
•
= , where H – is an amount of platelets on
1000 RBC; A – is an amount of RBC;.Method of count of amount of RBC see
in previouse lesson.
Conclusion
30

Practice examination type 1. Choose the correct answer:
Test 1. Hemorrhage punctate was found out in the patient after
application of a tourniquet. With disfunction of what blood cells is it
connected?
A. Monocytes
B. Eosinophiles
C. Neutrophiles
D. Lymphocytes
E. Platelets
Test 2. A 43-year-old patient has thrombocytopenia, reduction of
fibrinogen, products of degradation of fibrin presented in the blood,
petechial hemorrhage along with septic shock. What is the most likely
cause of the changes?
A. Autoimmune thrombocytopenia
B. DIC-syndrom
C. Exogenous intoxication
D. Disorder of thrombocytes production
E. Hemorrhagic diathesis
Test 3. There is an inhibited coagulation in the patients with bile ducts
obstruction, bleeding due to the low level of absorbtion of a vitamin. What
vitamin is in deficiency?
A. К
B. Е
C. D
D. А
E. Carotene
Test 4. A 6-months-old baby has got frequent and extensive subdermal
hemorrhages. The administration of the synthetic analogue of vitamin K
(vicasol) was effective. γ-carboxylation of glutamic acid of what protein of
blood coagulation system does this vitamin take part in?
A. Antihemophilic globulin A
B. Fibrinogen
C. Prothrombin
D. Hageman's factor
E. Rosental's factor
Test 5. A patient with tissue trauma was taken a blood sample for the
determination of blood clotting parameters. Specify the right sequence of
extrinsic pathway activation.
A. III – VIII: TF – Xa
B. III – VIIa – Xa
C. III – IV – Xa
D. IV – VIII: TF – Xa
E. IV – VIIa – Xa
Practice examination type 2. Give answer to the questions of the real-
life task:
Task. The patient was in surgical clinic because of thrombophlebitis of the
right leg. After careless sudden movement an acute dyspnoe to bother him, pain
in the chest and cyanosis appeared. Did these disorders associate with
thrombophlebitis of the leg? In what cases such consequences of
thrombophlebitis are possible? Are such complications occasional in the
31

patient? Is thrombophlebitis complication possible in the other organs - brain,
kidneys, spleen?
Answers for the task: ___________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed.byA.V.Kubyshkin–Vinn NovaKnuha Publ.–2011.–P.444–460.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne Publ. – 2010. – P. 322–338.
3. Copstead Lee-Ellen C. Pathophysiology /L.-E.C.Copstead,J.L.Banasic//Elsevier Inc.–2010.–P.330–346.
4. Pathophysiology, Concepts of Altered Health States/ C.M.Porth, G.Matfin.–NY,M.–2009.–P.262–278.Corwin Elizabeth J.
Handbook of Pathophysiology / Corwin Elizabeth J. – 3th
edition. Copyright В. – Lippincott Williams & Wilkins – 2008. –
Chapter 12. – P. 359–364, 387–390.
edition, USA. – 2008. – Ch. 11. – P. 726–741.
ed./Kumar,Abbas,Fauto.– 2007.–Ch12. –P.468–475.
Additional:
/ Carol Mattson Porth, Kathryn J. Gaspard. Chapter 12. – P. 205-215.
2. Silbernagl S. Color Atlas of Pathophysiology /S.Silbernagl,F.Lang//Thieme.Stuttg.NY.–2000.–P.60–65.
Topic 6. Practical skills for chapter “Pathophysiology of blood”.
1. Common changes of blood volume: hypo- and hypervolemia. Types, causes and
mechanisms of development, significance for organism.
2. Blood loss. Protective and adaptive responses of organism to bleeding: immediate
hemodynamic responses, restoration of blood volume, quantity of protein and blood cells.
3. Disorder of physiological functions caused by bleeding.
4. Hemorrhagic shock. Pathogenesis, consequences, principles of therapy.
5. Posthemotransfusion reactions and complications, mechanisms of their
development and preventive measures. Principles of therapy of bleeding: transfusion of
blood and blood substitutes, mechanisms of transfusion action.
6. Changes of physicochemical properties of blood: osmotic and oncotic pressure,
viscosity, erythrocyte sedimentation rate (ESR).
7. Principles of classification of hemolytic anemias. Etiology and pathogenesis of
acquired hemolytic anemias.
8. Hereditary hemolytic anemias: membrano-, enzymo- and hemoglobinopathies.
9. Mechanisms of intravascular and intracellular hemolysis of erythrocytes. Role of
immune processes in development of anemia.
10. Pathogenesis of main clinical manifestations of hemolytic anemia.
11. Anemias connected with disorder of erythropoiesis. Myelotoxic anemias. Etiology,
pathogenesis, blood picture.
12. Acquired and hereditary kinds of hypoplastic anemia, pathogenesis of clinical
manifestations.
13. Megaloblastic anemias. Causes of vitamin B12 and folic acid deficiency. Addison-
Biermer malignant anemia. B12-refractory megaloblastic anemias. Pathogenesis, blood
32

picture, mechanisms of development of main clinical manifestations of megaloblastic
anemias.
14. Iron-deficient anemia. Etiology, pathogenesis, blood picture, mechanisms of
development of main clinical manifestations. The main principles of pathogenetic therapy
of anemias.
15. Iron-resistant anemias. Anemias due to regulatory dysfunction. The main
principles of pathogenetic therapy of anemias.
16. Leukocytosis, principles of its classification.
17. Reasons and mechanisms of development of reactive and redistributional
leukocytosis. Disorders of structure and function of leukocytes.
18. Neutrophilic, eosinophilic, basophilic, lymphocytic and monocytic leukocytosis.
Concept of nuclear shift of neutrophilic granulocytes, its varieties.
19. Leukopenia, principles of its classification. Reasons and mechanisms of
leukopenia development. Pathogenesis of the main clinical manifestations of leukopenia.
20. Agranulocytosis, alimentary-toxic and hemorrhagic aleukia. Pathogenesis.
21. Definition of the concepts “hemoblastosis”, “leukemia”. Morphological
characteristics of myelopoiesis, lympho- and monopoiesis.
22. Etiology and pathogenesis of leukemia (role of viruses, physical and chemical
mutagens in origin of leukemia). Hereditary factors in leukemia origin. Principles of
leukemia classification.
23. Acute and chronic leukemia. Myeloproliferative diseases. Blood picture in acute
leukemia. Reasons of organism dysfunctions in leukemia.
24. A state of erythropoiesis and thrombocytopoiesis in leukemia. The reason for
weakening of protective properties of organism in leukemia. Blood picture in chronic
myeloleukemia. Blood picture in chronic lymphatic leukemia.
25. System of hemostasis. Vascular, thrombocyto-leucocytic and coagulative links of
hemostasis.
26. Antihemostatic system. Thromboresistance of a vascular wall, antithrombotic
factors of thrombocytes and leucocytes, system of plasma factors of fibrinolysis.
27. Pathogenesis of thrombosis. Causes and conditions of thrombus occurrence. Role
of thrombocytes and endotheliocytes in pathogenesis of thrombus formation.
28. Mechanisms of formation of white (agglutinative) and mixed (agglutinative-
coagulative) thrombi.
29. Hypercoagulation. Prethrombotic conditions. Local and common consequences of
thrombosis. Thrombosis of vitally important vascular regions of organism: brain vessels,
coronary vessels, portal vein.
30. Reasons and mechanisms of hemorrhage at the disorder in the vascular-
thrombocytic link of blood coagulation (thrombocytopenias and thrombocytopathies).
31. Coagulative hemostasis and antihemostasis, their disorders. Reasons of decrease of
blood coagulation system activity and increase of activity of coagulative and fibrinolytic
systems.
32. The main manifestations of disorders of some phases of blood coagulation, their
etiology and pathogenesis. Principles of correction of blood coagulation disorders.
33. Definition of the concepts “bleeding”, “hemorrhage”, “hematoma”, “suffusion”,
“petechiae”, “ecchymoses’, “purpura”. Mechanisms of bleedings. Consequences of
bleedings.
33

34. Vasopathies. Reasons, mechanisms of development, pathogenesis of main clinical
manifestations.
35. Thrombohemorrhagic syndrome. Syndrome of disseminated intravascular
coagulation (DIC-syndrome), its reasons, mechanisms and consequences.
Topic 7: Cardiac arrhythmias.
1. Actuality of the theme. The disorders of cardiac rhythm concern to
complex manifestations of pathology of heart. Its can arise in rather small
damage of the conducting system, and in some cases in structural changes.
More often arrythmia arise with infectious illnesses and intoxications as
consequence of miocarditis or dystrophy processes in cardiac muscle, and also
in heart ishemic disease, cardiosclerosis. The disorders of cardiac rhythm arise
also owing to reflex influences from various interreceptors areas (disease of
liver, intestinal tract, uterus), and also in hemodynamic disorders (arterial
hypertension). Not infrequently аrrythmia is a result of disturbance of functions
central and vegetative parts of nervous system. For example, the increase of
activity parasymphatic nervous system lead to delay of conductivity. Similar is
observed also by overdose of some medicin drugs (digitalis, quinidine,
morphine). If bradycardia is accompanied complete atrioventricular blockade,
can occur ischemia of brain with loss consciousness and occuring spasmes.
Arrythmia can be result in development of cardiac insufficiency.
3. Aim: To reproduce the models of basic forms of disorders of cardiac
activity of caused violation of excitability, to explain reasons and mechanisms
of origin in order to make ability to apply etiologic and pathogenetic treatment
of arrhythmias on the departments of clinical type.
To know: that ability to automatic formation of impulses depends on the
cells located in the conductive system of the heart (p-cells). A spontaneous
slow depolarization of the cellular membrane occurs in them during diastole.
- classification of arrhythmias and most widespread in clinical practice of
their form;
- mechanisms of violations of automatism, excitability and conductivity of
heart;
- signs of electrocardiographies of separate types of arrhythmias.
To be able:
- to reproduce in an experiment on animals separate types of violations of
cardiac rhythm;
34

- to explain changes on ECG at arrhythmias;
- to conduct electrocardiography research on animals (rabbit, frogs).
Conducting system of heart, its anatomy, histology and functional value.
Concept of “pace-maker”, mechanisms of origin of bioelectric potentials in
a cardiac muscle.
Basic electro-physiology properties of cardiac muscle.
Principle of electrocardiography. Basic taking which are used in medical
practice. Description of indexis of ECG.
To perform practical work: to analyse the mechanisms of the arrhythmias.
4. Basic level.
disciplines
1. Histology
2. Biochemistry
3. Physiology
4. Internal medicine
5. Stomatology
6. Intensive care
Structure of the conducting system of heart.
Histochemical structure of the myocardium. Main
properties of heart - automatism, irritability,
conductivity, contractivity, refractory. Specialities
of blood supply of heart. Principal components of
an electrocardiogram
1. Etiology of cardio-vascular diseases.
2. Arrhythmias of heart: definition, classification.
3. Etiology and pathogenesis of nomotopic and heterotopic violations of
automatism: sinus tachy-, brady- and arrhythmia.
4. Reasons and mechanisms of extrasystoles and paroxysmal tachycardia.
Basic signs of different types of extrasystoles on ECG .
5. Blocks of heart: kinds, reasons, mechanism of origin. Atrio-ventricular
block.
6. Blinking arrhythmia: principal reasons, description, mechanisms.
7. Flutter and fibrillation of atrium or ventricules; a mechanism of origin,
sign is on ECG.
8. Methods of experimental recreation of arrhythmias.
6. Independent audience work of student.
Protocol № 7 Date_____________________
Experimental work 1. Reproduce extrasystoles in a rabbit. A rabbit is
fixed in position on the back. Connect electrodes from electocardioscope on
front and back extremities. Take initial ECG. In a regional vein the ears of
35

rabbit enter 1 ml of a 10% solution of chlorous barium. Through 20-30 sec mark
appearance of single extrasystoles.
Study reflexion bradycardia in a rabbit. After normalization of
electrocardiogram to the nose of rabbit bring cotton wool, moistened the
concentrated solution of ammonia. Look after development bradycardia and
appearance different type of extrasystoles.
Conclusion:___________________________________________________________
Practical work 2. Changes of heart rhythm. Watching of movie by the
results of experiment: sinus tachycardia, reflectory sinus bradycardia,
extrasystole, atrium-ventricular block.
According to the documental movie students should graphicaly paint types
of arrithmias, make conclusions.
Conclusion:___________________________________________________________
Practical work 3. ECG analysis of the patients with arrhythmias
(registered in 12 Leeds).
Аnalyzing of the studding charts. It is necessary to do protocol by the
results of ECG analysis, answer on control questions.
Conclusion:___________________________________________________________
Test 1. Test 1. The arrow indicates
A. R wave
B. S wave
C. QS wave
D. Q wave
E. T wave
Test 2. The calcium canals of cardiomyocytes have been blocked on an
isolated rabbit's heart. What changes in the heart's activity can happen as
a result?
A. Decreased force of the contraction
B. Decreased heart beat rate
C. Decreased rate and force of heart beat
D. Heart stops in diastole E. Heart stops in systole
Test 3. In a 45-year-old patient on ECG it was revealed: sinus rhythm,
the number of auricular complexesexceeds number of ventricular
complexes; progressing extension of the P-Q interval from complex to
36

complex; fallout of some ventricular complexes; Р waves and QRST
complexes are without changes. Name the type of heart rhythm disfunction.
A. Complete atrioventricular block
B. Synoauricular block
C. Intraatrial block
D. Atrioventricular blockade of the I degree
E. Atrioventricular block of the II degree
Test 4. Person has stable HR (heart rate), not more than 40 bpm. What
is the pacemaker of the heart rhythm in this person?
A. His' bundle
B. Branches of His' bundle
C. Purkinye' fibers
D. Atrioventricular node
E. Sinoatrial node
Heart rate of a 30-year-old man under emotional stress reached 112
bpm. The reason for the heart rate increase is the altered condition of the
following conducting system of heart:
A. Purkinje's fibers
B. Sinoatrial node
C. His' bundle branches
D. Atrioventricular node
E. His' bundle
Test 5. A 45 year old patient was admitted to the cardiological
department. ECG data: negative P wave overlaps QRS complex, diastolic
interval is prolonged after extrasystole. What type of extrasystole is it?
A. Ventricular
B. Atrial
C. Atrioventricular
D. Sinus
E. Bundle-branch
Practice examination type 2. Give brief explanation for the real-life
tasks:
Task 1. In a football fan during match the heart rate has increased from 76
up to 96/min. 1. What is the name this change? 2. What is its mechanism? 3.
How does change the duration of slow diastolic depolarization of sinus node
pacemaker cells?
Task 2. The heart rate patient, which suffers from neurocirculatory
dystonia, increased up to 130/min in the. There are not symptoms of organic
damage of the heart. At doing of diagnostic vagus test (pressing on carotids
sinus), the frequency of heart beats decreased short time, and then has become
higher again.
1. What is the name of described cardiac rhythm disorder?
2. What is the mechanism of this arrythmia development?
37

3. Why carotid sinus irritation did normalize cardiac rhythm?
Answer for the task 2:__________________________________________________
Signature___________________
Literature:
Basic:
1. Robbins basic pathology / ed.by Vinay Kumar, Abul K. Abbas, Jon C. Aster.– 9th ed.Ch.10. – 2013. – P. 385 – 386.
2. General and clinical pathophysiology /Ed.byA.V.Kubyshkin–Vinn:Nova KnuhaPubl–2011.–P.460–780.
3. Pathophysiology / Ed. by N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 348–351.
4. Copstead L-El.C.Pathophysiology / L-E.C.Copstead, J.L. Banasic // Elsevier Inc. – 2010. – P. 396–427.
5. Pathophysiology,Concepts of Altered Health States/C.M.Porth,G.Matfin–NY,Milw.–2009.–P.584–606.
Wilkins – 2008. – Chapter 13. – P. 392–402, 414–426.
Additional:
7. 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. 217–221.
8. SilbernaglS.Color Atlas of Pathophysiology/S.Silbernagl,F.Lang//Thieme.Stuttg.NY.–2000.–P.176–294.
Topic 8: Insufficiency of circulation of blood. Heart failure.
1. Actuality of the theme. Adequate perfusion of body tissues depends on
the pumping ability of the heart, a vascular system that transports blood to the
cells and back to the heart, sufficient blood to fill the circulatory system, and
tissues that are able to extract and use the oxygen and nutrients from the blood.
Heart failure and circulatory shock are separate conditions that reflect failure of
the circulatory system. Both conditions exhibit common compensatory
mechanisms even though they differ in terms of pathogenesis and causes.
Strife with a heart insufficiency - major problem of national public health
services. Its national significance is determined by a high morbidity and death
rate, large labor losses, considerable traumatism. The heart insufficiency often
arises on ground of necrotic damages of cardiac muscle. Quantity both
coronarygenic and epinephrine and norepinephrine genesis damages of the
myocardium recently increases, which one result from a stress, mental
overstress, excessive phisical loads. The warning of necrotic, inflammatory,
metabolic, neuroendocrine and other damages of the myocardium is the
constituent of preventive maintenance of heart insufficiency. The new scientific
direction - preventive cardiology was now formed, problems by which one
include warning and early detection of cardiovascular system function
disorders.
3. Aim: Learn reasons, forms and mechanisms of development of cardiac
insufficiency. Acquaint students with the features of metabolism and
38

hemodynamics at condition insufficiency of blood circulation. Study concepts
and essence of hypertrophy of myocardium, features of its metabolism,
mechanisms of compensation and decompensation.
To know:
- types of insufficiency of heart and principal reasons of their
development;
- heterometric and homeometric mechanisms of compensation of
insufficiency of heart;
- hypertrophy of myocardium, its stage, feature of the hypertrophied heart;
To be able:
- to explain changes in an organism at the condition insufficiency of blood
circulation;
- to determine character of compensate reactions of myocardium on
experimental model of acute insufficiency of heart (depending on the type of
loading on a heart), discover and explain changes which pass here.
1. Structure of heart, its valves, circles of blood circulation [systemic and
pulmonary].
2. Features of innervation, metabolism and bloodstream of heart.
3. Phases of cardiac cycle, their description.
4. Physiology law of the heart [Frank-Starling's law]
5. Systolic [stroke volume] and minute volume [cardiac output] of heart,
methods of their determination.
6. Processes of energy supply of cardiac muscle.
To perform practical work: To analyse the compensatory mechanisms
cardio-vascular diseases.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
5. cardiology
6. intensive care
Histochemical structure of the myocardium. Specialities
of blood supply of heart. The main physiological features
of heart function. Principle of operation of the
electrocardiograph. Technique of record of an
electrocardiogram in three standard leads. Principal
components of an electrocardiogram.
1. Insufficiency of blood circulation: determination, classification.
2. The most widespread innate defects of heart. Mechanisms of
compensation.
3. Reasons and displays of acute cardiac insufficiency.
4. Pathogenesis of cardiac insufficiency at the overload of heart by the
39

volume of blood: reasons, essence of heterometric mechanism of compensation.
5. Pathogenesis of cardiac insufficiency at the overload of heart by
resistance of outflow of blood: reasons, essence of homeometric mechanism of
compensation.
6. Reasons and displays of chronic cardiac insufficiency.
7. Myocardial form of cardiac insufficiency. Molecular mechanisms of
violations of retractive function of myocardium.
8. Compensate hypertrophy of myocardium: determination, kinds and
stages.
9. Features of the hypertrophied heart, mechanisms of development of
cardiosclerosis.
10. Violation of hemo- and cardiodynamics at insufficiency of blood
circulation.
11. Vascular insufficiency. Unconsciousness, collapse: determinations,
reasons of origin.
Protocol № 8 Date_____________________
Experimental work 1. Modeling acute insufficiency of right ventricle in
a rat. Motion of work: Under easy ether anesthesia for a rat the section of skin
on the middle line of neck and separate external jugular vein. To front and back
extremities connect the electrodes of electrocardiographs. Tromboplastine inject
into a jugular vein for the recreation of acute right-ventricule insufficiency. Fix
a stop-watch time of offensive of shortness of breath, stop of breathing, cramps.
At the same time register changes on ECG: deep waves of QS and ST, getting
up of segment of RS-T into III leads, aVF, V1, V2 and decline of segment of
RS-T into I, aVL, V5, V6, appearance of negative waves of Q into III, aVF, V1
and V2 leads.
Conclusion:___________________________________________________________
Practical work 2. Secrets
of our heart. Watching of
movie and discuss the
pathology of the heart: sudden
40

heart death, acute and chronic heart failure. Method of treatment and
prophylaxys: cardioreanimation.
According to the documental movie students should graphicaly paint ECG
for Chagas’ heart disease according to movie explanation, make conclusions.
Conclusion:________________________________________________________
Test 1. The patient with acute miocardial infarction was given intravenously
different solutions during 8 hours with medical dropper 1500ml and oxygen
intranasally. He died because of pulmonary edema. What caused the pulmonary
edema?
A. Inhalation of the oxygen
B. Allergic reaction
C. Neurogenic reaction
D. Decreased oncotic pressure due to hemodilution
E. Volume overload of the left ventricular
Test 2. Dystrophic changes of the heart muscle are accompanied with cardiac
cavity enlargement, decrease of the strength of heart contraction, increased amount of
blood, which remains in the heart during systolic phase, overfilled veins. For what
state of heart is it characteristic?
A. Tonogenic dilatation
B. Tamponage of the heart
C. Myogenic dilatation
D. Cardiosclerosis
E. Emergency stage of hyperfunction and hypertrophy
Test 3. A patient ill with essential arterial hypertension had a hypertensic crisis
that resulted in an attack of cardiac asthm A. What is the leading mechanism of
cardiac insufficiency in this case?
A. Blood supply disturbance
B. Heart overload caused by high pressure
C. Heart overload caused by increased blood volume
D. Myocardium damage
E. Absolute coronary insufficiency
Test 4. A 63 year old male patient who had been suffering from chronic diffuse
obstructive disease, pulmonary emphysema, for 15 years died from cardiac
insufficiency. Autopsy revealed nutmeg liver cirrhosis, cyanotic induration of kidneys
and spleen, ascites, edemata of lower limbs. These changes of internal organs are
typical for the following disease:
A. General cardiac insufficiency
B. Acute left-ventricular insufficiency
C. Acute right-ventricular insufficiency
D. Chronic right-ventricular insufficiency
E. Chronic left-ventricular insufficiency
Test 5. A 35-year-old man developed acute heart failure while running for a long
time. What changes in ionic composition can be observed in the cardiac muscle?
41

A. Accumulation of Na+
and Ca2+
ions in the myocardium cells
B. Reduction of Na+
and Ca2+
C. Reduction of K+
and Mg2+
ions in the extracellular space
D. Accumulation of K+
and Mg2+
E. Reduction of Na+
and Ca2+
ions in the extracellular space
Practice examination type 2 Give answers to the questions of the real-
life task:
Task. After transferred 3 months back anginas patient begin to be disturb
by dyspnea, gravity in the right hypochondrium, attacks of difficult breathing.
The edemas of the lower extremitus have appeared. At objective examination:
dermal covers with icteric colour, labiums cyanotic leg swollen. The cervical
veins is pulsing. The borders of heart are enlarged for expense of both
ventricles, however it is more left. Arterial pressure – 90/60 mm Hg. A
respiration rate - 26/min. The myocarditis, cardiovascular insufficiency in stage
of compensation is detected. 1. What cause the damage of the myocardium in
this patient? 2. What disorder testify about heart insufficiency? 3. Explain their
pathogenesis? 4. What changes have compensatory – adaption significance? 5.
What is their mechanism?
Answer for the task:____________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed.by A.V.Kubyshkin–Vinn:NovaKnuha Publ–2011.–P.460–478.
2. Pathophysiology / Ed.by N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 348–351.
3. CopsteadL-E.C.Pathophysiology/L-E.C.Copstead,J.L.Banasic//ElsevierInc.–2010.–P.396–427,461–509.
Wilkins – 2008. – Chapter 13. – P. 392–298, 414–429, 447–460.
edition, USA. – 2008. – Ch. 4. – P. 166–207.
edition./ Kumar, Abbas, Fauto. – 2007. – Ch. 11. – P. 379–388, 400–
420.
Additional:
/ C. Mattson Porth, Kathryn J. Gaspard. – Ch.14, 17, 18. – P. 231–303, 308–338.
Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart.NY. – 2000. – P. 194–205,
224–233.
Topic 9: Insufficiency of coronary blood circulation.
Ischaemic heart disease.
42

1. Actuality of the theme. Among cardio-vascular diseases coronary heart
disease is the most frequent reason of loss of health, capacity and death rate.
From data of WHO, morbidity on CHD in the economic developed countries of
the world continues to be increased, striking all more persons of young age. In
this connection, obviously, there is a necessity of study of etiology,
pathogenesis, forms and complications of CHD, ability to reproduce on
experimental models, students, so both success of fight against ischemic illness
of heart in a considerable measure depends on correct diagnostics, medical and
prophylactic work as doctors of wide type and specialists of cardiologists.
3. Aim: To expose the mechanisms of different forms of coronal
insufficiency. To master the basic displays of CHD; to learn to analyze the
changes of ECG.
To know:
- reasons and mechanisms of development of violations of coronal
circulation of blood;
- functional, morphological, biochemical and electrocardiography changes
are at the heart attack of myocardium;
To be able:
- to reproduce in an experiment on animals coronal insufficiency;
- to analyse the changes of electrocardiography;
- to explain the mechanism of pain at angina pectoris and heart attack of
myocardium.
1. Anatomy of coronal circulation of blood.
2. Normal coronal blood circulation, its features.
3. Features of metabolism of cardiac muscle.
4. A concept is a heart “attack”, its reasons, kinds and consequences.
5. Approaches are to the experimental design of coronal insufficiency.
To perform practical work: To analyse the compensatory mechanisms
cardio-vascular diseases.
4. Basic level.
The name of the previous and future
disciplines
1. histology
2. biochemistry
3. physiology
5. intensive care
Histochemical structure of the
myocardium.
Specialities of blood supply of heart.
The main physiological features of
heart function.
Principle of operation of the
electrocardiograph.
Technique of record of an
43

electrocardiogram in three standard
leads.
Principal components of an
electrocardiogram.
Classification of coronary heart disease.
There are 4 main types clinical manifestations of coronary heart disease.
1. Stenocardia (angina pectoris)
a) Stenocardia of the stress;
b) Stenocardia of the rest
2. Myocardial infarction
3. Intermediate variants
a) Acute focal myocardial dystrophy;
b) Small focal myocardial infarction
4. Indolence CHD
a) Silent (asymptomatic) CHD;
b) Atherosclerotical cardiosclerosis
1. Features of coronal circulation of blood and metabolism of cardiac
muscle.
2. Classification of coronary heart disease. CHD: determination, reasons
and terms of origin, form.
3. Ischemic heart disease. Definition of the notion, risk factors, mechanisms
of development
4. Sudden coronary death: reasons, mechanisms of origin.
5. Angina pectoris: classification, pathogenesis of displays.
6. Heart attack of myocardium: kinds, description of functional and
biochemical violations in a cardiac muscle, mechanisms of pain syndrome.
7. Mechanisms of origin of spasms of coronary vessels.
8. Complication of heart attack of myocardium. Pathogenesis of cardiogenic
shock.
9. Experimental models of heart attack of myocardium.
10. Dressler’s syndrome, hibernal myocardium, methods of diagnosis, main
manifestations (blood tests, coagulogramm, ECG, SCG.
11. Noncoronary damages of myocardium: reasons, mechanisms of
development.
12. Damage of pericardium. Cardiac [pericardial] tamponade: reasons,
displays, mechanisms of indemnification.
44

Protocol № 9 Date_____________________
Experimental work 1. Recreate acute coronary insufficiency in a
rabbit. For a rabbit, fixed to the machine-tool, look after and analyze an
electrocardiogram. Then in a vein enter pituitrin (from a calculation 1 unit per
kg of mass). Immediately after introduction and during 3-5 min look after and
analyze an electrocardiogram. Mark bradycardia, displacement of segment of
ST in relation to a isoline, appearance of “coronal” T-wave, lengthening the PQ-
interval. Draw conclusions in relation to the mechanisms of development of
spasms of coronary vessels and changes which was observed on an
electrocardiogram.
Conclusion: ___________________________________________________________
Practical work 2.
Watching of movie
according to the
experimental work 1.
According to the
documental movie
students should
graphicaly paint ECG
with miocardial
infarction.
Conclusion:
_____________________
45

Test 1. Transmural myocardial infarction in the patient was
complicated with progressive acute left ventricle insufficiency. What is the
most typical for this state?
A. Edema of the extremities
B. Cyanosis
C. Edema of the lungs
D. Arterial hypertension
E. Ascites
Test 2. A 48-year-old patient after severe psychoemotional exertion
suddenly began feeling sharp pain in the heart region, irradiating into left
arm. Nitroglycerin releaved pain 10 minutes later. What pathogenetic
mechanism is responsible for the development of pain in this case?
A. Compression of coronary vessels
B. Spasm of coronary vessels
C. Dilation of peripheral vessels
D. Occlusion of coronary vessels
E. Increase of myocardial needs in oxygen
Test 3. A patient in three weeks after acute myocardial infarction has
pain in the heart and joints and pneumonia. What is the main mechanism
of development of post-infarction Dressler’s syndrome?
A. Ischemia of myocardium
B. Vessels' thrombosis
C. Secondary infection
D. Autoimmune inflammation
E. Resorption of enzymes from necrotized area of myocardium
Test 4. A patient presents high activity of LDH1,2, aspartate
aminotransferase, creatine phosphokinase. In what organ (organs) is the
development of a pathological process the most probable?
A. In the heart muscle (initial stage of myocardium infarction)
B. In skeletal muscles (dystrophy, atrophy)
C. In kidneys and adrenals
D. In liver and kidneys E. In connective tissue
Test 5. A patient suffering from stenocardia was taking nitroglycerine
which caused restoration of blood supply of myocardium and relieved pain
in the cardiac area. What intracellular mechanism provides restoration of
energy supply of insulted cells?
A. Intensification of RNA generation
B. Intensification of ATP resynthesis
C. Intensification of oxygen transporting into the cell
D. Increased permeability of membranes
E. Reduction of ATP resynthesis
Practice examination type 2 Give answers to the questions of the real-
life task: After transferred 3 months back anginas patient begin to be disturb by
46

dyspnea, gravity in the right hypochondrium, attacks of difficult breathing. The
edemas of the lower extremitus have appeared. At objective examination:
dermal covers with icteric colour, labiums cyanotic leg swollen. The cervical
veins are pulsing. The borders of heart are enlarged for expense of both
ventricles, however it is more left. Arterial pressure – 90/60 mm Hg. A
respiration rate - 26/min. The myocarditis, cardiovascular insufficiency in stage
of compensation is detected.
1. What cause the damage of the myocardium in this patient? 2. What
disorder testifies about heart insufficiency? 3. Explain their pathogenesis? 4.
What changes have compensatory – adaption significance? 5. What is their
mechanism?
Answer for the task:____________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology /Ed.by A.V.Kubyshkin–Vinn:NovaKnuha Publ–2011.–P.472-476.
2. Pathophysiology / Ed.by N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 344–348.
3. Copstead L-E.C. Pathophysiology / L-E.C. Copstead, J.L. Banasic // Elsevier Inc. – 2010. – P. 448–460.
Wilkins – 2008. – Chapter 13. – P. 345–347, 460–462.
edition, USA. – 2008. – Ch. 4. – P. 235–269.
ed./Kumar,Abbas,Fauto.–2007.–Ch.11.–P. 388–398.
Additional:
1. Faller A., Schunke M., Schunke G. The Human body: An Introduction to Structure and Function.-–Stuttgard, New York:
Thieme.–2004.– P. 536–553.
/ Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 17. – P. 294 – 302.
3. SilbernaglS. Color Atlas of Pathophysiology/S.Silbernagl, F.Lang//Thieme.Stut.NY.–2000.–P.216–224.
Topic 10: Disorders of vascular tone.
1. Actuality of the theme. Blood pressure is probably one of the most
variable but best regulated functions of the body. The purpose of the control of
blood pressure is to keep blood flow constant to vital organs such as the heart,
brain, and kidneys. Without constant flow to these organs, death ensues within
seconds, minutes, or days. Although a decrease in flow produces an immediate
47

threat to life, the continuous elevation of blood pressure that occurs with
hypertension is a contributor to premature death and disability due to its effect
on the heart, blood vessels, and kidneys.
2.Length of the employment – 1 h 30 min.
3.Aim: To pay attention of students to prevalence of defeat of vessels of
resistive and capacitive types. To expose the mechanisms of different types of
hypertension with the purpose of understanding of their pathogenesis in a clinic.
To familiarize with the basic experimental models of hypertension.
To know:
- basic types of symptomatic hypertension, their reasons, mechanisms of
development;
- etiology, pathogenesis, complication of hypertensive illness;
- basic experimental models of hypertension.
To be able:
- to explain the mechanisms of increase of arterial pressure at different
hypertension;
- to differentiate symptomatic hypertension and hypertensive illness.
A task for independent extracurricular work:
To think over the followings theoretical questions:
1. Mechanisms of regulation of vascular tone.
2. Functions of kidneys in regulation of blood pressure.
3. Methods of measuring of arterial pressure.
To perform practical work: to analyse the pathogenesis of the
hypertension and hypotension.
4. Basic level.
1. histology
2. biochemistry
3. physiology
5. intencive care
Histological structure of vessels wall.
Vascular tone.
Arterial pressure: the factors, defining it level.
Regulation of vascular tone and blood pressure.
Concept about the functional system of blood circulation.
Determinants of Blood Pressure
The systolic and diastolic components of blood pressure are determined by
the cardiac output and the peripheral vascular resistance and can be expressed as
a product of the two (blood pressure = cardiac output x peripheral vascular
resistance). The cardiac output is the product of the stroke volume (amount of
blood ejected from the heart with each beat) and the heart rate. The peripheral
vascular resistance reflects changes in the radius of the arterioles as well as the
viscosity or thickness of the blood. The arterioles often are referred to as the
48

resistance vessels because they can selectively constrict or relax to control the
resistance to outflow of blood into the capillaries. The body maintains its blood
pressure by adjusting the cardiac output to compensate for changes in peripheral
vascular resistance, and it changes the peripheral vascular resistance to
compensate for changes in cardiac output.
1. Factors which predetermine the level of blood pressure for a man, basal
tone of vessels.
2. Pressor and depressor systems of organism, their description.
3. Arterial hypertensions: kinds, classification. Degrees of high arterial
pressure.
4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.
5. Etiology and pathogenesis of endocrinal hypertension.
6. A role of the sympathetic nervous system in pathogenesis of neurogenic
hypertension.
7. Salt hypertension: etiology, mechanisms of development.
8. Etiology and pathogenesis of essential hypertension. Complication of
essential hypertension.
9. Reasons and mechanisms of arterial hypotension.
Protocol № 10 Date_____________________
Practical work 1. Study a role of the sympathetic and parasympathetic
nervous system in regulation of vascular tone (determination of Kerdyu
index). Measure arterial pressure on a hand, count up the number of cardiac
reductions. The index of Kerdyu (ІК) is calculated after a formula:
dyastolicBP
rateheart
IK
⋅
−=1 ; Norm of ІК = 0
The index of Kerdyu with the sign of “+” testifies to advantage of
sympathetic influences on a heart, and with the sign of “-“ – about
predominance of the parasympathetic influencing. The index of Kerdyu must be
calculated in the state of rest and after the physical loading.
To conduct such research for all students of group.
Conclusion: ___________________________________________________________
Practical work 2. Arterial hypertension. Watching documental movie
about risk factors and pathogenesis of blood pressure elevation.
49

Metod.stomat.f-ty 1st semester book Module 2

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