Metod. med 2st semester book 2018 Module 2

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 MEDICAL FACULTY
Prepared by:
GERASYMCHUK M. R.
CHERKASOVA V. V.
ZAIATS L. M.

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

«PATHOPHYSIOLOGY OF ORGANS AND SYSTEMS»
Training-methodical manual for class and out-of-class work for
students of medical faculty / M.R. Gerasymchuk, V.V. Cherkasova, L.M.
Zaiats // IFNMU. Department of pathophysiology. – 2018. – 90 p. Discussed
and approved by prophil commission of medical&biological disciplines
meeting of Ivano-Frankivsk National Medical University.
Protocol № __ from «__» _________________ 2018 year
4

CALENDAR PLAN OF PRACTICAL CLASSES
of pathological physiology for the students of the III course in the VI semester
Theme of practical classes Dates Hours
1. Pathophysiology of the blood system. Posthemorrhagic anemias. 15.01-19.01 2
2. Hemolytic anemia and anemia caused by violation of
erythropoiesis.
22.01-26.01 2
3. Leukocytosis and leukopenia. Leukemias. 29.01-02.02 2
4. Violation of hemostasis. 05.02-09.02 2
5. Pathophysiology of heart. Arrhythmias. 12.02-16.02 2
6. Pathophysiology of heart. Ischemic heart disease. 19.02-23.02 2
7. The pathophysiology of systemic circulation. Circulatory failure. 26.02-02.03 2
8. Pathophysiology of blood vessels. 05.03-09.03 2
9. Pathophysiology of external respiration. Respiratory failure. 12.03-16.03 2
10. Pathophysiology of the digestive system. Disorders of digestion
in the mouth, stomach and in the intestine.
19.03-23.03 2
11. Pathophysiology of the liver. Liver insufficiency. 26.03-30.03 2
12. Pathophysiology of kidneys. Main kidney disease. Renal failure. 02.04-06.04 2
13. Pathophysiology of the endocrine system. The general
adaptation syndrome. Dysfunction of the pituitary gland.
09.04-13.04 2
14. Dysfunction of the adrenal, thyroid, parathyroid and genital
glands.
16.04-20.04 2
15. Pathophysiology of the nervous system. Violation of sensory,
motor and trophic function of the nervous system.
23.04-27.04 2
16. Violation integrative function of the nervous system.
Experimental neuroses
30.04-04.05 2
17. Module 2 (practical part) 07.05-11.05 2
18. Module 2 (theoretical part) 14.05-18.05 2
Total hours 36
CALENDAR PLAN OF LECTURES
# THEME OF LECTURE
DATES
Hours
Ia1
Ia2
1. Leukocytosis, leukopenia. Leukemia. Etiology, pathogenesis
leukocytosis and leukopenias. Leukemia: principles of
classification, the main types, typical symptoms. The
etiology of leukemia. Features of the pathogenesis of acute
and chronic leukemia.
17.01.18 18.01.18 2
2. The pathophysiology of the heart. Coronary insufficiency:
etiology, pathogenesis, consequences, clinical
manifestations. Myocardial infarction.
22.01.18 26.01.18 2
3. Pathophysiology of blood vessels. Arterial hypertension:
types, etiology, and pathogenesis.
31.01.18 01.02.18 2
5

4. Pathophysiology of the digestive system. Violation of
secretory and motor functions of the digestive tract. Ulcer
disease. Indigestion associated with secretory insufficiency
of the pancreas.
05.02.18 09.02.18 2
5. Pathophysiology of the liver. Liver failure. 14.02.18 15.02.18 2
6. Pathophysiology of kidneys. Renal failure. Causes and
mechanisms of disorders of glomerular filtration, tubular
reabsorption, and secretion. Acute and chronic renal failure:
criteria, causes, mechanisms, common manifestations.
Glomerulonephritis. Nephrotic syndrome.
19.02.18 23.02.18 2
7. Pathophysiology of the endocrine system. General
mechanisms of disorders of the endocrine system.
Neuroendocrine disorders. Syndrome of general adaptation.
Pathophysiology of hypothalamic-pituitary and adrenal
system
28.02.18 01.03.18 2
8. Pathophysiology of the thyroid and parathyroid glands. 05.03.18 09.03.18 2
9. Pathophysiology of the nervous system. Violation of
sensitive function of the nervous system. Pain.
14.03.18 15.03.18 2
10. Pathophysiology of the nervous system. Violation of motor
and trophic functions of the nervous system. Pathogenesis of
neurogenic dystrophies.
19.03.18 23.03.18 2
11. Violation integrative function of the nervous system.
Neuroses.
28.03.18 29.03.18 2
12. Pathophysiology extreme conditions. Etiology, pathogenesis
of collapse and shock states. Etiology, pathogenesis coma.
02.04.18 05.04.18 2
Total hours 24
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 112 points, individual work is 8 points), on
results final module control are 80 points.
CONTROL OF THEORETICAL
& PRACTICAL PREPARATION
0 – 2 points – completely prepared homework;
0 – 4 points – oral answer;
0 – 1 points – test control during class.
Minimum – 0 points;
minimum positive – 4 points;
maximum – 7 points
6

Practical lessons are structured and provide a comprehensive assessment scores in
all learning activities (learning tasks) that students perform during practical classes:
"0" points – student just present in the class, but not fulfilled the task for self-
knowledge control, refuses to answer in the polling (quiz), does not participate in the
discussion of practical work and demonstration material, did not answer for the
question of the final test control. A student has not prepared homework.
"1" point – the student completed the task for self-knowledge, but can not explain
the solution of control tasks, do not know main part of the program material, does not
participate in the discussion of practical tasks, not solved the 50% of the final test
control tasks. A student has not prepared homework.
"2" points – the student completed the task for self-knowledge control, but has
difficulties in their interpretation, does not know large portions of the material, makes
significant errors; insecure, explains the practical tasks and display material just with
support, can not make the conclusion and findings, have not solved 50% the final test
control tasks. A student has not prepared homework properly.
"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 51-60% of the final test control tasks. A student has not
prepared homework properly.
"4" points – student is prepared to the lesson, knows the program material,
intelligently and good present it, able to explain the main idea of practical tasks,
correctly analyzes of displayed material, competently and logical makes conclusions,
solved 61-70% of the final test control tasks. The student has prepared homework
properly.
"5" points – student is prepared for class, knows the program material,
intelligently and logical explains it, is able to explain the practical tasks, correctly
analyzes of displayed material, competently and logical makes conclusions, solved
71-80% of the final test control tasks. The student has prepared homework properly.
"6" points – student mastered the program material thoroughly, consistently,
competently and logical makes explanations, tightly linking theory with practice, to
cope with the reasons of practical work, demonstration material, able to analyze and
make appropriate conclusions, solved 81 - 90% of the final test control tasks. The
student has prepared homework properly.
"7" points – student deeply learned program material, thoroughly, consistently,
competently and logical teaching, closely linking theory with practice, has no
difficulties in the response to changed tasks, easily cope with the reasons of practical
work, demonstration material, able to analyze and make the appropriate conclusions,
solved 91 - 100% final test control tasks. The student has prepared homework
properly.
7

Topic 1: Pathophysiology of the blood system. Posthemorrhagic anaemia
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. Duration of the class – 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 anemia.
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 hemoglobin, color index, amount of RBC in peripheral blood.
To be able: to describe the picture of blood at acute and chronic posthemorrhagic
anemia in its different stages; to estimate, using got in an experiment given, quantitative
changes of RBC, hemoglobin 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:
Normal content of erythrocytes (red blood cells - RBC) and hemoglobin in blood:
Erythrocytes: M — 4.0-5.0·1012
/l; F — 3.7-4.7·1012
/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 (Color Index, CI)
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.
4. Basic level.
The name of the previous
and future disciplines
The receiving of the skills
8

1. histology
2. biochemistry
3. physiology
4. Internal medicine
5. Haemathology
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. 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.Erytrocytosis. Polycythemia, its types, etiology, pathogenesis.
5.Determination of concept of “anaemia”. Classifications of anaemias.
6.Etiology of acute posthemorrhagic anaemia.
7.To give description of phases of compensation of organism on acute
hemorrhage.
8.A picture of peripheral blood is in the bone-cerebral phase of compensation
after hemorrhage.
9.Etiology and pathogenesis of chronic posthemorrhagic anaemia.
10. Hemorrhagic shock.
6. 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 the capillary by cotton wool
and out blood into the test tube with salt acid. A liquid is mixed and gives 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 are 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 color index.
9

Formula of calculation: Er
Нв
CI
•
=
2
Unit of Hb is mmol/l, Er is T/l. 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. Prepare vital stain drop of blood and count up the amount of
reticulocytes. On object-plate with the preliminary inflicted paint of brilliant (cresyl) blue
do the drop of blood and immediately place on 8-10 min in a water bath.
The sample of blood drop dried up on air is examined under the immersion increase of
microscope. The count of reticulocytes is conducted in the narrowed eyeshot. Determine
the number of reticulocytes on 1000 RBC. Draw a stroke.
Analyse information of practical works and draw a conclusion about a presence for the
rabbit of anemia. Classify this anemia after pathogenesis, color index, ability to
regeneration, by the type of hemopoiesis.
Conclusion: ____________________________________________________________
Experimental work 5. 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 75 0.71 9 6 0 2 - 5 61 28 4
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 % % % % % % %
3.2 100 0.58 7 7 1 3 1 4 57 29 5
Conclusion: __________________________________________________________
_____________________________________________________________________
Hemogram 3
Eryth-
rocytes
Hb CI Ht
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 % ∙109
/l % % % % % % %
8.5 130 1.05 67 12 0 2 2 8 58 24 6
Conclusion: __________________________________________________________
________________________________________________________________________________
7. Practice Examination.
10

Practice examination type 1: Choose the correct answer:
Test 1. "Extramedullar haemopoiesis" means:
A. Haemopoiesis occur outside the
medulla.
B. Spleen and liver resume
haemopoiesis.
С. Expansion of haemopoiesis
down the long bones.
D. Bonemarrow haemopoiesis.
E. None of the above.
Test 2. The pathogenesis of hypochromic anemia in lead poisoning is due
to:
A. Inhibition of enzymes involved in heme biosynthesis.
B. Binding of lead to transferrin, inhibiting the transport of iron.
С. Binding of leading to cell membrane of erythroid precursors.
D. Binding of lead to ferritin inhibiting their breakdown into hemosiderin.
Test 3. 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
Test 4. After the prolonged vomiting a pregnant 26-year-old woman was
found to have the reduced volume of circulating blood. What change in the
total blood volume can be the case?
A. Oligocythemic hypovolemia
B. Simple hypovolemia
C. Polycythemic hypovolemia
D. Polycythemic hypervolemia
E. Oligocythemic hypervolemia
Test 5. 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
Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. The victim is delivered in receiving branch of the hospital by the
casual transport through 8 minutes after a traffic incident. Complains about 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
a number of erythrocytes – 4.2×1012
/l, hemoglobin content - 122 g/l.
1. Analyse these data. What parameters deviate from the norm? 2. What is it
possible to think about in this case? 3. How does it explain painless of skin?
11

What does it mean this reaction? 4. How do you evaluate the increase in rate
pulse and breath?
Answer for the task 1: ___________________________________________________________
Task 2. Amount of RBC of the patient 3.5·1012
/l; contain Hb - 86g/l. 1.
What is this state name? 2. Define color index. 3. What does it testify 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.
2. Silbernagl S. Color Atlas of Pathophysiology /S.Silbernagl, F.Lang//Thieme.Stuttt.NY.–2000.–P.28–33.
Topic 2: Hemolytic anemia and anemia caused by violation of
erythropoiesis.
1. The actuality of the theme. Anemia is a hematological symptom of various diseases
(illnesses of the gastrointestinal pathway, kidneys, infectious and helmintosis, malignant
tumors, inherited and purchased diseases of children, different intoxications).
The qualitative features of erythrocytes of peripheral blood and bone marrow allow
determining a kind of anemia, to make a submission about the 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
(hypochromic erythrocytes), B12 (folic)-deficiency anemia (megaloblasts and
megalocytes), sickle-cell anemia (sickle-shaped erythrocytes), thalassemia (target-like
erythrocytes), Minkowski-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 hematological
displays, estimate the high-quality changes of RBC and hemoglobin as an index of the
tension of compensating mechanisms or pathological changes.
12

To know: 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 the red blood. 2. Functions of RBC, structure, and functions of
hemoglobin. 3. Able to explain a biosynthesis gem; the value of iron for a synthesis gem. 4.
To know the exchange of iron, a vitamin of B12 and folic acid in the organism. 5. To know
the normal indexes of a number of RBC, amount of hemoglobin, 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, the concentration of hemoglobin, color index and amount of
reticulocytes in blood.
To perform practical work:
In hereditary hemolytic anemia, hemolysis is caused by a 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 enzymopathy, for example, glucose-6-phosphate dehydrogenase deficiency
(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 (α2γ2) and their
synthesis begins after the 8th
week of the embryonal 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%HbA2(α2δ2) and 1-2% of HbF.
In sickle cell anemia HbS is formed (in 6 position of β-chain of globin glutamic acid is
substituted for valine) which in its restored condition falls out in crystals and causes
erythrocyte deformity (sickle cells); hypoxia contributes to the 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.
4. Basic level.
The name of the previous and future
disciplines
1. Histology; 2. Biochemistry
3. Physiology; 4 Haemathology
Scheme of erythropoiesis. Regulation of
erythropoiesis. Form and size of erythrocytes.
13

Structure of haemoglobin
1. Etiology of the purchased hemolytic anemias, their kinds.
2. To explain the mechanism of hemolysis at the purchased hemolytic
anemias.
3. To give a description of the 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], a picture of blood at this pathology.
6. To explain the pathogenesis of glucose 6-phosphate dehydrogenase
deficit anemia.
7. To name kinds, explain pathogenesis, a picture of peripheral blood at
inherited hemoglobinopathy. Thalassemias.
8. To explain the pathogenesis of sickle cell anemia, a picture of peripheral
blood.
9. To name kinds, make examples of anemias as a result of the violation of
erythropoiesis.
10. Etiology, pathogenesis, a picture of the blood of asiderotic [iron-
deficiency] anemia. Iron-refractory therapy.
11. Kinds and etiology of B12-folic acid deficit anemias.
12. Etiology, pathogenesis of Addison-Birmer’s anemia.
13. Explain the classic displays of pernicious [Biermer-Ehrlich] anemia.
14. To give a description of the 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 the ear of the rabbit, a skin has wiped an alcohol, dry out either and pricks a
regional vein. The drop of blood inflict on the edge of the preparatory glass, stretch on its
entire 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 Main-
Grunwald' and paint during 3 min. (fixing). Then inflict the same amount of drops of the
distilled water, mix up a waggle (coloring). A paint is united and, not washing water, a
stroke is inundated the divorced paint of Romanovsky (1 drop on 1 ml distilled water) on 6
min. Wash off a paint with water, dry out a stroke and study under an immersion increase.
Conclusion: __________________________________________________________
_____________________________________________________________________
14

Experimental work 2. To learn the picture of peripheral blood for an animal with
megaloblastic anemia. Daily, during 5 days, intraperitoneal 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 has wiped an alcohol and does an incision. Prepare
the thin stroke of blood, and after drying out dye after Pappengeym. A stroke is ready to
consider under an immersion increase.
Describe the picture of blood at hemolytic and megaloblastic anemias.
Conclusion: _________________________________________________________________
_____________________________________________________________________
Experimental work 3. Analysis of hemograms. 1. Analyse and estimate the quantity of
each indicator of red blood (erythrocytes, hemoglobin, CI): norm, more, less. 2. Select the
type of anemia according to color index: normochromic, hyperchromic, hypochromic. 3.
Give the examples of diseases in which this anemia occurs.
Conclusion: _______________________________________________________________________
_____________________________________________________________________
Hemogram 1
Eryth-
rocytes
Hb 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
3.25 120 1.22 7 7 1 3 1 4 55 31 5
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 2
Eryth-
rocytes
Hb 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
9.45 105 1.27 10 9 1 2 1 4 56 24 3
Conclusion: __________________________________________________________
_____________________________________________________________________
Experimental work 4. Microscope study the picture of blood and bone
marrow in various kinds of anemia: Slide 1. Iron-deficiency anemia – blood;
Slide 2. Pernicious (B12-deficiency) anemia – blood; Slide 3. Pernicious (B12-
deficiency) anemia – bone marrow
Conclusion: __________________________________________________________
_____________________________________________________________________
Test 1. A 34-year-old woman was diagnosed with hereditary
microspherocytic hemolytic anemia (Minkowsky-Shauffard disease). What
mechanism caused hemolysis of erythrocytes?
15

A. Autoimmune disorder
B. Bone marrow hypoplasia
C. Enzymopathy
D. Membranopathy
E. Hemoglobinopathy
Test 2. Substitution of the glutamic acid on valine was revealed while
examining the initial molecular structure. For what inherited pathology is
this typical?
A. Minkowsky-Shauffard
disease
B. Hemoglobinosis
C. Sickle-cell anemia
D. Favism
E. Thalassemia
Test 3. A 25-year-old Palestinian woman complains of weakness,
dizziness, and dyspnea. In anamnesis: periodically exacerbating anemia. In
blood: Hb - 60 g/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 4. A 47-year-old man walks into the emergency room because of
feeling very weak, tired, short of breath, and dizzy. He has numbness and
tingling in his fingers. He appears pale and sallow. On examination, his
heart rate is 132. His sclerae and nailbeds are pale. His heart is enlarged
and he has dependent edema of his ankles. Laboratory findings include a
negative Coombs’ test and hemoglobin of 4 g/dL. The likely diagnosis is?
A. Pernicious anemia
B. Autoimmune anemia
C. Blood loss
D. Traumatic hemolytic anemia
E. Iron-deficiency anemia
Test 5. A 55 y.o. woman consulted a doctor about having continuous
cyclic uterine hemorrhages for a year, weakness, dizziness. Examination
revealed skin pallor. Hemogram: Hb – 70 g/L, erythrocytes - 3.2*1012
/L,
color index - 0.6, leukocytes – 6.0*109
/L, reticulocytes - 1%; erythrocyte
hypochromic. What anemia is it?
A. B12-folate-deficiency anemia
B. Iron-deficiency anemia
C. Aplastic anemia
D. Chronic posthemorrhagic
anemia
E. Hemolytic anemia
Test 6. A 37-year-old female patient complains of a headache, vertigo,
troubled sleep, numbness of limbs. For the last 6 years, she has been
working at the gas-discharge lamp-producing factory in the lead-
processing shop. Blood test findings: low Hb & RBC level, serum iron
concentration exceeds the norm by several times. Specify the type of
anemia:
A. Iron-refractory anemia B. Iron-deficiency anemia
16

C. Minkowsky-Shauffard disease
D. Hypoplastic anemia E. Metaplastic anemia
Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. In a patient with anemia, there is the following picture of blood: a
number of erythrocytes – 1.4·1012
/l, hemoglobin content - 62 g/l; aniso- and
poikilocytes megaloblasts, megalocytes in the smear. 1. What type of anemia
are such changes characterized for? 2. Why does it develop? 3. Why in this case
is sharply expressed erythropenia? 4. Give the morphological characteristic to
megaloblasts and megalocytes. 5. Calculate Color Index (MCH).
Task 2. The blood of a patient with anemia is characterized by parameters:
the number of erythrocytes – 3.5·1012
/l, hemoglobin content - 50g/l; in blood
smear – annulocytes, poikilocytes, and microcytes. 1. For what kind of anemia
these parameters are characterized? 2. Calculate Color Index (MCH) and
determine, to what group (according to Color Index) this anemia concern. 3.
Why erythrocytes are acquired in rings form.
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed.by A.V.Kubyshkin–Vinn:Nova Knuha Publ–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 leukopenia. Leukemias.
1. The actuality of the theme. Leukocytosis is considered as a reaction hematopoietic
system due to the action of physiological and pathological irritations. Leukocytosis is a
pathological symptom of many diseases. In a basis of leukocytosis lay pathophysiological
mechanisms connected with proliferation, maturation going out of leukocytes and their
flow into vessels and redistribution.
17

Leukopenia may depend upon the oppressive influence of some toxins on the
maturation and outflow of leucocytes from the bone marrow. Often these phenomena are
observed during the infectious diseases. They have significance for the differential
diagnostic. If for the disease is characterized leukocytosis, the availability of leukopenia
testifies on depression of the hemopoietic system.
3. Aim: to analyze the pathogenesis of the quantitative and qualitative changes of
leucocytes in blood. The increase of leucocyte quantity is called leucocytosis, and the
decrease-leukopenia. The norm is 4-9G/l or 4-9*109
/l. The quantitative changes are
increased the quantity of immature forms in blood and degeneration of leucocytes.
Analyse of the pathogenesis of 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.
To know: types of the left nuclear deviation, leukemia – is a disease of tumor nature,
originating from blood cells with the initial affection of the bone marrow.
To be able: to analyze the quantitative and qualitative changes of leucocytes in blood,
blood data under acute and chronic leukemia.
The task for independent extracurricular work.
1. To know leukopoiesis in a norm, morphology of white blood cells.
2. Methods of determining the number of white blood cells in the blood.
3. Anatomy and functions of primary and secondary hematopoietic organs.
4. Basic level.
1. histology
2. biochemistry
3. physiology
4. haematology
Scheme of leucopoesis.
Leucocytes formula of blood.
Function of leucocytes.
Methods of counting of leucocytes maintenance in blood.
5. The advice for students.
Leukocytosis. Leucocytosis –is the increase of total leucocyte quantity in
blood – over 9G/l (9*109
/l).
Leukopenia. 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.
18

Pull film Push film
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
correspond to an absolute
lymphocyte count of 0.2 x 6.0
= 1.2 x 109
/L).
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")
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 is 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. Etiology of the
leukocytosis.
2. The mechanisms of leucocytosis. Blood picture under the leukocytosis.
3. What is leukopenia? Classification of the leukopenia. Etiology of the
leukopenia.
4. The mechanisms of leucopenia. What is aleukia?
5. Blood picture under the leukopenia.
6. Leucocyte degeneration in blood.
19

7. Determination and general definition of leukosis. Classification of leucosis
is after motion and morphological signs.
8. Modern theories of the origin of leukosis: the role of viruses, ionizing
radiation, chemical matters, inherited anomalies. Tumor nature of leukosis.
Basic displays of tumor progression.
9. Features of hemopoiesis, a picture of peripheral blood, leukogram at an
acute myeloleukosis [myeloleukemia].
10.Features of hemopoiesis, a picture of blood at chronic myeloleukosis.
11.Picture of blood, leukogram at an acute lympholeukosis.
12.Picture of blood, leukogram at a chronic lympholeukosis.
13.A mechanism of development of anemia at acute and chronic leukosis.
14.Violation of reactivity of organism is at leucosis. A role of the inherited
anomalies is in development of leucosis.
15.Plasma cell disorders. Multiple myeloma.
Protocol № 3 Date_____________________
Experimental work 1. Count up a leukocytic formula (leukogram) at an abscess. To
prepare the stroke of blood, taken from the vein of the ear of rabbit and to paint it after
Pappengeym. See the sample under an immersion increase. The drop of blood is mentally
divided into four fields, conducting the lines which are perpendicular one to one through
the center of the sample. Count up in every field 25 leukocytes, moving a stroke on the
broken line. Count up separate types of leukocytes 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____________________________________________________________________
______________________________________________________________________________
20

Experimental work 3. Counting of leukocytic formula in a smear of blood patient
with leukosis. a) Acute lymphoblastic leukosis; b) Acute myeloblastic leukosis; c) Chronic
myelocytic leukosis; d) Chronic lymphocytic leukosis
Study smear in immersion microscope objective. For determination of leucocytic
formula is necessary to calculate 100 leukocytes. 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, color,
granularity in protoplasm, form, and color of a nucleus. Put the results of counting in the
table:
Baso-
phi-
les
Eosi-
nophi-
les
Neutrophiles Lym-
pho-
blast
s
Lym-
pho-
cytes
Mono-
cytesMyelo-
blasts
Promy-
elocytes
Myelo-
cytes
Meta-
myelo-
cytes
Stabnuc-
leonic
Segmento-
nuclenic
1% 0% 0% 0% 1% 2% 5% 8% 80% 1% 2%
2% 0% 90% 0% 1% 0% 2% 1% 0% 3% 1%
2% 1% 3% 14% 10% 6% 7% 39% 0% 10% 8%
3% 2% 0% 0% 0% 2% 3% 7% 4% 75% 4%
Conclusion:_____________________________________________________________________
_______________________________________________________________________________
_______________________________________________________________________________
________________________________________________________________
Test 1. During the medical examination of a boy 5 years old were found
the significant increase of eosinophils in the blood. What from mentioned
below can be the cause of eosinophilia?
A. Helminthiasis
B. Obesity
C. Hypodynamia
D. Hypothermia
E. Physical strain
Test 2. A 16-year-old boy has performed an appendectomy. He has
been hospitalized for right lower quadrant abdominal pain within 18
hours. The surgical specimen is edematous and erythematous. Infiltration
by what of the following cells is the most typical for the process occurring
here?
A. Basophils
B. Eosinophils
C. Monocytes
D. Neutrophils
E. Limphocytes
Test 3. A patient operated on complicated appendicitis has the
following changes of blood count: erythrocytes-4.0x1012
/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
21

C. Regenerative left shift
D. Right shift
E. Degenerative left shift
Test 4. Lazy leucocyte syndrome is because of:
A. Disorder of phagocytosis
B. Cellular immunodeficiency
C. Combined immunodeficiency
D. Disorder of complement
Test 5. In a patient with leucosis parameters of white blood are the
following: the number of leucocytes – 100∙109
/l, from them basophils – 1 %,
eosinophils – 2%, stab neutrophils – 4%, segmental leucocytes – 7%,
lymphoblasts – 2%, lymphocytes – 80%, monocytes – 4%. In blood, there
are a lot of destroyed lymphocytes (Gymprehkt bodies). These parameters
are characterized by:
A. Acute myeloblastic leukosis
B. Chronic myelocytic leukosis
C. Chronic lymphocytic leukosis
D. Acute plasmoblastic leukosis
E. Chronic monocytic leukosis
Test 6. A patient with acute myeloblast leucosis has developed liver and
spleen enlargement, anemia, myeloblasts in peripheral blood. What
principal sign allows differing myeloblast leukosis from chronic one?
A. Leukemic gap
B. Pancytopenia
C. Anemia
D. Blast cells in peripheral blood
E. Thrombocytopenia
Test 7. A 23 y.o. a patient complains of weakness, a temperature rises
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, 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 8. Mongolism and Philadelphia chromosome (Phi) is commonly
associated with?
A. Acute lymphoblastic leukemia
B. Chronic lymphatic leukemia
C. Chronic myeloid leukemia
D. Acute myeloid leukemia
E. Erythroleukemia
Test 9. A patient has a cluster of matted together dense lymph nodes on
his neck. Histological examination of a removed lymph node revealed a
proliferation of reticular cells, the presence of Reed-Sternberg cells. What
disease is meant?
A. Myelocytic leukosis
B. Myeloblastic leukosis
C. Lymphocytic leukosis
D. Lymphoblastic leukosis
E. Lymphogranulomatosis
22

Practice examination type 2 Give answer to the questions of the real-
life tasks:
Task 1.
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 0 % 1 % - 1 % 3 % 72 % 21 % 2 %
1. Analyze above mentioned leucocytes formulas and indicate what changes
of total leukocytes and separate forms are present in each of them.
2. What pathological processes and diseases are typical for this type of
hemograms? Give examples.
Answer for the task 2:___________________________________________________
Task 2.
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?
Task 3.
Total
amount of
Baso-
philes
Eosi-
nophi-
Neutrophiles Lym-
pho-
Mono-
cytesMyelo- Promiel Myelo- Meta- Stab Seg-
23

leucocytes les
blasts ocytes cytes
myelo-
cytes
mental
cytes
75,0*109
/l 1% 1 % 78% - - - 3% 3% 10% 2%
54*109
/l - 1% 25% 0% 1% 3% 5% 43% 17% 5%
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 %
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–Vinn: Nova Knuha Publ– 2011.– P.286–287, 322–333.
2. Copstead L-E.C. Pathophysiology / L-E.C. Copstead, J.L. Banasic // Elsevier Inc. – 2010. – P. 242–262.
3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publ.–2010. – P.266–322.
4. 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.
Norman D. Harris // Published by the Pharmaceutical Press, 3rd
edition, USA. – 2008. – Chapter 11. – P. 725–726.
7. Robbins and Cotran Pathologic Basis of Disease8th
ed./Kumar,Abbas,Fauto.–2007. – Ch.12.–P.441–468.
Additional:
8. 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: Violation of hemostasis.
1. The 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. A 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 the coagulative ability of blood and origin of thromboses; 3) origin
of the thrombohemorragic syndrome, which shows up an increase of thrombosis and
hemorrhagic diathesis both.
2. Duration of the class – 1 h 30 min.
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 the pathology
of man.
To khow: etiologic factors which predetermine violation of producing blood clots; basic
phases of process of blood tromb formation; reasons and mechanisms of origin of
hemorrhagic diathesis; reasons and mechanisms of violation thrombocyte-vascular
24

hemostasis; etiology and pathogenesis of disseminated intravascular coagulation [DIC];
inherited violations of blood thrombosis.
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.
A task is to independent extracurricular work:
To think over the followings theoretical questions: 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. Von Willebrand factor functions as an adhesion bridge between subendothelial
collagen and the glycoprotein Ib (GpIb) platelet receptor. Aggregation is accomplished by
binding of fibrinogen to platelet GpIIb-IIIa receptors and bridging many platelets together.
Congenital deficiencies in the various receptors or bridging molecules lead to the diseases
indicated in the colored boxes. ADP, adenosine diphosphate.
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 pathology of hemostasis.
2.Normal hemostasis. The classical coagulation cascade.
3.Virchow's triad in thrombosis.
4.Decreasing of blood coagulation ability.
5.Thrombocytopenia and thrombocytopathy.
6.Increasing of blood coagulation ability.
7.Bleeding disorders related to defective platelet functions: Bernard–Soulier
syndrome, Glanzmann’s thrombasthenia.
8.Hemorrhagic diatheses related to abnormalities in clotting factors:
deficiencies of Factor VIII-vWF complex, Von Willebrand disease,
Hemophilia A, and B.
9.Generalized (disseminated) intravascular blood coagulation (DIC-syndrome).
10. Trombocytopenias: immune trombocytopenic purpura, drug-induced,
and HIV-associated trombocytopenia.
6. Independent audience work of student
Protocol № 4 Date_____________________
Experimental work 1. Define prothrombin time [PT] for a dog with the cirrhosis of
the liver. In advance, the oily solution of carbon tetrachloride has entered a dog from the
25

calculation of 4 ml per 1kg 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 a water bath at 38°C; 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 – a time of
coagulation of control plasma (seconds); B – the time of coagulation of experimental
plasma (seconds). A normal index of is equal 70-100%.
Conclusion:_______________________________________________________________________
Experimental work 2. Count up the number of thrombocytes for a rabbit with
radiation illness. Three days prior to lesson an animal is exposed to the X-rays. In 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 prepared mixture prepare a blood; dye it after Pappengeym (to repaint for the
best visibility of thrombocytes). A count is conducted under an immersion increase in the
narrowed eyeshot. Count up the number of thrombocytes on 1000 RBC.
Thef ormula of calculation: 1000
АН
Х
•
= , where H – is an amount of platelets on 1000 RBC;
A – is an amount of RBC; Method of count the number of RBC see in the previous lesson.
Conclusion:_______________________________________________________________________
Practice examination type 1. Choose the correct answer:
Test 1. In the patient in time accident on Chornobyl atomic power station
aroses hemorrhagic syndrome, which was showed by hemorrhage in skin
and mucous membrane, appearance of blood in urine, faces and phlegmon.
The mechanism of hemorrhagic syndrome consists of:
A. Activation of fibrinolytic system
B. Accumulation of heparin in blood
C. Decrease amount of thromocytes
D. Violation of structure of
fibrinogene
E. Lesion vascular wall
Test 2. A 43-year-old patient has thrombopenia, reduction of fibrinogen,
products of degradation of fibrin presented in the blood, petechial
haemorrhage 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. Haemorrhagic diathesis
Test 3. Prothrombin time is increased in:
A. Thrombocytopenia
B. Afibrinogenemia
C. Qualitative defect of platelets
D. Willebrand's disease
E. DIC syndrome
26

Test 4. Examination of a patient with frequent hemorrhages from
internals and mucous membranes revealed proline and lysine being a part
of collagen fibers. What vitamin absence caused disturbance of their
hydroxylation?
A. Vitamin A
B. Thiamine
C. Vitamin K
D. Vitamin E
E. Vitamin C
Test 5. A 2-year-old child has got intestinal dysbacteriosis, which results
in hemorrhagic syndrome. What is the most likely cause of hemorrhage of
this child?
A. Vitamin К insufficiency
B. Hypocalcemia
C. РР hypovitaminosis
D. Fibrinogen deficiency
E. Activation of tissue
thromboplastin
Practice examination type 2. Give answer to the questions of the real-life
task: The patient was in the surgical clinic because of thrombophlebitis of the
right leg. After careless sudden movement an acute dyspnea to bother him, pain
in the chest and cyanosis appeared.
1. Did these disorders associate with thrombophlebitis of the leg? 2. In what
cases such consequences of thrombophlebitis are possible? 3. Are such
complications occasional in the patient? 4. 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:
1. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003)
/ 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 5: Pathophysiology of heart. Arrhythmias.
1. The actuality of the theme. The disorders of cardiac rhythm concern to complex
manifestations of a pathology of heart. It can arise in rather small damage of the conducting
system, and in some cases in structural changes. More often arrhythmia arises with
27

infectious illnesses and intoxications as consequence of myocarditis or dystrophy processes
in cardiac muscle, and also in heart ischemic disease, cardiosclerosis. The disorders of
cardiac rhythm arise also owing to reflex influences from various interceptors areas
(disease of the 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 parasympathetic
nervous system leads to a delay of conductivity. Similar is observed also by an overdose of
some medicinal drugs (digitalis, quinidine, morphine). If bradycardia is accompanied
complete atrioventricular blockade, can occur ischemia of brain with loss consciousness
and occurring spasms. Arrhythmia can result in the 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 the ability to apply an etiologic and pathogenetic treatment of arrhythmias on the
departments of clinical type.
To know: that ability to the 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 electrocardiography of separate types of arrhythmias.
To be able: to reproduce in an experiment on animals separate types of violations of
cardiac rhythm;
- to explain changes on ECG at arrhythmias;
- to conduct electrocardiography research on animals (rabbit, frogs).
A task is to independent extracurricular work:
Conducting system of the heart, its anatomy, histology and functional value.
The concept of “pace-maker”, mechanisms of origin of bioelectric potentials in a cardiac
muscle. Basic electrophysiology properties of cardiac muscle. A principle of
electrocardiography. Basic taking which is used in medical practice. Description of indexes
of ECG.
To perform practical work: to analyze the mechanisms of the arrhythmias.
4. Basic level.
disciplines
5. Histology
6. Biochemistry
7. Physiology
8. Internal medicine
9. Cardiology
Structure of the conducting system of heart.
Main properties of heart - automatism, irritability,
conductivity, contractivity, refractory.
Mechanisms of occurrence and transfer of nervous
impulse on the conducting system of heart.
1. Etiology of cardiovascular diseases.
2. Arrhythmias of heart: definition, classification.
3. Etiology and pathogenesis of nomotopic and heterotopic violations of
automatism: sinus tachy-, brady- and arrhythmia.
28

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. Atrioventricular block.
6. Blinking arrhythmia: principal reasons, description, mechanisms.
7. Flutter and fibrillation of atrium or ventricles; a mechanism of origin, the
sign is on ECG.
8. Methods of experimental recreation of arrhythmias.
9. Sudden cardiac death.
6. Independent audience work of student.
Protocol № 5 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 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 the 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. 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:_____________
_____________________________
___________________________
Practical work 3. 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.
29

Conclusion:_____________________________________________________________________
Case 1. A 15-year-old female is brought to the emergency department (ED) after an
episode of syncope during a long-distance running event. She has no prior episodes of
syncope. Her ECG obtained in the ED is shown. She has no previous ECGs for comparison.
Which of the following have been identified as triggers of cardiac events in this family of
syndromes?
A. Loud noises
B. Exercise
C. Sleep
D. Swimming
E. Emotion
F. All of the above
Answer for the case 1:____________________________________________________________
Case 2. A 65-year-old
woman with a history of type 2
diabetes and previous MI presents
to her primary physician with a
chief complaint of nausea,
vomiting, and generalized
weakness since waking up. She
has no chest pain or dyspnea, and
this has never happened to her
before. She had been feeling well
prior to this episode. An ECG is
obtained (shown). Of note, this patient with symptoms of an MI is also having an inferior
and anterolateral ST-elevation MI (blue arrows). What is the AV conduction pattern
present?
A. Normal AV conduction
B. Atrial fibrillation
C. Accessory pathway
D. First-degree AV block
E. Second-degree Mobitz type I AV block
F. Second-degree Mobitz type II AV
block
G. Third-degree AV block
Answer for the case 2:___________________________________________________________
Case 3. A 52-year-old
woman is brought in by ambulance
to the ED with multiple episodes of
syncope within the past 30 minutes.
There were no advanced life
support paramedics available in the
field, and the patient has therefore
received no treatment other than
oxygen. She is conscious on arrival
but appears pale and anxious. She
complains of palpitations but is
30

unable to provide much more information. The ECG is displayed. What is the rhythm
shown?
A. Multifocal atrial tachycardia with LV
hypertrophy (LVH)
B. Sinus tachycardia with pre-excitation
(WPW syndrome)
C. Monomorphic VT
D. Polymorphic VT (torsade de pointes)
E. Atrial fibrillation with left bundle
branch block
F. Atrial flutter
Answer for the case 3:____________________________________________________________
Test 1. The arrow indicates
A. R wave
B. S wave
C. QS wave
D. Q wave
E. T wave
31

Test 2. Which of the following represent repolarization of the ventricles?
J point
A. P wave
B. QRS complex
C. T wave
D. J point
E. U wave
Test 3. After the trauma, the patient’s right n.vagus was damaged.
Which violation of the cardiac activity is possible in this case?
A. Violation of conductivity in the right auricle
B. Violation of the automatism of an atrioventricular node
C. Block of a conductivity in the atrioventricular node
D. Arrhythmia
E. Violation of the automatism of a Kiss-Fleck node
Test 4. An electrical cardiostimulator was implanted to a man 75 y.o.
with a heart rate of 40 bpm. After that heart rate rose up to 70 bpm.
Cardiostumulator assumed the function of the following heart part:
A. Sinoatrial node
B. His' bundle branches
C. His' bundle fibers
D. Atrioventricular node
E. Purkinje's fibers
Test 5. In a 45-year-old patient on ECG, it was revealed: sinus rhythm,
the number of auricular complexes exceeds the number of ventricular
complexes; progressing extension of the P-Q interval from complex to
complex; the fallout of some ventricular complexes; Р waves and QRST
complexes are without changes. Name the type of heart rhythm
dysfunction.
A. Complete atrioventricular block
B. Atrioventricular block of the II degree
C. Atrioventricular blockade of the I degree
D. Synoauricular block
E. Intraatrial block
32

Test 6. ECG of a patient with hyperfunction of thyroid gland showed
heart hurry. It is indicated by depression of the following ECG element:
A. QRS complex
B. P-T interval
C. P-Q interval
D. R-R interval
E. P-Q segment
Practice examination type 2. Give brief explanation for the real-life
tasks:
Task 1. In a patient with idiopathic hypertension the pulse rate during a
crisis decreases from 72 up to 52 beats per minute and within 10 days prolongs to
be retained at this level (48-56/minutes). The intramuscular injection 1 ml of
atropine, which was made for differentiation diagnosis, increased heart rate to 16
beats per minute. 1. What is the name of described disturbance of cardiac rhythm
and what group of arrhythmias does it concern? 2. What is its origin (cardiac –
organic damage of heart or extracardiac? 3. Why after injection of atropine heart
rate did increase?
Answer for the task 1:____________________________________________________________
________________________________________________________________________________
________________________________________________________________________________
Task 2. In a football fan during a 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 3. The heart rate patient, which suffers from neurocirculatory dystonia,
increased up to 130/min in the. There are no symptoms of organic damage to the
heart. In doing of diagnostic vagus test (pressing on carotids sinus), the
frequency of heartbeats 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 arrhythmia development? 3. Why did carotid sinus irritation
normalize cardiac rhythm?
_________________________________________________________________________________
_________________________________________________________________________________
_________________________________________________________________________________
Practice examination type 3
Q. What is the link between apnea and heart arrhythmias?
Answer for the question__________________________________________________________
_________________________________________________________________________________
_________________________________________________________________________________
_________________________________________________________________________________
33

_________________________________________________________________________________
_________________________________________________________________________________
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 6: Pathophysiology of heart. Ischemic heart disease.
1. The actuality of the theme. Among cardiovascular diseases, coronary heart disease
is the most frequent reason for loss of health, capacity and death rate. From data of WHO,
morbidity on CHD in the economically 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 successes 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 analyze
the changes of electrocardiography; to explain the mechanism of pain at angina pectoris and
heart attack of the myocardium.
A task is to independent extracurricular work: 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 analyze the compensatory mechanisms cardiovascular
diseases.
4. Basic level.
The name of the previous and future
disciplines
1. histology; 2. Biochemistry; 3. Physiology;
4. Internal medicine; 5. cardiology
Histochemical structure of the
myocardium. Specialities of blood
supply of heart. The main physiological
features of heart function. The principle
34

of operation of the electrocardiograph.
The technique of record of an
electrocardiogram in three standard
leads. Principal components of an
electrocardiogram.
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 the myocardium. Pathogenesis of
cardiogenic shock.
9.Experimental models of heart attack of the myocardium.
10.Dressler’s syndrome, hibernal myocardium, methods of diagnosis, main
manifestations, blood tests, coagulation, ECG, SCG.
11.Noncoronary damages of myocardium: reasons, mechanisms of
development.
12.Pericardium damage. Cardiac [pericardial] tamponade: reasons, displays,
mechanisms of indemnification.
Protocol № 6 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: _______________________________________________________________________
______________________________________________________________________________________
35

Practical work 3. ECG analysis of the patients with different kinds of miocardial
infarction (registered in 12 Leeds).
Conclusion: _______________________________________________________________________
Case 1. The paramedics call from the field requesting activation of the catheterization
laboratory for a ST-segment elevation myocardial infarction (STEMI) in a 50-year-old Asian
man complaining of difficulty breathing and palpitations. The paramedics express that the
ST-elevations look unusual in V1 and V2. Because they are 5 minutes away, you decide to
do a 12-lead ECG in the ED before activating the catheterization laboratory. The patient's
ECG is shown. He has no
previous ECGs for comparison.
What is your interpretation?
A. Confirmed STEMI
B. ST-segment ischemic
changes present but no STEMI
C. Benign early
repolarization
D. Depolarization /
repolarization abnormality
caused by channelopathy
E. Hyperkalemia
Answer for the case
_________________________________________________________
Test 1. A 59-year-old patient is a plant manager. After the tax inspection
of his plant, he felt intense pain behind his breastbone irradiating to his left
arm. 15 minutes later his condition came to normal. Which of the possible
mechanisms of stenocardia development is the leading in this case?
A. Functional heart overload
B. High catecholamine concentration in blood
C. Intravascular aggregation of blood corpuscles
D. Coronary thrombosis
E. Coronary atherosclerosis
Test 2. 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. Autoimmune inflammation
B. Vessels' thrombosis
C. Secondary infection
D. Ischemia of myocardium
E. Resorption of enzymes from
necrotized area of myocardium
Test 3. A 48-year-old patient after severe psychoemotional exertion
suddenly began feeling a sharp pain in the heart region, irradiating into left
36

arm. Nitroglycerin relieves 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 4. 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 5. A patient with an acute myocarditis has the clinic presentations of
cardiogenic shock. What pathogenetic mechanism plays the main part in
shock development?
A. Depositing of blood in veins
B. Decrease of diastolic flow to the heart
C. Disorder of pumping ability of heart
D. Increase of vascular tone
E. Decrease of vascular tone
Practice examination
type 2 Give answers to the
questions of the real-life
task: Interpret the 12-lead
ECG shown below in this
picture, obtained from a
patient who presented with
new-onset dyspnea. What
two clinical diagnoses
should come to mind in view
of the symmetric T wave inversion seen in leads V1,V2,V3 (arrows)?
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.
37

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.
2. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) /
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 7: The pathophysiology of the systemic circulation.
Circulatory failure.
1. The 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 a failure of the circulatory system. Both conditions exhibit
common compensatory mechanisms even though they differ in terms of pathogenesis and
causes.
3. Aim: Learn reasons, forms, and mechanisms of development of cardiac insufficiency.
Acquaint students with the features of metabolism and 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 for their development;
- heterometric and homeometric mechanisms of compensation of insufficiency of heart;
- hypertrophy of myocardium, its stage, a feature of the hypertrophied heart;
To be able: to explain changes in an organism at the condition insufficiency of blood
circulation; to determine the character of compensating reactions of myocardium on the
experimental model of acute insufficiency of heart (depending on the type of loading on a
heart), discover and explain changes which pass here.
A task is to independent extracurricular work: Structure of heart, its valves, circles of
blood circulation [systemic and pulmonary]. Features of innervation, metabolism, and
bloodstream of heart. Phases of the cardiac cycle, their description. Physiology law of the
heart [Frank-Starling's law]. Systolic [stroke volume] and minute volume [cardiac output] of
heart, methods of their determination. Processes of energy supply of cardiac muscle.
To perform practical work: To analyze the compensatory mechanisms cardio-vascular
diseases.
4. Basic level.
The name of the previous and
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. The principle of operation of the
electrocardiograph. A technique of record of an
electrocardiogram in three standard leads. Principal
components of an electrocardiogram.
38

1. Insufficiency of blood circulation: determination, classification.
2. The most widespread innate defects of the heart. Mechanisms of
compensation.
3. Reasons and displays of acute cardiac insufficiency.
4. Pathogenesis of cardiac insufficiency at the overload of heart by the volume
of blood: reasons, the essence of a heterometric mechanism of compensation.
5. Pathogenesis of cardiac insufficiency at the overload of heart by the resistance
of outflow of blood: reasons, the essence of a homeometric mechanism of
compensation.
6. Congenital heart failure. Congenital defects: ventricular & atrial septal defect,
patent ductus arteriosus, tetralogy of Fallot, transposition of the great vessels,
truncus arteriosus, tricuspid atresia, coarctation of the aorta.
7. Reasons and displays of chronic cardiac insufficiency. Rheumatic heart
disease. Valvular disorders.
8. A myocardial form of cardiac insufficiency. Molecular mechanisms of
violations of the retractive function of the myocardium.
9. Compensate hypertrophy of myocardium: determination, kinds, and stages.
10.Cardiomyopathy. Features of the hypertrophic, dilated, restrictive
cardiomyopathy.
11.Mechanisms of development of cardiosclerosis.
12.Violation of hemo- and cardiodynamics at the insufficiency of blood
circulation.
13.Vascular insufficiency. Unconsciousness, collapse: determinations, reasons of
origin.
14.Cardiac tumors: myxoma, rhabdomyoma.
Protocol № 7 Date_____________________
Experimental work 1. Modeling acute insufficiency of the right ventricle in a rat. A
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. Thromboplastin injects into a jugular vein for the
recreation of acute right- ventricular 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 heart death, acute and chronic heart failure. Method of treatment and
prophylaxys: cardioreanimation.
39

According to the documental movie, students should graphically paint ECG for Chagas’
heart disease according to movie explanation, make conclusions.
Conclusion:_____________________________________________________________
Practical work 3.
ECG analysis of the
patients with acute and
chronic heart failure
(registered in 12 Leeds).
Congestive heart
failureThis ECG is from
a patient with heart
failure with frequent
PVCs (Premature
Ventricular Complex)
Conclusion:______________________________________________________________________
Test 1. In course of a preventive examination of a miner, a doctor
revealed changes of cardiovascular fitness which was indicative of cardiac
insufficiency at the compensation stage. What is the main proof of cardiac
compensation?
A. Cyanosis
B. Myocardium hypertrophy
C. Dyspnea
D. Tachycardia
E. Rise of arterial pressure
Test 2. A patient ill with essential arterial hypertension had a
hypertensive crisis that resulted in an attack of cardiac asthma. 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 3. A patient who suffers from a severe disorder of water-salt
metabolism experienced cardiac arrest in diastole. What is the most
probable mechanism of cardiac arrest in diastole?
A. Hypokaliemia
B. Hypernatremia
C. Hyperkaliemia
D. Hyponatremia
E. Organism dehydratation
Test 4. Dystrophic changes of the heart muscle are accompanied with
cardiac cavity enlargement, a decrease of the strength of heart contraction,
40

an increased amount of blood, which remains in the heart during systolic
phase, overfilled veins. For what state of heart is it characteristic?
A. Myogenic dilatation
B. Cardiosclerosis
C. Tonogenic dilatation
D. Tamponage of the heart
E. Emergency stage of
hyperfunction and hypertrophy
Test 5. The patient with acute myocardial infarction was given
intravenously different solutions during 8 hours with medical dropper 1500
ml and oxygen intranasally. He died because of pulmonary edema. What
caused the pulmonary edema?
A. Inhalation of the oxygen
B. Decreased oncotic pressure due to hemodilution
C. Neurogenic reaction
D. Allergic reaction
E. Volume overload of the left ventricular
Practice examination type 2 Give answers to the questions of the real-life
task: After transferred 3 months back anginas patient begin to be disturbed by
dyspnea, gravity in the right hypochondrium, attacks of difficult breathing. The
edemas of the lower extremities have appeared. At objective examination: dermal
covers with icteric color, lips cyanotic and swollen legs. The cervical veins are
pulsing. The borders of the heart are enlarged for the expense of both ventricles;
however, it is more left. Arterial pressure – 90/60 mmHg. A respiration rate -
26/min. The myocarditis, cardiovascular insufficiency in the stage of
compensation is detected. 1. What causes the damage to 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:_______________________________________________________________
Practice examination type 3
A 75-year-old man has an active problem list, including coronary artery disease and
myocardial infarction with both initial and repeat coronary artery bypass graft surgeries,
cardiac arrest necessitating an implanted cardioverter defibrillator (ICD), chronic congestive
heart failure with a left ventricular ejection fraction of 20%, chronic atrial fibrillation,
hepatic cirrhosis with end-stage liver disease, and chronic renal failure.
His problems also include a coagulopathy due to end-stage liver disease, grade 1
esophageal varices, chronic iron deficiency anemia, hypothyroidism, & hyperlipidemia. As
expected, he is followed by a host of specialty services, including cardiology, hematology,
nephrology, hepatology, and gastroenterology.
His current medication list includes aspirin, folate, valsartan, isosorbide, furosemide,
digoxin, carvedilol, atorvastatin, amiodarone, levothyroxine, spironolactone, nadolol, and
esomeprazole. He is allergic to penicillin and cephalosporins.
41

The man was once a heavy smoker and alcohol user but has abstained for the past five
years. Family history is remarkable for coronary artery disease, hypertension, and aortic
dissection.
The review of
systems is notable for a
20-lb weight loss over
the past four months,
generalized weakness
with loss of muscle
tone, and easy bruising.
He has ascites that
require drainage on a
monthly basis. The
patient denies
gastrointestinal,
neurologic, or
pulmonary symptoms, and he has had no therapies from his ICD.
The ICD is a dual-chamber defibrillator. Pacing is programmed DDD at a lower rate of
60 beats/min and an upper rate of 120 beats/min. The paced AV delay is 150ms, and the
sensed AV delay is 120ms. Ventricular fibrillation (VF) detection is programmed to detect at
rates higher than 320ms (188 beats/min), and all therapies are programmed to deliver 35 J.
On physical examination, the man’s weight is 129 lb; blood pressure, 104/68 mm Hg;
pulse, 66 beats/min; temperature, 35.9°C; respiratory rate, 16 breaths/min; and O2 saturation,
97% on room air. The patient is a thin, frail man in no apparent distress.
Pertinent physical findings include clear lungs bilaterally; a regular heart rate and
rhythm with a grade II/VI systolic murmur and jugular venous distention to the jaw line, a
protuberant abdomen with a fluid wave present, a liver edge palpable 4 cm below the right
costal margin, and bilateral shoddy lymphadenopathy in both groins. Pitting edema is present
on both lower extremities, and he has multiple ecchymoses on his arms, chest, and right leg.
The patient is neurologically intact.
His ECG in clinic today includes the following: a ventricular rate of 61 beats/min; PR
interval, 464 ms; QRS duration, 192 ms; QT/QTc interval, 510/513 ms; R axis, 133; and T
axis, –34. What is your interpretation of this ECG?
Answer:_________________________________________________________________________
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.
42

edition, USA. – 2008. – Ch. 4. – P. 166–207.
edition./ Kumar, Abbas, Fauto. – 2007. – Ch. 11. – P. 379–388, 400–420.
Additional:
1. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) /
C. Mattson Porth, Kathryn J. Gaspard. – Ch.14, 17, 18. – P. 231–303, 308–338.
2. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart.NY. – 2000. – P. 194–205, 224–233.
Topic 8: Pathophysiology of blood vessels.
1. The 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 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.Duration of the class – 1 h 30 min.
3.Aim: To pay attention of students to the 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, a 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: Mechanisms of a regulation of vascular
tone. Functions of kidneys in regulation of blood pressure. Methods of measuring of arterial
pressure.
To perform practical work: to analyze the pathogenesis of hypertension and
hypotension.
4. Basic level.
1. histology
2. biochemistry
3. physiology
5. intensive care
Histological structure of vessels wall.
Vascular tone.
Arterial pressure: the factors, defining it level.
Regulation of vascular tone and blood pressure.
The concept of the functional system of blood circulation.
1.Factors which predetermine the level of blood pressure for a man, basal tone of
vessels.
2.Pressor and depressor systems of the organism, their description.
3.Arterial hypertension: kinds, classification. Degrees of high arterial pressure.
4.Nephrogenic hypertensions: reasons, kinds, pathogenesis.
43

5.Etiology and pathogenesis of endocrinal hypertension.
6.A role of the sympathetic nervous system in the pathogenesis of neurogenic
hypertension.
7.Salt hypertension: etiology, mechanisms of development.
8.Etiology and pathogenesis of essential hypertension.
9.Complication of essential hypertension.
10.Reasons and mechanisms of arterial hypotension.
Protocol № 8 Date_____________________
Practical work 1. Study a role of the sympathetic and parasympathetic nervous
system in the 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 by a formula:
dyastolicBP
rateheart
IK
⋅
−=1 ; Norm of ІК = 0
The index of Kerdyu with the sign of “+” testifies to the advantage of sympathetic
influences on a heart and with the sign of “-“ – about the 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 a group.
Conclusion: ________________________________________________________________________
____________________________________________________________________________________
Practical work 2. Arterial hypertension. Watching the documental movie about risk
factors and pathogenesis of blood pressure elevation. Students should discuss the main
ways of peer-educational explanation of arterial hypertension prevention and monitoring
blood pressure among patients.
Conclusion: _________________________________________________________________________
____________________________________________________________________________________
Test 1. Arterial hypertension is caused by the stenosis of the renal arteries
in the patient. Activation of what system is the main link in the pathogenesis
of this form of hypertension?
A. Parasympathetic
B. Kallikrein-kinin
C. Renin-angiotensin
D. Sympathoadrenal
E. Hypothalamic-pituitary
Test 2. In crisis period a 14-year-old child ill with diphtheria has AP -
70/50 mm Hg accompanied by abrupt fall in temperature and tachycardia.
What form of vascular tone disturbance is it?
A. Chronic hypotension
B. Essential arterial hypotension
C. Vegetovascular dystonia
D. Acute hypotension
44

Metod. med 2st semester book 2018 Module 2

Metod. med 2st semester book 2018 Module 2

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