Metod. pharm 2nd 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
PHARMACEUTICAL FACULTY STUDENTS
Prepared by:
GERASYMCHUK M. R.
CHERKASOVA V. V.
ZAIATS L. M.
Ivano-Frankivsk, 2018

Ministry of Public Health Service of Ukraine
Ivano-Frankivsk National Medical University
Department of Pathophysiology
PATHOPHYSIOLOGY OF ORGANS AND
SYSTEMS
(PHARMACEUTICAL FACULTY)
Training-methodical manual
for class and out-of-class work of students
Student 67 group of pharmaceutical 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
pharmaceutical faculty students / M.R. Gerasymchuk, V.V. Cherkasova,
L.M. Zaiats // IFNMU. Department of pathophysiology. – 2018. – 86 p.
Discussed and approved by profile commission of medical & biological
disciplines meeting of Ivano-Frankivsk National Medical University.
Protocol № __ from «__» _________ 2018 year
4

Calendar plan of practical classes
Theme of practical classes Dates Hours
1.
Pathophysiology of the blood system. Qualitative and quantitative
changes of erythrocytes. Anemia
18.01.2018 2
2. Leukocytosis. Leukopenia. Blood tumors (leukemia). 24.01.2018 2
3. Pathology of hemostasis. 01.02.2018 2
4. Arrhythmias of the heart. Circulatory insufficiency. 07.02.2018 2
5.
Insufficiency of coronary blood circulation. Coronary heart
disease.
15.02.2018 2
6. Pathology of vascular tone. Hypertensive disease. 21.02.2018 2
7. Pathophysiology of external respiration. 01.03.2018 2
8. Hypoxia. 07.03.2018 2
9.
Pathology of the digestive system. Etiology and pathogenesis of
peptic ulcer.
15.03.2018 2
10. Pathology of digestion in the intestine. 21.03.2018 2
11. Liver pathology. 29.03.2018 2
12. Main kidney disease. 04.04.2018 2
13. Disorders of functions of the pituitary and adrenal glands. 12.04.2018 2
14. Violation of the function of thyroid and parathyroid glands.. 18.04.2018 2
15. Pathophysiology of the nervous system. 26.04.2018 2
16. Module 2. Practical part 10.05.2018 2
17. Module 2. Theoretical part 16.05.2018 2
Total hours 34
Calendar plan of lectures
# Theme of lecture Dates Hours
1.
Leukocytosis. Leukopenia. Leukemias. Etiology, pathogenesis of
leukocytosis and leukopenia. Leukemia: principles of
classification, main types, typical manifestations. Etiology of
leukemia. Features of the pathogenesis of acute and chronic
leukemia.
17.01.2018 2
2.
Pathophysiology of the heart. Crown deficiency: etiology,
pathogenesis, consequences, clinical manifestations. Myocardial
infarction.
31.01.2018 2
3. Pathophysiology of vessels. Hypertonic disease. 14.02.2018 2
4.
Pathophysiology of the digestive system. Disturbance of secretory
and motor function of the digestive tract. Peptic ulcer. Digestive
disorders associated with secretory pancreatic insufficiency.
28.02.2018 2
5. Pathophysiology of the kidneys. Renal insufficiency. 14.03.2018 2
6.
Pathophysiology of the Endocrine system. General adaptation
syndrome.
28.03.2018 2
7. Pathophysiology of the nervous system. 11.04.2018 2
8. Pathophysiology of extreme states 25.04.2018 2
Total hours 16
5

The ESTIMATION FOR THE MODULE is defined as a sum of marks of
current educational activity (in points), which is proposed during the evaluation of
theoretical knowledges and practical skills. Maximal amount of points, which a
student can collect - 200 points during of every module study, including for current
educational activity – 120 points (minimum are 60 points, maximum are 120 points),
on results final module control are 80 points.
Criteria for assessing students' knowledge of module 2
Scale of
evaluation
Criteria for evaluation
Control of theoretical and practical preparation
0 – 2 points – completely prepared homework;
0 – 5 points – oral answer;
0 – 1 points – test control during class.
Minimum – 0 points; minimal positive – 4 points; maximum – 8 points
8
Exhibits for the correct, accurate implementation of the practical
skills and skills necessary for certain tasks, as well as for a thorough
grounded answer to the theoretical control and supplementary
questions.
7
Exhibited for the full implementation of the practical skills and skills
necessary for certain tasks, as well as for an incomplete answer to
control questions.
6
Exposed for minor inaccuracies in the implementation of the practical
skills and skills necessary for certain tasks, as well as for the
inaccurate response to control questions.
5
Is exposed for orientation in the concepts and definitions of the
subject and performance of practical work.
4
Exposed for orientation in terms and definitions of the subject, and
incomplete performance of practical work.
3
Is exposed for orientation in concepts and definitions from the
subject, but can not formulate his own opinion when solving
situational tasks.
2
Is exposed for orientation in the concepts and definitions of the
subject.
1
Demonstrate some ideas of the definition of concepts from the
subject, no homework.
0
Demonstrate the absence of input and output knowledge, no
homework.
6

Topic 1. Pathophysiology of the blood system. Qualitative and
quantitative changes of erythrocytes. Anemia
1. The actuality of the theme. The system of blood is the internal
environment of an organism. The normal state of blood, its cellular
composition, is in close interrelation with the 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 the
blood of different pathological factors. The qualitative features of erythrocytes
of peripheral blood and bone marrow allow to determine a kind of anemia, to
make a submission about the regenerative ability of bone marrow and to
inspect efficiency of treatment.
2. Length 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 red corpuscles,
hemoglobin and color index, indexes of physiology regeneration of marrow,
degenerative changes of RBC at posthemorrhagic anemia.
To know:
- determination of concept is “anemia” and principles of classification;
- etiology and pathogenesis of acute and chronic posthemorrhagic anemia;
- etiology, pathogenesis and displays of violation of general volume of
blood;
- method of determination of hemoglobin, color index, amount of RBC in
peripheral blood.
- principal reasons for origin and pathogenesis of hemolytic anemias and
anemias are as a result of the violation of erythropoiesis;
- basic clinical and hematological syndromes are at B12- and folic acid
deficit anemia.
To be able:
- to describe the picture of blood at acute and chronic posthemorrhagic
anemia in its different stages;
- to describe basic hematological indexes at hemolytic and megaloblastic
anemias;
- to estimate, using got in an experiment given, quantitative changes of
RBC, hemoglobin (Hb) and color index (CI), indexes of physiology
regeneration of marrow, degenerative changes of RBC at posthemorrhagic
anemia, hemolytic or megaloblastic anemias.
The task for independent extracurricular work.
1. To know erythropoiesis in a norm, morphology of cells of a red blood.
7

2. Able to analyze the value of the volume, will make and basic functions
of blood for support of normal vital functions.
3. Methods of determining the amount of hemoglobin, RBC in blood, the
color index.
4. Erythropoiesis in a norm, nomenclature, and morphology of red blood.
5. Normal indexes of the line of RBC: table of contents of RBC,
hemoglobin, color index, amount of reticulocyte.
6. To know the exchange of iron, the vitamin of B12 and folic acid in an
organism.
4. Basic level.
The name of the previous
and future disciplines
The receiving of the skills
1. histology
2. biochemistry
3. physiology
4. internal medicine
5. haematology
Scheme of erythropoiesis. Quantitative
parameters of red blood. The technique of
erythrocytes account. A technique of
determination of the hemoglobin content and a
color index.
5. The advice for students.
•To perform practical work: to analyze the normal content of blood
average:
•Normal content of erythrocytes (red blood cells - RBC) and
hemoglobin in blood:
o Erythrocytes: M — 4.0-5.0·1012
/l; F — 3.9-4.7·1012
/l; Newborn: 5-
6·1012
/l
•Hemoglobin (Hb): M - 135-160 g/l; F - 120-140 g/l;
•Mean corpuscular hemoglobin (MCH) = [Hb] / RBC count: 0.85-1.15
•Reticulocytes: 2-10 % (of total erythrocyte number)
•Erythrocytes sedimentation rate (ESR): M - 2-10 mm/h; F - 2-15mm/h
•Hematocrit: Adults: M - 40-48 %; F - 36-42 %; Newborn: 45-54 %
•Size of erythrocyte- 7-8 µm
•Lifespan 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.
•MBV – minute blood volume – 5L/min.
•VR – venous return – 5L/min.
•AP – arterial pressure – 120/80 mm Hg.
•CVP – central venous pressure – 65-120 mm of water (5-9 mm Hg)
8

•ABB (acid-base balance) pH of blood: arterial blood – 7.4, venous
blood – 7.35
6. Control questions of the theme:
1. The types of changes of general volume in blood.
2. To give a determination of “hypovolemia” and “hypervolemia”, its
kinds and examples.
3. Determination of concept is “anemia”. Classifications of anemias.
Etiology of acute posthemorrhagic anemia.
4. Description of phases of compensation of organism on the acute
hemorrhage. A picture of peripheral blood is in the bone-cerebral phase of
compensation after hemorrhage.
5. Etiology and pathogenesis of chronic posthemorrhagic anemia.
6. Etiology of the purchased hemolytic anemias, their kinds.
7. To explain the mechanism of hemolysis at the purchased hemolytic
anemias.
8. To give description of the picture of peripheral blood at the purchased
hemolytic anemia.
9. To name the types of the inherited hemolytic anemias. To explain
pathogenesis hereditary spherocytosis [globular cell anemia, Minkowsky-
Shauffard disease], a picture of blood at this pathology.
10. To explain the pathogenesis of glucose 6-phosphate dehydrogenase
deficit anemia.
11. To name kinds, explain pathogenesis, a picture of peripheral blood at
inherited hemoglobinopathy. To explain the pathogenesis of sickle cell anemia,
a picture of peripheral blood.
12. To name kinds, make examples of anemias as a result of the violation
of erythropoiesis.
13. Etiology, pathogenesis, a picture of the blood of a siderotic [iron-
deficiency] anemia.
14. Kinds and etiology of B12-folic acid deficit anemias.
15. Etiology, pathogenesis of Addison-Birmer’s anemia. To name the
classic displays of pernicious [Biermer’s, Biermer-Ehrlich] anemia.
16. To give a description of a picture of peripheral blood at pernicious
anemia.
7. Students’ practical activities
Protocol № 1 Date_____________________
Experimental work 1. Define the amount of hemoglobin 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.
9

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 with a glass stick until
the color of the liquid in a test tube will be equal to the color of the standard
solution of hemometer. The formula of calculation:
Hb = A×0,6206, where “A” is an amount of hemoglobin in g%; 0,6206 is a
coefficient of the count in the 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
the net of Goryaevs’ 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 colored index.
The 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 - 3 x 1012
/l. Then
1
32
2,6
≈
•
=CI
Conclusion: ________________________________________________________
___________________________________________________________________
Experimental work 4. 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 (CI): normochromic,
hyperchromic, hypochromic.
3. Give the examples of diseases in which this anemia occurs.
10

Hemogram 1
Eryth-
rocy-tes
Hb 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 60 0,62 9 6 1 2 - 5 56 31 5
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 2
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: ________________________________________________________
___________________________________________________________________
Hemogram 3
RBC 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
segmento
nucleonic
1012
/l g/l mm/h ∙109
/l % % % % % % %
3,79 131 1,03 8 5 1 4 - 2 59 28 6
Conclusion: ________________________________________________________
___________________________________________________________________
Hemogram 4
RBC 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
segmento
nucleonic
1012
/l g/l mm/h ∙109
/l % % % % % % %
3,27 142 1,37 5 7 1 5 1 6 53 30 4
Conclusion: ________________________________________________________
___________________________________________________________________
8. Practice Examination.
Practice examination type 1: Choose the correct answer:
Test 1. After massive blood loss victim had hypovolemic shock with
development of deep hypoxia. Its consequences will have an effect, first of
all, on activity of:
11

А. Lungs
В. Kidneys
С. Spleen
D. Brain
Е. Heart
Test 2. In the patient in time accident on Chornobyl atomic power
station arose 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 3. Substitution of the glutamic acid on valine was revealed while
examining 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 4. Patient 54 year-old, 5th day after surgical operation. Blood
count: Erythrocytes 3,6*1012
/l, Hemoglobin 95 g/l, Erythrocyte’s
hemoglobin content (color index) 0,78; Leukocytes 16*109
/l, Platelets
450*109
/l Blood picture: anizocytosis, poikilocytosis, reticulocytes- 3,8%.
What anemia does this patient have?
A. Chronic posthemorragic anemia
B. Acquired hemolytic anemia
C. Acute posthemorragic anemia
D. Anemia from iron deficiency
E. Hypoplastic anemia
Test 5. In the blood of a 26-year-old man - 18% of erythrocytes of the
spherical, ball-shaped, flat and thorn-like shape have been revealed. Other
erythrocytes were in the form of the concavo-concave disks. How is this
phenomenon called?
A. Physiological poikilocytosis
B. Erytrocytosis
C. Pathological poikilocytosis
D. Physiological anisocytosis
E. Pathological anisocytosis
Test 6. A 56 year old patient came to a hospital with complaints about
general weakness, tongue pain and burning, sensation of limb numbness.
In the past he underwent resection of fore stomach. In blood: Hb - 80 g/l;
12

erythrocytes - 2,0*1012
/l; color index (CI) - 1,2, leukocytes - 3,5*109
/l. What
anemia type is it?
A. Iron-deficient
B. Hemolytic
C. Aplastic
D. B12-folate deficient
E. Posthemorrhagic
Practice examination type 2. Give answer to the questions of the real-
life tasks:
Task 1. Victim is delivered in receiving branch of hospital by the casual
transport through 8 minutes after traffic incident. Complains on pain in
stomach with irradiation into the right shoulder. The skin is pale, is covered
with cold sweat. Arterial pressure - 95/70 mm Hg, pulse – 102 beats for 1
minute, breath - 28 for 1 minute. The blood was taken immediately on analysis
an amount of erythrocytes - 4,2×1012
/l, hemoglobin content - 122 g/l.
1. Analyse these data. What parameters deviate from norm? 2. What it is
possible to think about in this case? 3. How does it explained painless of skin?
What does it mean this reaction? 4. How do you evaluate the increase of rate
pulse and breath?
Answer for the task 1: _____________________________________________________________
Task 2. The blood of patient with anemia is characterized by parameters:
amount of erythrocytes – 3,5·1012
/l, hemoglobin content – 50 g/l; in blood
smear – annulocytes, poikilocytes, microcytes.
1. For what kind of anemia these parameters are characterized? 2.
Calculate color index and determine, to what group (according to color index)
this anemia concern. 3. Why erythrocytes are acquired of rings form?
Answer for the task 2: _____________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology. Edited by prof. A.V. Kubyskin. Simferopol. – 2011. – P. 362–409.
2. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010.
– P. 290–329.
3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 266–280.Russell J.
Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene, Norman D.
Harris // 3rd
edition, USA. – 2008. – Chapter 11. – P. 705–724.
Additional:
1. Robbins and Cotran Pathologic Basis of Disease 8th
edition / Kumar, Abbas, Fauto 2006. – Chapter 12. – P. 422–441.
2. Pathophysiology, Concepts of Altered Health States, C. M. Porth, G. Matfin. – NY, Milwaukee. – 2009. – P. 278–285.
13

3. 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.
4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students
and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P.167–178.
5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback
(2003) / Carol Mattson Porth, Kathryn J. Gaspard – Chapter 13. – P. 216-230.
Topic 2. Leukocytosis. Leukopenia. Blood tumors (leukemia).
1. The actuality of the theme. Leukocytosis is considered as a reaction
hematopoietic system due to 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 leucocytes and their flow into vessels and
redestribution.
Leucopenia may depend upon oppressive influence of some toxins on the
maturation and outflow of leucocytes from the bone-marrow. Often these
phenomenas are observed during the infectious diseases. They have
significanse for the differential diagnostic. If for the disease is characterised
leucocytosis, the availability of leukopenia testifies on depression of
hemopoietic system.
3. Aim: to analyse of the pathogenesis of the quantitative and qualitative
changes of leucocytes in blood. The increase of leucocyte quantity is called
leukocytosis, and the decrease-leukopenia. The norm is 4-9G/l or 4-9*109
/l.
The quantitative changes are increased quantity of immature forms in blood
and degeneration of leucocytes.
Analyse of the pathogenesis of the 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 initial affection of the bone
marrow.
To be able: to analyse of the quantitative and qualitative changes of
leucocytes in blood, blood data under acute and chronic leukemia.
Task for independent extracurricular work.
1. To know leukopoesis in a norm, morphology of white blood cells.
2. Methods of determining the amount of white blood cells in the blood.
3. Anatomy and functions of primary and secondary hematopoietic organs.
4. Basic level.
The name of the previous and
future disciplines
14

1. histology
2. biochemistry
3. physiology
4. haematology
Scheme of leukopoesis. Leucocytes formula of blood.
Function of leucocytes. Methods of counting of
leucocytes maintenance in blood.
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.
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 corresponds
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
15

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 leukopenia.
5. What is aleukia?
6. Blood picture under the leukopenia.
7. Leucocyte degeneration in blood.
8. Determination and general definition of leucosis. Classification of leukosis is after
motion and morphological signs.
9. Modern theories of origin of leucosis: role of viruses, ionizing radiation, chemical
matters, inherited anomalies. Tumor nature of leucosis. Basic displays of tumor
progression.
10. Features of hemopoiesis, picture of peripheral blood, leukogram at an acute
myeloleukosis [myeloleukemia].
11. Features of hemopoiesis, picture of blood at chronic myeloleukosis.
12. Picture of blood, leukogram at an acute lympholeukosis [lymphatic leukemia].
13. Picture of blood, leukogram at a chronic lympholeukosis.
14. A mechanism of development of anemia at acute and chronic leukosis.
15. Violation of reactivity of organism is at leucosis. A role of the inherited anomalies is
in development of leukosis.
Protocol № 2 Date_____________________
Experimental work 1. Count up a leukocyte formula (leukogram) at
an abscess. To prepare the stroke of blood, taken from the vein of ear of rabbit
and to paint it by the Pappengeym. See the stroke under an immersion increase.
The stroke of blood is mentally divided into four fields, conducting the lines
which are perpendicular one to one through the center of stroke. Count up in
every field 25 leucocytes, moving a stroke on the broken line. Count up
separate types of leucocytes using a meter.
Formula: LG
А
L
АА
/
20
/10
20
10
11600
204000 96
=•=•
•
••
,
А – amount of leucocytes in 100 big squares; 1600 – amount of small
squares; 4000
1
- a volume of small square is in microliter; 20 - is a degree of
16

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.
Conclusion:__________________________________________________
Experimental work 3. Counting of leukocyte formula in smear of
blood sick on leucosis.
a) Acute lymphoblastic leukosis; b) Acute myeloblastic leukosis
c) Chronic myelocytic leukosis; d) Chronic lymphocytic leukosis
Study smear in immersial microscope objective. For determination of
leucocytic formula is necessary to calculate 100 leucocytes. Counting should
be done in four various parts of smear, moving subject glass so that the fields
of sight were on sufficient distance from either and other. For it also necessary
pay attention to the form, sizes of cells, colour, granularity in protoplazma,
form and colour of a nucleus. Put the results of counting in the table:
Baso-
philes
Eosi-
nophi
les
Neutrophiles Lym-
pho-
blasts
Lym-pho-
cytes
Mono-
cytesMyelo-
blasts
Promy-
elocytes
Myelo-cytes
Meta-
myelo-cytes
Stab
nuc-leonic
Seg-ment
1% 0% 0% 0% 1% 2% 5% 8% 75% 6% 2%
2% 0% 90% 0% 0% 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%
Make a conclusion:____________________________________________________
17

Test 1. During the medical examination of a boy 5 years old were
founded the significant increase of eosinophiles in the blood. What from
mentioned below can be the cause of eosinophilia?
A. Helminthiasis
B. Obesity
C. Hypodynamia
D. Hypotermia
E. Physical strain
Test 2. Blood sampling for general analysis is recommended to be
performed on an empty stomach and in the morning. What changes in
blood count can occur if to perform blood sampling after food intake?
A. Increased plasma proteins
B. Increased contents of leukocytes
C. Increased contents of erythrocytes
D. Reduced contents of thrombocytes
E. Reduced contents of erythrocytes
Test 3. Lazy leucocyte syndrome is because of:
A. Disorder of phagocytosis
B. Cellular immunodeficiency
C. Combined immunodeficiency
D. Disorder of complement
Test 4. Earliest transient change following tissue injury will be:
A. Neutropenia
B. Neutrophilia
С. Monocytosis
D. Lymphocytosis
Test 5. In a patient with leucosis parameters of white blood are the
following: amount of leucocytes – 100∙109
/l, from them basophiles – 1%,
eosinophiles – 2%, stab neutrophils – 4%, segmental leukocytes – 7%,
lymphoblasts – 2%, lymphocytes – 80%, monocytes – 4%. In blood there
are a lot of desroyed lymphocytes (Gymprehkt bodies). These parameters
are characterized for:
A. Acute myeloblastic leukosis
B. Chronic mielocytic leukosis
C. Chronic lymphocytic leukosis
D. Acute plasmoblastic leukosis
E. Chronic monocytic leukosis
Test 6. A 23 y.o. patient complains of weakness, temperature rise up to
38-400
C. Objectively: liver and spleen are enlarged. Hemogram: Hb – 100
g/l, erythrocytes – 2.9*1012
/l, leukocytes – 4.4*109
/l, thrombocytes –
48*109
/l, segmentonuclear neutrophils – 17%, lymphocytes – 15%, blast
cells – 68%. All cytochemical reactions are negative. Make a hematological
conclusion:
A. Acute erythromyelosis
18

B. Acute myeloblastic leukosis
C. Chronic myeloleukosis
D. Undifferentiated leukosis
E. Acute lymphoblastic leukosis
Practice examination type 2 Give answer to the questions of the real-life tasks:
Task 1.
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 ites are characteristed for? Give examples.
Answer for the task 1: _______________________________________________
___________________________________________________________________
Task 2.
Amount of
leucocytes
Baso
-
phile
s
Eosino-
philes
Neutrophiles
Lym-
phocy
tes
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
18.3·109
/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 %
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 ites are characteristed for? Give examples.
Task 3.
Amount of
leuco-
cytes
Baso-
phi-
les
Eosino-
phi-
les
Neutrophiles
Lym
phocytes
Mono-
cytes
Mye-
lo-
cytes
Metamy-
elocytes
Stab
nucleonic
Segmento-
nucleonic
2.0·109
/l 1 % 2 % - 1 % 15 % 57 % 20 % 4 %
19

Total
amount of
leucocytes
Baso-
philes
Eosino-
philes
Neutrophiles Lympho-
blasts
Lympho-
cytes
Mono-
cytesMetamye
-locytes
Stab
Seg-
mental
100.0*109
/l 1 % 2 % - 4 % 7 % 2 % 80 % 4 %
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 leucogram is characterized for?
Task 4.
Total
amount of
leucocytes
Baso-
philes
Eosi-
nophi-
les
Neutrophiles
Lym
pho-
cytes
Mono-
cytes
Myelo-
blasts
Promie
locytes
Myelo
cytes
Meta-
myelo
cytes
Stab
Seg-
mental
75.0*109
/l 1 % 1 % 78 % 2 % - - 3 % 3 % 10% 2 %
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 leucogram is characterized for?
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. –
P.286–287, 322–333.
2. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, J. L. Banasic // Elsevier Inc. – 2010. – P. 242–262.
3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 266–322.
4. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York,
Milwaukee. – 2009. – P. 278–323.
5. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene,
Norman D. Harris // 3rd
Additional:
& Wilkins – 2008. – Chapter 12. – P. 357–359, 363, 366–367, 382–387.
edition./ Kumar, Abbas, Fauto. – 2007. – Chapter 12. – P. 441–468.
and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 179–191.
(2003) / Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 11. – P. 191-205.
Topic 3. Pathology of hemostasis.
20

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. Violation in the system of hemostasis can take
place in three directions: 1) decline of coagulative ability of blood and origin of
hemorragic diathesis; 2) increase of coagulative ability of blood and origin of thromboses;
3) origin of thrombohemorragic syndrome, which shows up increase of thrombosis and
hemorrhagic diathesis both.
2. Length of the 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
pathology of man.
To know:
- etiologic factors which predetermine violation of producing blood clots;
- basic phases of process of producing trombosis;
- reasons and mechanisms of origin of hemorrhagic diathesis;
- reasons and mechanisms of violation thrombocyte-vascular hemostasis;
- etiology and pathogenesis of disseminated intravascular coagulation [DIC];
- inherited violations of blood clotting.
To be able:
- to explain the mechanisms of interrelation of basic factors of coagulative and
anticoagulative systems in the process of clotting;
- to reproduce violation of blood clotting in an experiment;
- to calculate prothrombin time [PT] and prothrombin index;
- to count up the amount of platelets in peripheral blood.
A task is to independent extracurricular work:
To think over the followings theoretical questions:
1. Modern presentations about coagulative and anticoagulative system of blood.
2. Mechanisms of the physiology blood clotting.
3. Thrombosis as local violation of circulation of blood.
4. Stages of blood clotting.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
4. haemathology
Vesseles-thrombocytous and plasmatic factors,
which participate in coagulation of blood. Stage of
blood coagulation. Significance ancoagulative and
fibrinolytic systems of blood.
The term hemostasis refers to the stoppage of blood flow. The normal process of
hemostasis is regulated by a complex array of activators and inhibitors that maintain blood
fluidity and prevent blood from leaving the vascular compartment. Hemostasis is normal
when it seals a blood vessel to prevent blood loss and hemorrhage. It is abnormal when it
causes inappropriate blood clotting or when clotting is insufficient to stop the flow of
21

blood from the vascular compartment. Disorders of hemostasis fall into two main
categories: the inappropriate formation of clots within the vascular system (i.e.,
thrombosis) and the failure of blood to clot in response to an appropriate stimulus (i.e.,
bleeding).
What is hemostasis pathology? With the help of the system of hemostasis blood
carriers out one of its most significant functions – keeping itself in a liquid state and
coagulation in case of a vessel’s wall injury and, this way, stopping the bleeding and
keeping the initial volume and composition of blood. The system of hemostasis has many
components. These are platelets and other blood cells, vessel’s wall, extravascular tissue,
biological active substances, tissue factors (extrinsic pathway), plasma factors of blood
clotting (intrinsic pathway), begin in a close interaction with anticoagulational, fibrinolytic
and kallikrein-kinine systems. Disturbance of any of these components leads to hemostasis
pathology.
1. What is hemostasis pathology.
2. Classification of pathology of hemostasis.
3. Normal hemostasis.
4. The classical coagulation cascade.
5. Virchow's triad in thrombosis.
6. Decreasing of blood coagulation ability.
7. Thrombocytopenia and thrombocytopathy.
8. Increasing of blood coagulation ability.
9. Generalized (disseminated) intravascular blood coagulation (DIC-syndrome).
6. Independent audience work of student
Protocol № 3 Date_____________________
Experimental work 1. Define prothrombin time [PT] for a dog with the cirrhosis
of liver. In advance oily solution of carbon tetrachloride is entered a dog from the
calculation of 4 ml per 1 kg of mass. Before lesson for a dog take 4,5 ml of blood, add 0,5
ml of a 0,1% solution of oxalic sodium and spin, take the plasma. In test tube pour 0,2 ml
of plasma, warm up on an water bath at 38°N, add 0,2 ml warmed to a 38°N mixture from
equal parts of thromboplastin and 0,5% solution of calcium chloride. Carefully mix up a
glass stick, continuing to hold in a water bath. Calculate time from adding mixture to the
first signs of coagulation of plasma (in seconds).
Calculate the prothrombin indexes after formula: B
А
Х
•
=
100
, where A – time of
coagulation of control plasma (seconds); B – time of coagulation of experimental plasma
(seconds). A normal index of is equal 70-100%.
Conclusion:__________________________________________________
Experimental work 2. Count up the amount of thrombocytes for a rabbit with
radiation illness. Three days prior to lesson an animal is exposed to the X-rays.
22

On the area of regional vein ears inflict a few drops of a 14% solution of magnesium
sulphate, prick a vein; carefully mix up blood a glass stick with magnesia in correlation
2:10.
From the got mixture prepare a stroke; dye it after Pappengeym (to repaint for the
best visibility of trombocytes). A count is conducted under an immersion increase in the
narrowed eyeshot. Count up the amount of trombocytes on 1000 red corpuscles.
Formula of calculation: 1000
АН
Х
•
= , where H – is an amount of platelets on 1000 red
corpuscles; A – is an amount of red corpuscles; Method of count of amount of red
corpuscles see lesson 25.
Conclusion:__________________________________________________________
Practice examination type 1 Choose the correct answer:
Test 1. In the patient in time accident on Chornobyl atomic power
station arosed hemorrhagic syndrome, which was showed by hemorrhage
in skin and mucous membrane, appearance of blood in urine, faces and
phlegmone? 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 thrombocytopenia, 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. Punctate hemorrhage was found out in the patient after
application of a tourniquet. With disfunction of what blood cells is it
connected?
A. Eosinophiles
B. Lymphocytes
C. Monocytes
D. Neutrophiles
E. Platelets
Test 4. A 6-months-old baby has got frequent and extensive subdermal
hemorrhages. The administration of the synthetic analogue of vitamin K
23

(vicasol) was effective. γ-carboxylation of glutamic acid of what protein of
blood coagulation system does this vitamin take part in?
A. Antihemophilic globulin A
B. Fibrinogen
C. Prothrombin
D. Hageman's factor
E. Rosental's factor
Test 5. A 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 tasks:
Task. The patient was in surgical clinic because of thrombophlebitis of the
right leg. After careless sudden movement an acute dyspnia to bother him, pain
in the chest and cyanosis appeared. Did these disorders associate with
thrombophlebitis of the leg? In what cases such consequences of
thrombophlebitis are possible? Are such complications occasional in the
patient? Is thrombophlebitis complication possible in the other organs - brain,
kidneys, spleen?
Answers for the task: ________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – V.: Nova Knuha Publ. – 2011. – P. 444–460.
Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – NY. – 2009. – P. 262–278.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, J. L. Banasic // Elsevier Inc. – 2010. – P. 330–346.
edition, USA. – 2008. – Chapters 11. – P. 726–741.
Additional:
& Wilkins – 2008. – Chapter 12. – P. 359–364, 387–390.
and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 192–197.
(2003) / Carol Mattson Porth, Kathryn J. Gaspard. Chapter 12. – P. 205-215.
Topic 4. Arrhythmias of the heart. Circulatory insufficiency.
24

1. Actuality of the theme. The disorders of cardiac rhythm concern to complex
manifestations of pathology of heart. Its can arise in rather small damage of the conducting
system, and in some cases in structural changes. More often arrythmia arise with
infectious illnesses and intoxications as consequence of miocarditis or dystrophy processes
in cardiac muscle, and also in heart ishemic disease, cardiosclerosis. Arrythmia can be
result in development of cardiac insufficiency.
Adequate perfusion of body tissues depends on the pumping ability of the heart, a
vascular system that transports blood to the cells and back to the heart, sufficient blood to
fill the circulatory system, and tissues that are able to extract and use the oxygen and
nutrients from the blood. Heart failure and circulatory shock are separate conditions that
reflect failure of the circulatory system. Both conditions exhibit common compensatory
mechanisms even though they differ in terms of pathogenesis and causes.
3. Aim: To reproduce the models of basic forms of disorders of cardiac activity of
caused violation of excitability, to explain reasons and mechanisms of origin in order to
make ability to apply etiologic and pathogenetic treatment of arrhythmias on the
departments of clinical type. Learn reasons, forms and mechanisms of development of
cardiac insufficiency.
To know: that ability to automatic formation of impulses depends on the cells
located in the conductive system of the heart (p-cells). A spontaneous slow
depolarization of the cellular membrane occurs in them during diastole.
- classification of arrhythmias and most widespread in clinical practice of their
form;
- mechanisms of violations of automatism, excitability and conductivity of heart;
- signs of electrocardiographies of separate types of arrhythmias.
- types of insufficiency of heart and principal reasons of their development;
- heterometric and homeometric mechanisms of compensation of insufficiency of
heart;
- hypertrophy of myocardium, its stage, feature of the hypertrophied heart;
To be able:
- to 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).
- to explain changes in an organism at the condition insufficiency of blood
circulation;
- to determine character of compensate reactions of myocardium on experimental
model of acute insufficiency of heart (depending on the type of loading on a heart),
discover and explain changes which pass here.
1. Conducting system of heart, its anatomy, histology and functional value.
2. Concept of “pace-maker”, mechanisms of origin of bioelectric potentials in a
cardiac muscle.
3. Basic electro-physiology properties of cardiac muscle.
4. Principle of electrocardiography. Basic taking which are used in medical practice.
Description of indexis of ECG.
25

5. Structure of heart, its valves, circles of blood circulation [systemic and
pulmonary].
6. Features of innervation, metabolism and bloodstream of heart.
7. Phases of cardiac cycle, their description.
8. Physiology law of the heart [Frank-Starling's law]
9. Systolic [stroke volume] and minute volume [cardiac output] of heart, methods of
their determination.
10. Processes of energy supply of cardiac muscle.
To perform practical work: to analyse the mechanisms of the arrhythmias.
4. Basic level.
1. Histology
2. Biochemistry
3. Physiology
4. Internal medicine
5. Cardiology
Structure of the conducting system of heart.
Histochemical structure of the myocardium. Main
properties of heart - automatism, irritability, conductivity,
contractivity, refractory. Specialities of blood supply of
heart Mechanisms of occurrence and transfer of nervous
impulse on the conducting system of heart. Principle of
operation of the electrocardiograph. Technique of record
of an electrocardiogram in three standard leads. Principal
components of an electrocardiogram.
6. Control questions of the
theme:
1. Etiology of cardio-vascular
diseases. Arrhythmias of heart: definition, classification.
2. Etiology and pathogenesis of nomotopic and heterotopic violations of automatism:
sinus tachy-, brady- and arrhythmia.
3. Reasons and mechanisms of extrasystoles and paroxysmal tachycardia. Basic signs of
different types of extrasystoles on ECG.
4. Blocks of heart: kinds, reasons, mechanism of origin. Atrio-ventricular block.
5. Blinking arrhythmia: principal reasons, description, and displays.
6. Flutter and fibrillation of atrium or ventricules; a mechanism of origin, sign is on ECG.
7. Methods of experimental recreation of arrhythmias.
8. Insufficiency of blood circulation: determination, classification.
9. The most widespread innate defects of heart. Mechanisms of compensation.
26

10.Reasons and displays of acute cardiac insufficiency.
11.Pathogenesis of cardiac insufficiency at the overload of heart by the volume of blood:
reasons, essence of heterometric mechanism of compensation.
12.Pathogenesis of cardiac insufficiency at the overload of heart by resistance of outflow
of blood: reasons, essence of homeometric mechanism of compensation.
13.Reasons and displays of chronic cardiac insufficiency.
14.Myocardial form of cardiac insufficiency. Molecular mechanisms of violations of
retractive function of myocardium.
15.Compensate hypertrophy of myocardium: determination, kinds and stages.
16.Features of the hypertrophied heart, mechanisms of development of cardiosclerosis.
17.Violation of hemo- and cardiodynamics at insufficiency of blood circulation.
18.Vascular insufficiency. Unconsciousness, collapse: determinations, reasons of origin.
7. Independent audience work of student.
Protocol № 4 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 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:_______________________________________
______________________________________
Experimental work 2. Modeling acute insufficiency of right ventricle
in a rat. Motion of work: Under easy ether anesthesia for a rat the section of
skin on the middle line of neck and separate external jugular vein. To front and
back extremities connect the electrodes of electrocardiographs. Tromboplastine
inject into a jugular vein for the recreation of acute right-ventricule
insufficiency. Fix a stop-watch time of offensive of shortness of breath, stop of
breathing, cramps. At the same time register changes on ECG: deep waves of
QS and ST, getting up of segment of RS-T into III leads, aVF, V1, V2 and
27

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:________________________________________________________
Practice examination type 1. Choose the correct answer:
Test 1. In a 45-year-old patient on ECG it was revealed: sinus rhythm,
the number of auricular complexesexceeds number of ventricular
complexes; progressing extension of the P-Q interval from complex to
complex; fallout of some ventricular complexes; Р waves and QRST
complexes are without changes. Name the type of heart rhythm
disfunction.
A. Complete atrioventricular block
B. Atrioventricular block of the II degree
C. Atrioventricular blockade of the I degree
D. Synoauricular block E. Intraatrial block
Test 2. While a 24 year old woman was waiting for tooth extraction,
tonus of sympathetic part of autonomic nervous system rose. What
reaction will the patient display?
A. Hypersecretion of digestive juices
B. Bronchus constriction
C. Increased frequency of heartbeat
D. Miotic pupils E. Hyperperistalsis
Test 3. An electrical cardiostimulator was implanted to a 75 y.o. man
with heart rate of 40 bpm. After that heart rate rose up to 70 bpm.
Cardiostumulator assumed the function of the following heart part:
A. Purkinje's fibers
B. His' bundle branches
C. His' bundle fibers
D. Atrioventricular node
E. Sinoatrial node
Test 4. 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 5. 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?
28

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
Practice examination type 2. Give brief explanation for the real-life
tasks:
Task 1. In a patient with an 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 мl of atropine, which was made
for differentiation diagnosis, increased heart rate on 16 beat per minute.
1. What is the name of described disturbance of cardiac rhythm and what group of
arrhythmias does it concern to? 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 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?
Answer for the task 2:__________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – V: Nova Knuha Publ – 2011. – P.489–500.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 338–344, 348–351.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. – P. 396–427,
461–509.
Additional:
1. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – NY. – 2009. – P.584–633.
edition. Copyright В. – Lippincott Williams &
Wilkins – 2008. – Chapter 13. – P. 392–298, 414–429, 447–460.
ed./ Kumar, Abbas, Fauto. – 2007. – Ch11. – P. 379–388, 400–420.
4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and
practitioners. Edited by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 207–221.
5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003)
/ Carol Mattson Porth, Kathryn J. Gaspard. – Chapters 14, 17, 18. – P. 231–243, 302–338.
Topic 5: Insufficiency of coronary blood circulation.
Coronary heart disease.
1. The actuality of the theme. Among cardio-vascular diseases coronary heart disease
is the most frequent reason of loss of health, capacity and death rate. From data of WHO,
29

morbidity on CHD and hypertention in the economic developed countries of the world
continues to be increased, striking all more persons of young age. In this connection,
obviously, there is a necessity of study of etiology, pathogenesis, forms and complications
of CHD, ability to reproduce on experimental models, students, so both success of fight
against ischemic illness of heart in a considerable measure depends on correct diagnostics,
medical and prophylactic work as doctors of wide type and specialists of cardiologists.
3. Aim: To expose the mechanisms of different forms of coronal insufficiency. To
evaluate the basic displays of CHD; to learn to analyze the changes of ECG.
To know:
- reasons and mechanisms of development of violations of coronal circulation of
blood;
- functional, morphological, biochemical and electrocardiography changes are at the
heart attack of myocardium;
To be able:
- to reproduce in an experiment on animals coronal insufficiency;
- to analyse the changes of electrocardiography;
- to explain the mechanism of pain at angina pectoris and heart attack of myocardium.
A task for 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 analyse the compensatory mechanisms cardio-
vascular diseases.
4. Basic level.
The name of the previous and future
disciplines
1. histology
2. biochemistry
3. physiology
Histochemical structure of the
myocardium. Specialities of blood
supply of heart. The main physiological
features of heart function. Principle of
operation of the electrocardiograph.
Technique of record of an
electrocardiogram in three standard
leads. Principal components of an
electrocardiogram.
The classification of coronary heart disease. There are 4 main types clinical
manifestations of coronary heart disease.
1. Stenocardia (angina pectoris)
a) Stenocardia of the stress;
b) Stenocardia of the rest
30

2. Myocardial infarction
3. Intermediate variants
a) Acute focal myocardial dystrophy;
b) Small focal myocardial infarction
4. Indolence CHD
a) Silent (asymptomatic) CHD;
b) Atherosclerotical cardiosclerosis
1. Features of coronal circulation of blood and metabolism of cardiac muscle.
2. Classification of coronary heart disease. CHD: determination, reasons and terms of
origin, form.
3. Ischemic heart disease. Definition of the notion, risk factors, mechanisms of
development.
4. Sudden coronary death: reasons, mechanisms of origin.
5. Angina pectoris: classification, pathogenesis of displays.
6. Heart attack of myocardium: kinds, description of functional and biochemical
violations in a cardiac muscle, mechanisms of pain syndrome.
7. Mechanisms of origin of spasms of coronary vessels.
8. Complication of heart attack of myocardium. Pathogenesis of cardiogenic shock.
9. Experimental models of heart attack of myocardium.
10. Dressler’s syndrome, hibernal myocardium, methods of diagnosis, main
manifestations (blood tests, coagulogramm, ECG, SCG.
11. Noncoronary damages of myocardium: reasons, mechanisms of development.
12. Damage of pericardium. Cardiac [pericardial] tamponade: reasons, displays,
mechanisms of indemnification.
Protocol № 5 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:________________________________________________________
31

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:________________________________________________________
Test 1. A 48-year-old patient after severe psychoemotional exertion
suddenly began feeling sharp pain in the heart region, irradiating into left
arm. Nitroglycerin releaved pain 10 minutes later. What pathogenetic
mechanism is responsible for the development of pain in this case?
A. Compression of coronary vessels
B. Spasm of coronary vessels
C. Dilation of peripheral vessels
D. Occlusion of coronary vessels
E. Increase of myocardial needs in oxygen
Test 2. A patient presents high activity of LDH1,2, aspartate
aminotransferase, creatine phosphokinase. In what organ (organs) is the
development of a pathological process the most probable?
A. In the heart muscle (initial stage of myocardium infarction)
B. In skeletal muscles (dystrophy, atrophy)
C. In kidneys and adrenals
D. In liver and kidneys
E. In connective tissue
Test 3. 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 4. A patient suffering from stenocardia was taking nitroglycerine
which caused restoration of blood supply of myocardium and relieved pain
in the cardiac area. What intracellular mechanism provides restoration of
energy supply of insulted cells?
A. Intensification of RNA generation
B. Intensification of ATP resynthesis
C. Intensification of oxygen transporting into the cell
D. Increased permeability of membranes
E. Reduction of ATP resynthesis
32

Test 5. A patient in three weeks after acute myocardial infarction has
pain in the heart and joints and pneumonia. What is the main mechanism
of development of post-infarction Dressler’s syndrome?
A. Ischemia of myocardium
B. Vessels' thrombosis
C. Secondary infection
D. Autoimmune inflammation
E. Resorption of enzymes from necrotized area of myocardium
Practice examination type 2. Give answers to the questions of the real-
life tasks:
Task 1. The 24 years patient has addressed to clinic with the complaints to headache,
back pain, face edema, weakness. All previous years patient felt healthy but month before
hospitalization he has transferred tonsillitis. Data of inspection for hospitalization: amount
of erythrocytes – 3,1∙1012
/l, amount of leucocytes – 12,6∙109
/l, erythrocytes sedimentation
rate – 28 mm/hours, heart rate – 115/min, arterial pressure – 160/125 mm hg. In urine
expressed proteinuria, microhematuria, leukocyteuria. 1. What type of hypertension does
patient suffer from? 2. Explain the reason and mechanism of hypertension development in
this case.
Answer for the task:____________________________________________________
Task 2. After transferred 3 months back anginas patient begin to be disturb by
dyspnea, gravity in the right hypochondrium, attacks of difficult breathing. The edemas of
the lower extremitis have appeared. At objective examination: dermal covers with icteric
color, lips cyanotic, leg swollen. The cervical veins are pulsing. The borders of heart are
enlarged for expense of both ventricles, however it is more left. Arterial pressure – 90/60
mm Hg. A respiration rate - 26/min. The myocarditis, cardiovascular insufficiency in stage
of compensation is detected. 1. What cause the damage of the myocardium in this patient?
2. What disorder testifies about heart insufficiency? 3. Explain their pathogenesis? 4. What
changes have compensatory – adaption significance? 5. What is their mechanism?
Answer for the task:____________________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – V: Nova Knuha Publ – 2011. – P. 472-476.
1. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, J L. Banasic // Elsevier Inc. – 2010. – P. 448–460.
Additional:
edition. Copyright В. – Lippincott Williams &
Wilkins – 2008. – Chapter 13. – P. 345–347, 460–462.
33

4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and
practitioners. Edited by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 212–216.
1. Faller A., Schunke M.,Schunke G.The Human body: An Introduction to Structure and Function. – NY.–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
Topic 6. Pathology of vascular tone. Hypertensive disease.
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.
3.Aim: To pay attention of students to prevalence of defeat of vessels of resistive and
capacitive types. To expose the mechanisms of different types of hypertension with the
purpose of understanding of their pathogenesis in a clinic. To familiarize with the basic
experimental models of hypertension.
To know:
- basic types of symptomatic hypertension, their reasons, mechanisms of development;
- etiology, pathogenesis, complication of hypertensive illness;
- basic experimental models of hypertension.
To be able:
- to explain the mechanisms of increase of arterial pressure at different hypertension;
- to differentiate symptomatic hypertension and hypertensive illness.
A task for independent extracurricular work:
To think over the followings theoretical questions:
1. Mechanisms of regulation of vascular tone.
2. Functions of kidneys in regulation of blood pressure.
3. Methods of measuring of arterial pressure.
To perform practical work: to analyse the pathogenesis of the hypertension and
hypotension.
4. Basic level.
1. histology
2. biochemistry
3. physiology
5. intencive care
Histological structure of vessels wall.
Vascular tone.
Arterial pressure: the factors, defining it level.
Regulation of vascular tone and blood pressure.
Concept about the functional system of blood circulation.
Determinants of Blood Pressure
The systolic and diastolic components of blood pressure are determined by
the cardiac output and the peripheral vascular resistance and can be expressed as
34

a product of the two (blood pressure = cardiac output x peripheral vascular
resistance). The cardiac output is the product of the stroke volume (amount of
blood ejected from the heart with each beat) and the heart rate. The peripheral
vascular resistance reflects changes in the radius of the arterioles as well as the
viscosity or thickness of the blood. The arterioles often are referred to as the
resistance vessels because they can selectively constrict or relax to control the
resistance to outflow of blood into the capillaries. The body maintains its blood
pressure by adjusting the cardiac output to compensate for changes in peripheral
vascular resistance, and it changes the peripheral vascular resistance to
compensate for changes in cardiac output.
1. Factors which predetermine the level of blood pressure for a man, basal
tone of vessels.
2. Pressor and depressor systems of organism, their description.
3. Arterial hypertensions: kinds, classification. Levels of blood pressure
elevation.
4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.
5. Etiology and pathogenesis of endocrinal hypertension.
6. A role of the sympathetic nervous system in pathogenesis of neurogenic
hypertension.
7. Salt hypertension: etiology, mechanisms of development.
8. Etiology and pathogenesis of essential hypertension. Complications of an
essential hypertension.
9. Reasons and mechanisms of arterial hypotension.
Protocol № 6 Date_____________________
Practical work 1. Study a role of the sympathetic and parasympathetic
nervous system in regulation of vascular tone (determination of Kerdyu
index). Measure arterial pressure on a hand, count up the number of cardiac
reductions. The index of Kerdyu (ІК) is calculated after a formula:
dyastolicBP
rateheart
IK
⋅
−=1 ; Norm of ІК = 0
The index of Kerdyu with the sign of “+” testifies to advantage of
sympathetic influences on a heart, and with the sign of “-“ – about
predominance of the parasympathetic influencing. The index of Kerdyu must be
calculated in the state of rest and after the physical loading.
To conduct such research for all students of group.
Conclusion: ___________________________________________________________
35

Practical work 2. Arterial hypertension. Watching 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 hypertention is caused by the stenosis of the renal
arteries in the patient. Activation of what system is the main link in the
pathogenesys of this form of hypertension?
A. Parasympathetic
B. Kallikrein-kinin
C. Renin-angiotensin
D. Sympathoadrenal
E. Hypothalamic-pituitary
Test 2. In response to a change in body position from horizontal to
vertical blood circulation system develops reflectory pressor reaction.
Which of the following is its compulsory component?
A. Weakening of the pumping ability of heart
B. Decrease in the circulating blood volume
C. Increase in the heart rate
D. Systemic dilatation of the arterial resistive vessels
E. Systemic constriction of the venous vessels
Test 3. A 43-year-old-patient has arterial hypertension caused by
increase in cardiac output and general peripheral resistance. Specify the
variant of hemodynamic development of arterial hypertension in the given
case:
A. Hyperkinetic
B. Eukinetic
C. Hypokinetic
D. Combined
Test 4. An aged man had raise of arterial pressure under a stress. It
was caused by activation of:
A. Sympathoadrenal system
B. Functions of thyroid gland
C. Hypophysis function
D. Functions of adrenal cortex
E. Parasympathetic nucleus of vagus
Test 5. An adult man presents with systemic arterial pressure drop
from 120/70 to 90/50 mm Hg. This resulted in reflex vasoconstriction.
Vasoconstriction will be minimal in the following organ:
A. Bowels
B. Liver
C. Heart
D. Skeletal muscles
E. Skin
life tasks:
36

Task 1. The 24 years patient has addressed to clinic with the complaints to
headache, back pain, face edema, weakness. All previous years patient felt
healthy but month before hospitalization he has transferred tonsillitis. Data of
inspection for hospitalization: amount of erythrocytes – 3,1∙1012
/l, amount of
leucocytes – 12,6∙109
/l, erythrocytes sedimentation rate – 28 mm/hours, heart
rate – 115/min, arterial pressure – 160/125 mm hg. In urine expressed
proteiuria, microhematuria, leukocyteuria. 1. What type of hypertension does
patient suffer from? 2. Explain the reason and mechanism of hypertension
development in this case.
_____________________________________________________________________
Task 2. The patient has arrived on an inspection. There is durable and
stable increase of arterial pressure in anamnesis. They revealed in the patient
lowering concentration of renin in blood, increase of extracellular liquid
volume, increase of Na ions concentration and decrease of K one in saliva. The
treatment by saluretics has given positive result.
1. Analyse clinical biochemical parameters.
2. What mechanism of hypertension does testify it about (activation of
angiotensin synthesis or increase secretion of mineralocorticoids?
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology/Ed.by A.V.Kubyshkin–Vinn:NovaKnuha Publ–2011.–P.478–489.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne Publ. – 2010. – P. 372–387.
3. CopsteadL-E.C. Pathophysiology / L-E.C.Copstead, J.L.Banasic // ElsevierInc.–2010.–P. 374–395.
4. Pathophysiology, Concepts of Altered Health States/ C.M.Porth, G.Matfin.–NY,M.–2009.–P.50–532.
Norman D. Harris // IL 60030-7820, 3rd
edition, USA. – 2008. – Ch.4. – P. 208–234.
& Wilkins – 2008. – Chapter 13. – P. 399–412, 426–427, 431–435.
ed./Kumar,Abbas,Fauto.–2007.–Ch.11.–P.398–400.
Additional:
and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 222–229.
(2003) / Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 16 – P. 274–290.
2. Silbernagl S.Color Atlas of Pathophysiology/S.Silbernagl,F.Lang//Thieme.Stutt.NY.–2000.–P.206–215.
Topic 7. Pathophysiology of the external respiration.
37

The actuality of the theme. The major function of the lungs is to oxygenate and
remove carbon dioxide from the blood as a means of supporting the metabolic functions of
body cells. The gas exchange function of the lungs depends on a system of open airways,
expansion of the lungs, an adequate area for gas diffusion, and blood flow that carries the
gases to the rest of the body. This chapter focuses on diseases that disrupt ventilation and
gas exchange and on respiratory failure and hyperventilation.
Respiration insufficiency is a pathologic process developing due to the disturbance of
the external respiration. In respiration in sufficiency the maintenance of gas contents
adequate to organism requirements isn't ensured. Even at rest respiration insufficiency
may lead to hypoxia and gaseous acidosis or limit the organism abilities as fulfill physical
work. The main mechanisms of respiration insufficiency development consist in
disturbances of ventilation, perfusion, diffusion as well as their quantitative ratio.
3. Aim: To form understanding of mechanisms of violation of adjusting of the
external breathing for students, essence of pathological and protective-adaptive changes in
an organism, which arise up subject to the condition respiratory insufficiency.
To know: Characterize the periodical breath. Strenuous exercise or metabolic acidosis
induces Kussmaul respiration or hyperpnea. Kussmaul respiration is characterized by a slightly
increased ventilatory rate, very large tidal volumes, and no expiratory pause. Cheyne — Stokes
respirations are characterized by alternating periods of deep and shallow breathing. Apnea,
cessation of breathing lasting from 15 to 60 seconds, is followed by increased ventilation after
which ventilation decreases again to apnea. Cheyne — Stokes respirations occur in any
condition due to the slowing down of the blood flow to the brain stem or slowing down the
impulses causing death of the respiratory centers of the brain stem.
- reasons and types of respiratory insufficiency;
- pathophysiological variants of shortness of breath, mechanisms of their
development;
- types of the periodic and terminal breathing.
To be able: to analyse the mechanisms of the obstructive pulmonary diseases.
1. Basic processes which provide efficiency of the external breathing.
2. To explain the role of reflex of Gering-Breyer in adjusting of the external
breathing.
3. To interpret the adjusting of the external breathing.
4. To explain influence of change of frequency and depth of the external breathing on
its efficiency.
To perform practical work: to analyse the mechanisms of the pulmonary defenses.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
Lung defense mechanisms. The non-respiratory function
of the lungs. The structure of a normal bronchiole. The
normal structures of the acinus.
Microscopic structure of the alveolar wall.
TABLE. Lung Volumes and Capacities
38

Volume Symbol Measurement
Tidal volume (about 500
mL at rest)
TV
Amount of air that moves into and out of the lungs
with each breath
Inspiratory reserve
volume (about 3000 mL)
IRV
Maximum amount of air that can be inhaled from
the point of maximal expiration
Expiratory reserve
volume (about 1100 mL)
ERV
Maximum volume of air that can be exhaled from
the resting endexpiratory level
Residual volume (about
1200 mL)
RV
Volume of air remaining in the lungs after maximal
expiration. This volume cannot be measured with
the spirometer; it is measured indirectly using
methods such as the helium dilution method, the
nitrogen washout technique, or body
plethysmography.
Functional residual
capacity (about 2300 mL)
FRC
Volume of air remaining in the lungs at end-
expiration (sum of RV and ERV)
Inspiratory capacity
(about 3500 mL)
IC Sum of IRV and TV
Vital capacity (about
4600 mL)
VC
Maximal amount of air that can be exhaled from the
point of maximal inspiration
Total lung capacity (about
5800 mL)
TLC
Total amount of air that the lungs can hold; it is the
sum of all the volume components after maximal
inspiration. This value is about 20% to 25% less in
females than in males.
1. Respiratory insufficiency: determinations, basic kinds.
2. Obstructive and restrictive forms of respiratory insufficiency.
3. A role of violations of alveolar-capillary diffusion is in pathogenesis of respiratory
insufficiency.
4. A role of violation of perfusion of lungs and ventilating relations is in the origin of
the mixed type of breathing insufficiency.
5. Shortness of breath: determinations, kinds.
6. Bradipnoe, hyperpnoa, tachypnoa: reasonsand pathogenesis.
7. Mechanisms of shortness of breath are at the damage of parenchyma of lungs
(inflammation, was swollen).
8. Apnoe: definition, mechanisms of origin.
9. Inciter and expiration shortnesses of breath.
10. Periodic and terminal breathing: kinds, pathogenesis.
Protocol № 7 Date_____________________
Experimental work 1. Reflex apnoe at annoying the receptors of
mucus shell of overhead respiratory tracts. A rabbit is fixed to the preparing
dinner-wagon. Respiratory motions register by a kymograph. At the same time
by electrocardiograph write down cardiac activity.
39

In a role of irritant of receptors of mucus shell of overhead respiratory
tracts use an ammonia. After normalization of breathing in nasal motions bury
for 3-4 drops of a 0,5% solution of tetracaine (one drop through 1 min). Repeat
experience with an ammonia. Pneumogram sketch in protocol of experience.
Conclusion: ____________________________________________________________________________
Experimental work 2. A change of breathing rhythm is at the edema of
lungs. It is carried out test on two mice, it is desirable one weight. For them
count up the amount of breathings, and then a 0,1% solution of adrenalin is
entered hypodermic one mouse from the calculation of 0,2-0,3 ml per 100 g of
mass. Look after the common state of animal and through each 5 min. Count
up the amount of breathings. Through 40-50 min. both mice to decapitate,
unseal a thorax, pick out lights, weigh them on weight and determine a
pulmonary coefficient - relation of mass of lungs in mg to mass of body in
grammas.
Conclusion: ____________________________________________________________________________
Practical work 3. Watching movie about experimental respiratory
pathology in rats with discussing types of periodical and terminal
respiration. According to the documental movie students should graphicaly
paint types of periodical and terminal respiration (like in page 20-21 of this
methodical instruction), make conclusions.
Conclusion: ____________________________________________________________________________
Test 1. A 12 y.o. boy, who suffers from bronchial asthma, has an acute
attack of asthma: evident expiratory dyspnea, skin pallor. What type of
alveolar ventilation disturbance is it?
A. Throracodiaphragmatic
B. Central
C. Obstructive
D. Restrictive
E. Neuromuscular
Test 2. Lung of premature infant is presented on electronic
photomicrography of biopsy material. Collapse of the alveolar wall caused
by the deficiency of surfactant was revealed. Disfunction of what cells of
the alveolar wall caused it?
40

A. Fibroblasts
B. Alveolar macrophages
C. Secretory cells
D. Alveocytes type II
E. Alveocytes type I
Test 3. A 23 year patient was admitted to the hospital in grave
condition with craniocerebral trauma. His respiration is characterized by
a spasmodic long inspiration interrupted by a short expiration. What
respiration type is it typical for?
A. Apneustic
B. Cheyne-Stokes respiration
C. Gasping
D. Biot's respiration
E. Kussmaul's respiration
Test 4. Premature infants have syndrome of respiratory failure.
Failure of what aerohematic barriere component underlies this pathology?
A. Surfactant B. Alveolocytes
C. Basal membrane of alveolocytes
D. Basal membrane of endothelium
E. Capillary endothelium
Test 5. A 62 year old patient in grave condition was admitted to the
neurological department on account of cerebral hemorrhage. Objectively:
hyperpnoe and rising of respiratory rate, then it falls to apnea, after that
the cycle of respiratory movements restores. What respiratory type is it?
A. Kussmaul's respiration
B. Apneustic
C. Biot's respiration
D. Gasping respiration
E. Cheyne-Stokes respiration
life task:
Task. In the patient, who was on surgical table under narcosis, the sharp
oppression of breath has occured. The pulse has become rare and weak,
appeared cyanosis. The emergency measures accepted by the anaesthesiologist,
liquidated these disorders. 1. What can be connected the oppression of breath
with? 2. How, on yours opinion, the contents of oxygen and carbonic acid in
arterial of blood was changed in the patient? 3. Explain appearance of the
cyanosis. 4. How are you evaluating changes of the pulse in this case?
Answer for the task:____________________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – V: Nova Knuha Publ – 2011. – P. 500–519.
41

3. Copstead Lee-Ellen C. Pathophysiology / Lee-E. C. Copstead, J. L. Banasik // Elsevier Inc, 4th ed. – 2010.– P. 510–591.
Additional:
& Wilkins – 2008. – Chapter 14. – P. 464–514.
and practitioners. Edited by prof .Zaporozan, OSMU. – Odessa. – 2005.– P. 198–206.
(2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Chapter 19, 20. – P. 339–376.
4. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart. New York. – 2000. – P. 66–92.
Topic 8. Hypoxia.
1. Actuality of the theme. The study of hypoxia takes important place in
pathophysiology, so as accompanies almost all illnesses of man. A division of hypoxia is
on hypoxic, respiratory, circulatory, and urgent and the mixed is represented by the wide
circle of diseases which arises up at. A lot of types of professional activity are also related
to development of hypoxia. The study of pathogenesis of hypoxia, protective-adaptive
mechanisms and pathological changes is important for the choice of pathogenetic therapy
of the hypoxic states. Professional selection of high-resistant to hypoxia people, and also
adaptation to an oxygen insufficiency become relevant problem of medicine.
3. Aim: to study causes and pathogenesis of hypoxic conditions development and
mechanisms of compensatory and pathogenic reactions of organism in hypoxia, ways of
their pathogenetic correction.
To know: types of hypoxia (hypoxic, respiratory, haemic, circulatory, tissue and
combined hypoxia).
To be able: to analyse of the two stages of hypoxia-compensation and
decompensation specific and non-specific reactivity.
To perform practical work: to analase the causes of oxygen deficiency
4. Basic level.
1. Histology
2. Biochemistry
3. Physiology
4. Internal medicine
Indexes of respiratory function blood.
Construction of hemoglobin. The mechanism of
oxygen transport by hemoglobin. Enzymes of
respiratory chain. The mechanisms of transport of
electrons on respiratory chain.
Systems of oxygen supply of organism: system of external respiration - blood
system - circulatory system - microcirculatory vessels - tissues and cells.
Oxygen cascades of organism:
•Atmospheric air – pO2 - 160 mm Hg.
•Alveoli - pO2 - 100 mm Hg (13.6 kPa).
42

•Arterial blood - pO2 - 85-95 mm Hg (13.3 kPa).
•Mixed venous blood - pO2 - 40-50 mm Hg (5.3 – 6.7 kPa).
•Tissues - pO2 - 5-20 mm Hg (0.7 – 2.7 kPa).
•Hemoglobin (Hb) is protein with a molecular weight of 64800 Dalton. It
consists of four subunits containing Fe++
. Each of four molecules of Fe++
binds one
molecule of O2 (1 Mol Hb binds 4 Mol O2 or 1g Hb can attach 1.38 ml O2).
1. Hypoxia. Definition of the concept. Principle of classification of hypoxic
conditions.
2. Mechanisms of development of hypoxia: reduction of delivery of oxygen and
disorders of its utilization by cells.
3. Etiology and pathogenesis of the basic types of hypoxia: hypoxic, respiratory,
circulatory, hemic, tissue. Mixed forms of hypoxia.
4. Parameters of gas structure of arterial and venous blood at various types of oxygen
starvation.
5. Emergent and long-time adaptive reactions of the organism in hypoxia.
6. Mechanisms of hypoxic damage of cells. Pathogenesis of hypoxic necrobiosis.
7. Resistance of individual organs and tissues to hypoxia.
8. Oxygen therapy. Iso- and hyperbaric oxygenation.
9. Toxic effect of oxygen. Hyperoxia and free-radical reactions. Hyperoxia as a cause
of hypoxia.
Protocol № 8 Date_____________________
Experimental work 1. To of hemic by poisoning smoky gas. Mixture
serves as a source of smoky gas from equal parts of sulphuric and formic acids,
which is placed on the bottom of desiccator. Acids cover a grate, place on a rat
and densely close desiccator by lid, during 25-30 min. watch on the state an
animal (shortness of breath, cramps, death). At a section pay attention to the
color of blood and internal organs (raspberry blood) [crimson blood], as a
result of formation of carboxyhemoglobin).
Conclusion: __________________________________________________________
Experimental work 2. A express-method of determination of
carboxyhemoglobin is in blood. On subject glass inflict the drop of blood of
intact rat, and alongside drop blood of rat which poisoning smoky gas. To
every drop of blood add a 2% solution of sulphuric copper [bluestone] on a 1
43

drop, mixed them. After 1 minute the drop of blood of experimental rat
acquires a rich redder raspberry colour, and normal blood is greyish brown.
Conclusion: __________________________________________________________
Test 1. A 65-year-old patient suffers from aortic valve stenosis. She has
symptoms of heart failure such as dyspnea, cyanosis, and edema that
appeared after viral infection. She was admitted to the therapeutic
department. Which type of hypoxia is in the patient?
A. Tissue
B. Hemic
C. Circulatory
D. Respiratory
E. Mixed
Test 2. A 70-year-old patient underwent medical treatment for
ischemic heart disease, heart failure in cardiological department. Which
type of hypoxia was in the patient?
A. Tissue
B. Hemic
C. Circulatory
D. Respiratory
E. Mixed
Test 3. A 13-year-old girl undergoes treatment for iron-deficiency
anemia in hematological department. Which type of hypoxia does this
patient have?
A. Tissue
B. Hemic
C. Circulatory
D. Respiratory
E. Mixed
Test 4. A 56-year-old woman suffers from thyrotoxicosis for a long
time. Which type of hypoxia can develop in this patient?
A. Tissue
B. Hemic
C. Circulatory
D. Respiratory
E. Mixed
Test 5. Group of tourists ascended to the altitude of 4200 m. Three
alpinists complained of headache, pain in their ears and frontal sinuses,
somnolence, considerable muscular weakness, irritability during the
ascent. The possible reason for appearance of these symptoms was:
A. Gas saturation in blood
B. Hyperbaric oxygenetion
C. Caisson disease
D. Altitude sickness
E. Altitude decompression
life tasks:
Task . In one of the members of high-mountainous expedition the erose
increasing and deepening of breath has occured which was replaced by a
sudden oppression it and loss of consciousness. 1. Explain the mechanism of
increasing and deepening of breath for want of rise on height. 2. Why
44

stimulation of breath was replaced it by an oppression? 3. How the acid-base
balance in the climber was changed which has suffered? 4. What for him is
better - inhalation of pure oxygen or carbogen?
Answer for the task 1:__________________________________________________________________
Signature___________________
Literature:
Basic:
1. General and clinical pathophysiology / Ed. by A.V. Kubyshkin – V: Nova Kn.P. – 2011. – P. 121–134.
2. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS M-ne Publ. – 2010. – P. 160–174.
3. Copstead Lee-Ellen C. Pathophysiology / Lee-E. C. Copstead, J. L. Banasik // Elsevier Inc, 4th ed. – 2010. – P. 529–530.
4. Pathophysiology, Concepts of Altered Health States, C. M. Porth, G. Matfin.– NY, Milwaukee. – 2009. – P. 998–1007.
Additional:
and practitioners. Ed. by prof. Zaporozan, OSMU. – Odessa. – 2005.– P. 115–122.
(2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Chapter 19. – P. 351–356.
3. Silbernagl S. Color Atlas of Pathophysiology / S.Silbernagl, F.Lang // Th.St.NY.– 2000. – P. 122–131.
Topic 8. Pathology of the digestive system.
Etiology and pathogenesis of peptic ulcer.
1. The actuality of the theme. Number of patients, which suffer the different
diseases of stomach of, which are accompanied disorders of digestion, grows constantly,
resulting in the decline of capacity, invalidity of people. These diseases often cases death.
One of important and most early violations of functions of stomach there is violation of
gastric secretion, which can develop as a result of violation of the neuroendocrine
regulation, and also at pathological processes in a stomach. Secretory disorders of stomach
are characterized both quantitative and high-quality changes. Knowledge of basic
disorders of gastric secretion, high-quality changes of gastric juice, enables correctly to
conduct a prophylaxis and rational therapy of secretory disorders of stomach.
3. Aim: Explain reasons and pathogenetic mechanisms of violation of digestion in a
mouth cavity, stomach.
To know: structure and function of the digestive system; mechanisms of action of
digestive enzymes; basic mechanisms of the neuro-humoral regulation of function of the
digestive system; - normal types of gastric secretion;
To be able:
- to analyse the mechanism of development of hypo- and hypersecretion, hypoacidity
and hyperacidity states;
- to apply the got knowledges about the mechanisms of disorders of digestion in a
stomach for the correct understanding of their role in pathogenesis of diseases of gastro-
intestinal pathway.
A task to independent extracurricular work:
45

Describe component of saliva. Explain the process of digestion in the mouth of
cavities. Describe components of gastric juice. To interpret and explain the mechanisms of
regulators of gastric secretion. Physiology of digestion is in a duodenum and intestine.
External secretion of pancreas. Composition of bile and its role is in the processes of
digestion. A concept is about parietal digestion and cavity digestion in an intestine.
Mechanisms of suction of matters are in the different departments of digestive pathway.
To perform practical work: to analyse the mechanisms of the acute and chronic
gastritis.
4. Basic level.
future disciplines
1. histology
2. biochemistry
3. physiology
4. stomatology
Structure of gastrointestinal tract.
Digestion in stomach.
Digestion in an oral cavity.
List sequentially the parts of the alimentary canal from mouth to anus.
Table. Sites of and Requirements for Absorption of
Dietary Constituents and Manifestations of Malabsorption
Dietary
Constituent
Site of
Absorption
Requirements Manifestations
Water and
electrolytes
Mainly small
bowel
Osmotic gradient
Diarrhea
Dehydration
Cramps
Fat
Upper
jejunum
Pancreatic lipase
Bile salts
Functioning lymph
Weight loss
Steatorrhea
Fat-soluble vitamin deficiency
Carbohydrates
• Starch
• Sucrose
• Lactose
• Maltose
• Fructose
Small
intestine
Small
intestine
Small
intestine
Small
intestine
Small
intestine
Amylase
Maltase
Isomaltase α-dextrins
Sucrase
Lactase
Maltase
Diarrhea
Flatulence
Abdominal discomfort
Protein
Small
intestine
Pancreatic enzymes
(e.g., trypsin,
chymotrypsin, elastin)
Loss of muscle mass
Weakness
Edema
Vitamins
• A Upper
jejunum
Bile salts Night blindness
Dry eyes
46

• Folic
acid
• B12
• D
• E
• K
Duodenum
and jejunum
Ileum
Upper
jejunum
Upper
jejunum
Upper
jejunum
Absorptive; may be
impaired by some
drugs (i.e.,
anticonvulsants)
Intrinsic factor
Bile salts
Bile salts
Bile salts
Corneal irritation
Cheilosis
Glossitis
Megaloblastic anemia
Glossitis
Neuropathy
Megaloblastic anemia
Bone pain
Fractures
Tetany
Uncertain
Easy bruising and bleeding
Calcium Duodenum
Vitamin D and
parathyroid hormone
Bone pain
Fractures
Tetany
Iron
Duodenum
and jejunum
Normal pH
(hydrochloric acid
secretion)
Iron-deficiency anemia
Glossitis
1. List sequentially the parts of the alimentary canal from mouth to anus.
2. Caries. Etiology. Pathogenesis. Prevention.
3. Paradontitis. Etiology. Pathogenesis. Prevention.
4. Describe the structure and function of the esophagus, stomach.
5. Characterize the common signs and symptoms of gastrointestinal dysfunction.
6. Compare the various disorders of digestive motility.
7. Hormonal and secretory function of GIT, digestion and absorbtion.
8. Types of violations of secretory function of stomach. Etiology and pathogenesis of
chronic gastritis’s (type A, B, C). Reasons and displays of violations of motive and suction
function of stomach.
9. Etiology of ulcerous illness of stomach and duodenum. A role of aggressive and
protective factors in ulcer creating.
10.A role of emotion and stresses in pathogenesis of ulcerous illness. A value of local
factors in pathogenesis of ulcerous illness (violation of diet and inherited inclinations).
11.Theories of pathogenesis of ulcerous illness. Experimental design of ulcerous illness.
Protocol № 9 Date_____________________
Experimental work 1. Recreate in the rat of stress damage of stomach.
To the rat which starved 24 hours, enter mixture of alcohol and hydrochloric
acid in correlation 1:1 by probe. Then the rat immobilize during 2 hours. Then
47

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