Circulation 2016

EUROPOS SJUNGA
Europos Socialinis Fondas
Program of Medicine Studies
MODULE
CIRCULATION
Second Year
Fourth Semester
Faculty of Medicine
Kaunas University of Medicine
Contents
1. General information...................................................................................................5
2. General content of the module...................................................................................6
3. Aim and objectives of the module..............................................................................6
4. Tutorials......................................................................................................................7
4.1. Case 1. Breathless artist......................................................................................7
Aim.......................................................................................................................8
Learning objectives and contents..........................................................................8
4.2. Case 2. Rapid heart beating..............................................................................12
Aim.....................................................................................................................13
Learning objectives and contents........................................................................13
4.3. Case 3. Lamely smoker....................................................................................16
Aim.....................................................................................................................17
4.4. Case 4. Chest pain............................................................................................20
Aim.....................................................................................................................21
4.5. Case 5. Mysterious pain....................................................................................25
Aim.....................................................................................................................26
4.6. Case 6. Fatigue, fatigue....................................................................................29
Aim.....................................................................................................................30
5. Lectures....................................................................................................................33
5.1. Development and peculiarities of the structure of the heart and blood vessels
(2 hrs).......................................................................................................................33
5.2. Electrical and mechanical activity of the heart (3 hrs).....................................33
5.3 Antiarrhytmic drugs (2 hrs)...............................................................................33
5.4. Heart metabolism in normal and ischemic conditions (2 hrs)..........................34
5.5. Coronary circulation and regulation of local blood flow. Pathophysiological
mechanisms of myocardial ischemia and infarction (3 hrs)....................................34
5.6. Introduction to patient clinical examination. Primary and secondary arterial
hypertension. The main clinical morphological syndromes of cardiovascular
system. Functional syndromes (acute and chronic heart failure) (2 hrs).................35
5.7. Regulation of the fluidity of blood and pathological anatomy of hemostasis (2
hrs)...........................................................................................................................35
5.8. Drugs used in heart failure (2 hrs)....................................................................35
5.9. Types, causes and consequences of bleeding. Temporary and definitive
hemostasis. Hemorrhagic shock (2 hrs)...................................................................36
5.10. Pathological anatomy of the heart failure and insufficiency of peripheral
blood circulation (2 hrs)..........................................................................................36
5.11. Arterial blood pressure regulatory mechanisms and their alterations (3 hrs). 36
5.12. Hypertension disease and symptomatic hypertension. Atherosclerosis (2 hrs)
.................................................................................................................................37
5.13. Drugs used in hypertension. Drugs used in the treatment of angina pectoris (2
hrs)...........................................................................................................................37
5.14. Thrombosis of deep vein. Pulmonary thromboembolism. Understanding
about peripheral arterial disease. (2 hrs)..................................................................38
5.15. ECG disorders of automatism and excitability. Heart conduction
abnormalities. Rhythm disturbances of mixed genesis. Enlargement and
hypertrophy of heart chambers. ECG changes in ischaemic heart disease (2 hrs). .38
5.16. Understanding of ischaemic heart disease: stable angina pectoris unstable
angina pectoris, myocardial infarction. Causes, clinical signs, diagnostic principles.
Understanding of peripheral arterial disease (2 hrs)................................................38
6. Practicals..................................................................................................................39
6.1. Microstructure of the heart wall (2 hrs)............................................................39
6.2. Electrical activity of the heart (4 hrs)...............................................................40
6.3. Mechanical activity of the heart (4 hrs)............................................................41
6.4. Understanding of patient clinical examination (3 hrs).....................................42
6.5. ECG interpretation. Abnormalities of automatism and excitability. Rhythm
disturbances of mixed genesis. Conduction abnormalities. Enlargement and
hypertrophy of heart chambers. (3 hrs)...................................................................42
6.6. Anatomy of arteries of the lower limb (2 hrs)..................................................43
6.7. Microstructure of the wall of the blood vessels (2 hrs)....................................44
6.8. Arterial pulse and blood flow regulation (4 hrs)...............................................46
6.9. Anatomy of heart and coronary circulation (2 hrs)...........................................47
6.10. Anatomy of venous and lymphatic circulation (2 hrs)...................................48
6.11. Primary and secondary hemostasis: determination of bleeding and clotting
time. Microcirculation. Alterations in microcirculation. (4 hrs)..............................49
6.12. ECG changes of myocardial necrosis, damage and ischaemia (3 hrs)...........49
6.13. Peripheral arterial disease and deep vein thrombosis. Pulmonary
thromboembolism (3 hrs)........................................................................................50
6.14. Morphology of the disorders of hemostasis and fluidity of blood (3 hrs)......51
6.15. Bleeding. Temporary and definitive hemostasis. Hemorrhagic shock. (3 hrs)
.................................................................................................................................52
6.16. Regulation of the arterial blood pressure (4 hrs)............................................53
6.17. Pathological anatomy of the heart failure and insufficiency of the peripheral
blood circulation (3 hrs)..........................................................................................53
6.18. Syndromes and diseases of the cardiovascular system (3 hrs).......................54
6.19. Understanding of ischaemic heart disease (stable angina pectoris, unstable
angina pectoris, acute myocardial infarction). Causes, clinical signs, diagnostic
principles. Clinical understanding of cardioechography, exercise ECG,
angiographic examination of cardiovascular system, radiological investigations of
cardiovascular system, chest X-ray picture (3 hrs)..................................................56
6.20. The main cardiovascular syndromes (arrhythmia, arterial hypertension, heart
valvular diseases) (3 hrs).........................................................................................57
6.21. The main functional clinical syndromes of the cardiovascular system (acute
and chronic heart failure). Peripheral arterial disease (3 hrs)..................................57
7. Seminars...................................................................................................................59
7.1. Antiarrhytmic drugs (2 hrs)..............................................................................59
7.2. Metabolism of lipoproteins (2 hrs)...................................................................59
7.4 Drugs used in hypertension, angina pectoris and heart failure (2 hrs)..............60
8. Examination programme..........................................................................................62
1. General information
Supervisor of the module: prof. Edgaras Stankeviius, Department of Physiology

(edgaras@gmail.com)
Coordinator of the module: assoc. prof. Genuvait Civinskien, Department of
Physiology (genuvaite.civinskiene@med.kmu.lt; civgen78@gmail.com)
Subjects and responsible persons:

Human Anatomy (assoc. Prof. Vidmantas Aelis, tel.: 327238, e-mail:
vidmantas.azelis@med.kmu.lt)
Human Histology and Embryology (prof. Angelija Valanit, e-mail:
angval@kmu.lt, assoc. prof. Ingrida Balnyt, tel.: 327282, e-mail:
balnyte@itc.kmu.lt)
Biochemistry (assoc. prof. Ramun Morknien, tel.: 327367, e-mail:
ramunemo@delfi.lt )
Physiology (prof. Edgaras Stankeviius, tel.: 327257, e-mail:
edgaras@gmail.com, assoc. prof. Genuvait Civinskien, tel.: 396053, e-mail:
genuvaite.civinskiene@med.kmu.lt; civgen78@gmail.com)
Pathological Physiology (lect. Dalia Akramien, tel.: 327285, e-mail:
dalia.akramiene@lsmuni.lt)
Pathological Anatomy (prof. Dalia Pangonyt e-mail:
dalia.pangonyte@med.kmu.lt, prof. Romualdas Gailys, tel.: 327013, e-mail:
patanat@kmu.lt)
Pharmacology (assoc. prof. Arvydas Milaius, assoc. prof. Rugil
Pilvinien, tel.: 327242, e-mail: rugile.pilviniene@gmail.com)
Essentials of Medical Diagnosis (lect. Daiva Emilija Rkien, tel.:
306093, e-mail: daiva.rekiene@gmail.com)
General Surgery (prof. Donatas Venskutonis, tel.: 306066, e-mail:
donas@medi.lt)
2. General content of the module
By analyzing the problems of this module the students gain new knowledge and apply
it to the following domains:
Morphology and physiology of the cardiovascular system;
Development of the cardiovascular system and fetal blood circulation;
Stoppage of the bleeding (primary hemostasis) and blood clotting (secondary
hemostasis), principles of treatment of blood loss;
Metabolism of lipoproteins and the peculiarities of the metabolism in the
heart;
Pathology of the cardiovascular system (most common) and
pathophysiological mechanisms;
Fundamentals of drug pharmacology affecting the cardiovascular system;
Essentials of clinical evaluation of the cardiovascular system.
3. Aim and objectives of the module
The student after have studied this module should know how to define, analyze,
explain and relate phenomena to the cases analyzed in the module. Attaining this
aim, students must gain knowledge about the structure, function and disorders in
pathological conditions, mechanisms and principles of their examination and
treatment:
heart as a pump;
conducting system of the heart;
coronary circulation;
arterial circulation;
microcirculation;
lymphatic circulation;
venous circulation;
primary hemostasis and blood clotting;
transport of oxygen (O2) and carbon dioxide (CO2);
fetal blood circulation.
4. Tutorials
4.1. Case 1. Breathless artist
The artist J.D. is 34 years old. When he was 19 years old, during medical
inspection for the military service, the aortic valve insufficiency was found. From
this time he did not feel any signs that could limit his physical activity. However,
6 months ago he has noticed that during active physical exercise (basketball) he
became breathless for a longer than usually time. The breathlessness after each
physical exercise became stronger and stronger. During medical examination, it
was found that the diastolic murmur could be best heard in the second intercostal
space at the right side of the sternum and the systolic murmur at the apex of the
heart. After the chest X-ray examination, it was found that the size of the heart has
significantly increased as compared with the chest X-ray picture of J.D. two years
ago. During echocardioscopic examination, a high degree of aortic regurgitation
and a decrease in cardiac ejection fraction down to 35% (normal 55-75%) were
found.
Medical doctor has proposed J.D. to have a cardiac operation in order to change
the aortic valve. J.D. has agreed and an artificial aortic valve was implanted.
During first hours after the cardiac surgery, dopamine was injected and after 6
hours following the cardiac operation J.D. cardiac output has increased from 3
L/min to 5 L/min.
Please, explain the course and signs of the disease.

What is the mechanism of action of dopamine?
Concept of the problem: heart as a mechanical pump.
Clinical symptoms: dyspnea and cardiac dysfunction.
Aim
To know the structure of the heart and to understand the cardiac mechanical
activity and regulation, morphological and clinical signs of heart valve insufficiency
(regurgitation), mechanisms of action of inotropic drugs and their effect on
electromechanical coupling.
Learning objectives and contents

To complete an analysis of this problem the students must know:
Development of the heart and developmental defects, structure of the heart
wall.
Subject Human Histology and Embryology
Department of Histology and Embryology
References:
L.C. Junqueira, J. Carneiro. Basic Histology. 11th edition. McGraw-Hill
Companies, 2005. p. 217-221.
T.W. Sadler. Langmans Medical Embryology. 10th edition. Lippincott Williams
& Wilkins, 2006. p. 159-180, 189-194.
Supplementary readings:
B. Young, J.S. Lowe, A. Stevens, J.W. Heath. Wheaters Functional Histology.
5th edition. Churchill Livingstone Elsevier, 2006.
D.W. Fawcett, R.P. Jensh. Bloom & Fawcetts Concise Histology. 2nd edition.
Arnold, a member of the Hodder Headline Group, 2002.
www.mc.vanderbilt.edu/histology/labmanual2002/labsection2/Cardiovascular03.htm
www.siumed.edu/~dking2/crr/cvguide.htm
www.portfolio.mvm.ed.ac.uk/studentwebs/session1/group51/ embryology.htm
www.cellbio.emory.edu/courses/medi510/Lecture09.doc
Anatomy of heart valves and heart chambers.

Subject Human Anatomy
Institute of Anatomy
References:
Grays anatomy. The antomical basis of clinical practice. Edinburg-London. 2005. p.
1014-1019.
Peculiarities of the action and electromechanical coupling in the myocardium,
mechanical activity of the heart and cardiac cycle, pressure-volume changes
during the cardiac cycle, preload and afterload, cardiac output and cardiac
index, ejection fraction, work of the heart, origin of the heart sounds and their
origin, phonocardiography, intracardiac and extracardiac regulatory
mechanisms of the heart, factors affecting the cardiac output.
Subject Physiology
Department of Physiology
References:
Review of Medical Physiology. Twenty-third edition. Ganong W.F. Lange Medical
Books, New York, 2010. p. 507-520.
Textbook of Medical Physiology. Eleventh edition. Guyton A.C. and Hall J.E.
Elsevier Saunders, Philadelphia, 2006. p. 103-115, 269-277.
Review of Medical Physiology. Twenty-second edition. Ganong W.F. Lange
Medical Books, New York, 2005. p. 565-576.
Medical Physiology. Eleventh edition. Boron W.F., Boulpaep E.L. Elsevier
Saunders, Philadelphia, 2005. p. 483- 488, 508-513, 519-533, 547.
Effects of increased preload and afterload on mechanical function of the heart,
pathophysiological mechanisms of dyspnea and heart failure.
Subject Pathological Physiology
Institute of Physiology and Pharmacology
References:
Copstead L. E., Banasik J. L. Pathophysiology, Elsevier Saunders. 2013. p. 409
417.
McCance K., Huether S. E. Pathophysiology, Elsevier Mosby. 2010. p. 1189

1196.
Morphological changes of the damaged valves and pathological anatomy of

heart hypertrophy and failure.
Subject Pathological Anatomy
Clinic of Pathological Anatomy
References:
Pathologic Basis of Disease. Robbins and Cotran/Eds I.L. Robbins,R.S. Cotran. 7 th
edition, 2005, p.560-563, 592-597.
Mechanisms of action of inotropic drugs.

Subject Pharmacology
Department of Basic and Clinical Pharmacology
References:
Mycek M. J. Champe P.C. et al. Lippincott's Illustrated Reviews: Pharmacology,
3rd (2nd) edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p. 181-185;
189-193.
Katzung B.G. Basic and Clinical Pharmacology Seventh Edition. Stamford:
Appleton & Lange, 1998, p. 197-213.
Rang H.P. Dale M.M. et al. Pharmacology. Fifth edition. Edinburgh: Churchil Liv-
ingstone, 2003, p.278-279 .
Changes of heart sounds, characteristics of heart murmurs, principles of

echocardiography, changes of arterial blood pressure in aortic valve disease.
Subject Essentials of Medical Diagnostics
Clinic of Internal Diseases
References:
P. Kumar & M. Clark. Clinical medicine. Sixth edition. Elsevier Saunders.
Edinburgh, London, New York, Oxford, Philadelphia, St. Louis, Sydney, Toronto,
2005, p. 738-741, 784-790, 824-825.
E. Baceviius. Propedeutics to internal medicine. Kaunas, 1998.
R. M. Babarskien, R. Benetis, J. Bradionyt, S. Giedraitis, R. Jonkaitien ir kt.
Cardiology. The essentials. 3rd edition. KMU, 2006.
P. Ramrakha, J. Hill. Oxford handbook of cardiology. Oxford University Press,
New York, 2006.
J. S. Alpert, G. A. Ewy. Manual of cardiovascular diagnosis and therapy. Fifth edi-
tion. Lippincott Williams & Wilkins, Philadelphia Baltimore New York London
Buenos Aires Hong Kong Sydney Tokyo, 2002.
E. R. Beck, R. L. Souhami, M. G. Hanna, D. R. Holdright. Tutorials in differential
diagnosis. Fourth edition. Churchill Livingstone. Edinburgh London New York
Oxford Philadelphia St Louis Sydney Toronto, 2003.
L. S. Bickley. Bates Pocket guide to physical examination and history taking.
Fifth edition. Lippincott Williams & Wilkins, Philadelphia Baltimore New York
London Buenos Aires Hong Kong Sydney Tokyo, 2007.
4.2. Case 2. Rapid heart beating
In the evening, 31 years old schoolmistress S.T. during correction of the test of her
pupils drank 3 cups of coffee and felt bad. She had the feeling of rapid heart
beating and pulsation of blood vessels in the neck.
On the next day, the bad feeling has not changed and she went to the doctor.
During medical examination, it was found that the arterial pulse was weak,
frequent, and rhythmical, 180 beats/min. The increased pulsation was found by
palpation of the veins in the neck. On the electrocardiogram (ECG) P waves were
negative before every normal QRS complex, RR intervals were even and short.
The medical doctor did the short compression in the region of the carotid sinus on
the right side of the neck. However, the heart rate did not become normal. Then
the doctor prescribed a fast bolus injection of adenosine intravenously. After the
bolus injection of adenosine, the heart rate became normal and a normal sinus
rhythm was recorded on the ECG.
Please, explain the origin and mechanisms of disorders.

What are the mechanisms of action of carotid sinus compression and bolus
injection of adenosine?
Concept of the problem: cardiac rhythm and impulse propagation in the heart.
Clinical symptoms: tachycardia.
Aim
To understand the automaticity of the heart and regulation, propagation of
electrical impulses in the heart, the origin of the electrocardiogram (ECG) and to
know the mechanisms, clinical signs and diagnostic principles of cardiac arrhythmias,
action of antiarrhytmic drugs.

Anatomy of the conducting system of the heart.
References:
1014-1019.
Cardiac automacity, ionic mechanism of cardiac pacemaker potencial,

propagation of electrical impulse in the heart, nervous and humoral regulation
of the cardiac electrical activity: chronotropic and dromatropic effects, the
origin of the electrocardiogram (ECG), unipolar and bipolar leads of the ECG,
vectorcardiography, electrical axis of the heart.
Subject Physiology
References:
Review of Medical Physiology. Twenty-third edition. Ganong W.F.. Lange
Elsevier Saunders, Philadelphia, 2006. p. 116-140.
Review of Medical Physiology. Twenty-second edition. Ganong W.F.. Lange
Medical Physiology. Eleventh edition. Boron W.F., Boulpaep E.L., Elsevier
Saunders, Philadelphia. 2005. p. 489-499.
Pathophysiological mechanisms of cardiac arrhythmias.

References:
430.

1200.
McPhee S. J., Ganong W. F. Pathophysiology of disease. Introduction to clinical

medicine. McGraw-Hill 2006. p. 269-272.
Mechanisms of action of antiarrhythmic drugs.

References:
3rd edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p. 195-205.
Rang H.P. Dale M.M. et al. Pharmacology.Fifth edition. Edinburgh: Churchil Liv-
ingstone, 2003, 247-278.
Clinical signs and ECG changes in cardiac arrhythmia.

References:
2005, p. 744-749, 770-784.
R. M. Babarskien, R. Benetis, J. Bradionyt, S. Giedraitis, R. Jonkaitien et al.
New York, 2006.
R. Haberl. ECG pocket. 2nd edition. Brm Bruckeier publishing. China, 2006.
4.3. Case 3. Lamely smoker
The patient C.I. is 60 years old and he smokes nearly 40 years 1 pack of cigarettes
per day on the average. Recently he felt the pain in the right ankle and was forced
to stop after 50 meters of the walk. The pain became quiet during the still standing
and C.I. was able to continue walking again for about 50 meters. He complained
that in the nighttime the pain in the right ankle and toes of the right feed awakened
him several times. However, the pain did not become quiet when the patient C.I.
sat in the bed and took the legs down.
During medical examination, the doctor found that pulsations of a. tibialis
posterior and a. dorsalis pedis in the left leg were decreased. In the right leg it
was impossible to feel the pulsations of a. dorsalis pedis. Arterial systolic pressure
in the brachial artery was 160 mmHg, in a. tibialis posterior of the left leg was 90
mmHg, and in a. tibialis posterior of the right leg was 60 mmHg. Blood test: total
cholesterol 6,8 mmol/l (normal < 5,2 mmol/l), high density lipoprotein (HDL)
cholesterol 0,8 mmol/l (normal > 1,0 mmol/l).
Please, explain the course and signs of the disease.

What do you suggest for the treatment of the patient C.I.?
Concept of the problem: peripheral arterial circulation and atherosclerosis.
Clinical symptoms: claudicatio intermittens, cramps of the legs.
Aim
To know the microstructure and anatomy of peripheral arteries and to understand
the regulation of arterial circulation and disturbances of the regulation, metabolism of
lipoproteins and their role in the pathogenesis of atherosclerosis, morphological signs
and sequences, clinical signs and diagnostic principles of peripheral arterial disease.

Anatomy of arteries in the legs.
References:
1. Grays anatomy. The anatomical basis of clinical practice. Edinburgh-London.
2005. p. 1412-13, 1436-37, 1450-51, 1453-54.
2. T.H.Schiebler. W.Schmidt. Anatomie. Berlin-Heidelberg. 1991. p. 376-380.
3. K.L.Moor. Clinical oriented anatomy. Baltimore-Hong Kong. 1985. 450-451.
4. C.D.Clemente. Anatomy. A regional atlas of the human body. Williams & Wilkins.
Philadelphia-Baltimore. 2007. p. 376-426.
Microstructure of the arteries and arterioles.

Subject Human Histology and Embryology
References:
L.C. Junqueira, J. Carneiro. Basic Histology. 11th edition. McGraw-Hill Companies,
2005. p. 205-216.
T.W. Sadler. Langmans Medical Embryology. 10th edition. Lippincott Williams &
Wilkins, 2006. p. 180-194.
B. Young, J.S. Lowe, A. Stevens, J.W. Heath. Wheaters Functional Histology. 5th
edition. Churchill Livingstone Elsevier, 2006.
www.portfolio.mvm.ed.ac.uk/studentwebs/session1/group51/embryology.htm
Metabolism of lipoproteins and their role in the formation of atherosclerosis.

Subject Biochemistry
Department of Biochemistry
References:
1. R.K. Murray, D.K. Granner, P.A. Mayes, V.W. Rodwell. Harpers Biochemistry,
23 ed., Appleton and Lange, Norwalk, Connecticut, 1993, p. 250-258, 271-
273, 275.
2. P.C. Champe, R.A. Harvey, D.R. Ferrier. Lippincotts Illustrated Reviews:
Biochemistry, 3 ed. Lippincott Williams and Wilkins, 2005, p. 225-235.
Physiological characteristics of arterial circulation, arterial pulse and velocity

of arterial pulse, laminar and turbulent blood flow, regulatory mechanisms of
local blood flow.
Subject Physiology
References:
1. Review of Medical Physiology. Twenty-third edition. Ganong W.F. Lange
Medical Books, New York, 2010. p. 535-545, 563-566.
2. Textbook of Medical Physiology. Eleventh edition. Guyton A.C. and Hall J.E.
Elsevier Saunders, Philadelphia, 2006. p. 161-166, 171-174, 195-203.
1. Review of Medical Physiology. Twenty-second edition. Ganong W.F. Lange
2. Medical Physiology, Updated Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadelphia, 2005. p. 426-436, 477-482.
Morphological structure of the atherosclerotic plaques, their kinds,

complications and causes of death.
References:
Pathologic Basis of Disease. Robbins and Cotran/Eds I.L. Robbins,R.S. Cotran. 7th
edition, 2005, p.516-524.
Complaints in chronic limb ischemia, arterial pulse palpation, principles of

vascular ultrasound investigation, clinical signs and diagnostic principles of
peripheral arterial disease.
References:
Edinburgh London New York Oxford Philadelphia St. Louis Sydney Toronto,
2005, p 866-868.
Fifth edition. Lippincott Williams & Wilkins; Philadelphia, Baltimore, New York,
London, Buenos Aires, Hong Kong, Sydney, Tokyo, 2007. p. 240-249.
tion. Lippincott Williams & Wilkins; Philadelphia, Baltimore, New York, London,
Buenos Aires, Hong Kong, Sydney, Tokyo, 2002.
4.4. Case 4. Chest pain
The taxi-driver M.I., 52 years old, is a smoker since the age of 20 years and he
smokes about 20 cigarettes/day. The only physical exercise for M.I. after the job was
to go upstairs to his flat on the second floor. One day M.I. felt the pain on the left side
of the chest when he was going home upstairs. The pain disappered after a few
minutes of rest. Keeping in mind that his father died at the age of 54 years due to the
heart attack, on the next day M.I. went to the doctor. The arterial blood pressure of
M.I. was 145/90 mmHg, pulse rate 76 beats/min, the heart sounds were without
pathological changes, and electrocardiogram (ECG) at rest was normal. The doctor
has prescribed to do the veloergometer exercise test in a month.
Following a few weeks after the medical consultation, M.I. had a hot dispute with
another taxi-driver and suddenly felt a strong pain on the left side of the chest. The
pain spread to the left shoulder and arm. Because the pain did not disappear for 1.5
hour, the co-workers called the emergency medical service. When the ambulance
arrived, the doctor found M.I. excited, sweaty, and breathless. He complained to the
doctor of a strong pain in the chest. The arterial pressure of M.I. was 170/100 mmHg,
pulse rate 84 beats/min. By auscultation of the heart and lungs pathological changes
were not found. On the ECG the elevation of ST segment in the II and III leads was
determined. The patient M.I. was immediately transported to the hospital for the
urgent treatment.
Please, explain what has happened to M.I.?

Please, explain the changes on the ECG and what additional tests are needed for
M.I.?
Concept of the problem: coronary circulation and atherosclerosis.
Clinical symptoms: angina pectoris, dyspnea.
Aim
To know anatomy and regulation of coronary circulation, to understand the
influence of atherosclerosis on coronary circulation, metabolic peculiarities of
ischemic myocardium, mechanisms of action of antianginal drugs, pathogenesis,
clinical signs and diagnostic principles of myocardial infarction.

Anatomy of coronary circulation.
References:
1. Grays anatomy. The anatomical basis of clinical practice. Edinburgh-London.
2005. p. 1014-1019.
4. C.D.Clemente. Anatomy. A regional atlas of the human body. Williams & Wikins.
The principles and regulation of metabolism in the cardiac muscle cells, disor-
ders of metabolism during heart ischemia, basic types and mechanisms of cell
death.
Subject Biochemistry
References:
1. R.K. Murray, D.K. Granner, P.A. Mayes, V.W. Rodwell. Harpers Biochem-
istry, 23 ed., Appleton and Lange, Norwalk, Connecticut, 1993, p. 654-656,
658-660, 760-762.
2. C.M. Smith, A. Marks, M.A. Lieberman. Marks Basic medical biochemistry
2nd ed., 2005, p. 865, 866-869.
3. http://www.celldeath.de/encyclo/aporev/aporev.htm
4. http://www.apoptosisinfo.com/cardiomyocyte-apoptosis/
Functional characteristics of coronary circulation and mechanisms of

regulation.
Subject Physiology
References:
2. Medical Physiology, Updated Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadephia, 2005. p. 558-559, 562-564.
Pathophysiological mechanisms of myocardial ischemia and infarction.

References:
390.

1176.
Peculiarities of atherosclerosis of the coronary arteries, local complications,

inducing developing of the myocardial infarction, its stages, morphology,
References:
edition, 2005, p.571-586.
Characteristics and reasons of angina pectoris and myocardial infarction,

evaluate health history, past history, family history, risk factors, ECG
changes in acute myocardial infarction - necrosis, damage and ischemia,
heart contractility abnormalities in echocardiography, angiographic
changes stenosis or occlusion, myocardial damage markers (troponin T,
troponin I) elevation in unstable angina pectoris and acute myocardial
infarction.
References:
P. Kumar & M. Clark. Clinical medicine. Sixth edition. Elsevier Saunders. Edinburgh
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005, p.798-810.
P. Ramrakha, J. Hill. Oxford handbook of cardiology. Oxford University Press, New
York, 2006.
J. S. Alpert, G. A. Ewy. Manual of cardiovascular diagnosis and therapy. Fifth edition.
Lippincott Williams & Wilkins, Philadelphia Baltimore New York London Buenos
Aires Hong Kong Sydney Tokyo, 2002.
diagnosis. Fourth edition. Churchill Livingstone. Edinburgh London New York Ox-
ford Philadelphia St Louis Sydney Toronto, 2003.
L. S. Bickley. Bates Pocket guide to physical examination and history taking. Fifth
edition. Lippincott Williams & Wilkins, Philadelphia Baltimore New York London
Mechanisms of action of antianginal drugs.

References:
3rd (2nd) edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p. 207-211;
219-221; 221-222.
Appleton & Lange, 1998, 179-194.
Rang H.P. Dale M.M. et al. Pharmacology.Fifth edition. Edinburgh: Churchil Liv-
ingstone, 2003, 270-272.
4.5. Case 5. Mysterious pain
A young woman T.E., 25 years old, called the family doctor following two weeks
after the birth of her first baby. She complained about increasing pain and swelling in
the right calf. Last night she waked up because of a sudden pain in the chest on the
right side and dyspnea. When she was 19 years old, medical doctors diagnosed
pulmonary thromboembolism one month from the onset of using peroral contraceptic.
Her mother died suddenly a few days after her birth. A sister of her mother, who took
care of T.E., had complaints about ulcers her legs.
During medical inspection of T.E., the doctor found that the right calf was cyanotic
and swollen. The measurement with the tape showed that the diameter of the right calf
was bigger than that of the left one. The doctor urgently sent T.E. to the hospital for
the treatment.
Please, explain the complaints of T.E. and the course of the disease.
What treatment do you suggest for T.E?
Concept of the problem: venous circulation and thromboembolism.
Clinical symptoms: leg and chest pain, dyspnea.
Aim
To know the anatomy and physiology of venous circulation, to understand the
microcirculation and hemostasis, clinical signs and diagnostic principles of venous
circulation abnormalities, pulmonary thromboembolism.

Anatomy of venous circulatory system.
References:
1014-1019.
Physiological characteristics of venous circulation and regulatory

mechanisms, mechanisms of blood clotting.
Subject Physiology
References:
2. Medical Physiologt, Updated Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadelphia, 2005. p. 446-446g, 456.
Pathophysiological mechanisms of alterations in microcirculation.

References:
Copstead L. E., Banasik J. L. Pathophysiology, Elsevier Saunders. 2013. p. 314-
331.
McCance K., Huether S. E. Pathophysiology. Elsevier Mosby. 2010. p. 1142-1144,
98-101.
Thrombosis in deep veins of the lower extremity, its causative factors,

clinicomorphological peculiarities of thromboembolism, pathology of right
heart failure.
References:
edition, 2005, p.134-136, 588.
Clinical signs and diagnostic principles of venous circulation abnormalities,

pulmonary thromboembolism.
References:
P. Kumar & M. Clark. Clinical medicine. Sixth edition. Elsevier Saunders. Edin-
burgh, London, New York, Oxford, Philadelphia, St. Louis, Sydney, Toronto,
2005, p. 844-846, 870-871.
New York, 2006.
4.6. Case 6. Fatigue, fatigue
Ms H.F., 72 years old, knows that for about 30 years her arterial blood pressure is
increased, however, she used medicines irregularly. During last few months, she
complained about increased weakness and fatigue in addition to increased dyspnea.
Recently the weather was hot and Ms H.F. could not sleep because of breathlessness,
however, she did not feel any pain in the chest.
Next day she called the doctor because of very expressed fatigue and weakness. The
arterial blood pressure in the brachial artery was found to be 180/115 mmHg, and
pulse rate 130 beats/min. The gallop sounds and systolic murmur in the mitral valve
projection place on the chest were heard on auscultation. Moist rales over the lung
bases were heard on auscultation. Edema of the legs was found by inspection. The
lower margin of the liver was found about 5 cm below the costal arch by palpation of
the abdomen. ECG showed the electrical signs characteristic of left ventricular
hypertrophy. Echocardioscopy showed that the ejection fraction was 30%. The chest
X-ray showed changes characteristic of the left-sided heart failure.
Please, explain the course of the disease and reasons of the fatigue for Ms H.F.
What tests and treatment do you suggest?
Concept of the problem: regulation of arterial blood pressure and chronic heart
failure.
Clinical symptoms: arterial hypertension, chronic heart failure.
Aim
To know the regulation of arterial blood pressure and pathophysiological
mechanisms of arterial blood pressure regulation alterations, to understand the
morphological and clinical signs, complications, diagnostic principles of arterial
hypertension, morphological and clinical signs, diagnostic principles of chronic heart
failure, and mechanisms of action of arterial blood pressure lowering drugs.

Regulatory mechanisms of arterial blood pressure.
Subject Physiology
References:
Review of Medical Physiology. Twenty-third edition. Ganong W.F. Lange
Medical Books, New York, 2005. p. 588-591, 600-610, 630-634.
2. Meidcal Physiology, Updated Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadelphia, 2005. p. 534-547, 554-557.
Pathophysiological mechanisms of arterial blood pressure regulation

alterations.
References:
346, 432-447.
1696 1713.
Primary and secondary hypertension, its mechanism of developing,

peculiarities of systemic damage of the arterioles, morphological damage of
the internal organs, complications and causes of death.
References:
Pathologic Basis of Disease. Robbins and Cotran/Eds I.L. Robbins,R.S. Cotran. 7 th
edition, 2005, p.525-530,587.
Mechanisms of action of arterial blood pressure lowering drugs.

References:
Rang H.P. Dale M.M. et al. Pharmacology. Fifth edition. Edinburgh: Churchil Liv-
ingstone, 2003, 285-300.
Clinical signs, complications, diagnostic principles of arterial hypertension,

the classification of arterial hypertension, clinical signs, diagnostic principles
of chronic heart failure.
References:
2005, p.784-790, 857-861.
New York, 2006.
5. Lectures
5.1. Development and peculiarities of the structure of the heart and

blood vessels (2 hrs)

In charge assoc. prof. I. Balnyt, professor A. Valanit
Description
Structure of the heart wall. Peculiarities of the structure of the epicardium,
myocardium, and endocardium. Microstructure of the heart conducting system.
Development of the heart. Heart developmental defects, their classification and
causes. Classification of the blood vessels. Peculiarities of the structure of the arteries
and veins. Microstructure of the lymphatics. Development of the arteries, veins and
lymphatics. Fetal blood circulation.
5.2. Electrical and mechanical activity of the heart (3 hrs)

In charge lect. I. Korotkich (Physiology), lect. D. Akramien (Pathological
Physiology)
Description
Ionic mechanisms of cardiac automaticity. Propagation of electrical impulse in the
heart. Electromechanical coupling and mechanisms of myocardial contraction and
relaxation. Pressure-volume diagram of cardiac cycle. Parameters of mechanical
activity of the heart. Intracardiac and extracardiac regulatory mechanisms. Factors
controling cardiac output. Pathophysiological mechanisms of the heart failure due to
increased preload and afterload. Compensatory mechanisms. Functional properties of
the hypertrophied myocardium.
5.3 Antiarrhytmic drugs (2 hrs)
In charge - lect. V. Liukaitis, assoc. prof. R. Pilviniene

Description
Antiarrhytmic drugs. Drug classification. Mechanism of action of each drug class,

triggered pharmacological effect are discussed. Information about the properties of the
most important representatives of separate classes of drugs, indications and side
effects are presented.
5.4. Heart metabolism in normal and ischemic conditions (2 hrs)
In charge assoc. prof. R. Morknien
Description
Energy sources and reserves in cardiac muscle cell. Peculiarities of regulation of
energy metabolism in myocardium. Disorders of metabolism in cardiac muscle cell
during ischemia and its consequences. Apoptosis and necrosis main types of heart
cell death. Stages of apoptosis. Enzymes (caspases), its specificity, ways of
activation, substrates. Extrinsic or death receptor pathway of apoptosis. Intrinsic or
mitochondrial pathway of apoptosis.
References:
1. C.M. Smith, A. Marks, M.A. Lieberman. Marks Basic medical biochemistry
2nd ed., 2005, p. 865 - 871, p. 329-331
2. R.K. Murray, D.K. Granner, P.A. Mayes, V.W. Rodwell. Harpers Biochemistry,
23 ed., Appleton and Lange, Norwalk, Connecticut, 1993, p. 654-656,
658-660, 770-776.
3. E. Newsholme. T. Leech. Functional Biochemistry in Health and Disease. 2009. p.
524 527.
5.5. Coronary circulation and regulation of local blood flow.

Pathophysiological mechanisms of myocardial ischemia and
infarction (3 hrs)

In charge lect. A. Laukeviien (Physiology), lect. D. Akramien (Pathological
Physiology)
Description
Local blood flow regulation: metabolic, myogenic and endothelial factors.
Physiological characteristics of coronary circulation, regulatory mechanisms of
coronary flow. Pathophysiological mechanisms of myocardial ischemia and
infarction. Coronarogenic and non-coronarogenic injury of the myocardium.
Reversible and irreversible alterations of cardiac myocytes during myocardial
ischemia.
5.6. Introduction to patient clinical examination. Primary and

secondary arterial hypertension. The main clinical morphological
syndromes of cardiovascular system. Functional syndromes (acute
and chronic heart failure) (2 hrs)

In charge lect. D. E. Rkien
5.7. Regulation of the fluidity of blood and pathological anatomy of

hemostasis (2 hrs)

In charge prof. R.Gailys, prof. V.Lesauskait
Description
Biological essence of thrombosis and mechanisms of its formation, morphology,
outcome, significance; peculiarities in separate parts of blood circulation,
disseminated intravascular coagulation (DIC). Thromboembolism, its peculiarities,
morphology, and significance. Hemorrhage, its mechanisms, morphology,
compensatory mechanisms, outcome, and significance.
5.8. Drugs used in heart failure (2 hrs)
In charge - lect. V. Liukaitis, assoc. prof. R. Pilvinien

Description
Dopamine, dobutamine; cardiac glycosides; inhibitors of phosphodiesterase. Other

drugs used in congestive heart failure (angiotensin antagonists). Mechanism of action
of each drug group, site of effect and triggered pharmacological effect are discussed.
Information about the properties of the most important representatives of separate
classes of drugs, indications and side effects are presented.
5.9. Types, causes and consequences of bleeding. Temporary and

definitive hemostasis. Hemorrhagic shock (2 hrs)
Clinic of general Surgery

In charge prof. D. Venskutonis
Description
Bleeding: causes, classification, consequences. Hemostasis. Preoperative assessment
of hemostasis. Disturbances of blood coagulation, implications on surgical operation.
Syndrome of acute bleeding. Pathogenesis and compensatory mechanisms of central
hemodynamics, microcirculation and tissue metabolism disturbances during acute
bleeding. Hemorrhagic shock, principles of treatment. Blood components. Indications
for transfusion of blood components. First aid for bleeding, ways of temporary and
definitive hemostasis.
5.10. Pathological anatomy of the heart failure and insufficiency of

peripheral blood circulation (2 hrs)

Description
The causes, pathogenetic and compensatory mechanisms, morphology of left-sided,
right-sided and total heart failure. Ischemic factors, compensatory mechanisms,
morphology; kinds of the infarctions, its morphology, outcome, and results,
peculiarities, and significance of the infarctions in different parts of the arterial
system.
5.11. Arterial blood pressure regulatory mechanisms and their

alterations (3 hrs)

In charge lect. A. Laukeviien (Physiology), lect. D. Akramien (Pathological
Physiology)
Description
Neural and humoral regulation of arterial blood pressure. Short-term and long-term
regulatory mechanisms. Baroreceptor reflex, chemoreceptor reflex, ischemic CNS
reaction (Cushing reflex). Rennin-angiotensin-aldosteron system. Action of
antidiuretic hormone (ADH) and atrial natriuretic peptide (atriopeptin). Primary and
secondary arterial hypertension. Arterial blood pressure regulation alterations.
Hypotension. Shock.
5.12. Hypertension disease and symptomatic hypertension.

Atherosclerosis (2 hrs)

Description
The essence, morphology and causes of death of the hypertension disease and
symptomatic hypertension. Atherosclerosis, its essence, morphogenesis, morphology,
peculiarities and significance of main arteries, complications and causes of death.
Sudden coronary death. Cardiomyopathies.
5.13. Drugs used in hypertension. Drugs used in the treatment of

angina pectoris (2 hrs)

In charge - lect. V. Liukaitis, assoc. prof. R. Pilviniene
Description
Nitrates, beta-blockers, calcium blockers; sympatoplegic-blockers of alpha and beta

receptors; vasodilators. Mechanism of action of each drug group, site of effects and
triggered pharmacological effects are discussed. Information about the properties of
the most important representatives of separate classes of drugs, indications and side
effects are presented.
5.14. Thrombosis of deep vein. Pulmonary thromboembolism.

Understanding about peripheral arterial disease. (2 hrs)

In charge - prof. A. Naudinas, lect. E. Kalinauskien
Description
Thrombosis of deep vein: reasons, clinical signs, and diagnostic principles.
Pulmonary thromboembolism. Understanding about peripheral arterial disease:
reasons, clinical signs, and diagnostic principles.
5.15. ECG disorders of automatism and excitability. Heart

conduction abnormalities. Rhythm disturbances of mixed genesis.
Enlargement and hypertrophy of heart chambers. ECG changes in
ischaemic heart disease (2 hrs)

In charge lect. L. Jankauskien
5.16. Understanding of ischaemic heart disease: stable angina

pectoris unstable angina pectoris, myocardial infarction. Causes,
clinical signs, diagnostic principles. Understanding of peripheral
arterial disease (2 hrs)

In charge assoc. prof. P. Leiyt
6. Practicals
6.1. Microstructure of the heart wall (2 hrs)

Description
Aim: 1. To learn and understand the structure of the heart wall.
2. To find out the structure of the conducting system elements of the heart.
3. To find out consistent patterns of the heart development.
Histological micropreparations:
Myocardium. Using high magnification recognize and draw longitudinal
section of the striated cardiac muscle cells cardiomyocytes. These cells are
connected one to other end-to-end by junctional complex intercalated discs.
Distinguish intercalated discs: they are black-staining transverse lines that cross the
chains of cardiac cells at irregular intervals. Cardiac cells can attach to the
neighboring cardiac cells side-to-side and they form fibers network. Oval shape
nucleus is in the centre of the cardiac myocyte.
Wall of the heart. Using lower magnification recognize the layers of the heart
wall: epicardium, myocardium and endocardium.
Using high magnification distinguish and draw endocardium (it is composed
of a single layer of squamous endothelium and subendothelial layer of loose
connective tissue). Recognize myocardium: cardiac myocytes and between them
septum of the connective tissue with blood vessels, lymphatics and nerves can be
found in this layer. Find and draw epicardium, which is composed of: mesothelium (it
covers epicardium from the surface) and subepicardial layer (it consists of loose
connective tissue with blood vessels, nerves and adipose cells).
Atrioventricular valve of the heart. Using lower magnification look at the
surfaces of the valve: the atrial surface is plane and ventricular surface rough.
Roughness of the ventricular surface is explained by the fact that tendons of papillary
muscles insert into the valve. The atrioventricular valves are attached to the annuli
fibrosi, the connective tissue of which extends into valve to form its core.
The valve is covered on both sides by the endocardium (it is thicker on the
ventricular side). Scattered smooth myocytes are present on the atrial side of the
valve, while on the ventricular side elastic fibers are prominent. Using high
magnification distinguish endothelium, subendothelial connective tissue (in the atrial
surface it is thicker than in the ventricular surface) on the atrial surface, and
subendothelial connective tissue with elastic and collagen fibers on the ventricular
surface.
Conducting system of the heart (Purkinje cells). Using lower magnification
recognize Purkinje cells of the heart conducting system in the subendocardial layer.
These cells are bigger than usual (contractile) cardiac myocytes, they have one or two
nuclei (which can be located eccentrically in the cell), rich in mitochondria and
glycogen. The myofibrils are sparse and restricted to the periphery of the cytoplasm.
Using high magnification distinguish Purkinje cells, that are pale-pink, packed
in bundles and covered by connective tissue.
References:
2005. p. 217-221.
Wilkins, 2006. p. 159-180, 189-194.
6.2. Electrical activity of the heart (4 hrs)
Description
The electrocardiogram (ECG) recorded at rest. Distinguish between bipolar and
unipolar leads. Designate the waves in the different leads (for example, II, V 1, V4).
Define the parameters of the ECG (P wave, PQ interval, QRS complex, ST segment,
T wave, QT interval, amplitude of R wave). The ECGs recorded by Cabrera circle.
Use them for defining the electrical axis of the heart. Define electrical axis of the
heart by using the Einthoven triangle. The vectorcardiogram. By the use of the
computer program EKG define the projection points of the vectorcardiogram for the
waves R and S of each Einthoven (standard limb) leads.
References:
Review of Medical Physiology. Twenty-third edition. Ganong W.F.. Lange Medical
Books, New York, 2010. p. 492-496.
Review of Medical Physiology. Twenty-second edition. Ganong W.F.. Lange Medical
Books, New York, 2005. p. 549-554.
6.3. Mechanical activity of the heart (4 hrs)
Description
The phonocardiogram. Heart sounds. Designate the 1st and 2nd heart sounds on the
phonocardiogram. Mechanical events of the cardiac cycle. Using the simultaneous
phonocardiogram and ECG recording, define the phases of the cardiac cycle. Define
the length of systole and diastole. By the use of the computer program EKG analyze
hemodynamic parameters in high pressure parts in low parts of the cardiovascular
system, obtained from healthy patients. Compare tyem with data obtained from
patients with aortic stenosis, aortic regurgitation (insufficiency of aortic valve), mitral
stenosis, and pulmonary stenosis. Distinguish various cardiac murmurs in each case.
References:
Books, New York, 2010. p. 511-513.
Books, New York, 2005. p. 565-570.
6.4. Understanding of patient clinical examination (3 hrs)

Description
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005, p. 738-741,
817-827.
York, 2006.
6.5. ECG interpretation. Abnormalities of automatism and

excitability. Rhythm disturbances of mixed genesis. Conduction
abnormalities. Enlargement and hypertrophy of heart chambers. (3
hrs)

Description
Students must learn to interpret ECG and know abnormalities of automatism and
excitability, rhythm disturbances of mixed genesis, conduction abnormalities
(sinoatrial block second degree type I, type II; atrioventricular block I, II, III
degree; intraventricular block- right bundle branch block, left bundle branch block),
enlargement and hypertrophy of heart chambers (left atrial and ventricular, right atrial
and ventricular).
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005, p. 744-749,
764-783, 817-821.
York, 2006.
6.6. Anatomy of arteries of the lower limb (2 hrs)

Description
1. Internal iliac artery, its location and parietal branches: iliolumbar artery, lateral
sacral artery, obturator artery. Vascularization regions of these branches.
2. External iliac artery, its location and branches: inferior epigastric artery and deep
circumflex iliac artery. Vascularization regions of these branches.
3. Femoral artery and its branches: superficial epigastric artery, superficial
circumflex iliac artery, external pudendal artery, deep femoral artery.
Vascularization regions of these branches.
4. Popliteal artery and its branches: lateral, medial, superior genicular arteries,
middle genicular artery, inferior genicular arteries.
5. Anterior tibial artery and its branches: posterior and anterior tibial recurrent
arteries, anterior medial malleolar artery, anterior lateral malleolar artery.
6. Posterior tibial artery, its branches: circumflex fibular artery, medial malleolar
branches.
7. Plantar arteries, dorsalis pedis artery, their vascularization regions.
8. Collateral arteries of the lower limb.
References:
1. Grays anatomy. The anatomical basis of clinical practice. Edinburg-London.
2005. p. 1412-13, 1436-37, 1450-51, 1453-54.
2. R.L. Drake, W. Vogl, A.W.M. Mitchell. Gray's Anatomy for Students. Elsevier,
Churchill Livingstone, Philadelphia- Toronto. 2005. p363-605.
6.7. Microstructure of the wall of the blood vessels (2 hrs)

Description
Aim: 1. To find out the peculiarities of the structure of the different size blood
vessels wall.
2. To learn and understand the main periods of the development of the blood
vessels.
3. To be able to distinguish the blood vessels of the various types.
Histological micropreparations:
Precapillary arteriole. Using lower and high magnification find and draw the
precapillary arteriole in the field of the loose connective tissue. It is translucent and
without formed elements of blood.
Using high magnification recognize the wall of the arteriole. Its wall consists
of inner layer (endothelium and thin subendothelial layer), an intermediate layer
(smooth muscle cells) and outer layer (several pericytes, branched processes of which
cover the surface of the arteriole and connect with surrounding loose connective
tissue.
Thin elongated nuclei of the endothelial cells are located parallel and
elongated nuclei of smooth muscle cells are perpendicular to the axis of arteriole.
Nuclei of the pericytes are rounded and bigger than the nuclei of the endothelial and
smooth muscle cells.
In this micropreparation you can find blood capillaries also. Their wall is
made of endothelium, basal lamina, and pericytes.
Muscular artery. Using lower magnification find the artery. Using lower and
high magnification distinguish and draw layers of the wall of the artery: inner (tunica
intima) the thinnest, an intermediate (tunica media) the thickest, and outer (tunica
adventitia).
Tunica intima consists of endothelium, thin subendothelial connective tissue
and wavy internal elastic lamina. An internal elastic lamina is the outermost layer of
the tunica intima and separates this layer from tunica media. Tunica media consists of
smooth myocytes and collagen and elastic fibers between them, and external elastic
lamina (if it is visible). An external elastic lamina is the last component of the media
(separates media and tunica adventitia) and is present only in the larger muscular
arteries (it is more difficult to distinguish this lamina in lower magnification). Tunica
adventitia consists of the connective tissue. Lymphatic capillaries, vasa vasorum and
nerves also can be found in the adventitia, and these structures may penetrate to the
outer part of the media.
Vein. Using lower and high magnification distinguish and draw layers of the
wall of the vein: inner (tunica intima) the thinnest, an intermediate (tunica media)
and outer (tunica adventitia) the thickest. It is more difficult to distinguish the layers
of the wall of the vein than those of the artery.
Endothelial cells of the tunica intima of the vein are less flat, more rounded
and more prominent in the lumen than those in the artery. Subendothelial connective
tissue layer contains sparse smooth muscle cells. In the tunica media you can find
more collagen fibers, a little elastic fibers and a lot of smooth myocytes, oriented
longitudinally and circularly. Pay attention to the tunica adventitia: there are a lot of
collagen fibers (in comparison to elastic fibers), sparse smooth muscle cells and vasa
vasorum also can be found.
Aorta (H+E). Using lower magnification recognize and draw layers of the
wall of the artery: inner (tunica intima) the thinnest, an intermediate (tunica media)
the thickest, and outer (tunica adventitia). Pay attention to the subendothelial layer,
which is thicker than in the muscular artery.
Using high magnification distinguish and draw endothelium in the tunica
intima. Pay attention at the size, shape and nuclei of the endothelial cells; the
subendothelial layer, which is composed of thin fibers of the connective tissue, of
star-like fibroblasts and smooth myocytes. In the tunica media find circularly oriented
elastic fibers and membranes, in between them small amount of the smooth muscle
cells and collagen fibers. Collagen and elastic fibers, smooth myocytes, adipose cells
and vasa vasorum can be found in the tunica adventitia.
Internal and external elastic laminae are also present in the aorta, but it is
difficult to distinguish them from the many other elastic laminae in the tunica media.
Aorta (azan). Distinguish elastic laminae and elastic fibers in the tunica media
(this staining method enables us to see elastic fibers clearly). Tunica adventitia is
blue.
References:
2005. p. 205-216.
Wilkins, 2006. p. 180-194.
6.8. Arterial pulse and blood flow regulation (4 hrs)

Description
By the use of the computer program PULS record the sphygmogram of the central
pulse (a. carotis) and peripheral pulse (a. radialis). Describe the properties of the
central and peripheral pulse. Define the duration of systole and diastole from the
sphygmogram of a. carotis. Calculate the velocity of the pulse wave. Compare
quantitatively the sphygmograms of the carotid artery at rest and after physical
exercise.
Venous occlusion pletismography. By the use of the computer program COGEV
measure the blood flow in the forearm at rest, during reactive hyperemia, and active
hyperemia.
References:
Books, New York, 2010. p. 544-546, 563-566.
Elsevier Saunders, Philadelphia, 2006. p. 161-166, 171-174, 195-203, 246-247.
Books, New York, 2005. p. 582-587, 597-599.
Medical Physiology, Update Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadelphia, 2005. p. 477-482.
6.9. Anatomy of heart and coronary circulation (2 hrs)

Description
1. Right coronary artery, its location and branches:
a) branches of the 1st segment, their locations and vascularization regions;
b) branches of the 2nd segment, their locations and vascularization regions;
c) posterior interventricular branch, its location, branches and vascularization regions.
2. Left coronary artery, its location and branches:
a) anterior interventricular artery, its location, branches, vascularization regions;
b) circumflex branch, its location, branches, vascularization regions;
3. Anastomoses and revascularization of coronary arteries.
4. Cardiac veins. Their variations.
5. Cardiac walls and valves.
References:
11 Grays anatomy. The anatomical basis of clinical practice. Edinburg-London.
2005. p. 1014-1019.
11 R.L. Drake, W. Vogl, A.W.M. Mitchell. Gray's Anatomy for Students. Elsevier,
Churchill Livingstone, Philadelphia- Toronto. 2005. p157-180.
1. T.H.Schiebler, W.Schmidt. Anatomie. Berlin-Heidelberg. 1991. p. 537-538.
6.10. Anatomy of venous and lymphatic circulation (2 hrs)

Description
1. System of the inferior vena cava and its inlets: lumbar veins, diaphragmatic veins,
hepatic veins, renal veins, testicular veins, ovarian veins.
2. Internal iliac vein and its inlets: sacral veins, rectal veins, veins of bladder,
prostate, uterus and vagina.
3. External iliac vein and its inlets: inferior epigastric vein, deep circumflex iliac
vein.
4. Veins of lower limb. Deep veins: anterior and posterior tibial veins, popliteal and
femoral veins. Superficial veins: vena saphena parva, vena saphena magna.
Superficial epigastric vein, superficial circumflex iliac vein, external pudendal
and accessory saphenous vein.
5. Cava-caval and porto-caval anastomoses of the inferior vena cava.
6. Lymphatic circulation of the lower limb: lymphatic vessels and lymph nodes
References:
1. Grays anatomy. The anatomical basis of clinical practice. Edinburg-London.
2005. p. 1121-1122.
2. R.L. Drake, W. Vogl, A.W.M. Mitchell. Gray's Anatomy for Students. Elsevier,
Churchill Livingstone, Philadelphia- Toronto. 2005. p.109-111, 130-132, 303-307,
331-336, 498-500.
6.11. Primary and secondary hemostasis: determination of bleeding

and clotting time. Microcirculation. Alterations in microcirculation.
(4 hrs)
Description
Primary and secondary hemostasis. The clotting and anticlotting mechanisms. The
microcirculation and Typical alterations in microcirculation:
1. intravascular alterations with aggregation of formed elements and cells and
disturbances of blood rheological properties;
2. injury of endotheliocytes and blood vessels wall;
3. extravascular alterations. Role of microcirculation alterations during athero-
sclerosis, arterial hypertension, diabetes mellitus, DIC (disseminated intravas-
cular coagulation) syndrome, shock, multiple organ dysfunction syndrome.
References:
Review of Medical Physiology. Twenty-second edition. Ganong W.F. Lange Medical
Books, New York, 2005. p. 542-545, 590-594.
Copstead L. E., Banasik J. L. Pathophysiology, Elsevier Saunders. 2013. p. 314-
331, 432-447.
98-101, 1696 1713.
6.12. ECG changes of myocardial necrosis, damage and ischaemia (3

hrs)
Description
Students must learn ECG changes in cases of myocardial necrosis, injury, and
ischemia. They must know ECG changes of Q-wave infarction and non Q-wave
infarction. The students must learn the stage of myocardial infarction on the ECG and
location of myocardial infarction.
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005, p.808-817.
R. Haberl. ECG pocket. 2nd edition. Brm Bruckeier publishing. China, 2006, p.87-
117.
York, 2006.
6.13. Peripheral arterial disease and deep vein thrombosis.

Pulmonary thromboembolism (3 hrs)
Description
Induction course with clinical signs and diagnostic principles of peripheral
arterial disease, deep vein thrombosis, and pulmonary thromboembolism.
.
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005, p.866-871,
844-846.
York, 2006.
6.14. Morphology of the disorders of hemostasis and fluidity of blood

(3 hrs)

Description
Aim: study and illustrate by macropreparations the pathogenetic mechanisms of
thrombus formation, morphology, outcome, and significance. Studying
macropreparations evaluate and point out peculiarities of the thromboembolism,
illustrate morphology of bleeding caused by damage of blood vessel wall and
increased permeability of the wall.
Electron micrographs and histological slides:
Thrombocyte adhesion and aggregation. Electron micrographs (x 8 500, 32 000).
Observe adherent thrombocytes to exposed collagen in the lumen of vessel (I phase);
fibrous fibrin and erythrocytes attached to degranulated thrombocytes (II phase).
Thrombus recens venae (arteriae). Histological slide (H+E). Find thrombus forming
components: pink fibrous, a scarlet homogenous mass of thrombocytes, erythrocytes
and leukocytes.
Thrombus in organisatione. Histological slide (H+E). Observe the growing
connective tissue and endothelial cells from vessel wall into the periphery of recent
thrombus.
Thrombus organisatus et recanalisatus. Histological slide (H+E). Note that the
thrombus is organized by connective tissue, formed fissures are covered with the
endothelium and filled with blood and macrophages with hemosiderin could be seen
in the connective tissue.
References:
Pathologic Basis of Disease/Eds I.L. Robbins, R. S. Cotran. 7 th edition, 2005. p. 124-
138.
Laboratory practice on general and special pathological anatomy. R. Butkus, J.
eponis, R. Gailys, Kaunas 2004.
6.15. Bleeding. Temporary and definitive hemostasis. Hemorrhagic

shock. (3 hrs)
Clinic of General Surgery

Description
Aim: to help the students get acquainted with:
- conception, causes, classification, consequences and Latin terminology of

bleeding;
- hemostasis, mechanisms of spontaneous hemostasis, preoperative assessment
of hemostasis;
- disturbances of blood coagulation, their implications on bleeding during the
operation;
- syndrome of acute bleeding;
- pathogenesis and compensatory mechanisms of central hemodynamics,
microcirculation and tissue metabolism disturbances during acute bleeding;
- detection of internal bleeding (clinical, laboratory and instrumental findings)
and the first aid;
- acute anemia, clinical findings;
- principles of treatment of hemorrhagic shock, compensation of blood loss;
- principles of blood saving during surgical operations;
- hematomas: types, their impact and consequences;
- first aid for bleeding, ways of temporary and definitive hemostasis.
References:
S.S. Schwartz. Principles of Surgery. Sixth edition. McGraw-Hill, Inc. 1998. p. 95-
145.
O. J. Garden, A.W. Bradbury, J Forsythe. Principles and practice of surgery. Fourth
edition. 2002, p. 20-36, 48-49.
6.16. Regulation of the arterial blood pressure (4 hrs)
Description
Measurement of the arterial blood pressure by palpation and auscultatory method.
Using computer program FANY, measure the arterial blood pressure and
pulse/heart rate during the orthostatic test and physical exercise. Analyze and discuss
the changes of the cardiovascular parameters. Draw graphs showing changes of the
arterial blood pressure and pulse/heart rate.
References:
Review of Medical Physiology. Twenty-third edition. Ganong W.F. Lange Medical
Books, New York, 2010. p. 544-546, 555-563.
Elsevier Saunders, Philadelphia, 2006. p. 166-167, 175-176, 204-226, 247-249.
Review of Medical Physiology. Twenty-second edition. Ganong W.F. Lange Medical
Books, New York, 2005. p. 588-591, 600-610, 630-634.
Medical Physiology, Updated Edition. Boron W.F., Boulpaep E.L. Saunders,
Philadelphia, 2005. p. 577-579, 582-585.
6.17. Pathological anatomy of the heart failure and insufficiency of

the peripheral blood circulation (3 hrs)

Description
Studying macropreparations, point out mostly frequent causative factors of heart
failure, group them according pathogenetical mechanisms. Evaluate and mark in the
notebooks macro and micropreparations, illustrating morphological features of left-
sided and right-sided heart failure.
Hypertrophy of the myocyte (phase of decompensation). Electron micrograph (x
20000). Pay attention to the ultrastructural changes of myocytes: lesser amount of
mitochondrial crists, some of them disintegrated, swelling of sarcoplasm, destruction
of myofibrils.
Hyperaemia venosa acuta et oedema pulmonum. Histological slide (H+E). Find the
dilated and filled with blood interalveolar capillaries, abundant accumulation of
stained-in-pink edematous fluid (transudate), mixed with some erythrocytes.
Hyperaemia venosa chronica pulmonum. Histological slide (H+E and reaction of
Berlin blue used for revealing iron). Find some full-blooded capillaries of fibrotic
interalveolar septi, a little amount of proteinous fluid in some alveoli and lots of
macrophages with hemosiderin granules (siderophages).
Hyperaemia venosa chronica hepatis. Histological slide (H+E). Find the dilated
central vein and central lobular sinusoids, with compressed and atrophic hepatocytes
between them. Pay attention to the normal structures in the peripheral regions of the
lobules and determine the cause.
References:
Pathologic Basis of Disease/Eds. I.L. Robbins, R. S. Cotran. 7 th edition, 2005. p. 137-
138, 554-563, 592.
6.18. Syndromes and diseases of the cardiovascular system (3 hrs)

Description
Aim: to learn and illustrate morphogenesis and morphology of atherosclerosis of
different locations blood vessels, its clinicomorphological manifestations
(infarctions), morphological background of arterial hypertension disease and
secondary symptomatic hypertension, rheumatic endocarditis, its main complications
and causes of death.
Ultrastructure of atherosclerotic plaque. Electron micrograph (x 9000). Find and
draw components of the plaque.
Rheumatic damage of the glomerular filter. Electron micrograph (x 29 300). Find
out and mark schematically immune complexes (deposits) located in the basal
membrane of the glomeruli.
Irreversible cellular damage due to recent myocardial infraction. Electron
micrograph (x 20 000). Find decayed mitochondria, myofibrils, sarcoplasmic
reticulum.
Atherosclerosis (stenosis x%) a. coronariae cum thrombosi. Histological slide
(H+E). Find atherosclerotic plaque narrowing the lumen of artery and draw the
components of this plaque: lipids, connective tissue, deposits of calcium; evaluate the
percent of the lumen narrowing. Pay attention to the components of thrombus:
aggregated thrombocytes, fibrin, erythrocytes and leukocytes; evaluate and point out
approximate age of the thrombus.
Infarctus myocardii recens. Histological slide (H+E). Find the necrotic focus:
cardiomyocytes without nuclei and striation, pay attention to the acidophilic
sarcoplasm. Find the myocardium without damage. Pay attention to the line of
demarcation between the necrotic focus and the normal myocardium. There is
inflammation response with dilated vessels and neutrophilic infiltration at the margins
of the infarct.
Nephrocirrhosis arteriolosclerotica. Histological slide (H+E). In the cortex of kidney
find arterioles with thick walls, insudated by proteinous material, and the narrowed
lumen, small foci of connective tissue, atrophic tubules with proteinous plugs in the
lumen. Show compensatory enlarged glomeruli.
Nodulus rheumaticcus (necrosis fibrinoides textus connectivi). Histological slide
(H+E). Find a focus of necrosis of collagen fibers insudated by fibrin and surrounded
by macrophages.
Endocarditis verrucosa recurrens. Histological slide (H+E). Find and mark for
yourself morphological changes indicating recurrent character of endocarditis acute
fresh verrucous endocarditis: thrombotic mass on the injured valvular endothelial
surface and in subendothelial tissue elements of specific immune reactions
(macrophages, lymphocytes, plasmocytes).
References:
Pathologic Basis of Disease/Eds I.L. Robbins, R. S. Cotran. 7 th edition, 2005. p. 512-
530, 587. 592-597.
6.19. Understanding of ischaemic heart disease (stable angina

pectoris, unstable angina pectoris, acute myocardial infarction).
Causes, clinical signs, diagnostic principles. Clinical understanding of
cardioechography, exercise ECG, angiographic examination of
cardiovascular system, radiological investigations of cardiovascular
system, chest X-ray picture (3 hrs)

Description
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005. p.741-759,
798-817.
R. Haberl. ECG pocket. 2nd edition. Brm Bruckeier publishing. China, 2006. p. 117-
124.
York, 2006.
6.20. The main cardiovascular syndromes (arrhythmia, arterial
hypertension, heart valvular diseases) (3 hrs)

Description
The students must learn the reasons, clinical signs and ECG changes of cardiac
arrhythmia and arterial hypertension.
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005. p.764-784,
857-864.
York, 2006.
6.21. The main functional clinical syndromes of the cardiovascular

system (acute and chronic heart failure). Peripheral arterial disease
(3 hrs)

Description
References:
London New York Oxford Philadelphia St. Louis Sydney Toronto, 2005. p.784-798.
York, 2006.
7. Seminars
7.1. Antiarrhytmic drugs (2 hrs)
Description
Drug classification. Mechanism of action of each drug class, site of effects and
triggered pharmacological effects are discussed. Information about the properties of
the most important representatives of separate classes of drugs, indications and side
effects.
References:
1. Mycek M. J. Champe P.C. et al. Lippincott's Illustrated Reviews: Pharmacol-
ogy, 3rd (2nd) edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p.
195-206 (at the department).
1. Katzung B.G. Basic and Clinical Pharmacology Seventh Edition. Stamford:
Appleton & Lange, 1998, p. 216-240 (at the department).
2. Rang H.P. Dale M.M. et al. Pharmacology. Fifth edition. Edinburgh: Churchil
Livingstone, 2003, p. 264-279.
7.2. Metabolism of lipoproteins (2 hrs)
Description
1. Lipid transport function of lipoproteins in blood plasma.
2. Classification of Lipoproteins. Characteristics of the major apoproteins.
Chylomicrons. Alimentary lipemia. Metabolism of Chylomicrons. ApoE
receptors. Tissue lipoproteinlipases (LPL).
3. Metabolism of very low density lipoproteins (VLDL) and low density
lipoproteins (LDL). LDL as a source of cell cholesterol. The LDL
receptors. Biochemical aspects of atherosclerosis.
4. High density lipoproteins. Reverse cholesterol transport.
5. Dislipoproteinemias: Hyper- and hypolipopreteinemias.
References:
1. 1. C.M. Smith, A. Marks, M.A. Lieberman. Marks Basic medical
biochemistry 2nd ed., 2005, p. 586-591, p. 631-643
2. 2. Lippincott's illustrated reviews: Biochemistry: By P C Champe and R
A Harvey. 2nd ed. 1994. p. 225-235.
7.4 Drugs used in hypertension, angina pectoris and heart failure (2

hrs)
Description
Positive inotropic drugs. Other drugs used in congestive heart failure. Drugs used in
hypertension. Drugs used in the treatment of angina pectoris. Mechanism of action of
each drug group, site of effect and triggered pharmacological effect are discussed.
Information about the properties of the most important representatives of separate
classes of drugs, indications and side effects.
References:
1. Mycek M. J. Champe P.C. et al. Lippincott's Illustrated Reviews: Pharmacol-
ogy, 3rd (2nd) edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p.
181-194; 207-212; 213-226 (at the department).
1. Katzung B.G. Basic and Clinical Pharmacology Seventh Edition. Stamford: Ap-
pleton & Lange, 1998 p. 153-179; 179-196; 197-215 (at the department).
2. Rang H.P. Dale M.M. et al. Pharmacology. Fifth edition. Edinburgh: Churchil
Livingstone, 2003, p. 264-284; 285-305.
8. Examination programme
Module CIRCULATION
8.1. Anatomy
1. External iliac artery, femoral and popliteal arteries, their locations and
vascularization regions.
2. Arteries of leg and foot, their locations and vascularization regions.
3. Veins of lower limb.
4. Vena cava inferior, its location, inlets. Cava-caval and porto-caval anastomoses of
the inferior vena cava.
5. Coronary arteries of heart.
6. Veins of heart.
7. Lymphatic circulation of the lower limb: lymphatic vessels and lymph nodes.
8.2. Histology and Embryology

1. Structure of different diameter blood vessels wall and peculiarities of their
development.
2. Structuse of the heart wall and peculiarities of its development.
3. Heart developmental defects: their classification and causes.
4. Heart conducting system.
5. Structure of the lymphatic and peculiarities of their development.
6. Fetal blood circulation.
8.3. Biochemistry
1. Metabolism of low density lipoproteins and its disorders.
2. Peculiarities of energy metabolism of the cardiac muscle cells
3. Changes in myocardial metabolism during ischemia.
4. Mechanism of apoptosis involving cell surface death receptors and mitochondria.
8.4. Physiology
1. Electrical activity of the heart. Ionic mechanism of cardiac pacemaker automaticity.
2. Propagation of electrical impulse in the heart. The origin of the electrocardiogram
(ECG) and vectocardiogram.
3. Electromechenical coupling in the myocardium. Mechanical activity of the heart
and cardiac cycle. The pressure-volume changes during the cardiac cycle.
4. Intracardiac regulatory mechanisms of the heart.
5. Extracardiac regulatory mechanisms of the heart.
6. Velocity of blood flow. Laminar and turbulent blood flow. The compliance
(capacitance) and tension of vascular wall.
7. Physiological characteristics of arterial circulation. Arterial pulse, the velocity of
arterial pulse and its measurement.
8. Microcirculation. Capillary fluid exchange mechanisms.
9. Physiological characteristics of venous circulation and regulatory mechanisms.
10. Local blood flow regulation. Myogenic, metabolic and endothelial regulatory
mechanisms.
11. Systemic regulation of circulation: nervous regulation.
12. Systemic regulation of circulation: humoral regulation.
13. Rapid and short term regulatory mechanisms of arterial blood pressure.
14. Long-term regulatory mechanisms of arterial blood pressure.
15. Functional characteristics of coronary circulation and mechanisms of regulation.
16. Primary and secondary hemostasis: mechanisms and physiological role.
17. Balance between blood clotting and fibrinolysis. Factors important for the
balance.
8.5. Pathological Physiology

1. Functional unit of microcirculation. Typical disorders of microcirculation.
2. Left- and right-sided heart failure etiology and pathogenesis.
3. Intracardiac compensatory mechanisms during the changes of preload and
afterload.
4. Myocardial ischemia, etiology, risk factors and pathogenesis.
5. Primary arterial hypertension, etiology and pathogenesis.
6. Secondory arterial hypertension, etiology and pathogenesis.
7. Hypotension, etiology and pathogenesis.
8. Shock: classification, etiology and pathogenesis.
9. Typical disorders of microcirculation (arterial hyperemia, venous hyperemia, stasis,
edema): etiology, pathogenesis and outcomes.
8.6. Pathological anatomy

1. Thrombosis, its definition, pathogenesis, morphology, outcomes and results.
2. Thrombosis in the chambers of the heart, arteries, and veins, its results.
3. Disseminated intravascular coagulation, its causes, pathogenesis, morphology.
4. Embolism, its definition and regularities. Sources of thromboemboli in major et
minor circles of blood circulation, morphology and results.
5. Hemorrhage, its kinds, mechanisms, terminology morphology, compensatory
mechanisms and results.
6. Congestive heart failure, its causes, pathogenetic mechanisms and expression of
compensation.
7. Left-sided acute and chronic heart failure, its causes, and morphology.
8. Right-sided acute and chronic heart failure, its causes and morphology.
9. Cell injury, its causative agents, reversible and irreversible damages.
10. Cellular death and necrosis, its clinicomorphological forms, outcomes. Gangrene,
its causes.
11. Causes of insufficiency of arterial blood circulation, its pathogenesis,
compensatory mechanisms and results - ischaemia and necrosis (infarction).
12. Infarction, its definition and causes, morphology, and outcomes.
13. Peculiarities and results of infarction in brain, heart, spleen, kidneys, intestine, and
lungs.
14. Insufficiency of local venous blood circulation, its pathogenesis, morphology,
results. Postthrombotic syndrome.
15. Edema and insufficiency of lymphatic circulation: pathogenesis and morphology.
16. Atherosclerosis risk factors and pathogenesis.
17. Morphology of atherosclerotic lesions, its complications. Results of
atherosclerosis of aorta, cerebral, mesenteric, and renal arteries.
18. Atherosclerosis of coronary arteries, its morphology and complications.
19. Myocardial infarction, its definition and pathogenesis, morphology, complications
and causes of death.
20. Classification of primary cardiomyopathies, clinical morphological forms,
21. Common features of pathogenesis, morphology and course of systemic connective
tissue diseases. Definition of rheumatic fever, its etiology, pathogenesis, morphology
of affected connective tissue.
22. Cardiovascular pathology in rheumatic fever, morphology of rheumatic
endocarditis, myocarditis and pericarditis, complications and causes of death.
23. Infective endocarditis, its etiology, pathogenesis, morphology, complications.
24. Essence of hypertension disease and symptomic hypertension, morphology,
25. Hypertension of the minor ratio (pulmonary) blood circulation: causative factors,
pathogenetic mechanisms, morphology and causes of death (cor-pulmonale
syndrome).
8.7. Pharmacology
1. Inotropic agents. Mechanism of action, pharmacokinetics, therapeutic uses, adverse
effects.
2. Nitrates. Mechanism of action, pharmacokinetics, therapeutic uses, adverse effects.
3. Calcium channel blockers. Mechanism of action, pharmacokinetics, therapeutic
uses, adverse effects.
4. Angiotensin antagonists. Mechanism of action, pharmacokinetics, therapeutic uses,
adverse effects.
5. Classification of antiarrhytmic agents. Quinidine, procainamide, disopyramide.
Pharmacodynamics, therapeutic uses, adverse effects.
6. Classification of antiarrhytmic agents. Lidocaine, mexiletine. Pharmacodynamics,
therapeutic uses, adverse effects.
7. Classification of antiarrhytmic agents. Beta adrenoreceptors blockers.
Pharmacodynamics, therapeutic uses, adverse effects.
8. Classification of antiarrhytmic agents. Amiodarone, sotalol. Pharmacodynamics,
9. Other antiarrhytmic drugs (not included in the classification of antiarrthytmics):
adenosine, digoxin. Pharmacodynamics, therapeutic uses, adverse effects.
10. Classification of antihypertensive drugs. Describe main effects drugs in each
group. Representatives, pharmacokinetics, therapeutic uses, adverse effects.
11. Drugs acting on blood coagulation. Anticoagulants. Mechanism of action,
12. Drugs acting on blood coagulation. Platelet antiagregants. Mechanism of action,
13. Drugs acting on blood coagulation. Fibrinolytic agents. Mechanism of action,
8.8. General Surgery

1. Preoperative assessment of hemostasis.
2. Bleeding: types and causes, conservative treatment. Local hemostasis.
3. Possibilities of blood saving during the operation.
5. Pathogenesis of blood loss.
6. Signs and diagnosis of blood loss, classes of blood loss.
7. Principles of treatment of blood loss.
8. Blood components, use of blood components.
9. Possibilities of use of autologous blood.
10. Blood substitutes, use of blood substitutes.
8.9. Priciples of Medical Diagnostic

1. Understanding about primary arterial hypertension. Clinical signs , complication,
diagnostic principles. Organs marks damages.
2. Understanding about ischaemic heart disease: stable angina pectoris, acute
myocardial infarction. Clinical signs, diagnostic principles.
3. Understanding about peripherial arterial disease: causes, clinical signs, diagnostic
principles.
4. Understanding about primary and secondary pulmonary hypertension: causes,
clinical signs, diagnostic principles.
5. Understanding about deep veonons thrombosis and pulmonary thromboembolism:
causes, clinical signs, diagnostic principles.
6. Heart arrhytmia syndrome: clinical signs, diagnostic priciples.
7. Mitral stenosis: causes, clinical signs, diagnostic principles.
8. Mitral regurgitation: causes, clinical signs, diagnostic principles.
9. Aortic stenosis: causes, clinical signs, diagnostic principles.
10. Aoritc regurgitation: causes, clinical signs, diagnostic principles.
11. Acute left ventricular failure: pulmonary oedema. Causes, clinical signs,
diagnostic principles.
12. Chronic left ventricular failure: causes, clinical signs, diagnostic principles.
13. Chronic right ventricular failure: causes, clinical signs, diagnostic principles.
14. Electrocardiographic criterions of left ventrical hypretrophy, meanings.
15. Electrocardiographic criterions of atrioventrical junctional escape rhythm and
ventricular escape rhythm.
16. Electrocardiographic criterions of ventricular premature beats and atrial
fibrillation.
17. Electrocardiographic criterions of supraventricular tachycardia and ventricular
tachycardia.
18. Electrocardiographic criterions of intraventricular conduction disorders: left
bundle branch block, rignt bundle branch block.
19. Electrocardiographic criterions of q wave myocardial infarction: hyperacute,
acute, subacute, old myocardial infarction.

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EUROPOS SJUNGA

Europos Socialinis Fondas

Program of Medicine Studies

Supervisor of the module: prof. Edgaras Stankeviius, Department of Physiology

Subjects and responsible persons:

3. Aim and objectives of the module

Please, explain the course and signs of the disease.

Learning objectives and contents

Anatomy of heart valves and heart chambers.

McCance K., Huether S. E. Pathophysiology, Elsevier Mosby. 2010. p. 1189

Morphological changes of the damaged valves and pathological anatomy of

Mechanisms of action of inotropic drugs.

Changes of heart sounds, characteristics of heart murmurs, principles of

Please, explain the origin and mechanisms of disorders.

Learning objectives and contents

Cardiac automacity, ionic mechanism of cardiac pacemaker potencial,

Pathophysiological mechanisms of cardiac arrhythmias.

McCance K., Huether S. E. Pathophysiology, Elsevier Mosby. 2010. p. 1197

McPhee S. J., Ganong W. F. Pathophysiology of disease. Introduction to clinical

Mechanisms of action of antiarrhythmic drugs.

Clinical signs and ECG changes in cardiac arrhythmia.

Please, explain the course and signs of the disease.

Learning objectives and contents

Microstructure of the arteries and arterioles.

Metabolism of lipoproteins and their role in the formation of atherosclerosis.

Physiological characteristics of arterial circulation, arterial pulse and velocity

Morphological structure of the atherosclerotic plaques, their kinds,

Complaints in chronic limb ischemia, arterial pulse palpation, principles of

Please, explain what has happened to M.I.?

Learning objectives and contents

Functional characteristics of coronary circulation and mechanisms of

Pathophysiological mechanisms of myocardial ischemia and infarction.

McCance K., Huether S. E. Pathophysiology, Elsevier Mosby. 2010. p. 1165

Peculiarities of atherosclerosis of the coronary arteries, local complications,

Characteristics and reasons of angina pectoris and myocardial infarction,

Mechanisms of action of antianginal drugs.

Learning objectives and contents

Physiological characteristics of venous circulation and regulatory

Pathophysiological mechanisms of alterations in microcirculation.

Thrombosis in deep veins of the lower extremity, its causative factors,

Clinical signs and diagnostic principles of venous circulation abnormalities,

Learning objectives and contents

Pathophysiological mechanisms of arterial blood pressure regulation

Primary and secondary hypertension, its mechanism of developing,

Mechanisms of action of arterial blood pressure lowering drugs.

Clinical signs, complications, diagnostic principles of arterial hypertension,

5.1. Development and peculiarities of the structure of the heart and

Department of Histology and Embryology

5.2. Electrical and mechanical activity of the heart (3 hrs)

Institute of Physiology and Pharmacology

5.3 Antiarrhytmic drugs (2 hrs)

Department of Basic and Clinical Pharmacology

In charge - lect. V. Liukaitis, assoc. prof. R. Pilviniene

Antiarrhytmic drugs. Drug classification. Mechanism of action of each drug class,

5.4. Heart metabolism in normal and ischemic conditions (2 hrs)

5.5. Coronary circulation and regulation of local blood flow.

Institute of Physiology and Pharmacology

5.6. Introduction to patient clinical examination. Primary and

Clinic of Internal Diseases

5.7. Regulation of the fluidity of blood and pathological anatomy of

Clinic of Pathological Anatomy

Department of Basic and Clinical Pharmacology

In charge - lect. V. Liukaitis, assoc. prof. R. Pilvinien