MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 1 : GENERAL PATHOLOGY.
Contenting module 2. Typical pathological processes.
Theme15: Final control-2.
Chernivtsi – 2008
1.Actuality of the theme. Necrosis is local cell death and involves the
process of cellular self-digestion known as autodigestion or autolysis. As necrosis
progresses, most organelles are disrupted and karyolysis, nuclear dissolution from
the action of hydrolytic enzymes, becomes evident. There are four major types of
necrosis: coagulative, liquefactive, caseous, and fat. Gangrenous necrosis is not a
distinctive type of cell death but refers to large areas of tissue death.
The two pathways of apoptosis differ in their induction and regulation, and both
culminate in the activation of "executioner" caspases. The induction of apoptosis is
dependent on a balance between pro- and anti-apoptotic signals and intracellular
proteins. The figure shows the pathways that induce apoptotic cell death, and the
anti-apoptotic proteins that inhibit mitochondrial leakiness and cytochrome cdependent caspase activation and thus function as regulators of mitochondrial
apoptosis.
Hereditary factors play an essential role in human pathology. About 2000
different hereditary diseases are known now. 4 % of new-born suffer from these or
other genetically conditioned defects. This testifies importance of ability to
participate in exposure methods of hereditary diseases, study ways of their
prophylaxis and cure principles. Heredity pathology plays an important role in
development of such hereditary conditioned diseases, as atherosclerosis, essential
hypertension, rheumatism, diabetes mellitus, gout.
Reactivity is the characteristic of the organism to react in a certain way on the
influence of the environment. It is the same as growing up, feeding, metabolism.
Reactivity is formed in the process of evolution in phylogenes and ontogenes,
reflects specific, group and individual peculiarities of reaction.
Arterial hyperemia as a typical pathological process is observed in
inflammation, many infectious diseases (measles, spotted fever, scarlet fever),
damages of nervous plexus, neuralgias etc. Knowledge of causes, mechanisms and
symptoms of arterial hyperemia matters practically. Doctors use the surgical,
pharmacological, physiotherapeutic influences, which cause artificial arterial
hyperemia. The aim of these influences is improve metabolism, blood and
lymphatic circulation in damaged area.
Knowlege of clinical features of inflammation is necessary for differential
diagnostic of inflammational illnesses. It is necessary to remember that appearance
of all five classical features is typical only for acute inflammation of the skin and
mucous membranes. If inflammation arises in the inner organs these features are
expressed weakly. In those cases it is necessary to take into consideration general
sings of inflammation. Some features can be absent in chronic inflammation and it
makes the right interpretation of the inflammation character much difficult.
In all hospitals it is obligatory is carried out patients’ thermometria. In the case
history there is a temperature list where is the morning and evening temperature, as
well as the diagram of its changes. According to type of the curve they define the
fever type. It has diagnostical significance because a lot of infectious diseases are
accompanied with fever with tupical temperature curve. Fever has mainly
protective role. Only in the persons with serious disorders of cardiovascular,
nervous and other systems and in children the high temperature (abov 39 °C) can
be dangerous. The doctor must evaluate the fever significance in the patient and
will plan the treatment.
The problem of an oxygen deficiency causes practical interest in clinic of
internal illnesses (prophylaxis and treatment of myocardium infarction, diseases
of the system of breathing, anemias), in neurologic clinic (prophylaxis and
treatment of ischemic damages of the brain), in surgical clinic (treatment obliteric
endarteriitis, operations on vital important organs), in obstetric practice (struggle
with hypoxia of fetus and neonatal). Professional selection of high-resistant to
hypoxia people, and also adaptation to an oxygen insufficiency become relevant
problem of medicine.
2.Length of the employment – 2 hours.
3.Aim:
To khow: that are cell injury, pathophysiology of peripheral blood
circulation, reactivity, inflammation, fever, hypoxia.
To be able: to analyse the pathogenesis of the cell injury, pathophysiology
of peripheral blood circulation, reactivity, inflammation, fever, hypoxia.
To perform practical work: to analyse the tests,
clinicalpathophysiological schemes, tables with pathology of the cell injury,
pathophysiology of peripheral blood circulation, reactivity, inflammation,
fever, hypoxia.
Control questions of the theme:
1.
2.
3.
4.
5.
6.
7.
8.
Vicious circle.
Cellular atrophy.
Hypertrophy.
Hyperplasia.
Dysplasia.
Metaplasia.
Identification the mechanism of cellular injury for the following causes:
hypoxia, chemicals; infectious agents, immunological and inflammatory
responses.
9. Identification the mechanism of cellular injury for the following causes:
10.genetic factors, nutritional imbalances, ionizing radiation and physical
trauma.
11.Coagulative necrosis.
12.Liquefactive necrosis.
13.Caseous necrosis.
14.Fat necrosis.
15.Gangrenous necrosis.
16.Description of the mechanisms of apoptosis.
17.Cellular Accumulations.
18.Describe theories of aging.
19.Identify the criteria used to define multifactorial disease.
20.Complex genetic diseases.
21.Characterize chromosome abnormalities.
22.Describe inheritance and environmental interactions.
23.Cite well-known examples of chromosome disorders.
24.Cite the well-known examples of single-gene disorders.
25.Describe the normal and abnormal phenylalanine metabolism (molecular
hereditary disease)
26.What is constitution?
27.What is the role of constitution in pathology?
28.Define reactivity ant its types.
29. What is specific and non-specific reactivity?
30. Pathologic reactivity.
31.Resistance. Types. Interaction with reactivity.
32.Reactivity by Bogomolets.
Explain term “physiological system of
connecting tissue” and name elements of this system by Bogomoletz. What
is role of this system in maintenance of organisms homeostasis?
33.The theory of Hans’a Seley of diseases of adaptation.
34.Reactivity and biological barriers.
35.Describe the microcirculation bed is function, and the mechanism of
regulation.
36.Name the main disturbances of microcirculation.
37.What does the arterial hyperemia mean?
38.Define venous hyperemia.
39.Define ischemia.
40.Define stasis.
41.Thrombosis
42.Embolism.
43.Define what is inflammation.
44.Name and describe the systemic and local signs of inflammation.
45.Name exogenic and endogenic flogogenic factors.
46.Identify mechanism of alteration, microcirculation disorders in inflammatory
focus.
47.Identify the plasma protein systems and their roles in inflammation.
48.Identify the role for mast cells, platelets, neutrophils, monocytes,
macrophages and eosinophils in the acute and chronic inflammatory process.
49.State the roles for lymphokines, interferon, and interleukins; note their
relationships within the immune system.
50. Identify mechanism of exudate formation.
51. Describe disturbance of microcirculation in inflammatory focus.
52.Normal thermoregulation.
53.Principal mechanisms of human thermoregulation.Common mechanism of
termoregulation.
54.Hypothalamic processing in thermoregulation.
55.What does it fever mean?
56.What is the etiology of fever?
57.Classify the pyrogens.
58.Characterize the pathogenesis of fever.
59.Describe the alterations occurring in fever, hypothermia, and hypothermia.
60.What is the role of fever?
61.Pharmaceutical intervention in fever.
62.Three stages of fever.
63.Define hypoxia
64.The types of hypoxia.
65.Pathogenesis of hypoxia.
66.The mechanisms of long term adaptation to hypoxia.
67.The pathological disorders by hypoxia.
68.The disturbances in the organs and physiological systems under hypoxia.
69.How does it correct hypoxia?
Literature:
1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical
pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.P.35-91.
2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study
guide for medical students and practitioners.-Odessa, 2003.- P.27-98, 129-136.
3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar,
Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.