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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.


Theme8: Cell injury-2 Apoptosis.


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 c-dependent caspase activation and thus function as regulators of mitochondrial apoptosis.


^ 2.Length of the employment – 2 hours.


3.Aim:


To khow the major types of cellular necrosis.

To be able: two pathways of apoptosis.

To perform practical work: to analyse of the mechanisms of apoptosis.





4. Basic level.


The name of the previous disciplines


The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

Fluid mosaic model of the plasma membrane.

Cell populations and cycle landmarks.

Lipid peroxidation.

Erythrocytes in hypertonic, isotonic, and

hypotonic solutions.



^ 5. The advices for students.


1.Coagulative necrosis occurs primarily in the kidneys, heart, and adrenal glands and usually results from hypoxia caused by severe ischemia. Protein denaturation causes coagulation. An increased intracellular level of calcium may be a critical event in coagulation necrosis.

^ 2. Liquefactive necrosis is common following ischemic injury to neurons and glial cells in the brain. Because brain cells are rich in digestive hydrolytic enzymes and lipids, the brain cells are digested by their own hydrolases. The brain tissue becomes soft, liquefies, and is walled off from the healthy tissue to form cysts. Liquefactive necrosis can also result from bacterial infections. Here, the hydrolases are released from the lysosomes of phagocytic neutrophils that are attracted to the infected area to kill the bacteria; these hydrolases also destroy brain tissue. The accumulation of pus is present in liquefaction necrosis.

^ 3. Caseous necrosis is commonly seen in tuberculous pulmonary infection and is a combination of coagulative and liquefactive necrosis. The necrotic debris is not digested completely by hydrolases, so tissues appear soft, granular, and resemble clumped cheese. A granulomatous inflammatory wall may enclose the central areas of caseous necrosis.

4.Fat necrosis found in the breast, pancreas, and other abdominal structures is a specific cellular dissolution caused by lipases. Lipases break down triglycerides and release free fatty acids that then combine with calcium, magnesium, and sodium ions to create soaps, or saponification. The necrotic tissue appears opaque and chalk white.

^ 5.Gangrenous necrosis refers to death of tissue, usually in considerable mass and putrefaction. It results from severe hypoxic injury subsequent to arteriosclerosis or blockage of major arteries followed by bacterial invasion. Dry gangrene is usually due to a coagulative necrosis, and wet gangrene develops when neutrophils invade the site and cause liquefactive necrosis. Gas gangrene, a special type of gangrene, is due to bacterial infection of injury tissue by a species of Clostridium. These anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and the cellular membrane; bubbles of gas likely form in the muscle cells.

^ 6. Describe the mechanisms of apoptosis.

Apoptosis is an important, distinct type of cell death that differs from necrosis. It is an active process of cellular self-destruction in both normal and pathologic tissue changes. Apoptosis likely plays a role in deletion of cells during embryonic development and in endocrine-dependent tissues that are undergoing atrophic change. It may occur spontaneously in malignant tumors and in normal, rapidly proliferating cells treated with cancer chemotherapeutic agents and ionizing radiation. Unlike necrosis, apoptosis affect scattered, single cells and results in shrinkage of a cell; whereas in necrosis, cells swell and lyse.

^ 7. Cellular Accumulations





8. Describe theories of aging.

(1) Genetic, environmental, and behavioral factors produce cellular aging change; (2) changes in regulatory mechanisms. There are two general theories of aging: (1) aging is caused by the accumulation of injurious events, sometimes termed damage-accumulation theories, or (2) aging is the result of a genetically controlled developmental program. In support of these two categories, threе mechanisms of aging have emerged: three cells of the endocrine, immune, and central nervous systems, are responsible for aging; and (3) degenerative extracellular and vascular alterations cause aging.

Regardless of injurious environmental factors, some believe that each cell may have a finite life span during which it can replicate. Fibroblasts have been demonstrated to be limited to 40 to 60 cell doublings. Alternatively, an intrinsic program within the human genome progressively slows or shuts down mitosis.

Alterations of cellular control mechanisms include increased hormonal degradations, decreased hormonal synthesis and secretion, and decreased receptors for hormones and neuromodulators. This suggests that a genetic program for aging is encoded in the brain and relayed through hormonal and neural agents because of shared common receptors within these systems.

Immune function declines with age and the number of autoantibodies that attack body tissues increases with age. These observations implicate the immune system in aging.

A degenerative extracellular change that affects the aging process is collagen cross-linking, which makes collagen more rigid and results in decreased cell permeability to nutrients. Free radicals of oxygen are believed to damage tissues during aging. These reactive species not only permanently damage cells but also may lead to cell death. Damage accumulates over time and reduces the body’s ability to maintain a steady state.

^ 5.1. Content of the theme. Coagulative necrosis. Liquefactive necrosis.

Caseous necrosis. Fat necrosis. Gangrenous necrosis. Description of the mechanisms of apoptosis. Cellular accumulations.Describe theories of aging.


5.2. Control questions of the theme:


  1. Coagulative necrosis.

  2. Liquefactive necrosis.

  3. Caseous necrosis.

  4. Fat necrosis.

5. Gangrenous necrosis.

6. Description of the mechanisms of apoptosis.

7. Cellular accumulations.

8. Describe theories of aging.


^ 5.3. Practice Examination.

I

Task 1.

Hemorrhagic syndrome arose in victim in the time of accident on Chornobyl atomic electric station. It displayed by hemorrhage in skin and mucous membranes, appearance of blood in urine, in feces and in sputum. Mechanism of hemorrhagic syndrome concludes in




A. Activation of fibrinolysis system B. Heparin accumulation in blood C. Decrease of thrombocytes amount D. Disturbance of fibrinogen structure Е. Disorder of vessels wall

Task 2.

A victim was affected by the radiation in dose 6 grey (600 Rad) at time of atomic submarine accident. Disorders of what cells structure and function should be waited in this case?




A. Skin epithelium B. Bowels epithelium C. Spleen pulp D. Thyroid gland Е. Bone marrow


II

Task 1.

There are the following SMP cells in liver:







A. Hystiocytes B. Kupfer’s cells C. Оsteoclasts D. Glial cells

Е. Peritoneal macrophages




Task 2.

There are the following SMP cells in connective tissue:







A. Оsteoclasts B. Alveolar macrophages C. Glial cells D. Kupfer’s cells Е. Hystiocytes





III

Task 1.

Phagocytes are




A. Lymphocytes B. Trombocytes C. Eosinophils D. Myocytes

Е. Hepatocytes

Task 2.

Phagocytes named macrophages are




A. Lymphocytes B. Basophils C. Monocytes D. Eosinophils

Е. Neutrophils

Task 3.
^

Suppression of phagocytosis by monoidine acetate as a result of





A. Destruction of phagocytes membrane B. Disorder of energy generation C. Exhaustion of enzymes reserve D. Oppression of chemotaxis Е. Stabilization of lysosomal membranes

Task 4.

Patient with chronic granulomatosis has an acute oppression of phagocytosis. This is related to deficit of




A. Cytochromoxidase B. NADP-oxidase C. Adenosintriphosphatase

D. Glucose-6-phosphatase Е. Piruvatkinase

Task 5.

Patients which suffer from Chediac-Higasi’s syndrome have decreased activity of phagocytes. The base of this hereditary disease is




A. Defect of lysosomes formation B. Decrease of enzymes in lysosomes C. Inactivation of enzymes in lysosomes D. Thickening of lysosomal membranes Е. Oppression of energy generation in leucocytes
^

Real-life situations to be solved:


Emissions of radioactive elements arose in the result of one atomic station block breakdown. In zone of raised radiation activity was three men. They got about 250-300 Rad. They were immediately delivered in clinic.

  1. What consequences should wait in victim?

  2. What stages pick out in development of radial disease?

  3. What researches should you make for clearing up of lesion degree?

  4. How would be differ state irradiated being received 50 R? 500 R? 600 R?

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. 44-50.

2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study guide for medical students and practitioners.-Odessa, 2003.- P. 27-39.

3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar, Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.

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