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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.


Theme12: Inflammation.


Chernivtsi – 2008

1.Actuality of the theme. 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.


2.Length of the employment – 2 hours.

3.Aim:

To khow: 1. Definition of the notion "inflammation". 2. Causes of the inflammation. 3. The role of mediators in inflammation development. 4. The meaning of the organism reactivity in inflammation development. 5. General manifestation of inflammatory reaction. 6. Clinical symptoms of the inflammation.

7. Causes and mechanisms of the vascular permeability disorder in inflammation.

8. Methods of the vascular permeability study in the area of inflammation.

To be able: To analyse of the pathogenesis :1. heat (calor), 2. redness (rubor), 3. swelling (tumor), 4. pain (dolor), 5. loss of function (function laesa.

To perform practical work: to analyse of the pathogenesis of inflammation: disorders and after effect.




4. Basic level.


The name of the previous disciplines


The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

Meaning of mechanical, physical, chemical, biological and mental factors in etiology of inflammation.

Physical and chemical indexes of metabolism in tissues.

Structure of the microcirculatory stream.

Main data about allergy and immunity.

Meaning of an organism reactivity in pathology.




^ 5. The advices for students.

  1. Define what is inflammation.

Inflammation is a biochemical and cellular process that occurs in vascularized tissues. Most of the essential components of the inflammatory process are found in the circulation, and most of the early mediators (facilitators) of inflammation affect the vascular bed so as to increase the movement of plasma and blood cells from the circulation into the tissues surrounding the injury. These substances, known collectively as exudate, defend the host against infection and facilitate tissue repair and healing.

As described in antiquity, the superficial hallmarks of inflammation include redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function (functio laesa). The development of the microscope, however, enabled investigators to detect inflammatory changes at the cellular level. In the nineteenth century, Julius Cohnheim observed three characteristic changes in the microcirculation (arterioles, capillaries, and venules) near the site of an injury. He saw that (1) blood vessels dilated, increasing blood flow to the area; (2) vascular permeability increased, resulting in the outward leakage of plasma, which formed an inflammatory exudate; and (3) white blood cells adhered to the inner walls of vessels and then emigrated through vessel walls to the site of injury.

Inflammation and repair can be divided into several phases. The characteristics of the early inflammatory response differ from those of the later response, and each phase involves different biochemical mediators and cells that function together to (1) destroy injurious agents and remove them from the inflammatory site, (2) wall off and confine these agents so as to limit their effects on the host, (3) stimulate and enhance the immune response, and (4) promote healing.

In contrast to the immune system, which is antigen specific and has memory, the inflammatory response is nonspecific because it takes place in about the same way, no matter what the stimulus, and occurs in the same manner, even on second exposure to the same stimulus. The acute response is self-limiting; that is, it continues only until the threat to the host is eliminated. This usually takes 8 to 10 days, from onset to healing. Inflammation is considered chronic if it persists longer than 2 weeks.

^ 2. Name and describe the systemic and local signs of inflammation.

Inflammation hallmarks

Systemic

Leukocytosis

Leukopenia (in inflammation of viral origin)

Fever

Change of protein composition of blood:

acute phase protein (acute inflammation)

 - and -globulins (chronic inflammation)

Change of ferment composition of blood: increase of transaminase, hyaluronidase, trombokinase activity

Increase of erythrocyte sedimentation

Change of hormone content:

catecholamins

corticosteroids

Immune system alterations and allergization of organism:

antibody titre

— appearance of sensibilizing lymphocytes in blood

— development of allergic reactions

Local

redness (rubor)

heat (calor)

pain (dolor)

swelling (tumor)

loss of function (functio laesa)

Legend:  — increase

^ 3. Name exogenic and endogenic flogogenic factors.

Etiology of inflammation (flogogenic factors).

Exogenic: infectious, bacteria, viruses, rickettsiae, parasites, fungi, non-infectious, physical, mechanical trauma, thermal, electrical, radiation, chemical, acids, alkalies, biological, foreign protein, animal insect poisons, psychogenic factors.

Endogenic: products of tissue decay, malignant tumour, trombi, infarctions, hemorrhages, salt deposition, saprophytic microflora.

  1. ^ Identify mechanism of alteration, microcirculation disorders in inflammatory focus.

Alteration. Primary injury. Secondary injury. Exudation. Vascular reactions: ischemia, arterial hyperemia, venous hyperemia, prestatic state, stasis. Extravasation of fluid. Margination of leukocytes. Emigration of leukocytes. Extravascular processes: chemotaxis, phagocytosis. Proliferation

5. ^ Identify the plasma protein systems and their roles in inflammation.

A) Inflammation is mediated by three key plasma protein systems: the complement system, the clotting system, and the kinin system. The components of all three systems are a series of inactive proteins (proenzymes) that are activated in cascade fashion.

B) The complement system can be activated by antigen-antibody reactions (through the classic pathway) or by other products, especially bacterial polysaccharides (through the alternative pathway), resulting in the production of biologically active (anaphylatoxic or chemotactic) fragments and target cell lysis.

C) The clotting system stops bleeding, localizes microorganisms, and provides a meshwork for repair and healing.

D) Bradykinin is the most important kinin protein and causes vascular permeability, smooth muscle contraction, and pain.

^ 6. Identify the role for mast cells, platelets, neutrophils, monocytes, macrophages and eosinophils in the acute and chronic inflammatory process.

A) The most Frequent activator of the inflammatory response is the mast cell, which initiates inflammation (1) by releasing biochemical mediators (histamine, chemotactic factors) from preformed cytoplasmic granules and (2) by synthesizing other mediators (prostaglandins, leukotrienes) in response to a stimulus.

B) Histamine and serotonin, produced by platelets are the major vasoactive amines of inflammation. Both cause constriction of bronchial smooth musde and vessels.

C) Phagocytic cells engulf and destroy microorganisms by enclosing them in phagocytic vacuoles (phagolysosomes), within which toxic products (especially metabolites of oxygen) and degradative lysosomal enzymes kill and digest the microorganisms.

D) Opsonins, such as antibody and complement component C3b, coat microorganisms and make them more susceptible to phagocytosis by binding them more tightly to the phagocyte.

E) The polymorphonuclear neutrophil (PMN), the predominant phagocytic cell in the early inflammatory response, exits the circulation by diapedesis through the retracted endothelial cell junctions and moves to the inflammatory site by chemotaxis.

F) The macrophage, the predominant phagocytic cell in the late inflammatory response, is highly phagocytic, responsive to lymphokines, and responsible for antigen processing and presentation to lymphocytes.

G) Eosinophils release products that control the inflammatory response and are induced by IgE-mediated mechanisms of hypersensitivity to kill parasitic organisms directly

^ 7. State the roles for lymphokines, interferon, and interleukins; note their relationships within the immune system.

A) The cells involved in immunity and inflammation stimulate other cells by secreting cytokines, especially interferons or interleukins.

B) Lymphokines are cytokines produced by T cells and have their most important effects on macrophages. These effects include chemotaxis, inhibition of migration once the macrophage has entered the inflammatory site, and activation of the macrophage, which makes it a more powerful phagocyte.

C) Interferons are produced by host cells that are already infected by viruses. Once released from infected cells, interferons can stimulate neighboring healthy cells to produce substances that prevent viral penetration.

D) Interleukins are produced by leukocytes that have been stimulated by an antigen. Interleukins stimulate other leukocytes to proliferate or otherwise increase their immune functions. The chief effect of interleukins is to accelerate the immune response.

8. ^ Identify mechanism of exudate formation.

Mechanism of exudate formation

Increased vessel wall permeability

Increase of filtrational pressure in venous part of capillaria and venuli

Intensification of ultrapinocytosis

Increase of osmotic and oncotic pressure in inflammatory focus

9. ^ Describe disturbance of microcirculation in inflammatory focus.

Transitory vascular spasm

Arterial hyperemia

Venous hyperemia

Prestatic condition

Stasis

Irritation of vasoconstrictors

Inflammatory mediators – irritation of vasodilation

Paralysis of vasoconstrictors

Acidosis

Decreased elasticity of connective tissue, surrounding vessels

Blood factors: erythrocyte swelling, leukocyte margination, exudation and pachyemia, activation of clotting system

Vascular wall factors: swelling of vascular endotelium

Surrounding tissue factors: exudate leukocytic infiltration of tissues

^ 5.1. Content of the theme. Define what is inflammation. Name and describe the systemic and local signs of inflammation. Name exogenic and endogenic flogogenic factors. Identify mechanism of alteration, microcirculation disorders in inflammatory focus. Identify the plasma protein systems and their roles in inflammation. Identify the role for mast cells, platelets, neutrophils, monocytes, macrophages and eosinophils in the acute and chronic inflammatory process. State the roles for lymphokines, interferon, and interleukins; note their relationships within the immune system. Identify mechanism of exudate formation.

Describe disturbance of microcirculation in inflammatory focus.

^ 5.2. Control questions of the theme:

  1. Define what is inflammation.

  2. Name and describe the systemic and local signs of inflammation.

  3. Name exogenic and endogenic flogogenic factors.

  4. Identify mechanism of alteration, microcirculation disorders in inflammatory focus.

  5. Identify the plasma protein systems and their roles in inflammation.

  6. Identify the role for mast cells, platelets, neutrophils, monocytes, macrophages and eosinophils in the acute and chronic inflammatory process.

  7. State the roles for lymphokines, interferon, and interleukins; note their relationships within the immune system.

  8. Identify mechanism of exudate formation.

  9. Describe disturbance of microcirculation in inflammatory focus.


^ 5.3. Practice Examination.


I. Circle the correct answer or answers for each question.

1. Inflammation: A. Destroys injurious agents B. Confines injurious agents C.Stimulates and enhances immunity D. Promotes healing E. All of the above are correct.

2. Inflammatory microcirculation changes involve all of the following except: A. Vasodilation B. Blood Flow rate increase C. Increased vascular permeability D. Emigration of leukocytes to the injury site.

3. A phagocyte’s role begins with an inflammatory response. The sequence for phagocytosis:

A. Margination or pavementing, recognition of the target, adherence or binding, and fusion with lysosomes inside the phagocyte D. Diapedesis, margination or pavementing, phagosome formation, recognition of the target, and fusion with lysosomes inside the phagocyte C. Recognition of the target, margination or pavementing, and destruction of the target by lysosomal enzymes D. Margination, diapedesis, recognition, adherence, ingestion, fusion with lysosomes inside the phagocyte, and destruction of the target

4. Chemotactic factors for phagocytes include all of the following except: A.Complement components D. Streptolysins C. Plasminogen activator D.Prostaglandins E. Mast cell degranulation products.

5. Which is not a local manifestation of inflammation? A. Swelling B. Pain C.Heat D. Leukocytosis E. Redness.

6. Complement is: A. A series of proteins in the blood B. An antibody C. A hormone D. A lymphokine.

7. Diapedesis is a process in which: A. Neutrophils migrate from the bloodstream to an injured tissue site. B. Phagocytes stick to capillary and venule walls C. Bacteria are “coated” with an opsonin D. There is oxygen-dependent killing of cells

8. Interferon: A. Interferes with the ablity of bacteria to cause disease B.Prevents viruses from infecting healthy host cells C. Inhibits macrophage migration from inflamed sites D. Increases the phagocytic activity of macrophages E. Increases the number of circulating neutrophils.

9. The complement system can be activated by: A. The binding of complement 1 to a complement binding site of an antibody B. Components of other plasma protein systems C. The binding of complement 3 to bacteria D. Both A and C are correct E. A, B, and C are correct.

10. Which is not a systemic manifestation of inflammation? A. Leukocytosis B.Fever C. Increased acute-phase reactants D. Exudation.

11. The inflammatory response: A. Prevents blood from entering the injured tissue B. Elevates body temperature to prevent spread of infection C. Prevents formation of abscesses D. Minimizes injury and promotes healing.

12. Scar tissue is: A. Nonfunctional collagenous and fibrotic tissue B.Functional tissue that follows wound healing C. Regenerated tissue formed in the area of injury D. Fibrinogen which has entrapped phagocytes and neurons.

13. Which mast cell mediator is not preformed? A. Histamine B. Leukotriene C. Neutrophil chemotactic factor D. Eosinophil chemotactic factor of anaphylaxis.

14. Swelling during acute inflammation is caused by: A. Collagenase B. The fluid exudates C. Lymphocytic margination D. Neutrophilic margination E.Anaerobic glycolysis.

15. Which is not released from mast cells during degranulation?

A. Chemotactic factors B. Histamine C. Complement D. Vasoactive amines.

16. Chronic inflammation is characterize by: A. Hypertrophy B. Metaplasia C.Neutrophilic infiltration D. Lymphocytic and macrophagic infiltration All of the above are correct.

17. Interferons: A. Specifically kill viruses B. Attach to receptors on neighboring host cells C. Are host specific D. Both B and C are correct E. A, B, and C are correct.

18. Intracellular adhesion molecules (ICAMs): A. Include integrins B. Promote adhesion of leukocytes to endothelium C. Are membrane bound proteins D. A, B, and C are correct.

19. Which is not true of interleukins? A. They provide messages between leukocytes B. They are produced in response to tissue injury C. They stimulate cells to produce antiviral substances D. They increase antibody production and populations of T cells E. All of the above are true of interleukins.

20. Eosinophils: A. Are agranulocytes B. Control the vascular effects of serotonin and histamine by lysosomal mediators C. Have a lysosomal protein that can dissolve the surface membranes of parasites

D. All of the above are correct E. Both B and C correct.

II. Match the term with the definition or characteristic.

21. Resolution 22. Bradykinin 23. Granulation tissue 24. Fibroblasts 25. Scar

A. Increases the phagocytic activity of macrophages B. Restores original structure and physiologic function C. Inhibits macrophage migration from the inflamed area D. Increases vascular permeability

E. Forms new capillaries, fibroblasts, and macrophages F. Does not create vascular reactions

G. Synthesize and secrete collagen H. Proliferate antigen-specific clones of B and T cells


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. 70-80.

2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study guide for medical students and practitioners.-Odessa, 2003.- P. 68-82.

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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