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Questions to control basic knowledge.

1. Give the definition of inflammation.

2. Give the characteristic of the inflammation phases.

3. Name the main mediators of inflammation.

4. Give the classification of inflammation.

5. Give the comparative characteristic of exudate and transudate.

6. Describe morphology and consequences of the different kinds of exudative inflammation.

Visual aids.

Gross specimens: croupous pneumonia (gray hepatization), fibrinous pericarditis, suppurative nephritis, diphtheritic colitis, liver abscess.

Microscopic specimens: serous hepatitis, fibrinous pericarditis, focal bronchopneumonia, croupous (fibrinous) pneumonia, liver abscess.

Electron micrographs: micropinocytosis of endotheliocyte, migration of leukocyte through the capillary wall, labrocyte degranulation, fibrinous pericarditis, acute catarrhal bronchitis, migration of erythrocyte out of the capillary.

Annotatedtables (pictures, schemes, classifications): classification of inflammation, acute ulcerophlegmonous cholecystitis, focal bronchopneumonia, classification of the inflammation mediators, fibrinous pericarditis, kidney abscess, serous dermatitis.

Slides: liver abscess, pneumonia complicated by an abscess, purulent cerebrospinal leptomeningitis, fibrinous pericarditis (“hairy heart”), diphtheritic colitis, fibrinous tonsillitis, acute catarrhal bronchitis, inflammatory hyperemia of the brain tunic.

Theoretical part.

Inflammation is a severe, predominantly local vessel-mesenchymal reaction, which occurs in the response to the action of different pathogenic agents or aggressive stimuli. Inflammation has a defensive character, because it is aimed for the liquidation either causative agents, or the consequences of their destructive activity. But an inflammation could be unhealthy, because it can cause the hypersensitivity reactions, can lead to sclerosis or fibrosis.

Five basic symptoms of inflammation include redness (rubor), swelling (tumour), heat (calor), pain (dolor) and impaired function (functio laesa) have been known since the ancient Greek and Roman era. These signs are due to extravasation of plasma and infiltration of leukocytes into the site of inflammation.

There are three factors in the basis of inflammation: impairment of metabolism, that appears as alteration; changes of the microvessels system, that appear as exudation and as the cells elements migration; reproduction, differentiation and transformation of cells in the injury zone (proliferation).

The alteration appears as the different kinds of the dystrophy, in more advanced cases — by the restricted or extended necrosis. The inflammatory liquid (exudate) and cellular infiltration form in the exudation phase as a result of blood redistribution in the microvessels system and increase of their permeability in the injury zone. The proliferation phase is characterized by the processes aimed for recovery of the injured zone. It consists of the differentiation and transformation of different hematogenous and histiogenous cell elements.

The histological evidences of the inflammation are severe, but it is possible to ascertain the type of inflammatory reaction by the cells characteristic and distribution of the inflammatory infiltration. For example, polymorphonuclear leukocytes predominance proves an exudative inflammation; on the other hand, the infiltration consisting mostly of lymphocytes and histiocytes gives evidence of the productive inflammation; and the presence of plasmocytes in the infiltration is observed in lingering chronic inflammation.

In exudative inflammation, the pressure in postcapillary venules may overcome the osmotic pressure of plasma proteins. Therefore fluid and low molecular substances have the tendency to penetrate into the surrounding area. These processes are related to accumulation of inflammation mediators in the alteration zone (histamine, serotonin, kinins, active globulins, nucleus acids).

An important role in production of mediators belongs to the labrocytes, which contain histamine, serotonin, heparin. The granule matrix of the labrocytes is formed with the participation of ribosomes (protein synthesis) and Golgi apparatus (heparin synthesis). Histamine connects to protein-polysaccharide granules matrix of labrocytes (the mitochondrion makes this process).

Increasing of tissue-vascular permeability is provided by appearance of the labrocytes near the capillaries and production histamine and serotonin by them. These processes contribute to accumulation of heparin (inhibitor of coagulants and hyaluronidases) and indicate the involvement of these cells into vasotonic regulation, blood clotting process and fibrinolysis, capillary and tissue permeability, and as a result, exudate forms in the alteration zone.

According to inflammation character and its localization, we differentiate serous, fibrinous, purulent, putrefactive, hemorrhagic, catarrhal and mixed types of the inflammation. The hemorrhagic inflammation is not a separate type, here the erythrocytes are added to the other blood formed elements. The catarrhal inflammation is described as admixtures of mucus and desquamated epithelial cells to serous or purulent exudates.

In summary, inflammation — is protective and adaptive reaction aimed for removal of pathogenic agent, restriction of the injury zone and regeneration of the tissue or organ structure.

The alteration is initial phase, characterized by onset of the mediators, which determine all further inflammation development phases. There are two kinds of the mediators: plasmatic and cellular. They act as autocatalytic system by the reverse link principle. There are four phases in the exudation process, they are: microvasculature reaction; increasing microvascular permeability; the fluid and plasmatic proteins logging out, penetrate into the tissue; cells also migrate to the site of injury.

During the proliferation takes place the reproduction of cells: macrophages, cambial mesenchymal cells, smooth muscle cells and epithelium; differentiation and transformation of the cells: macrophage-epithelioid cell, giant cell, B- lymphocyte, plasmocyte, cambial mesenchymal cell, fibroblast. Proliferation and differentiation of cell elements occur by means of cytosines and multitudinous growth factor.

Practical part

Fibrinous pericarditis. Gross specimen.

It is the most essential for acute rheumatic polyarthritis. Pericarditis develops due to the process in the myocardium and cardiac valves. Besides this pericarditis can occurs in the course of the other diseases, it results from its spread from such organs and tissues as lungs, pleura, mediastinum or as the result of the spread of infection with blood to the pericardium vessels.

Fibrinous exudate as a rule forms on the both laminas of the pericardium, and fills the whole pericardial cavity. Fibrin is coagulated on the epicardial surface, in the course of time it hardens so the heart acquires a special look — “cor villosum” or “hairy heart”.

Liver abscess.Gross specimen.

The purulent inflammation germs penetrate into the liver throuth the blood vessels or the bile ducts, seldom — throuth the lymphatic vessels or as a result of immediate contact with the neighbouring organs. This inflammation has self-limited character, that is characterized by abscess formation. A small abscess has embolic origin in those cases when pyogenic bacteria penetrate with blood-tinged exudate. Abscesses look like yellow-gray nodules, the contents of these nodules looks like porridge, on its periphery they are separated from the parenchyma.

A big abscess appears in case of generalized infection spread throuth the branchlet of the v.portae (pylephlebitic abscess) or throuth the bile ducts (cholangiolitic abscess). A single liver abscess could exist during a long time and has chronic character. In these cases abscess is the pus-filled cavity which has granulation tissue paries.

Fibrinous pericarditis. Microscopic specimen.

An inflammation begins as the vessels widening, which occurs in fatty or connective tissue in the pericardium. The most of fibrin is deposited on the pericardium surface and looks like fine-filamented plexuses on the surface, then it has homogeneous structure containing leukocytes.

Mesothelium edemas, gradually desquamated. The number of fibrin augments, it becomes thicker than the pericardium and the border between the exudate and tissues disappears. Then the leukocytes come out of the vessels, they are accumulated in the tissue and in the fibrin composition. Fibrin fibers merge with each other and look like homogeneous mass. Then the pericardium undergoes another process: so-called “organization”. Histiocytes which enter in between fibrin fibers appear adjuncent to the vessels and in the epicardial connective tissues. New vessels appear, connective tissuesgrow up that influences fibrin organization. Mesotelicytes don’t reproduce, and the result is adhesions of the both pericardium leaves.

Liver abscess.Microscopic specimen.

Liver abscess occurs respectively to blood vessels and bile ducts location in the connective tissue. The onset is assotiated with infiltration of leukocytes in the vessels or duct walls, followed by their necrosis. Necrosis site is surrounded by coming leukocytes from the adjacent parenchyma vessels.

Cells are locate between the connective tissue fibers and between liver cords, here hepatocytes are destroyed. Microorganisms grow among the destroyed leukocytes, they perish the new liver cords and it makes the abscess bigger.

Thus the structure of the liver lobule is destroyed. The abscess looks like a part of oval or circular in form intensively colored by hematoxylin and infiltrated by many leukocytes. Sometimes the central divisions of these parts are not so colored, it is connected with nuclear chromatin dissolution. Bacterial accumulation often occurs in this sites. On the abscess periphery the liver cords are squeezed, their cells are depressed, there are many hepatocytes with pyknotic nucleus. The cells that are adjacent to the abscess have the signs of fatty degeneration. Polymorphonuclear leukocytes are found in the capillaries. In chronic process granulation tissue grows on the abscess periphery. There are many new microvessels and different cells in the granulation tissue.

Phlegmon of subcutaneous fat.Microscopic specimen.

The purulent inflammation allows the staphylococcal or streptococcal infection to spread from the penetration place. The change of epidermis is not so significant. Small perivascular infiltrations in the derma vessels occur. The most considerable changes are in the depth of the tissue. Many leukocytes are found here so the fibers contours disappear. The most leukocytes have nucleus with signs of karyorrhexis and karyopicnosis. Sometimes leukocytes overlap the lymphatic vessels lumens.

Fibrinous tonsillitis.Microscopic specimen.

The fibrinous film on the tonsil surface is closely connected with the tonsil tissue and it is infiltrated with leukocytes.

Serous dermatitis.Microscopic specimen.

Serous exudate contains about 2% of protein and some cell elements. In skin this process appears as the bubbles with desquamation of the epidermis, swelling of the derma structure, discirculatory changes in the microvessel system.

Fibrinous (croupous) pneumonia.Microscopic specimen.

Alveoli are filled with exudate. Exudate consists of fibrin, polymorphonuclear leukocytes, macrophages, between alveolar septum with oedema character.

Acute ulcerophlegmonous cholecystitis.Microscopic specimen.

Gallbladder wall has the signs of oedema, desquamation of the mucous shell epithelium, focal destruction, diffusinfiltration of polymorphonuclear leukocytes, and dyscirculatory disturbance in the microvessel system.

Micropinocytosis of endotheliocyte.Electron micrograph.

There are multiplicity of small vesicles spread along the plasmolemma in the endothelial cytoplasm. The capillary lumen is narrowed, the nuclear structure is not changed, basal membrane is swollen.

Migration of leukocyte through the capillary’s wall.Electron micrograph.

One segmental leukocyte is seen on the endothelial surface of the capillary, cytoplasm of the other leukocyte is in the subendothelial layer.

Migration of erythrocyte from the capillary.Electron micrograph.

There are erythrocytes with deformations in the pericapillary zone near labile interendothelial cleft.

The classification of inflammation. Table.

The classification of mediators. Table.

Purulent cerebrospinal leptomeningitis.Slide.

Purulent inflammation of the meninx vasculosa has extended character because perivascular space connects with subarachnoidal one along the brain vessels. The tissue isn’t changed, but sometimes there are small hemorrhage and softening areas. Exudate fills in subarachnoidal and perivascular spaces. It contains leukocytes, fibrin, erythrocytes. Meninx vasculosa is thickened, the connective tissue fibers cann’t be detected.

Acute catarrhal bronchitis.Slide.

Bronchial mucous tunic is thickened, the mucus is accumulated in cell the cytoplasm. There are a lot of polymorphonuclear leukocytes in and at the surface of the bronchial shell and between the epithelial cells.

Blood vessels are full of blood. There are negligible cell infiltrations around the vessels. This infiltrations are located in the wall of the major bronchi near the glands and between muscular fibers, in the small bronchi the infiltrations are not big, with the nucleus chromatin consolidation.

Inflammatory hyperemia of the brain tunic.Slide.

A big plethora and swelling of the brain shells (serous meningitis).

Date: 2016-03-03; view: 1058

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