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Questions to control basic knowledge.

1. Give definition, causes and mechanisms of productive inflammation.

2. Give classification of productive inflammation.

3. Give classification of granulomas.

4. Explane morphological characteristic of tuberculosis, syphilitic, leprous and rinoscleroma inflammation.

5. Explane morphology and consequences of the productive inflammation.

6. Give definition and classification of immunopathologic processes.

7. Give classification and morphology characteristic of autoimmune diseases.

8. Name phases of immune inflammation.

9. Give characteristic of humoral immune reaction.

10. Give characteristic of cell immune reaction.

11. Give morphologcal characteristic of immune inflammation.

12. Give classification and morphological characteristic of immunodeficiency syndromes.

Visual aids.

Gross specimens: miliary tuberculosis of the lungs, kidneys in systemic lupus erythematosus.

Microscopic specimens: miliary tuberculosis of the liver, miliary pulmonary tuberculosis, tuberculosis lymphadenitis, hepatic gumma, lepromatous form of leprosy, actinomycosis, foreign body granuloma.

Electron micrographs: Pirogov-Langhans’ giant cell, Mikulich’s cell.

Annotatedtables (pictures, schemes, classifications): the classification of granulomas, morphogenesis of granuloma, the classification of productive inflammation, the phases of granuloma development, the of immune inflammation.

Slides: multichamber Echinococcus in the liver, pulmonary actinomycosis.

Algorithm of the topic.

Theoretical part.

Productive inflammation is characterized by the reproduction (proliferation) of cellular elements in the alteration zone, their differentiation and transformation. These processes are observed in the local cells, or histiogenic origin (cambial epithelial and mesenchymal elements) and hematogenic - (monocyte, lymphocyte).

The agent causing productive inflammation stimulates the cell proliferation but does not cause any essential metabolic and blood supply disturbances. Therefore, cell proliferation is gradual, and the inflammation itself is not acute. So the proliferation phase is more pronounced than exudative.

Its acute form is observed in the cases of inflammation originating in the organs with a high level of regenerative activity. They include lymphoid tissue (lymph nodes, intestinal lymphoid follicles). The morphological changes occurring in those tissues resemble hyperplasia, though they are different from it in such signs of inflammation as alteration and exudation. Acute productive inflammation may be observed in the kidneys (glomerulonephritis) and in the cardiac valves (rheumatic endocarditis).

The proliferation and transformation processes caused by productive inflammation may form focal alterations, or granulomas. They are formed around foreign bodies or unviable products of tissue decay, thus creating giant multinuclear cells. This phenomenon is observed in fatty tissue necroses (murine typhus), in the tissues around the operative sutures, near dermatozoons, etc. The giant cells forming a part of an inflammatory infiltrate are in close contact with the above structures and sometimes surround them almost completely.



The granulomas formed as a result of microbial penetration into the body are the most important clinically. These granulomas are named infectious (specific). They cause penetration of the infectious agent (leprosy bacillus, Koch's bacillus, treponema pallidum) to different inner organs through the blood stream, which in turn causes granulomatous inflammation.

Getting into the body, the pathogenic agent does not always cause the same cell reaction. In these cases the degree of immunity defense and the immuno-biological reactivity state of the organism are of utmost importance. The body sensitivity may be increased or decreased, therefore the tissue alterations may be absolutely different.

Sometimes their course differs from productive inflammation which causes granuloma formation but has exudative character, represented as small focal necroses. In some cases (tuberculosis, syphilis) the pathogenic agent may be found in the body in the latent phase, causing no visible changes. This is mostly connected with the immune system and the peculiarities of its cellular and humoral reactions, that is the development of immunopathological processes.

These are the processes which onset is connected with functional disturbances of the immunocompetent system. They form the basis for immunopathology – the science studying the diseases originating from immunological homeostasis disturbances.

One of the kinds of immunopathological processes is autoimmunization, bazed on the autoantibody formation and (or) sensitized lymphocyte; their activity is directed against the antigens of the body tissues.

Diseases developing on the basis of autoimmune processes are called autoimmune diseases. Immunodeficiency syndrome is an extreme manifestation of the immune system deficiency. These syndromes may be primary, caused by the immune system hypoplasia (aplasia) – hereditary and congenital immunodeficiency

syndromes – and secondary ones originating due to disease or resulting from its treatment – acquired immunodeficiency syndromes.

The morphology of immunopathologic processes is represented by: a) immunocompetent tissue changes caused by antigen stimulation and immunodeficiency; b) local immune reactions or hypersensitivity reactions, immediate and delayed reactions included, and transplantation immunity reactions (rejection reaction).

According to the mechanism of their development, hypersensitivity reactions are referred to several groups: anaphylactic reactions of immediate type, cytotoxic reactions connected with toxic immune complexes (immunocomplex), reactions connected with the effector cells action, granulomatous reactions. Immediate-type hypersensitivity reactions (ITH) cause acute immune inflammation, while delayed-type hypersensitivity reactions (DTH) cause chronic immune inflammation.

Thus, productive inflammation develops in case of a pathogenic agent’s persistence and is connected with imperfect exudative reactions (often caused by polymorphonuclear leukocytes defects) or with peculiar properties of the causative agent (its resistence against phagocytes – incomplete phagocytosis or endocytobiosis). The inflammation is accompanied with the appearance of focal or diffuse infiltrates including macrophages, lymphocytes and plasmocytes. Transformation of macrophages into epithelioid cells, as well as that of all the other cells – into giant cells (foreign body or Pirogov-Langhans’) is characteristic, as well as increased fibroblast activity. Inflammation mediators appear in the process of monocyte-macrophage interaction with lymphocytes.

Monocytes appear in the productive inflammation zone as a result of chemotaxic factor activity and their transmutation into macrophages – the central cells of this process. Macrophages secrete cytokins which activate lymphocytes; these also secrete cytokins which, in their turn, activate monocytes and macrophages, causing their proliferation and transformation. Monocytes (macrophages) also secrete growth factors that cause fibroblasts proliferation, and vegetations of the vessels and connective tissue.

Granulomatous inflammation is characterized by formation of granulomas, in which activated macrophages are dominating. Here the agent (exciter) of resistence to phagocytes (inability of monocytic phagocytes in respect to the agent) is of utmost importance.

In the process of granuloma development the antigen which is not considered completely harmless constitutes a macrophage to lymphocyte (helper). The latter excretes cytokins which stimulate monocyte and macrophage transformation into epithelioid and giant foreign body or Pirogov-Langhans’ cells. In the transformation process the phagocyte activity of the macrophage is diminished, but its secretory activity is growing, and involves more and more monocytes into the granuloma.

Practical part.

Miliary tuberculosis of the lungs. Gross specimen.

The lungs are chubby, there are small greyish nodules in their tissue. In chronic miliary tuberculosis the nodules are disseminated all over the lung parenchyma.

Kidneys in systemic lupus erythematosus. Gross specimen.

The kidneys are enlarged, their surface is motley, with patches of hematomas of irregular shapes. The parenchyma is dull on section, the cortex layer is greyish, the medullary layer is cyanotic.

Miliary tuberculosis of the liver. Microscopic specimen.

Specific granulomas, or tubercles, are characteristic. The process of their formation is gradual: first Mycobacterium tuberculosis causes alteration of an area in the invasion zone accompanied with exudation, further – a small amount of fibrin and separate leukocytes appear. At the same time, there is proliferation of cell elements. The cells forming granuloma are represented with lymphoid and epithelioid elements and are of hematogenic origin:

Monocytehistiocyte macrophage

Pirogov-Langhans’giant cell

Macrophage epithelioid cell

Epithelioid cells are of oval or irregular bullet-like shape, their nuclei are elongated, light. The majority of giant cell nuclei are situated on the periphery and form a ring or a horseshoe shape. Their structure resembles epithelioid cell nuclei; their cytoplasm is homogeneous, pale in colour. The number of giant cells in the granuloma varies, sometimes they are completely absent. At first these cells are located in the central sectors of the granuloma, on the border of the caseous necrosis zone, later on they move to the periphery. Lymphocytes appear on the granuloma periphery, and therefore these sections seem more intensively coloured.

In the liver the granulomas may be situated both inside the hepatic particles and outside them, that is in the interparticle layers, close to the blood vessels and bile ducts. Due to the fact that the granulomas are scattered all around the parenchyma and do not reach considerable sizes the organ structure remains the same.

There are certain distinctions between the granulomas in the interparticle layers and inside the particles. So, the granulomas localized beyond the particles consist of epithelioid and lymphoid cells, and the number of lymphocytes may be larger than the number of epithelial cells. Giant cells are rare. In the periportal tissue there are secondary inflammatory alterations characterized by infiltrates containing lymphocytes and histiocytes. Connective tissue layers become rough and thickened.

If the granulomas are localized inside the particles, hepatocyte destruction is noted in the central regions of the particles. Epithelial cell formation is more pronounced, while necrotic changes in the cell are less pronounced. Besides epithelial cells, these granulomas contain fewer lymphocytes; sometimes one can observe single leukocytes, as well as fibrin.

The intraparticle granulomas vary in size: they may be represented by rather considerable aggregations of epithelioid cells, or they may look like small foci of necrosis. Their contours are not clear, owing to the absence of the peripheral ridge of lymphoid elements.

Miliary pulmonary tuberculosis. Microscopic specimen.

This is characterized with the onset of tuberculous granulomas (nodules) in the lungs. In the centre of such a granuloma there is a detritus surrounded with a ridge of epithelioid and lymphoid cells with an admixture of macrophages and plasmocytes. A frail network of argyrophile fibers can be distinguished among epithelioid cells due to impregnation with silver. The circulatory capillaries are absent. The granuloma cells are of hematogenic and histiogenic origin. The presence of the giant cells of Pirogov-Langhans is characteristic; these cells appear as a result of epithelial cell fusion, division of these cells without the cytoplasm division, or as a result of proliferation and hemocapillary endotheliocyte fusion, situated in the outer zone of the granuloma in small amounts.

Tuberculosis lymphadenitis. Microscopic specimen.

Tuberculous granulomas of characteristic productive-type structure are found in the node tissue. They incorporate giant cells of Pirogov-Langhans with a great number of nuclei in the peripheral zone.

Hepatic gumma. Microscopic specimen.

The basis for productive inflammation lies in specific granuloma, or gumma, the formation observed in the tertiary period of syphilis; it may be single (solitary gumma) or multiple (miliary gummas). The latter are small and are most frequently observed in children with congenital syphilis.

Unlike tuberculous granuloma, gumma is rich in blood vessels surrounded with small cellular infiltrates composed of polymorphonuclear leukocytes, lymphocytes and plasmocytes. The latter are characteristic of syphilis.

The infiltrates also contain epithelial cells, sometimes – giant cells of a foreign body type. A characteristic feature of syphilis is very early, almost simultaneous with the appearance of epithelioid cells, appearance of fibroblasts, collagen fibers and newly formed blood capillaries.

The blood vessel walls (small arteries, veins) are infiltrated with lymphoid elements, their lumens are narrowed due to the intimal thickening caused by an inflammatory process (endarteritis, endophlebitis).

The necrotic alterations with further connective tissue growth are gradually develops in the gumma. Their development is caused by vessel obliteration and toxic action of the Spirochaeta pallidus poison. Caseous necrosis is found in the central part of the gumma; first cellular elements undergo destruction, while collagen and elastic fibers remain intact for a long time. That is why the necrotic area is not homogeneous and structureless, unlike that of tuberculous granuloma, but keeps the tissue contours, which is characteristic of gumma.

While in the central part of gumma caseous necrosis is developed, the cellular elements on the periphery, represented by lymphocytes and plasmocytes, remain intact. The tendency to considerable connective tissue development, characteristic of syphilitic granulomas, may also appear when there is no gummal necrosis. In such cases the collagen fiber proliferation causes gradual disappearance of cellular elements, and the granuloma is substituted with connective tissue.

Microscopically: liver gumma is composed of the necrotic zone, specific granulation tissue, and adjacent altered parenchyma sites. The nuclei of the destroyed cells are almost never encountered in the necrotic zone, this zone is microgranular or fibrous in structure, sometimes there are calcareous deposits on its periphery (in old gummas).

Adjacent to the necrotic zone, there is indurated fibrous tissue with fibroblasts and histiocytes in it. Their amount grows while the necrotic masses resolve. Lymphocytes and plasmocytes form small aggregations in gumma. Giant and epithelial cells are rarely encountered. Inside the granuloma one can also find newly formed vessels, capillaries, veins, arteries and bile ducts. Their walls are thickened, their lumens are narrowed. Hepatocytes situated on the periphery of gumma have pyknomorphous nuclei, signs of lipid dystrophy and dcomposition, the trabecular structure of the particles is broken.

Lepromatous form of leprosy.Microscopic specimen.

This form is characterized by the appearance of separate nodules or granulomas in the skin (derma). The granuloma mostly consists of macrophages with a small amount of lymphocytes, plasma cells, histiocytes. There is a large number of leprous mycobacteria, especially in the macrophageal cytoplasm. These cells are gradually enlarged, separate vacuoles and lipid drops appear in them – the Virchov’s cells, characteristic of leproma, appear.

Actinomycosis. Microscopic specimen.

Actinomycosis is characterized by granulation tissue composed of epithelioid and round cells with occasional xanthomic cells, Russel’s corpuscles. One should note the appearance of small pustules, each containing a druse of radiant fungus. In the intervals between the pustules and on the periphery the granulation tissue displays the ability to fibrous transformation.

Foreign body granuloma. Microscopic specimen.

This granuloma appears as a productive-type inflammatory process in response to penetration of foreign bodies into tissues. The granuloma is composed of remnants of a foreign body (catgut, etc.), large amounts of giant multinuclear cells of Pirogov-Langhans type, lymphoid-histiocytic elements and fibroblasts.

Pirogov-Langhans’ giant cells. Electron micrograph.

There is a large number of nuclei situated on the periphery of the cell cytoplasm. Lipid vacuoles are encountered in the endoplasmatic network tubules.

Mikulich’s cell. Electron micrograph.

There are large vacuoles in the cytoplasm, containing the disease agent (Volkovich-Frisch bacilla).

Multichamber echinococcus in the liver. Slide.

Necrotic cites with remnants of parenchyma containing single cavities of various sizes and shapes are determined microscopically. Their edges are clearly limited (chitin membrane of the finna). There are rare scolexes on the inner surface. They may be revealed only by round or oval structures having a corolla of more intensively coloured tenacula.

Pulmonary actinomycosis. Slide.

The disease develops as a result of the fungus getting into the lungs in the blood flow and is characterized by granuloma formation. The process is spread widely, so the lung structure is greatly changed.

There are separate granulomas (nodules) of various sizes in the lung tissue, with druses of fungi. The central granular part of the actinomycotic druse is of light purple colour while their ends are pinkish-red; therefore the coloured druse has a specific radiant shape. The nodule borders are not clear due to considerable infiltration; there is also a considerable spread of collagenous fibres forming hyalinized fascicles.

Tasks for self-control.

Task ¹ 1. Prolonged injection of camphor has caused a small induration in the right buttock soft tissues of the patient with chronic cardiovascular failure (lower extremity edema, ascites, anasarca). Histologic investigation of the bioptate of subcutaneous tissue nodule taken from the extremity revealed aggregations of macrophages, leukocytes, as well as cells with lipid drops in the cytoplasm: a)put the diagnosis; b) name the cells that contain lipid; c) name the disease in which an analogous process is observed.

Task ¹ 2. The autopsy of the patient who died of chronic tuberculosis has revealed many greyish nodules of a millet grain size in the lungs: a) put the diagnosis; b) name the morphological substrate of the disease; c) describe the micromorphology of the process.

Task ¹ 3. The bioptate of the muscle has been taken from the patient with cardiac insufficiency during the operation of commissurotomy. The microscopic study of the left atrium auricle has revealed aggregation of macrophages, plasmocytes, separate lymphocytes and leukocytes. There is also a moderate growth of connective tissue along small caliber vessels: a) put the diagnosis; b) establish the character of the pathological process; c) name one of the consequences of this process.

Task ¹ 4. During the last four months the patient noticed general weakness, fatigue after physical exercise, progressive weight loss (he lost nine kilograms during the last three months), aversion to meat products. An autopsy revealed carcinoma of the stomach with metastases into the liver, a crater-like depression with dence edges, of gray colour, 3,5-2,5 cm in diameter, in the anterior wall of the left ventricle of the heart: a) what changes in the heart muscle may be supposed? b) Name the cells characteristic of this pathological process. c) State the period in which the characteristic features of the process appear.

 

Final revision 1


Date: 2016-03-03; view: 662


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