Общая патологическая анатомия животных = Introduction to the pathological anatomy of animals. Учебно-методическое пособие

Morphological scheme of inflammation

Zone of lymphoid cells

The fibroblast zone is

connective tissue

Functional diagram of the inflammation

Zone of alteration (necrosis, dystrophy)

Zone of arterial hyperemia (mediators of inflammation, exudate)

Zone of venous hyperemia (hypoxia,

transudate)

Scheme of the relationship of venous stagnation and inflammation.

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Venous congestion

Stagnant Hypoxia Transudate phenomena

(increased vascular porosity)

Inflammation

Proliferation (organization, encapsulation, sequestration, scarring)

Purulent inflammation

Causes – cocci, dwarven microorganisms, brucella, fungi, helminths. Depending on the infection that caused purulent inflammation, the following types of pus can be distinguished:

1.Staphylococcal pus: whitish-yellow, creamy-like, sometimes with fibrin flakes.

2.Streptococcal pus: liquid, fetid, gray-yellow or gray-brown (due to blood impurities).

3.Pus induced by E. coli: green-brown, has a specific lovely smell.

4.Pus induced by Pseudomonas aeruginosa: thick, fetid, pale or gray - green color.

5.Tuberculosis pus (typical for tuberculosis in dogs): liquid, with whitish flakes (curd pus).

6.Brucellosis pus: is a purulent hemorrhagic exudate of an oily consistency of gray-yellow color.

7.Actinomycosis pus: thick, sourcream, and then plasticine-like. While palpating does not stain your hands, odorless, when rubbing

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through your fingers in the mass of grains palpated – it's druses fungus that induce pus.

Depending on the localization of pus we distinguish:

1. Abscess: a newly formed cavity filled with pus, formed as a result of the lytic action of pus serum enzymes on the tissue. Elevated enzyme activity in the wall of the abscess may lyse. The contents of the abscess enter the bloodstream and forms purulent embolism, which leads to the formation of purulent metastases – daughter abscesses. Most often these abscesses are formed in the lungs, liver, kidneys. The size of abscesses is very variable: furuncle, carbuncle, and under the epidermis

– pustule (all this – skin rashes).

Morphogenesis abscess formation: initially, the tissue is penetrated by pyogenic micro-organisms and the lysis of tissue with the formation of tissue impregnated with pus. Then, around the dwarven microorganisms abundance of cells begin to accumulate (micro - and macrophages, which are designed to phagocytize dwarven microorganisms). Dying micro-and macrophages form pus. Then, around the mass of pus cell elements multiply and form capsule-abscess encapsulates.

2.Empyema is a purulent inflammation of serous cavities. Purulent pleurisy, purulent peritonitis, etc.The main cause is injury or breakthrough of the abscess into the serous cavity. Thus inflamed serous integument are covered with pus, dull, swollen, hyperemic, with hemorrhages.

3.Phlegmon is a diffuse purulent inflammation with infiltration of the tissues with pus. It is observed in organs and tissues, where there is a lot of loose fiber – most often in the intermuscular. The phlegmon area is swollen, without clear boundaries, doughy consistency, bluishred. From the surface of a cut a turbid pussy mass flows down which is a mixture of pus and blood. In severe cases, there is a melting of the tissue and the formation of an abscess. Phlegmon of subcutaneous fat is called cellulite. The outcome and clinical value depend on the volume, severity of purulent inflammation, reactivity of the body. Extensive suppuration leads to protein deficiency, depletion of the body and a sharp violation of reactivity.

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Hemorrhagic inflammation

This is a severe form of inflammation that occurs with the formation of exudate, which is dominated by red blood cells. It accompanies severe changes in the microcirculatory bed. It is characterized by an increase in the permeability of the vessel wall, through which blood passes easily: red blood cells.

Etiology: the main cause is septic infections (anthrax, pasteurellosis, plague, etc.).

Morphologically, there is hyperemia of tissues, hemorrhagic exudate accumulates in natural cavities, there are foci of erosions, ulcers, necrosis.

Examples:

1.Hemorrhagic inflammation – anthrax carbuncle. The site of the lesion is swollen, dark red, from the surface of the incision bloody exudates flows, in the future there is necrosis of tissues and mutation (tissue rejection) with the formation of bleeding ulcers.

2.Hemorrhagic pneumonia – hemorrhagic exudate accumulates in the lumen of the alveoli, bronchioles and can affect slices and whole lobes. Pneumatic hearth is dark red in color, resembles liver in consistency (hepatization), bloody liquid flows from the cut surface.

3.Hemorrhagic enteritis – hemorrhagic inflammation of the intestine. Mucosa is swollen, increased in volume, impregnated with blood, covered with effusion, which is a mixture of mucus, blood and chyme, because of what the mucosa becomes of dirty-coffee color. In the large intestine the contents turn black (melena). The mucous membrane is often necrotic. Erosion, ulceration, and sometimes perforation areas form.

4.Hemorrhagic lymphadenitis – inflammation of the lymph node. Lymph nodes are swollen, increased in volume, bloody red, with necrosis foci. The section has a marble pattern due to the alternation of inflamed foci with gray-white foci of its own tissue.

Hemorrhagic inflammation is the most severe form of inflammation. The outcome is unfavorable. The clinical significance lies in the deep disruption of the functioning of the inflamed organ. Many forms of inflammation, especially vital organs, lead to death.

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Putrid (ichorous, gangrenous) inflammation

This is a severe form of inflammatory reaction, which is often gangrene, when exudative type of inflammation is complicated by the putrefactive microflora, primarily anaerobes (clostridia). Multiplying, microorganisms emit gases, lead to the lysis of tissues, inflamed areas liquefy, dirty-green or gray color, they easily disintegrate, smell foully and pose a tremendous danger for the body.

Catarrhal (from the Greek. “catarrheo” – “draining”)

It is an inflammation of the mucous membranes, which is characterized by the formation of a liquid exudate of any kind, except fibrinous. Catarrhal exudate consists of blood cells, desquamated epithelium and mucus.

Etiology: all types of irritations that exceed the natural resistance of the mucous and can cause an inflammatory reaction.

Morphology: depends on the course of the process. In acute catarrh:

1.Serous catarrh is characterized by the formation of opalescent or turbid aqueous exudate. Mucous in this is glassy, swollen, dropsical, hyperemic with petechial hemorrhages.

2.Mucous catarrh: says about the alterative catarrhal inflammation. It is characterized by a powerful mucous dystrophy of the epithelial lining with desquamation of the epithelium. This is a descriptive catarrh. The mucous membranes are dull, swollen, hyperemic, permeated with hemorrhages and covered, depending on the intensity of the process, with a thick viscous muddy mucus mass.

3.Purulent catarrh: on the surface of the mucous membrane there is a purulent exudate, with the removal of which the swollen dull mucosa of dark red color erodes, hyperemic, with hemorrhages.

4.Hemorrhagic catarrh: characterized by powerful hyperemia and swelling of the mucous membrane. Mucosa is bright, brilliant, bloodsoaked, swollen, necrotic foci and also foci of erosions and ulcers are found.

In chronic catarrh, there is a attenuation of exudative phenomena, there is a growth of CT. The mucous thickens, becomes dense, wrinkled, pale, becomes grayish.

The clinical significance and outcome of catarrhal inflammation depends on the extent and extent of damage. If they are high, then there

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is a sharp decrease in the functional ability of the organ, chronic insufficiency is noted.

Proliferative (productive) type of inflammation

In this type, proliferation prevails, i.e., the reproduction of cellular elements. Alteration and exudation are weakly expressed and are present in the background. As a result of proliferative inflammation, tissue growth is formed with the formation of limited or diffuse cellular tissue infiltrates.

Types of infiltrates:

1.Polymorphic cell infiltrates: composed of polymorphonuclear leukocytes (PALS), as well as round cell components, consisting of lymphocyte and histiocytic cells.

2.Macrophage infiltrates.

3.Epithelio-cellular infiltrates.

4.In case of infestations – eosinophilic infiltrates.

Types of proliferative inflammation and their characteristics

Proliferative inflammation includes the following types:

a)interstitial inflammation

b)granulomatous.

c)inflammation around foreign objects.

d)inflammation around the helminths and their larvae.

e)inflammation with formation of polyps and warts.

f)hyperplastic inflammation in lymphoid tissue

Interstitial inflammation

A type of productive inflammation, in which cell infiltrates are formed in the stroma of the body, while mono-, lymph - histiocytes, macrophages, fibroblasts accumulate. This is the chain of differentiation of cells and tissues. In the outcome of this inflammation, a mature fibrous CT is formed in the stroma, i.e., there is sclerosis of the organ (pneumosclerosis, cardiosclerosis, etc.).

A kind of interstitial inflammation is cirrhosis of the liver (from lat. "cirros" - red). It's a hepatic CT growth. The liver in this brown-grey color, in connection with CT growth.

Morphologically there are two forms of liver cirrhosis:

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1)Hypertrophic cirrhosis – with it, each slice accretes with CT, after which CT penetrates into the hepatic lobule. The body is compacted, becomes gray-brown. Then, in the body areas of hypertrophy of hepatic cells – areas of regeneration form. The liver thus acquires a knotty appearance, an uneven surface.

2)Atrophic cirrhosis – the growth of CT only around the lobules with their atrophy. Liver tissue with whitish, muscat, granular. It is compacted, increased in volume. A variety of atrophic liver cirrhosis is biliary cirrhosis. It begins with the growth of CT in the triad, i.e. in the locations of the bile ducts. The reason is helminths.

Granulomatous inflammation

A feature of this inflammation is that it has a specific pathogen. This inflammation occurs with the formation of granules.

Granuloma – a nodule, in the center of which is the mass of necrosis, and around several areas of cells are located. Directly to the necrosis area are adjacent epithelial cells. Their main function is phagocytosis. Phagocytic function of epithelial cells is enhanced by giant cells Pirogov-Langhans (tuberculosis). This is followed by a powerful shaft of round-cell elements – lymphoid cells. They perform at-forming function and detoxification function. Over time, these cells mature and turn into fibrous CT, that is, a capsule is formed around the focus of necrosis. Granulomatous inflammation is observed in tuberculosis, glanders, some fungal diseases (actinomycosis, botryomicosis), and a man with syphilis, leprosy, etc.

Productive inflammation around parasites and foreign bodies

Migrating into the tissue of the parasite and its larvae cause exudative and proliferative changes, which are replaced by the growth of granulation tissue around the parasite or larvae. The same is observed around foreign bodies. Over time the parasite dies, around CT capsule forms. The process of capsule formation is similar to granulomatous inflammation.

Inflammation with formation of polyps and condylomata acuminata

It is observed on the mucous membranes with damage to the epithelium. Polyps in the form of tree-like dilutions are formed on the

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mucous membranes of the respiratory tract. condylomata acuminata develop at the site of the transitional epithelium, that is, in the urinary tract.

Hyperplastic inflammation of lymphoid tissue

It is observed in the lymph nodes, tonsils, spleen. It is characterized by the proliferation of young cells of the lymphoid series, which leads to an increase in the volume of the body and the formation of reactive centers. Hyperplastic lymphadenitis, hyperplasia of the spleen develop.

Immunomorphology. Immunopathology Immunopathology is a branch of morphology that studies

morphological manifestations of immunological processes in animals and humans.

In the immune system, central and peripheral organs are distinguished. The central organs include the thymus, red bone marrow, to the peripheral-spleen, l/n, lymphoid formation of the digestive tract (tonsils, Peyer's plaques, solitary follicles).

In birds to the central organs we refer the bone marrow, thymus, Fabricius bag. To the peripheral – spleen, lymphoid tissue of the intestine, as well as cells of the mononuclear phagocyte system.

Immunogenesis cells or immunocompetent cells are formed in the central organs. To the cells of immunogenesis we refer:

1. Lymphocytes. The source is the bone marrow stem cell. The first group of lymphocytes migrates from bone marrow to thymus, where it is processed by hormones and then goes to the peripheral organs of the immune system. This forms the so – called thymus-dependent cell populations – T-lymphocytes. The second group of cells of bone marrow is sent in birds to Fabricius bag, in mammals – the probable analogue of the bag of the lymph tissue of the digestive tract. Here bursae lymphocytes – B-lymphocytes are formed.

T-lymphocytes are responsible for cellular immune responses. Among them T-killers, T-helpers and T-suppressors are distinguished. T-killers destroy target cells. They support the genetic constancy of the body. T-helpers promote the transformation of B-lymphocytes into plasma cells, followed by the production of antibodies. T-suppressors inhibit the transition of B-lymphocytes into plasma cells and suppress humoral reactions.

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B-lymphocytes are responsible for humoral immunity. Under the action of T-helpers, they are transformed into plasma cells that synthesize antibodies – B-lymphocytes into low-living cells. Only one clone of these cells lives for a very long time and is called immune memory cells.

2. Non-specific cells: PNM (neutrophils) and macrophages – monocytes.

Immunomorphogenesis

Humoral immune response. Stages.

1.In contact with the body of AG phagocytosis occurs by AG phagocytes, including cells, belonging to the system of mononuclear phagocytes.

2.Phagocytes digest AG and with the help of T-helpers transmit information about the AG in the thymus. There it is processed and transmitted to the lymphocytes.

3.B-lymphocytes turn into plasma cells that produce antibody to the

AG.

Cellular immune response. Stages.

1.AG is in contact with lymphocyte. Information is transmitted by T-lymphocytes to lymphoid tissue.

2.In lymphoid tissue cell proliferation occurs.

3.T-killer activation occurs with the interaction of these cells with AG. T-killer cells can directly kill AG-bearing cell, which activates the compliment, to convey AG to phagocytes.

Immune reactions in the body occur with the development of the following changes:

1. Immune inflammatory response. It develops in immunocompetent organs. L / u increased in volume, full-blooded, juicy, blood vessel walls are swollen, due to the appearance of young cells of the lymphoid series - white pulp (l/n follicles)- increased in volume. Their reactive centers are enlarged, light. This is due to the fact that young cells do not have time to accumulate nuclear chromatin. The spleen is enlarged in volume, juicy, grainy on the section, due to the increase in follicles, under the microscope, reactive centers are observed.

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2. Development of cellular immune responses in chronic infections. For example, with tuberculosis, glanders, brucellosis. At the same time, infectious granulomas develop, the cellular composition of which is immunocompetent cells. They accumulate and multiply in the inflammation, they prevent the outbreak and prevent microorganisms spread to the relatively healthy tissue.

Immunopathology

The most important among immunopathological processes are: allergic reactions, transplantation immunity, autoimmune diseases, immunodeficiency.

Allergic reactions are immune reactions in a sensitized organism. There is hypersensitivity of delayed and immediate types.

Hypersensitivity of immediate type is an acute immune response associated with humoral immunity. There is an acute alteration with the presence of acute fibrinous or fibrin hemorrhagic exudate. Accompanies erysipelas, Glasser's disease, pasteurellosis.

Hypersensitivity of the delayed type proceeds according to the type of cellular immunity and accompanies chronic infections – tuberculosis, glanders, paratuberculosis, helminthiasis. In this case, cell infiltrates are formed with the formation of serous fibrinous exudate and granulomas.

Transplantation immunity is a reaction to a genetically alien transplant with its subsequent rejection. T-killers and macrophages are involved in this reaction. These cells penetrate into the foreign tissue, multiply in it, infiltrate it, absorb the cells resulting in the transplant dies and is rejected.

Autoimmune diseases develop as the action of the immune system against their own cells and tissues. Under the influence of pathogenic factors in the body, clones of autoantibodies are formed, that is, immunoglobulins, which consider their own cells as foreign, and interacting with them, form immune complexes, which are destroyed by macrophages, complement system, T-killers. Morphologically, it is manifested by foci of hyperedge inflammation, which leads to severe dystrophy and tissue necrosis followed by sclerosis.

Immunodeficiency is a congenital or acquired deficiency of immune system, humoral or cellular mechanisms.

Primary immunodeficiency is congenital or hereditary. They are manifested by underdevelopment of the thymus, brain, lymphoid tissue.

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