Classification of inflammation by stages of development. Stage acute inflammation. Chronic exudative inflammation

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Pathological anatomy of inflammation

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Inflammation (inflammatory response, inflammatio, flogosis) - protective and adaptive mechanism that provides the necessary conditions for the restoration of damaged tissue. The inflammatory response is also briefly defined as a tissue reaction to damage.

Inflammation in itself is not a pathological process, but under certain conditions, like any other protective-adaptive reaction (thrombosis, stress, immune response, regeneration, etc.), can proceed pathologically. Therefore, it is advisable to distinguish inflammation and pathology of inflammation (pathological variants of the inflammatory response).

Peculiarities of inflammation. Unlike other protective and adaptive mechanisms (non-logogenic response of scavenger cells, non-inflammatory encapsulation, immune response), during inflammation occurs delimitation (demarcation) of damaged tissues from healthy (due to vascular changes and cellular infiltration), cleansing phagocytes of the focus of damage from detritus and phlogogen (for example, microorganisms), and most importantly - the creation of conditions for further recovery the integrity of the damaged tissue (i.e. for reparative regeneration). The inflammatory response is a mandatory intermediate between tissue damage and its repair.

Classical theory of morphogenesis of inflammation

With the formation of fibroepithelial polyps (reactive papillomas)
With the formation of hyperplastic polyps
Papillary synovitis
Papillary serositis
With the formation of viral warts.

Interstitial inflammation

Interstitial (interstitial) inflammation - productive inflammation, in which the cells of the inflammatory infiltrate are distributed more or less evenly in the tissue, without the formation of focal accumulations. Infiltration in interstitial inflammation is formed mainly by lymphocytes and ordinary macrophages (histiocytes), so it is called lymphohistiocytic. Often in the infiltrate derivatives of B-lymphocytes (plasma cells) are detected, and then it is designated as lymphohistioplasmocytic. The presence of plasma cells reflects the formation of humoral immunity.

A characteristic outcome of a long-term interstitial inflammation is widespread fibrosis in the affected organ. Against the background of post-inflammatory fibrosis, parenchyma atrophy develops and, as a result, functional deficiency syndrome body. Often the body is deformed ( "Cicatricial wrinkling", or cirrhosis). Interstitial inflammation is the basis of chronic pyelonephritis (without exacerbation of the process), chronic hepatitis, many forms of myocarditis (thyrotoxic myocarditis, toxic myocarditis in diphtheria, myocarditis in tertiary syphilis), interstitial pneumonia.

Granulomatous inflammation

Granulomatous inflammation - productive inflammation, in which the infiltrate cells form focal accumulations ( granulomas). Granulomas are sometimes called "knots", however this designation is inaccurate, because granulomas can be not only nodules, but also nodes (for example, gum or leproma). Granulomas form under conditions of excessive activity of the immune system ( allergies), therefore, granulomatous inflammation is also defined as one of the types of allergic reactions (type VI in the S. Sell classification, type V in the O. Günther classification). The severity of the immunopathological reaction in the formation of granulomas is different: from the minimum ( non-immune granulomas) up to significant ( immune granulomas).

Classification of granulomas

Granulomas are classified according to their composition, pathogenetic features, speed of change of cell generations and morphological specificity.

I. Cell composition

Phagocytoma (mature macrophage granuloma)
Epithelioid cell granuloma
Giant cell granuloma (with langans cells or with foreign cells)
Lymphocytic granuloma [for example, in viral encephalomyelitis, typhus fever]
Granuloma "with suppuration" [for example, with sape].

Ii. Features of pathogenesis

Immune granuloma
Non-immune granuloma.

Iii. The intensity of the change of cells in the granuloma

High exchange granuloma
Low exchange granuloma.

Iv. The specificity of the structure

Nonspecific granulomas
Specific granulomas.

Specific granulomas (tubercles and sapna granulomas are not specific):

Gumma
Leproma
(scleroma)
Granulema Ashoff-Talalayev (specific rheumatic granuloma)
.

The composition of granulomas are divided into five main types: phagocytomas (granulomas from ordinary phagocytic macrophages), epithelioid cell granulomas (granulomas with epithelioid macrophages), giant cell (granulomas with giant multi-core macrophages), lymphocytic (formed mainly by lymphoid cells) and suppuration granulomas (granulomas with centrally located disintegrating neutrophilic granulocytes and phagocytic macrophages located on the periphery).

Epithelioid macrophages differ from the usual larger size, light cytoplasm than resemble some epithelial cells (hence the term "epithelioid"). Their main function is not phagocytosis, but the formation, like neutrophilic granulocytes, of active oxygen metabolites. Epithelioid macrophages often appear in lesions with the presence of an aggressive phlogogen and an insufficient number of neutrophils, for example, in tuberculosis.

Giant multi-core macrophages formed by the merger of conventional phagocytic macrophages. Epithelioid cells practically do not participate in this process. In pathological anatomy, two types of multinuclear macrophages occur in granulomas: (1) langans cells and 2) foreign body cells. The difference between them lies in the location of the nuclei. In the cells of Langans, the nuclei are located on the periphery of the cytoplasm, near the plasmolemma, forming the “crown” (“crown”) figure, the cell center from the nucleus is free (there are collected centrioles of all the fused histiocytes). In foreign cells, the nuclei are distributed throughout the cytoplasm, located both on the periphery and in the center. Langans cells are characteristic of lesions in tuberculosis, cells of foreign bodies (as the name implies) - for granulomas of foreign bodies.

Granulomas "with suppuration" - conditional term, since purulent exudate in the center of the granuloma is not formed due to the numerous macrophages on the periphery, phagocytic neutrons destroyed. However, in diseases involving the formation of such granulomas, purulent inflammation may develop, for example, with sapa.

According to the features of pathogenesis emit immune (formed on the background of severe allergies) and non-immune granulomas. The term "non-immune granulomas" can not be considered successful, because all granulomas are the essence of the manifestation of an allergic process, only for them it does not play a decisive role, it is less pronounced. The morphological marker of immune granulomas are epithelioid macrophages, non-immune granulomas are cells of foreign bodies.

According to the rate of change of cell generations, granulomas are distinguished with a high (the cells in the granuloma die quickly, they are replaced by new ones) and with a low level of cell metabolism. The first are mainly infectious granulomas, the second - the granulomas of foreign bodies.

By morphological specificity, granulomas are subdivided into non-specific (the same structure of granulomas in different diseases) and specific (the structure of granulomas is characteristic only for one disease). In diseases for which specific granulomas are typical, non-specific granulomas may also be formed. For example, rheumatism is characterized by a specific granuloma (granuloma Aschoff-Talalayeva), but this does not mean that with this disease in the tissue there are only specific granulomas; along with them, granulomas of non-specific structure are detected. Currently, specific granulomas are considered leproma (granuloma with lepromatous leprosy), gumma (granuloma with tertiary syphilis), granuloma Ashofa-Talalayev (with rheumatism), specific granuloma with rhinosclerosis and specific granuloma in actinomycosis. Until recently, the specific attributed tubercle (granuloma in tuberculosis), but a similar structure may have granulomas in sarcoidosis, some mycoses, berylliosis and a number of other diseases. In old textbooks, the group of specific granulomas also included a granuloma with glanders, which has a “suppuration” granuloma morphology, but granulomas of the same structure were found in many diseases (yersiniosis, atypical mycobacterioses, some mycoses, etc.).

Gumma

A specific granuloma for syphilis is called gumma. Gumma are found in tertiary syphilis. Macromorphologically, it is a dense gray knot. A typical gumma in the center contains a gray translucent sticky mass (“fibrous necrosis”), around which granulation tissue is located, ripening along the periphery into cicatricial. Necrosis in the center of the gum was called “fibrous” in classical pathological anatomy, since In the detritus, the first researchers constantly found retained reticular fibers, but later it turned out that this type of fibers remains in the focus of any necrosis longer than other tissue structures. The main cells of the inflammatory infiltrate are plasma cells and B lymphocytes. Gumma marker cells - plasma cells (some authors call the gum's plasma cells unny-Marshalko-Yadasson cells). Pathogen ( Treponema pallidum) can be detected in tissue sections with levaditi silver impregnation (bacterial cells are stained black and have a convoluted shape).

Leproma

Specific leprosy granuloma ( leproma) is found only in the case of lepromatous leprosy (a form with lesions of the internal organs). Leproma, like gum, outwardly represents a knot, it is formed mainly by phagocytic macrophages (phagocytoma), called virchow cells. The cytoplasm of Virchow cells contains fat droplets and pathogen ( Mycobacterium leprae), which is stained by the Ziel-Nielsen method with a basic magenta in red color, similar to the causative agent of tuberculosis. Bacteria are usually arranged parallel to each other, like "matches in a box" or "cigarettes in a pack."

Specific granuloma in rhinosclerosis (scleroma)

Specific granuloma with rhinosclerosis (scleroma) as well as leproma, is mainly formed by phagocytic macrophages ( mikulich cells), in the cytoplasm of which are found light vacuoles that do not contain fat, and the causative agent of the disease ( Klebsiella rhinoscleromatispreviously called bacillus Volkowicz-Frisch). The typical localization of granulomas in this disease is the upper respiratory tract; the characteristic outcome of granulomas in rhinosclerosis is scarring, sometimes so pronounced that obliteration of the trachea and bronchi occurs.

Specific actinomycotic granuloma

Specific granuloma in actinomycosis formed around druze (so called colonies of hyphae-forming bacteria). It consists of granulation tissue rich in neutrophilic granulocytes and large macrophages with light, frothy cytoplasm ( "Foam cells"). Numerous closely located “frothy macrophages” are granuloma marker cells. Over time, the druse is surrounded by purulent exudate, which is formed during the disintegration of neutrophilic granulocytes, and the granulation tissue matures into coarse-fibered tissue, determining the density of the tissue in the lesion. Pathogen (some species of the genus Actinomyces) is painted in red-purple with PAS reactions. Actinomycosis is more often localized in the orofacial region, neck tissues and in the female genital organs (uterus, tubes), but the process can develop in any organ.

Tubercle

A characteristic morphological sign of productive inflammation in tuberculosis is the formation of tuburkulov (epithelioid cell tuberculosis granulomas), which until recently were considered as specific, but granulomas similar in structure can be detected in other diseases (mycoses, sarcoidosis, berylliosis, etc.). Macromorphologically, the tubercle is a dense, whitish foci. Microscopic examination in a typical tubercle around the central caseous necrosis cells are located inflammatory infiltrate. Marker cells of the tubercle are langans cells (inaccurately called pirogov-Langans cells) - giant multinuclear macrophages, the central part of which is free from nuclei. The predominant elements in the tubercle are epithelioid macrophages. On the periphery of the granuloma, T-lymphocytes are detected ( lymphocytic cuff). In macrophages, it is possible to identify the causative agent ( Mycobacterium tuberculosis, M. bovis, M. africanum), they turn red with basic fuchsin when dyeing the Zil-Nielsen tissue section. Tubercules are not formed in cases of tuberculosis without signs of productive inflammation, for example, in caseous pneumonia.

Granuloma with sapa

Granuloma with sapa (an infectious disease mainly among horses; when a person is infected, it usually proceeds as septicopyemiawas first studied by pathologists granuloma "with suppuration"therefore, for a long time was considered as specific. It has been established that such granulomas are found in many diseases (atypical mycobacterioses, intestinal yersiniosis and pseudotuberculosis, some mycoses, etc.). Disintegrating neutrophilic granulocytes are located in the center of the granuloma, along the periphery are numerous phagocytic macrophages. Despite the name, purulent exudate in the granuloma itself is not formed, because disintegrating neutrophils are rapidly phagocytosed by macrophages.

Granulomatous diseases (granulomatosis)

Classification of granulomatous diseases:

I. Etiological principle

Idiopathic granulomatosis [sarcoidosis, Wegener's granulomatosis, Horton's disease, etc.]
Granulomatous infections and invasions [some viral and bacterial infections, mycoses, protozoa, helminth infections (for example, alveococcosis)]
Pneumoconiosis (dust diseases of the lungs) [silicosis, berylliosis]
Drug granulomatosis [drug hepatitis]
Granulomatous reactions to foreign bodies [surgical talcosis, granulomas around suture material]
Lipogranulomatosis.

Ii. With the flow

Acute granulomatosis [eg typhoid fever]
Chronic granulomatosis.

Granulating inflammation

Granulating inflammation - productive inflammation, in which granulation tissue grows in the lesion. Examples of processes with the development of granulating inflammation are granulating pulpite and granulating periodontitis. Granulation tissue usually matures into coarse-fibrous (scar) tissue.

Productive inflammation of integumentary tissues (skin, mucous membranes, synovial and serous membranes) is accompanied by the formation of connective tissue outgrowths of these tissues, covered with a typical or metaplastic epithelium. Outgrowths of epithelial tissues due to productive inflammation are hypertrophic growths. Depending on the location, hypertrophic growths have different names: (1) fibroepithelial polyps, or reactive papillomas (on the skin and mucous membranes covered with stratified squamous epithelium), (2) hyperplastic polyps (on mucous membranes covered with a single layer of the epithelium). Analogs of fibroepithelial polyps arising under the influence of DNA containing human papillomavirus from the family Papovaviridae traditionally denoted viral warts, among which there are (1) ordinary (verrucae vulgares), (2) plantar, (3) juvenile warts and (4) genital warts. The latter are formed in zones bordering the skin and mucous membranes (perineum, genitals, face around the openings of the mouth and nose). The previously distinguished "giant genital warts of the Auschke-Lowenstein" is currently regarded as verrucous squamous cell carcinoma.

ACUTE INFLAMMATION

Stage of acute inflammation

There are interrelated phases of acute inflammation: damage (alteration), exudation, and proliferation. It is usually difficult to grasp the line between tissue damage and the release of inflammatory mediators by cells. However, without morphobiochemical changes in case of damage, the vascular reaction that occurs after a very short latent period cannot be included.

DAMAGE STAGE

EXIT STUDIO

This stage occurs at different times after damage to cells and tissues in response to the action of inflammatory mediators, especially plasma mediators, arising from the activation of three blood systems - kinin, complementary and coagulating. All components of these systems exist in the blood in the form of precursors and begin to function only after exposure to certain activators. In the blood plasma is present and the system of inhibitors, balancing the action of activators.

The mediators of the kinin system are bradykinin and kallikrein. Bradykinin increases vascular permeability, causes a feeling of pain, has a pronounced hypotensive effect. Kallikrein performs leukocyte chemotaxis, but its main value is the activation of the Hageman factor, i.e. inclusion in the inflammatory process of blood coagulation and fibrinolysis. The Hageman factor initiates blood coagulation, activates plasma mediators of inflammation and acts as a mediator itself, increasing vascular permeability, enhancing neutrophil migration, and platelet aggregation. As a result, the blood coagulation system becomes a component of the inflammatory response. The complement system consists of special plasma proteins that cause lysis of bacteria and cells. In addition, a number of complement components, first of all, C 3b and C 5b, increase vascular permeability, enhance the chemotactic activity of neutrophils and macrophages. The complex action of cellular and plasma mediators of inflammation, other products accumulating in the zone of local disturbance of homeostasis and causing changes in the permeability of the walls of microcirculatory vessels, the cellular elements entering the zone of inflammation from the blood leads to the development of an exudation stage. This stage has the following components, leading to the formation of exudate:

∨ vascular reactions in the inflammation;

∨ exudation itself;

∨ emigration of blood corpuscles.

The vascular reactions that occur during the development of inflammation mean dilation of the vessels of the microcirculatory bed, increased blood flow to the site of inflammation (active hyperemia), and slower venous outflow (passive hyperemia). Slowing blood flow is associated with intravascular and extravascular factors.

Intravascular factors: violation of the rheological properties of blood (sludge, microthrombosis, hemoconcentration), parietal standing of leukocytes, changes in the properties of the vascular wall and increasing its permeability.

Extravascular factors: edema and exudate, compressing venules.

As a result, blood flow slows down, capillaries and venules expand, and hydrodynamic pressure increases in them. All this causes a decrease in the partial tension of oxygen and the development of hypoxia in the area of \u200b\u200binflammation. Against the background of venous hyperemia exudation, leukocyte emigration, phagocytosis are most pronounced. The increasing slowing down of the blood flow in the jerky and pendulum-like movement of blood leads to its complete stop - venous stasis. In addition, the cessation of blood flow contributes to the isolation of the area of \u200b\u200binflammation from surrounding tissues, reducing the absorption of substances from this area. Active hyperemia enhances the oxygenation of the inflammatory focus, which contributes to the formation of reactive oxygen species, the influx of humoral protection factors (complement, properdin, fibronectin, etc.), leukocytes, monocytes, platelets and other blood cells. The development of exudation contribute to the following factors.

The increase in hydrodynamic and, therefore, filtration pressure with active hyperemia.

The increase in the area of \u200b\u200bexudation associated with the expansion of blood vessels, an increase in the number of functioning capillaries.

The increase in osmotic and oncotic pressure in the inflammation, which ensures the movement of fluid along the concentration gradient from the zone of lower pressure to the region of higher.

The increase in the permeability of the vascular wall as a result of the destruction of glycosaminoglycans, basement membrane proteins, the main substance, necrosis and endothelial exfoliation under the influence of inflammatory mediators, oxygen radicals, enzymes, cationic proteins, cytokines.

Increased transport through the cytoplasm of endothelial cells by micropinocytosis.

Simultaneously with exudation of blood plasma, leukocytes emigrate from vessels into tissues, which leads to the formation of exudate — a protein-rich fluid (more than 2.5 g / l of protein, specific gravity more than 1020 g / l), containing blood cells, the remnants of decayed tissues, often inflammatory pathogens. The exudation has several stages: marginal standing of leukocytes and passage of leukocytes through the wall of microvessels.

Regional standing of leukocytes. The action of the chemotactic factors of the source of inflammation, slowing blood flow velocity, increasing hydrodynamic pressure leads to the movement of leukocytes, which are less dense than other blood cells, from the axial cylinder and bring them closer to the vascular wall. This stage precedes the emigration of leukocytes into the surrounding tissue. Pre-leukocytes must go into an activated state in order to perceive the signals of chemoattractants.

◊ Under normal conditions, the adhesion of leukocytes to the vascular endothelium prevents the negative charge of those and other cells, their repulsion from each other. With the development of exudation under the influence of inflammatory mediators, bivalent plasma cations enter into the process: Ca 2 +, Mn 2 + and Mg 2 +. They change the negative endothelium charge to a positive one, which is promoted by the disruption of the Na + -K + -dependent ATPase, the accumulation of H + and K + ions in the area of \u200b\u200binflammation. As a result, negatively charged leukocytes are attracted to the vascular wall. The main mechanism of leukocyte adhesion to the endothelium is the ligand-receptor interaction between leukocytes and the vascular wall, and the appearance of receptors (adhesion molecules) induce inflammatory mediators. Before leukocyte activation, adhesion molecules are found in intracellular granules, their release occurs under the influence of leukotriene B 4, IL-1, 8, α-interferon, TNF-α, and bacteria lipopolysaccharides. Leukocyte adhesion is also provided by complement (C 5a, C 1, C 3 fractions) and IgG Fc fragments. They bind the corresponding receptors on the membranes of leukocytes, causing their activation and chemoattraction to the vascular endothelium. The prolapse of fibronectin on endotheliocytes and collagen fibers of the vascular basement membrane also contributes to the targeted attraction of leukocytes and mononuclear cells. These substances stimulate leukocyte adhesiveness and endothelial stickiness.

◊ Endotheliocytes during inflammation express cell adhesion molecules, they are a source of procoagulants, anticoagulants and acute phase mediators. The cell adhesion molecules include selectins, receptors expressed on the surface of leukocytes and endothelium. Ligands for selectins are complementary adhesion molecules on the surface of contacting cells. Selectins mediate the earliest stage of adhesion - reversible adhesion. First, there is a release from the endothelium of E-selectin for neutrophils, which explains their early emigration from the vascular bed. This is followed by isolation of the integrins and the intercellular adhesion molecules (ICAM-1 and VCAV-1) responsible for the late stages of adhesion of activated leukocytes and platelets to the endothelium. Endotheliocytes are important as regulators of the local manifestation of inflammation and a link between local and general body reactions. In case of inflammation with severe intoxication, deposition of immune complexes or aggregated immunoglobulin in the vascular wall, polymorphonuclear leukocytes can degranulate directly in the vessel lumen, damaging their vascular wall hydrolases. This enhances the secretion of biologically active substances by endotheliocytes and exudation. Endotheliocytes can perform an antigen-presenting function and regulate the development of cells of the immune system.

The passage of leukocytes through the wall of microvessels is the next stage, which occurs after the activation of leukocytes under the action of cytokines. All types of white blood cells are capable of active movement. After the marginal standing of leukocytes due to the action of their enzymes on the inner lining of blood vessels, a reduction of endothelial cells and the opening of interendothelial slits occur, and leukocytes are transferred to them after adhesion.

◊ To pass through the endothelial lining, the leukocyte forms a pseudopodia entering the interendothelial gap and then under the endotheliocyte. Then the whole leukocyte moves there, located between the endothelium and the basement membrane of the vessel. Molecular changes in the basement membrane allow blood cells to overcome it and emigrate to the area of \u200b\u200binflammation. This mechanism is characteristic of all blood cells, including red blood cells (Fig. 4-1). The process of leukocyte out of the vessel takes several hours. In acute inflammation, neutrophilic leukocytes are released into the inflammatory focus for the first 6–24 hours. In 24-48 hours, monocyte and lymphocyte emigration prevails. Such a sequence is associated with the sequence of the selection of adhesion molecules and chemoattractants. The order of cell emigration depends on other factors, in particular, on the cause of inflammation. For example, in viral infections and tuberculosis, lymphocytes migrate first to the zone of inflammation, and for immune inflammation, eosinophils. Nevertheless, inflammatory mediators play a crucial role in exudation and its features.

Fig. 4-1. Red blood cell diapedesis from a vessel (x18,000).

◊ Participation in the process of inflammation of the blood and lymphatic vessels occurs simultaneously. In the venular section of the microvascular bed, there is a pronounced cell migration and plasma sweating, the next stage is the involvement of the lymphatic system component in the process - the interstitial channels. This leads to impaired blood flow balance, changes in the extravascular circulation of tissue fluid, swelling and swelling of the tissue, which increase with the development of lymphostasis. At the same time, damage to the endothelium of the lymphatic capillaries, their overfilling of the lymph, the expansion of the interendothelial crevices is typical. The lymph enters the tissue, and at the very beginning of the exudative stage, acute lymphatic edema occurs, which persists until the end of the inflammation.

The emergence of blood cells from the vessel into the zone of inflammation and the formation of one or another type of exudate are important for phagocytosis in cells. In addition, leukocytes can cause tissue destruction by enzymes, toxic oxygen compounds, resulting in inflammatory detritus.

Phagocytosis - the biological process of absorption by phagocytes and the digestion of foreign material and its own damaged cells. There are two groups of phagocytes:

∨ microphages - granulocytes (neutrophils, eosinophils, basophils);

∨ macrophages - monocytes and tissue macrophages (Kupffer's cells in the liver, Langerhans cells in the skin, alveolar macrophages, microglia cells, macrophages of lymph nodes and spleen, bone osteoblasts) formed after migration from the blood to the tissues.

Blood monocytes live for about a day, tissue macrophages last several months. According to their ability to move, phagocytes are divided into motile and fixed. Neutrophils are particularly effective in phagocytosis of bacteria. The possibilities of macrophages are wider, but the mechanism of phagocytosis is the same for all phagocytes.

The following stages of phagocytosis are distinguished:

∨ approach of phagocyte to the object of phagocytosis;

∨ adhesion of the object to the surface of the phagocyte;

∨ immersion of the object in the cytoplasm of phagocyte;

∨ intracellular digestion.

Phagocyte exhibits positive chemotaxis, thermotaxis, galvanotaxis, hydrotaxis. Phagocyte migration to the inflammatory focus occurs in a certain sequence: first, neutrophil movement prevails, and monocytes, which begin movement with them, reach the maximum number in the infiltrate later. Lymphocytes migrate last. The sequence of phagocytic movements is associated with the appearance of adhesion molecules and chemoattractants in a certain sequence.

The most important mechanism of adhesion - opsonization - the attachment of specific substances to the object of phagocytosis and their recognition by phagocytic receptors. These substances are called opsonins.

Opsonins include immunoglobulins G 1, G 3, M that make contact with the phagocyte Fc receptor and the phabocytosis object Fab receptor. The adherence of the phagocytosis object to the phagocyte causes the activation of the latter. In phagocyte, a metabolic explosion occurs with the formation and release of biologically active substances, adhesion molecules and receptor expression. Oxygen consumption increases with the formation of free radicals, glycolysis and the pentose pathway are activated. Phagocyte activation is possible without phagocytosis under the influence of cytokines (IL-2, 3, TNF-α, α-interferon).

Immersion occurs due to the coverage of the object of phagocytosis with pseudopodia; as a result, it appears in the cytoplasm of the phagocyte, surrounded by a phagosome formed by invagination and closure of a fragment of the cell membrane. This is followed by the merger of the phagosome with the lysosome with the formation of the phagolysosome, in the latter there is an intracellular digestion.

Mechanisms of destruction of the absorbed material:

∨ oxygen-dependent - digestion due to the formation of reactive oxygen species, free radicals and peroxides;

∨ oxygen-independent - due to lysosomal hydrolases, cathepsins, cationic bactericidal proteins, lactoferrin, lysozyme.

Active oxygen-containing radicals (singlet oxygen, hydroxyl radical, superoxide anion, nitric oxide), as well as hydrogen peroxide can destroy the intact bacterial cell walls and cell membranes, therefore the oxygen-dependent mechanism is much more important than the hydrolytic one. Neutrophilic myeloperoxidase converts hydrogen peroxide in the presence of chlorine ions into hypochloride anion with pronounced bactericidal properties. During phagocytosis, neutrophils emit many substances: inflammatory mediators, including those with bactericidal and cytotoxic properties, a chemotactic factor that attracts monocytes. After phagocytosis, the phagocyte dies, not coping with the consequences of this process. During phagocytosis and phagocytic death, inflammatory mediators are released from them. On the one hand, it causes tissue damage, on the other hand, it enhances the bactericidal and cytolytic properties of exudates. The release of biologically active substances makes it possible to destroy an object without its seizure, especially if it is larger than the phagocyte, or to influence it before absorption, weakening its damaging effect.

If the absorbed microorganisms do not perish during digestion, this kind of phagocytosis is called incomplete. Incomplete phagocytosis, or endocytobiosis, usually depends on the biological properties of the microorganisms, and not on the phagocyte. The following factors affect endocytobiosis:

∨ disruption of phagosome and lysosome fusions (influenza viruses, mycobacterium tuberculosis, whooping cough, and toxoplasma that produce antilectins have this effect);

∨ resistance of pathogens to lysosome enzymes (gonococci, staphylococci);

∨ the ability to leave the phagosome after absorption and long exist in the cytoplasm (rickettsia, chlamydia, the causative agent of leprosy);

∨ the ability to produce catalase that destroys hydrogen peroxide (staphylococcus, aspergilla), which violates the destruction of microorganisms and the antigen presenting function of phagocyte.

Thus, incomplete phagocytosis is an important mechanism for the chronic and recurrent course of infections. The release of viable microorganisms from leukocytes leads to recurrent suppurative inflammation. The location in the phagocytes of living microorganisms makes it difficult to access bactericidal substances of the body and medicines, and therefore, the treatment of the patient.

Incomplete phagocytosis, obviously, may be the mechanism of adaptation of the organism. For tuberculosis and other chronic infections with non-sterile immunity using incomplete phagocytosis, the body keeps the pathogens alive (endocytobiosis). It constantly stimulates the immune system and prevents the spread of pathogens throughout the body. In this process, macrophages are transformed into epithelioid and gigantic cells, forming granulomas together with T-lymphocytes. However, this is possible only after the macrophage phagocytes the mycobacterium of tuberculosis, digests it, identifies antigenic determinants and presents them to the immune system. When transformed into an epithelioid cell, the macrophage loses most of the lysosomes, which prevents it from completing phagocytosis by digesting the pathogens.

A more frequent occurrence is phagocytic insufficiency - inability of phagocytic cells to perform their functions. It is based on the following mechanisms:

∨ decrease in the number of phagocytes;

∨ dysfunction of phagocytosis;

∨ dysregulation of phagocytosis.

The decrease in the number of phagocytic cells can be hereditary and acquired (as a result of physical, chemical and biological effects). In both cases, the processes of proliferation and maturation of bone marrow cells are violated. The weakening of the phagocytic reaction causes a violation of the function of adhesion, movement, digestion.

Digestion disorders are associated with hereditary deficiency of the enzyme NADP-dependent oxidase in monocytes and granulocytes, which causes a decrease in the formation of reactive oxygen species, peroxides and the preservation of bacteria in phagocyte. Defect of metabolic explosion is possible with deficiency of pyruvate kinase or glucose-6-phosphate dehydrogenase. Myeloperoxidase deficiency of neutrophils leads to a decrease in the formation of hypochlorite, which has pronounced bactericidal properties. The adhesion process is disrupted by hereditary insufficiency of integrins and selectins.

Phagocytosis is important for the destruction of foreign objects, own damaged cells, immune complexes, the isolation of inflammatory mediators, the presentation of antigens to lymphocytes, the development of the immune response in general.

Cell cooperation, which has arisen in the inflammatory focus as a result of tissue alteration and exudation, is characterized by autoregulatory mechanisms, cyclical development and division of functions between cells. The main protection against microorganisms, especially with purulent infection, is carried out by neutrophils. Their emigration occurs simultaneously with the vascular reaction. Neutrophils are the first to come into contact with an infectious pathogen and block its penetration into the body. Polymorphonuclear leukocytes are not specific to the pathogenic stimulus: they react to any pathogen, destroying it with the help of phagocytosis and exocytosis, and at the same time they die. Polymorphonuclear leukocytes - "duty" cells of the system of nonspecific resistance of the organism. Neutrophilic granulocytes and macrophages entering the inflammation site perform bactericidal and phagocytic functions. They also synthesize biologically active substances that provide a variety of effects, but, above all, enhancing the vascular response and chemoattraction of inflammation. Often, early neutrophilic infiltration with a high concentration of the corresponding chemoattractants quickly leads to inflammation of the inflammation zone. Later, monocytic and macrophage are added to the neutrophilic infiltration, which characterizes the beginning of the encapsulation, the delimitation of the inflamed zone due to the formation of the cell wall along its periphery.

An important component of inflammation is the development of tissue necrosis. Necrotized tissue performs several functions. From the standpoint of biological expediency, the development of necrosis is beneficial for the organism, since the pathogenic factor must die in the necrosis focus. The sooner necrosis develops, the fewer the complications of inflammation will be, and the dead tissue will then regenerate with the restoration of its function. This explains not only the formation by cells of various hydrolases in the focus of inflammation, but also the development of vascular thrombosis around the inflamed area. It is likely that the thrombosis of small vessels, which occurs after the emigration of leukocytes to the focus of damage, not only separates the inflamed area, but also contributes to the development of tissue hypoxia and their necrosis. Therefore, in the midst of an exudative inflammatory reaction, when the entire field of inflammation is infiltrated by leukocytes and the concentration of hydrolytic enzymes in it is obviously very high, macrophages practically do not enter the focus, concentrating on its periphery. Otherwise, macrophages will simply die in the center of the center of inflammation, while their function is much more complicated than simple phagocytosis of the pathogen.

Macrophages play a special role in inflammation, acting as both a local regulator of inflammation and a link between the local manifestations of this process and the general body reactions to it. In addition, macrophages are important as the first link in the development of immunity in the development of inflammation. The task of phagocytosis, carried out by a macrophage, apparently, is not only the destruction of the infecti to reduce its concentration in the inflammatory focus, but the identification of its antigenic determinants and the subsequent transmission of information about this to the immune system. From this perspective, it is clear why the phagocytic activity of macrophages in relation to purulent infection is significantly lower than neutrophilic leukocytes. It is also clear why macrophages do not enter the focus of purulent inflammation in the midst of exudation and the most pronounced leukocyte infiltration, but are located on the periphery of the inflammatory zone, participating in the formation of the second barrier, which isolates the inflamed tissue. This expediency is also confirmed by the peculiarity of the pathogenesis of aseptic inflammation, when in the focus of damage there are not alien, but “altered” antigens. After 18-24 hours, leukocytes leave the damage zone, and only after that it is filled with macrophages, without being exposed to the danger of lysis under the action of neutrophil hydrolases. It is also explained that in chronic, especially granulomatous, inflammation, when the antigenic structure of the pathogen is already known, incomplete phagocytosis is often characteristic of macrophages, and that when the immune system is stimulated, the number of macrophages involved in delimiting the source of inflammation significantly increases.

Thus, when inflammation occurs locally, extremely complex processes occur. They serve as a signal for inclusion in the inflammatory response of various body systems.

PROLIFERATION STAGE

EXUDENT INFLAMMATION

The formation of exudates is typical, their composition is mainly due to the cause of inflammation and the body’s response to a damaging factor. The nature of the exudate determines the name of the form of acute exudative inflammation. The causes of its development are viruses (herpes, chicken pox), thermal, radiation or chemical burns, the formation of endogenous toxins. Exudative inflammation can be serous, fibrinous, purulent, putrid.

SEROUS INFLAMMATION

Fibrinous inflammation

Characterized by the formation of exudate, in addition to polymorphonuclear leukocytes, lymphocytes, monocytes, macrophages, disintegrating cells of inflamed tissue, a large amount of fibrinogen. The latter under the action of thromboplastin falls in the tissues in the form of fibrin bundles. For this reason, the protein content in fibrinous exudate is higher than in serous one. This form of inflammation causes a significant increase in vascular permeability, which is facilitated by the presence in the stroma of substances with procoagulant properties.

Etiological factors: diphtheria corynebacterium, coccal flora, mycobacterium tuberculosis, viruses, dysentery pathogens, allergic, exogenous and endogenous toxic factors. Fibrinous inflammation is more common on mucous membranes or serous membranes. The exudation is preceded by tissue necrosis and platelet aggregation in the lesion. Fibrinous exudate infiltrates dead tissues, forming a light-gray film, under it are microorganisms that emit a large number of toxins. The thickness of the film depends on the depth of necrosis, and the latter depends on the structure of the epithelial lining and the characteristics of the underlying connective tissue. Depending on the depth of necrosis and the thickness of the fibrinous film, croupous and diphtheritic fibrinous inflammation is isolated.

Lobar inflammation (from scotl croup - film) develops on mucous membranes or serous membranes, covered with a single-layer epithelium, located on a thin dense connective tissue basis. Under these conditions, the necrosis cannot be deep; therefore, a thin fibrinous film appears, it is easy to remove. Croupous inflammation occurs on the mucous membranes of the trachea and bronchi, serous membranes (fibrinous pleurisy, pericarditis, peritonitis), with fibrinous alveolitis, croupous pneumonia (Fig. 4-2).

Fig. 4-2. Croupous pneumonia. Fibrinous exudate in the alveoli. Stained with hematoxylin and eosin (x200).

Diphtheritic inflammation (from the Greek diphteria - skin) develops on a multilayer flat non-keratinized epithelium, transitional or single-layer epithelium with a loose broad connective tissue basis of the body, which contributes to the development of deep necrosis and the formation of a thick, difficult to remove fibrinous film, after its removal, deep ulcers remain. Diphtheritic inflammation occurs in the oropharynx, on the mucous membranes of the esophagus, uterus, vagina, stomach, intestines, bladder, skin and mucous membrane wounds (Fig. 4-3).

Fig. 4-3. Dysentery. Diphtheritic inflammation of the colon. Necrosis and imbibition by fibrinous exudate of the mucous membrane and submucous layer of the intestine. Stained with hematoxylin and eosin (x150).

The outcome of the fibrinous inflammation of the mucous membranes is the melting of fibrinous films with the help of hydrolases of polymorphonuclear leukocytes. Croupous inflammation of mucous and serous membranes, as a rule, ends with the restitution of damaged tissues. Diphtheritic inflammation occurs with the formation of ulcers and subsequent substitution, with deep ulcers in the outcome scars are possible. Since fibrin activates fibroblasts, undissolved fibrinous exudate undergoes organization and replacement with connective tissue. On serous membranes often spikes, moorings, often fibrinous inflammation of the membranes of the body cavities causes their obliteration.

Purulent Inflammation

For purulent inflammation is characterized by the formation of purulent exudate. It is a creamy mass consisting of cells and detritus of tissues of the inflammatory focus, microorganisms, and blood cells. The number of the latter - 17-29%, mostly viable and dead granulocytes. In addition, the exudate has lymphocytes, macrophages, often eosinophilic granulocytes. Pus has a specific smell, bluish-greenish color of various shades, its protein content is more than 3-7%, globulins usually prevail, pH of pus is 5.6-6.9.

Purulent exudate contains various enzymes, primarily proteases, capable of cleaving dead and dystrophically altered structures in the focus of damage, including collagen and elastic fibers, therefore tissue lysis is characteristic of purulent inflammation. Along with polymorphonuclear leukocytes that can phagocytize and kill microorganisms, bactericidal factors are present in the exudate (immunoglobulins, complement components, etc.). Bactericidal factors produce viable leukocytes, they also arise from the breakdown of dead leukocytes and enter the exudate along with the blood plasma. In this regard, pus inhibits the growth of bacteria and destroys them. Neutrophilic pus leukocytes have a varied structure depending on the time they arrive from the blood in the suppuration zone. After 8-12 hours, polymorphonuclear leukocytes in the pus die and turn into "purulent bodies".

The cause of purulent inflammation is pyogenic (pyogenic) staphylococci, streptococci, gonococci, typhoid bacilli, etc. Purulent inflammation occurs in almost any tissue and organ. Its course can be acute and chronic. The main forms of purulent inflammation: abscess, phlegmon, empyema, purulent wound, acute ulcers.

Abscess - delimited purulent inflammation with the formation of a cavity filled with purulent exudate. It occurs in viable tissues after strong exposure to microorganisms or in dead tissues, where autolysis processes are growing.

◊ Within a few hours after the onset of purulent inflammation, a shaft of blood cells is visible around the accumulation of exudate: monocytes, macrophages, lymphocytes, eosinophils, fibrin clusters containing polymorphonuclear leukocytes. At the same time, fibrin, which has chemotaxis to polymorphonuclear leukocytes, stimulates their emigration from the vessels and entry into the focus of inflammation. Fibrin precipitates circulating immune complexes - chemoattractants for complement, which has pronounced histolytic properties. After three days, the formation of granulation tissue begins around the abscess and a pyogenic membrane appears. Through the vessels of the granulation tissue, leukocyte abscess enters the abscess cavity and partially removes decomposition products from it. With immunodeficiency, the patient has a tendency to melt the tissues surrounding the abscess. In chronic abscess, the granulation tissue matures, and two layers appear in the pyogenic membrane: the inner layer facing the cavity consisting of granulations, fibrin, detritus, and the outer layer of mature connective tissue.

Phlegmon - purulent diffuse inflammation with the impregnation and delamination of tissues with purulent exudate. The formation of cellulitis depends on the pathogenicity of the pathogen, the state of the body's defense systems, the structural characteristics of the tissues, where the cellulitis has arisen and where there are conditions for the spread of pus. Cellulitis usually occurs in the subcutaneous fatty tissue, intermuscular layers, the appendix wall, the meninges, etc. (fig. 4-4). Cellulitis fibrous fat is called cellulite.

◊ Phlegmon is of two kinds:

∨ soft, if lysis of necrotic tissue prevails;

∨ hard when coagulative necrosis and gradual tissue rejection occurs in the inflamed tissue.

Fig. 4-4. Purulent leptomeningitis and encephalitis. Stained with hematoxylin and eosin (x150).

◊ Complications phlegmon Arterial thrombosis is possible, and necrosis of the affected tissues occurs, for example, gangrenous appendicitis. Often the spread of purulent inflammation in the lymphatic vessels and veins, in these cases, purulent thrombophlebitis and lymphangitis occur. Phlegmon of a number of localizations under the influence of gravity of pus can drain along the muscle-tendon sheaths, neurovascular bundles, fat layers in the lower divisions, forming clusters there, not enclosed in a capsule (cold abscesses, or slivers). More often, this spread of pus causes acute inflammation of organs or cavities, for example, purulent mediastinitis - acute purulent inflammation of the mediastinal cellulose. Rejection of necrotic and coagulated tissues with solid phlegmon can lead to bleeding. Sometimes there are complications associated with severe intoxication, always accompanying purulent inflammation.

◊ Outcomes. Healing of phlegmonous inflammation begins with its delimitation with the formation of a rough scar. Usually phlegmon is removed surgically with subsequent scarring of the surgical wound. If the outcome is unfavorable, generalization of infection with the development of sepsis is possible.

Empyema - purulent inflammation of body cavities or hollow organs. The causes of empyema are both purulent foci in adjacent organs (for example, lung abscess, empyema of the pleural cavity), and impaired outflow of pus during purulent inflammation of hollow organs (gallbladder, appendix, fallopian tube, etc.). At the same time, local defense mechanisms are violated (constant updating of the contents of hollow organs, maintaining intracavitary pressure, which determines blood circulation in the wall of the hollow organ, synthesis and secretion of protective substances, including secretory immunoglobulins). With a long course of purulent inflammation, obliteration of hollow organs occurs.

Purulent wound is a special form of purulent inflammation that occurs as a result of suppuration of a traumatic, including surgical wound, or when opening to the external environment of a center of purulent inflammation with the formation of a wound surface. There are primary and secondary suppuration in the wound.

◊ Primary suppuration occurs immediately after trauma and traumatic edema.

◊ Secondary suppuration - recurrent purulent inflammation.

The involvement of bacteria in suppuration is part of the process of wound biological cleansing. Other features of a purulent wound are related to the conditions of its occurrence and course.

◊ Complications of purulent wounds: phlegmon, purulent resorptive fever, sepsis.

◊ Outcome of a purulent wound - its healing by secondary tension with scar formation.

Acute Ulcers most often in the gastrointestinal tract, less frequently on the surface of the body. By origin, primary, secondary and symptomatic acute ulcers are distinguished.

◊ Primary acute ulcers occur on the surface of the body, in the esophagus or stomach, with direct effects on the skin or mucosa of damaging factors (acids, alkalis, heat, microorganisms). Sometimes primary acute ulcers are a consequence of dermatitis (erysipelas, contact dermatitis, etc.). Purulent-necrotic changes in tissues are characteristic, and the predominance of one or another component depends on the etiological factor. The healing of such ulcers usually leaves scars.

◊ Secondary acute ulcers occur with extensive body burns, ischemia of the gastrointestinal tract, etc.

◊ Symptomatic and acute ulcers occur under stress, endocrinopathies, medication, neuro-reflex, trophic, vascular, specific.

The morphology of secondary and symptomatic acute ulcers is in many ways similar. Their localization is mainly the stomach and duodenum. Often there are several such ulcers. Their size is initially small, but multiple ulcers tend to merge. At the bottom of the ulcer is necrotic detritus, saturated with fibrin and covered with mucus. In the submucosal layer is expressed neutrophilic, sometimes eosinophilic infiltration. Steroid ulcers are characterized by a mild inflammatory reaction around the ulcer and intense hardening.

◊ Complications acute ulcers: arrosion of the vessel and gastrointestinal bleeding, with steroid ulcers sometimes perforation of the organ wall.

◊ The outcome of uncomplicated secondary acute ulcers is usually tissue healing.

Rotting inflammation

SPECIAL TYPES OF INFLAMMATION

Special types of inflammation - hemorrhagic and catarrhal are not considered independent forms.

Hemorrhagic inflammation is a variant of serous, fibrinous or purulent inflammation. Very high permeability of microcirculatory vessels, erythrocyte diapedesis, their admixture to exudate (serous hemorrhagic, purulent hemorrhagic inflammation) are characteristic. With the breakdown of red blood cells and the corresponding transformations of hemoglobin exudate can become black. Typically, hemorrhagic inflammation occurs with severe intoxication with a sharp increase in vascular permeability. It is characteristic of many viral infections, especially severe forms of influenza, plague, anthrax, smallpox. When purulent inflammation is also possible arrosia of the blood vessel and bleeding, but this does not mean that the inflammation becomes hemorrhagic in nature. In this case we are talking about the complication of purulent inflammation. Hemorrhagic inflammation usually worsens the course of the disease, the outcome depends on its etiology.

Catarrh develops on mucous membranes. Characteristic admixture of mucus to any exudate. Causes of catarrhal inflammation - various infections, allergies, thermal and chemical factors. In allergic rhinitis, mucus may be admixed to serous exudate. Often see purulent catarrh of the mucous membrane of the trachea and bronchi. Acute catarrhal inflammation lasts 2-3 weeks, usually leaving no traces. Atrophic or hypertrophic changes of the mucous membrane are possible in the outcome of chronic catarrhal inflammation. The value of catarrhal inflammation for the body depends on its location and the nature of the course.

PRODUCTIVE INFLAMMATION

Characteristic is the predominance of the proliferation of cellular elements over the alteration and exudation. Apparently, this is facilitated by the special reactivity of the organism. In addition, the etiological factor itself determines the proliferative cell response, which is especially typical for viruses and rickettsiae. The main forms of acute productive inflammation are granulomatous and interstitial diffuse.

Granulomatous inflammation is important mainly in the chronic course of the process. However, it can also be acute, for example, in acute infectious diseases (typhus and typhoid fever, rabies, epidemic encephalitis, acute anterior poliomyelitis, etc.). The basis of granulomas that occur in the nervous tissue are necrosis of groups of neurons or ganglion cells. Small focal necrosis of the gray or white matter of the brain or spinal cord, surrounded by glial elements with the function of phagocytes, are possible. After the resorption of necrotic tissue, glial cells are involved in the formation of glial scars in the central nervous system. The pathogenetic basis of necrosis is most often inflammation of microcirculatory vessels with infectious agents or their toxins with the development of perivascular tissue hypoxia. In typhoid fever, granulomas appear in the lymphoid formations of the small intestine and look like clusters of phagocytes transformed from reticular cells ("typhoid cells"). These large, round cells with bright cytoplasm phagocytize S. typhiand also detritus in solitary follicles. Typhoid granulomas are subject to necrosis, which is associated with salmonella phagocytosed typhoid cells. When recovering, sharp granulomas disappear without a trace, as in typhoid fever, or glial scars are left, as in neuroinfections. In the latter case, the outcome of the disease depends on the location and volume of scars.

Interstitial diffuse (interstitial) inflammation is caused by various infectious agents or develops as a reaction of the active mesenchyme of the organs to marked toxic effects, intoxication by microorganisms. It can occur in the stroma of all parenchymatous organs, where inflammatory and immunocompetent cells accumulate. The peculiarities of this inflammation in the acute phase are a significant amount of mononuclears (monocytes) in the infiltrate, dystrophic and necrobiotic changes of the parenchyma of the organ. The most vivid picture of interstitial productive inflammation occurs in acute and chronic interstitial pneumonia, interstitial hepatitis, interstitial nephritis, interstitial myocarditis.

Interstitial, or interstitial myocarditis occurs more often with infectious or toxic effects. Mainly exudative and predominantly productive forms of interstitial myocarditis are distinguished (Fig. 4-5). With productive myocarditis, lymphohistiocytic and monocytic infiltrate is visible in the stroma of the myocardium. By interstitial myocarditis include myocarditis Abramov-Fidler, having an allergic nature. Interstitial nephritis often occurs in violation of the outflow of urine from the renal pelvis and the development of acute pyelonephritis, as well as with long-term use of drugs of phenacetin series. Acute interstitial inflammation in the liver leads to the appearance of mononuclear infiltrates in portal waste, sometimes with a small number of polymorphonuclear leukocytes, always in combination with dystrophy of the parenchyma. Possible transformation of acute interstitial hepatitis of various etiologies into chronic hepatitis, which causes sclerosis of the portal tracts.

Fig. 4-5. Acute interstitial myocarditis. Stained with hematoxylin and eosin (x120).

CHRONIC INFLAMMATION

Chronic inflammation is a pathological process that proceeds with the persistence of the pathological factor, the development in this connection of the immunological deficiency, which causes the originality of the morphological changes of tissues in the area of \u200b\u200binflammation, the course of the process according to the principle of "vicious circle", the difficulty of repair and restoration of homeostasis.

As stated above, the biological meaning of inflammation is the delimitation, destruction and elimination of the pathogenic factor, after which the inflammation ends with the repair and restoration of homeostasis. However, often for various reasons, the pathogenic stimulus is not destroyed. In this case, the inflammation becomes chronic. Chronic inflammation is a manifestation of a defect in the system of protection and adaptation of the organism to the environment.

The reasons chronic inflammation are numerous. However, the main reason is the persistence of the damaging factor, which is associated both with its features and with the insufficient response of the inflammation of the organism itself. Thus, the pathogenic factor may have high immunogenicity, increased resistance against hydrolases of leukocytes and macrophages, and a large amount of stimulus (for example, echinococcus) also prevents the completion of inflammation. Defects in the protection of the organism itself may be due to congenital leukocyte pathology, primarily neutrophilic, impaired mononuclear phagocytic formation, inhibition of chemotaxis, impaired tissue innervation in the area of \u200b\u200binflammation, autoimmunization of these tissues, genetic increase in sensitivity to the action of pathogenic factors. These and other causes hinder tissue repair in the area of \u200b\u200binflammation and the restoration of homeostasis, so inflammation loses its adaptive value.

Inflammation and the immune system are closely related. Naturally, immune mechanisms play a major role in the pathogenesis of chronic inflammation. For a long time the current inflammatory process affects all body systems, which can be judged by changes in blood and immunity parameters. Thus, patients suffering from chronic inflammatory diseases, especially chronic wounds, usually have lymphocytopenia, a decrease in the level of all T-lymphocytes, including T-helpers and T-suppressors, their ratio is disturbed, which indicates the development of secondary immune deficiency . Increased antibody production, especially IgA and IgG. In most patients, the level of circulating immune complexes (CIC) in the blood is clearly increased, which is associated not only with their increased formation, but also with a violation of elimination. At the same time, the ability of neutrophils to chemotaxis decreases, which is associated with the accumulation in the blood of inhibitors of this process (decomposition products of cells, microorganisms, toxins, immune complexes), especially when inflammation worsens.

Chronic inflammation has features that depend on the etiology of the process, the structure and function of the affected organ, the reactivity of the organism and other factors. Obviously, the persistence of the stimulus is of primary importance. Constant antigenic stimulation of the immune system, intoxication caused by a stimulus, other microorganisms and constant tissue necrosis in the inflammatory focus not only increase the functional load on the immune system, but also damage it. It is possible that in these conditions the granulation tissue itself may acquire auto-antigenic properties, becoming an additional constant stimulus to the hyperfunction of the immune system. Prolonged last voltage after some time leads to the disruption of its functions. There are pathological changes that reflect the pronounced dysfunction of the immune system, gradually increasing immune deficiency. At the same time, a decrease in the bactericidal and phagocytic functions of leukocytes, along with the suppression of their chemotaxis, violates phagocytosis, which contributes to the persistence of infection. There is a "vicious circle." While maintaining the causes and conditions of chronic inflammation, a complete repair of the inflammatory focus and restoration of homeostasis are impossible.

Morphology. A common morphogenetic symptom of chronic inflammation is a violation of the cyclical course of the process in the form of continuous layering of alteration and exudation stages at the proliferation stage. This leads to a constant recurrence of inflammation and the impossibility of reparation. Granulation tissue in chronic inflammation has the features of formation and maturation. It is characterized by constantly emerging focal necrosis, lymphoplasmacytic infiltrate with a reduced number of polymorphonuclear leukocytes, macrophages and a relatively small number of active fibroblasts. In the walls of blood vessels and perivascular granulation tissue reveal CIC, immunoglobulins, complement. The development of productive vasculitis, the proliferation of the endothelium in larger vessels, up to the obliteration of their lumen, is observed (Fig. 4-6). During exacerbation of the disease, vasculitis is purulent (Fig. 4-7). The endothelium destruction increases in them and pinocytosis falls.

Fig. 4-6. Thickening of the walls and narrowing of the lumen of the vessels of granulation tissue. Stained with hematoxylin and eosin (x120).

Fig. 4-7. Purulent vasculitis of vessels of granulation tissue. Stained with hematoxylin and eosin (x120).

The number of capillaries is usually reduced, which increases the hypoxia of granulation tissue and metabolic disorders in it. At the same time endotheliocytes - secretory cells involved in intercellular interactions - suffer. They synthesize a number of mediators of immunity, including IL-1, enhancing the proliferation of fibroblasts and the synthesis of collagen. Damage to the vascular endothelium of granulation tissue contributes to the violation of its maturation and intercellular regulation. For a long time, granulation tissue remains at the stage of loose connective tissue, unstable collagen type III prevails in it, the formation of elastic fibers is impaired. These changes are aggravated by hypoxia, which increases with the decrease in the number of altered vessels. Reducing the partial oxygen tension in the tissue also impairs the function of fibroblasts, including the synthesis of collagen and elastin. Defective elastic fibers, which play a large role in reparation, form shapeless clusters that prevent them from performing their functions. Reducing the amount of type I collagen in the inflammation center makes epithelization of the granulating wound difficult.

Conditions for the development of chronic inflammation.

Persistence of the damaging factor.

Immunological deficiency and the development of secondary immunodeficiency as a result of humoral or cellular disorders.

◊ Violations of humoral immunity:

∨ changing the concentration of IgA, IgG, IgM in the blood, increasing their level in the tissues;

∨ increased concentration of CIC in blood and tissues.

◊ Disruption of cellular immunity:

∨ lymphocytopenia;

∨ reduction of the total population of T-lymphocytes;

∨ decrease in the level of T-helper and T-suppressors;

∨ change in the ratio of T-helper and T-suppressors;

∨ reduction of leukocyte chemotactic activity;

∨ impaired regeneration in the focus of chronic inflammation;

∨ process of the process on the principle of a vicious circle;

∨ difficulty restoring homeostasis.

Considering the above features of chronic inflammation, the treatment of such patients should be directed not only at fighting infection and destroying the persistent damaging factor, but also at normalizing the function of the entire immune system.

There is chronic exudative and productive inflammation.

Chronic exudative inflammation: osteomyelitis, abscesses, purulent salpingitis, chronic wounds (trophic ulcers and bedsores), chronic ulcers (inflammation in ulcers, ulcerative colitis, etc.).

Chronic productive inflammation:

∨ diffuse (chronic hepatitis, idiopathic fibrosing alveolitis);

∨ granulomatous - immune (tuberculosis, syphilis, leprosy) and non-immune granulomas (around dust particles);

∨ inflammatory hyperplastic (hyperregenerative) growths;

Chronic Exudative Inflammation

Characterized by the presence of a moderate amount of exudate, often purulent, often purulent-fibrinous. Infiltration of inflamed tissues is predominantly lymphoplasmacytic, but neutrophilic leukocytes are also present in the infiltration, and monocytes, macrophages and fibroblasts are present along the periphery of the inflammatory zone. A connective capsule arises around a chronic abscess, a focus of osteomyelitis. In chronic purulent salpingitis, the cavity of the uterine tube is filled with pus, its wall is sclerotic, infiltrated with leukocytes. Such a process may be the cause of the development of pelvioperitonitis or ovarian abscesses and pelvic tissues. In chronic abscess, with osteomyelitis, fistulas are often found that connect the inflammatory focus with a cavity or open outwards. Through them, purulent exudate leaves the zone of inflammation. After healing of such inflammation a scar is formed.

Trophic ulcers, usually of the lower limbs, occur in chronic progressive circulatory disorders as a result of sclerosis of microcirculatory vessels in diabetes mellitus, disorders in tissue trophism in decompensated varicose veins, sometimes in atherosclerosis. Circulatory disorders are associated with impaired lymph circulation and the development of lymphostasis, which, along with hypoxia, stimulates fibroblasts. At bedsores, disturbance of the nervous trophism and secondary disturbance of the blood supply to the tissues prevail. For trophic ulcers and bedsores, the development of an immature granulation tissue is characteristic. The described general and local biochemical and immunological changes in trophic ulcers and bedsores explain the low efficiency of skin transplantation in this pathology.

The morphology and pathogenesis of chronic peptic ulcer and nonspecific ulcerative colitis are described in Chapter 13. General and local factors that support chronic inflammation in the stomach and intestines constantly stimulate fibroblasts and pronounced development of sclerotic changes in the area of \u200b\u200binflammation, including sclerosis of arteries with stenosis of their lumen . This leads to a progressive deterioration in the blood supply to the area of \u200b\u200binflammation, an increase in hypoxia. The latter, in turn, prevents the development of the productive phase of inflammation and, in addition, stimulates fibroblasts. All this contributes to a pronounced sclerosis of the stomach wall and leads to stenosis of the intestinal lumen.

CHRONIC PRODUCTIVE INFLAMMATION

CHRONIC DIFFUSIVE INFLAMMATION

An example of chronic diffuse inflammation is chronic hepatitis and interstitial pneumonia (see chapters 11 and 14). Often they are caused by viruses that cause serous inflammation at the beginning, and then the prevalence of the productive component of the inflammatory process. Characterized by the development of patho-and morphogenesis on the principle of "vicious circle", the progression of productive inflammatory reactions. The outcome is cirrhosis of the liver and septo-alveolar sclerosis of the lung tissue.

GRANULATED INFLAMMATION

The formation of granulomas (nodules) resulting from the proliferation and transformation of cells capable of phagocytosis is characteristic. Chronic granulomatous inflammation occurs when, for some reason, damaging factors cannot be removed from the body.

Granuloma morphogenesis consists of the following stages:

∨ accumulation in the focus of damage to monocytic phagocytes;

∨ maturation of monocytes into macrophages and the formation of macrophage granulomas;

∨ transformation of macrophages into epithelioid cells and the formation of epithelioid cell granulomas;

∨ fusion of epithelioid cells, the formation of giant foreign body cells (Pirogov-Langhans cells), the possible formation of giant cell granulomas.

Thus, in granulomatous inflammation, macrophage (phagocytoma or simple granuloma), epithelioid cell and giant cell granulomas can occur. Depending on the level of metabolism, the following types of granulomas are distinguished:

∨ with a low level of metabolism, arising under the action of relatively inert substances (foreign bodies), forming, in the main, giant cell granulomas;

∨ with a high level of metabolism, resulting from toxic effects (usually microorganisms), with the formation of epithelioid cell granulomas.

The etiology of granulomatous inflammation is diverse. According to etiology, the following types of granulomas are distinguished:

∨ granulomas with established etiology - infectious (with tuberculosis, syphilis, leprosy, rheumatism, scleroma) and non-infectious;

Granulomas with unidentified etiology (for sarcoidosis, Crohn's disease, etc.).

Pathogenesis. The following conditions are necessary for the development of granulomas:

∨ presence of substances capable of stimulating the system of mononuclear phagocytes;

∨ resistance of the stimulus to phagocytosis.

Such an irritant is a powerful antigenic stimulator of the immune system, primarily activating macrophages. The latter, with the help of IL-1, attract lymphocytes to the focus of inflammation, promote their stimulation and proliferation. The mechanisms of cellular immunity, primarily HRT, begin to operate. In this case, they say about the immune granuloma, which usually has morphology of the epithelioid cell with giant Pirogov-Langhans cells. For such a granuloma, unfinished phagocytosis (endocytobiosis) is characteristic.

Non-immune granulomas occur mainly around foreign bodies, including particles of organic dust. In these cases, phagocytosis is often more complete and chronic inflammation is represented by phagocytoma, less often - giant cell granuloma from cells of foreign bodies.

Granulomas are also divided into the following groups:

∨ specific, reflecting features of the disease (tuberculosis, syphilis, leprosy, scleroma);

∨ nonspecific, not having characteristic etiological signs, arising from infectious diseases (echinococcosis, alveoliococcosis, brucellosis, etc.), ingestion of foreign bodies.

Specific immune granulomas have the greatest epidemiological and diagnostic value. Their function is to fix the pathogens in one place to prevent their spread throughout the body and, obviously, to stimulate the immune system. In the pathogenesis and morphogenesis of these granulomas, epithelioid cells play a special role. Diseases with the formation of epithelioid cell granulomas have non-sterile immunity, i.e. The resulting immunity is maintained until the pathogen persists in the body. This persistence and allows the epithelioid cell. The transformation of a macrophage into an epithelioid cell occurs when, due to the complete phagocytosis, the antigenic structure of the pathogen is known and immune reactions take place. After that you need a cell that retains the ability to phagocytosis, but is unable to complete this phagocytosis. As a result, live pathogens constantly stimulate the immune system, supporting non-sterile immunity. In the epithelioid cell there are few lysosomes, its bactericidal activity is reduced, but it retains the ability to stimulate the immune system, synthesizing IL-1, fibroblast growth factor and transforming growth factor.

It is believed that the transformation of epithelioid cells into giant cells is possible either by dividing the nuclei while preserving the cytoplasm, or by merging the cytoplasm of several epithelioid cells into one giant cell with many nuclei. Giant cells are distinguished from each other by the number and location of nuclei: in giant cells of Pirogov-Langhans there are up to 20 nuclei located on the periphery of the cell as a horseshoe, and in giant cells of foreign bodies up to 80 nuclei randomly located in the center of the cell. In giant cells of both types there are no lysosomes, therefore they possess selective phagocytosis and endocytobiosis or their functions are not associated with phagocytosis. The cellular composition of specific granulomas is the same, but the ratio of cells and their location in the granuloma depends on the cause of the disease.

Tuberculosis granuloma has a characteristic structure. Its center is a zone of caseous necrosis surrounded by epithelioid cells located in the form of a paling. This granuloma is called epithelioid cell. For epithelioid cells - a shaft of sensitized T-lymphocytes. Between epithelioid and lymphoid cells - 1-3 giant Pirogov-Langhans cells. Fibroblasts located behind the lymphocyte shaft restrict the granuloma (Figure 4-8). When stained with Tsil-Nielsen, phagocytosed mycobacteria are often detected in epithelioid and giant cells, and upon impregnation with silver salts in granulomas, a thin network of argyrophil fibers is seen. There are no vessels in the tuberculous granuloma, therefore there are no leukocytes in it. Only in the outer zones of the tubercle are small vessels visible. With a favorable course of the disease, fibrosis and petrification of granulomas occur, however, mycobacteria persist in petrifications, which provides non-sterile immunity.

Fig. 4-8. Epithelioid cell granuloma in tuberculosis. In the center of the granuloma - caseous necrosis, surrounded by a shaft of epithelioid and lymphoid cells. One can see the giant cells of Pirogov-Langhans. Stained with hematoxylin and eosin (x120).

Syphilitic granuloma (gumma) contains a zone of coagulation necrosis, neutrophilic leukocyte hydrolases give it stickiness. The area of \u200b\u200bnecrosis is surrounded by lymphocytes, plasma cells, neutrophilic leukocytes, fibroblasts, as well as single epithelioid cells, macrophages and giant Pirogov-Langans-type cells. Connective tissue is intensively developing around the granuloma, forming a capsule. Near the capsule in the inflammatory infiltrate are many small vessels with symptoms of productive endovasculitis. The reason for this is the incubation of pale spirochaetes predominantly in the vessels, therefore, microorganisms act primarily on the inner lining of the vessels. Around the gum is a diffuse infiltrate of lymphocytes, fibroblasts and leukocytes (Fig. 4-9).

Fig. 4-9. Syphilitic gumma in the liver. Stained with hematoxylin and eosin (x120).

◊ In addition to gum, tertiary syphilis is characterized by the development of gummy infiltration, most often in the ascending aorta and the aortic arch, mainly in the middle envelope. The composition of the infiltrate is the same as in gum, there are many small vessels and capillaries in it, including vasa vasorum, with the phenomena of vasculitis, however, a capsule does not appear around the infiltrate. Syphilitic mesaortitis develops (Fig. 4-10). Necrosis in the aortic wall causes the destruction of elastic and the growth of granulation tissue. The latter, ripening, turns into a coarse connective tissue. The result is uneven hardening of the aortic wall, its inner membrane is uneven, wrinkled, and bumpy (“shagreen” skin).

Fig. 4-10. Syphilitic mesaortitis: a - gummy infiltration of the aortic middle membrane, caseous necrosis, inflamed vasa vasorum, lymphocytic leukocyte infiltration (stained with hematoxylin and eosin, x120) are visible; b - destruction of elastic fibers in the middle aortic membrane (fuxselin for Shueninov, x100).

◊ Complications of syphilitic mesaortitis - the formation of aneurysm of the ascending part and the aortic arch, its rupture leads to sudden death. The value of gum depends on its localization (in the brain or spinal cord, liver, etc.).

◊ Exodus gumma. During treatment, healing is possible with the formation of coarse scars of stellate form. Gummy destructive lesions of the roto-and nasopharynx lead to impaired speech, swallowing, breathing, deform the face, destroying the nose and hard palate. At the same time immunity is lowered, which creates the possibility of re-infection with syphilis.

Leprosy granuloma (leproma) has the same cellular composition of the infiltrate as other specific granulomas: macrophages, epithelioid cells, lymphocytes, plasma cells, fibroblasts. Large cells with large fatty inclusions (leprous balls) are seen among macrophages; after cell destruction, these inclusions phagocyte giant cells. Macrophages contain mycobacterium leprosy, located in the form of cigarettes in a pack. Such giant cells are called Virchow leprous cells (Fig. 4-11). Mycobacterium leprosy destroys these cells and falls into the cellular infiltrate of the leproma, apparently stimulating the immune system. Such a granuloma is more characteristic of the leprous form of leprosy, when granulomatous inflammation mainly affects the skin and peripheral nerves. However, individual granulomas are found in almost all internal organs. The tuberculoid form of leprosy is characterized by the development of HRT with the formation of epithelioid cell granulomas. They reveal mycobacterium leprosy in an amount less than that of leprous form (see Chapter 17).

Fig. 4-11. Leprosis granuloma. The giant Virchow leprous cells are visible. Stained with hematoxylin and eosin (x120).

Scleroma granuloma - a cluster of macrophages, lymphocytes, plasma cells and their degradation products - Roussel's eosinophilic bodies. Macrophages capture diplobacilli Volkovich-Frisch, but phagocytosis in them is incomplete. Increasing in size, they turn into giant cells of Mikulich. When these cells are destroyed, pathogens enter the tissues and, probably, stimulate not only the immune system, but also fibrillogenesis. For this reason, the development of connective tissue is characteristic of scleroma granulomas. Scleroma granulomas are mainly located in the mucous membrane of the upper respiratory tract. Rapid hardening leads to stenosis of the nasal larynx, larynx, trachea and even the bronchi, which makes it difficult for air to enter the lungs and carries the threat of asphyxiation.

Thus, all specific immune granulomas have much in common in their morphology, immunological processes and biological expediency.

Non-immune granulomas arise around foreign bodies and as a result of the action of dusts, fumes, aerosols, suspensions. It is possible the formation of phagocyte or giant cell granulomas. A mandatory element of such granulomas is a macrophage that performs phagocytosis, a small number of leukocytes, including eosinophils, as well as giant cells of foreign bodies. As a rule, in such granulomas there are no epithelioid cells, many vessels. Non-immune granulomas are characteristic of a number of occupational diseases.

Granulomatous diseases - a group of diseases of various etiologies with the formation of granulomas, often in combination with vasculitis. The pathogenesis of diseases with the presence of immune granulomas determine the reactions of the immune system, and diseases with the formation of non-immune granulomas determine the nature of the damaging factor. Those and other diseases flow chronically, with the development of sclerotic processes in the organs that violate their functions.

Hyperplastic (hyperregenerative) growths - productive inflammation in the stroma of the mucous membranes. Against the background of the proliferation of stromal cells, an accumulation of eosinophils, lymphocytes, and hyperplasia of mucosal epithelium are observed. When this occurs, polyps of inflammatory origin - polypous rhinitis, polypous colitis, etc. Hyperplastic growths are also on the border of flat or prismatic epithelium and mucous membranes as a result of the constant irritant action of their discharge, for example, in the rectum or female external genital organs. When this occurs, maceration of the squamous epithelium, and in the stroma occurs chronic productive inflammation, leading to the growth of the stroma, epithelium and the formation of genital warts. Most often they occur around the anus and external genital organs, especially in women.

IMMUNE INFLAMMATION

PATHOLOGY OF THERMAL REGULATION

Body temperature is an important physiological constant, since the normal course of metabolic processes, the performance of various functions and the stability of cell structures are possible only at a certain temperature of the internal environment. The constancy of body temperature is ensured by the balance between heat transfer and heat production. Thermoregulation disorders are manifested by fever, hypo-and hyperthermia.

Fever

Fever (lat. febrisfrom Greek pirexia - fever) - a typical pathological protective-adaptive reaction to the effects of pyrogenic stimuli, manifested by a restructuring of heat regulation and an increase in body temperature. It is often accompanied by changes in the metabolism and functions of various organs.

ETIOLOGY

The cause of the febrile reaction are pyrogens (from the Greek. rUr - the fire, gennao - create) - substances that change the regulation of temperature homeostasis and cause fever. Pyrogens are conventionally divided into infectious (exogenous) and non-infectious (endogenous). The cause of infectious fever are bacteria, and non-infectious - substances formed during the destruction of the tissues of the organism. Exogenous bacterial pyrogen, being a lipopolysaccharide that is part of endotoxins, is especially active in gram-negative and some gram-positive bacteria. Protein components of a number of other infectious agents can also cause fever. Pyrogenic activity is characteristic of the vital products of viruses, fungi, protozoa and helminths. Endogenous pyrogens can form in body tissues under the influence of infectious agents, as well as with dystrophies, aseptic inflammation, allergies, myocardial infarction, mechanical tissue damage, radiation and burn cell decay, tumor necrosis, etc. By their nature, they can be low molecular weight proteins, polypeptides, nucleic acids, other compounds and take part in the development of fever along with exopyrogenic. Pyrogenic, which causes fever, is formed in the body and under the influence of immune stimuli, in particular immune complexes, C 5 component of complement, allergy mediators (cytokines), etc. Obviously, the influence of exogenous lipopolysaccharides and tissue pyrogens is mediated through specialized fever mediators synthesized by leukocytes. Endogenous pyrogens secreted by macrophages are cytokines (IL-1, 6 and 8, as well as TNF-α).

IL-1 has the most pronounced pyrogenic activity, it has an affinity for thermoregulating neurons, rearranges the work of the thermoregulation system and directly causes fever. IL-1 is a protein that is synthesized by almost all cells of the body, with the exception of erythrocytes, however, mononuclear phagocytes, including fixed liver and spleen macrophages, alveolar and peritoneal macrophages, as well as granulocytes, are the most active. The ability to synthesize IL-1 is also possessed by B-lymphocytes and various cells of the skin, mesangium, astrocytes of brain microglia, endothelial cells, vascular myocytes, Kupffer cells, etc. Blood monocytes are less active in this regard.

In the evolutionary aspect, IL-1 is one of the most ancient factors released by phagocytes, which exhibits the properties of a mediator of inflammation in various lesions. As the organisms are improved, IL-1 not only provides adequate coordination of local reactions - cellular (expression of endothelial receptors to neutrophils, adhesion, chemotaxis), vascular (vasodilation and increased permeability) and mesenchymal (stimulation of fibroblasts, collagenogenesis) - but also determines the formation of common changes in the body. Among the latter, fever, leukocytosis, switching of the synthetic activity of hepatocytes are of the greatest importance, as a result of which the formation of “acute phase proteins” (C-reactive protein, serum amyloid A, fibrinogen and other hemostasis proteins, complement, etc.) is increased and albumin synthesis is reduced. With the advent of IL-1 in the evolution of immunogenesis, it becomes a factor linking inflammation with immune restructuring, stimulates the reproduction and maturation of immunocytes, ensures the activity of natural killer cells and stimulation of mononuclear cells, i.e. affects all immunity systems. Thus, fever is only one of the many-sided adaptive reactions of the body to damage, which are activated by one compound - IL-1.

However, with the excessive formation of IL-1, it has negative effects: drowsiness, loss of appetite, myalgia and arthralgia, enhanced catabolism of muscle tissue proteins.

PATHOGENESIS

The isolated IL-1 interacts with specific receptors on the membrane of the neurons of the thermoregulation center. Due to the activation of receptors, the activity of the enzyme conjugated with them, phospholipase A 2, increases. This enzyme releases from the phospholipids of the plasma membrane arachidonic acid, from which prostaglandins of the E group are formed. The prostaglandins E 1 and E 2 inhibit the synthesis of the phosphodiesterase enzyme, resulting in an increase in the amount of cyclic adenosine monophosphate (cAMP), which changes the sensitivity of the neurons of the thermoregulation to the temperature and cold patterns. Sensitivity to cold signals increases, decreases to heat signals. As a result, the heat transfer center is inhibited (physical heat regulation) and the heat production center is activated (chemical heat regulation). Commands of thermoregulating neurons are realized to target organs via neuroendocrine channels through locomotor, vegetative and endocrine connections. An increase in locomotor and sympathoadrenal effects leads to an increase in contractile and non-contractile thermogenesis; sympathetic neurohormones (catecholamines) not only increase heat production by stimulating oxidative processes, but also limit heat transfer due to spasm of small arterial vessels of the skin. The limitation of heat transfer can also be associated with the weakening of parasympathetic influences that increase sweating, salivation, blood circulation in the skin and mucous membranes. An increase in the increment of thyroid hormone - T 3 and T 4 plays an important role in the onset of fever. They increase heat production due to increased oxidative processes in tissues, in large doses it is possible because of the dissociation of oxidative phosphorylation, and possibly due to the increased sensitivity of thermoneurons to pyrogenic effects. With an increase in body temperature, the incoming reverse afferent influences by humoral (blood temperature) and reflex (from thermoreceptors of the skin and other organs) carry information about the effectiveness of command implementation, the degree of temperature rise. This information is compared with the new program of work of the heat control center, if necessary, the temperature is corrected and set at the required level. Such a set of mechanisms is only the most general scheme for the formation of a febrile reaction, in which there are still many unknown and debatable positions.

DEVELOPMENT STAGES

Regardless of the nature of the primary pyrogens and the form of fever, there are three stages of a febrile reaction: elevation ( stadium incrementi) holding ( stadium fasgtigii) and reductions ( stadium decrementi) body temperature. Each of these stages of fever is formed due to a regular change in the heat balance of the body, which, in turn, is determined by the activity of the thermoregulation center.

◊ For stage I fever characterized by a positive heat balance, i.e. the predominance of heat production over heat emission. Heat accumulates in the body and the body temperature rises.

◊ Stage II is characterized by the formation of an equilibrium between heat production and heat transfer, although both of them are maintained at a higher level than normal. Body temperature remains increased and maintained at the same level; however, the temperature regulation is maintained.

◊ During stage III fever, the negative heat balance increases, i.e. the predominance of heat transfer over heat production; the body loses heat and body temperature drops to normal.

Although the heat balance at each stage of fever is a regular phenomenon recorded during any febrile reactions, the absolute values \u200b\u200bof heat production and heat transfer compared with the norm may be different and determine the rate of increase, the degree of rise and the rate of temperature drop at the corresponding stages of fever.

Stage I fever develops differently: perhaps a rapid, within a few hours, increase in body temperature, usually to high numbers (for example, with lobar pneumonia, influenza, etc.). There may be a slow increase to relatively moderate body temperature (over several days), as in bronchopneumonia, typhoid fever, etc. In such cases, heat production prevails over heat emission, but this positive heat balance is achieved in different ways. The rapid (acute) increase in body temperature is primarily due to the sharp limitation of heat transfer; at the same time, heat production also increases, but gradually and only slightly. In the skin and mucous membranes there may be a spasm of small vessels and restriction of blood flow in them, which leads to a decrease in the temperature of these tissues. A corresponding afferentation from thermoreceptors is formed, a person feels chills, although the temperature of the blood increases progressively (the “chills” stage). A peculiar situation arises: the heat accumulates in the body, and the temperature of the internal environment increases, but as a result of a decrease in the sensitivity of thermoregulating neurons, cooling is felt, heat transfer is increasingly limited, and even to some extent, heat production is provided by muscle tremor and contraction of smooth muscles of the skin ("goose bumps "). With a gradual rise in body temperature, heat production increases moderately and heat output is limited; there are no bright manifestations of changes in heat balance and chills. There are other options for changes in heat production and heat transfer.

Stage II fever is characterized by the cessation of growth in body temperature, which stabilizes at an elevated level that corresponds to the setting point of the thermoregulation center. Stabilization of temperature in this stage is associated with the establishment of an equilibrium between heat production and heat transfer, equally increased. The feeling of cold and chills at this time disappear, and a person may experience a feeling of heat, often visible redness of the skin and mucous membranes (the stage of "heat"). During this period, the body actively maintains body temperature and afferent or humoral effects, which are aimed at its additional increase or decrease, are less effective than normal. In other words, under fever conditions, temperature-controlled neurons are to some extent isolated from additional influences. The elimination of disturbances in the thermoregulation system determines the adequacy of raising the temperature of the intensity of the pyrogenic effect. At the same time, isolation from additional thermoregulatory influences is not “hard”, since the regulation of the heat center still remains. In particular, daily temperature fluctuations persist, although under fever conditions they can change significantly, forming types of temperature curves.

The third stage of fever is to some extent connected with the first one: often with a rapid rise in temperature, a rapid (critical) decrease in temperature is observed, and with a slow one, a slow (lytic) decrease is also observed. With a rapid drop in temperature, a negative heat balance occurs, first of all, due to a sharp increase in heat transfer with a slow decrease in heat production. Sometimes the heat emission remains increased for a long time and even increases somewhat. At the same time, the heat release is accelerated due to a sharp increase in sweating (the “sweat” stage), although other ways of increasing heat transfer are possible due to the rapid expansion of small vessels of the skin and mucous membranes with increasing blood flow. With a gradual decrease in body temperature, heat transfer returns to normal, and heat production decreases.

The question of what caused the characteristics of heat transfer and heat production, and, accordingly, variations in the rate of rise and fall in temperature, is not fully resolved, however, the important role in the nature of the primary pyrogen is obvious, since the critical rise and critical drop in temperature are most often observed in certain infections for example, with lobar pneumonia and flu. The high lability of the mechanisms of physical thermoregulation as a younger, evolutionary, education that reacts faster to various stimuli than chemical thermoregulation may also be of considerable importance. The individual features of the organism can also play a significant role, in particular its sensitivity to primary pyrogens and the sensitivity of temperature-controlled neurons to secondary ones, i.e. leukocyte pyrogens, the level and activity of mononuclear phagocytes, the state of the vegetative nervous and endocrine regulation systems, etc. In addition, some primary pyrogenic compounds (for example, salmonella endotoxin, etc.), in addition to stimulating the production of leukocytes IL-1, can have a direct uncoupling effect on the oxidative phosphorylation in mitochondria of cells of various tissues. All these factors cause variations and determine the peculiarities of temperature changes at different stages of fever.

CLASSIFICATION

Each febrile reaction has its own characteristics, determined by the nosological form of the disease, the properties of the primary pyrogen and the individual capabilities of the organism. This applies not only to the rate of rise and fall of temperature, but also the degree of maximum rise in the holding stage, as well as the type of temperature curve. Moreover, the type of temperature curve can be so associated with the nosological form of the disease that it sometimes serves the purpose of its diagnosis.

For the classification of fever use the etiological principle, and therefore isolated infectious and non-infectious fevers.

Depending on the degree of maximum temperature rise, the fever may be:

∨ subfebrile (not above 38 ° C);

∨ febrile or moderate (38-39 ° C);

∨ pyretic, or high (39-41 ° C);

∨ hyperpyretic, or excessive (above 41 ° C).

Taking into account the peculiarities of daily temperature fluctuations, the following types of temperature curves and, accordingly, the forms of fever determine.

◊ Constant fever, in which morning and evening fluctuations in body temperature do not exceed 1 ° C, often occurs in typhoid fever, typhus, croupous pneumonia, etc.

◊ laxative fever, when the morning-evening fluctuations in body temperature are 1.5-2 ° C, but do not reach the norm; it is found in tuberculosis, viral infections, exudative pleurisy, etc.

◊ Intermittent fever - fluctuations in body temperature are more than 2 ° C, and in the morning it can be normal and even below normal, which is also observed in tuberculosis, severe purulent infections, malaria, lymphomas, etc.

◊ Exhausting fever is characterized by a high rise in body temperature and its decrease by 3-5 ° C, as in severe purulent infections and sepsis.

◊ Return fever - periods of increased body temperature lasting from one to several days are repeated against the background of normal temperature; such fever is observed in relapsing fever, Hodgkin's disease, malaria, etc.

◊ Atypical fever is characterized by several temperature rises (falls) during the day, i.e. with violation of the morning-evening rhythmics (for example, in sepsis).

◊ Ephemeral fever. In the case of chronic infectious diseases, a short-term low temperature rise (37.5-38 ° C) occurs with unstable morning-evening fluctuations.

It should be noted that at present, due to the widespread use of antibiotics and antipyretics, typical forms of temperature curves are rare.

The specific physiological mechanisms of diurnal bias in the regulation of temperature homeostasis are not known, although it is obvious that they, like seasonal regulation bias, reflect rhythmic processes occurring in the body due to changes in habitat. It is also clear that fluctuations in metabolism and functions have an adaptive value and correspond to the total body activity formed in the evolution. During fever, this rhythm of temperature regulation is retained, although in some cases it becomes more pronounced (fluctuations reach 2-3 ° C), and sometimes the daily rhythm is distorted. Such disturbances of the diurnal rhythm, arising during toxic-infectious processes (some forms of tuberculosis, sepsis, etc.), are manifested by a rise in temperature in the morning, sometimes repeated rises and falls to the norm and lower during the day, etc. Changes in the daily rhythm of temperature during fever, being a prognostically unfavorable sign, indicate the onset of toxic damage to brain thermo-neurons, their transition from adaptive activation to exhaustion. Such situations usually arise in cases where the etiological factor, in addition to the usual pyrogenic effect, causes a direct increase in heat production in the tissues, for example, due to the dissociation of biological oxidation, i.e. fever and hyperthermia are both possible.

CHANGES IN ORGANS AND SYSTEMS

Metabolism, physiological processes and morphological changes in organs during fever are quite complex in their origin. They can be different for different types of fever, depend on its stage, previous and associated diseases and other factors. The basis of the peculiarity of metabolism and the functions of different organs and systems, as well as morphological changes in them, are at least three groups of mechanisms. The former form the actual fever, which is associated with changes in neuroendocrine influences, metabolism and physiological processes; the second ones are caused by the effect on the organism of the most elevated body temperature in case of a fever that has already arisen; the third are the result of intoxication, which can be with infectious and non-infectious fever. At a height of fever, as a rule, there is a negative nitrogen balance due to enhanced proteolysis, the level of residual nitrogen in the blood and the proteolytic activity of its serum increase. The amount of glycogen decreases in the liver and muscles, the concentration of lactate and pyruvate increases in the blood, hyperglycemia is observed. Lipolysis is enhanced in the body and hyperketonemia is registered. Hyperlactacidemia and hyperketonemia lead to the occurrence of metabolic acidosis, which is associated with an increase in the body's need for oxygen and the occurrence of relative hypoxia. Equally important in increasing the body's need for oxygen is the activation of the sympathoadrenal system and thyroid function of the thyroid gland. However, enhanced protein breakdown may not be associated with the fever itself, but with accompanying loss of appetite, starvation and intoxication, since the introduction of purified pyrogen (pyrogenal) or a mixture of bacterial toxin with the corresponding antitoxic serum does not cause this phenomenon.

The restructuring of the central nervous system is often proactive, i.e. occurs when leukocyte pyrogen is exposed before the body temperature rises. It is assumed that early changes in the function of the higher parts of the brain develop under the influence of the direct action of IL-1 and only later, at the stage of temperature, does the effect of the actual high temperature, metabolic deviations and homeostasis parameters manifest. Most often, apathy, weakness, drowsiness, weakening of reflexes, decreased concentration, general physical inactivity, decreased appetite, and sometimes headache are recorded during the temperature rise stage. In the stage of standing body temperature with moderate fever, changes in the central nervous system become less pronounced with some increase in the excitability of neurons, but with high and prolonged fever, the oppression of excitability remains or even increases. At the height of fever, with its high level, nausea and vomiting are possible, and with severe intoxication - delusions, hallucinations, convulsions, and even loss of consciousness, especially in children.

Pyrogens and fever are stressors and cause activation of the sympathoadrenal and pituitary-adrenal systems, with some authors considering IL-1 as one of the mediators of stress. The activation of the sympathoadrenal system and hypercatecholaminemia during the temperature rise stage are of great importance in the redistribution of blood with a decrease in blood flow through the vessels of the skin and mucous membranes, which contributes to limiting heat transfer. Under the influence of pyrogens, hypertrophy and hyperplasia of the adrenal cortex occur as a result of increased output from the anterior lobe of the pituitary ACTH, and the level of glucocorticoids increases in the blood. Their increase under the influence of primary and secondary pyrogens occurs earlier than the rise in body temperature is recorded. When fever increases the activity of the thyroid gland and the increment of thyroid hormones, there is stimulation of external respiration, which is especially pronounced with high fever in the stage of standing temperature, when breathing becomes frequent and shallow.

It is believed that an increase in body temperature of 1 ° C increases the frequency of respiratory excursions by 3 in 1 min. However, the frequency and depth of respiration during fever are subject to large variations and depend on the degree of temperature rise, stage of fever, severity of infectious intoxication and deviations of gas and acid-base blood parameters.

The febrile reaction is accompanied by significant changes in the central, peripheral and microcirculatory blood circulation, which are involved in the formation of fever. The most characteristic is the centralization of blood circulation with limited regional and microcirculatory blood flow through the superficial vessels of the skin and mucous membranes, as a result of which the heat transfer is reduced. In this case, regional blood circulation in the brain, liver and kidneys may increase. Fever is accompanied by an increase in heart rate; an increase in body temperature of 1 ° C increases the pulse by 8-10 heartbeats per 1 minute. However, in some infections, such as typhoid fever, bradycardia occurs on the background of fever. The increase in the frequency of cardiac contraction is associated with the activation of sinus node cells under the influence of elevated temperature, but it is difficult to exclude a certain role of increasing sympathetic-adrenal effects on the heart and the level of thyroid hormones in the blood. In the stage of raising the temperature, the blood pressure rises, and in the stage of standing, and especially the fall in body temperature, it decreases. However, for some infections, such as typhus and typhoid fever or dysentery, blood pressure decreases. Especially dangerous is the sharp drop in high body temperature in stage III fever, when acute vascular insufficiency can develop - collapse.

When pyrogenal fever initially appears leukopenia, and later - usually neutrophilic leukocytosis with absolute or relative eosinosis and monocytopenia. IL-1 stimulates neutrophilopoiesis, therefore a regenerative nuclear shift to the left is possible. In severe infectious intoxication, a nuclear left shift can occur, and sometimes a leukemoid reaction of the myeloid type can occur.

When fever increases the formation of coarse protein fractions (prothrombin, fibrinogen, globulins), "acute phase proteins" appear, the blood fibrinolytic activity increases, but albumin level usually decreases. These changes in the composition of the blood are largely due to the effect of IL-1 on the liver.

During fever, digestion activity decreases, appetite decreases, secretion and activity of saliva enzymes are weakened, and dry mouth occurs. The secretory function of the stomach is usually impaired in both the reflex and neurochemical phases, especially in stage I fever; in stage II of its gastric secretion may increase. Motor and evacuation functions of the stomach are reduced. The exocrine function of the pancreas, the biliary formation and biliary function of the liver, and the secretory and motor activity of the intestine are weakened. Often there are constipation, fermenting and putrefying processes in the intestine are intensifying, meteorism is possible. However, in intestinal infectious diseases against a background of fever due to organotropicity of the pathogen (dysentery, salmonellosis, etc.) there is an increase in intestinal motility, diarrhea, nausea and vomiting, usually at the height of fever due to intoxication. Vomiting and diarrhea can be the causes of hypovolemia, electrolyte abnormalities, and CBS (enteral acidosis).

The urinary and urinary functions of the kidneys during fever are subject to considerable fluctuations and can lead to marked disorders (toxic-infectious kidney) during severe infectious processes. Usually, an increase in diuresis occurs during the temperature rise stage, probably as a result of an increase in renal blood flow and filtration, and with significant hyperglycemia and osmotic diuresis. While the temperature is high at a high level, diuresis usually falls due to hypovolemia and a decrease in renal blood flow. Enhanced proteolysis and the retention of chlorides in the tissues, as well as hypoalbuminemia, lead to an increased influx of water into the tissues, which is accompanied by a decrease in its excretion by the kidneys and sweat glands. In contrast, diuresis rises to the stage of temperature drop; simultaneous critical drop in temperature, increased excretion of water and sodium chloride can cause a decrease in body weight and the so-called chlorine crisis with the development of collapse.

With a high fever, glycogen disappears in myocardial cells, liver and skeletal muscles, mitochondria vacuolize, their cristae are observed, their mitochondria are possibly destroyed. Appear cell edema and extracellular matrix. Often, high fever in the cells of parenchymal organs develops protein and fatty degeneration.

THE IMPORTANCE OF FEVER FOR THE ORGANISM

Hyperthermia

Hyperthermia is an increase in the temperature of the body or part of it, due to the insufficiency of the thermoregulation system in the body. Hyperthermia can be common and local, and each of them is divided into exogenous and endogenous by origin.

Exogenous hyperthermia occurs when the whole body is overheated, and the local one - of its individual parts. Endogenous hyperthermia occurs with stress, an excess of a number of hormones (thyroid, catecholamines, corticosteroids), the action of uncouplers of oxidative phosphorylation, and local - with arterial hyperemia, in the focus of inflammation, etc. General hyperthermia develops with a significant increase in ambient temperature or a sharp increase in the production of heat in the body during intense exercise. High humidity and low speed of air movement contribute to overheating, as this reduces heat emission by convection, excretion and evaporation of sweat. Hyperthermia goes through a series of stages.

The first stage is the adaptation of the organism to an increase in the temperature of the environment. In this situation, due to the regulatory increase in heat transfer and the restriction of heat production, body temperature is maintained in the physiological range.

The second stage is a partial adaptation of the organism (more often when the temperature of the medium rises to 50 ° C). At the same time, a number of adaptation mechanisms are preserved, for example, increased sweating and heat release by hyperventilation of the lungs. At the same time, the efficiency of heat transfer decreases as compared with the previous period, the heat production of the body increases, and the body temperature begins to rise. In such a state, the function of external respiration and blood circulation is sharply increased due to the increased need of the body for oxygen. Pulse rate increases by 40-60 beats per 1 min. There is a sharp feeling of heat, there is a flushing of the face and motive anxiety.

The third stage - the breakdown of the body's adaptation - usually develops at a high ambient temperature (above 50 ° C). At this time, heat transfer is significantly limited, heat accumulates in the body and the body temperature rises significantly (often up to 40 ° C and higher). Pulmonary hyperventilation continues to increase, the pulse may be doubled, but the minute volume of blood flow is reduced due to the fall in the stroke volume of the heart. General motor excitement develops, severe headache, noise or tinnitus, palpitations, and a feeling of lack of air appear. There are dry mucous membranes, facial flushing, nausea and vomiting.

A comatose hyperthermic condition usually occurs at a body temperature of 41 ° C and above. There is confusion or total loss of consciousness, possible clonic and tonic convulsions. The periods of motor excitement are replaced by the periods of oppression. Characterized by the development of collapse with long-term preservation of tachycardia. Breathing is frequent and shallow, periodic forms of breathing are possible.

An important mechanism for the development of hyperthermic coma are disorders of water and electrolyte metabolism due to significant loss of water and salts, primarily sodium chloride, due to increased perspiration, increased diuresis, and later vomiting. Extracellular dehydration leads to thickening of the blood, an increase in its viscosity, and in connection with this - to impaired blood circulation. Blood coagulation and changes in its physicochemical properties cause hemolysis of erythrocytes and an increase in plasma K + level. Hemic, circulatory and respiratory disorders cause hypoxia, which from a certain stage of hyperthermia becomes a factor determining the severity of the patient's condition.

HEAT & SUNNY IMPACT

The peculiar forms of hyperthermia, which quickly lead to the development of coma, are heat and sunstroke.

Heat stroke usually develops with a significant increase in ambient temperature simultaneously with an increase in heat production and a sharp limitation of heat transfer (work in hot shops, a military march, etc.). With thermal shock, the stages of complete and partial adaptation are practically absent, the insufficiency of the thermoregulation system and the coma quickly develop.

Sunstroke occurs as a result of direct action of intense solar radiation on the head. Essential in the pathogenesis of sunstroke is arterial hyperemia of the brain, leading to increased intracranial pressure, compression of the venous vessels and the development of secondary venous congestion. This is accompanied by swelling of the membranes and brain tissue, multiple point hemorrhages and neurological disorders. Violations of the hypothalamic centers of thermoregulation contribute to a secondary increase in body temperature and general hyperthermia. Thus, at a certain stage, thermal and solar impacts on their mechanisms and manifestations come closer.

Hypothermia

Hypothermia is a decrease in body temperature or part of it, due to the inadequate system of thermoregulation in the body. Hypothermia can be common and local; each of these forms is divided into exogenous and endogenous by origin.

◊ Exogenous general hypothermia occurs when the entire body is cooled, and local hypothermia occurs in its individual parts.

◊ Endogenous general hypothermia occurs with hypodynamia and deficiency in the body of a number of hormones (corticosteroids, thyroxin, etc.), and local - with ischemic conditions, venous hyperemia, etc.

General hypothermia occurs at low ambient temperatures, especially if there is a decrease in heat production in the body. The development of hypothermia is promoted by high air humidity, strong wind, and wet clothing, i.e. factors contributing to heat transfer. Supercooling occurs especially quickly while the body is in the water. Sensitivity to cold increases with alcohol intoxication, physical fatigue, starvation and other conditions that lower the adaptive abilities of the body. Acute hypothermia, in which death occurs within 1 hour, occurs relatively rarely (usually in disasters).

With gradual cooling, three stages are detected.

The first stage is a complete adaptation of the body, which is achieved by limiting heat transfer (reducing sweating, blood flow in skin vessels and heat radiation, etc.) and increasing heat production (increasing muscle thermogenesis and the inclusion of neuroendocrine regulation). Body temperature in this case is maintained at a normal level.

The second stage is a relative device, when heat transfer begins to increase due to the expansion of skin vessels, but the heat production remains increased. Body temperature at this time begins to decrease.

The third stage is the breakdown of the device. In this state, along with increased heat transfer, a decrease in heat production occurs, and the body temperature drops rapidly. As hypothermia rises and the body's metabolism decreases, the activity of neurons of the central nervous system decreases, drowsiness, indifference to the environment and adynamia appear. In the future, the development of external respiratory depression and hypoventilation of the lungs, a decrease in the stroke volume of the heart, bradycardia and a decrease in the minute volume of blood flow develop. Disorders of external respiration and blood circulation lead to the development of hypoxia, despite the decrease in the body's need for oxygen during hypothermia. Metabolic acidosis occurs, the rheological properties of blood change. Along with the loss of vascular muscle wall tone, this leads to widespread microcirculation disorders, which further aggravate hypoxia.

Symptoms of coma appear already at body temperature from 30 ° C to 25 ° C. Drowsiness and apathy are replaced by loss of consciousness, convulsive tonic contractions of the muscles of the limbs and masticatory muscles (trisism) are possible. There are floating movements of the eyeballs, the pupils are narrowed, the corneal reflex is weakened or lost. Vomiting and involuntary urination are possible. Respiratory rate and contractions of the heart are reduced. HELL dramatically reduced or not defined. Death occurs when you stop breathing; sometimes it is preceded by a form of periodic breathing.

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Inflammation

Professor M.K. Nedzved

Inflammation is a pathological process, which is a compensatory defense response of the body to the effects of a pathogenic agent (irritant), which is realized at the microcirculatory level. Morphologically, inflammation is characterized by a different combination of three main components: alteration, exudation and proliferation. The morphological type of the inflammatory process depends on the severity of one or another component. Inflammation is aimed at eliminating the products of tissue damage and the pathogenic agent.

These components are considered as successive stages of inflammation. All blood cells (neutrophils, basophils, eosinophils, monocytes, platelets and even erythrocytes), endothelial cells, connective tissue cells (labrocytes, macrophages, fibroblasts) are involved in the inflammatory process, resulting in one or another cell cooperation, the elements of which interact with each other. a friend.

Inflammation is characterized by five clinical features: redness - rubor, swelling - tumor, pain - dolor, temperature increase - calor, dysfunction - functio laesa, which are caused by morphological changes in the area of \u200b\u200bthe inflammatory process.

Alteration morphologically it represents various types of damage to tissues and individual cells, in mild cases being limited to dystrophic changes, in severe cases to the appearance of common or focal necrosis. Alteration arises as a result of the direct action of a pathogenic agent, and the effects of inflammatory mediators. At the same time, the alteration can be secondary - as a consequence of circulatory disorders.

Alteration is the trigger mechanism of inflammation, which determines its kinetics, since in this phase there is a release of biologically active substances - inflammatory mediators.

Mediators are divided by their origin into humoral (plasma) and cellular.

Humoral mediators (kinins, kallikreins, components of C3 and C5 complement, XII coagulation factor (Hageman factor), plasmin) increase vascular permeability of ICR, activate chemotaxis of polymorphonuclear leukocytes (PML), phagocytosis and intravascular coagulation. The spectrum of their action is wider than cellular mediators, whose action is local.

Mediators of cellular origin (histamine, serotonin, granulocyte factors, lymphokines and monokines, derivatives of arachidonic acid / prostaglandins /) increase vascular permeability, ICR and phagocytosis, have a bactericidal effect, causing secondary alteration. These mediators include immune mechanisms in the inflammatory response, regulate the proliferation and differentiation of cells in the inflammatory focus. The conductor of intercellular interactions in the inflammation are macrophages.

Macrophages have properties that allow them to act not only as a local regulator of the inflammatory process, but also to determine the severity of general body reactions.

One of the most important mediators of inflammation are histamine, which is formed in labrocytes, basophils and platelets from the amino acid histamine and deposited in the granules of these cells. After release, histamine is rapidly destroyed by the enzyme histaminase.

The release of histamine is one of the first tissue reactions to damage, its effect manifests itself after a few seconds as an instant spasm, alternating with vasodilation and the first wave of increasing vascular permeability at the level of the ICR, increases the adhesive properties of the endothelium. It activates kininogenesis, stimulates phagocytosis. In the outbreak of acute inflammation, histamine causes pain. Since histamine is rapidly destroyed, further microcirculation changes are supported by other inflammatory mediators.

Inclusion of kinins in the pathogenesis of acute inflammation means the beginning of the activity of the second cascade of mediators. Kinins are formed from a2 -globulin plasma (kininogen), the splitting of which occurs under the influence of plasma proteolytic enzymes (kallikrein I) and tissues (kallikrein II). These enzymes are activated by coagulation factor XII (Hageman factor).

In the focus of inflammation, kinins dilate blood vessels, increase their permeability, increasing exudation. Kinins are destroyed by kininases, which are contained in erythrocytes, PMNs, and are also inhibited by a1-antitrypsin, an inactivator of the C-fraction of the complement.

Kallikrein, plasmin, thrombin, proteases of bacteria and its own cells activate complement, fragments of which are the most important mediators of inflammation. Activated C2 fragment of complement has the properties of kinins, C3 fragment increases the vascular permeability and is a granulocyte chemoattractant. The C5 fragment is more active, since, having similar properties, it releases lysosomal hydrolases of neutrophils and monocytes, stimulates the lipoxygenase arachidonic acid decomposition pathway, and contributes to the generation of oxygen radicals and lipid hydroperoxide. C5-9 fragments provide reactions aimed at the lysis of foreign and own cells.

Arachidonic acid is released from phospholipid cell membranes as a result of the action of the enzyme phospholipase A2. The activators of this enzyme, in addition to the C5 fragment of the compliment, are microbial toxins, kinins, thrombin, antigen-antibody complexes, and Ca 2+.

Splitting of arachidonic acid goes in two ways: the first is cyclooxygenase, with the formation of prostaglandins, the second is lipoxygenase, with the formation of leukotrienes.

In the morphogenesis of inflammation, oppositely acting prostacyclin and thromboxane A2 are important. Prostacyclin is synthesized by the endothelium and inhibits platelet aggregation, maintains the liquid state of the blood, and causes vasodilation. Thromboxane is produced by platelets, causing their aggregation and vasoconstriction.

Leukotrienes are formed in the membranes of platelets, basophils, endotheliocytes and have a chemotactic effect, cause vasoconstriction and increase the permeability of the vascular walls, especially venules.

In the focus of inflammation in the mitochondria and microsomes of cells, especially phagocytes, various oxygen radicals are formed, which damage the membranes of microbes and their own cells, contribute to the splitting of antigens and immune complexes.

In acute inflammation, histamine and serotonin promote the release of platelet activating factor (PAF) from platelets. This mediator enhances the release of hydrolytic enzymes from the lysosomes of polymorphoncellular leukocytes (PMNs), stimulates free radical processes in them.

In the focus of inflammation of PMN, special substances for them (granulocyte factors) are emitted: cationic proteins, neutral and acid proteases. Cationic proteins are able to release histamine, possess chemotactic properties for monocytes, and inhibit granulocyte migration. Neutral proteases in the focus of inflammation cause the destruction of the fibers of the basal membrane of blood vessels. Acid proteases are active in conditions of acidosis and affect the membranes of microorganisms and their own cells.

Monocytes and lymphocytes also secrete mediators (monokines and lymphokines), which are actively involved in the development of immune inflammation.

The impact of mediators in the dynamics of the inflammatory process is diverse. Separate mediators are deposited together in the same cells. When released, they form various manifestations of inflammation. Thus, when alterations from labrocytes and basophils, histamine and PAF are released, which leads not only to an increase in vascular permeability, but also to activation of the hemostasis system and the appearance of blood clots in ICRs. In contrast, with severe immune inflammation, the release of heparin and histamine from labrocytes leads to a decrease in blood clotting.

In turn, the neurotransmitters in the inflammatory focus promote the accumulation of enzymes that destroy these mediators. Thus, the release of chemotactic eosinophil factor (CPE) from labrocytes attracts these cells, which contain a large amount of enzymes that destroy the mediators, to the inflammatory focus.

Inflammation is a dynamic process and proceeds in stages, replacing each other. At each stage of inflammation a certain group of mediators matters. Thus, in acute inflammation, biogenic amines play the initial role: histamine and serotonin. In other forms of inflammation, other patterns of inclusion of mediators are possible. For example, the release of histamine can immediately lead not only to the activation of the kinin system, but also to the inclusion of free radical mechanisms and leukocyte infiltration. PMNs in some cases (especially when the course of the process deteriorates) additionally stimulate labrocytes, activate the kinin system, generate oxygen radicals, increase the formation of prostaglandins and leukotrienes. Such feedbacks prolong the inflammatory process, worsen its course or cause its exacerbation from time to time.

Excessive accumulation of inflammatory mediators and their entry into the blood can lead to shock, collapse, DIC.

At all stages of inflammation, substances that prevent the excessive accumulation of mediators or inhibit their effects are released and act. These substances constitute a system of anti-mediators of inflammation. The ratio of mediators and antimediators determine the features of the formation, development and termination of the inflammatory process.

An important role in the formation and delivery of anti-medications to the inflammatory focus is played by eosinophils, which perform functions to end the inflammatory process. Eosinophils not only absorb antigens and immune complexes, but also secrete almost all anti-mediator enzymes: histaminase, carboxypeptidase, esterase, prostaglandine dehydrogenase, catalase, arylsulfatase. Anti-mediator function can be performed by humoral and neural effects, maintaining an optimal mediator mode of inflammation. This role is played by a1-antitrypsin, which is formed in hepatocytes. Plasma antiproteases inhibit the formation of kinins. The antimediators of inflammation include glucocorticoid hormones (cortisone, corticosterone). They reduce the manifestations of inflammation, vascular reactions, stabilize the vascular membranes of the ICR, reduce exudation, phagocytosis and leukocyte emigration.

Corticosteroids also have an anti-mediator effect: they reduce the formation and release of histamine, decrease the sensitivity of H1-histamine receptors, stabilize the lysosomal membranes, reduce the activity of acidic lysosomal hydrolases, the production of kinins and prostaglandins. In immune inflammation, they reduce the inclusion of mediators in the pathochemical stage of allergy. As a result, T-killer activity is reduced, proliferation and maturation of T-lymphocytes is inhibited.

The system of inflammatory mediators ensures the transition of the inflammatory process to the exudation phase and ensures the development of the proliferation phase.

Depolymerization in the focus of protein inflammation-glycosaminoglycan complexes leads to the appearance of free amino acids, polypeptides, uranic acid, polysaccharides, resulting in an increase in osmotic pressure in the tissues, their further swelling and retention of water by the tissues. The accumulation of products of fat and carbohydrate metabolism (fatty acids, lactic acid) leads to tissue acidosis and hypoxia, which further enhances the alteration phase.

Considering the fact that alteration can develop at any stage of the inflammatory process, including chronic inflammation, and can prevail over other components of inflammation, it is completely unjustified to exclude an alterative form from inflammation.

Morphologically, exudation goes through several stages: 1) microcirculatory bed reaction and disturbance of rheological properties of blood, 2) increased vascular permeability of the microcirculatory bed, 3) exudation of plasma components, 4) emigration of blood cells, 5) phagocytosis 6) formation of exudate and inflammatory cell infiltrate. These stages correspond to the phases of cellular interactions in the inflammatory process.

In morphogenesis exudation there are two stages - plasma exudation and cell infiltration.

After a short-term vasoconstriction, not only arterioles expand, but venules also expand, which increases the inflow and outflow of blood. However, the inflow exceeds the outflow, as a result of which the hydrodynamic pressure in the vessels rises in the inflammation center, which causes the liquid part of the blood to exit from the vessels.

Inflammatory hyperemia eliminates acidosis, increases tissue oxygenation, increases biological oxidation in tissues, promotes the influx of humoral factors of body defense (complement, properdin, fibronectin), leukocytes and antibodies to the center of inflammation, is accompanied by enhanced leaching of the products of disturbed metabolism and toxins of microorganisms.

Increased vascular permeability becomes an important factor in the release of liquid blood into the tissue, emigration of leukocytes and red blood cell diapedesis. When inflammation occurs, the flow of fluid from the blood into the tissue, not only in the arterioles, but also in the venules.

There are two ways of passing substances through the walls of the vessel, which complement each other: interendothelial and transendothelial. When the first is the reduction of endothelial cells, the intercellular cracks widen, exposing the basement membrane. At the second stage, plasmolemosis invasions appear in the cytoplasm of the endothelium cells, turning into vesicles, which move to the opposite cell wall. They then unfold, freeing the contents. On both sides, vesicles can merge, forming channels through which various substances pass (microvesicular transport).

A moderate increase in permeability leads to the release of fine fractions of proteins (albumin), then globulins, which usually occurs during serous inflammation. With a significant increase in permeability, fibrinogen is released, which in the focus of inflammation forms fibrin clots (fibrinous inflammation). Severe damage to the walls of blood vessels in the form of fibrinoid necrosis leads to erythrocyte diapedesis.

When inflammation is often observed selective increased permeability for certain substances or cells, the mechanism of which is still unknown. Such selectivity determines the development of various forms of exudative inflammation: serous, fibrinous, hemorrhagic, purulent.

In the focus of inflammation, microcirculation changes and the behavior of blood cells undergo six phases. AT first phase Blood cells retain their position in the center of the vessel. In second phase leukocytes approach the vessel wall and roll along the surface of the endothelium, then begin to attach to it. AT third phase leukocyte adhesion occurs, which form muffs along the walls. In the II and III phases, adhesive molecules play an important role, providing the interaction between the endothelium and leukocytes: integrins, immunoglobulins, selectins. PMN integrins and selectins provide adhesion of circulating cells to the endothelium, and selectins and immunoglobulins on the endothelium serve as ligands for leukocyte receptors.

Neurophils constantly express adhesive molecules (2 -integrin and -selectin) on their surface, the number and function of which rapidly change depending on the action of a specific stimulus. 2-integrins (they are established three types) are constantly present in the plasma membrane of neutrophils. The adhesive ability of these cells increases dramatically when they are activated due to the movement of the integrin CD 11a / CD18 and CD 11c / CD 18, which are usually located in leukocyte granules.

Activated endothelium cells synthesize a number of biologically active molecules, of which platelet activation factor (PAF) is of great importance. Normally, this factor is not present in endothelial cells. It appears only after stimulation of the endothelium by thrombin, histamine, leukotriene C4 and other agonists. PAF is expressed on the surface of the cell membrane as an associated mediator and activates neutrophils by acting on their surface receptors. This is what enhances the expression of CD 11a / CD18 and CD 11c / CD 18 in leukocytes. Consequently, PAF acts as a signal inducing adhesion of neutrophils through the 2-integrin system. This phenomenon of adhesion and activation of target cells by membrane-bound molecules of other cells is called juxtacrin activation (J. Massague, 1990). This activation of neutrophils is highly targeted. PAF in the activated endothelium rapidly disintegrates, which limits the duration of the signal.

Under the influence of another group of agonists (IL-1, TNF6, lipopolysaccharides / LPS /), endothelial cells synthesize another signaling molecule, IL-8 (neutrophilic activating factor), which takes 4-24 hours to synthesize. IL-8 is a potential chemoattractant for neutrophils, facilitates their passage through the vascular wall.

Unlike PAF, IL-8 is secreted in the liquid phase and is associated with the basal surface of endothelial cells. IL-8 activates neutrophils by binding to a specific receptor belonging to the G-protein family. As a result, the density of 2-integrins increases, leukocyte adhesion to endothelial cells and the extracellular matrix increases, but adhesion to cytokine-activated endothelium expressing α-selectin decreases.

Like neutrophils, endothelial cells also express a number of adherent molecules on their surface. In addition to the ligands for -selectin and 2 -integrin, p and -selectins are identified on these cells.

Transient expression of p-selectin, which is formed from secretory granules activated by histamine or thrombin of the endothelium, occurs in parallel with the adhesion of neutrophils to the endothelium. Activation of the endothelium by some oxidants prolongs the expression of p-selectin on the cell surface. It should be noted that p-selectin can bind to non-activated leukocytes without the participation of the 2-integrin system. This effect is inhibited by monoclonal antibodies that identify the Ca 2+ -dependent lectin domain epitopes.

-selectin is synthesized by endothelium, stimulated by IL-1, TNF2 and LPS. Its surface expression takes about 1 hour. -selectin adhesion is also carried out without activation of the 2-integrin system.

Ligands for p and -selectins at the molecular level are not yet sufficiently characterized. However, it is known that sialic acid is an important part of their structure.

In endothelial-leukocyte interaction, different molecular systems act complexly in a specific combination sequence.

For the initial stage of adhesion of neutrophils to histamine or thrombin-stimulated endothelium, co-expression of PAF and p-selectin is necessary, followed by active interaction of PAF with its receptor on neutrophils. Coexpression of these two molecular systems provide for the specificity of the interaction, since other blood cells, such as platelets, have receptors for PAF only and do not have receptors for p-selectin.

The involvement of the 2-integrin system and PAF increases the adhesion density, since the expression of p-selectin is transient. At the same time, prolonged expression of p-selectin causes tight adhesion without the participation of 2-integrins.

A combination of molecular systems is used for the adhesion of eosinophils and basophils that bind to the endothelium via 2-integrins. Eosinophils also express 1 -integrin (VLA-4), which is not found on neutrophils. With it, adhesion of neutrophils to cytokine-activated endothelium cells occurs.

Coexpression of selectin and IL-8 regulates the degree of neutrophil binding to activated endothelial cells. IL-8 can change the activity of the -selectin ligand and, together with PAF, provide for the process of migration of neutrophils from the vascular bed.

Inflammation is a dynamic process. After 4 hours, the number of neutrophils decreases in the vascular bed and the number of monocytes and lymphocytes increases, which completely corrects with the change of phenotin of adhesive molecules expressed by endothelial cells. So after 6-8 hours the expression of α-selectin (ELAM-1) begins to decrease due to a decrease in its synthesis and degradation. The synthesis of intercellular adherence molecules (ICAM-1), on the contrary, increases dramatically and reaches a stable level of expression 24 hours after the onset of inflammation. Another adhesive molecule appears on the surface of endothelial cells (V-SAM — a vascular cell adhesion molecule). The ligand for it is the 2 -integrin molecule (VZA-4), which is expressed on monocytes. The binding of T-lymphocytes to the endothelium provides an adhesive molecule CD 44. Like neutrophils, T-lymphocytes appear in the focus of inflammation as a result of the action of IL-8. In contrast, monocytes appear later, as they are insensitive to the action of IL-8, however, they react to the JE gene product (monocytic chemotactic protein - MCP-1) expressed by endothelium during stimulation of IL-1 and TNF.

In the development of marginal standing and adhesion of leukocytes with endothelial cells, the elimination of their negative charge is of great importance, which in normal conditions prevents adhesion. The negative charge of the membrane of the endothelial cell decreases due to the accumulation in the focus of inflammation of H + and K + and cationic proteins secreted by activated leukocytes. The divalent plasma cations (Ca 2+, Mn 2+ and Mg 2+) also reduce the negative charge of the endothelium and leukocytes.

In the development of the inflammatory process, there is a rigid control system in the form of a mechanism of positive feedbacks that limit its development. This control is carried out by a balanced system of cytotoxic and inhibitory factors. If the inflammatory process is not controlled by feedback mechanisms, the synthesis and release of inflammatory mediators is enhanced, the level of inhibitors is critically reduced, as a result of which local inflammatory reactions develop into extensive processes. The result is significant damage to the endothelium, excessive cellular infiltration, and increased vascular permeability.

Fourth phase exudation is the passage of leukocytes through the vascular wall and their emigration into the tissue.

After adhesion with the membrane of the endothelial cell, the leukocyte moves along its surface to the interendothelial gap, which, after the reduction of the endothelium, expands significantly.

Not only granulocytes, but also monocytes and, to a lesser extent, lymphocytes, with different speeds, react to the chemotactic stimulus.

At present, some mechanisms are known as a leukocyte, “sees” or “feels” a chemotactic agent, and what determines its movement.

The association of the chemotactic factor with specific receptors on the cell membrane of a leukocyte leads to the activation of phospholipase C through protein G and hydrolysis of cell phosphates and diacylglycerol. This leads to the release of Ca, first from the cellular stock, then to the entry of extracellular Ca into the cell, which includes the complex of contractile elements responsible for cell movement.

White blood cell moves ( 5 phase exudation) by throwing pseudopodia in the direction of motion. This pseudopodia consists of a network of filaments constructed from actin and a contractile protein, myosin. Actin monomers are rearranged into linear polymers directed to the edge of the pseudopodia. This process is controlled by the action of Ca ions and phosphoinositol on actin-regulated proteins: filamin, gelsolin, profilin, calmodulin.

The process of leukocyte passage through the basement membrane is associated with the action of leukocyte and endothelial enzymes. Such cytokines as IL-1, TNF, IFN, TGF alter the protease / antiprotease balance, which leads to damage to the proteins of the basement membrane. Cytokine-activated endothelium also synthesizes a large number of glycosaminoglycans, which is a characteristic feature of areas of increased migration of leukocytes.

Enhancing or weakening the expression of various cytokines and adhesive molecules has a time dependence and regulates the evolution of the inflammatory process.

When activated, leukocytes form metabolites arachidonic acid, an increase in intracellular Ca occurs. Activation of protein kinase leads to degranulation and secretion of lysosomal enzymes and subsequent oxidative burst.

Intravascular movement, including marginal standing, takes several hours, passing through the vessel wall - 30 min-1 hour. In the first 6-24 hours, neutrophils are dominant, in 24-48 hours - monocytes. This is due to the fact that when neutrophils are activated, chemotactic substances for monocytes are released. However, there are known conditions in which the main role in emigration is played by lymphocytes (viral infections, tuberculosis) or eosinophils (in allergic reactions).

Phagocytosis follows emigration ( 6 phase exudation), which takes place in three distinct interdependent stages: 1) recognition and attachment of leukocytes pathogenic particles, 2) their absorption with the formation of a phagocytic vacuole, 3) death or degradation of the absorbed material.

Most microorganisms are not recognized by leukocytes until they are absorbed by a substance, opsonins, which bind to specific leukocyte receptors. There are two main types of opsonins: 1) Fc fragment of immunoglobulin G (lgG) and 2) Szv, the so-called opsonin fragment C3, formed by activation of complement. There is also nepsonin phagocytosis, when some bacteria are recognized by their lipopolysaccharides.

The binding of opsonized particles to leukocyte receptors triggers absorption, in which the cytoplasmic current surrounds the object, followed by its imprisonment in the phagosome formed by the cytoplasmic cell membrane and the release of leukocyte granules into the vacuole formed.

The death of bacteria is carried out mainly with the help of oxygen-dependent processes, the result of which is the formation of H2O2, which is converted into HOCl-, which is the result of the action of the enzyme myeloperoxidase contained in neutrophil azurophilic granules. It is this substance that destroys bacteria by halogenation or oxidation of proteins and lipids. A similar mechanism is carried out against fungi, viruses, protozoa and worms. Myeloperoxidase-deficient white blood cells also have, but to a lesser extent, bactericidal properties, forming hydroxyl radicals, superoxides and free oxygen atoms.

Membrane changes in neutrophils and monocytes during chemotaxis and phagocytosis are not only accompanied by the entry of substances into phagolysosomes, but also into the extracellular space. The most important of these are: 1) lysosome enzymes represented by neutrophilic granules; 2) active metabolites of oxygen; 3) products of arachidonic acid metabolism, including prostaglandins and leukotrienes. All of them are the strongest mediators and cause damage not only to the endothelium, but also to the tissue. If this effect of leukocytes is long and massive, then leukocyte infiltration itself becomes dangerous, which underlies many human diseases, for example, rheumatoid arthritis and certain types of chronic lung diseases. The exocytosis of such mediators occurs in the case of non-closing of the phagocytic vacuole, or in the case of phagocytosis of membranolytic substances, such as urats. There is evidence that specific granules of neutrophils can be secreted by exocytosis.

Genetic and acquired defects in the function of leukocytes are the cause of increased human sensitivity to infections.

For example, Chediak-Higashi syndrome (an autosomal recessive mode of inheritance) is based on impaired microtubule function, which form the basis of leukocyte azurophilic granules. The disease manifests itself only in cases of invasion of bacteria in the body.

Lymphokine-activated macrophages already in the exudation phase secrete not only chemotactic and tissue-damaging factors, but also growth factors, angiogenesis, and fibrogenic cytokines that influence the modeling of the proliferation phase.

Proliferation characterized by the release into the focus of inflammation of a large number of macrophages that multiply and secrete monokines that stimulate the multiplication of fibroblasts. Other cells take an active part in proliferation: lymphocytes and plasma cells, eosinophils and labrocytes, endothelium and epithelium. Proliferation is the final stage of inflammation, providing tissue regeneration at the site of the lesion.

Proliferation occurs a few hours after the onset of inflammation and after 48 hours in the inflammatory infiltrate, monocytes are the main cell type. The release of monocytes from the vessels of the ICR is regulated by the same factors as the emigration of neutrophils (adhesive molecules and mediators with chemotactic and activating properties). After release, the monocyte is transformed into a large phagocytic cell - the macrophage. Activation signals, including cytokines, are produced by sensitized E-lymphocytes, bacterial endotoxins, other chemical mediators, fibronectin. After activation, the macrophage secretes a large number of biologically active substances.

In cases of acute inflammation, when the pathogenic agent is dead or eliminated, macrophages also die or enter the lymphatic vessels and nodes.

In cases of chronic inflammation, macrophages do not disappear, continue to accumulate and secrete toxic products that damage not only pathogenic agents, but also their own tissues. These are primarily metabolites of oxygen and arachidonic acid, proteases, neutrophil chemotactic factors, nitrogen oxides, coagulation factors. Consequently, tissue damage is one of the most important signs of chronic inflammation.

During proliferation, epithelioid cells appear in the focus of inflammation, which are more often formed from macrophages in the foci of granulomatous inflammation, starting from the 7th day of the formation of granulomas and perform mainly secretory function. Aggregation of epithelioid cells with the formation of close (interdigital) clutches of the zipper type is characteristic of this type of inflammation. These cells are considered hyperstimulated “super-mature” macrophages. Epithelioid cells have less phagocytic ability compared to macrophages, but their bactericidal and secretory properties are much stronger.

In cases of fusion of macrophages with each other or division of their nuclei without separation of the cytoplasm, two types of multinuclear giant cells are formed: Pirogov-Lanhans cells and resorption cells of foreign bodies. The merger of macrophages occurs always in the part of the cells where the lamellar complex and the concave part of the nucleus are located. In HIV and herpes infections, a third type of multinucleated giant cell occurs when the nuclei are grouped at opposite poles of the cell.

Antigen-activated lymphocytes produce lymphokines, which stimulate monocytes and macrophages. The latter form monokines that activate lymphocytes. Plasma cells form antibodies against the antigen at the site of inflammation, or against components of the damaged tissue.

The morphological marker of healing is the formation of granulation tissue, signs of which appear on day 3-5 of the inflammatory process.

The repair process consists of 4 components: 1) formation of new blood vessels (angiogenesis), 2) migration and proliferation of fibroblasts, 3) formation of an intercellular matrix, 4) maturation and organization of connective tissue.

Angiogenesis is carried out in the following ways: 1) proteolytic degradation of the basal membrane of the ICR vessel. 2) migration of endothelial cells to an angiogenic stimulus, 3) proliferation of endothelial cells, and 4) maturation of these cells and organization into capillary tubes. This process is regulated by activated macrophages that secrete endothelial and other growth factors.

The migration and proliferation of fibroblasts is also due to growth factors and fibrogenic cytokines produced by inflammatory macrophages. On the first day of the inflammatory process, low-differentiated fibroblasts appear in the vessels and in the exudate, which turn into young fibroblasts capable of secreting acid glycosaminoglycans and synthesizing collagen. Young forms are transformed into mature fibroblasts.

Mature fibroblasts lose their ability to reproduce, but continue to intensively synthesize and secrete collagen. Most of the mature fibroblasts die; preserved cells are transformed into long-lived fibroblasts.

Angiogenesis and proliferation of fibroblasts leads to the formation of the extracellular matrix, through the formation of young (granulation) connective tissue with its subsequent maturation. These processes delimit the inflamed area from healthy tissue. With a favorable course, granulation tissue completely replaces the foci of alteration or purulent inflammation. In the formation and restructuring of the scar in the inflammation, a large role is played by fibroblasts (cells of the fibroblastic series), which phagocytize and lyse collagen fibers. This balances synthesis and catabolism of collagen, which are alternative functions of fibroblasts.

Proliferation is the final stage of the inflammatory process, in which both the cells of the blood system and the cells of the tissue in which inflammation develops take part.

Terminology and nomenklatour inflammation

inflammation alternation angiogenesis exudative

The name of inflammation of a particular tissue or organ is formed from their name, to which is added the ending - it, to the Latin or Greek name - the ending - it. For example, inflammation of the brain - encephalitis (encephalitis)., Inflammation of the stomach - gastritis (gastritis). Latin names are more commonly used, more rarely Greek, for example, inflammation of the pia mater - leptomeningitis. There are exceptions to this rule. So, pneumonia is called pneumonia, and pharynx inflammation is called sore throat.

The nomenclature of inflammation is represented by the names of the inflammatory processes of various parts of a particular body system. For example, inflammation of various parts of the gastrointestinal tract: cheilitis, gingivitis, glossitis, pharyngitis, esophagitis, gastritis, enteritis (duodenitis, fever, ileitis), colitis (tiflit, sigmoiditis, proctitis), hepatitis, pancreatitis.

Inflammation classification

The classification of inflammation takes into account the etiology, the nature of the process and the predominance of a particular phase of inflammation.

According to etiology, inflammation is divided into a banal (caused by any etiological factor) specific (has characteristic morphological manifestations and is caused by a certain infectious agent).

By the nature of the course of inflammation is acute, subacute and chronic.

According to the predominance of the phase of inflammation: alterative, exudative and proliferative (productive) inflammation.

Alterative inflammation

Alterative inflammation is characterized by a predominance of dystrophic and necrotic changes, exudation and proliferation are also present, but are weakly expressed. Such inflammation is most often observed in parenchymatous organs - myocardium, lungs, liver, kidneys. According to the type of course, alterative inflammation refers to acute.

Causes of alterative inflammation can be poisoning with chemical poisons and toxins, infectious agents. Examples of alterative inflammation include caseous pneumonia in tuberculosis, fulminant (necrotic) hepatitis B and C, acute alterative encephalitis of herpetic etiology, alterative myocarditis in diphtheria. Alterative inflammation is usually a manifestation of a hyperergic reaction of the immediate type (Arthus phenomenon) or prevails in the early stages of the development of autoimmune diseases (for example, with rheumatism). Such inflammation can also develop with a decrease in the body's defenses and in secondary and primary immunodeficiencies (acute tuberculosis sepsis in hematogenous generalized tuberculosis, necrotizing tonsillitis in acute leukemia, severe scarlet fever, and in acute form of radiation sickness.

The outcome of alterative inflammation depends on the location, extent and severity of alterative changes. With a favorable outcome, foci of necrosis with alterative inflammation undergo organization.

The exjudative inflammation

Exudative inflammation is characterized by the predominance of the exudative phase in which the liquid part of the blood leaves the vascular bed and the formation of exudate occurs. The composition of the exudate may be different. The classification takes into account two factors: the nature of the exudate and the localization process. Depending on the nature of the exudate emit: serous, fibrinous, purulent, putrid, hemorrhagic, mixed inflammation. The peculiarity of the process localization on the mucous membranes determines the development of one type of exudative inflammation - catarrhal.

Serous inflammation It is characterized by the formation of exudate containing a small amount of protein (2-3%), single white blood cells and desquamated cells of the affected tissue. Serous inflammation can develop in any organs and tissues: serous cavities, pia mater, skin, heart, liver, etc.

Causes of serous inflammation can be infectious agents, physical factors, auto-intoxication. For example: serous inflammation in the skin with the formation of vesicles (vesicles) caused by the herpes simplex virus ..

Serous inflammation can be acute and chronic.

The outcome of acute serous inflammation is usually favorable: the exudate is absorbed, there is a complete restoration of the structure of tissues. However, quite often this type of inflammation serves only as a transitional stage, the onset of fibrinous, purulent, or hemorrhagic inflammation. For example, the transition of serous pneumonia in purulent. In some cases, serous inflammation is life threatening: serous enteritis with cholera, serous encephalitis with rabies. Chronic serous inflammation can lead to organ sclerosis.

Fibrinous inflammation.It is characterized by exudate, rich in fibrinogen, which turns into fibrin in tissues, which is a grayish filamentous tissue. Fibrinous inflammation often localized on the serous and mucous membranes.

Causes of fibrinous inflammation - bacteria, viruses, chemicals of exogenous and endogenous origin. An example of fibrinous inflammation is the occurrence of polyserositis, including pericarditis, with uremia. At the same time, but filamentary overlays of fibrin appear in sheets of the pericardium, in connection with which such a macroscopic career is called the "hairy" heart.

Depending on the depth of necrosis, the film can be loosely or firmly connected with the underlying tissues, and therefore there are two types of fibrinous inflammation: croupous and diphtheritic.

Croupous inflammation often develops on a monolayer epithelium of the mucous or serous membrane. Necrosis with this type of inflammation is shallow, and the fibrinous film is thin, easily removed. With the separation of such a film, surface defects are formed. Fibrinous inflammation in the lung with the formation of exudate in the alveoli of the lobe of the lung is called lobar pneumonia.

Dipheritic inflammation develops in organs covered with stratified squamous epithelium. In this case, there are deep necrosis, and the fibrinous film is thick, it is difficult to remove, when it is rejected, a deep tissue defect occurs.

The dependence of the occurrence of a particular type of fibrinous inflammation can be traced by the example of diphtheria. On the mucous membranes of the pharynx, tonsils, which are lined with stratified squamous epithelium, Leffler's wand causes diphtheria inflammation, and on the mucous membranes of the larynx, trachea and bronchi, lined with a single-layered prismatic epithelium, the lobar. In this case, since fibrin films are easily removed, they can block the respiratory tract and cause choking (true croup). However, in a disease such as dysentery, diphtheria inflammation occurs in the intestine lined with a single-layer epithelium, since the sticks of dysentery can cause deep tissue necrosis.

The outcome of fibrinous inflammation may be different. Fibrinous exudate can melt, then the structure of the organ can be fully restored. But the fibrin filaments germinate with connective tissue, and if the inflammation is localized in the cavity, then adhesions form there, or the cavity is obliterated.

Purulent inflammation characterized by the presence in the exudate of a large number of neutrophils, both unchanged and lost and dead. Along with neutrophils, purulent exudate is rich in proteins. The pus contains many decay products of diseased tissues rich in enzymes that carry out the lysis of necrotic tissue elements. Macroscopically, pus is a thick, creamy mass of yellow-green color.

The causes of purulent inflammation can be various factors, but more often these are microorganisms (staphylococci, streptococci, gonococci, meningococci, etc.).

The course of purulent inflammation is acute and chronic.

Purulent inflammation can occur in any organs and tissues. The main forms of purulent inflammation are abscess, phlegmon, empyema.

Abscess - focal purulent inflammation, characterized by the melting of the tissue with the formation of a cavity filled with pus. The tissue located around the cavity turns into a pyogenic membrane - a large number of vessels appear in it, from the lumen of which there is a constant emigration of leukocytes. An abscess can be located both in the thickness of tissues and organs, and in their superficial parts. In the latter case, it can break out to form a fistulous course. In chronic course, the abscess wall thickens and grows connective tissue.

Cellulitis - diffuse purulent inflammation, in which purulent exudate diffuse into tissues, dissecting and melting tissue elements. Typically, cellulitis develops in tissues where there are conditions for the easy spread of pus — in the fatty tissue, in the areas of tendons, fascia, along the neurovascular bundles. Diffuse purulent inflammation can also be observed in parenchymal organs.

Empyema is a purulent inflammation characterized by the accumulation of pus in the natural cavity. In the cavities of the body empyema can be formed in the presence of purulent foci in adjacent organs (for example, empyema in the abscess of the lung). Empyema of the hollow organs develops in violation of the outflow of pus with purulent inflammation (empyema of the gallbladder, appendix).

Outcomes of purulent inflammation may be different. Purulent exudate can sometimes completely dissolve. With extensive or prolonged inflammation, it usually ends with sclerosis with scar formation. With an unfavorable course, purulent inflammation can spread to the blood and lymph vessels with further generalization of infection and the development of sepsis. Long-term chronic suppurative inflammation is often complicated by secondary amyloidosis.

Putrid inflammation.It develops when putrefactive microorganisms get into the focus of inflammation (group of clostridia, causative agents of anaerobic infection).

The putrid inflammation develops when the putrid microflora enters the center of inflammation. The outcome is usually unfavorable, due to the massiveness of the lesion and the decrease in resistance of the microorganism.

Hemorrhagic inflammation is characterized by the prevalence of red blood cells in the exudate. This type of inflammation is characteristic of some serious infectious diseases - plague, anthrax, smallpox.

Mixed inflammation is observed in cases when another type is attached to one type of exudate. As a result, serous-purulent, serous-fibrinous, purulent-hemorrhagic and other types of inflammation occur.

Catarrh develops on the mucous membranes and is characterized by abundant exudate secretion. A distinctive feature of catarrhal inflammation is the admixture of mucus to any exudate (serous, purulent, hemorrhagic).

The course of catarrhal inflammation can be acute and chronic. Acute inflammation may result in complete recovery. Chronic inflammation can lead to atrophy or hypertrophy of the mucous membrane.

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