Which is released at the site of inflammation. Inflammation. Tension of the muscles of the anterior abdominal wall

General characteristics of inflammation

Inflammation- protective and adaptive reaction of the whole organism to the action of a pathogenic stimulus, manifested by the development of changes in blood circulation at the site of damage to a tissue or organ and an increase in vascular permeability in combination with tissue degeneration and cell proliferation. Inflammation is a typical pathological process aimed at eliminating a pathogenic stimulus and restoring damaged tissues.

The famous Russian scientist I.I. Mechnikov at the end of the 19th century showed for the first time that inflammation is inherent not only in humans, but also in lower animals, even unicellular, albeit in a primitive form. In higher animals and humans, the protective role of inflammation is manifested:

a) in the localization and delimitation of the inflammatory focus from healthy tissues;

b) fixation in place, in the focus of inflammation of the pathogenic factor and its destruction; c) removal of decay products and restoration of tissue integrity; d) the development of immunity in the process of inflammation.

At the same time, I.I. Mechnikov believed that this protective reaction of the body is relative and imperfect, since inflammation is the basis of many diseases, often ending in the death of the patient. Therefore, it is necessary to know the patterns of inflammation development in order to actively intervene in its course and eliminate the threat of death from this process.

To denote inflammation of an organ or tissue, the ending "itis" is added to the root of their Latin name: for example, inflammation of the kidneys - nephritis, liver - hepatitis, bladder - cystitis, pleura - pleurisy, etc. etc. Along with this, medicine has preserved the old names for inflammation of some organs: pneumonia - inflammation of the lungs, panaritium - inflammation of the nail bed of the finger, tonsillitis - inflammation of the throat, and some others.

2 Causes and conditions of inflammation

The occurrence, course and outcome of inflammation largely depend on the reactivity of the body, which is determined by age, gender, constitutional features, the state of physiological systems, primarily immune, endocrine and nervous, the presence of concomitant diseases. Of no small importance in the development and outcome of inflammation is its localization. For example, an abscess of the brain, inflammation of the larynx in diphtheria are extremely life-threatening.

According to the severity of local and general changes, inflammation is divided into normergic, when the body's response corresponds to the strength and nature of the stimulus; hyperergic, in which the body's response to irritation is much more intense than the action of the stimulus, and hyperergic, when inflammatory changes are mild or not at all pronounced. Inflammation may be limited, but may extend to an entire organ or even to a system, such as the connective tissue system.

3 Stages and mechanisms of inflammation

Characteristic of inflammation, which distinguishes it from all other pathological processes, is the presence of three successive stages of development:

1) alterations,

2) exudation; and 3) cell proliferation. These three stages are necessarily present in the area of ​​any inflammation.

Alteration- tissue damage - is a trigger for the development of the inflammatory process. It leads to the release of a special class of biologically active substances called inflammatory mediators. In general, all the changes that occur in the focus of inflammation under the influence of these substances are aimed at the development of the second stage of the inflammatory process - exudation. Inflammatory mediators change metabolism, physicochemical properties and functions of tissues, rheological properties of blood and functions of formed elements. Inflammatory mediators include biogenic amines - histamine and serotonin. Histamine is released by mast cells in response to tissue damage. It causes pain, expansion of microvessels and an increase in their permeability, activates phagocytosis, enhances the release of other mediators. Serotonin is released from platelets in the blood and alters the microcirculation at the site of inflammation. Lymphocytes secrete mediators called lymphokines, which activate the most important cells of the immune system - T-lymphocytes.

Blood plasma polypeptides - kinins, including kallikreins and bradykinin, cause pain, dilate microvessels and increase the permeability of their walls, activate phagocytosis.

Inflammatory mediators also include some prostaglandins that cause the same effects as kinins, while regulating the intensity of the inflammatory response.

inflammation protective pathogenic

The restructuring of metabolism in the zone of alteration leads to a change in the physicochemical properties of tissues and the development of acidosis in them. Acidosis increases the permeability of blood vessels and lysosome membranes, the breakdown of proteins and the dissociation of salts, thereby causing an increase in oncotic and osmotic pressure in damaged tissues. This, in turn, increases the output of fluid from the vessels, causing the development of exudation, inflammatory edema and tissue infiltration in the area of ​​inflammation.

Exudation- exit, or sweating, from the vessels into the tissue of the liquid part of the blood with the substances in it, as well as blood cells. Exudation occurs very quickly after alteration and is provided primarily by the reaction of the microvasculature in the focus of inflammation. The first reaction of microcirculation vessels and regional blood circulation in response to the action of inflammatory mediators, mainly histamine, is spasm of arterioles and a decrease in arterial blood flow. As a result, tissue ischemia occurs in the area of ​​inflammation, associated with an increase in sympathetic influences. This reaction of vessels is short-lived. The slowdown in the rate of blood flow and a decrease in the volume of flowing blood leads to metabolic disorders in tissues and acidosis. Spasm of arterioles is replaced by their expansion, an increase in blood flow velocity, the volume of flowing blood and an increase in hydrodynamic pressure, i.e. the appearance of arterial hyperemia. The mechanism of its development is very complex and is associated with a weakening of sympathetic and an increase in parasympathetic influences, as well as with the action of inflammatory mediators. Arterial hyperemia promotes an increase in metabolism in the focus of inflammation, increases the influx of leukocytes and antibodies to it, promotes the activation of the lymphatic system, which carries away the decay products of tissues. Hyperemia of the vessels causes an increase in temperature and redness of the site of inflammation.

Arterial hyperemia with the development of inflammation is replaced by venous hyperemia. The blood pressure in the venules and postcapillaries increases, the blood flow slows down, the volume of flowing blood decreases, the venules become tortuous, and jerky blood movements appear in them. In the development of venous hyperemia, the loss of tone by the walls of the venules is important due to metabolic disorders and tissue acidosis in the focus of inflammation, thrombosis of the venules, and compression of their edematous fluid. The slowing of the blood flow velocity in venous hyperemia promotes the movement of leukocytes from the center of the blood flow to its periphery and their adherence to the walls of blood vessels. This phenomenon is called the marginal standing of leukocytes, it precedes their exit from the vessels and the transition to the tissues. Venous hyperemia ends with a stoppage of blood, i.e. the occurrence of stasis, which manifests itself first in the venules, and later becomes true, capillary. Lymphatic vessels are overflowing with lymph, the lymph flow slows down, and then stops, as thrombosis of the lymphatic vessels occurs. Thus, the focus of inflammation is isolated from intact tissues. At the same time, blood continues to flow to it, and the outflow of it and lymph is sharply reduced, which prevents the spread of damaging agents, including toxins, throughout the body.

Exudation begins during the period of arterial hyperemia and reaches a maximum during venous hyperemia. The increased release of the liquid part of the blood and substances dissolved in it from the vessels into the tissue is due to several factors. The leading role in the development of exudation is the increase in the permeability of the walls of microvessels under the influence of inflammatory mediators, metabolites (lactic acid, ATP decay products), lysosomal enzymes, imbalance of K and Ca ions, hypoxia and acidosis. The release of fluid is also due to an increase in hydrostatic pressure in microvessels, hyperonkia and hyperosmia of tissues. Morphologically, an increase in vascular permeability is manifested in increased pinocytosis in the vascular endothelium, swelling of the basement membranes. As vascular permeability increases, blood cells begin to leak from the capillaries into the focus of inflammation.

The fluid that accumulates in the focus of inflammation is called exudate. The composition of exudate differs significantly from transudate - accumulation of fluid during edema. In the exudate, the protein content is much higher (3-5%), and the exudate contains not only albumins, like transudate, but also proteins with a high molecular weight - globulins and fibrinogen. In exudate, unlike transudate, there are always blood cells - leukocytes (neutrophils, lymphocytes, monocytes), and often erythrocytes, which, accumulating in the focus of inflammation, form an inflammatory infiltrate. Exudation, i.e. the flow of fluid from the vessels into the tissue towards the center of the focus of inflammation, prevents the spread of pathogenic irritants, waste products of microbes and decay products of their own tissues, promotes the entry of leukocytes and other blood cells, antibodies and biologically active substances into the focus of inflammation. The exudate contains active enzymes that are released from dead leukocytes and cell lysosomes. Their action is aimed at the destruction of microbes, melting the remnants of dead cells and tissues. The exudate contains active proteins and polypeptides that stimulate cell proliferation and tissue repair at the final stage of inflammation. At the same time, exudate can compress the nerve trunks and cause pain, disrupt the function of organs and cause pathological changes in them.

Inflammation- a complex local reaction of the body to damage, aimed at destroying the damaging factor and restoring damaged tissues, which is manifested by characteristic changes in the microvasculature and connective tissue.

Signs of inflammation were known to the ancient doctors, who believed that it was characterized by 5 symptoms: redness (rubor), tissue swelling (tumor), heat (calor), pain (dolor) and dysfunction (functio laesa). To denote inflammation, the ending “itis” is added to the name of the organ in which it develops: carditis is inflammation of the heart, nephritis is inflammation of the kidney, hepatitis is inflammation of the liver, etc.

The biological meaning of inflammation consists in the delimitation and elimination of the source of damage and the pathogenic factors that caused it, as well as in the restoration of homeostasis.

Inflammation is characterized by the following features.

Inflammation- this is a protective-adaptive reaction that arose in the course of evolution. Thanks to inflammation, many body systems are stimulated, it gets rid of an infectious or other damaging factor; usually in the outcome of inflammation, immunity arises and new relationships with the environment are established.

As a result, not only individual people, but also humanity, as a biological species, adapts to changes in the world in which it lives - the atmosphere, ecology, microcosm, etc. However, in a particular person, inflammation can sometimes lead to serious complications, up to until the death of the patient, since the course of the inflammatory process is influenced by the characteristics of the reactivity of the organism of this person - his age, the state of the defense systems, etc. Therefore, inflammation often requires medical intervention.

Inflammation- a typical general pathological process with which the body responds to a variety of influences, therefore it occurs in most diseases and is combined with other reactions.

Inflammation can be an independent disease in cases where it forms the basis of the disease (for example, croupous pneumonia, osteomyelitis, purulent leptomeningitis, etc.). In these cases, inflammation has all the signs of the disease, i.e., a specific cause, a peculiar mechanism of the course, complications and outcomes, which requires targeted treatment.

Inflammation and immunity.

There is both a direct and an inverse relationship between inflammation and immunity, since both processes are aimed at “cleansing” the body’s internal environment from a foreign factor or a changed “own” factor, followed by rejection of a foreign factor and elimination of the consequences of damage. In the process of inflammation, immune reactions are formed, and the immune response itself is realized through inflammation, and the course of inflammation depends on the severity of the body's immune response. If immune defenses are effective, inflammation may not develop at all. When immune hypersensitivity reactions occur (see Chapter 8), inflammation becomes their morphological manifestation - immune inflammation develops (see below).

For the development of inflammation, in addition to the damaging factor, it is necessary to combine various biologically active substances, certain cells, intercellular and cellular-matrix relationships, the development of local tissue changes and general changes in the body.

Inflammation is a complex set of processes that consists of three interrelated reactions - alteration (damage), exudation and polyferation.

The absence of at least one of these three components of the reactions does not allow us to speak of inflammation.

Alteration - tissue damage, in which various changes in cellular and extracellular components occur at the site of the damaging factor.

Exudation- the entry of exudate into the focus of inflammation, i.e., a protein-rich liquid containing blood cells, depending on the amount of which various exudates are formed.

Proliferation- reproduction of cells and the formation of an extracellular matrix, aimed at restoring damaged tissues.

A necessary condition for the development of these reactions is the presence of inflammatory mediators.

Inflammatory mediators- biologically active substances that provide chemical and molecular links between the processes occurring in the focus of inflammation and without which the development of the inflammatory process is impossible.

There are 2 groups of inflammatory mediators:

Cellular (or tissue) inflammatory mediators, with the help of which the vascular reaction is turned on and exudation is provided. These mediators are produced by cells and tissues, especially mast cells (mast cells), basophilic and eosinophilic granulocytes, monocytes, macrophages, lymphocytes, cells of the APUD system, etc. The most important cellular mediators of inflammation are:

biogenic amines, especially histamine and serotonin, which cause acute dilatation (expansion) of the vessels of the microvasculature, which increases vascular permeability, promotes tissue edema, increases mucus formation and contraction of smooth muscles:

• acidic lipids, which are formed when cells and tissues are damaged and are themselves a source of tissue mediators of inflammation;
• slow regulating substance of anaphylaxis increases vascular permeability;
• eosinophilic chemotactic factor A increases cocydisty permeability and release of eosinophils into the focus of inflammation;
• platelet activating factor stimulates platelets and their multifaceted functions;
• prostaglandans have a wide spectrum of action, including damage to microcirculation vessels, increase their permeability, enhance chemotaxis, promote fibroblast proliferation.

Plasma mediators of inflammation are formed as a result of activation under the influence of a damaging factor and cellular mediators of inflammation of three plasma systems - complement systems, plasmin systems(kallekrin-kinin system) and blood coagulation system. All components of these systems are in the blood as precursors and begin to function only under the influence of certain activators.

• mediators of the kinin system are bradykinin and kallikrein. Bradykinin enhances vascular permeability, causes a feeling of pain, and has a hypotensive property. Kallikrein carries out leukocyte chemotaxis and activates the Hageman factor, thus including the blood coagulation and fibrinolysis systems in the inflammatory process.
• Hageman factor, a key component of the blood coagulation system, initiates blood clotting, activates other plasma mediators of inflammation, increases vascular permeability, enhances the migration of neutrophilic leukocytes and platelet aggregation.
• Complement system consists of a group of special blood plasma proteins that cause lysis of bacteria and cells, complement components C3b and C5b increase vascular permeability, increase the movement of polymorphonuclear leukocytes (PMNs), monocytes and macrophages to the site of inflammation.

Acute phase reactants- biologically active protein substances, due to which inflammation includes not only the microcirculation system and the immune system, but also other body systems, including the endocrine and nervous systems.

Among the reactants of the acute phase, the most important are:

• C-reactive protein, the concentration of which in the blood increases by 100-1000 times during inflammation, activates the cytolytic activity of T-killer lymphocytes. slows down platelet aggregation;
• interleukin-1 (IL-1), affects the activity of many cells of the focus of inflammation, especially T-lymphocytes, PNL, stimulates the synthesis of prostaglandins and prostacyclins in endothelial cells, promotes hemostasis in the focus of inflammation;
• T-kininogen is a precursor of plasma inflammatory mediators - kinins, inhibits (cysteine ​​proteinases.

Thus, a gamut of very complex processes occurs in the focus of inflammation, which cannot proceed autonomously for a long time, without being a signal to turn on various systems of the body. Such signals are the accumulation and circulation of biologically active substances, kinins, in the blood. complement components, prostaglandins, interferon, etc. As a result, the hematopoietic system, immune, endocrine, and nervous systems, i.e., the body as a whole, are involved in inflammation. Therefore, broadly speaking inflammation should be considered as a local manifestation of the general reaction of the body.

Inflammation usually accompanies intoxication. It is associated not only with the inflammation itself, but also with the characteristics of the damaging factor, primarily the infectious agent. As the area of ​​damage and the severity of alteration increase, the absorption of toxic products increases and intoxication increases, which inhibits various defense systems of the body - immunocompetent, hematopoietic, macrophage, etc. Intoxication often has a decisive influence on the course and nature of inflammation. This is primarily due to the lack of effectiveness of inflammation, for example, in acute diffuse peritonitis, burn disease, traumatic disease and many chronic infectious diseases.

PATHOPHYSIOLOGY AND MORPHOLOGY OF INFLAMMATORY

In its development, inflammation goes through 3 stages, the sequence of which determines the course of the entire process.

STAGE OF ALTERATION

Stage of alteration (damage)- the initial, starting stage of inflammation, characterized by tissue damage. Cheluattraction develops at this stage, i.e. attraction to the focus of damage of cells that produce inflammatory mediators necessary for inclusion in the process of the vascular reaction.

Chemoattractants- substances that determine the direction of movement of cells in tissues. They are produced by microbes, cells, tissues, contained in the blood.

Immediately after damage, chemoattractants such as proserinesterase, thrombin, kinin are released from tissues, and in case of damage to blood vessels - fibrinogen, activated complement components.

As a result of cumulative chemoattraction in the damage zone, primary cooperation of cells, producing inflammatory mediators - accumulation of labrocytes, basophilic and eosinophilic granulocytes, monocytes, cells of the APUD system, etc. Only being in the focus of damage, these cells ensure the release of tissue mediators and the onset of inflammation.

As a result of the action of tissue mediators of inflammation in the area of ​​damage, the following processes occur:

• increases the permeability of the vessels of the microvasculature;
• biochemical changes develop in the connective tissue, leading to water retention in the tissues and swelling of the extracellular matrix;
• initial activation of plasma inflammatory mediators under the influence of a damaging factor and tissue mediators;
• development of dystrophic and necrotic tissue changes in the area of ​​damage;
• hydrolases (proteases, lipases, phospholipases, elastase, collagenases) and other enzymes released from cell lysosomes and activated in the focus of inflammation play a significant role in the development of damage to cells and non-cellular structures:
• violations of functions, both specific - of the organ in which the alteration occurred, and non-specific - thermoregulation, local immunity, etc.

EXUDATION STAGE

B. The stage of exudation occurs at different times following tissue damage in response to the action of cellular and especially plasma mediators of inflammation, which are formed during the activation of the kinin, complementary and coagulation systems of the blood. In the dynamics of the stage of exudation, 2 stages are distinguished: plasmatic exudation and cellular infiltration.

Rice. 22. Marginal state of a segmented leukocyte (Lc).

Plasma exudation due to the initial expansion of the vessels of the microvasculature, increased blood flow to the focus of inflammation (active), which leads to an increase in hydrostatic pressure in the vessels. Active contributes to the development of oxygenation of the focus of inflammation, resulting in the following processes:

• formation of reactive oxygen species;
• the influx of humoral protection factors - complement, fibronectin, properdin, etc.;
• an influx of PMNs, monocytes, platelets and other blood cells.

Cellular infiltration- entry into the inflammation zone of various cells, primarily blood cells, which is associated with a slowdown in blood flow in the venules (passive) and the action of inflammatory mediators.

At the same time, the following processes develop:

• leukocytes move to the periphery of the axial blood flow;
• blood plasma cations Ca 2+ , Mn and Mg 2+ remove the negative charge of endothelial cells and leukocytes and leukocytes adhere to the vessel wall (adhesion of leukocytes);
• arises marginal state of leukocytes, i.e., stopping them at the wall of the vessels (Fig. 22);

Rice. 23. Emigration of a segmented leukocyte from the lumen (Pr) of the host.

The segmented leukocyte (Lc) is located under the endothelial cell (En) near the basement membrane (BM) of the vessel.

• prevents the outflow of exudate, toxins, pathogens from the focus of inflammation and the rapid increase in intoxication and the spread of infection.

Thrombosis of the vessels of the inflammation zone develops after the emigration of blood cells to the focus of inflammation.

Interaction of cells in the focus of inflammation.

1. Polymorphonuclear leukocytes usually the first to enter the focus of inflammation. Their functions:
   • delimitation of the focus of inflammation;
   • localization and destruction of the pathogenic factor,
   • creation of an acidic environment in the focus of inflammation by ejection (exocytosis) of granules containing hydrolases
2. macrophages, especially resident, appear in the focus of damage even before the development of inflammation. Their functions are very diverse. what is he doing macrophage and one of the main cells of the inflammatory response:
   • they carry out phagocytosis of the damaging agent;
   • reveal the antigenic nature of the pathogenic factor;
   • induce immune responses and participation of the immune system in inflammation;
   • provide neutralization of toxins in the focus of inflammation;
   • provide diverse intercellular interactions, primarily with PMNs, lymphocytes, monocytes, fibroblasts;
   • interacting with NAL, provide phagocytosis of the damaging agent;
   • the interaction of macrophages and lymphocytes contributes to the development of a delayed-type hypersensitivity reaction (DTH) in the form of immune cytolysis and granulomatosis;
   • the interaction of macrophages and fibroblasts is aimed at stimulating the formation of collagen and various fibrils.
3. Monocytes are precursors of macrophages, circulate in the blood, enter the focus of inflammation, transforming into macrophages.
4. Cells of the immune system - T- and B-lymphocytes, plasma cells:
   • different subpopulations of T-lymphocytes determine the activity of the immune response;
   • T-lymphocytes-killers ensure the death of biological pathogenic factors, have a cytolytic property in relation to the body's own cells;
   • B-lymphocytes and plasmocytes are involved in the production of specific antibodies (see Chapter 8), which ensure the elimination of the damaging factor.
5. fibroblasts are the main producers of collagen and elastin, which form the basis of connective tissue. They appear already at the initial stages of inflammation under the influence of macrophage cytokines, and to a large extent ensure the restoration of damaged tissues.
6. Other cells (eosinophils, erythrocytes) , the appearance of which depends on the cause of inflammation.

All these cells, as well as the extracellular matrix, components of the connective tissue interact with each other due to numerous active substances that determine cellular and extracellular reception - cytokines and growth factors. By reacting with cell and extracellular matrix receptors, they activate or inhibit the functions of cells involved in inflammation.

Lymphatic microvascular system participates in inflammation synchronously with the hemomicrocirculatory bed. With pronounced infiltration of cells and sweating of blood plasma in the area of ​​the venular link of the microcirculatory bed, the roots of the "ultracirculatory" system of the interstitial tissue are soon involved in the process - interstitial channels.

As a result, in the area of ​​​​inflammation occurs:

• violation of blood tissue balance;
• change in extravascular circulation of tissue fluid;
• the occurrence of edema and swelling of the tissue;
• lymphedema develops. as a result of which the lymphatic capillaries overflow with lymph. It goes into the surrounding tissues and acute lymphatic edema occurs.

tissue necrosis is an important component of inflammation, as it has several functions:

• in the focus of necrosis, along with dying tissues, the pathogenic factor must die;
• at a certain mass of necrotic tissues, biologically active substances appear, including various integrative mechanisms for regulating inflammation, including acute phase reactants and the fibroblast system;
• contributes to the activation of the immune system, which regulates the utilization of altered "own" tissues.

PRODUCTIVE (PROLIFERATIVE) STAGE

The productive (proliferative) stage completes acute inflammation and provides repair (restoration) of damaged tissues. The following processes take place in this stage:

• decreases inflamed tissue;
• the intensity of emigration of blood cells decreases;
• the number of leukocytes in the area of ​​inflammation decreases;
• the focus of inflammation is gradually filled with macrophages of hematogenous origin, which secrete interleukins - chemoattractants for fibroblasts and stimulate, in addition, neoplasm of blood vessels;
• Fibroblasts multiply in the focus of inflammation:
• accumulation in the focus of inflammation of cells of the immune system - T- and B-lymphocytes, plasma cells;
• the formation of an inflammatory infiltrate - the accumulation of these cells with a sharp decrease in the liquid part of the exudate;
• activation of anabolic processes - the intensity of the synthesis of DNA and RNA, the main substance and fibrillar structures of the connective tissue:
• "purification" of the field of inflammation due to the activation of hydrolases of lysosomes of monocytes, macrophages, histiocytes and other cells;
• proliferation of endotheliocytes of preserved vessels and the formation of new vessels:
• the formation of granulation tissue after the elimination of necrotic detritus.

Granulation tissue - immature connective tissue, characterized by an accumulation of inflammatory infiltrate cells and a special architectonics of newly formed vessels, growing vertically to the surface of the damage, and then again descending into depth. The site of vessel rotation looks like a granule, which gave the tissue its name. As the focus of inflammation is cleared of necrotic masses, granulation tissue fills the entire area of ​​damage. It has a great resorption capacity, but at the same time it is a barrier to inflammatory pathogens.

The inflammatory process ends with the maturation of granulations and the formation of mature connective tissue.

FORMS OF ACUTE INFLAMMATION

Clinical and anatomical forms of inflammation are determined by the predominance in its dynamics of either exudation or proliferation over other reactions that make up inflammation. Depending on this, there are:

• exudative inflammation;
• productive (or proliferative) inflammation.

According to the flow, they distinguish:

• acute inflammation - lasts no more than 4-6 weeks;
• chronic inflammation - lasts more than 6 weeks, up to several months and years.

By pathogenetic specificity allocate:

• ordinary (banal) inflammation;
• immune inflammation.

EXUDATIVE INFLAMMATION

Exudative inflammation characterized by the formation of exudates, the composition of which is determined mainly by:

• cause of inflammation
• the body's response to the damaging factor and its features;
• exudate determines the name of the form of exudative inflammation.

1. Serous inflammation characterized by the formation of serous exudate - a cloudy liquid containing up to 2-25% protein and a small amount of cellular elements - leukocytes, lymphocytes, desquamated epithelial cells.

The causes of serous inflammation are:

• the action of physical and chemical factors (for example, exfoliation of the epidermis with the formation of a bubble during a burn);
• the action of toxins and poisons that cause severe plasmorrhagia (for example, pustules on the skin with smallpox):
• severe intoxication, accompanied by hyperreactivity of the body, which causes serous inflammation in the stroma of parenchymal organs - the so-called intermediate inflammation.

Localization of serous inflammation - mucous and serous membranes, skin, interstitial tissue, glomeruli of the kidneys, peri-sinusoidal spaces of the liver.

The outcome is usually favorable - the exudate resolves and the structure of damaged tissues is restored. An unfavorable outcome is associated with complications of serous inflammation, for example, serous exudate in the meninges (serous leptomeningitis) can compress the brain, serous impregnation of the alveolar septa of the lungs is one of the causes of acute respiratory failure. Sometimes after serous inflammation in the parenchymal organs develops diffuse sclerosis their stroma.

2. fibrinous inflammation characterized by education fibrinous exudate, containing, in addition to leukocytes, monocytes, macrophages, decaying cells of inflamed tissue, a large amount of fibrinogen, which precipitates in the form of fibrin bundles. Therefore, in fibrinous exudate, the protein content is 2.5-5%.

The causes of fibrinous inflammation can be a variety of microbial flora: toxigenic corynebacterium diphtheria, various cocci, Mycobacterium tuberculosis, some Shigella - causative agents of dysentery, endogenous and exogenous toxic factors, etc.

Localization of fibrinous inflammation - Mucous and serous membranes.

Morphogenesis.

Exudation is preceded by tissue necrosis and platelet aggregation in the focus of inflammation. Fibrinous exudate impregnates dead tissues, forming a light gray film, under which microbes that secrete toxins are located. The thickness of the film is determined by the depth of necrosis, and the depth of necrosis itself depends on the structure of the epithelial or serous integuments and the characteristics of the underlying connective tissue. Therefore, depending on the depth of necrosis and the thickness of the fibrinous film, 2 types of fibrinous inflammation are distinguished: croupous and diphtheritic.

Croupous inflammation in the form of a thin, easily removable fibrinous film, it develops on a single-layer epithelial cover of mucous or serous membranes located on a thin dense connective tissue base.

Rice. 24. Fibrinous inflammation. Diphtheritic angina, croupous laryngitis and tracheitis.

After removing the fibrinous film, no defect of the underlying tissues is formed. Croupous inflammation develops on the mucous membrane of the trachea and bronchi, on the epithelial lining of the alveoli, on the surface of the pleura, peritoneum, pericardium with fibrinous tracheitis and bronchitis, lobar pneumonia, peritonitis, pericarditis, etc. (Fig. 24).

Diphtheritic inflammation , developing on surfaces lined with squamous or transitional epithelium, as well as other types of epithelium located on a loose and wide connective tissue basis. This tissue structure usually contributes to the development of deep necrosis and the formation of a thick, difficult-to-remove fibrinous film, after the removal of which ulcers remain. Diphtheritic inflammation develops in the pharynx, on the mucous membranes of the esophagus, stomach, intestines, uterus and vagina, bladder, in wounds of the skin and mucous membranes.

Exodus fibrinous inflammation can be favorable: with croupous inflammation of the mucous membranes, fibrinous films melt under the influence of leukocyte hydrolases and the original tissue is restored in their place. Diphtheritic inflammation results in the formation of ulcers, which can sometimes heal with scarring. An unfavorable outcome of fibrinous inflammation is the organization of fibrinous exudate, the formation of adhesions and the mooring between the sheets of serous cavities up to their obliteration, for example, the pericardial cavity, pleural cavities.

3. Purulent inflammation characterized by education purulent exudate, which is a creamy mass consisting of tissue detritus of the inflammation focus, dystrophically altered cells, microbes, a large number of blood cells, the bulk of which are living and dead leukocytes, as well as lymphocytes, monocytes, macrophages, often eosinophilic granulocytes. The protein content in pus is 3-7%. The pH of the pus is 5.6-6.9. Pus has a specific odor, a bluish-greenish color with various shades. Purulent exudate has a number of qualities that determine the biological significance of purulent inflammation; contains various enzymes, including proteases, that break down dead structures; therefore, tissue lysis is characteristic in the focus of inflammation; contains, along with leukocytes capable of phagocytizing and killing microbes, various bactericidal factors - immunoglobulins, complement components, proteins, etc. Therefore, pus retards the growth of bacteria and destroys them. After 8-12 hours, pus leukocytes die, turning into " purulent bodies".

The cause of purulent inflammation are pyogenic microbes - staphylococci, streptococci, gonococci, typhoid bacillus, etc.

Localization of purulent inflammation - any tissues of the body and all organs.

Forms of purulent inflammation.

Abscess - delimited purulent inflammation, accompanied by the formation of a cavity filled with purulent exudate. The cavity is limited by a pyogenic capsule - granulation tissue, through the vessels of which leukocytes enter. In the chronic course of an abscess, two layers are formed in the pyogenic membrane: the inner one, consisting of granulation tissue, and the outer one, which is formed as a result of the maturation of granulation tissue into mature connective tissue. An abscess usually ends with emptying and exit of pus to the surface of the body, into hollow organs or cavities through a fistula - a channel lined with granulation tissue or epithelium that connects the abscess to the surface of the body or to its cavities. After a breakthrough of pus, the abscess cavity is scarred. Occasionally, the abscess undergoes encapsulation.

Phlegmon - unlimited, diffuse purulent inflammation, in which purulent exudate impregnates and exfoliates tissues. Phlegmon is usually formed in the subcutaneous adipose tissue, intermuscular layers, etc. Phlegmon can be soft if lysis of necrotic tissues predominates, and solid when coagulative necrosis of tissues occurs in the phlegmon, which are gradually rejected. In some cases, pus can drain under the influence of gravity into the underlying sections along the muscle-tendon sheaths, neurovascular bundles, fatty layers and form secondary, so-called cold abscesses, or leakers. Phlegmonous inflammation can spread to the vessels, causing thrombosis of arteries and veins (thrombophlebitis, thrombarteritis, lymphangiitis). The healing of phlegmon begins with its limitation, followed by the formation of a rough scar.

empyema - purulent inflammation of body cavities or hollow organs. The cause of empyema is both purulent foci in neighboring organs (for example, lung abscess and empyema of the pleural cavity), and a violation of the outflow of pus in case of purulent inflammation of hollow organs - the gallbladder, appendix, fallopian tube, etc. With a long course of empyema, obliteration occurs hollow organ or cavity.

festering wound - a special form of purulent inflammation, which occurs either as a result of suppuration of a traumatic, including surgical, wound, or as a result of opening a focus of purulent inflammation into the external environment and the formation of a wound surface covered with purulent exudate.

4. Putrid or ichorous inflammation develops when putrefactive microflora enters the focus of purulent inflammation with severe tissue necrosis. Usually occurs in debilitated patients with extensive, long-term non-healing wounds or chronic abscesses. In this case, the purulent exudate acquires a particularly unpleasant smell of decay. In the morphological picture, tissue necrosis prevails without a tendency to delimitation. Necrotized tissues turn into a fetid mass, which is accompanied by increasing intoxication.

5. Hemorrhagic inflammation is a form of serous, fibrinous or purulent inflammation and is characterized by a particularly high permeability of the microcirculation vessels, diapedesis of erythrocytes and their admixture to the existing exudate (serous-hemorrhagic, purulent-hemorrhagic inflammation). The admixture of erythrocytes as a result of hemoglobin transformations gives the exudate a black color.

The cause of hemorrhagic inflammation is usually a very high intoxication, accompanied by a sharp increase in vascular permeability, which is observed, in particular, in such infections as plague, anthrax, many viral infections, smallpox, severe forms of influenza, etc.

The outcome of hemorrhagic inflammation usually depends on its etiology.

6. Catarrh develops on the mucous membranes and is characterized by an admixture of mucus to any exudate, so it, like hemorrhagic, is not an independent form of inflammation.

The cause of catarrh can be various infections. products of disturbed metabolism, allergic irritants, thermal and chemical factors. For example, with allergic rhinitis, mucus is mixed with serous exudate (catarrhal rhinitis), purulent catarrh of the mucous membrane of the trachea and bronchi (purulent-catarrhal tracheitis or bronchitis) is often observed, etc.

Exodus. Acute catarrhal inflammation lasts 2-3 weeks and, ending, leaves no traces. Chronic catarrh can lead to atrophic or hypertrophic changes in the mucosa.

PRODUCTIVE INFLAMMATION

Productive (proliferative) inflammation characterized by the predominance of proliferation of cellular elements over exudation and alteration. There are 4 main forms of productive inflammation:

Rice. 25. Popov's typhoid granuloma. Accumulation of histiocytes and glial cells at the site of the destroyed vessel.

1. Granulomatous inflammation can proceed acutely and chronically, but the most important is the chronic course of the process.

Acute granulomatous inflammation observed, as a rule, in acute infectious diseases - typhus, typhoid fever, rabies, epidemic encephalitis, acute anterior poliomyelitis, etc. (Fig. 25).

Pathogenetic basis acute granulomatous inflammation is usually inflammation of the microcirculatory vessels when exposed to infectious agents or their toxins, which is accompanied by ischemia of the perivascular tissue.

Morphology of acute granulomatous inflammation. In the nervous tissue, the morphogenesis of granulomas is determined by the necrosis of a group of neurons or ganglion cells, as well as by small-focal necrosis of the substance of the brain or spinal cord, surrounded by glial elements that carry the function of phagocytes.

In typhoid fever, the morphogenesis of granulomas is due to the accumulation of phagocytes that have transformed from reticular cells in group follicles of the small intestine. These large cells phagocytize S. typhi, as well as detritus formed in solitary follicles. Typhoid granulomas undergo necrosis.

The outcome of acute granulomatous inflammation can be favorable when the granuloma disappears without a trace, as in typhoid fever, or small glial scars remain after it, as in neuroinfections. The unfavorable outcome of acute granulomatous inflammation is mainly associated with its complications - intestinal perforation in typhoid fever or with the death of a large number of neurons with severe consequences.

2. interstitial diffuse, or interstitial, inflammation is localized in the stroma of parenchymal organs, where there is an accumulation of mononuclear cells - monocytes, macrophages, lymphocytes. At the same time, dystrophic and necrobiotic changes develop in the parenchyma.

The cause of inflammation can be either various infectious agents, or it can occur as a reaction of the mesenchyme of organs to toxic effects or microbial intoxication. The most striking picture of interstitial inflammation is observed in interstitial pneumonia, interstitial myocarditis, interstitial hepatitis and nephritis.

The outcome of interstitial inflammation can be favorable when there is a complete restoration of the interstitial tissue of organs and unfavorable when the stroma of the organ is sclerosed, which usually occurs in the chronic course of inflammation.

3. Hyperplastic (hyper-regenerative) growths- productive inflammation in the stroma of the mucous membranes, in which there is a proliferation of stromal cells. accompanied by accumulation of eosinophils, lymphocytes, as well as hyperplasia of the epithelium of the mucous membranes. At the same time, they form polyps of inflammatory origin- polypous rhinitis, polypous colitis, etc.

Hyperplastic growths also occur at the border of the mucous membranes with a flat or prismatic epithelium as a result of the constant irritating action of the discharge of the mucous membranes, for example, the rectum or female genital organs. In this case, the epithelium macerates, and chronic productive inflammation occurs in the stroma, leading to the formation of genital warts.

immune inflammation A type of inflammation that is initially caused by an immune response. This concept was introduced by A.I. Strukov (1979), who showed that the morphological basis of reactions immediate type hypersensitivity(anaphylaxis, Arthus phenomenon, etc.), as well as delayed type hypersensitivity(tuberculin reaction) is inflammation. In this regard, tissue damage by antigen-antibody immune complexes, complement components and a number of immune mediators becomes the trigger for such inflammation.

In an immediate hypersensitivity reaction these changes develop in a certain sequence:

1. formation of antigen-antibody immune complexes in the lumen of venules:
2. binding of these complexes with complement;
3. chemotactic effect of immune complexes on PMNs and their accumulation near veins and capillaries;
4. phagocytosis and digestion of immune complexes by leukocytes;
5. damage to the walls of blood vessels by immune complexes and lysosomes of leukocytes, with the development of fibrinoid necrosis in them, perivascular hemorrhages and edema of surrounding tissues.

As a result, in the zone of immune inflammation develops exudative-necrotic reaction with serous-hemorrhagic exudate

With a delayed-type hypersensitivity reaction, which develops in response to an antigen in the tissues, the sequence of processes is somewhat different:

1. T-lymphocytes and macrophages move into the tissue, find the antigen and destroy it, while destroying the tissues in which the antigen is located;
2. in the zone of inflammation, a lymphomacrophage infiltrate accumulates, often with giant cells and a small amount of PMNs;
3. changes in the microvasculature are weakly expressed;
4. this immune inflammation proceeds as a productive, most often granulomatous, sometimes interstitial and is characterized by a protracted course.

CHRONIC INFLAMMATION

chronic inflammation- a pathological process characterized by the persistence of a pathological factor, the development of immunological deficiency in connection with this, which causes the originality of morphological changes in tissues in the area of ​​​​inflammation, the course of the process according to the principle of a vicious circle, the difficulty of repair and restoration of homeostasis.

In essence, chronic inflammation is a manifestation of a defect that has arisen in the body's defense system to the changed conditions of its existence.

The cause of chronic inflammation is primarily the constant action (persistence) of a damaging factor, which can be associated both with the characteristics of this factor (for example, resistance against leukocyte hydrolases), and with the lack of mechanisms of inflammation of the body itself (pathology of leukocytes, inhibition of chemotaxis, impaired innervation tissues or their autoimmunization, etc.).

Pathogenesis. The persistence of the stimulus constantly stimulates the immune system, which leads to its disruption and the appearance at a certain stage of inflammation of a complex of immunopathological processes, primarily the appearance and growth of immunodeficiency, sometimes also to autoimmunization of tissues, and this complex itself determines the chronicity of the inflammatory process.

Patients develop lymphocytopathy, including a decrease in the level of T-helpers and T-suppressors, their ratio is disturbed, at the same time the level of antibody formation increases, the concentration of circulating immune complexes (CIC) and complement in the blood increases, which leads to damage to microcirculation vessels and the development of vasculitis . This reduces the body's ability to remove immune complexes. The ability of leukocytes to chemotaxis also decreases due to the accumulation in the blood of cell decay products, microbes, toxins, immune complexes, especially during exacerbation of inflammation.

Morphogenesis. The zone of chronic inflammation is usually filled with granulation tissue with a reduced number of capillaries. Productive vasculitis is characteristic, and with an exacerbation of the process, vasculitis is purulent. The granulation tissue contains multiple foci of necrosis, lymphocytic infiltrate, a moderate amount of neutrophilic leukocytes, macrophages and fibroblasts, and also contains immunoglobulins. In the foci of chronic inflammation, microbes are often found, but the number of leukocytes and their bactericidal activity remain reduced. Regenerative processes are also disturbed - there are few elastic fibers, unstable type III collagen predominates in the forming connective tissue, and there is little type IV collagen necessary for building basement membranes.

common feature chronic inflammation is violation of the cyclic flow of the process in the form of constant layering of one stage onto another, primarily the stages of alteration and exudation to the stage of proliferation. This leads to constant relapses and exacerbations of inflammation and the impossibility of repairing damaged tissues and restoring homeostasis.

The etiology of the process, features of the structure and function of the organ in which inflammation develops, reactivity and other factors leave an imprint on the course and morphology of chronic inflammation. Therefore, the clinical and morphological manifestations of chronic inflammation are diverse.

Chronic granulomatous inflammation develops in cases where the body cannot destroy the pathogenic agent, but at the same time has the ability to limit its spread, localize it in certain areas of organs and tissues. Most often it occurs in infectious diseases such as tuberculosis, syphilis, leprosy, glanders and some others, which have a number of common clinical, morphological and immunological features. Therefore, such inflammation is often called specific inflammation.

According to the etiology, 3 groups of granulomas are distinguished:

1. infectious, such as granulomas in tuberculosis, syphilis, actinomycosis, glanders, etc.;
2. granulomas of foreign bodies - starch, talc, suture, etc.;
3. granulomas of unknown origin, such as in sarcoidosis. eosinophilic, allergic, etc.

Morphology. Granulomas are compact collections of macrophages and/or epithelioid cells, usually giant multinucleated cells of the Pirogov-Langhans type or foreign body type. According to the predominance of certain types of macrophages, macrophage granulomas are distinguished (Fig. 26) and epitpelluid-cell(Fig. 27). Both types of granulomas are accompanied by infiltration by other cells - lymphocytes, plasma, often neutrophilic or eosinophilic leukocytes. The presence of fibroblasts and the development of sclerosis are also characteristic. Often, caseous necrosis occurs in the center of the granulomas.

The immune system is involved in the formation of chronic infectious granulomas and most granulomas of unknown etiology, so this phanulomatous inflammation is usually accompanied by cell-mediated immunity, in particular HRT.

Rice. 27. Tuberculous nodules (granulomas) in the lungs. Caseous necrosis of the central part of the granulomas (a); on the border with necosis foci, epithelioid cells (b) and Pirogov-Langhans giant cells (c) of the periphery of the granulomas are accumulations of lymphoid cells.

Outcomes of granulomatous inflammation, which, like any other, proceeds cyclically:

1. resorption of the cellular infiltrate with the formation of a scar at the site of the former infiltrate;
2. calcification of the granuloma (for example, Gon's focus in tuberculosis);
3. progression of dry (caseous) necrosis or wet necrosis with the formation of a tissue defect - cavities;
4. granuloma growth up to the formation of a pseudotumor.

Granulomatous inflammation underlies granulomatous diseases, i.e., such diseases in which this inflammation is the structural and functional basis of the disease. An example of granulomatous diseases are tuberculosis, syphilis, leprosy, glanders, etc.

Thus, all of the above allows us to consider inflammation as a typical and at the same time unique reaction of the body, which has an adaptive character, but depending on the individual characteristics of the patient, it can aggravate his condition, up to the development of fatal complications. In this regard, inflammation, especially the basis of various diseases, requires treatment.

Lecture #6

INFLAMMATION: DEFINITION, ESSENCE, BIOLOGICAL SIGNIFICANCE. INFLAMMATORY MEDIATORS. LOCAL AND GENERAL MANIFESTATIONS OF INFLAMMATION. ACUTE INFLAMMATION: ETIOLOGY, PATHOGENESIS. MORPHOLOGICAL MANIFESTATION OF EXUDATIVE INFLAMMATION. OUTCOMES OF ACUTE INFLAMMATION

Inflammation is a biological general pathological process, the expediency of which is determined by its protective and adaptive function, aimed at eliminating the damaging agent and restoring damaged tissue.

To designate inflammation, the ending "itis" is added to the name of the organ in which the inflammatory process develops - myocarditis, bronchitis, gastritis, etc.

The Roman scientist A. Celsus singled out the main symptoms of inflammation, redness (rubor), tumor (tumor), heat (color) and pain (dolor). Later, K. Galen added another sign - dysfunction (functio laesa).

The biological meaning of inflammation lies in the delimitation and elimination of the focus of damage and the pathogenic factors that caused it, as well as in the repair of damaged tissues.

Features of inflammation depend not only on the immune, but also on body reactivity. In children, the ability to delimit the inflammatory focus and repair the damaged tissue is not sufficiently expressed. This explains the tendency to generalization of inflammatory and infectious processes at this age. In old age, a similar inflammatory response occurs.

Inflammation is a complex complex process that consists of three interrelated reactions - alteration (damage), exudation and proliferation.

Only the combination of these three reactions allows us to speak of inflammation. Alteration attracts to the site of damage inflammatory mediators - biologically active substances that provide chemical and molecular links between the processes occurring in the focus of inflammation. All these reactions are directed to delimit the lesion, fixation in it and the destruction of the damaging factor.

In any type of inflammation, polymorphonuclear leukocytes (PMNs) are the first to arrive at the site. Their function is aimed at localization and destruction of the pathogenic factor.

In the inflammatory reaction, lymphoid and non-lymphoid cells, various biologically active substances interact, multiple intercellular and cell-matrix relationships arise.

Inflammation- This localnpophenomenon of the general reaction of the body. At the same time, they stimulate the inclusion of other body systems in the process, contributing to the interaction of local and general reactions during inflammation.

Another manifestation of the participation of the whole organism in inflammation is the clinical systemic inflammatory response syndrome - SIRS (systemic Inflammatory Response Syndrome), development of which may result in the appearance of multiple organ failure.

This reaction is manifested by: 1) an increase in body temperature above 38 ° C, 2) a heart rate of more than 90 beats / min, 3) a respiratory rate of more than 20 per minute, 4) peripheral blood leukocytosis more than 12000 μl or leukopenia less than 4000 μl, possibly also the appearance of more than 10% of immature forms of leukocytes. A diagnosis of SIRS requires the presence of at least two of these features.

With the flow inflammation may be acute and chronic.

Stages of inflammation . Stage of alteration (damage) - this is the initial, starting stage of inflammation, characterized by tissue damage. It includes a variety of changes in cellular and extracellular components at the site of action of the damaging factor.

Exudation stage. This stage occurs at different times following damage to cells and tissues in response to the action of inflammatory mediators and especially plasma mediators that occur during the activation of three blood systems - kinin, complementary and coagulation.

In the dynamics of the stage of exudation, two stages are distinguished: 1) plasma exudation, associated with the expansion of the vessels of the microvasculature, increased blood flow to the focus of inflammation (active hyperemia), which leads to an increase in hydrostatic pressure in the vessels. 2) cell infiltration, associated with slowing blood flow in the venules and the action of inflammatory mediators.

Arises marginal standing of leukocytes, prior to their emigration into the surrounding tissue.

The process of leaving leukocytes outside the vessel takes several hours. During the first 6-24 hours, neutrophilic leukocytes enter the inflammatory focus. After 24-48 hours, the emigration of monocytes and lymphocytes dominates.

Further, platelet activation occurs and a short thrombosis of small vessels develops in the area of ​​inflammation, ischemia of the vessel walls increases, which increases their permeability, as well as ischemia of inflamed tissues. This contributes to the development of necrobiotic and necrotic processes in them. Obturation of the microcirculatory bed prevents the outflow of exudate, toxins, pathogens from the focus of inflammation, which contributes to the rapid growth of intoxication and the spread of infection.

Neutrophilic granulocytes and macrophages that have arrived at the site of inflammation perform bactericidal and phagocytic functions, and also produce biologically active substances. Later, monocytic and macrophage join neutrophilic infiltration, which characterizes the beginning of encapsulation, delimitation of the inflamed zone due to the formation of a cell wall along its periphery.

An important component of inflammation is the development of tissue necrosis. In the focus of necrosis, the pathogenic factor must die, and the sooner necrosis develops, the fewer complications of inflammation will be.

Productive (proliferative) stage completes inflammation. The hyperemia of the inflamed tissue and the intensity of the emigration of neutrophilic leukocytes are reduced.

After purification of the inflammation field by phagocytosis and digestion of bacteria and necrotic detritus, the inflammation focus is filled with macrophages of hematogenous origin. However, proliferation begins already during the exudative stage and is characterized by the release of a large number of macrophages into the focus of inflammation.

The accumulation of cells in the focus of inflammation is called inflammatory infiltrate. It reveals T- and B-lymphocytes, plasmocytes and macrophages, i.e. cells associated with the immune system.

The endothelium of the vessels of the microvasculature takes an active part. The cells of the infiltrate are gradually destroyed, and fibroblasts predominate in the focus of inflammation. In the dynamics of proliferation, the formation of granulation tissue occurs.

The inflammatory process ends with the maturation of granulations and the formation of mature connective tissue. When substitutions granulation tissue matures to a connective tissue scar. If the inflammation ends restitution then the original tissue is restored.

Forms of acute inflammation. Clinical and anatomical forms of inflammation are determined by the predominance of exudation or proliferation in its dynamics.

Inflammation feel sharp , if it lasts no more than 4-6 weeks, however, in most cases it ends within 1.5-2 weeks.

Acute inflammation consider exudative, which has several types: 1) serous, 2) fibrinous, 3) purulent, 4) putrefactive, 5) hemorrhagic. With inflammation of the mucous membranes, mucus is mixed with the exudate, then they talk about catarrhal inflammation, which is usually combined with other types of exudative inflammation. 6) a combination of different types of exudative inflammation is called mixed.

Exudative inflammation characterized by the formation of exudate, the composition of which is determined by the cause of the inflammatory process and the corresponding reaction of the body to the damaging factor. The exudate also determines the name of the form of acute exudative inflammation.

Serous inflammation occurs as a result of the action of chemical or physical factors, toxins and poisons. An option is infiltrates in the stroma of parenchymal organs with severe intoxication of the body (intermediate inflammation) . It is characterized by a cloudy exudate with a small amount of cellular elements - PMN, deflated epithelial cells and up to 2-2.5% protein. It develops in the mucous and serous membranes, interstitial tissue, skin, in the capsules of the glomeruli of the kidneys.

The outcome of serous inflammation is usually favorable - the exudate resolves and the process ends by restitution. Sometimes, after serous inflammation of parenchymal organs, diffuse sclerosis develops in them.

fibrinous inflammation characterized by the formation of exudate containing, in addition to PMN, lymphocytes, monocytes, macrophages, decaying cells, a large amount of fibrinogen, which precipitates in the tissues in the form of fibrin bundles.

Etiological factors can be diphtheria corynebacterium, various coccal flora, mycobacterium tuberculosis, some viruses, dysentery pathogens, exogenous and endogenous toxic factors.

More often develops on mucous membranes or serous membranes. Exudation is preceded by tissue necrosis and platelet aggregation. Fibrinous exudate impregnates dead tissues, forming a light gray film, under which microbes are located, releasing a large amount of toxins. The thickness of the film is determined by the depth of necrosis, and the latter depends on the structure of the epithelial integuments and the characteristics of the underlying connective tissue.

Depending on the depth of necrosis and the thickness of the fibrinous exudate, two types of fibrinous inflammation are distinguished. With a single-layer epithelial cover of the mucous or serous membrane of the organ and a thin dense connective tissue base, a thin, easily removable fibrinous film is formed. This fibrinous inflammation is called croupy .

It occurs on the mucous membranes of the trachea and bronchi, serous membranes, characterizing fibrinous pleurisy, pericarditis, peritonitis, and also in the form of fibrinous alveolitis, which captures a lobe of the lung, develops with lobar pneumonia.

Stratified squamous non-keratinizing epithelium, transitional epithelium or loose broad connective tissue base of the organ contribute to the development of deep necrosis and the formation of a thick, hard-to-remove fibrinous film, after removal of which deep ulcers remain.

This fibrinous inflammation is called diphtheritic . It develops in the pharynx, on the mucous membranes of the esophagus, uterus and vagina, intestines and stomach, bladder, in wounds of the skin and mucous membranes.

The outcome of fibrinous inflammation mucous membranes is the melting of fibrinous films. Diphtheritic inflammation ends with the formation of ulcers, followed by substitution, with deep ulcers, scars may form. Croupous inflammation of the mucous membranes ends with the restitution of damaged tissues. On the serous membranes, fibrinous exudate is more often organized, resulting in the formation of adhesions, moorings, and often fibrinous inflammation of the membranes of the body cavities ends with their obliteration.

Purulent inflammation characterized by the formation of purulent exudate. It is a creamy mass, consisting of detritus of tissues of the focus of inflammation, cells, microbes. Most of the formed elements are viable and dead granulocytes, lymphocytes, macrophages, and often eosinophilic granulocytes are contained. Pus has a specific odor, a bluish-greenish color with various shades.

Purulent inflammation is caused by pyogenic microbes - staphylococci, streptococci, gonococci, typhoid bacillus, etc. It occurs in almost any tissue and in all organs. Its course can be acute and chronic.

The main forms of purulent inflammation are 1) abscess, 2) phlegmon, 3) empyema, 4) purulent wound.

Abscess - delimited purulent inflammation, accompanied by the formation of a cavity filled with purulent exudate.

The accumulation of pus is surrounded by a shaft of granulation tissue. The granulation tissue that borders the abscess cavity is called pyogenic capsule . If it becomes chronic, two layers are formed in the pyogenic membrane: the inner one, facing the cavity and consisting of granulations, and the outer one, which is formed as a result of the maturation of granulation tissue into mature connective tissue.

Phlegmon - purulent, unrestricted diffuse inflammation, in which purulent exudate impregnates and exfoliates tissues. The formation of phlegmon depends on the pathogenicity of the pathogen, the state of the body's defense systems, as well as on the structural features of the tissues.

Phlegmon is usually formed in the subcutaneous fat, intermuscular layers, etc. Phlegmon of fibrous fatty tissue is called cellulite.

May be soft , if lysis of necrotic tissue predominates, and solid , when coagulative tissue necrosis occurs in phlegmon. Pus can drain along the muscle-tendon sheaths, neurovascular bundles, fatty layers into the underlying sections and form secondary ones there, the so-called cold abscesses, orsills .

Complicated by thrombosis of blood vessels, with necrosis of the affected tissues. Purulent inflammation can spread to the lymphatic vessels and veins, and in these cases, purulent thrombophlebitis and lymphangitis occur.

The healing of phlegmonous inflammation begins with its delimitation, followed by the formation of a rough scar. With an unfavorable outcome, generalization of infection with the development of sepsis may occur.

empyema - This is a purulent inflammation of body cavities or hollow organs.

The reason for the development of empyema are: 1) purulent foci in neighboring organs (for example, lung abscess and empyema of the pleural cavity), 2) violation of the outflow of pus in case of purulent inflammation of hollow organs - the gallbladder, appendix, fallopian tube, etc.

With a long course of purulent inflammation, obliteration of hollow organs occurs.

festering wound - a special form of purulent inflammation, which occurs either as a result of suppuration of a traumatic, including surgical, or other wound, or as a result of opening a focus of purulent inflammation into the external environment and the formation of a wound surface.

Distinguish primary and secondary suppuration in the wound. The primary occurs immediately after trauma and traumatic edema, the secondary is a relapse of purulent inflammation.

putrid or ichorous , inflammation develops mainly when putrefactive microflora enters the focus of purulent inflammation with severe tissue necrosis.

Occurs in debilitated patients with extensive, long-term non-healing wounds or chronic abscesses. Purulent exudate acquires a particularly unpleasant smell of decay.

The morphological picture is dominated by progressive tissue necrosis without a tendency to delimitation. Necrotic tissues turn into a fetid mass, which is accompanied by increasing intoxication, from which patients usually die.

Hemorrhagic inflammation is not an independent form, but a variant of serous, fibrinous or purulent inflammation and is characterized by a particularly high permeability of microcirculation vessels, diapedesis of erythrocytes and their admixture to the existing exudate (serous-hemorrhagic, purulent-hemorrhagic inflammation).

With the breakdown of red blood cells, the exudate may become black. Usually, hemorrhagic inflammation develops in cases of very high intoxication, accompanied by a sharp increase in vascular permeability, and is also characteristic of many types of viral infection.

Typical of plague, anthrax, smallpox, and severe forms of the flu. In the case of hemorrhagic inflammation, the course of the disease usually worsens, the outcome of which depends on its etiology.

Catarrh , like hemorrhagic, is not an independent form. It develops on the mucous membranes and is characterized by the admixture of mucus to any exudate.

The cause of catarrhal inflammation can be various infections, metabolic products, allergic irritants, thermal and chemical factors.

Acute catarrhal inflammation lasts 2-3 weeks and ends without leaving traces. As a result of chronic catarrhal inflammation, atrophic or hypertrophic changes in the mucous membrane may develop. The value of catarrhal inflammation for the body is determined by its localization and the nature of the course.

Alterative inflammation

Alteration - damage to tissue and cells - can be considered as a result of the direct action of a pathogenic factor and general disorders that occur in damaged tissue.

In all cases of inflammation, alteration is the first phase of the process. Morphologically, this type of inflammation can be defined as swelling and swelling of tissues and cells. Formed elements of the blood, with the exception of erythrocytes, do not sweat from the capillaries during alteration. The period of edema and tissue swelling is considered a reversible stage of alterative inflammation. But the reversibility of the alteration in most cases limited to two weeks. If during this time the process is not stopped, irreversible tissue changes develop in the form of necrobiosis, dystrophies, connective tissue degeneration.

Exudative inflammation

In contrast to the alternative, with exudative inflammation, the vascular reaction is noted not only in the venous part of the capillaries; but also in the arterial, with vasodilatation and an increase in their permeability. This leads not only to profuse sweating of blood plasma and its free accumulation. In the subcutaneous tissue, intermuscular spaces, serous cavities, organs, etc., but also to the release of leukocyte blood elements into the exudate. Predominantly small, uniform elements of blood sweat: eosinophils and lymphocytes. The appearance and growth of neutrophils in the exudate, as a rule, indicates the transition of exudative inflammation to purulent.

Clinically, exudative inflammation is accompanied by: severe swelling of soft tissues (for example, subcutaneous tissue); free accumulation of exudate in the serous cavities; sweating into hollow organs (for example, into the tracheobronchial tree with bronchitis and pneumonia). In most cases, the very fact of exudation for diagnosis is not difficult. A difficult problem is to identify the cause of its development and differential diagnosis with purulent inflammation.

Proliferative (productive) inflammation

It is formed in the form of two forms: reproduction (recovery) of atypical, with an outcome in degeneration.

Morphologically, it is characterized by: the formation of a liquid transudate containing proteins, fibrin filaments, decomposed cellular elements of the blood; the presence of tissue detritus; dead and viable microorganisms. This product of inflammation is called pus.

Purulent inflammation develops only in the presence of pathogenic microflora, which is the starting point of the body's reaction to the effects of both exogenous and endogenous infections. The process of purulent inflammation is staged. Primarily introduced microflora itself is inert, in addition, it is exposed to protective factors of the body (phagocytosis, complement fixation reaction, etc.) and can be destroyed by them. This period proceeds in the form of alteration. Clinically, it may not manifest itself in any way (incubation period) or manifest itself slightly: itching, slight pain irritation in the form of bursting, fuzzy hyperemia. Palpation determines: local pastosity; seals, as a rule, are not present; slight local increase in skin temperature, moderate pain. There are no changes in general condition.

The second stage - infiltration, in fact, is the phase of exudative inflammation. It is formed when the microflora begins to develop in the focus, releasing toxins that cause a neuroreflex reaction with the release of inflammatory mediators that determine the formation of a typical vascular reaction. Due to the increase in vascular permeability, plasma effusion is massive, with blood cells.

Clinically, this stage is characterized by: increased pain, they become bursting; expansion and increase in edema; the appearance of bright hyperemia with blurry edges. In the depth of the edema, a painful seal is palpated - elastic, more often, round or oval.

The third stage is suppuration; vascular reactions with it are pronounced. Vessels become empty and thrombose, mostly venous trunks, with the blood flow cut off in the tissues of the infiltrate (Arthus phenomenon). They become necrotic and a pyogenic capsule forms around them. Around it, granulations and scar tissue from fibroblasts grow from healthy tissues. A restrictive barrier is formed that determines the course of the purulent process. It may proceed as an abscess when the delimitation is sufficient; or phlegmon - when the delimitation is either weak or absent altogether. Thus, an abscess is a delimited typical purulent inflammation, and phlegmon is not a delimited typical purulent inflammation. The general manifestations of a purulent infection depend on the nature of the microflora, since the gram-positive microflora gives more local manifestations, and the gram-negative one causes a greater degree of intoxication.

The second important point is the tension of the microflora in the focus, and the critical number is up to myriads per cm3 of tissue. At a lower voltage of the microflora, the process proceeds as a local one. Greater tension causes a breakthrough of microflora into the blood, with the development of: with preserved resistance of the organism - purulent-resorptive fever; in cases of its decrease and immunodeficiency - intoxication syndrome.

The third point is determined by the prevalence of the focus of purulent infection and its delimitation. Abeceding forms of purulent inflammation, as a rule, proceed as a local process; and phlegmonous - prone to intoxication. But its localization should also be taken into account, for example, with a relatively small abscess of the brain, severe functional disorders are formed.

The fourth point, and perhaps the leading one, is the state of the macroorganism. The presence of: vitamin deficiency, alimentary depletion, malignant tumors, diabetes mellitus, immunosuppression - determine the decrease in a person's natural resistance to the effects of pathogenic microflora. This significantly aggravates both the local manifestation of inflammation and the general reaction of the body to purulent inflammation. The general response to a purulent infection according to the state of the body's reactivity can be of three types.

1. Normergic - with preserved resistance and normal immunity, i.e. in a practically healthy person, when an adequate protective reaction to purulent inflammation is formed according to the type of local and general manifestations, depending on its nature.
2. Hypoergic (up to anergic) is due to a decrease in resistance due to the pathological conditions listed above. Figuratively speaking, the body simply has nothing to fight the infection with and an opportunity is formed for its generalization, but there is no response protective effect on pronounced purulent inflammation (blood reactions in the form of leukocytosis, as well as the development of local restrictive barriers are not noted).
3. A hyperergic reaction proceeds in the form of an autoallergy, since the modern microflora is in most cases allergen-active and causes a general reaction with the release of a large amount of histamine and serotonin, up to the development of anaphylactic shock, even with "small" abscesses.

Clinically, in the normergic state of the body, the general manifestations of a purulent infection give 4 pictures.

• Purulent (infectious) toxicosis. This is a typical reaction of the body to "small" forms of purulent inflammation with preserved reactivity of the body. It is formed when the tension of the microflora in the focus of inflammation is less than the critical number (10 myriads per cm3). In this case, the release of microflora into the bloodstream does not occur, and the process proceeds in the form of local purulent inflammation. The general reaction is manifested: headaches, malaise, weakness. The body temperature is kept at the subfebrile level (37.0-37.5 degrees). There is a slight increase in leukocytes in the blood, there is a leukocyte, a shift of the formula to the left, but the leukocyte index of intoxication is normal, the ESR is accelerated. Organ function is not impaired.
• Purulent-resorptive fever. It develops frequently and complicates up to 30% of all purulent-inflammatory diseases. It is caused by the tension of the microflora in the focus above 10 myriads per cm 3, which determines the periodic release of microflora into the blood directly from the abscess, or through the lymphatic system. But with the preserved resistance of the organism, it is destroyed in the blood by cellular elements.

Clinically, purulent-resorptive fever is accompanied by: high body temperature with a daily range of up to one degree; chills with heavy sweats, especially at the time of entry of microflora into the blood; weakness, malaise. In blood tests: high leukocytosis, increased ESR is detected; in the leukocyte formula, a shift to the left, a slight increase in the intoxication index and an increase in the fraction of medium molecules. Functional changes in the internal organs are not particularly pronounced, with the exception of tachycardia.

• Syndrome of intoxication
• bacterial shock. In literary sources, many authors understand bacterial shock as intoxication syndrome, which is fundamentally wrong. The issue was discussed at an international conference in Chicago (1993), and the decision made on this issue does not differ from our opinion.

Bacterial shock develops only when the blood-brain barrier is broken, mainly during superinfection with a viral passage, which determines the role of penetration of toxins. At the same time, the functions of the cerebral cortex are blocked with a violation of the central regulation of the activity of all internal organs, including vital ones. Cerebral edema develops intensively in the form of exudative inflammation, up to the wedging of the medulla oblongata into the foramen magnum. A distinctive clinical feature is a sudden loss of consciousness against the background of a purulent-inflammatory disease with complete areflexia - there are not even convulsions. Death in such patients occurs quickly, within an hour. Resuscitation measures are hopeless.

Inflammation I Inflammation (inflammatio)

protective and adaptive local organism to the action of various damaging factors, one of the most frequent forms of the body's response to pathogenic stimuli.

V.'s reasons are diverse. It can be caused by various factors: biological (for example, bacteria, viruses), physical (high and low temperatures, mechanical, etc.), chemical (for example, exposure to acids, alkalis). The classic signs of V. are redness, fever, swelling, and dysfunction. However, in many cases only a part of these signs is expressed.

Inflammation begins with alteration (cells and tissues), which is the result of the direct action of the etiological factor. At the same time, a number of changes occur in the cell - ultrastructural, arising in the components of the cytoplasm, the cell nucleus and its membrane, to pronounced dystrophic processes and even complete destruction of cells and tissue. Phenomena of alteration are observed both in the parenchyma and in the stroma. Primary entails the release of biologically active substances (inflammatory mediators) in the affected tissues. These substances, differing in origin, chemical nature and features of action, play the role of a starting link in the chain of mechanisms for the development of the inflammatory process and are responsible for its various components. The release of inflammatory mediators may be a direct result of the damaging action of pathogenic factors, but to a large extent this is an indirect process that occurs under the influence of lysosomal hydrolytic enzymes that are released from lysosomes when their membrane is destroyed. Lysosomes are called the "launching pad of inflammation", because. lysosomal hydrolytic break down all types of macromolecules that make up animal tissues (, nucleic acids, lipids). Under the influence of lysosomal hydrolytic enzymes, the connective tissue framework of microvessels continues. inflammation, both of cellular and humoral origin, accumulating as V. develops, more and more deepens tissue alteration. So, the most powerful histamine causes the expansion of microvessels, an increase in their permeability. contained in the granules of mast cells (mast cells), as well as in basophils, and is released during the granulation of these cells. Another cellular mediator - Serotonin , increases vascularity. Its source is . The cellular mediators of V. include prostaglandins, etc., which are formed in lymphocytes. Of the humoral mediators, the most important are (, kallidin), which expand the precapillary arterioles, increase the permeability of the capillary wall and participate in the formation of pain sensations. - a group of neurovasoactive polypeptides formed as a result of a cascade of chemical reactions, the trigger mechanism of which is the activation of factor XII of blood coagulation. Lysosomal hydrolytic enzymes can also be attributed to V.'s mediators, tk. they not only stimulate the formation of other mediators, but also act as mediators themselves, participating in phagocytosis and chemotaxis.

Under the influence of V. mediators, the following, the main link in the mechanism of inflammation, is formed - a hyperemic reaction (see Hyperemia) , characterized by an increase in vascular permeability and a violation of the rheological properties of the blood. The vascular reaction in V. is expressed in a sharp expansion of the microvascular bed, primarily capillaries, both active and passive (see Microcirculation) . It is this vascular reaction that determines the first sign of V. - redness and its features (diffusion, delimitation from neighboring tissues, etc.). Unlike various types of arterial hyperemia (thermal, reactive, etc.), capillary expansion in V. depends not so much on blood flow through the arterial segments as on local (primary) mechanisms. The latter include the expansion of precapillary microvessels under the influence of V.'s vasodilator mediators and an increase in pressure in them, which causes an increase in the lumen of active capillaries and the opening of the lumen of previously non-functioning ones. This is facilitated by a change in the mechanical properties of the loose connective tissue framework of the capillary bed. The diffuse expansion of the capillaries is joined by the reflex arterial both in the focus of inflammation and along its periphery, which develops according to the mechanism of the axon reflex (i.e., a reflex carried out along the branches of the axon). In this initial period of the inflammatory process (after 2-3 h after exposure to a damaging factor), due to an increase in the total cross-sectional area of ​​the vascular bed in the affected area, the intensity of blood flow (volume velocity) increases, despite a decrease in its linear velocity. At this stage, increased blood flow in the area of ​​inflammation determines the second sign of V. - an increase in local temperature (fever).

The subsequent links of the process are characterized by the appearance of not only chain reactions, but also "vicious circles", in which pathological phenomena follow one another, accompanied by a deepening of their severity. This can be seen in the example of such a rheological phenomenon inherent in V. as erythrocytes (the formation of conglomerates of erythrocytes) in microvessels. Slowing blood flow creates conditions for erythrocyte aggregation, and erythrocyte aggregation, in turn, further reduces the circulation rate.

With V., other changes in rheological properties also occur, which ultimately lead to an increase in blood clotting and thrombosis. Erythrocyte aggregates and thrombi (platelet clots), partially or completely closing the lumen of the vessels, are one of the main reasons that slowed down in some places turns into prestasis and. Increasing phenomena of venous hyperemia and stagnation gradually join the arterial hyperemia. The development of venous hyperemia is also associated with compression of the veins and lymphatic vessels (up to lymphostasis) by the inflammatory fluid accumulated in the surrounding tissues - Exudate om . The third sign of V., swelling, depends on the accumulation of exudate in the tissues. With an increase in tissue volume, nerve endings occur, as a result of which the fourth symptom of V. arises - pain. manifested by the release of blood components - water, salts, proteins, as well as formed elements (emigration) from the blood vessels of the tissue. The emigration of leukocytes is due to both purely physical (hemodynamic) and biological patterns. When blood flow slows down, the transition of leukocytes from the axial layer of blood cells to the parietal (plasma) layer occurs in full accordance with the physical laws of particles suspended in the flowing fluid; a decrease in the difference in the speeds of movement in the axial and near-wall layers causes a decrease in the pressure difference between them, and, as it were, lighter compared to erythrocytes are thrown to the inner shell of the blood vessel. In places of especially strong slowing down of the blood flow (transition of capillaries to venules), where the blood becomes wider, forming "bays", the marginal arrangement of leukocytes passes into the marginal standing, they begin to attach to the wall of the blood vessel, which becomes covered with a flocculent layer during V. After that, leukocytes form thin protoplasmic processes - with the help of which they penetrate through the interendothelial gaps, and then through the basement membrane - outside the blood vessel. Perhaps there is also a transcellular way of leukocyte emigration, i.e. through the cytoplasm of endothelial cells, the leukocytes that have emigrated in the focus of V. continue active (migration), and mainly in the direction of chemical irritants. They can be products of tissue proteolysis or vital activity of microorganisms. This property of leukocytes to move towards certain substances (chemotaxis) I.I. Mechnikov attached leading importance at all stages of the movement of leukocytes from the blood into tissues. Later it turned out that during the passage of leukocytes through the vascular wall, it plays a secondary role. In V.'s focus, the main leukocyte is the absorption and digestion of foreign particles ().

Exudation primarily depends on an increase in the permeability of microvessels and an increase in the hydrodynamic pressure of blood in them. An increase in the permeability of microvessels is associated with the deformation of the normal permeability pathways through the endothelial wall of the vessels and the appearance of new ones. Due to the expansion of microvessels and, possibly, the contraction of contractile structures (myofibrils) of endothelial cells, the gaps between them increase, forming the so-called small pores, and even channels, or large pores, may appear in the endothelial cell. In addition, with V., the transfer of substances is activated by microvesicular transport - active "swallowing" by endothelial cells of the smallest bubbles and drops of plasma (micropinocytosis), passing them through the cells to the opposite side and pushing them out of it. The second factor that determines the process of exudation - an increase in blood pressure in the capillary network - is primarily the result of an increase in the lumen of the precapillary and larger adducting arterial vessels, from which the resistance and energy consumption (i.e. pressure) in them decrease, and therefore remain more "unused" energy.

An indispensable link in V. is () cells, which is especially pronounced in the final stages of inflammation, when recovery processes come to the fore. Proliferative processes involve local cambial cells (progenitor cells), primarily mesenchymal cells, which give rise to fibroblasts that synthesize (the main part of scar tissue); adventitial, endothelial cells, as well as cells of hematogenous origin - B- and T-lymphocytes and monocytes multiply. Some of the cells that make up, having fulfilled their phagocytic function, die, the other undergoes a series of transformations. for example, monocytes transform into histiocytes (macrophages), and macrophages can be the source of epithelioid cells from which so-called giant mono- or multinucleated cells (see Mononuclear phagocyte system) are derived. .

Depending on the nature of the prevailing local changes, alterative, exudative and productive V. are distinguished. With alterative V., the phenomena of damage and necrosis are expressed. They are more often observed in parenchymal organs (liver, kidneys, etc.).

Exudative V. is characterized by the predominance of exudation processes. Depending on the nature of the exudate, serous, catarrhal, fibrinous, purulent and hemorrhagic inflammation are distinguished. With serous V., it contains from 3 to 8% of blood serum protein and single leukocytes (serous exudate). Serous V., as a rule, acute, is localized more often in serous cavities; serous exudate is easily absorbed, V. practically leaves no traces. Catarrhal V. develops on the mucous membranes. Occurs acutely or chronically. A serous or purulent exudate with an admixture of mucus is released. Fibrinous V. occurs on serous or mucous membranes; usually sharp. contains a lot of fibrin, which in the form of a film can lie freely on the surface of the mucous or serous membrane or be soldered to the underlying surface. Fibrinous V. is one of the severe forms of inflammation; its outcome depends on the localization and depth of tissue damage. Purulent V. can develop in any tissue and organ; the course is acute or chronic, may take the form of an abscess or phlegmon; the process is accompanied by histolysis (melting) of the tissue. The exudate contains mainly leukocytes that are in a state of decay. When the exudate contains a large number of red blood cells, the inflammation is called hemorrhagic. It is characterized by a sharp increase in the permeability of blood vessels and even a violation of the integrity of their walls. Any V. can take on a character.

Productive (proliferative) V., as a rule, proceeds chronically : the phenomena of reproduction of cellular elements of the affected tissues predominate. Scar formation is a common outcome.

Inflammation depends on the immunological reactivity of the body, so it can have a clinically completely different course and outcome. If the inflammatory reaction is of a normal nature, i.e. one that is observed most often, they speak of normergic V. If the inflammatory process proceeds sluggishly, acquires a protracted character with mildly expressed main signs of V., it is called hypoergic inflammation. In some cases, the damaging agent causes an extremely violent inflammatory reaction, inadequate to its strength and dose. Such V., called hyperergic, is most characteristic of the state of allergy (Allergy) .

The outcome of V. is determined by the nature and intensity of the inflammatory agent, the form of the inflammatory process, its localization, the size of the affected area and the reactivity of the body (Reactivity of the body) . V. is accompanied by the death of cellular elements in the event that necrosis covers significant areas, especially in vital organs; consequences for the body can be the most severe. More often, the focus is delimited from the surrounding healthy tissue, tissue decay products undergo enzymatic cleavage and phagocytic resorption, and the inflammatory focus is filled with granulation tissue as a result of cell proliferation. If the area of ​​damage is small, complete restoration of the previous tissue may occur (see Regeneration) , with a more extensive lesion at the site of the defect is formed.

From the point of view of biological expediency, the inflammatory process has a dual nature. On the one side. V. is a protective and adaptive reaction developed in the process of evolution. Thanks to it, it delimits itself from the harmful factors that are in the focus of V., prevents the generalization of the process. This is achieved through various mechanisms. So, venous and lymphatic stagnation and stasis, the occurrence of blood clots prevent the process from spreading beyond the affected area. The resulting exudate contains components that can bind, fix and destroy bacterial; phagocytosis is carried out by emigrated leukocytes, the proliferation of lymphocytes and plasma cells contributes to the production of antibodies and an increase in local and general immunity. In the proliferation stage, a protective shaft of granulation tissue is formed. At the same time, V. can have a destructive and life-threatening effect on the body. In V.'s zone always there is a death of cellular elements. The accumulated exudate can cause enzymatic melting of the tissue, their compression with impaired blood circulation and nutrition. exudate and tissue breakdown products cause intoxication, metabolic disorders. The inconsistency of the value of V. for the body dictates the need to distinguish between phenomena of a protective nature from the elements of disruption of compensatory mechanisms.

Bibliography: Alpern D.E. Inflammation. (Issues of pathogenesis), M., 1959, bibliogr.; General Human, ed. A.I. Strukova et al., M., 1982; Strukov A.I. and Chernukh A.M. Inflammation, BME, 3rd ed., vol. 4, p. 413, M, 1976; Chernukh A.M. Inflammation, M., 1979, bibliogr.

1. Small medical encyclopedia. - M.: Medical Encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic dictionary of medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

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