The disease is accompanied by an inflammatory process. Inflammatory process: how the body's defense reactions become chronic diseases and how to avoid it. How to treat inflammation in a feminine way

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 temperature, 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 reflex arterial both in the focus of inflammation and along its periphery joins the diffuse expansion of the capillaries, developing 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 symptom 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 particularly 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, with V., becomes covered with a flocculent layer. 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 the hearth V. main leukocyte consists in 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, during 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 is an increase 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, which means that more "unused" energy remains.

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 uninuclear 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 are expressed - and necrosis. 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 the vital important 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, there may be full recovery previous tissue (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. 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 decay 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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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, lobar 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 feedback relationship between inflammation and immunity, since both processes are aimed at "cleansing" internal environment organism from a foreign factor or a changed "one's own" with the subsequent rejection of a foreign factor and the 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 cocystic 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;
• released from cell lysosomes and activated in the focus of inflammation hydrolases (proteases, lipases, phospholipases, elastase, collagenases) and other enzymes 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;
• with 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 that grow vertically to the surface of the damage, and then again descend 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%.

Causes fibrinous inflammation there may be a diverse 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 are melted 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 hard 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 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 tissue autoimmunization, and this complex itself causes 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 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.

INFLAMMATION- a complex, complex local vascular tissue (mesenchymal) protective and adaptive reaction of the whole organism to the action of a pathogenic stimulus. This reaction is manifested by the development of changes in blood circulation at the site of damage to a tissue or organ, mainly in the microcirculatory bed, an increase in vascular permeability in combination with tissue degeneration and cell proliferation.

General pathology

Brief historical information and theories

The question of the meaning and essence of V. has always been given a large place in medicine. Even Hippocrates believed that V. has a neutralizing value for the body, that harmful principles are destroyed in the purulent focus, and therefore the formation of pus is useful, healing, unless a certain limit of the intensity of the inflammatory process is exceeded. Hippocrates' views on the nature of inflammation dominated until the 18th century, supplemented by a description of the "cardinal signs" of inflammation.

A. Celsus described four main wedges, V.'s sign: redness ( rubor), swelling ( tumor), pain ( dolor), temperature rise ( calories). The fifth sign is dysfunction ( functio laesa) described by K. Galen; he spoke about an inflammation as about local fever and pointed to a variety of etiol, factors, to-rye it can cause.

The first close to the modern idea of ​​V. was formulated by the English. surgeon J. Gunter, to-ry defined V. as the reaction of the body to any damage. Gunter considered V. a protective process that always occurs at the site of damage, with the help of which the normal function of the damaged tissue or organ is restored.

The doctrine of V. began to develop after the improvement of the light microscope (mid-19th century), as well as in the first half of the 20th century. in connection with the development of biochemical, biophysic, and histochemical. methods and methods of electron microscopic study of tissues. R. Virchow (1859) drew attention to damage to the parenchyma of organs ( dystrophic changes cells) at V. and created the so-called. nutritional ("nutritional") theory B. This theory has lost its significance in connection with the studies of Samuel (S. Samuel, 1873) and Y. Kongeym (1887), to-rye main importance in the pathogenesis of V. was given to the reaction of small vessels (vascular theory B .).

AS Shklyarevsky (1869) applied an experimental method for studying of a blood-groove at V. and gave physical. explanation of the phenomenon of "marginal standing of leukocytes". A. G. Mamurovsky (1886) noted thrombosis and blockade of lymph, vessels in the focus of V.

Especially great contribution to the development of the problem of V. was made by I. I. Mechnikov, who in 1892 formulated the biological theory of V., developed the doctrine of phagocytosis (see), laid the foundation for the comparative pathology of V. and the theory of cellular and humoral immunity ( cm.). The process of absorption of foreign particles by phagocytes, including bacteria, was recognized by I. I. Mechnikov as the main, central process characterizing B. In his lectures on the comparative pathology of inflammation, I. I. Mechnikov wrote about the process of intracellular digestion carried out in the cytoplasm of phagocytes .

The development of the idea of ​​I. I. Mechnikov on the importance of phagocytosis for protecting the body from a pathogenic factor and the formation of immunity was obtained in the works of H. N. Anichkov, A. D. Ado, Kohn (E. J. Cohn, 1892 - 1953) and many other scientists . With the discovery in 1955 of cytoplasmic organelles - lysosomes (see) - the teachings of I. I. Mechnikov about cytases as carriers of the digestive function of the cell received further confirmation.

V. V. Voronin in 1897 established the importance of the state of the interstitial tissue and vascular tone in V. Assigning a secondary role to the process of phagocytosis, he considered the processes occurring in the interstitial substance of the connective tissue to be the main mechanisms underlying V., and gave a difference from Mechnikov's interpretation of the phenomenon of emigration, cell wandering and phagocytosis. Voronin's theory did not reveal biol, the essence of inflammation. V. V. Podvysotsky in "Fundamentals of General and Experimental Pathology" (1899) wrote that with V. there is a divergence of endothelial cells, as a result of which holes are formed between them, through which leukocytes penetrate from the vessel into the perivascular space.

In 1923 H. Schade put forward fiz.-chem. V.'s theory: in his opinion, V.'s basis is tissue acidosis, the Crimea and the whole set of changes is determined. Ricker (G. Ricker, 1924) considered V.'s phenomena as a manifestation of neurovascular disorders (V.'s neurovascular theory).

The works of A. A. Maksimov (1916, 1927), A. A. Zavarzin (1950) and other scientists who created experimental models of V. and studied the transformation of cell forms in the focus B.

comparative pathology

The classical description of the comparative pathology of V. was given by I. I. Mechnikov, who showed that V. is always an active reaction of the organism, at whatever stage of evolutionary development it may be. I. I. Mechnikov traced the development of all phases of the inflammatory reaction at different stages of phylogenesis - alteration, exudation and proliferation, described phagocytosis in detail; in highly organized animals, a large role in phagocytosis was assigned to neuroregulatory mechanisms. The organism, I. I. Mechnikov points out, is protected by the means it has. Even the simplest unicellular organisms do not passively treat harmful stimuli, but fight them by phagocytosis and the digestive action of the cytoplasm. However, even in the simplest unicellular organisms, when exposed to a pathogenic factor, alterations occur that are similar to certain dystrophic processes in multicellular organisms. In multicellular organisms, the reaction to damage is complicated by cell proliferation and the formed vascular system; the body can already "send" a significant number of phagocytes to the site of damage. At later stages of phylogenesis, cell emigration occurs in organisms. With the formation of the endocrine and nervous systems in organisms, neurohumoral factors for the regulation of the inflammatory response appear.

In highly organized animals, other protective and adaptive processes join phagocytosis: blockade of venous and lymph vessels that drain blood from the focus of V., exudation of serous fluid that dilutes toxic products, and the formation of antibodies by proliferating plasma cells that neutralize the pathogenic factor.

Data on the phases of V., obtained in the study of the inflammatory response in phylogenesis, show its complication as the evolution of organisms; V.'s phases are repeated to a certain extent in the prenatal period of a person. Yu. V. Gulkevich (1973) showed that the embryo has a significantly lower reactivity compared to the adult organism and that at the earliest stages of development the embryo reacts to harmful effects only by death, however, cell proliferation can also be observed already at the early stages of development. Exudation with the presence of leukocytes was found in the fetal part of the placenta and the fetal membrane by 10-12 weeks. and is the latest ontogenetic component of the inflammatory response. Phagocytosis at a germ of the person is carried out by hl. arr. connective tissue macrophages, and later segmented granulocytes.

The development of an inflammatory response in human ontogenesis is closely related to the formation of immunol, reactivity, which is morphologically expressed by the appearance of a large number of plasma cells producing immunoglobulins, the number of which increases markedly when an inflammatory focus occurs in the body of the embryo. Studies show that an inflammatory reaction with the presence of all signs of V. is established on the 4-5th month of intrauterine life. In the postnatal period at V. influence on an organism of antigenic irritants of the environment and immunol amplifies, processes complicate kliniko-morfol even more. profile B.

Etiology and pathogenetic mechanisms

The inflammatory reaction consists of several interconnected phases: a) alteration of tissues and their constituent cells; b) the release of physiologically active substances (the so-called mediators of V.), which constitutes V.'s trigger mechanisms and entails a reaction of microcirculation vessels; c) increasing the permeability of the walls of capillaries and venules; d) reactions of the blood system to damage, including changes in the rheological properties of the blood (see Blood, Rheology); e) proliferation - reparative stage B.

For practical purposes, it is advisable to conditionally divide the three main interrelated components of V., which have a bright clinical morphol. expression: alteration with release of mediators, vascular reaction with exudation and proliferation. The classification of the main morphol, V.'s forms is based on the predominance of one or another of these components.

Alteration (damage to tissue and cells) can be considered as a result of the direct action of the pathogenic factor and metabolic disorders that occur in the damaged tissue. This is the first phase of V.; it characterizes the initial processes and morphologically manifests itself from barely noticeable structural and functional disorders to complete destruction and death (necrobiosis, necrosis) of tissues and cells (see Alteration). Alternative changes in V. are especially pronounced in highly differentiated tissues that perform complex functions, for example, in neurons; in the fabrics which are carrying out hl. arr. support function and constituting the stroma of an organ, for example, in the connective tissue, alterative changes are often difficult to detect. In parenchymal organs, alteration is manifested by various types of proteinaceous degeneration (see) and fatty degeneration (see), in their stroma, Mucoid and fibrinoid swelling can occur up to fibrinoid necrosis (see Fibrinoid transformation).

In c. n. With. alteration is expressed by a change in ganglion cells (neurocytes) in the form of lysis of the basophilic (tigroid) substance, pushing the nuclei to the periphery and pycnosis (see), swelling or wrinkling of the cells. In mucous membranes, alteration is expressed by damage to the epithelium, desquamation (see) with exposure of the basement membrane; mucous glands intensively secrete mucus, desquamated epithelium is added to the cut, the lumens of the glands expand (see Mucous degeneration).

Ultrastructural changes in V. occur both in the components of the cytoplasm and in the cell nucleus and its membrane. Mitochondria increase in size, swell; some mitochondria, on the contrary, shrink, cristae are destroyed; the shape and size of the cisterns of the endoplasmic reticulum changes (see), vesicles, concentric structures, etc. appear. Ribosomes also change (see). In the cell nucleus, damage is manifested by the marginal location of chromatin, ruptures of the nuclear membrane.

In many cases, alteration develops through the so-called. lysosomal effect: when the membranes of lysosomes are destroyed (see), various, especially hydrolytic, enzymes are released, which play a significant role in damaging cell structures.

Inflammatory mediators- a number of physiologically active substances considered as triggers of V., under the influence of which the main link of V. arises - the reaction of the vessels of the microcirculatory bed and flowing blood with a violation of the rheological properties of the blood, which constitutes the initial phase of the inflammatory reaction. V.'s mediators contribute to an increase in the permeability of the vessels of the microcirculatory system, especially its venular section, with subsequent exudation of plasma proteins, emigration of all types of leukocytes, as well as erythrocytes through the walls of these vessels. These physiologically active substances play an important role in V.'s manifestations, and some researchers call them "internal engines" of V.

Spector and Willoughby (W. G. Spector, D. A. Willoughby, 1968) give 25 names of physiologically active substances (chemical mediators) of a different spectrum of action that appear after tissue damage. Especially a lot of work on V.'s mediators appeared after the discovery of histamine and leukotaxin. Although leukotaxin turned out to be a substance of a heterogeneous nature in subsequent verification works, its study served as a stimulus for further studies of endogenous chem. V.'s mediators, the most important of which are considered to be histamine, serotonin, plasma kinins, decay products of RNA and DNA, hyaluronidase, prostaglandins, etc.

One of the main sources of chem. V.'s mediators are mast cells (see), in granules to-rykh histamine, serotonin, heparin, etc. are found; in the cytoplasm of mast cells, cytochrome oxidase, acid and alkaline phosphatases, enzymes for the synthesis of nucleotides, proteases, exterases, leucine aminopeptidases, and plasmin were found.

Spector and Willoughby most convincingly showed the especially important role of histamine (see) in trigger mechanisms B. Histamine is the first vasoactive substance that appears immediately after tissue damage; it is with him that the starting stages of vasodilation, increased vascular permeability and exudation are associated; histamine has a predominant effect on venules. Serotonin is also of great importance (see).

Among V.'s mediators, it is necessary to note the globulin permeability factor (PF / dil.), discovered in the blood plasma of a guinea pig by Miles (A. A. Miles) et al. (1953, 1955) and T. S. Paskhina (1953, 1955) in aseptic inflammatory exudate, blood serum of rabbits, dogs and humans; this factor promotes the release of bradykinin with the help of kallikrein. Spector believes that the globulin permeability factor has a close relationship with the mechanism of blood coagulation, and in particular with the Hageman factor (see Blood coagulation system). According to Miles, the Hageman factor activates the globulin precursor PF/dil., an active PF/dil. is formed, and then a chain of successive reactions is switched on: prekininogenase - kininogenase - kallikrein - kininogen - kinin.

Nek-ry nucleosides take part in inflammatory reaction; adenosine can cause an increase in the permeability of the walls of microvessels and local accumulation of leukocytes; nek-ry nucleosides are liberators (releasing) a histamine.

Vascular reaction with exudation plays a very important role in the mechanisms of V. A number of authors argue that the entire “appearance of inflammation”, all its features, the entire range of tissue changes are determined by the vascular reaction, the permeability of the vessels of the microcirculatory bed, and the severity of its damage.

In the earliest phases of V. activation of functions of an endothelium of capillaries is noted. In the cytoplasm of the endothelium, the number of microvesicles increases, accumulations of cytogranules appear, polyribosomes are formed, mitochondria swell, and the cavities of the endoplasmic reticulum expand. Endothelial cells change their configuration somewhat, swell, their membranes become loose (see Permeability).

The mechanisms of passage of substances of various molecular weights and blood cells through the endothelial lining and basement membrane of capillaries and venules remained unclear for a long time. With the use of electron microscopy methods, it was found that endothelial cells in capillaries with continuous endothelium, closely adjacent to each other, are only in some places linked to each other with the help of desmosomes (tight junctions). The cell is fixed on the basement membrane and fastened to neighboring cells with a colloidal mass such as calcium proteinate in combination with mucopolysaccharides. In patol, conditions the cell body can be reduced, change the form and move. The complex of endothelial cells lining the inner surface of microcirculation vessels is a mobile system, during the functioning of a cut, gaps can appear in the gaps between endothelial cells, and even channels in the body of cells. Interendothelial gaps should be attributed to the so-called. small pores, and the channels in the body of the endothelial cell (microvesicular transport) - to the so-called. large pores, through which transcapillary transport is carried out. Dynamic Electron Microscope Observations

A. M. Chernukha et al. showed that, for example, in pneumonia, microvesiculation of the capillary endothelium and the formation of larger endothelial microbubbles are significantly increased, indicating an increase in tissue metabolism.

In V.'s focus, pronounced disorders of blood flow and lymph circulation occur. After tissue damage, the earliest change in an acute inflammatory reaction is a rapidly passing (from 10-20 seconds to several minutes) reduction of arterioles. Most researchers do not attach much importance to this phenomenon, but Spector and Willoughby consider it a protective reaction caused by catecholamines. Soon two phases of vasodilation develop. The first phase (immediate vasodilation), accompanied by an increase in permeability to blood proteins, reaches a maximum after an average of 10 minutes; the second phase, much longer, is measured in several hours. Owing to the second phase of expansion of vessels there is an infiltration of fabrics by leukocytes, an inflammatory hyperemia (see), rheological properties of blood change, there are stasises, local hemorrhages, thrombosis of small vessels; in V.'s focus, metabolism increases, to-ry is expressed by an increase in the concentration of hydrogen ions, acidosis, hyperosmia. In limf, microvessels the lymphostasis and a lymphothrombosis develop.

Shifts in the rheological properties of blood begin with a change in the speed of blood flow, a violation of the axial current, the release of white blood cells from it and their location along the walls of postcapillary venules (the so-called marginal standing of leukocytes); aggregates of platelets and erythrocytes, stasis and thrombosis of venules and capillaries are formed. Thrombosis occurs due to the activation of the Hageman factor, an important component of the blood coagulation system. Then there is an exudation (see), ie an exit from vessels in fabrics of components of blood - waters, proteins, salts and blood cells. In V.'s focus, metabolic products, toxins released from the blood stream are found, that is, V.'s focus performs, as it were, a drainage eliminative function. Substances (eg, paints) that have been exuded or introduced directly into V.'s focus are poorly excreted due to thrombosis of venous and lymph vessels in inflamed tissues.

The exudation of proteins occurs in sequence, which is explained by the size of the molecules (the smallest molecule of albumin, the largest of fibrinogen): with a slight increase in permeability, albumins are released, as permeability increases, globulins and fibrinogen. Exudation of proteinaceous molecules happens hl. arr. through channels in the endothelial cell body (large pores) and, to a lesser extent, through gaps between endothelial cells (small pores).

To an exit from a current of blood through a wall of venules and capillaries of cellular elements of blood, hl. arr. leukocytes (segmentonuclear granulocytes and monocytes), preceded by the marginal standing of leukocytes, gluing them to the vessel wall. AS Shklyarevsky (1869) showed that the release of leukocytes from the axial current is in full accordance with physical. the law of behavior of particles suspended in a flowing fluid when its speed slows down. After gluing to endothelial cells, segmented granulocytes form pseudopodia penetrating through the vessel wall, the contents of the cell overflow towards the stem extended beyond the vessel, and the leukocyte is outside the vessel. In the perivascular tissue, segmented granulocytes continue to move and are mixed with the exudate.

The process of emigration of leukocytes is called leukodiapedesis. It has been established that the emigration of segmented granulocytes and mononuclear cells is somewhat different. So, segmented granulocytes (neutrophils, eosinophils and basophils) emigrate between endothelial cells (interendothelial), and agranulocytes (large and small lymphocytes and monocytes) - through the cytoplasm of the endothelial cell (transendothelial).

Rice. 1. Interendothelial emigration of leukocytes through the vessel wall during inflammation: a - segmented granulocytes (1) penetrated into the space under the endothelial cell and are located between the endothelium (2) and the basement membrane (3). Joints of endothelial cells (4), collagen fibers (5), nuclei of granulocytes (6) are visible; x 20,000; b - two segmented granulocytes (1) are located in the perivascular connective tissue (the basement membrane has recovered into a dense gel). The endothelium (2) is not changed, the joints (4) of its cells and collagen fibers of the perivascular connective tissue (5) are visible; vessel lumen (7); x 12,000.

Interendothelial emigration occurs as follows. In the very initial phase of B., the segmented granulocyte adheres to the endothelial cell and, as it were, threads are stretched between it and the leukocyte. Then comes the contraction of the endothelial cell and pseudopodia rush into the gap formed between the two cells; with their help, the segmented granulocyte quickly penetrates into the space under the endothelial cell, exfoliates, as it were, and the hole above it is closed by reconnecting endothelial cells - the segmented granulocyte is between the endothelium and the basement membrane (Fig. 1, a). The next barrier - the basement membrane - is overcome by the segmented granulocyte, apparently, by the mechanism of thixotropy (isothermal reversible decrease in the viscosity of the colloidal solution), i.e., the transition of the membrane gel into a sol with a slight touch of the granulocyte to the membrane. The granulocyte easily overcomes the sol, finds itself in the tissue outside the vessel (Fig. 1b), and the basement membrane is again restored into a dense gel.

At transendothelial emigration agranulocytes initially stick to an endothelial cell, activity a cut at the same time sharply increases; the finger-like processes arising at the membrane of the endothelial cell, as it were, capture the mononuclear cell from all sides, absorb it by forming a large vacuole, and throw it onto the basement membrane. Then, by the mechanism of thixotropy, mononuclear cells penetrate through the basement membrane into the perivascular space and admixture with the exudate.

With V., erythrocytes also come out of the vessels into the tissue (see Diapedesis). They pass the vessel wall passively with a sharp increase in vascular permeability, which is observed with highly toxic infections (plague, anthrax), damage to the vessel walls by a tumor, radiation sickness, etc.

I. I. Mechnikov explained the exit from the vessel of segmented granulocytes and movement towards the focus of damage by chemotaxis, i.e., the effect on leukocytes of substances that caused V. or formed in the focus of V. (see Taxis). Menkin (V. Menkin, 1937) singled out the so-called inflammatory tissue. leukotaxin, which causes positive chemotaxis of segmented granulocytes; positive chemotaxis is more pronounced in segmented granulocytes, less in agranulocytes.

The most important phenomenon of V. is phagocytosis (see), carried out by cells - phagocytes; these include segmented granulocytes - microphages and agranulocytes - macrophages (see), in the cytoplasm to-rykh, the process of intracellular digestion is carried out. Revealed a positive role in the processes of phagocytosis of aluminum ions, chromium, iron and calcium, opsonins (see).

It has been established that various particles and bacteria invaginate the phagocyte membrane; in the cytoplasm of the phagocyte, the invaginated part of the membrane with the material enclosed in it is split off, forming a vacuole, or phagosome. When the phagosome merges with the lysosome, a phagolysosome (secondary lysosome) is formed, which, with the help of acid hydrolases, performs intracellular digestion. At the time of phagocytosis, the activity of lysosomal proteolytic enzymes sharply increases, especially acid phosphatase, collagenase, cathepsins, arylsulfatase A and B, etc. Thanks to the same enzymes, dead tissues are split; removal of decay products from V.'s focus occurs by phagocytosis.

With the help of the phenomena of pinocytosis, liquid droplets and macromolecules are absorbed, for example, ferritin, protein, antigen (see Pinocytosis). Nossel (G. Nossal, 1966) showed that the Salmonella antigen labeled radioactive iodine and introduced into the body of a rabbit, is absorbed by macrophages in the order of micropinocytosis. Antigen molecules in the macrophage cytoplasm are exposed to lysosomal hydrolases, which leads to the release of antigenic determinants. The latter are complexed with macrophage RNA, and then information about the antigen is transmitted to lymphocytes, which are transformed into plasma cells that form antibodies. So, intracellular digestion of antigen comes to the end with immunogenic process (see. Immunomorphology ), and protective and immunogenic function of inflammatory reaction is carried out, in the course a cut there is a cellular and humoral immunity.

However, along with complete phagocytosis in macrophages, for example, with certain infections, phagocytosis is incomplete, or endocytobiosis, when phagocytosed bacteria or viruses are not completely digested, and sometimes even begin to multiply in the cytoplasm of the cell. Endocytobiosis is explained by the lack or even absence of antibacterial cationic proteins in macrophage lysosomes, which reduces the digestive capacity of lysosomal enzymes.

As a result of changes in microcirculation, an increase in vascular permeability and the subsequent exudation of plasma proteins, water, salts and emigration of blood cells, a cloudy, protein-rich (from 3 to 8%) liquid is formed in the tissues - exudate (see). Exudate can accumulate in the serous cavities, between the fibrous structures of the stroma of the organ, in the subcutaneous tissue, which leads to an increase in the volume of the inflamed tissue. The exudate consists of a liquid part and a cell mass, contains tissue decay products. The nature of the exudate is not homogeneous: with a small degree of vascular permeability, albumins predominate in the exudate, few cells, with significant permeability - globulin, fibrin, many cells.

The dynamics of cellular changes in the exudate shows that under the influence of treatment, the number of neutrophils initially decreases, and the number of monocytes increases, and a large number of macrophages appear. The change in the exudate of segmented granulocytes to agranulocytes is considered a favorable prognostic sign.

Proliferation (multiplication) of cells is the final, reparative phase B. Reproduction of cells occurs hl. arr. due to mesenchymal elements of the stroma, as well as elements of the parenchyma of organs. Connective tissue stem cells multiply - polyblasts, or lymphoid cells, adventitial and endothelial cells of small vessels, reticular cells of lymph nodes, small and large lymphoblasts (see Granulation tissue, Connective tissue). With their differentiation, mature and specialized cells appear in V.'s focus: fibroblasts, fibrocytes, mast and plasma cells, to-rye differentiate from their predecessors - plasmablasts and large and small lymphocytes; new capillaries appear. With proliferation (see), exudation of neutrophilic, eosinophilic, basophilic leukocytes and lymphocytes, etc. is also observed; in this regard, lymphoid, plasma cell, eosinophilic and other infiltrates are distinguished.

Cellular elements in the inflammatory focus undergo transformation processes. Segmentonuclear granulocytes that have completed their phagocytic function die rather quickly. Lymphocytes partly die, partly transform into plasma cells, which gradually die, leaving the product of their secretion - hyaline balls. Mast cells die, blood monocytes that have entered the tissues become macrophages, clearing V.'s focus of cellular detritus, and are carried away by the lymph flow to regional lymph nodes, where they also die. The most persistent cellular forms in the inflammatory focus are polyblasts and the products of their differentiation - epithelioid cells, fibroblasts and fibrocytes. Occasionally, multinucleated giant cells appear, arising from epithelioid and proliferating endothelial cells. With the participation of fibroblasts, there is an active synthesis of collagen. The cytoplasm of fibroblasts becomes pyroninophilic, that is, it is enriched with ribonucleoproteins that form a matrix for collagen. V. ends with the formation of mature fibrous connective tissue.

The exchange disturbances arising in V.'s center, according to Lindner (J. Lindner, 1966), can be subdivided into catabolic and anabolic processes.

Catabolic processes are manifested by violations of fiziol, the balance of the main substance of the connective tissue: there are processes of depolymerization of protein-mucopolysaccharide complexes, the formation of decay products, the appearance of free amino acids, uronic acids (which leads to acidosis), amino sugars, polypeptides, low molecular weight polysaccharides. Such disorganization of the interstitial substance enhances vascular tissue permeability, exudation; this is accompanied by the deposition of blood proteins, including fibrinogen, between collagen fibrils and protofibrils, which, in turn, contributes to a change in the properties of collagens.

Protective reactions of the body are largely determined by anabolic processes and their degree of intensity. These processes in V. are expressed by an increase in the synthesis of RNA and DNA, the synthesis of the main intermediate substance and cellular enzymes, including hydrolytic ones. Histochem. studies conducted by Lindner on the study of enzymes in cells in the focus of V. showed that a particularly large enzymatic activity from the moment V. appears in the focus, monocytes, macrophages, giant cells, and segmented granulocytes show. The activity of hydrolases enzymes, which are markers of lysosomes, increases, which suggests an increase in the activity of lysosomes in focus B. In fibroblasts and granulocytes, the activity of redox enzymes increases, thereby enhancing the associated process of tissue respiration and oxidative phosphorylation.

The early appearance of cells rich in hydrolases (lysosomes), and primarily segmented granulocytes, can be considered as one of the manifestations of catabolic processes due to the need for increased processing of decay products; however, it promotes anabolic processes.

Regulatory factors and course

V. is considered as a local tissue reaction, however, its occurrence and course are largely determined by the general state of the organism. The general principle of self-regulation with information feedback is already presented at the cell level. However, adaptive reactions within the cell have independent significance as long as functional systems of the whole organism, reflecting a complex complex of self-regulation of cells and organs, retain their relatively stable state. When this state is disturbed, adaptive and compensatory mechanisms are activated, representing complex neurohumoral reactions. This should be kept in mind when analyzing the local features of the development of the B.

Both hormonal and nervous factors can influence V.'s character. Nek-ry hormones, hl are of great importance for inflammatory reaction. arr. hormones of the adrenal cortex and pituitary gland, which was convincingly shown in the experiment and in the clinic by the Canadian pathologist G. Selye. It has been established that the pituitary somatotropic hormone deoxycorticosterone acetate and aldosterone are able to increase the inflammatory "potential" of the body, i.e., strengthen V., although they cannot cause it by themselves. Mineralocorticoids, affecting the electrolyte composition of tissues, have a pro-inflammatory effect (activate V.). Along with this, glucocorticoids (hydrocortisone and others), adrenocorticotropic hormone, without bactericidal properties, have an anti-inflammatory effect, reducing the inflammatory response. Cortisone, delaying the development of the earliest signs of V. (hyperemia, exudation, cell emigration), prevents the occurrence of edema; This property of cortisone is widely used in practical medicine. Cortisone deprives the connective tissue of precursors of mast cells (large lymphocytes and polyblasts), in connection with this, the connective tissue is depleted of mast cells. It is possible that the anti-inflammatory effect of cortisone is based on this, because in the absence of mast cells, the activity of triggering factors of B., for example, histamine, which is formed from mast cell granules, is significantly reduced.

The influence of nervous factors on V. has not been studied enough. However, it is known that in case of violation of peripheral innervation, especially sensitive, V. becomes sluggish, protracted. For example, trophic ulcers of the extremities that occur when the spinal cord or sciatic nerve are injured take a very long time to heal. This is due to the fact that in tissues devoid of sensitive innervation, metabolic processes are disturbed, alterative changes intensify, vascular permeability increases and edema increases.

Wedge, V.'s current depends on set of factors. The state of reactive readiness of the organism, the degree of its sensitization, is of particular importance for V.'s course. In some cases, especially with hypersensitivity, V. is acute, in others it takes a protracted course, acquiring the character of subacute or chronic. An undulating course of V. is also observed, when periods of the process's remission alternate with exacerbations; outbreaks of the inflammatory process are possible over a number of years, for example, with brucellosis, tuberculosis, collagen diseases. In these cases, during the course of the disease, the period (phase) of immediate-type hypersensitivity is replaced by a period of delayed-type hypersensitivity. Exudative and even necrotic changes predominate in the phases of hypersensitivity with a pronounced reaction of the microcirculation system. In process of V.'s remission or transition of process to a subacute form the vascular phenomena subside and the proliferation phenomena dominating at hron come to the fore. B. At hron, abscess, for example, along with formation of pus there are the expressed proliferative phenomena up to development of mature connecting fabric. At the same time, proliferative nodules with a very mild vascular-exudative reaction occur primarily in certain infectious diseases with an acute course (typhoid and typhus, malaria, tularemia).

At hron, an inflammation with a wavy current a wedge, a picture can be very motley depending on predominance of this or that phase of V., and in fabrics both old, and fresh morfol, changes are possible.

Main clinical signs

Five classical a wedge, the signs characteristic of acute V. of external covers keep the value, having passed test of time and having received modern patofiziol. and morfol, characteristic: redness, swelling, pain, fever, dysfunction. At hron. V. and V. of internals nek-ry from these signs can be absent.

Redness- a very bright wedge, a sign of V., caused by inflammatory hyperemia, expansion of arterioles, venules, capillaries, slowing down of blood flow; as the blood flow slows down, the scarlet-red color of the inflamed tissue becomes cyanotic. Inflammatory hyperemia is combined with tissue alteration, increased vascular tissue permeability, exudation and cell proliferation, i.e. with the whole complex of tissue changes characteristic of B.

Swelling with V. it is caused in the initial period by the consequences of a vascular reaction and the formation of an infiltrate and perifocal edema, which develops especially easily around the center of V., surrounded by loose tissue; in the later periods of V., proliferation also matters.

Pain- a constant companion of V., resulting from exudate irritation of the endings of sensory nerves or some physiologically active substances, for example, kinins.

Temperature rise develops with an increased inflow of arterial blood, as well as as a result of an increase in metabolism in the focus B.

Impaired function on the basis of V. arises, as a rule, always; sometimes this may be limited to a disorder of the functions of the affected tissue, but more often the whole organism suffers, especially when V. occurs in the vital organs.

The main forms of inflammation

On morfol, to signs distinguish three forms of V.: alternative, exudative, productive (proliferative).

Alterative inflammation

Alterative inflammation is characterized by a predominance of tissue damage, although exudation and proliferation also occur. This type of V. is also called parenchymal, since it is observed most often in parenchymal organs (myocardium, liver, kidneys, skeletal muscles).

Alteration is expressed by various types of dystrophy of the cells of the parenchyma of the organ and stroma, ranging from cloudy swelling of the cytoplasm and ending with necrobiotic and necrotic changes, which can occur in the parenchyma of the organ and in the interstitial tissue in the form of fibrinoid swelling and fibrinoid necrosis.

Alternative V. with a predominance of necrobiotic changes is called necrotic V. This type of V. is observed during an allergic reaction of an immediate type (see Allergy), as well as when exposed to highly toxic substances. When exposed to the body of toxins of bacteria, for example, diphtheria, there is an alternative V. of the myocardium, a cut is expressed by the appearance in various layers of the myocardium, especially in the subendocardial zone, foci of fatty degeneration, clumpy disintegration of myofibrils up to the occurrence in severe cases of foci of necrosis; the same is observed in allergic myocarditis (tsvetn. fig. 1). Vascular-mesenchymal and proliferative reactions are weakly expressed.

In the liver, alternative V. is observed with infectious hepatitis, when exposed to, for example, chloroform, carbon tetrachloride and is expressed by cloudy swelling and fatty degeneration of hepatocytes, an increase in their size and the size of the liver as a whole.

In the kidney, alternative V. is expressed by granular degeneration of the epithelium of the proximal and distal parts of the nephron up to epithelial necrosis with a mild vascular-mesenchymal reaction.

The outcomes of alternative V. are determined by the intensity and depth of tissue damage. With a mild degree of dystrophy, after the elimination of the cause that caused V., complete tissue restoration occurs; areas of irreversible damage to the parenchyma are replaced by connective tissue (for example, cardiosclerosis develops after diphtheria myocarditis).

Exudative inflammation

The exudative inflammation is characterized by dominance of reaction of system of microcirculation, hl. arr. its venular department, over the processes of alteration and proliferation. The exudation of the liquid parts of the plasma, the emigration of blood cells, i.e., the formation of exudate, comes to the fore. For exudative V., a variety of morfol, and a wedge, manifestations are typical, since, depending on the degree of violation of vascular permeability, the nature of the exudate may be different. In this regard, exudative V. can be serous, catarrhal, fibrinous (croupous and diphtheritic), purulent, putrefactive, hemorrhagic, mixed.

Serous inflammation characterized by the accumulation in the tissues, more often in the serous cavities, of a slightly cloudy, almost transparent exudate containing from 3 to 8% of serum protein, and in the sediment - single segmented granulocytes and desquamated cells of the serous membranes.

Serous V. can be caused by thermal (burns), chemical, infectious (especially viruses), endocrine, and allergic agents. This form of V. more often develops in serous cavities (serous pleurisy, peritonitis, pericarditis, arthritis, etc.), less often in parenchymal organs - the myocardium, liver, and kidneys.

Serous V. of the myocardium is expressed by the accumulation of exudate between the bundles of muscle fibers, around the capillaries; in the liver - in the around-sinusoidal spaces (Disse spaces); in the kidneys (with serous glomerulitis) - in the lumen of the glomerular capsule (Shumlyansky-Bowman capsule). AT lung serous exudate accumulates in the lumen of the alveoli (tsvetn. Fig. 2). When the skin burns, serous effusion accumulates under the epidermis, which leads to the formation of large blisters. In the serous membranes, hyperemia is noted, they become dull, lose their characteristic luster.

A serous effusion may occur around the foci of purulent V. (eg, with periostitis of the jaw) or around the tuberculous focus, increasing the area of ​​the lesion, the so-called. perifocal B.

Serous V. usually proceeds sharply. With a large amount of effusion, cardiac activity becomes difficult, respiratory failure occurs, joint mobility is limited, etc.

The outcome of serous V., if it has not turned into purulent or hemorrhagic, is mostly favorable. Serous exudate is easily absorbed and does not leave any traces or a slight thickening of the serous membranes is formed. In the myocardium and liver, small areas of sclerosis may occur due to the proliferation of fibroblasts and the formation of collagen fibers.

catarrh (catarrh) develops on the mucous membranes and is characterized by the formation of a liquid, often transparent exudate with an admixture of a large amount of mucus, to-ruyu secrete mucous glands in an increased amount. The exudate contains leukocytes, lymphocytes, and desquamated epithelial cells and usually runs down the mucosa. These are catarrhal rhinitis, rhinosinusitis, gastritis, enterocolitis. By the nature of the exudate, i.e., by the predominance of certain elements in the exudate, they speak of serous, mucous or purulent catarrhs. Century of a mucous membrane quite often begins with serous catarrh, to-ry passes in mucous, then in purulent.

The reasons are very varied. Of great importance are microbes, thermal and chemical. irritants, etc. Catarrhs ​​can occur when the body's defenses are weakened, when saprophytic bacteria vegetating on the mucous membranes become pathogenic.

Catarrhal V. can proceed acutely and chronically. At acute course the mucous membrane looks full-blooded, swollen, covered with liquid exudate. Acute serous and mucous catarrh lasts two to three weeks and usually passes without leaving any consequences. With purulent catarrh, erosions and ulcers may occur on the mucous membrane. With hron, catarrh, in some cases, the mucous membrane can remain swollen for a long time and become thickened, polyps of various sizes may appear on it (hypertrophic catarrh), in other cases, the mucous membrane becomes very thin (atrophic catarrh).

fibrinous inflammation it is characterized by liquid exudate, in Krom fibrinogen accumulates in a short time, passing into fibrin in contact with damaged tissues, as a result of which the exudate thickens. The etiology of fibrotic V. is diverse: it can be caused by microbes (diphtheria bacillus, dysentery microbes, mycobacterium tuberculosis, etc.), viruses, poisons of endogenous (eg, with uremia) and exogenous (eg, sublimate) origin. Fibrinous V. is localized on the serous and mucous membranes, less often in the depths of the organ. Fibrinous V. usually happens acute, but in nek-ry cases can accept hron, a current or proceed in waves.

Rice. 12. Croupous inflammation of the lung in the stage of gray hepatization.

Fibrin falls on the surface of the serous membranes in the form of villous masses, and on the surface of the mucous membranes - in the form of a continuous film (printing. Fig. 3). In the lumen of the lung alveoli, fibrin falls out in the form of fibrinous plugs, for example, with croupous pneumonia (printing. Fig. 7), as a result of which the lung tissue becomes dense and resembles a liver in its consistency (printing. Fig. 12).

The serous membranes acquire a dull appearance, villous overlays of fibrin are formed on them, soldered to the serous membrane (eg, fibrinous pericarditis - Fig. 2). On the mucous membranes, fibrinous deposits in some cases are located loosely, superficially, easily separated, in others they are tightly soldered to the underlying tissue, which depends on the depth of the damage and on the nature of the epithelium of the mucous membrane. So, the connection of the prismatic epithelium with the underlying tissue is weak and fibrin, even if it has fallen out in the depth of the submucosal layer, forms a loosely sitting film (for example, on the mucous membrane of the stomach, intestines, trachea, bronchi).

Rice. 10. Diphtheritic tonsillitis and croupous tracheitis. The surface of the tonsils and the mucous membrane are covered with membranous overlays.

The squamous epithelium is tightly connected to the underlying connective tissue, and the fibrin film is therefore tightly soldered to the mucous membrane, although fibrin falls out in the surface layer of the squamous epithelium (between cells preserved during damage), which is observed, for example, on the mucous membrane of the tonsils, oral cavity, esophagus. In connection with these features, fibrinous V. (tsvetn. Fig. 10) is divided into diphtheria (tightly sitting films) and croupous (loosely sitting films).

diphtheria B. proceeds more severely: microbes multiply under tightly-fitting films, releasing a large amount of toxin; films can close the airways, for example, with diphtheria of the pharynx, which can cause asphyxia. With croupous V., the films are easily separated, intoxication is less pronounced, but the risk of blockage of the respiratory tract is also not excluded.

Fibrinous V. is one of the severe forms of V.; its prognosis is largely determined by the localization of the process and the depth of tissue damage, and the outcome of fibrinous V. of serous and mucous membranes is different. On the serous membranes, fibrin masses are partially subjected to enzymatic melting, most of them to organizational processes, i.e., germination by young connective tissue from the side of the cambial layers of the visceral and parietal serous membranes, in connection with which connective tissue adhesions (adhesions) are formed, which can disrupt organ function.

On the mucous membranes, fibrinous films are usually rejected due to autolysis (see), which develops around the focus, and demarcation V. In place of the torn off film, a mucosal defect, an ulcer, is formed, the depth of which is determined by the depth of fibrin prolapse. The healing of ulcers sometimes occurs quickly, but in some cases (especially in the large intestine with dysentery) it is delayed for a long time. In the pulmonary alveoli, fibrinous exudate, with a favorable course of croupous pneumonia, undergoes lytic decay and resolves, in rare cases, the exudate germinates with cells of young connective tissue, gradually matures, and fields of sclerosis appear, which is referred to as carnification of the lung.

Purulent inflammation characterized by a liquid exudate containing albumins and globulins, and sometimes fibrin threads; in the sediment - neutrophils, mostly decayed (purulent bodies). Such a product of V. - a turbid liquid with a greenish tinge - is called pus (see). The etiology of purulent V. is diverse: it can be caused by bacteria (staphylococci, streptococci, gonococci, meningococci, less often salmonella typhoid, tuberculosis mycobacteria, etc.), pathogenic fungi, or be aseptic, caused by chemical. substances. Purulent V. can occur in any tissue and organ, serous cavities, in the skin (Fig. 3). Its current can be acute and chronic, in nek-ry cases very heavy.

Morphologically, purulent V. can have two forms - an abscess (see) and phlegmon (see) and be accompanied by histolysis (tissue melting). An abscess may occur primarily (its cavity is formed as a result of tissue melting), as well as by embolism with septicopyemia, for example, focal purulent B. of the myocardium with the formation of an abscess (printing. Fig. 8).

Acute diffuse purulent V. (phlegmon) has a tendency to spread along the interfascial layers, interstitial fissures (tsvetn. Fig. 4); at phlegmon of bodies went. - kish. a path in infiltrate it is a lot of eosinophils (tsvetn. fig. 5).

At hron, V.'s form the purulent center is surrounded by a dense fibrous capsule; in the exudate along with purulent bodies are in a small amount lymphocytes, macrophages and plasma cells. There may be periods of exacerbation of V., the formation of a fistula with the expiration of pus. Accumulation of purulent exudate in nek-ry cavities of an organism is designated as empyema (see).

In the outcome of acute purulent V., in favorable cases, the process is delimited, it is possible to heal even large abscesses by replacing their cavity with granulation tissue, gradually maturing into a scar, which remains at the site of the abscess. Hron, purulent V. can proceed for a very long time and lead to amyloidosis (see). In adverse cases, the purulent focus is not limited, the purulent process passes to the lymph, vessels and veins, which leads to a generalization of the process, sometimes up to sepsis (see).

Putrid inflammation(gangrenous, ichorous) develops as a result of the participation of putrefactive bacteria (pathogenic anaerobes) in one form or another of exudative V.. Putrid V. poses a great danger to the body and can occur in those organs that come into contact with the environment (see Gangrene, Ludwig's angina). Inflamed tissues undergo putrefactive decomposition, acquire a dirty green color, become flabby, as if creeping away with the formation of foul-smelling gases (see Anaerobic infection).

Hemorrhagic inflammation characterized by the presence in the exudate of a different number of erythrocytes. Hemorrhagic character can take any type of V. (serous, fibrinous, purulent), which depends on a high degree of increase in permeability, up to the destruction of microcirculation vessels. This type of V. occurs when exposed to highly virulent microbes; with plague, anthrax, toxic influenza, the hemorrhagic focus of V. resembles a hemorrhage. Hemorrhagic exudate is observed in serous cavities in malignant tumors. This type of V. is a sign of a very serious illness; its outcome depends on the underlying disease.

Mixed forms of inflammation are observed when the body's defenses are weakened, secondary infection, eg. staphylococci. In these cases, purulent or fibrinous can join the serous exudate, then V. is called serous-purulent, serous-fibrinous, etc. Catarrhal exudate can also have a mixed character. A particularly unfavorable prognostic sign is the transformation of serous exudate into hemorrhagic, which always indicates on the attachment of a severe infection or the progression of a malignant tumor.

Productive inflammation

This form is also called proliferative inflammation, since it is characterized by the predominance of reproduction (proliferation) of the cellular elements of the affected tissue. Alteration and exudation are poorly expressed, hardly recognized; segmented granulocytes are rare.

Productive V. can be caused primarily by biol., physical. and chem. factors or observed during the transition of acute V. to chronic.

Productive V. proceeds, as a rule, chronically, but can be acute, for example, granulomatous V. with typhoid and typhus, with vasculitis of various etiologies, etc.

Productive V. is based on the reproduction of young cells of the local connective tissue, as well as cambial cells of the blood capillaries, which form new capillaries during differentiation. All cells multiplying during productive V. have both local, histiogenic, and hematogenous origin. For example, in V.'s focus, one can see large and small lymphocytes, monocytes, as well as a small amount of eosinophils and basophils that have come from the blood stream. As the cells mature, macrophages, fibroblasts, fibrocytes, lymphoid, single plasmatic, and mast cells remain in the V.'s focus. Productive V., as it were, is completed by fibroblasts; they secrete tropocollagen, a collagen precursor of fibrous connective tissue, which remains at the site of the focus of productive B.

The outcomes of productive inflammation are different. Complete resorption of the cellular infiltrate may occur; however, more often at the site of the infiltrate, as a result of the maturation of the mesenchymal cells included in the infiltrate, connective tissue fibers are formed and scars appear.

There are two types of productive V.: nonspecific and specific. With nonspecific productive V., proliferating cells are diffusely located in the inflamed tissue; morfol, there is no specific picture characteristic of the causative agent that caused V.. With specific productive V., the cellular composition of the exudate, the grouping of cells and the cycle of the process are characteristic of the pathogen V. Specific V. for the most part has the character of the so-called. infectious granulomas - nodules consisting of elements of granulation tissue.

Interstitial inflammation, or interstitial, usually has a hron, a course and is characterized by the fact that the inflammatory infiltrate is formed in the stroma of the organ surrounding the vessels (myocardium, liver, kidneys, lungs, striated muscles, uterus, endocrine glands). The infiltrate, consisting of a variety of cells, is located diffusely, capturing the entire organ, or in separate foci mainly around the vessels (tsvetn. Fig. 9). In some cases, any type of cells predominates; sometimes the infiltrate consists of lymphocytes and macrophages and resembles B. on an immune basis. At nek-ry types of interstitial V. the large number of the plasmocytes secreting gamma globulins collects. With the death of plasma cells, the products of their vital activity remain in the tissues in the form of free-lying fuchsinophilic spherical formations - the so-called. hyaline balls or Roussel bodies. In the outcome of interstitial productive V. develops sclerosis (see) or cirrhosis (see).

Formation of granulomas(nodules) occurs as a result of cell proliferation in the interstitial tissue of the organ under the influence of a pathogenic factor. These nodules may be composed of a variety of mesenchymal cells or a single cell type; sometimes they are located in close connection with small vessels and even form in the wall of the artery. The diameter of the granuloma usually does not exceed 1-2 mm, but can reach 2 cm. In the center of the granuloma, cellular or tissue detritus is sometimes found, in Krom it is sometimes possible to identify the causative agent of the disease, and on the periphery of the detritus, lymphoid, epithelioid, and plasma macrophages are located in different proportions. and mast cells, among which multinucleated giant cells can be found. Usually granulomas are poor in capillaries.

Formation in fabrics of granulomas reflects protective and immune processes, to-rye develop at infectious diseases, and to a certain extent determines dynamics immunol, process from the beginning of damage of fabric to the final stage of the disease which is expressed by scarring of granulomas.

The formation of granulomas is observed in a number of acute infectious diseases (typhoid and typhus, tularemia, viral encephalitis, rabies) and certain hron, diseases (rheumatism, brucellosis, mycosis, sarcoidosis, tuberculosis, syphilis, etc.).

At nek-ry hron, infectious diseases granulomas get morfol, a structure and dynamics of development, characteristic of this illness, to a certain extent. In this regard, they are designated as follows: tubercle - with tuberculosis, gumma - with syphilis, leproma - with leprosy, nodules - with glanders and rhinoscleroma. With the listed diseases, V. proceeds in a specific way, that is, it is characteristic only of this disease; in specific B.'s granulomas, the cellular composition is quite similar, the most characteristic are epithelioid and multinucleated giant cells: Pirogov-Langhans cells - in tuberculous granuloma; cells, or balls, Virchow - in leprosy; Mikulich cells - with scleroma, etc.

Rice. 11. Miliary tuberculous granulomas of the lung.

Specificity of granulomas is defined not only by their morfol, a structure (tsvetn. fig. 6), but also features a wedge. currents and pathoanatomical manifestations of V. (tsvetn. fig. 11). In nek-ry cases granulomas at tuberculosis, syphilis and leprosy have so much in common in a structure that without special coloring of the causative agent the diagnosis can be difficult; therefore at morfol, specific V.'s diagnosis the kliniko-anatomical analysis of a disease as a whole is very important.

In typhoid fever, granulomas are formed in group limf, follicles (Peyer's patches), in ileocecal limf, nodes, liver, spleen, bone marrow. They arise from proliferating reticular cells capable of phagocytizing typhoid salmonellae; these nodular accumulations then undergo necrosis. The process of granuloma formation, including scar formation, takes 4-5 weeks. (see Typhoid fever).

Granulomas with typhus occur in c. n. N of page, especially in a medulla oblongata at the level of olives, in close connection with small vessels, in to-rykh productive and destructive endotrombovaskulit, characteristic of a sapropyra, is observed (see. Epidemic typhus). Granulomas similar in structure, but with a less pronounced vascular lesion, occur in c. n. With. with viral encephalitis and rabies.

With rheumatism, granulomas occur in the connective tissue of the myocardium, heart valves, in the periarticular tissue, in the capsule of the tonsils; they are built from large cells with basophilic cytoplasm of the macrophage type, the accumulation of which is considered as a reaction to the processes of disorganization of the connective tissue (see Rheumatism).

At a tularemia the granuloma develops in regional to the center of defeat of skin of limf, nodes. In the center of the granuloma there is a focus of necrosis, along the periphery there is a shaft of epithelioid and lymphoid cells and a large number of segmented granulocytes; sometimes there are multi-nuclear giant cells (see Tularemia).

With brucellosis, granulomas have a different structure. In some cases, in the center of the granuloma and around the circumference, there is an accumulation of epithelioid and giant multinucleated cells, in others, there is necrosis in the center of the granuloma and epithelioid and giant cells along the periphery (see Brucellosis); morfol, the picture is very similar to tuberculous granuloma.

Sarcoidosis is characterized by the formation of granulomas in the lymph nodes, built from epithelioid and giant cells without signs of necrosis in the center (see Sarcoidosis).

When healing granulomas, small, barely noticeable scars form (see Granuloma).

Formation of polyps and genital warts- productive V. of mucous membranes. At the same time, cells of the stroma and prismatic epithelium grow, polyps of inflammatory origin are formed (hypertrophic catarrh); such are, for example, polyposis rhinitis, colitis, etc. On the mucous membranes, on the border of the prismatic and squamous epithelium, for example, in the anus, on the genitals, genital warts are formed from the growths of the squamous epithelium (see Warts). Mucosal discharge irritates and macerates squamous epithelium, in a stroma causes hron. V., a cut stimulates the stroma and epithelium to further growth (see Papilloma, Polyp, polyposis).

The favorable course of V. is determined by the perfection of the processes of phagocytosis, the formation of antibodies, the proliferation of connective tissue cells, and the delimitation inflammatory focus. Such an adequate reaction is characteristic of a healthy organism and is called normergic. However, the development of all components of V., the course and outcome also depend on the state of the organism: on previous diseases, age, metabolic rate, etc.

Wedge, observations show that often the same pathogen in one person does not cause any reaction, and in another - a very violent local and general reaction, sometimes even leading to death.

For example, cases of diphtheria have been described, when one person in a family died from a severe toxic manifestation of the disease, while other family members either did not get sick at all, or their infection manifested itself in an erased form of the disease, although they all had one source of infection.

It has been established that, depending on the reactivity of the organism, V. can be hyperergic, arising in a sensitized organism (see Allergy), or hypoergic, a cut is observed in the presence of immunity to agent V.

There are many observations when V.'s picture does not correspond to the usual, normergic type and depends not so much on the toxicity of the pathogen, but on the inadequately violent reaction of the affected organism, which may be caused by preliminary sensitization (see). This type of V. is called allergic inflammation.

In the experiment, in animals infected with diphtheria bacillus after sensitization with horse serum, the disease proceeds very rapidly and in a peculiar way compared to non-sensitized animals. The fact that such a different from normergic course of the disease is associated with sensitization of the body was noted in the works on anaphylaxis by G. P. Sakharov (1905), on the tuberculin reaction of K. Pirke (1907), in studies on the morphology of allergic reactions by A. I. Abrikosov (1938) and R. Ressle (1935), in the works on the development of V. in ontogenesis by H. N. Sirotinin (1940).

Immune Based Inflammation

The studies of F. Burnet (1962), R. V. Petrov (1968) found that the rate of V. can increase or slow down depending on the state of cellular and humoral immunity, i.e., with an altered reactivity of the body, V. acquires features that distinguish it from normergic B. Thus, the introduction of a protein substance into the body as an antigen leads to the development of hypersensitivity and, with repeated administration of even an insignificant dose of the same substance, an inadequate general or local reaction develops with a pronounced difference from the normergic reaction - a discrepancy between a small dose of the antigen and a very violent reaction of the body (see Anaphylaxis, Arthus phenomenon).

Such a reaction is called hyperergic, V. - hyperergic, or an immediate hypersensitivity reaction: it develops in the tissue 1-2 hours after the re-introduction of the antigen. V.'s reason at hypersensitivity of immediate type are immune complexes, to-rye consist of the antibody circulating in blood on the antigen entered earlier, the antigen again entered into fabric and the activated complement. Kokrin (Ch. Cochrane, 1963) showed that immune complexes have a cytopathic and leukotactic effect: they are fixed in the vessel wall, especially postcapillary venules, damage it, increasing permeability and leukodiapedesis.

With allergic V., which proceeds according to the type of immediate hypersensitivity reaction, the so-called. inflammatory protease (rich in sulfhydryl groups), which sharply increases vascular permeability and stimulates the emigration of segmented granulocytes. With this type of V., both in the experiment and in pathology, a person experiences significant tissue damage, a very pronounced reaction of the microvasculature, abundant emigration of segmented granulocytes, plasma impregnation and fibrinoid necrosis of the walls of small vessels and tissues surrounding the vessels, edema, hemorrhages, i.e. e. develops characteristic picture necrotic V. The immune nature of this V. is confirmed by the detection of immune complexes in the focus, determined by the Koons method (see Immunofluorescence).

Electron microscopy and immunochem. studies of Shirasawa (H. Schirasawa, 1965) show the following sequence of tissue changes in the focus of ischerergic V. of the immediate type: 1) the formation of immune precipitates (antigen-antibody complexes) in the lumen of venules; 2) binding to complement; 3) chemotactic effect of precipitates on segmented granulocytes and their accumulation near veins and capillaries; 4) phagocytosis and digestion of immune complexes by segmented granulocytes with the help of lysosome enzymes; 5) release of lysosomal enzymes and formation of vasoactive substances; 6) damage to the vascular wall by them, followed by hemorrhage, edema and necrosis.

Hyperergic inflammation, i.e., V., proceeding on an immune basis, is observed in patients prone to allergic reactions, nair, with drug intolerance, in the acute phase of the course of collagen diseases, with hay fever, etc.

There is another type of increased sensitivity of the body - delayed-type hypersensitivity; it is based on manifestations of not humoral, but cellular immunity. In this case, a local reaction in the tissues of the sensitized organism occurs 12 or more hours after the repeated administration of the corresponding antigen. Such a reaction is usually observed in children infected with mycobacterium tuberculosis after intradermal administration of tuberculin, therefore, a delayed-type hypersensitivity reaction is also called a tuberculin-type reaction. The main role in the focus of such V. belongs to T-lymphocytes and macrophages. Lymphocytes are representatives of the thymic lymphocyte population, they migrate from the lymphoid organs to the blood and back (recirculating lymphocytes), as if they find an antigen in the tissues and carry out a pathogenic effect on the tissues. Lymphocytes come into contact with macrophages rich in acid phosphatase and, as it were, mutually inform each other about the nature of the antigen. Changes in the microcirculatory bed in the focus of V. with this type of reaction are very weakly expressed, segmented granulocytes are absent, signs of V. are not clearly expressed. Meanwhile, V., which proceeds according to the type of delayed hypersensitivity, is observed in a number of severe autoimmune diseases (in the skin, liver, kidneys, etc.). having poorly expressed wedge, and morfol, dynamics, and comes to an end with a sclerosis.

Quite often gistol, a picture at hron, interstitial V. at the person reminds reaction of the delayed type (predominance in infiltrate of lymphocytes and macrophages); V. takes a protracted course, reflecting the autoimmune processes occurring in the body. The same type of V. is observed during the formation of granulomas. In some cases, granulomas perform the function of macrophages in relation to the antigen, in others, the granuloma is, as it were, intended for resorption of tissue decay products in the focus of immune damage (for example, rheumatic granuloma).

V., developing on an immune basis, can manifest itself in a mixed form, when it is difficult to establish the boundaries between two types of hyperergic V..

Differentiation of inflammation and morphologically similar processes

In the developed form V. does not represent big difficulties for a wedge, and morfol, diagnostics. However only morfol, it is impossible to be limited to criterion at V.'s recognition, especially its separate forms; it is necessary to take into account the whole complex of manifestations, including the wedge, data. In the body, such tissue and vascular-cellular reactions are observed, such as, for example, with delayed-type hypersensitivity, when it is difficult to detect all signs of V. in the tissues: for example, there is no pronounced reaction of microcirculation vessels, there are no segmented granulocytes, or, as is observed in the wall stomach in the midst of digestion, a lot of segmented granulocytes as a manifestation of distributive leukocytosis. It is known that during postpartum involution of the uterus in the glandular organs it is possible to detect infiltrates from lymphoid cells as an expression of metabolic changes. The expressed proliferation of plasmoblasts and plasmocytes in organs of immunogenesis (bone marrow, limf, nodes, spleen, thymus gland) not related to V. is described as an expression of a protective reaction manifested by the production of antibodies. In the peripelvic tissue, foci of extramedullary hematopoiesis are described, resembling an inflammatory infiltrate.

Great difficulties arise in distinguishing between inflammatory and dystrophic processes, inflammatory cell proliferation and non-inflammatory cell proliferation, in particular tumor.

Outcomes and significance of inflammation for the body

V.'s outcomes are different and depend on the cause, the state of the organism and the structure of the organ. The death of vital tissues is possible with the most severe consequences for the body. However, usually the inflamed tissue is gradually delimited from the surrounding healthy tissue, the products of tissue decay undergo enzymatic cleavage and are resorbed by phagocytosis, absorbed by the capillaries of the newly formed lymph. networks. Due to cell proliferation, V.'s focus is gradually replaced by granulation tissue (see). If there was no significant tissue damage, their full recovery may occur. With a significant defect at the site of V.'s focus, a scar is formed as a result of maturation of the granulation tissue (see). In organs and tissues, certain patol, changes (thickening and adhesions of serous membranes, overgrowth of serous cavities, scars in organs) can remain, which in severe cases disrupt the function of a regional organ, sometimes the whole organism. So, for example, a fibrinous effusion on the surface of the serous membranes, in the lumen of the alveoli, can dissolve or, with its significant accumulation, undergoes organization and connective tissue transformation. Diffuse interstitial productive V. usually ends with diffuse sclerosis of the organ (eg, cardiosclerosis). With the healing of a large number of granulomas, for example, in the myocardium with rheumatism, significant fields of cardiosclerosis are formed, which negatively affect the activity of the heart. In cases where the emerging connective tissue shrinks and compresses the parenchyma, the organ is deformed, which is usually accompanied by a restructuring of its structure and regeneration phenomena (see). Such a process is referred to as organ cirrhosis, for example, cirrhosis of the liver, nephrocyrrhosis, pneumocirrhosis.

Inflammation is an important protective and adaptive and, in general biological terms, quite expedient reaction developed in the process of phylogenesis; this reaction gradually became more complicated in the process of evolution of living organisms (see Protective reactions of the body, Adaptive reactions). V. bears protection against influence of a pathogenic factor in the form of a peculiar biol, a barrier that is expressed by the phenomenon of phagocytosis and development of cellular and humoral immunity. However, this reaction is automatic, it is carried out by the mechanisms of self-regulation with the help of reflex and humoral influences. Arising as an adaptive reaction, V. under certain conditions can sometimes acquire a harmful value for the body: with V., tissue damage occurs, in some forms up to necrosis.

Due to the inflammatory reaction, the focus of damage is delimited from the whole organism, the emigration of white blood cells to the focus of V. and phagocytosis, the elimination of harmful principles. The proliferation of lymphocytes and plasma cells contributes to the production of antibodies and an increase in local and general immunity. At the same time, it is well known that the accumulation of exudate in V. can be very dangerous. So, for example, exudate in the alveoli with pneumonia from the very beginning of its occurrence has a harmful effect on the body, because gas exchange is disturbed, the formation of a fibrinous effusion on the mucous membrane of the larynx causes a narrowing of the lumen, irritates the receptors of the larynx, which is accompanied by a spasm of the muscles of the larynx and can lead to asphyxia (see). Phagocytosis may be incomplete: a phagocyte that has absorbed a bacterium but is unable to digest it becomes a carrier of infection throughout the body.

Violations at V. not only local; usually there is also a general reaction of the body, expressed by fever, leukocytosis, accelerated ESR, changes in protein and carbohydrate metabolism, phenomena of general intoxication of the body, which in turn changes the reactivity of the body.

I. I. Mechnikov wrote in 1892: “... the healing power of nature, the main element of which is inflammatory reactions, is not at all an adaptation that has reached perfection. Private illnesses and cases of premature death prove this enough. And further: "This imperfection made necessary the active intervention of a man dissatisfied with the function of his natural healing power." The imperfection of the "healing power" of nature necessitates surgical intervention and the use of therapeutic agents, aimed at strengthening the protective and compensatory reactions of the body and the elimination of V.

Century is the cornerstone of many diseases therefore is one of the most important problems experimental and a wedge, medicine. It is studied at all levels biol, structures, since molecular, subcellular, cellular and finishing with a complete organism. Etiol, factors, biochemical, changes, morphophysiol are investigated. characteristics, reactivity of tissues and the organism as a whole, wedge, picture B. A special section arose in the development of the problem of V. - V. pharmacology - the study of the mechanisms of action of V.'s mediators, with the participation of which various stages of the inflammatory reaction are realized; active anti-inflammatory drugs are being sought that inhibit the release of these mediators, and therefore contribute to the subsidence of B.

Bibliography: Ado A. D. Pathophysiology of phagocytes, M., 1961, bibliogr.; Alekseev O. V. and Chernukh A. M. Neuro-capillary connections in the myocardium of rats, Bull. Experiment, biol, and medical, t. 74, No. 12, p. 96, 1972, bibliogr.; Alpern D. E. Inflammation (Issues of pathogenesis), M., 1959, bibliogr.; Voronin VV Inflammation, Tbilisi, 1959, bibliogr.; Inflammation, immunity and hypersensitivity, trans. from English, ed. G. 3. Moveta, M., 1975; Kongeim I. General pathology, trans. from German, vol. 1, St. Petersburg, 1887; M e n-to in V. Dynamics of inflammation, trans. from English, M., 1948, bibliography; Mechnikov II Essay on the current state of the issue of inflammation, SPb., 1897; he, Lectures on the comparative pathology of inflammation, M., 1947; Paskhina T. S. The role of humoral factors of peptide and protein nature in the regulation of capillary permeability, Vestn. USSR Academy of Medical Sciences, No. 9, p. 21, 1962; Pigarevsky VE Cytochemistry of antibacterial cationic proteins of leukocytes in phagocytosis and inflammation, Arkh. patol., t. 37, No. 9, p. 3, 1975, bibliogr.; Polikar A. Inflammatory reactions and their dynamics, trans. from French, Novosibirsk, 1969, bibliography; Strukov AI Controversial issues in the doctrine of inflammation, Arkh. patol., t. 34, No. 10, p. 73, 1972, bibliogr.; Chernukh A. M. Infectious focus of inflammation, M., 1965, bibliogr.; Chernukh A. M., Alexandrov P. N. and Alekseev O. V. M! microcirculation, M., 1975, bibliogr.; C o t r a n R. S. The fine structure of the microvasculature in relation to normal and altered permeability, in: Physical bases of circulatory transport, ed. by E. B. Reeve a. A. C. Guyton, p. 249, Philadelphia-L., 1967, bibliogr.; H i r s c h J. G. Phagocytosis, Ann. Rev. Microbiol., v. 19, p. 339, 1965, bibliogr.; The inflammatory process, ed. by B. W. Zweifach a. o., v. 1 - 3, N. Y.--L., 1974 ; Mediators of inflammation, ed. by G. Weissmann, N. Y., 1974; M i 1 e s A. A. Large molecular substances as mediators of the inflammatory reaction, Ann. N. Y. Acad. Sc., v. 116, p. 855, 1964; M i 1 es A. A. a. Wilhelm D. L. Globulins affecting capillary permeability, in: Polypeptides which effect smooth muscles a. blood vessels, ed. by M. Schachter, p. 309, Oxford a. o., 1960, bibliogr.; Rocha e Silva M. Chemical mediators of the acute inflammatory reaction, Ann. N. Y. Acad. Sc., v. 116, p. 899, 1964; Selye H. The mast cells, Washington, 1965, bibliogr.; Spector W. G. Activation of a globulin system controlling capillary permeability in inflammation, J. Path. Bact., v. 74, p. 67, 1957, bibliogr.; aka, Substances which affect capillary permeability, Pharmacol. Rev., v. 10, p. 475, 1958, bibliogr.; Spector W. G. a. Willoughby D. A. The inflammatory response, Bact. Rev., v. 27, p. 117.1963; they, The pharmacology of inflammation, L., 1968; Willoughby D. A. a. Walters M. N. The effect of ribonucleic acid (RNA) on vascular permeability and its possible relation to LNPF, J. Path. Bact., v. 90, p. 193, 1965.

A. I. Strukov, A. M. Chernukh.

Instruction

There are 2 types of inflammation: chronic and acute. Acute process develops as a result of the body's reaction to irritation, injury, infection or an allergen. Contributes to chronic inflammation increased load on certain organs, aging of the body, general overload. Inflammation is manifested by pain, fever. The process proceeds in 3 stages. On the 1st, a reaction develops in response to damage. At the same time, adjacent blood vessels expand, and blood flow to the affected area increases. Together with the blood, nutrients and cells of the immune system enter the site of inflammation.

At the 2nd stage, phagocyte cells fight pathogenic microorganisms. They secrete special substances that destroy pathogenic flora, and also produce antioxidants necessary to protect against possible damage by free radicals. In this case, damaged and dead cells of the body are removed. At the 3rd stage, the focus of inflammation is separated from the surrounding tissues. At the same time, mast cells release histamine, which increases the permeability of blood vessels. As a result, the damaged area is cleared of toxins and toxins.

The most noticeable manifestation of the inflammatory process is fever. A rise in temperature occurs when the immune system acts at its limit in response to inflammation. The following symptoms appear: rapid pulse, rapid breathing, increased sweating. At a high temperature, a cascade of reactions occurs in the body aimed at eliminating the causes of its occurrence. This symptom can last up to 3 days. During this period, the body fights infectious pathogens. Elevated temperature leads to the fact that the ability to reproduce bacteria drops sharply, and the number of protective phagocyte cells increases. As a result, they eliminate pathogenic microorganisms.

An increase in temperature is considered an alarming symptom, and the patient does not experience the most pleasant sensations. However, taking antipyretics is still not recommended, as this leads to an interruption of the natural process of fighting infection. In this case, the disease acquires a protracted course and often recurs. Undesirable preparations at temperatures up to 38.5 ° C. The relief of the condition is facilitated by an increase in the amount of fluid consumed, the intake of vitamin C. With a sharp rise in temperature, you should immediately call a doctor.

Any increase in the optimal body temperature in a person without visible signs and reasons serves as a certain protective reaction of the body to infection. A similar affliction may lead to some disease. Often, experts warn that an increase in temperature indicates that the body has entered the fray with the infection, producing interferon and protective antibodies.

Hyperthermia or fever

Thermoregulation of the human body occurs at a special reflex level. The hypothalamus, which belongs to the departments, is responsible for its optimal performance. diencephalon. Its functions also include control of the nervous and endocrine systems. It is in it that the centers are located that regulate the cycle of wakefulness and sleep, the feeling of thirst and hunger, body temperature and a large number of other psychosomatic and physiological processes.

Pyrogens, protein substances, take part in the increase in body temperature. They are both secondary (internal) and primary (external - in the form of microbes, bacteria and toxins). When a focus of the disease appears, external pyrogens force the cells of the body to produce secondary protein substances, which send an impulse to the thermoreceptors of the hypothalamus. In turn, he gradually begins to adjust the temperature of the body for the natural mobilization of its protective functions. Thus, until the hypothalamus regulates the existing disturbed temperature balance, the person suffers from fever.

Also, the temperature without symptoms can be with hyperthermia. This happens when the hypothalamus does not take part in its increase: it does not receive a signal to protect the body from infection. This increase in body temperature often occurs as a result of a violation of the heat transfer process, for example, at certain physical activity.

The main reasons for the rise in temperature

Fever or fever occurs in almost any acute infectious disease. In addition, a similar relapse can be observed during an exacerbation of certain chronic diseases. In the absence of symptoms, a qualified specialist can establish the cause of the elevated body temperature by isolating the pathogen from the blood or the source of infection.

It is much more difficult to identify the cause of elevated body temperature without symptoms if the disease has arisen due to exposure to the body. conditionally pathogenic microbes(microplasma, fungi, bacteria) - against the background of a local or general decrease in the immune system. In this case, a detailed laboratory study of mucus, sputum, bile and silence should be carried out.

Causes of fever without symptoms can be associated with the following diseases:

Cervicitis is an inflammation of the vaginal part of the cervix, which acts as a protective barrier between the body of the uterus and the external environment. Depending on the location, cervicitis can be internal (endocervicitis) or external (exocervicitis). The nature of the course is acute and chronic.

Causes of cervicitis

This disease rarely occurs on its own. Its companions can be any inflammation or infection of the reproductive system. More often, against the background of weakened immunity, they attack the mucous membrane of the cervix. The causative agents of infections can be:
- staphylococcus;
- ;
- chlamydia;
- treponema;
- gonococcus (more often with endocervicitis);
- candida (with exocervicitis);
- ureplasma;
- human papillomavirus.

The causes of cervicitis can be the use of contraceptives, mechanical damage cervix during, abortion or installation, active sex life.

If a woman becomes ill with cervicitis during pregnancy, she must notify her doctor about this. Some drugs that are used in the treatment can affect the development of the embryo.

Signs and symptoms of cervicitis

Obvious signs of cervicitis can occur in the acute course of the disease. These symptoms are:
- slight increase in body temperature;
- purulent, bad vaginal discharge;
- smearing discharge of a dark color;
- hot flashes in the pelvic organs;
- pain in the lumbar region;
- Drawing pain at rest or pain during intercourse;
- burning and itching in the vaginal area;
- Pain when urinating.

Chronic cervicitis does not have such bright severe symptoms, goes unnoticed. A gynecologist can detect and diagnose it with scheduled inspection or dealing with another problem.
As a rule, women of childbearing age are exposed to the disease, less often it occurs during the menopause.
The danger of cervicitis is that the infection can spread very quickly to nearby organs - appendages, peritoneum, bladder.

Before going to the doctor, you need to refrain from sexual intercourse for 1-2 days. Stop taking medications and using suppositories. Genital hygiene should be performed in the evening, on the eve of the appointment, without douching and detergents.

Treatment of cervicitis

Depending on which infection provoked cervicitis, the doctor prescribes a specific treatment. The course of treatment is also prescribed for the sexual partner, even in the absence of symptoms of the disease, after which tests are prescribed.
If left untreated, cervicitis thickens, there is a risk of miscarriage, low birth weight, postpartum maternal infections.

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Bartholinitis symptoms

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Diagnosis of bartholinitis

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The main symptoms of gastritis

You should know that such an ailment is initially asymptomatic. The first signs of such a disease begin to appear when, along with inflammation of the internal surfaces of the stomach, their integrity is violated. A person may experience discomfort in the abdomen after eating. Before eating, spasms in the upper lobe of the epigastrium are often noted. A patient with such an ailment can observe frequent belching and bad breath. Moreover, such symptoms may not be present in a person on an ongoing basis, as a rule, they first appear for a while, and then disappear for a certain period. Therefore, many people who have such an ailment attribute the first signs of gastritis to the usual malaise of the body and are in no hurry to seek help from specialists.

Additional symptoms of gastritis

When the disease progresses to a more serious form, a person may begin to experience nausea and vomiting before and after meals. At the same time, undigested food with a very sour taste will come out at first. Subsequently, along with her, the patient can observe bile and mucus. Along with this, body weight will decrease, frequent and severe dizziness, general weakness and pain in the pit of the stomach, which are acute, will occur. At the same time, there may be cramps in the upper abdomen, which will be quite difficult to relieve with analgesics.

Symptoms of acute gastritis

This form of the disease has the above symptoms, and it also manifests itself with other symptoms. So, the patient may experience diarrhea or severe constipation, persistent migraines, tachycardia, fever, excessive production of saliva, due to a violation of food processing by the body. Also, a person can observe a loss of appetite, belching with fetid discharge, heaviness in the stomach, pulling pain after a meal in the stomach and gurgling in it, flatulence. With this disease, the nails become yellow, brittle and exfoliating, and the hair is faded. There may not be enough hemoglobin in the blood, because of this, you will constantly want to sleep.

Having discovered the symptoms of gastritis, it is necessary to visit a specialist as soon as possible. He will conduct a comprehensive examination and identify at what stage the disease is. Depending on this, a comprehensive and effective treatment will be selected that will ensure a speedy recovery.

Protective and adaptive reaction of the body to the action of a pathogenic stimulus, manifested by the development of changes in blood circulation and an increase in vascular permeability in combination with tissue degeneration and cell proliferation at the site of damage to a tissue or organ.

Symptoms of inflammation are familiar to each of us: there is hardly at least one person who has not had a burn or injury, an infectious disease, he has never rubbed his feet with uncomfortable shoes, has not frozen or dived so that water got into his ears.

Meanwhile, in all these situations, the development of an inflammatory process is possible:

• Inflammation of the eye - if dust gets into it or you catch an infection.
• Inflammation of the appendages threatens women with hypothermia, etc.

What is inflammation? This is a kind of distress signal, a universal reaction of the body to damage or irritation of its tissues. Such a reaction is aimed at neutralizing the negative impact of damaging factors and restoring the normal functioning of the affected organs.

Inflammation is the body's response to damaged or irritated cells. In response to this, he tries to get rid of the consequences of the harmful effects and recover. With inflammation, pain can be very severe, because in this way the body gives a signal of serious ill health. What are possible symptoms inflammation other than pain?

• Redness of the skin (including those caused by dilated capillaries).
• Puffiness, swelling in the disturbing area.
• Local temperature increase (feeling of heat in a sore spot, while it occurs not necessarily with inflammation of the skin, but also with other inflammatory phenomena).

The chain of appearance of symptoms is as follows: first, in the place where damage or irritation of cells occurs, the vessels dilate, due to which the blood flow becomes slower. The damaged area is filled with blood. The temperature in the area of ​​inflammation rises. The walls of the capillaries become more permeable, and through them leukocytes, macrophage cells, and plasma penetrate into the surrounding tissues. There is a local edema and swelling that affect the nerve endings - they are infringed, provoking an attack of inflammatory pain.

In the pathological process of inflammation are involved:

• Special proteins are inflammatory mediators (serotonin and cytokine).
• Macrophages are cells that capture and digest foreign proteins, bacteria, and the body's own dead cells.
• White blood cells (leukocytes) and lymphocytes.
• Cytokines are special molecules that are released to the cell surface, through which interaction with other cells occurs (bradykinin, interleukin-1, anti-inflammatory protein provocateur of tumor decay TNF, kallidin).
• Proteins that affect the process of blood clotting.

Inflammation in adults

inflammation in women

Inflammation in women during pregnancy is associated with a decrease in immunity. What signs indicate pathology?

• Pain of varying intensity.
• Discharge with an unpleasant odor.

It should be remembered that acute inflammation of the genital area can cause irreparable damage to pregnancy:

• It causes anembryony, when an embryo does not form in the fertilized egg.
• May contribute to embryonic death and miscarriage
• Spontaneous abortion or premature birth is possible.
• Another possible complication is infection of the fetus in the womb and even its death.

If a woman has chronic inflammation, it affects the immune system. At the same time, the endometrium tries to reject the embryo, perceiving it as something alien, and even if the embryo manages to gain a foothold, its location close to the cervix has a bad effect on gestation.

Chronic inflammation of the ovaries leads to the formation of adhesions and proliferation of connective tissue, disrupts the functioning of the cilia lining the tubes from the inside, reduces their lumen - all this increases the risk of ectopic pregnancy.

What else is dangerous chronic inflammation of the reproductive sphere? Immune failure contributes to the production of antibodies to their own tissues, and because of this, microthrombosis of the placenta occurs, which leads to its detachment, abnormalities in the development of the fetus, preeclampsia.

How to avoid inflammatory complications during pregnancy?

• Dress warmly, avoid hypothermia.
• Observe personal hygiene, use special intimate cosmetics.
• Do not swim in questionable waters.
• Before the onset of pregnancy, it is necessary to cure the existing inflammation of the reproductive sphere.

Inflammation in breastfeeding mothers

Inflammation in women during breastfeeding is usually associated with stagnation of milk (lactostasis) due to impaired patency of the ducts of the mammary gland. An acute inflammatory process develops in the chest, and if infection with staphylococcus or streptococcus is added to this, infected mastitis is obtained. The situation is aggravated by improper attachment of the baby to the breast and injury to the nipples.

As a rule, inflammation in a woman develops rapidly:

• Suddenly, and to high numbers (39-40 ° C), the body temperature rises, the young mother is in a fever, she has a headache.
• Symptoms of inflammation of the mammary gland appear: severe pain, seals are felt when palpated, the skin becomes hot to the touch, hyperemic (red) areas may appear on it.

Mastitis requires urgent treatment, otherwise there is a risk of starting the disease and even losing part of the breast: difficult cases end with the removal of the affected sector of the mammary gland.

Do I need to stop breastfeeding during treatment? Modern recommendations of doctors boil down to the fact that the ban on HB with mastitis is not justified. On the contrary, a diseased breast requires high-quality emptying, and the baby will do it better than any breast pump or manual pumping. If mastitis has taken a purulent form, before feeding, you need to express milk until the pus ceases to stand out. However, specialist advice is required.

How can a young mother be treated so as not to harm the child? When a slight stagnation appears, it will be useful to apply cool compresses from cabbage and cottage cheese, but alcohol and warming ointments are not recommended. A warm shower can be taken in order to improve milk flow from the breast and empty it as best as possible.

If the temperature continues to rise, and chest pains increase, there is pus, you should immediately consult a doctor. Self-medication is unacceptable. The doctor must prescribe the medicine. In the absence of the effect of antibiotic therapy for two days, surgical assistance is required - puncture and pumping out of pus or removal of the diseased area.

To prevent inflammation of the mammary gland during breastfeeding, you need to observe hygiene, wear comfortable underwear, and prevent stagnation of milk in the chest.

inflammation in men

"Male" inflammation is a delicate topic. It is aggravated by the fact that men do not like to seek help from a doctor, they drag it to the last, and as a result they get an appointment with an already fairly advanced disease. The following inflammatory diseases of the genital area are typical for men:

• Prostatitis (inflammation of the prostate)

The most famous ailment that affects many of the fair sex. Inflammation of the gland occurs due to infection (bacterial, viral, fungal) or stagnation of the prostate secretion or blood in it. Patients are concerned about mild pain and an unpleasant sensation in the perineum, difficulty urinating, discharge from the penis. Prostatitis without proper therapy can lead to male infertility. Treatment consists in prescribing antibiotics, a course of massage, physiotherapy, antispasmodics and drugs to improve the outflow of urine and prostate secretion.

• Balanitis and balanoposthitis

Inflammation of the head and foreskin of the penis. Most often, inflammation develops in a child, especially if he has phimosis, but sometimes the disease occurs in adults. Patients are concerned about itching, redness and swelling of the head, pain, sometimes the lymph nodes in the groin increase. In the absence of proper treatment, the disease can be complicated by narrowing of the urethra, paraphimosis, sclerosing balanitis. The cause of inflammation is a fungus or a pathogenic bacterium, an infection from the urethra. The disease is treated with antibiotics and local antiseptics. If necessary, a surgical operation (circumcision of the foreskin) is performed.

• Urethritis

Inflammation affecting the urethra. It is due to the presence of genital infections. Much less often, an allergy or injury can be the cause. The main symptoms of urethritis are burning in the urethra, pain and pain when trying to urinate, purulent purulent-mucous discharge. The danger of inflammation is that along the ascending path, the infection can reach the prostate, testicles, appendages and even the kidneys, and lead to their diseases. Treatment of urethritis consists in the appointment of antibiotics, immunomodulators, the introduction of drugs into the urethra, with a narrowing of the urethra - expansion through special bougies.

• Inflammation of the testicles and appendages

It is provoked by injuries and infectious diseases (mumps, scarlet fever, influenza), but in most cases the infection comes from other organs. genitourinary system. Inflammation begins with an acute stage, which is characterized by severe pain, an increase in the scrotum and stretching of the skin on it, and a rise in temperature. Perhaps the development of a purulent process and blockage of the ducts, fraught with infertility. If the disease is not treated, after 10-14 days it can go into a chronic stage: the pain will subside, the temperature will subside, but when the testicle is palpated, a painful formation will be felt. Inflammation is treated with antibiotics, bed rest is required with the scrotum in an elevated state. If necessary, a surgical operation is performed (opening the cavity and removing pus, and in severe cases, removing the testicle).

Inflammation in a child

Inflammation in a child during the neonatal period is a dangerous phenomenon, so it should be controlled by a pediatrician. What inflammatory diseases can overtake a baby who has barely been born?

• Dacryocystitis is an inflammation of the lacrimal sac located between the nose and inside corner eyes.

It occurs due to the obstruction of the nasolacrimal canal due to the overgrowth of its lumen with the remains of embryonic tissue. Inflammation in a child is manifested by purulent discharge, aggravated by pressure on the inner corner of the eye, redness, relapses after antibiotics are discontinued.

Treatment consists of two stages: conservative and surgical (used if conservative does not help). A conservative way is to massage the lacrimal sac to improve the outflow and patency of the canal, instillation of antibacterial drops into the eye. In the absence of the effect of such treatment, probing of the canals is done. It is performed by an ophthalmologist local anesthesia. AT tear duct a probe is inserted, and then the lacrimal ducts are washed with an antiseptic. In addition, the baby is assigned eye drops with an antibiotic, which must be instilled for several days after probing. For a complete cure, one procedure is usually enough.

• Inflammation of the ear (otitis) is another scourge of newborns.

There are several reasons for the appearance of otitis media. Babies cry a lot, and mucus forms in the nasopharynx, which can clog the Eustachian tube. In addition, they often regurgitate excess milk after feeding, and this excess also contributes to tube blockage. The anatomical structure of the baby's Eustachian tubes also contributes to the development of inflammation: they are rather narrow and short, and the liquid easily clogs them.

A sign of otitis media in babies is anxiety and crying, refusal to suck, fever. Another symptom: if you press on the tragus, the pain intensifies and the child worries more.

Treatment of ear inflammation in newborns has its own characteristics and should only take place under the supervision of a physician. If the eardrum is not damaged, ear drops and turundas with medicine are allowed. To improve the outflow of fluid and relieve swelling, the baby is prescribed vasoconstrictor drops. Sometimes it is possible to act on the Eustachian tube with the best effect with drops in the nose, and not in the ear.

• Omphalitis (inflammation of the skin and tissue around the navel).

The navel of a newborn, until completely healed, is a large "entrance gate" for infection. Inflammation in this area is quite dangerous, because it can lead to the development of enterocolitis, lymphangitis, peritonitis and other serious complications. The reason for its occurrence is infection due to poor hygiene, intrauterine infection or other diseases of the newborn.

Omphalitis is manifested by fever, restlessness or lethargy, decreased weight gain. Discharge appears from the umbilical wound, the skin around it turns red and becomes hot, and if the vessels are involved in inflammation, red stripes diverge from the navel. Omphalitis can take four forms:

• catarrhal (slight redness, light discharge from the navel),
• purulent (discharge from the wound is purulent, the child has a slightly elevated temperature),
• phlegmonous (at the site of the umbilical wound - an ulcer in which pus accumulates, the baby feels unwell, he has a high body temperature)
• necrotic - the most severe, when tissue necrosis occurs.

Treatment consists in treating the umbilical wound with antiseptics, with a purulent process, antibiotic ointments are used, the wound is drained. The necrotic form is treated by excision of dead tissue. In addition, antibiotics are prescribed in the form of injections, vitamins, and in case of severe intoxication, intravenous injections of glucose.

Symptoms of inflammation

) – dangerous disease, which is an inflammation of the lung tissue. Pneumonia can be caused by bacteria, fungi and viruses. Sometimes it also occurs for other reasons - for example, when blood vessels are clogged with blood clots, the nutrition of the lung is disrupted, and the so-called heart attack-pneumonia occurs. Depending on the prevalence of the process, pneumonia can be focal, segmental, lobar and total (capturing the entire lung). When two lungs are affected, the inflammation is called bilateral, the disease of one lung is called "unilateral pneumonia".

Symptoms of inflammation depend on the form of the disease. Classical bacterial pneumonia manifests itself

• high temperature,
• severe cough with phlegm
• shortness of breath.

There is an atypical course of the disease, when the cough is not strong and dry, and the patient is more worried about general malaise, headache and weakness.

Pneumonia is diagnosed by auscultation and percussion, X-ray chest, sputum analysis, complete blood count and blood gas testing.

Treatment for pneumonia depends on the underlying cause: bacterial form requires the appointment of antibiotics, viral - antiviral agents, fungal - antifungal drugs. Since the causative agent of severe forms of bacterial pneumonia is Haemophilus influenzae and pneumococcus, vaccination is recommended (especially in risk groups - children, the elderly, debilitated people).

Inflammation of the lymph nodes

Inflammation of the lymph nodes is due to a general or local infection, oncological diseases, connective tissue diseases, injuries. Inflamed lymph nodes signal the body's struggle with foreign proteins, bacteria, viruses, and its own altered cells. The increase in size of the nodes means that the immune system has increased the number of lymphocytes produced to destroy proteins, bacteria, viruses and pathological cells.

How does inflammation of the lymph nodes manifest itself? Depending on the cause that caused it, and the severity of the process, patients complain of

• fever and chills,
• headache and fatigue,
• a significant increase in the size of the lymph nodes
• pain in them.

Reddened skin, discomfort when pressed around may indicate that suppuration has begun.

In a child, inflammation of the lymph nodes on the head and neck is often accompanied by a cold.

Treatment of inflammation consists in treating the underlying disease that caused it. If the lymph node is festering, antibiotics are prescribed (a place in the form of ointment dressings and tablets inside), and if there is no effect, it is opened and drained.

Inflammation of the prostate

Inflammation of the prostate, or prostatitis is a common male disease. The reason is infection in the genitals or stagnation in the pelvis, which provokes a sedentary lifestyle, wearing tight underwear, decreased immunity, long sexual abstinence.

Inflammation of the gland is acute, and in the absence of proper treatment, the process becomes chronic. The complaints that the patient makes are usually the following: fever and chills, pain in the lower back, groin, and lower abdomen. Sometimes pain occurs in the anus, perineum and scrotum. Men have difficulty urinating, there are false nocturnal urges to go to the toilet. Inflammation of the prostate gland can lead to male infertility.

It is necessary to treat prostatitis with the help of antipyretic and anti-inflammatory drugs, diuretics, antispasmodics.

Nerve inflammation is a pathology caused by trauma, impaired blood flow, infection, exposure to toxic substances, and metabolic disorders.

Inflammation of the nerve can occur in two forms:

• Neuralgia

Irritation of nerve fibers, due to which the patient has a feeling of pain, tingling and numbness at the site of nerve damage, as well as pressure. The skin in the area of ​​the diseased nerve turns red or, conversely, becomes very pale. The most famous variant of neuralgia is the defeat of the trigeminal nerve, when a person complains of a strong short term pain on one side of the face. The cause of this inflammation is infections, diseases of the sinuses and teeth, individual anatomical features (small openings of the skull through which the nerves pass).

• Neuritis

It is characterized by changes in the nerve itself (sheath, trunk). Symptoms are paralysis, paresis, trophic disorders, changes in sensitivity, if the optic nerves are affected - strabismus, immobility of the eyeball, drooping of the eyelids, loss of vision up to complete blindness.

Treatment of inflammation of the nerves is aimed at the cause that caused it: a bacterial lesion is treated with antibiotics, a viral one - antiviral drugs. If the nerve has become inflamed due to injury, the diseased limb is immobilized. Violation related to insufficient blood supply, requires the appointment of vasodilators. With neuralgia, blockade of the inflamed nerve helps well. In all cases, medications are added to the treatment to reduce swelling and inflammation, painkillers, vitamins of group B. After 12-14 days from the onset of the disease, anticholinesterase drugs and hyaluronidase-based agents are prescribed. A good effect is also given by massage and exercise therapy, physiotherapy (electrophoresis with lidase or novocaine, UHF, pulsed currents, etc.)

Sometimes surgical treatment is used to treat neuritis: decompression, plastic surgery, or suturing of damaged nerves. Neuralgia is treated by cutting the affected nerve endings and decompressing.

Erysipelas

Erysipelas is an infectious disease that causes hemolytic streptococcus. The disease begins with symptoms of intoxication: nausea and vomiting, headache, fever. Later, the skin begins to burn and “pull”, it becomes hot, red spots and swelling appear, with a bullous form - blisters with liquid contents. Lymph nodes enlarge, lymphatic vessels become inflamed.

Treatment of erysipelas consists of taking antibiotics, to which hemolytic streptococcus is sensitive. Additionally, ultraviolet irradiation of the skin and laser therapy can be prescribed.

Inflammation of the gums

Inflammation of the gums occurs in many people. Symptoms of the disease are redness and swelling of the gums, putrid breath, pain and bleeding of the gums. The last sign is hard to miss: as a rule, blood oozes every time you brush your teeth or bite into solid food. The pain is sometimes mistaken by patients for a toothache, but when examined by a periodontist, it turns out that the gum still hurts.

Gum inflammation has three degrees:

• Gingivitis

The mildest form, which is expressed by redness and bleeding of the gums. The cause of inflammation is poor hygiene and the lack of a full chewing load on the teeth. Treatment at this stage consists of proper brushing of the teeth, regular professional care, and exercising the teeth and gums by chewing solid foods.

• Periodontitis

Inflammation of the gums of moderate severity. To the red bleeding gums is added bad smell from the mouth, swelling and pain, pockets appear between the teeth and gums, where the remnants of food are clogged, and pathogenic microbes multiply there. The cause of periodontitis can be improper prosthetics, gastrointestinal diseases and others. common diseases, lack of proper hygiene. Treatment of inflammation, in addition to eliminating the cause of its occurrence, consists in medical procedures: special medications are placed in the periodontal pockets.

• periodontal disease

The third and most severe degree of inflammation. Here, the inflammation affects the tissue of the tooth and the bone underneath, causing the teeth to become loose and then fall out. Treatment of periodontal disease is carried out in different ways: tartar is removed, periodontal pockets are sanitized, injections are made into the gums, splinting is performed (attachment of a loose tooth to stable neighboring teeth).

Doctors call inflammation of the joints (if one joint is affected, it is monoarthritis, if several - polyarthritis). Pathology begins with inflammation of the internal joint bag, and then spreads to the cartilage and bone heads, tendons and ligaments surrounding the joint tissue.

The causes of arthritis are many: it can be injuries, infections, autoimmune diseases, allergies. Symptoms of joint inflammation include:

• Pain of varying intensity.
• Redness and swelling.
• Local increase in temperature in the area of ​​​​the diseased joint.
• An increase in the size of the joint.
• Limited mobility.

Arthritis treatment focuses on addressing the cause of the inflammation. A good effect is given by physiotherapy, intra-articular injections of hormonal drugs, anti-inflammatory therapy.

Inflammation of the appendages is a process that affects the fallopian tubes and ovaries. In medical practice, such inflammation is called salpingo-oophoritis. It occurs when pathogenic microbes enter the tubes and ovaries. Salpingo-oophoritis can be acute or chronic. Patients complain of pain in the lower abdomen and in the groin, aggravated at the end of the chicle before menstruation, discomfort during intercourse and decreased libido, fever (in acute or exacerbation of a chronic process), weakness and fatigue.

Inflammation of the appendages is dangerous because it can lead to female infertility, so women pay close attention to its treatment. Depending on the severity of the process, salpingo-oophoritis is treated with antibiotics, anti-inflammatory drugs, mud applications, physiotherapy (electrophoresis, ozone therapy, etc.). A good effect gives a sanatorium recovery. If the disease is not amenable to therapy and the diagnosis is in doubt, they resort to therapeutic and diagnostic laparoscopy.

Inflammation of the gallbladder

Inflammation of the gallbladder (cholecystitis) can be stoneless and against the background of cholelithiasis. Stagnation of bile due to impaired outflow, trauma to the walls with stones, the formation of bedsores - all this leads to inflammation of the bladder.

The main symptom of cholecystitis is pain of varying intensity. It can be very strong and short-term with biliary colic or weak, aching, but constant. In addition, patients may be concerned

• skin itch,
• feeling of bitterness in the mouth,
• stool disorder.

The best way to get rid of inflammation of the bladder is its surgical removal (in the presence of stones in the gallbladder). Acalculous cholecystitis is treated conservatively. The most sparing method of removal is laparoscopic, it is used during surgery without exacerbation. If the gallbladder needs to be removed in the midst of acute cholecystitis, surgeons prefer laparotomy.

Inflammation of the ovaries

Inflammation of the ovaries is called oophoritis. The cause of the pathological process is the penetration of pathogenic bacteria and microorganisms into the reproductive organs. The course of the disease can be acute, subacute and chronic. In the case of acute inflammation, pain in the lower abdomen, a rise in temperature are disturbing; when palpated, tension and soreness are felt in the lower abdomen. Subacute and chronic inflammation is manifested by aching pain in the groin, menstrual irregularities, and general malaise.

Ophoritis and salpingo-oophoritis are treated in the acute stage mainly with antibiotics, in the subacute stage physiotherapy is added. In a chronic process, the entire arsenal of means is used: antibiotics during an exacerbation, physiotherapy, mud therapy, immunostimulants, spa treatment, vitamins.

Inflammation of the ear (otitis media) can be external, middle and internal. The reason in all three cases is the same - the ingress of microbes or fungus, sometimes - an allergy.

Otitis externa is an inflammatory process in the auricle, the symptoms of which are swelling, itching and liquid discharge. Sometimes external otitis is manifested by an abscess located inside the auricle.

Otitis media is a deep-seated inflammation of the inner ear, which is expressed by tinnitus, vomiting and nausea. Patients feel dizzy, their sense of balance suffers.

The most common type of ear inflammation is otitis media. It begins with tolerable pain, which gradually increases and becomes acute. Sometimes the body temperature rises. Pus accumulated in the ear presses on eardrum, can break through it and go outside - in this case, the patient immediately experiences relief.

Treatment of ear inflammation depends on the form in which it occurs. For the treatment of external otitis, ointments are enough, and if there is an abscess in the auricle, alcohol lotions will help. With otitis media, local anesthetics and antibiotics, turundas with boric alcohol, and vasoconstrictor drops in the nose are prescribed. Inflammation of the inner ear requires the patient to be in the hospital, compliance bed rest, detoxification therapy and prescription of antibiotics.

Inflammation of the ear is considered by many to be a frivolous disease, with which it is not necessary to consult a doctor - and completely in vain. The fact is that improper treatment can lead to sad consequences up to deafness, especially when it comes to internal otitis media. Therefore, it is better to entrust the treatment to a doctor.

skin inflammation

Inflammation of the skin can take many forms:

• Dermatitis of various origins (contact, seborrheic, allergic)
• Purulent inflammation (boils, carbuncles, abscesses)
• Psoriasis
• Eczema
• Erysipelas

Symptoms of the inflammatory process are different: boils, carbuncles and abscesses cause severe pain when pressed, the skin around the center of the formation becomes red and hot. Eczema is characterized by a burning sensation and itching. Dermatitis occurs with the appearance of blisters, swelling, severe redness.

Treatment depends on the type of inflammation. Purulent processes are treated with ointment dressings with an antibiotic, if necessary, the formation is opened surgically. In psoriasis, local treatment is prescribed in the form of ointments, sometimes psychotropic drugs. Allergic dermatitis and eczema are treated sedatives, ointments based on hormones, naftalan, etc.

Inflammation of the eye has several forms, it can be both acute and chronic. What types of inflammatory eye diseases are most common?

• Conjunctivitis

Inflammation of the mucous membrane of the eye (conjunctiva) due to infection or allergy. Conjunctivitis can be acute or chronic. The symptoms of inflammation are quite pronounced - swelling and redness of the conjunctiva, tears, fear of light, reddening of the eye protein, and in the case of a purulent process - discharge of pus from the eye. Conjunctivitis is treated based on its form: bacterial - with antibiotics, viral - with antiviral drops, artificial tears, antiviral tablets. allergic form conjunctivitis requires limiting contact with the allergen and prescribing antihistamine eye drops. If they do not help, hormone-based drops can be used.

• Uveitis

Inflammation of the choroid of the eyes. The most dangerous form is inflammation of the iris and ciliary body of the eye. Uveitis is characterized by photophobia, redness of the eyes, blurred vision. Self-treatment is categorically contraindicated: you need to urgently consult an ophthalmologist, because the disease threatens with complete blindness. Therapy for uveitis consists in the appointment of painkillers and drugs to dilate the pupil (atropine), anti-inflammatory drugs and antibiotics.

• Barley

Acute purulent inflammation of the eye (ciliary follicle or sebaceous gland next to the follicle). It is manifested by redness, pain when pressed, and in the case of a large size of barley - and at rest, swelling. A few days later, a yellow “head” appears, which then opens and pus drains out. In most cases, the culprit is Staphylococcus aureus. To prescribe treatment, you should contact an ophthalmologist. As a rule, ointments or drops with an antibiotic are prescribed, with an increase in temperature, antibiotic tablets are taken orally. Sometimes the formation of an abscess requires the help of a surgeon - he opens it and removes the pus.

• halazion

Chronic inflammatory process affecting the cartilage and sebaceous gland at the edge of the eyelid. It is a formation similar to barley both in appearance and symptoms, but differs from it in a recurrent course. The chalazion is first treated conservatively (with drops, ointments, steroid injections), and if there is no effect, the formation is removed surgically.

Pain with inflammation

Inflammatory pain is the body's distress signal. It is caused by irritation of nerve endings by special substances (inflammatory mediators), irritation of the endings due to edema and swelling, changes in pH and osmotic pressure, imbalance of calcium and potassium ions. However, one is closely related to the other: inflammation increases pain, and pain increases the production of inflammatory mediators.

The nature of pain during inflammation changes over time. If you burn your hand, the pain is unbearable and sharp at first. Over time, it decreases, but at the same time it becomes more common: it can hurt not only at the site of the burn, but also the intact skin around. Why is this happening? The reason is inflammation. The burn provokes the formation of mediators of the inflammatory process, and they contribute to the expansion of capillaries and a more abundant flow of blood, which causes a feeling of warmth and the skin turns red. Due to the excessive release of neurotransmitters, the sensitivity of neurons increases so much that even a simple touch to the skin near the burn causes discomfort. It turns out that pain provokes inflammation, and it causes an increase in pain. a poet for best effect, along with the treatment of the inflammatory process, attention should be paid to high-quality anesthesia.

There are only two causes of inflammation:

• Cell damage.
• Exposure to irritants of any kind.

But the circumstances under which contact with stimuli occurs and cells are damaged are much greater:

• Mechanical injury resulting from impact, friction, compression.
• Thermal or chemical burns.
• Frostbite.
• Electric shock.
• All kinds of microorganisms are pathogens. Depending on the type of microbes, inflammation can occur in different forms. The most acute form is suppuration.

In medicine, there is a classification of inflammation according to the causes of occurrence:

• The infectious-inflammatory process is caused by microbes that have penetrated into the tissues: anaerobic ones provoke putrefactive inflammation, aerobic ones - purulent. infectious inflammation may have an acute or chronic course.
• Toxic inflammation occurs due to damage to the cells of the body by harmful substances.
• The autoimmune process is associated with such a pathology of immunity, in which the body begins to produce antibodies against its own healthy tissues. These antibodies damage tissues and cause inflammation.
• Purulent-septic inflammation
• Paraneoplastic syndrome occurs in cancer patients due to the fact that organs and systems react to the presence of a tumor and its release of biologically active substances. As a result, a person develops symptoms similar to, for example, rheumatic lesions or scleroderma (hardening of connective tissues).
• Traumatic and post-traumatic inflammation - any injury is accompanied by a reaction of the body, manifested by pain, swelling and limitation of the functions of the damaged organ or part of the body. So, inflammation of the joints after a blow or pressure leads to the development of post-traumatic arthritis, which causes severe pain, stiffness, crunching and swelling in the area of ​​damage.

Diagnosis for inflammation

Collection of anamnesis

Diagnostic procedures for suspected inflammation begin with anamnesis. The doctor finds out from the patient all the circumstances under which he had pain, how they developed, what worries him this moment. Examination and history taking is the main means of initial diagnosis of inflammation. As a rule, doctors are interested in:

Anamnesis of a person's life - what chronic diseases does he have, whether there were operations, injuries, in what domestic and social conditions a person lives. Such information is very important - for example, when diagnosing erysipelas, the doctor needs to know whether the patient has had this before, whether he has diabetes, skin fungus or immune disorders.

History of the disease - how it began, how it develops at the moment, whether the person sought medical help, what treatment was prescribed, how it worked. For example, if a patient is concerned about inflammation of the joints, you need to find out what caused it (whether there was an injury or a blow), what it expressed - whether the limb became worse to bend, swollen, reddened, how and how the patient was treated on his own before going to the hospital .

An epidemiological history is important in the diagnosis of an infectious and inflammatory process. The doctor is interested in whether the patient has been in contact with sick infectious diseases, whether there have been trips to epidemiologically disadvantaged countries or regions, and if we are talking about an intestinal infection, what and where he ate.

If we are talking about inflammation in women in the reproductive area, a gynecological history is collected: what diseases and gynecological operations used to be, abortions, the nature of the menstrual cycle, etc.

Family history - the presence of cases of the same disease in blood relatives, whether there are hereditary diseases in the family and how many people they affected. A family history suggests that a person has a particular pathology - for example, if there are cases of celiac disease (genetically determined chronic inflammation of the small intestine with impaired absorption of food) in the family, the likelihood of developing the disease increases.

Allergic history makes it possible to establish the presence of inflammation characteristic of allergies. Interrogating the patient, the doctor finds out whether a person has a reaction to food, plants, medicines, vaccinations, how it manifests itself, what medicines are removed.

A nutritional history is relevant when it comes to inflammation of the gastrointestinal tract, gallbladder and biliary tract. Here the doctor is interested in the regimen and diet of the patient - how many times a day, what food he eats, in what quantity.

Laboratory tests make it possible to determine the presence of inflammation and clarify its nature. What studies are needed to diagnose the inflammatory process?

• Erythrocyte sedimentation rate (ESR)

A universal marker of acute inflammation, in which changes occur in the blood. The procedure for conducting the analysis is as follows: a tube with an anticoagulant is filled with blood, and then it is left vertically for an hour. During this time, the erythrocytes fall to the bottom of the tube, and the plasma remains at the top. The unit of measurement of ESR is millimeters per hour, that is, how many millimeters of a layer of settled erythrocytes formed in one hour at the bottom of the tube. When the blood is changed under the influence of an acute inflammatory process, the globulins and fibrinogens present in its composition envelop the red blood cells, they stick together and fall down. The more acute the inflammation, the more such agglutinated red blood cells settle to the bottom. It turns out that a high ESR indicates the presence of acute inflammation.

By the rate of erythrocyte sedimentation, it is impossible to understand which organ is affected by the pathological process. In addition, ESR is a non-specific analysis: the indicator can increase not only with inflammation (an increased level occurs during pregnancy, anemia, the use of certain drugs, and even against the background of complete health, it is usually higher in women than in men). Sometimes it happens that inflammation occurs without an increase in ESR at all.

Given all this, other laboratory tests are also used for diagnosis in conjunction with the determination of ESR - for example, an analysis is carried out for C-reactive protein.

• C-reactive protein (CRP) indicates the acute phase of inflammation and appears in the blood within a few hours after the onset of the pathological process.

The protein is synthesized by the liver, which receives information about the need to increase its production from macrophages (cells responsible for digesting foreign cells, microbes, toxins, own dead cells). CRP is determined by blood serum. The peculiarity of this protein is a short half-life (from half a day to a day), therefore, by its fluctuations, one can quickly judge the effectiveness of the treatment started: if CRP decreases, then the therapy has the desired effect.

CRP is a more specific analysis than ESR. It does not depend on many indicators. which affect the fluctuation of ESR. In addition, ESR responds to an increase or, conversely, a decrease in the intensity of the inflammatory process much more slowly than CRP.

There are other markers of inflammatory processes, but due to their relatively high cost in mass diagnostics, they are used less frequently:

• Haptoglobin is a plasma protein responsible for the binding of hemoglobin. An increase in its level indicates the presence of acute inflammation.
• Antistreptolysin - indicates a past acute streptococcal infection and the presence of rheumatism or glomerulonephritis.
• Rheumatoid factor is an indicator of rheumatoid arthritis, autoimmune diseases, and chronic inflammation. The analysis shows the presence of immunoglobulin antibodies that destroy tissues.

In addition to specific markers of inflammation, other laboratory tests are also used in the diagnosis:

A general blood test with a leukocyte formula - by changes in the proportions and number of leukocytes of various types, one can judge the presence of an inflammatory process. So, a significant increase in the level of neutrophils indicates acute bacterial inflammation.

Sometimes a biochemical blood test is useful - with some types of inflammation, the main indicators change. For example, with pancreatitis, the level of amylase, lipase, trypsin increases. Sometimes an increase in blood glucose indirectly indicates inflammation of the pancreas.

Urinalysis: the appearance of mucus and leukocytes in it is an indicator of the inflammatory process. If an analysis after scarlet fever shows red blood cells, this may indicate the development of glomerulonephritis, a chronic inflammatory disease of the kidneys.

A coprogram (fecal analysis) helps to diagnose an inflammatory process in the intestine: it is indicated by the presence of mucus, epithelium and undigested food, the presence of leukocytes and iodophilic (iodine-stained) flora.

When it is necessary to determine gynecological inflammation in women, laboratory tests of vaginal secretions and smears from the cervical, urethra and cervix come to the aid of the doctor. Sometimes the endometrium is taken from the uterine cavity. The study helps to determine the presence of an inflammatory process, the presence of pathogenic microflora, infectious agents.

"Male" inflammation (prostatitis, urethritis, balanoposthitis, etc.) helps to determine the bacteriological culture of prostate juice, a smear for genital infections.

To diagnose the inflammatory process in the lungs, a general sputum analysis is used. Quantity, color, appearance, the presence of certain cells and fibers can be judged on the presence of bronchitis, pneumonia, tuberculosis, purulent lesions of the lungs.

By smear and bacteriological culture from the nasopharynx, inflammation in this area can be determined. For example, in frequently ill children, the Epstein-Barr virus, which is responsible for constant colds and the development of infectious mononucleosis, is usually sown. Mononucleosis is accompanied by high fever, damage to the spleen, inflammation and enlargement of the lymph nodes.

To diagnose the inflammatory process, it is useful to conduct instrumental studies. What are the main types of research?

• Radiology (X-ray, CT (MSCT - a type of CT))

One of the most common ways instrumental diagnostics inflammation. What is its advantage? He attracts patients with the absence of pain and speed of execution, and doctors love X-rays, MRI and MSCT for good information content: in a correctly taken picture, you can see the diseased organ, determine how inflamed it is, whether the inflammation has affected the surrounding organs. This method is quite accurate - especially MRI and MSCT, where the image of the internal organs is recorded in layers with a step of several millimeters. With the help of X-ray, MRI and MSCT, inflammation of the pelvic organs, abdominal cavity, chest, limbs, and joints can be diagnosed.

• Endoscopy

Examination of internal organs by means of a special optical instrument(endoscope). Endoscopic examination is good because it allows the doctor to see the surface of organs in multiple magnification, to determine the presence of inflamed areas of the mucosa, and, if necessary, to biopsy the suspicious area. What are the types of endoscopic diagnostics? If pneumonia, tuberculosis or bronchitis is suspected, bronchoscopy is performed, FGDS and colonoscopy are used to diagnose inflammatory diseases of the gastrointestinal tract, cystitis and urethritis can be seen on cystoscopy, and diseases of the female genitalia on hysteroscopy. Laparoscopic endoscopy is used to diagnose inflammation in the abdominal cavity.

• Ultrasound procedure

Modern ultrasound helps to see inflammation of the lymph nodes, joints, gallbladder, changes in the liver, kidneys, suggest inflammatory diseases of the female genital area.

• Functional diagnostics

Allows you to identify a violation in the work of an organ or system. For example, if pneumonia or bronchial asthma is suspected, peak flowmetry (shows the maximum expiratory flow of a person), spirometry (estimates the volume and speed of exhalation) is used.

Treatment of inflammation

For the treatment of inflammation, several groups of medicines are used:

• Antibiotics are prescribed if the bacterial nature of the pathology is proven.

This can be done using a special analysis - seeding with the determination of sensitivity to drugs, when the material is placed in a nutrient medium and wait for the growth of bacteria, and then they check which of the antibiotics kills the grown colonies the fastest. The more accurately and promptly prescribed antibiotics, the greater the chance that the disease will be cured quickly and without consequences. Be sure to require antibiotic therapy for erysipelas of the skin, pneumonia of bacterial origin, advanced inflammation of the ovaries and all diseases in which rapid multiplication of microbes is possible with negative consequences for the patient.

• Non-steroidal anti-inflammatory drugs (NSAIDs) are fever-reducing drugs that have analgesic and anti-inflammatory effects.

They suppress the production of a special cyclooxygenase enzyme, which disrupts the production of prostaglandins (they affect the development of inflammation). NSAIDs are prescribed to reduce the severity of the inflammatory process, anesthetize and reduce the temperature.

• Antihistamines - As the name suggests, they suppress the production of histamine in the body.

Histamine is a substance that regulates the transmission of nerve impulses between cells. It can provoke a spasm of large vessels, expansion and increase in capillary permeability, spasm of smooth muscles, release of adrenaline, increased secretion of digestive enzymes and mucus in the bronchi. Usually, antihistamines are prescribed for allergic inflammation and as a means to relieve symptoms during a cold.

• Hormones are an emergency remedy that is used only for severe inflammation due to the fact that it has contraindications and serious side effects.

The action of hormones is to counteract the production of prostaglandins, block enzymes that destroy cells, reduce the permeability of vascular walls and inhibit the formation of exudate and the growth of connective tissue in the area of ​​inflammation.

Physiotherapy for inflammation

Physical therapy is usually used to treat inflammation in the convalescent stage or chronic disease. Depending on the type of pathology, different types of physiotherapy treatment can be used:

• Electrophoresis (administration of drugs with the help of electric current).
• Pulsed electric current therapy (diadynamic therapy) is used to treat inflammation of the nerve.
• Cryotherapy (cold treatment) - local and general.
• Laser therapy - its effect is based on the beneficial effects of light radiation with one fixed wavelength.
• Ultrasound Therapy– the effect is based on the impact of ultrasound, which accelerates the process of tissue regeneration, dissolves edema, restores nerve conduction, eliminates spasm. Ultrasound therapy has a pronounced anti-inflammatory effect.
• Mud therapy is a method of physiotherapy, which is used mainly for the treatment of gynecological inflammation in women. Muds have a strong anti-inflammatory effect, stimulate the immune system, improve blood flow in the area of ​​application of mud applications.

Depending on the cause of the inflammation, the treatment of the acute form can be surgical or conservative. Conservative therapy consists in the appointment:

• antibiotics.
• Non-steroidal anti-inflammatory drugs.
• If necessary, antihistamines.
• If the inflammation is very active, and other drugs do not help well - a short course of hormones (mainly used in autoimmune and allergic processes).

All forces must be directed to the treatment of the acute stage of inflammation, because:

• It is possible to develop complications that are life-threatening.
• Untimely or poor-quality therapy can lead to the fact that the process becomes chronic, with frequent exacerbations.

Surgical treatment of inflammation is required when it is not possible to cope with a conservative way. This usually happens with acute cholecystitis, gynecological diseases, appendicitis, purulent inflammation of the fiber (phlegmon) and abscesses.

Treatment of chronic inflammation

The causes of inflammation can be different. Sometimes it is provoked by a chronic infection or other chronic diseases. In this case, the inflammation lasts for a long time constantly repeating and escalating. It is treated surgically and conservatively. Conservative treatment includes medication, physiotherapy, exercise therapy, balneological procedures. Surgical methods are used when a more impressive effect is expected from them than from conservative therapy, and a radical cure for the patient. They try to carry out operations outside the stage of exacerbation in order to reduce possible negative consequences.

What types of chronic inflammation are common, and how are they treated?

• Pathologies of the gastrointestinal tract - appendicitis, pancreatitis, colitis, etc.

The method of treatment depends on the specific disease - for example, with pancreatitis, a starvation diet, enzymes, painkillers, antioxidants and toxins are first prescribed, and in the absence of effect, surgical removal of part of the gland is performed. Appendicitis is treated mainly immediately surgically, as patients come with acute pain, and it is necessary to remove the source of inflammation as soon as possible.

• Inflammation of the biliary system (liver, biliary tract and bladder) - most often manifested by cholecystitis.

Acalculous nonpurulent cholecystitis is treated conservatively. In the presence of stones, surgical removal of the gallbladder is often used, and in the acute stage, doctors prefer laparotomy surgery, and in the absence of an exacerbation, a more gentle laparoscopy is possible.

• Chronic inflammation of the eye (eyelid) due to blockage of the sebaceous gland - chalazion.

Treatment begins conservatively, prescribing hormone injections into the chalazion cavity, eye drops, ointments. If this does not help, the formation is removed surgically on an outpatient basis.

• Chronic inflammation of the urinary system (pyelonephritis, cystitis, urethritis)

Requires the appointment of local antiseptics (uroseptics), proper drinking regimen, drugs to improve blood circulation in the kidneys.

• Chronic inflammation of the gynecological sphere

They are treated with an increase in general and local immunity, antibiotics and antimicrobial agents, physiotherapy (ozone therapy and mud therapy help well). If a woman has symptoms of sluggish inflammation of the ovaries, uterus, tubes, but it was not possible to accurately identify the disease using conventional methods, the patient may be prescribed a diagnostic and at the same time therapeutic laparoscopy, during which the diagnosis will become clear and surgical treatment will be performed (dissection of adhesions, resection of the ovaries, restoration patency of pipes).

There are cases when the treatment of inflammation is impossible without surgical intervention. As a rule, the patient is brought to the operating table acute diseases and medical assistance should be provided immediately:

• Acute cholecystitis is an inflammatory process in the gallbladder that affects its walls.

The operation to remove the gallbladder is performed in the presence of stones and the absence of the effect of conservative therapy. Inflammation of the bladder occurs due to a violation of the outflow of bile and infection of it pathogenic bacteria. Untimely treatment of cholecystitis can lead to serious complications when the pathological process captures the surrounding tissue or leads to bladder gangrene. Surgical care is to remove the diseased organ.

• Acute inflammation of the pancreas - acute pancreatitis.

Severe inflammation of the gland can be fatal. Surgical treatment of pancreatitis consists in removing the inflamed tissues of the pancreas if conservative treatment is ineffective.

• Appendicitis

Acute inflammation of the appendix of the caecum, which is currently treated with laparoscopic surgery: the appendix is ​​removed with instruments that are inserted through small punctures, under the control of a video camera.

• Purulent inflammation of the lymph node (lymphadenitis)

It also requires surgical treatment - suppuration is opened, drained, and then antibiotics are prescribed.

• Gynecological diseases: acute purulent inflammation of the appendages, ovaries

The reason for an emergency operation, because the rupture of organs and the spread of a purulent process to the abdominal cavity threatens the life of a woman.

• Purulent diseases of the skin and tissues: boils, abscesses, phlegmon (diffuse inflammation of the fiber without a clear localization).

In this case, the surgeon opens the focus, cleans the cavity of pus, puts drainage, and then the patient is prescribed antibiotic treatment.

• Acute inflammation of the ENT organs: otitis media, sinusitis, ethmoiditis, etc.

The essence of all operations in this case is to ensure the outflow of purulent contents from closed cavities to the outside. So, if a patient has a purulent inflammation of the ear, he is incised with a tympanic membrane. In the case of acute ethmoiditis and the formation of an abscess, cells of the bone lattice are opened, pus is removed.

• Pathology of the oral cavity - this includes the treatment of periodontitis, inflammation of the periosteum, osteomyelitis, inflammation of the salivary glands.

Prevention of inflammation

Prevention of inflammatory diseases can be different:

An increase in general immunity is always necessary, regardless of what kind of inflammation we are talking about. Thanks to a strong immune system, pathogens cannot multiply when they enter the body.

In order not to get pneumonia, it is necessary to treat ARVI in a timely manner, not to overcool, and if a person is at risk for pneumococcal infection and diseases caused by Haemophilus influenzae, he is shown a preventive vaccination. The risk group includes patients with immune diseases, chronic diseases of the lungs and the cardiovascular system, the elderly (especially those who live in boarding schools) and patients in need of hemodialysis.

To prevent inflammation of the skin of various types (erysipelas, boils, abscesses), you need to properly observe personal hygiene: take a shower daily, use pH-neutral detergents. It is very important to avoid the occurrence of wounds, chafing and diaper rash, and if they do appear, the skin should be treated with antiseptics. Sunburns also damage the skin, damaging the upper protective layer and reducing immunity - therefore, they should be treated without fail (panthenol-based preparations help well). Since erysipelas usually occurs against the background of chronic diseases, attention should be paid to their treatment: diabetes mellitus, thrombophlebitis, trophic ulcers, endocrine diseases require close monitoring. To improve blood circulation and lymph flow, it is recommended to undergo massage courses twice a year.

To prevent inflammatory diseases of the gallbladder and biliary tract, you need to follow a reasonable diet with a restriction of animal fats, fried and cold foods, an increase in the proportion of fiber in the diet and fractional meals. Such a diet prevents the formation of stones and the appearance of gallstone disease, which is often the cause of bladder inflammation.

Prevention of acute pancreatitis is to follow the principles healthy eating, giving up bad habits, healthy lifestyle.

To avoid inflammation of the gums and oral cavity, you need to observe hygiene, treat your teeth in a timely manner, use rinses and good toothpastes.

Prevention of appendicitis is based on the fight against stool disorder and other disorders in the digestive tract, preventing infection from entering the body. This can be achieved by proper nutrition with a high content of fiber, the establishment of a diet. Hygiene will also help - washing vegetables, fruits, berries, washing hands thoroughly before eating.

Inflammatory diseases of the female genital area (inflammation of the appendages, ovaries, vagina and cervix) can be avoided if casual sexual intercourse is avoided, infections are protected, abortions are abandoned in favor of civilized contraceptives. In order not to "limp" local immunity, it is important not to overcool. Hygiene is also required - a regular shower, the rejection of daily pads, it is advisable to use detergents for intimate hygiene.

Inflammation of the joints can be avoided if you engage in physical education, monitor your posture, avoid injuries and excessive load, watch your weight.

Since acute inflammation of the lymph nodes usually occurs when they are injured or injured, traumatic situations should be avoided. If the lymph nodes become inflamed due to any chronic infection, you should fight it - after all, as long as it exists, the inflammation will recur.

Inflammation can occur in any organ, and this is not surprising: an inflammatory reaction is a variant of protecting the body from destructive or pathogenic effects on it. The body itself gives a distress signal, which must be responded to in a timely manner, otherwise the untreated disease becomes chronic, and worsens over and over again.

The cause of inflammation can be not only a disease, but also an injury: physical, chemical, temperature. Sometimes even the sun is guilty of malaise - from an excessively long stay under its rays, the skin becomes inflamed and reddens.

Inflammation is treated differently depending on what caused it. Treatment can be surgical (surgery) or conservative (tablets, ointments, physiotherapy, massage, injections). The specific plan of procedures in each case is determined by the doctor, based on the results of the examination. Self-medication for inflammation is not only pointless, but also dangerous - without proper experience and qualifications, it is impossible to accurately diagnose and prescribe competent therapy to oneself. As a result, you waste precious time in vain, and risk getting serious complications. Therefore, you need to remember: any inflammation is a reason for an urgent visit to the doctor!