Gives inflammation. What is inflammation? Causes, symptoms and treatment. Causes and conditions of inflammation

General characteristics of inflammation

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

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

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

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

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

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

2 Causes and conditions of inflammation

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

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

3 Stages and mechanisms of inflammation

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

1) alterations,

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

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

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

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

inflammation protective pathogenic

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

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

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

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

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

1. Inflammation-definition of the concept, etiology.

Until now, there is no single idea about the essence of inflammation. Therefore, there is no exhaustive definition of this process yet. Some researchers, giving the definition of inflammation, do not indicate at all which category of biological processes it belongs to [Chernukh AM, 1979; Sarkisov D.S., 1988], others, considering inflammation as an adaptive reaction, nevertheless, emphasize its relative expediency [Strukov A.I., Serov V.V., 1985], others consider inflammation as a pathological reaction associated, before in total, with congenital and acquired defects in leukocytes. There is a point of view according to which inflammation is only a reaction to tissue damage. The most complete definition of the essence of inflammation was given by G.Z. fabrics." Currently, most experts believe that inflammation is a protective, adaptive, homeostatic reaction. Inflammation is the most ancient and complex vascular-mesenchymal response to injury. The biological meaning of inflammation is the elimination or delimitation of the focus of damage and the pathogenic agents that caused it, which, ultimately, is aimed at preserving the species. Inflammation as a medical category is both a manifestation of a disease and a pathological process aimed at eliminating the damaging onset and reparation, i.e. for healing from illness.

2. Morphogenesis and pathogenesis of inflammation.

Inflammation develops in several stages. There are three phases of inflammation: 1) alteration, 2) exudation, 3) proliferation and differentiation of cells.

Damage (alteration) is an essential component of inflammation. This is initially what the vascular-mesenchymal reaction occurs, which is the essence of inflammation. However, the question of whether alteration can be considered a phase of inflammation remains open. Some modern pathologists do not distinguish alteration as such, replacing it with microcirculation disorders and blood rheological properties. Most pathologists advocate the need to identify an alternative phase of inflammation, which characterizes the initial processes (dystrophy, necrosis) and the release of mediators, which has a specific morphological and biochemical expression. It should be noted that the preservation of the alterative phase of the inflammatory response does not justify the identification of an alternative form of inflammation, in which the vascular-mesenchymal reaction to damage itself is practically absent. Therefore, one should agree with the majority of modern pathologists that the recognition of alternative inflammation contradicts the essence of the inflammatory reaction in its modern interpretation.

Damage and mediation are inseparable components of inflammation morphogenesis, since mediators appear in the damage itself. Allocate plasma mediators, represented primarily by the kallikrein-kinin system, the complement system and the blood coagulation system. They also secrete cellular mediators associated with many cells: mastocytes, platelets, basophils, macrophages, lymphocytes, fibroblasts, etc. Products that accumulate in the area of ​​local homeostasis disturbance cause a change in the permeability of the walls of the vessels of the microvasculature in the area of ​​inflammation and entry into this area from blood of cellular elements, primarily various leukocytes, some of which are capable of proliferation. From this moment, the inflammation passes into the exudative stage. It distinguishes two stages - plasmatic exudation and cellular infiltration. Consequently, the stage of exudation involves not only the passive passage of plasma and blood cells through the vascular wall, but also cell infiltration, i.e. active introduction of cells, mainly leukocytes, into altered tissues.

At the beginning stages of exudation a reaction of the microvasculature develops, which is manifested by a reflex spasm, and then by vasodilation. Further, a violation of the rheological properties of the blood develops - neutrophilic leukocytes leave the axial blood flow, collect in the marginal zone and are located along the vessel wall (marginal standing). In the lumen of postcapillaries and venules, stases and microthrombi occur. Under the influence of mediators, the permeability in the vessels of the microvasculature increases, which is manifested primarily by the activation of the endothelium (the appearance of polyribosomes in the cytoplasm, swelling of mitochondria, increased pinocytosis). Due to an increase in vascular permeability, exudation of plasma components develops, and then the emigration of blood cells. In the exudation phase, phagocytosis occurs - absorption by cells (phagocytes) of various bodies, both living and inanimate nature. During inflammation, neutrophils, monocytes and histiocytes mainly become phagocytes. Neutrophils phagocytize small bodies (microorganisms), therefore they are called microphages, and monocytes and histiocytes are large particles, and therefore they are called macrophages. Phagocytosis may be complete or incomplete. With completed phagocytosis, intracellular digestion of absorbed particles is carried out, and with incomplete phagocytosis, microorganisms are not digested by phagocytes and can stay in them for a long time and even multiply. Exudation ends with the formation of exudate and inflammatory cell infiltrate.

Third stage of inflammation called productive or proliferative. Proliferation begins already against the background of the exudative stage. It is characterized by the release of a large number of macrophages into the focus of inflammation, which not only multiply in this zone, but also secrete biologically active substances - monokines, which attract fibroblasts and stimulate their reproduction, as well as activating neoangiogenesis. In the infiltrate, lymphocytes are usually detected, sometimes plasmocytes. However, the cells of the infiltrate are gradually destroyed and fibroblasts begin to predominate in the focus of inflammation. As a result, a young connective tissue is formed - granulation tissue, characterized by a special architectonics of vessels with the formation of capillary loops near the focus of inflammation (Fig. 1).

3. Classification of inflammation.

The classification of inflammation takes into account the nature of the course of the process and morphological forms, depending on the predominance of the exudative or proliferative phase of inflammation.

According to the nature of the course, inflammation is divided into acute, subacute and chronic. Criteria for the allocation of subacute inflammation are very conditional. One speaks of chronic inflammation when the reparative phase fails.

According to the predominance of the inflammation phase, exudative and proliferative (productive) inflammation are distinguished. The failure to isolate an alternative form of inflammation has already been mentioned. The division of inflammation into banal and specific is not justified, since any form of inflammation that develops as a result of exposure to one or another damaging agent can be called specific.

4. Exudative inflammation.

Exudative inflammation is characterized by the predominance of the exudative phase. Depending on the degree of damage to the walls of capillaries and venules and the intensity of the action of mediators, the nature of the resulting exudate may be different. With mild damage to the vessels, only low molecular weight albumins seep into the focus of inflammation, with more severe damage, large molecular globulins appear in the exudate and, finally, the largest molecules of fibrinogen, which turn into tissues into fibrin. The composition of the exudate also includes blood cells emigrating through the vascular wall, as well as cellular elements of damaged tissue. Thus, the composition of the exudate may be different. The classification takes into account two factors: the nature of the exudate and the localization of the process. Depending on the nature of the exudate, there are: serous, fibrinous, purulent, putrefactive, hemorrhagic, mixed inflammation. The peculiarity of the localization of the process on the mucous membranes determines the development of one type of exudative inflammation - catarrhal.

Types of exudative inflammation.

Serous inflammation(Fig.2). It is characterized by the formation of exudate containing up to 2% protein, single polymorphonuclear leukocytes and desquamated epithelial cells. Serous inflammation develops most often in the serous cavities, mucous membranes, pia mater and skin.

Causes of serous inflammation: infectious agents, thermal and physical factors, autointoxication. For example: serous inflammation in the skin with the formation of vesicles caused by the herpes simplex virus. Thermal burns are characterized by the formation of blisters in the skin filled with serous exudate.

Morphologically, during inflammation of the serous membranes, a cloudy liquid accumulates in the serous cavities, poor in cellular elements, among which desquamated mesothelial cells and single leukocytes predominate. The same picture is observed in the soft meninges, which become thickened, swollen. In the liver, serous exudate accumulates perisinusoidally, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule. Serous inflammation of the skin is characterized by the accumulation of effusion in the thickness of the epidermis, sometimes the exudate accumulates under the epidermis, exfoliating it from the dermis with the formation of blisters. With serous inflammation, vascular plethora is observed.

The outcome of serous inflammation is usually favorable. The exudate is well absorbed.

fibrinous inflammation. It is characterized by an exudate rich in fibrinogen, which is converted into fibrin in tissues. In addition to fibrin, exudate also contains polymorphonuclear leukocytes and fragments of necrotic tissues. Fibrinous inflammation is more often localized on the serous and mucous membranes.

The causes of fibrinous inflammation are bacteria, viruses, chemicals of exogenous and endogenous origin. Of the bacterial agents, the development of fibrinous inflammation is most typical for diphtheria corynebacterium, shigella, mycobacterium tuberculosis. It can also be caused by pneumococci, streptococci and staphylococci, some viruses. Typical development of fibrinous inflammation in uremia. The development of fibrinous inflammation is determined by a sharp increase in vascular permeability, which may be due to both the characteristics of bacterial toxins (for example, the vasoparalytic effect of diphtheria corynebacterium exotoxin) and the hyperergic reaction of the body.

Morphologically, a grayish film appears on the surface of the mucous or serous membrane. Depending on the type of epithelium and the depth of necrosis, the film can be loosely or firmly connected to the underlying tissues, in connection with which two types of fibrinous inflammation are distinguished: croupous and diphtheritic.

Croupous inflammation often develops on a single-layer epithelium of the mucous or serous membrane. At the same time, the fibrinous film is thin and easily removed. When such a film is separated, surface defects are formed. The mucous membrane is swollen, dull. The serous membrane is dull, covered with gray fibrin filaments resembling hair. For example, fibrinous inflammation of the pericardium is called "hairy heart" (Fig. 3, 4). Fibrinous inflammation in the lung with the formation of exudate in the alveoli of the lobe of the lung is called croupous pneumonia.

Diphtheritic inflammation develops in organs covered with stratified squamous epithelium or a single-layer epithelium with a loose connective tissue base, which contributes to the development of deep tissue necrosis. In such cases, the fibrinous film is thick, difficult to remove, and when it is rejected, a deep tissue defect occurs. Diphtheritic inflammation occurs in the pharynx, on the mucous membrane of the uterus, vagina, bladder, intestines.

The outcome of fibrinous inflammation on the mucous and serous membranes is different. On the mucous membranes, fibrin films are rejected with the formation of ulcers - superficial with lobar inflammation and deep with diphtheria. Superficial ulcers usually regenerate completely, while deep ulcers heal with scarring. In the lung with croupous pneumonia, the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils, connective tissue (carnification) appears at the site of the exudate, with excessive activity of neutrophils, an abscess and gangrene of the lung may develop. On serous membranes, fibrinous exudate may melt, but more often it undergoes organization with the formation of adhesions between serous sheets.

Purulent inflammation(Fig.5, 6). It develops with the predominance of neutrophils in the exudate. Pus is a thick mass of yellow-green color.

Purulent exudate is rich in proteins. Neutrophils die 8-12 hours after entering the focus of inflammation, such decaying cells are called purulent bodies. In addition, the exudate contains lymphocytes, macrophages, elements of destroyed tissues, as well as colonies of microbes. Purulent exudate contains a large number of enzymes, primarily neutral proteinases, released from the lysosomes of decaying neutrophils. Neutrophil proteinases cause the melting of the body's own tissues, increase vascular permeability, promote the formation of chemotactic substances and enhance phagocytosis. Pus has bactericidal properties. Non-enzymatic cationic proteins contained in specific granules of neutrophils are adsorbed on the membrane of a microbial cell, resulting in the death of the microorganism, which is then lysed by lysosomal proteinases.

The causes of purulent inflammation are microbes (staphylococci, streptococci, gonococci, meningococci, Frenkel's diplococcus, etc.). Aseptic purulent inflammation is possible when certain chemical agents (turpentine, kerosene) enter the tissues.

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

Abscess - focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus (Fig. 7, 8).

A shaft of granulation tissue is formed around the abscess, through numerous capillaries, through which leukocytes enter the abscess cavity and partially remove decay products. The pus-producing abscess is called the pyogenic membrane. . With a long course of inflammation (chronic abscess), the granulation tissue that forms the pyogenic membrane matures, and two layers are formed: the inner one, consisting of granulation tissue, and the outer one, represented by mature fibrous connective tissue (Fig. 9).

Phlegmon is a diffuse purulent inflammation, in which purulent exudate diffusely spreads into tissues, exfoliating and melting tissue elements. Usually, phlegmon develops in tissues where there are conditions for easy spread of pus - in fatty tissue, in the area of ​​\u200b\u200btendons, fascia, along the neurovascular bundles. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, an important role is played by the pathogenicity of the pathogen and the state of the body's defense systems. There are soft and hard phlegmon. Soft phlegmon is characterized by the absence of visible foci of necrosis in the tissues, with hard phlegmon, foci of necrosis are formed in the tissues, which do not undergo melting, but are gradually rejected.

Empyema is a purulent inflammation of hollow organs or body cavities with accumulation of pus in them. In body cavities, empyema can form in the presence of purulent foci in neighboring organs (for example, pleural empyema with lung abscess). Empyema of hollow organs develops when there is a violation of the outflow of pus during purulent inflammation (empyema of the gallbladder, appendix).

A purulent wound occurs when a traumatic wound suppurates or as a result of opening a focus of purulent inflammation into the external environment and the formation of a wound surface.

The course of purulent inflammation is acute and chronic.

Outcomes and complications of purulent inflammation. An abscess usually ends with spontaneous emptying of pus into the external environment or into adjacent cavities. If the communication of the abscess with the cavity is insufficient and its walls do not collapse, a fistula is formed - a channel lined with granulation tissue or epithelium, connecting the abscess cavity with a hollow organ or body surface. In some cases, pus spreads under the influence of gravity along the muscle-tendon sheaths, neurovascular bundles, fatty layers to the underlying sections and forms clusters there (swelling) . Such accumulations of pus are usually not accompanied by noticeable hyperemia, a feeling of heat and pain, therefore they are also called cold abscesses. Extensive streaks of pus cause severe intoxication and lead to depletion of the body. In chronic purulent inflammation, the cellular composition of exudate and inflammatory infiltrate changes. In pus, along with neutrophilic leukocytes, a relatively large number of lymphocytes and macrophages appear, and infiltration by lymphoid cells predominates in the surrounding tissue.

When the abscess is emptied, its cavity collapses and is filled with granulation tissue, which matures with the formation of a scar. Less often, the abscess becomes encapsulated, the pus thickens and may undergo petrification. With phlegmon, the process is delimited, followed by the formation of a rough scar. With an unfavorable course, purulent inflammation can spread to the blood and lymphatic vessels, while bleeding and generalization of infection with the development of sepsis are possible. With thrombosis of the affected vessels, tissue necrosis may develop. Long-term chronic purulent inflammation is often complicated by secondary amyloidosis.

Putrid inflammation. It develops when putrefactive microorganisms enter the focus of inflammation. Causes - putrefactive inflammation is caused by a group of clostridia, pathogens of anaerobic infection.

Morphological characteristic. Putrefactive inflammation develops most often in wounds with extensive crushing of the tissue, with disturbed blood supply conditions. The resulting inflammation is called anaerobic gangrene. The wound with anaerobic gangrene has a characteristic appearance: its edges are cyanotic, there is a gelatinous swelling of the tissue. Cellulose and pale, sometimes necrotic muscles bulge out of the wound. When feeling in the tissues, crepitus is determined, the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is first determined, which is replaced by widespread necrotic changes. Neutrophils that enter the focus of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign, indicating the attenuation of the process.

The outcome is usually unfavorable, which is associated with the massiveness of the lesion and a decrease in the resistance of the macroorganism.

Hemorrhagic inflammation. It is characterized by the predominance of erythrocytes in the exudate. In the development of this type of inflammation, the main significance belongs to a sharp increase in the permeability of microvessels.

Hemorrhagic inflammation is characteristic of some serious infectious diseases - plague, anthrax, smallpox.

Macroscopically, areas of hemorrhagic inflammation resemble hemorrhages. Microscopically, a large number of erythrocytes, single neutrophils and macrophages are determined in the focus of inflammation. Significant tissue damage is characteristic.

The outcome of hemorrhagic inflammation depends on the cause that caused it, often unfavorable.

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

A change in the composition of the exudate is observed during inflammation: the onset of the inflammatory process is characterized by the formation of serous exudate, later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change in the qualitative composition of leukocytes: neutrophils are the first to appear in the focus of inflammation, they are replaced by monocytes and later by lymphocytes. In addition, when a new infection joins an already ongoing inflammation, the nature of the exudate often changes. For example, when a bacterial infection is attached to a viral respiratory infection, a mixed, more often mucopurulent exudate is formed on the mucous membranes.

The morphological characteristic is determined by a combination of changes characteristic of various types of exudative inflammation.

The outcomes of mixed inflammation are different. In some cases, the development of mixed inflammation indicates a favorable course of the process, in others it indicates the addition of a secondary infection or a decrease in the body's resistance.

Catarrh. It develops on the mucous membranes and is characterized by an abundant release of exudate flowing from the surface of the mucous membrane. A distinctive feature of catarrh is the admixture of mucus to any exudate (serous, purulent, hemorrhagic).

The causes of catarrhal inflammation are diverse: bacterial and viral infections, allergic reactions to infectious and non-infectious agents (allergic rhinitis), the action of chemical and thermal factors, endogenous toxins.

Morphologically, the mucous membrane is edematous, full-blooded, exudate flows from its surface. The nature of the exudate can be different (serous, mucous, purulent), but its essential component is mucus, as a result of which the exudate takes the form of a viscous, viscous mass. Microscopic examination in the exudate determines leukocytes, desquamated cells of the integumentary epithelium and mucous glands; the mucous membrane is edematous, hyperemic, infiltrated with leukocytes, plasma cells.

The course of catarrhal inflammation can be acute and chronic. Acute catarrh is characteristic of acute respiratory viral infections, while there is a change in the types of catarrh: serous catarrh is usually replaced by mucous, then - purulent, less often - purulent-hemorrhagic. Chronic catarrh can occur in both infectious and non-infectious diseases. Chronic inflammation in the mucous membrane is often accompanied by a violation of the regeneration of epithelial cells with the development of atrophy or hypertrophy.

Exodus. Acute catarrh usually ends in recovery. Chronic catarrh leads to atrophy or hypertrophy of the mucous membrane.

Note: the attached file contains the full version of the lecture with pictures.

Inflammation

Inflammation develops in response to injury, infection, or the introduction of some kind of irritant. Most people regard inflammation, which is accompanied by pain, swelling and redness, as a misfortune or a necessary evil. However, inflammation is actually a defensive reaction that the body needs to recover.

The immune system is the main body guard; at the slightest need, she enters the battle. It destroys bacteria and viruses, promotes recovery from injuries and diseases, adequately responds to external influences, and also to such an irritant as important for the human body as food. To all these influences, the immune system responds with a cascade of complex reactions, one of which is inflammation.

Plenty of evidence suggests that our diet has a lot to do with how the immune system functions. For example, a diet high in fruits, vegetables, unsaturated fatty acids, and whole grains is good at controlling inflammation, while a lean diet, based on fast food, meat, and dairy products, in contrast, promotes unwanted inflammatory responses.

Certain foods, particularly strawberries and lentils, have anti-inflammatory effects. Others, such as tomatoes and potatoes, on the contrary, increase the inflammatory response.

Types of inflammation

There are two types of inflammation: acute and chronic. Acute inflammation develops as a response of the body to injury (injury, wound), irritation, infection or allergen (from chemical agents to food). Chronic inflammation is a protracted process. Contribute to it: increased load on certain organs, general overload, as well as aging.

The first signs of acute inflammation are pain, swelling, redness, and heat. This is due to the expansion of blood vessels adjacent to the site of injury, as well as the involvement of soluble immunological factors in the focus that oppose the pathogenic stimulus. This is the initial stage of the healing process. In the event that healing does not occur for some reason, chronic inflammation develops, the cause of which is either hyperstimulation of the immune system, or its overactivity, or its inability to turn off (any combination of these three factors is possible). An example is systemic lupus erythematosus, an autoimmune disease that damages many organs.

Inflammatory process

Inflammation is the most common occurrence. Imagine what happens when we just cut or even pinch a finger: it immediately turns red, swells, we feel pain - in other words, the finger temporarily fails. The same thing happens when any part of the body is damaged, regardless of the location and nature of the damaging or irritating factor.

When this happens, most people rush to take some kind of anti-inflammatory pain reliever. This explains why such commonly available medicines have come out on top in the world in terms of sales. And yet we want to emphasize that inflammation is a positive phenomenon. It indicates that your immune system is functioning normally.

Characterization of the inflammatory response

• Redness
• Swelling
• Rise in temperature (sensation of warming)
• Loss of function

What it is?

Simply put, the suffix "it" (Greek "itis") is used to refer to inflammation in a particular place. For example, "arthritis" means inflammation of the joint ("artro" in Greek means "joint"). "Dermatitis" - inflammation of the skin ("derma" - "skin").

But not only the suffix "it" is used to denote inflammation. Inflammatory reactions are also characteristic of asthma, Crohn's disease (see), psoriasis and other diseases.

So, with signs of inflammation, you should not go into the first-aid kit, but it is better to remember that the inflammatory process reflects the natural reaction of your immune system, which has mobilized to fight the cause that caused it. Give your body freedom, and it will overcome the disease itself!

Three stages of inflammation

The process of inflammation is unusual in that three forces of the body (skin, blood, cells of the immune system) combine their efforts to overcome it and renew damaged tissues. The process proceeds in three stages.

At the first stage, in response to damage, the reaction develops almost instantly. Adjacent blood vessels dilate to increase blood flow to the affected area, and essential nutrients and immune system cells are supplied with the blood.

Inflammation

In the process of phagocytosis, not only bacteria are destroyed. Damaged and dead cells are removed in exactly the same way. And this leads to the third stage, in which the focus of inflammation is isolated from the surrounding tissues. It, as a rule, becomes painful, and may even pulsate, which is why there is a desire to protect this place from any contact. In this case, the so-called mast cells release histamine, which increases the permeability of blood vessels. This allows you to more effectively clean the damaged area from toxins and toxins.

Give me a fever!

The most noticeable manifestation of the inflammatory process is, of course, fever or fever. This occurs when the immune system is pushed to its limits in response to an infection. Many are frightened when a patient develops a high temperature, however, having figured out what is its cause, you can easily overcome your fears. At a high temperature in the body, a whole cascade of reactions begins, aimed at eliminating the causes of fever. These reactions and the causes that cause them are listed on.

As the fever progresses, body temperature rises sharply, peaking at the peak of the fight against infection. At the same time, we may feel trembling and chills, a desire to lie down in bed and wrap ourselves in something warm. The body aches, one does not want to move from weakness, the appetite disappears, all feelings can be dulled, and in general life does not seem to be a joy. The body itself seems to tell us that it needs rest and time to restore strength. These symptoms can last up to 3 days - about the time it takes for the immune system to magically renew the body.

Throughout this period, the body is engaged in a continuous battle with infectious pathogens. At 37 C (normal human body temperature), bacteria live in clover and reproduce perfectly. But at elevated temperatures, bacteria feel uncomfortable, and their ability to reproduce decreases. On the contrary, the number of phagocytic cells increases, they flock to the inflammatory focus from all sides. As the temperature continues to rise, the balance of power is rapidly shifting in favor of the defenders, with fewer bacteria and more and more white blood cells. It becomes clear that a turning point has occurred, and the battle is finally won. The temperature is dropping.

Why heat is good

A feverish state, according to external manifestations, looks rather alarming, and the patient himself experiences far from the most pleasant sensations. In the arsenal of modern doctors there are many antipyretic drugs, however, by abruptly interrupting the fever, we thereby interrupt the natural process of fighting the infection, which leads to the fact that the disease becomes more protracted and often recurs. This is typical, for example, for children's infections of the ear, throat and nose.

Of course, we do not urge you to ignore the high temperature. In adult patients, for example, the temperature often rises to 40 C. If such an increase is short-term, then there is nothing wrong with it, but it is advisable that your doctor be aware of what is happening.

Useful advice. Vitamin C helps to eliminate toxins and reduce fever. Make sure your sick child drinks more diluted orange juice.

Diseases and means of their treatment

Warning

In children, a sharp rise in temperature is observed more often than in adults, and such cases cannot be ignored. If the fever persists, if the child is drowsy, delusional, nauseous, or in pain, you should call a doctor. Especially beware if the child develops skin rashes that do not disappear when pressed against the background of a high temperature - such symptoms are characteristic of meningitis, and the child will need immediate medical attention. With fever, epileptic seizures are possible - then the temperature should be brought down with the help of rubdowns.

Causes of inflammation

An inflammatory reaction can develop under the influence of a wide variety of stimuli: external, metabolic, nutritional, digestive, infectious, or, for example, in response to a drug. Five leading factors take part in the inflammatory process: histamine, kinins, prostaglandins, leukotrienes and complement. Some of them help the body, while others do not bring benefits. Foods that help or counteract these factors are listed.

The body's response to high body temperature

• Reaction
• temperature rise
• Rapid breathing
• Rapid pulse
• sweating
• Meaning
• Reduced activity of bacteria that multiply at normal temperatures.
• Increasing the supply of oxygen to the body.
• Pumping blood to the site of inflammation, delivering more nutrients needed to heal.
• Accelerated removal of toxins and slags through the skin, thermoregulation.

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Inflammation It's an attempt at self-defense. Its purpose is to remove negative factors, including pathogenic cells and irritants, and start the healing process.

When something harmful or irritating enters the body, it happens. Signs and symptoms show that the body is trying to heal itself.

Inflammation does not mean infection, even if infection is the cause. Infection is caused by, or, while inflammation is the body's response to them.

Quick Facts About Inflammation

• Inflammation is the body's attempt at self-defense, eliminating harmful stimuli and starting the regeneration process.
• The process is part of the body's immune response.
• The first stage of inflammation is often referred to as irritation, which then becomes inflammation.
• The process is accompanied by suppuration (excretion of pus). Then comes the granulation stage, the formation of tiny, round masses of tissue in the wounds during healing.
• Acute process - begins quickly and very soon becomes serious.
• Chronic inflammation is long-term inflammation that can last for months or even years.
• Infections, wounds and any tissue damage would never heal without inflammation - the tissue would become more and more damaged and the body (or any organism) would eventually die.
• The chronic process leads to a number of diseases and conditions, including certain types of cancer, rheumatoid arthritis, atherosclerosis, periodontitis, and fever.
• Although scientists know that inflammation plays a key role in heart disease and several other diseases, the immediate cause of inflammation remains a mystery.
• It should be remembered that inflammation is part of the healing process. Therefore, it is not always necessary to stop it.

What is inflammation?

is part of the body's defense response. This is initially useful when, for example, your knee is getting hit and the tissues need care and protection.

However, in some cases the inflammation may progress to become self-perpetuating, resulting in a more severe reaction.

Inflammation Helps Wound Healing

Our immediate response to - . Given that inflammation is an integral part of the body's attempt to heal itself, patients and clinicians need to be confident that treatment to reduce swelling is absolutely necessary and should not undermine or slow down the healing process.

The first stage of inflammation is often called irritation, which then becomes inflammation- direct healing process. Inflammation is accompanied suppuration(discharge of pus). Then comes the stage granulation, the formation in wounds of tiny rounded masses of tissue during healing. Inflammation is part of a complex biological response to noxious stimuli. Without inflammation, infections and wounds would never heal.

Neuroscientists at the Lerner Research Institute at the Cleveland Clinic in Ohio have found that inflammation does help heal damaged muscle tissue. They are researching how athletes with inflammation are treated - medical professionals are always trying to control inflammation to encourage healing.

The researchers say their findings could lead to new treatments for acute muscle injuries caused by freeze damage, drugs, chemicals and trauma.

Inflammation is part of innate immunity

innate immunity is something that is naturally present in the body from birth, and not adaptive immunity, which we get after or. Innate immunity is usually non-specific, while adaptive immunity is specific to a single pathogen:

Pertussis vaccine - an example of immunity specific to a single pathogen

After vaccination against we develop immunity to Bordetella pertussis or , the types of bacteria that cause whooping cough.

This is an example of adaptive immunity - after all, there was no immunity before the vaccine was received. The process is the mechanism of innate immunity.

What is the difference between chronic and acute inflammation?

Acute inflammation- starts suddenly and becomes severe in a short period of time. Symptoms last for several days, in rare cases - up to several weeks.

• Bronchi;
• Skin cuts;
• Appendix;
• Leather;
• palatine tonsils;
• Meninges;
• Frontal sinuses.

chronic inflammation It's a process that can take months or even years.

• Impossibility to eliminate damaging factors;
• A protective response to the antigen itself - the immune system infects its own cells, mistaking them for negative pathogens;
• Weak damaging factor.

• Bronchial asthma;
• Chronic ulcer of the stomach and duodenum;
• Periodontitis;
• Colon ulcer and Crohn's disease;
• Sinusitis;
• Hepatitis.

Infections and any tissue injury would never heal without inflammatory changes - the tissue would become more and more damaged and the organism would eventually die.

However, chronic inflammation can eventually lead to a number of diseases and conditions, including some types, and.

What happens in acute inflammation?

• Arterioles, small branches of arteries that lead to capillaries, dilate, resulting in increased blood flow.
• The capillaries become more permeable so that plasma and blood proteins can move into the spaces between cells.
• Neutrophils and possibly some macrophages migrate out of capillaries and venules (small veins that run from capillaries to veins) and move into the spaces between. The neutrophil is a type of granulocyte (leukocyte) filled with tiny sacs that contain enzymes that digest microorganisms. Macrophages are also white blood cells that engulf foreign material.

are the first line of defense of the human body. They are the main cells that protect us from. Their protective function is positive, however, they also possess, which can eventually lead to various things, such as. Effective manipulation of neutrophils is vital in the fight against inflammatory diseases.

When the skin is scratched, a pale red line can be seen. Soon the area around this scratch will turn red, this is due to the fact that the capillaries have expanded and filled with blood and become more permeable, allowing fluids and blood proteins to move into the space between the tissues.


Edema The area then swells as additional fluid builds up in the interstitium.

• Pain - the area of ​​injury becomes painful, especially when touched. Chemicals that irritate nerve receptors are released, resulting in pain.
• Redness - due to increased blood supply, dilated capillaries and arterioles.
• Immobility - there may be loss of function.
• Swelling - caused by the accumulation of fluid.
• Heat.

Comparison of acute and chronic inflammation

The following lists show the difference between chronic and acute inflammation in relation to pathogens, which include the main cells:

:

• Miscellaneous pathogens - non-degradable pathogens that cause persistent inflammation, infection with certain types of viruses, persistent foreign bodies, overactive immune system responses;
• The main cells involved are macrophages, lymphocytes, plasma cells (these three are mononuclear cells), and fibroblasts;
• Primary mediators - reactive oxygen species, hydrolytic enzymes, IFN- and other cytokines, growth factors;
• Duration - from several months to several years;
• Outcomes - destruction of tissue, thickening and scarring of connective tissue (fibrosis), death of cells or tissues (necrosis).

Why does inflammation cause pain?

Pain- this is a very subjective sign, and the only person who can describe it correctly is the one who feels it.

Pain may or may not It can also be:

nociceptive pain

Specific ones are stimulated to make us feel this type of pain. These receptors sense changes that lead to cell damage. " Nociceptive" means causing or reacting to pain - the cause of pain comes from outside the nervous system, and the nervous system reacts to it.

Somatic pain

This is a type of nociceptive pain. Feels in and on. is. Pain receptors are sensitive to: stretching in the muscles, vibration, temperature, and inflammation. When present, it can be painful.

Somatic pain is sharp and localized - touching or moving the affected area will result in more intense pain.

Visceral pain

This is a type of nociceptive pain. The pain is felt deep in the body, in, such as, and. Nociceptors (pain receptors) sense oxygen starvation ( ischemia), stretching and inflammation. The pain can be described as deep. and are examples of visceral pain.

Inflammation mainly causes pain because the swelling interferes with sensitive nerve endings that send pain signals to the brain. Nerve endings send pain signals to the brain all day long. However, the brain learns to ignore most of them unless the pressure on the nerve endings increases.

During inflammation, other biochemical processes also occur that affect the state of the nerve fibers, causing pain.

The risk of inflammation is much higher if you are obese

Fat men have more inflammatory markers () than men of the same age who are not obese or overweight.

Elevated levels of white blood cells- markers that are associated with an increased risk of developing various diseases, including.

In a recent study, a team at the Pennington Center for Biomedical Research in Baton Rouge, Louisiana, focused on specific types of white blood cells; Neutrophils, lymphocytes, monocytes, basophils and eosinophils.

They measured adult male resting white blood cell levels, as well as their fitness levels and BMIs (body mass indexes), and adjusted the results for age.

• Unhealthy men had higher levels of white blood cells than healthy men.
• In men with a higher BMI, the level of leukocytes is increased.
• The combination of fitness levels and body weight significantly affected white blood cell levels and ultimately inflammation.

Although scientists know that inflammation plays a key role in heart disease and several other diseases, the immediate cause of inflammation remains a mystery.

Inflammation decreases when women lose weight - scientists at the Fred Hutchinson Cancer Research Center in Seattle, Washington found that overweight or obese postmenopausal women who lost 5% or more of their body weight experienced marked drops in levels of inflammatory markers .

Team leader Anne McTiernan, Ph.D., said: "Both obesity and inflammation have been shown to be associated with several types of cancer, and this study shows that if you lose weight, you can also reduce inflammation."

Autoimmune disorders and inflammation

autoimmune reaction, also known as autoimmune disease, is a disease in which the body initiates an immune response against healthy tissues, mistaking them for harmful pathogens or irritants. The immune response also causes an inflammatory response.

• Rheumatoid arthritis- inflammation of the joints, tissues surrounding the joints, and sometimes some other organs in the body;
• Ankylosing spondylitis- there is inflammation of the vertebrae, muscles, ligaments, as well as sacroiliac joints;
• celiac disease- inflammation and destruction of the inner lining of the small intestine;
• Crohn's disease- the gastrointestinal tract becomes inflamed. Inflammation is most common in the small intestine and anywhere in the tract;
• fibromyalgia- often a set of symptoms associated with an autoimmune disease such as lupus or rheumatoid arthritis. Pain in various parts of the body. The location and presence of the process is unclear;
• Graves syndrome- sign of goiter. The thyroid gland becomes inflamed. Exophthalmos. Grave's dermopathy, inflammation of the skin, usually of the lower legs and thighs;
• Idiopathic pulmonary fibrosis The role of inflammation is unclear. Experts used to think that the disease is mainly caused by inflammation in the alveoli (tiny sacs in the lungs). However, treatment to reduce inflammation is often disappointing. Therefore, although there is inflammation, its effect on disease is a mystery;
• Systemic lupus erythematosus- Inflammation may occur in the joints, lungs, heart, kidneys and skin;
• Psoriasis- inflammation of the skin. In some cases, as in psoriatic arthritis, the joints and tissue surrounding the joints may also become inflamed;
• Type 1 diabetes- inflammation in various parts of the body, likely if diabetes is poorly controlled;
• Addison's disease- inflammation of the adrenal glands. The stress on the body caused by this disease can also lead to inflammation elsewhere;
• Vasculitis- refers to a group of diseases in which inflammation eventually destroys blood vessels, both arteries and veins;
• transplant rejection- There is already significant inflammation caused by the graft operation. If the organ recipient's immune system rejects the new organ, inflammation usually occurs in and around the donor organ;
• Various allergies All allergies cause inflammation. In asthma, the airways become inflamed; in hay fever, the mucous membranes of the nose, ear, and throat become inflamed; people who are allergic to bee stings can have severe, life-threatening inflammation that affects the entire body (anaphylaxis);
• Vitamin A deficiency- Inflammatory reactions are much more likely if a person is deficient in vitamin A.

The disorders mentioned above are just a tiny example of the hundreds of autoimmune disorders in which inflammation is one of their hallmarks.

Treatment of inflammation

As mentioned earlier in this article, patients (and many healthcare professionals) need to remember that inflammation is part of the healing process. Sometimes reducing inflammation is necessary, but not always.

Anti-inflammatory drugs

NSAIDs(non-steroidal anti-inflammatory drugs) are taken to relieve pain caused by inflammation. They oppose COX(cyclooxygenase) an enzyme that synthesizes prostaglandins and creates inflammation. If prostaglandin synthesis can be blocked, pain is either eliminated or reduced. Examples of NSAIDs include, and.

People should not use NSAIDs for a long time without being under medical supervision because there are risks and life threatening. NSAIDs can also worsen symptoms and cause. Drugs, with the exception of aspirin, can also increase the risk of and ().

Acetaminophen(paracetamol, tylenol) may reduce pain associated with inflammatory conditions but has no anti-inflammatory effects. These drugs may be ideal for those who only want to treat the pain while letting the inflammation take its course.

Corticosteroids is a class of steroid hormones naturally produced in the cortex (outer part) of the adrenal glands. They are synthesized in laboratories and added to drugs.

Corticosteroids such as are anti-inflammatory. They prevent the release of phospholipids, which undermines the action of eosinophils and several other mechanisms involved in inflammation.

• Glucocorticoids, which are produced as a response to stress, and are also involved in the metabolism of fats, proteins and carbohydrates. Synthetic glucocorticoids are prescribed for joint inflammation (arthritis), inflammatory bowel disease, systemic lupus erythematosus, hepatitis, asthma, allergic reactions, and sarcoidosis. Creams and ointments may be prescribed for inflammation of the skin, eyes, lungs, intestines, and nose.
• Mineralocorticoids that regulate the balance of salt and water. Medicines with mineral corticoids are used to treat meningitis and to replace the missing aldosterone (hormone) in patients with adrenal insufficiency.

more likely if taken than with inhalers or injections. The higher the dose and/or the longer they are taken, the greater the risk of side effects. The severity of side effects is also related to the dosage and duration of treatment. Patients taking oral corticosteroids for more than three months are significantly more likely to experience unwanted side effects.

Inhaled drugs, such as long-term medications, increase the risk of developing - rinsing your mouth with water after each use can help prevent thrush.

Glucocorticoids can also call, while mineralocorticoids can call (), (), (), and.

Herbs with anti-inflammatory properties

Harpagophytum- also known as devil's claw, originally from South Africa and refers to sesame plants. The European colonists used the devil's claw to heal, and. Devil's claw has diuretic, sedative and analgesic properties.

Hyssop officinalis- added to cologne and Chartreuse (liquor). It is also used to color some drinks. Hyssop is mixed with other herbs to treat certain lung conditions, including inflammation. Beware of hyssop essential oils as they can cause life-threatening seizures in laboratory animals.

Ginger, also known as ginger root- used as medicine or spice. Jamaican ginger was the traditional medicinal form of this root and was used as a carminative and stimulant. It has been used for hundreds of years to treat other gastrointestinal problems as well as pain. Ginger supplements reduce markers of colon inflammation. Chronic inflammation of the colon is associated with a higher chance of developing it. Ginger supplements help reduce the chance of neoplasms.

- also a plant of the ginger family. Current research is looking at the possible beneficial effects of turmeric in treating some other inflammatory conditions. Curcumin, a substance found in turmeric, is being researched to treat a number of diseases and disorders, including inflammation.

cannabis- contains a cannabinoid called cannabichromene, which has been shown to have anti-inflammatory properties.

Other Treatments for Inflammation

Ice application- do not place the ice in direct contact with the skin, wrap it in a cloth or an ice bag. Ice application has been shown to reduce inflammation. Athletes commonly use ice therapy to treat pain and inflammation. Inflammation may decrease more quickly if you rest, apply ice, and squeeze and lift the affected area (for example, if there is swelling).

(Omega 3) - Daily consumption of fish reduces both inflammation and anxiety.

Green tea- Regular consumption of green tea improves bone health and reduces inflammation in postmenopausal women.

If you notice these five signs of inflammation in yourself, you urgently need to see a doctor.

The inflammatory process is a serious pathology that cannot be treated on its own.

From a young age in the office of an uncle or aunt in a white coat, a frightened child hears these strange words: rhinitis, sinusitis, or, for example, tonsillitis. With age, mysterious diagnoses with the ending "it" are added to the medical record of almost every person. Did you know that all these "its" mean one thing: inflammation of one or another organ. The doctor says nephritis means that the kidneys have caught a cold, arthritis means your joint hurts. Absolutely every structure in the human body can be affected by the inflammatory process. And your body starts to tell you about it quite early and actively.

Five signs of inflammation were identified in ancient times, when not only special medical devices for diagnostics did not exist, but even a simple blood test was out of the question.

Knowing these five characteristic signs of inflammation, you too can determine your disease without any additional methods:

1. Tumor - swelling

Any inflammatory process in the human body begins with the penetration of a provoking agent into it. It can be a bacterium, a virus, a foreign body, a chemical, or another "provocateur". The body immediately reacts to an unexpected guest, sending its guards to him - leukocyte cells, which are completely unhappy with him and instantly join the battle. In the place of accumulation of exudate, an infiltrate is formed. In the area of ​​the inflammatory process, you will definitely see swelling.

2. Rubor - redness

As a result of the death of damaged cells in the body, special substances are released - inflammatory mediators. First of all, the blood vessels located in the surrounding tissues react to them. To slow down the flow of blood, they expand, fill with blood and the result is the appearance of redness. In this way, redness is another characteristic sign of inflammation.

3. Calor - temperature increase

Vasodilation is an indispensable component of any inflammatory process, also because it must be cleaned up on the battlefield. The blood flow brings oxygen and the necessary building materials to the site of inflammation, and takes away all the decay products. As a result of such active work in the area of ​​​​inflammation, it becomes very hot. The third mandatory sign of inflammation is fever.

4. Dolor - pain

The fact that somewhere in the body there is an active fight against the pest must be communicated to the brain, and the best way to do this is some kind of bright and expressive signal. To do this, in almost every part of our body there are special bells - nerve endings. Pain is the best signal for the brain, as a result of which a person understands that something is going wrong in a certain area of ​​his body.

5. Functio laesa - dysfunction

The above signs of inflammation in total give another important symptom of this pathological process - dysfunction of the affected structure.In a combat area, life cannot continue in the usual way. Therefore, inflammation is always accompanied by functional insufficiency of the affected organ. In some cases, this can be very dangerous for the body, for example, in inflammatory processes of the heart, kidneys or other vital organs.

If you notice these five signs of inflammation in yourself, you urgently need to see a doctor.

Remember that the inflammatory process is a serious pathology that cannot be treated on its own. Consultation with a qualified specialist and the selection of an effective treatment regimen will help your body become a winner in the battle against inflammation.published