General characteristics of inflammation

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

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

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

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

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

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

2 Causes and conditions of inflammation

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

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

3 Stages and mechanisms of inflammation

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

1) alterations,

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

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

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

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

inflammation protective pathogenic

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

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

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

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

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

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

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

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

Inflammation is characterized by the following features.

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

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

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

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

Inflammation and immunity.

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

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

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

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

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

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

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

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

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

There are 2 groups of inflammatory mediators:

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

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

• acidic lipids, which are formed when cells and tissues are damaged and are themselves a source of tissue mediators of inflammation;
• slow regulating substance of anaphylaxis increases vascular permeability;
• eosinophilic chemotactic factor A increases 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;
• hydrolases (proteases, lipases, phospholipases, elastase, collagenases) and other enzymes released from cell lysosomes and activated in the focus of inflammation play a significant role in the development of damage to cells and non-cellular structures:
• violations of functions, both specific - of the organ in which the alteration occurred, and non-specific - thermoregulation, local immunity, etc.

EXUDATION STAGE

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

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

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

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

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

At the same time, the following processes develop:

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

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

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

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

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

Interaction of cells in the focus of inflammation.

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

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

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

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

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

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

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

PRODUCTIVE (PROLIFERATIVE) STAGE

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

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

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

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

FORMS OF ACUTE INFLAMMATION

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

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

According to the flow, they distinguish:

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

By pathogenetic specificity allocate:

• ordinary (banal) inflammation;
• immune inflammation.

EXUDATIVE INFLAMMATION

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

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

1. Serous inflammation characterized by the formation of serous exudate - a cloudy liquid containing up to 2-25% protein and not a large number of cellular elements - leukocytes, lymphocytes, desquamated epithelial cells.

The causes of serous inflammation are:

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

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

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

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

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

Localization of fibrinous inflammation - Mucous and serous membranes.

Morphogenesis.

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

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

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

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

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

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

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

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

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

Forms of purulent inflammation.

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

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

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

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

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

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

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

The outcome of hemorrhagic inflammation usually depends on its etiology.

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

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

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

PRODUCTIVE INFLAMMATION

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

CHRONIC INFLAMMATION

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Physiologist I. Mechnikov in the 19th century suggested that any inflammation is nothing more than an adaptive reaction of the body. And modern research proves that a small inflammation in itself is not terrible if it is not prolonged. The reaction of the body is really aimed at protecting and recovering from exposure to negative factors.

The treatment of inflammation is reduced to the establishment of the factor that provokes it, and the direct elimination of the negative impact and its consequences. The reactions of the body are diverse, and it is not easy to understand the complex processes inside the focus of the disease. But let's try anyway.

What is inflammation? Causes. Pain processing in the brain

Inflammation is a reaction that is characterized by the emergence of pathological processes and adaptive mechanisms.

The causes of such reactions are various environmental factors - chemical irritants, bacteria, injuries. It is characterized by an active process of protecting the body, the appearance in the blood of a large number of biologically active substances - intracellular and plasma mediators. Therefore, to diagnose inflammation of the internal organs, they take blood for a general and biochemical analysis, where they study such indicators as the level of ESR, the number of leukocytes, and others.

In the process of inflammation, the necessary antibodies to viruses and bacteria are produced. Without them, our immune system would not develop, would not be strengthened with age.

The first reaction to tissue damage is, of course, a sharp pain. This sensation of pain, nerve endings, irritated by neurotransmitters, are poisoned in the central nervous system.

Pain signals are transmitted to the medulla oblongata, and from there to the cerebral cortex. And they are already being processed here. Damage to the areas of the cortex responsible for somatosensory signals leads to a decrease in the ability not only to feel pain, but also to perceive the temperature of one's own body.

Autoimmune reactions

Separately, it must be said about the autoimmune causes of the inflammatory process. What is autoimmune inflammation? The disease is characterized by the production of antibodies to one's own cells, not foreign ones. This reaction of the body is not well understood. But it is believed that some kind of genetic failure plays a role here.

Widely known is such an autoimmune disease as systemic lupus erythematosus. It is impossible to cure the disease completely, but a person can stop the inflammation by constantly taking medications.

Discoid lupus affects only the skin. Its main symptom is butterfly syndrome - bright red spots with swelling on the cheeks.

And systemic - affects many systems, the lungs, joints, heart muscle suffer, and it happens that the nervous system.

The joints are especially affected by rheumatoid arthritis, which is also an autoimmune disease. The onset of the disease is most likely at the age of 20-40 years, and women are affected more often by about 8 times.

Stages of inflammation

The stronger the protective complex in a person, that is, his immune system, the faster the body will cope in stressful situations without outside help.

For example, a person cut his finger or drove a splinter into his hand. At the site of damage, of course, an inflammatory process will begin, which is conditionally divided into 3 stages. There are the following stages:

1. Alterations (from lat. altere - change). At this stage, when tissues are damaged, structural, functional and chemical changes begin. Distinguish between primary and secondary alteration. This stage automatically starts the 2nd phase.
2. Exudation. During this period, emigration of blood cells and active phagocytosis are observed. In this phase, exudate and infiltrate are formed.
3. Proliferation is the separation of healthy tissues from damaged ones and the beginning of the repair process. There is a cleansing of tissues and restoration of the microcirculatory bed.

But when the soft subcutaneous tissues are inflamed, a different inflammation takes place, and the stages are different.

1. The stage of serous impregnation.
2. Infiltration.
3. Suppuration - when an abscess or phlegmon appears.

In the first and second stages, cold or hot compresses are usually used. But in the stage of suppuration, the intervention of a surgeon is already necessary.

Types and forms

In medicine, there is a special classification that determines how dangerous inflammation is and how long it takes to treat it.

There are such types of reactions of the body:

• local or systemic inflammation - by localization;
• acute, subacute, chronic - by duration;
• normergic and hypergic - in severity.

The concept of hyperinflammation means that the reaction to the stimulus exceeds the norm.

Consider also the forms in which an acute reaction occurs.

• Granulomatous inflammation is a productive form in which the main morphological substrate of the granuloma is a small nodule.
• Interstitial - the second type of productive form, in which an infiltrate is formed in some organs (kidneys, lungs).
• Purulent - with the formation of a thick fluid, which includes neutrophils.
• Hemorrhagic - when red blood cells pass into the exudate, which is typical for severe forms of influenza.
• Catarrhal - inflammation of the mucous membranes, with the presence of mucus in the exudate.
• Putrid - characterized by necrotic processes and the formation of a bad odor.
• Fibrinous - with the defeat of mucous and serous tissues. It is characterized by the presence of fibrin.
• Mixed.

The doctor must definitely clarify this part of the diagnosis at the appointment and explain what is happening with the patient's body and why these manifestations must be treated to the end, and not just relieve the symptoms.

Common Symptoms

A few simple, well-known signs accompany any inflammation. We list the symptoms, starting with the most famous - fever.

1. Raising the temperature in the inflamed tissue by 1 or 2 degrees is natural. After all, there is an influx of arterial blood to a sore spot, and arterial blood, unlike venous blood, has a slightly higher temperature - 37 0 C. The second reason for overheating of tissues is an increase in metabolic rate.
2. Pain. Many receptors located near the affected area are irritated by mediators. As a result, we experience pain.
3. Redness is also easily explained by a rush of blood.
4. The tumor is explained by the appearance of exudate - a special fluid that is released from the blood into the tissues.
5. Violation of the functions of the damaged organ or tissue.

Inflammation that is not immediately cured becomes chronic, and then the treatment will be even more difficult. Science now knows that chronic pain travels to the brain through other, slower nerve pathways. And getting rid of it over the years is more and more difficult.

In addition to the main signs, there are also general symptoms of inflammation, visible only to a doctor, when studying a blood test:

• changes in hormonal composition;
• leukocytosis;
• changes in blood proteins;
• change in the enzyme composition;
• an increase in the erythrocyte sedimentation rate.

Mediators that are in an inactivated state in the blood are very important. These substances provide a regularity in the development of a protective reaction.

The production of mediators during tissue inflammation

Mediators include histamine, prostaglandin, and serotonin. Mediators are released when stimuli occur. Microbes or special substances that are released from dead cells activate a certain type of mediators. The main cells that produce such biological substances are platelets and neutrophils. However, some smooth muscle cells, the endothelium, are also capable of producing these enzymes.

Mediators of plasma origin are constantly present in the blood, but must be activated through a series of cleavages. Plasma active substances are produced by the liver. For example, the membrane attack complex.

The complement system, which is also synthesized in our biological filter, always resides in the blood, but is in an inactive state. It is activated only through a cascade process of transformations, when it notices a foreign element that has entered the body.

In the development of inflammation, mediators such as anaphylotoxins are indispensable. These are glycoproteins involved in allergic reactions. This is where the name anaphylactic shock comes from. They release histamine from mast cells and basophils. And they also activate the kallikrein-kinin system (KKS). In inflammation, it regulates the process of blood clotting. It is the activation of this system that leads to reddening of the skin around the damaged area.

Once activated, mediators rapidly decompose and help cleanse living cells. The so-called macrophages are designed to absorb waste, bacteria and destroy them inside themselves.

In connection with this information, we can answer the question of what inflammation is. This is the production of protective enzymes and the disposal of decomposition waste.

Inflammation of the glands

Let's start with a review of inflamed tissues. There are many glands in the human body - pancreas, thyroid, salivary glands, male prostate - this is a connective tissue that can also be affected by inflammation under certain conditions. Symptoms and treatment for inflammation of individual glands are different, since these are different body systems.

Let's talk, for example, about sialadenitis - inflammation of the gland with saliva. The disease occurs under the influence of various factors: due to structural changes, diabetes or bacterial infection.

Symptoms are:

• temperature increase;
• pain during chewing;
• feeling of dryness in the mouth;
• painful formation and swelling in the area of ​​​​the location of the glands, another.

However, the salivary glands do not often bother people. Much more often they complain of thyroiditis - inflammation of the gland, which is responsible for most hormonal functions - this is the thyroid gland.

Thyroiditis, or inflammation of the thyroid gland, is accompanied by weakness, mood swings from apathy to anger, swelling in the neck, increased sweating, decreased sexual function, and weight loss.

Thyroiditis is more common in women than in men, almost 10 times. According to statistics, every 5th woman suffers from goiter disease. Inflammation in men of the thyroid gland occurs much more often at the age of 70 years or more.

Due to neglect, the disease progresses and leads to the fact that the gland sharply reduces its functions.

Recall the importance of the pancreas for the body. Damage to this organ impairs digestion and occurs, in fact, due to malnutrition. A person with pancreatitis, a chronic inflammation of the pancreas, has to constantly drink the enzymes of this gland, which itself is already functioning poorly.

Pyelonephritis

Nephrites are various inflammatory diseases of the kidneys. What are the causes of inflammation in this case? Pyelonephritis occurs when the urinary organs are affected by some kind of infection. What is pyelonephritis in fact and how it manifests itself? Microorganisms grow in the renal tangle, and the patient feels severe pain and weakness.

The tissues of the organ gradually damaged by microorganisms become overgrown with scars, and the organ performs its functions worse. Both kidneys can be damaged, then kidney failure quickly develops and the person will eventually be forced to undergo dialysis from time to time to cleanse their body.

Acute pyelonephritis should be suspected when pain, discomfort begin in the kidney area, and the temperature rises. A person experiences severe pain in the lower back, and the temperature can rise up to 40 0 ​​C, severe sweating. Excruciating muscle weakness, sometimes nausea.

A doctor can determine the exact cause of a fever by examining the composition of urine and blood tests. The acute stage of the disease must be treated in a hospital, where the doctor will prescribe antibiotic therapy and antispasmodics for pain.

Toothache and osteomyelitis

Improper care of the teeth or damage to the crowns provokes a condition such as inflammation of the tooth root. What is tooth inflammation? This is a very painful condition that requires special treatment, and immediate.

Penetration into the root of the tooth infection has serious consequences. Sometimes such inflammation in an adult begins after an incorrect rough treatment by a dentist. You need to have your own highly qualified dentist that you trust.

If, against the background of the inflammatory process, osteomyelitis develops in the jaw area, the pain will be so severe that most classic analgesics will not help either.

Osteomyelitis is a nonspecific purulent-inflammatory process that affects both bone tissue, periosteum, and even surrounding soft tissues. But the most common cause of the disease is bone fracture.

Facial nerve and manifestations of inflammation

What is inflammation? This is primarily a violation of the physiological functions of the tissue. Nervous tissue is also sometimes affected due to certain circumstances. The most well-known is such an inflammatory disease as neuritis - a lesion of the facial nerve. The pain from neuritis is sometimes simply unbearable, and a person has to drink the strongest painkillers.

To take any steps in the treatment, you must first determine the cause. This may be due to chronic inflammation of the sinuses or meningitis. Such inflammation leads to exposure to a draft or ordinary infections. There are many reasons.

If the facial or trigeminal nerve is damaged, there is a hum in the ears, pain. In the acute form of inflammation, the corner of the mouth rises slightly, and the eyeball protrudes.

Of course, inflammation of the nerve does not go unnoticed. And that means that immediately, at the first symptoms, you need to consult a doctor and choose the appropriate treatment.

Treatment of inflammation of the nerve lasts at least 6 months. There are special preparations of both the old and the new generation to relieve symptoms. A neurologist should choose a medicine. Without a doctor, it is impossible to choose an anesthetic medicine, because each drug has its own contraindications and can damage the heart or nervous activity of the body.

Pathological processes of the reproductive system

The genitourinary system in women and men today also suffers from constant stress and fatigue. Women are increasingly diagnosed with oophoritis - inflammation of the appendages. Invariably, this pathological process, without treatment, spreads to the fallopian tubes, and adnexitis begins.

Inflammation of the fallopian tubes is also accompanied by severe pain and weakness. The monthly cycle is disturbed: in some women, menstruation becomes too plentiful, with the release of lumps. And the first 2 days of menstruation are very painful. Others have the exact opposite effect. That is, menstruation is waning. Pain and specific discharge with a smell are the main signs of inflammation of the female genital organs.

The infection penetrates in various ways: sometimes through damage to neighboring organs, from the external genital organs, and much less often enters the appendages with the bloodstream.

Chronic adnexitis, which led to scarring, can lead to infertility. Therefore, the treatment of inflammation in women should take place on time and under the supervision of a gynecologist.

In men, due to weakened immunity and infection in the urethra, urethritis occurs. The causes of inflammation are various biological microbes: the herpes virus, staphylococci, Candida fungus. Due to the fact that the urethra of men is longer, the inflammatory process in them is more difficult and takes longer to heal. Symptoms of inflammation of the urethra - frequent trips to the toilet at night and the presence of blood in the urine, pain.

Another common and painful problem that comes to men is prostatitis. Inflammation of the prostate is hidden, and not many men are aware of the early manifestations of the disease. Representatives of the stronger sex should pay attention to pain in the lower abdomen, frequent trips to the toilet and incomprehensible chills.

Running chronic prostatitis is complicated by suppuration. Then the patient needs to be operated on.

Treatment of inflammation of various origins

As we have understood, inflammation plays an important role. This reaction should save the whole body, sacrificing some of the damaged cells, which are gradually replaced by connective tissue.

But large-scale long-term inflammation draws all the forces from the body, depletes a person and can lead to complications. Due to the risk of complications, all measures must be taken on time.

Treatment of any inflammation occurs after determining the cause. It is necessary to pass all the required tests and tell the doctor about the complaints, that is, give an anamnesis. If antibodies to bacteria are found in the blood, then the doctor will prescribe antibacterial drugs. High temperature must be brought down by any antipyretic agents.

If the reaction is caused by chemical irritants, you need to cleanse the body of the poison.

For the treatment of autoimmune diseases and allergic manifestations, drugs called immunosuppressants are needed, which should reduce the excessive immune response.

There are several groups of such drugs, some of them have a greater effect on cellular immunity, others on humoral. The best known prednisone, betamethazole, cortisone are glucocorticoids. There are also cytostatic drugs and immunophile agonists. Some of them have a toxic effect on the body. Children, for example, are shown chlorambucil, since others will be unsafe for them.

Antibiotics

Modern antibiotics are divided into 3 main types: natural, synthetic and semi-synthetic. Natural ones are made from plants, mushrooms, tissues of some fish.

While taking antibiotics for inflammation, it is imperative to take probiotics - “life-restoring” agents.

Antibiotics are also divided into groups according to their chemical composition. The first group is penicillin. All antibiotics of this group cure pneumonia and severe tonsillitis well.

Cephalosporin preparations are very similar in composition to penicillins. A lot of them have already been synthesized. They help fight viruses well, but can cause allergies.

The group of macrolides is designed to combat chlamydia and toxoplasma. Separately invented antibiotics aminoglycosides, which are prescribed when sepsis has begun, and there is an antifungal group of drugs.

The cause of many diseases, including heart disease, obesity, etc. is chronic inflammation in the body. Chronic inflammation is an enemy that knows how to disguise itself well, because it is very difficult to independently detect signs of an inflammatory process in the body.

However, it is possible to identify this initiator of disease processes if you look closely at the signs of the inflammatory process and consult a doctor in time to undergo the necessary tests. the site will help you bring the inflammatory process to clean water.

What are the signs of inflammation in the body

Inflammation is the body's response to injury. As a rule, we recognize inflammation in the body by typical signs: redness, fever and swelling of the damaged area, as well as restriction of mobility, for example, in the case of a sprained ankle or bruised finger.

Chronic inflammation accompanies all diseases ending in "it" - arthritis, hepatitis, bursitis, etc. The inflammatory process can proceed “quietly” inside the body, and a person may not be aware of its presence.

However, your body gives you some clues, and if you ignore them, you can face some pretty serious health problems in the future.

6 Common Signs of an Inflammatory Process

1. Pain. If your muscles, joints are constantly aching, or your body is aching in general, you can bet on the inflammatory process in the body. When your immune cells or fat cells release inflammatory chemicals called cytokines, you feel more pain and aches. Fibromyalgia and arthritis are classic symptoms of severe inflammation in the body, but extensive body pain while getting out of bed in the morning is also a sign of an inflammatory process. Pain in the soles (plantar fasciitis) is also a sign of inflammation in the body.

2. Fatigue.

Fatigue can be caused by various factors, one of which is the inflammatory process in the body. When your immune cells are constantly busy producing antibodies, you are overcome by fatigue. For example, when you have the flu, a cold, or another illness that causes inflammation.

3. Overweight.

It was once believed that fat cells store extra calories and keep you warm in winter. It is now also known that fat cells play the role of chemical factories.

They are capable of producing a variety of chemicals, some of which can be compared to those produced by immune cells in the process of fighting infection. The more fat in your body, the more of these substances they produce.

The problem is that such chemicals lead to insulin resistance, which makes it difficult to lose weight.

4. Redness and / or itching of the skin.

Redness and itching are classic signs of chronic inflammation in the body. These symptoms can be caused by allergies, autoimmune diseases, or a weakened liver.

Itchy skin accompanies people with hepatitis, but it can occur in case of inflammation of the liver for various reasons. An inflamed liver produces large amounts of an inflammatory chemical called C-reactive protein.

5. Diagnosed autoimmune disease.

Chronic inflammation is largely responsible for the symptoms of most autoimmune diseases - pain, fatigue and poor sleep. Typical examples of autoimmune diseases are:

• psoriasis;
• disorders of the thyroid gland;
• rheumatoid arthritis;
• lupus.

6. Allergies and infections. If you suffer from allergic reactions, the inflammatory process in the body is manifested by swelling, redness, itching and pain.

Such symptoms are the result of an immune response to harmful, harmless substances. Infections are also a typical cause of inflammatory processes, especially if they become chronic. Some viruses and bacteria live in your body for years, constantly stimulating the immune system and releasing toxins into the bloodstream. Among them:

Chronic infections are a very big burden on the immune system and liver, so you need to take care of strengthening the immune system.

If you have found the above signs in yourself, you need to consult a doctor who, based on the tests, will prescribe the necessary treatment and nutrition for inflammation.

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?

A few seconds or minutes after tissue starts. The damage may be physical, or it may be caused by an immune response.

• 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 inflicting or reacting to pain - the cause of pain comes from outside nervous system and the nervous system responds 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- becomes inflamed gastrointestinal tract. 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.