Medical educational literature. Serous inflammation

Serous inflammation (i. serosa) exudative V., characterized by the formation of serous exudate in the tissues; observed more often in serous cavities.

Big Medical Dictionary. 2000 .

See what "serous inflammation" is in other dictionaries:

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It is characterized by the predominance of exudation processes and the formation of exudate in the area of ​​inflammation. Depending on the nature of the exudate, the following types of exudative inflammation are distinguished: serous; fibrinous; purulent; putrid; hemorrhagic; ... ... Wikipedia

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. Exudative inflammation characterized by the predominance of the second, exudative, phase of inflammation. As is known, this phase occurs at different times following damage to cells and tissues and is due to the release of inflammatory mediators. Depending on the degree of damage to the walls of capillaries and venules and the intensity of the action of mediators, the nature of the resulting exudate may be different. With mild vascular damage, only low molecular weight albumins seep into the inflammation site, with more severe damage, large molecular globulins appear in the exudate and, finally, the largest fibrinogen molecules that turn into tissues into fibrin. The composition of the exudate also includes blood cells emigrating through the vascular wall, and cellular elements of damaged tissue. Thus, the composition of the exudate may be different.

Classification. The classification of exudative inflammation takes into account two factors: the nature of the exudate and the localization of the process. Depending on the nature of the exudate, serous, fibrinous, purulent, putrefactive, hemorrhagic, mixed inflammation is isolated (Scheme 20). The peculiarity of the localization of the process on the mucous membranes determines the development of one type of exudative inflammation - catarrhal.

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

The reasons. The causes of serous inflammation are varied: infectious agents, thermal and physical factors, auto-intoxication. Serous inflammation in the skin with the formation of vesicles is a characteristic sign of inflammation caused by iiruses of the Herpesviridae family (herpes simplex, chickenpox).

Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella) can also cause serous inflammation. Thermal, less often chemical burns characterized by the formation of blisters in the skin filled with serous exudate.

With inflammation of the serous membranes in the serous cavities, a cloudy fluid accumulates, poor in cellular elements, among which deflated mesothelial cells and single PMNs predominate. The same picture is observed in the soft meninges, which become thickened, swollen. In the liver, serous exudate accumulates perisinusoidally, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule. Serous inflammation of parenchymal organs is accompanied by degeneration of parenchymal cells. Serous inflammation of the skin is characterized by the accumulation of effusion in the thickness of the epidermis, sometimes exudate accumulates under the epidermis, exfoliating it from the dermis with the formation of large blisters (for example, with burns). With serous inflammation, there is always a plethora of blood vessels. Serous exudate helps to remove pathogens and toxins from the affected tissues.

Exodus. Usually favorable. The exudate is well absorbed. The accumulation of serous exudate in parenchymal organs causes tissue hypoxia, which can stimulate the proliferation of fibroblasts with the development of diffuse sclerosis.

Meaning. Serous exudate in the meninges can lead to disruption of the outflow of cerebrospinal fluid (liquor) and cerebral edema, pericardial effusion makes it difficult for the heart to work, and serous inflammation of the lung parenchyma can lead to acute respiratory failure.

fibrinousinflammation. It is characterized by an exudate rich in fibrinogen, which is converted into fibrin in the affected tissue. This is facilitated by the release of tissue thromboplastin. In addition to fibrin, PMN and elements of necrotic tissues are also found in the exudate. Fibrinous inflammation is more often localized on the serous and mucous membranes.

The reasons. The causes of fibrinous inflammation are diverse - bacteria, viruses, chemicals of exogenous and endogenous origin. Among bacterial agents, diphtheria Corynebacterium, Shigella, Mycobacterium tuberculosis are the most conducive to the development of fibrinous inflammation. Fibrinous inflammation can also be caused by Frenkel diplococcus, pneumococcus, streptococcus and staphylococcus, and some viruses. Typically, the development of fibrinous inflammation during autointoxication (uremia). The development of fibrinous inflammation is determined sharp rise permeability vascular wall, which may be due, on the one hand, to the characteristics of bacterial toxins (for example, the vasoparalytic effect of diphtheria corynebacterium exotoxin), on the other hand, to a hyperergic reaction of the body.

Morphological characteristic. A light gray film appears on the surface of the mucosa or serous membrane. Depending on the type of epithelium and the depth of necrosis, the film can be loosely or firmly associated with the underlying tissues, and therefore there are two types of fibrinous inflammation; croupous and diphtheritic.

Croupous inflammation often develops on a single-layer epithelium of the mucous or serous membrane, which has a dense connective tissue base. At the same time, the fibrinous film is thin and easily removed. When such a film is separated, surface defects are formed. The mucous membrane is swollen, dull, sometimes it seems that it is, as it were, sprinkled with sawdust. The serous membrane is dull, covered with gray fibrin filaments resembling a hairline. For example, fibrinous inflammation of the pericardium has long been figuratively called a hairy heart. Fibrinous inflammation in the lung with the formation of cru. postural exudate in the alveoli of the lobe of the lung is called croupous pneumonia.

Diphtheritic inflammation flutters and organs covered with multilayer squamous epithelium or a single-layered epithelium with a loose connective tissue base, contributing to the development of deep tissue necrosis. In such cases, the fibrinous film is thick, difficult to remove, and when it is rejected, a deep tissue defect occurs. Diphtheritic inflammation occurs on the walls of the pharynx, on the mucous membrane of the uterus, vagina, Bladder, stomach and intestines, in wounds.

Exodus. on mucous membranes and serous membranes the outcome of fibrinous inflammation is not the same. On the mucous membranes, fibrin films are rejected with the formation of ulcers - superficial with croupous inflammation and deep with diphtheria. Superficial ulcers usually regenerate completely, while deep ulcers heal, scars form. In the lung with croupous pneumonia, the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils at the site of exsu. connective tissue appears (organization of exudate occurs), with excessive activity neutrophils may develop abscess and gangrene of the lung. On serous membranes fibrinous exudate may melt, but more often it is subject. organization with the formation of adhesions between the serous sheets. There may be a complete overgrowth of the serous cavity - obliteration.

Meaning. The value of fibrinous inflammation is largely determined by its type. For example, in diphtheria of the pharynx, the fibrinous film containing pathogens is tightly associated with the underlying tissues (diphtheritic inflammation), while severe intoxication of the body with corynebacteria toxins and decay products of necrotic tissues develops. With diphtheria of the trachea, intoxication is slightly expressed, however, easily rejected films close the lumen of the upper respiratory tract, which leads to asphyxia (true croup).

Purulent inflammation. It develops with the predominance of neutrophils in the exudate. Pus is a thick cream-like mass of yellow-green color with a characteristic odor. Purulent exudate is rich in proteins (mainly globulins). Formed elements in purulent exudate make up 17-29%; these are living and dying neutrophils, a few lymphocytes and macrophages. Neutrophils die 8-12 hours after entering the focus of inflammation, such decaying cells are called purulent bodies. In addition, in the exudate, you can see elements of destroyed tissues, as well as colonies of microorganisms. Purulent exudate contains a large number of enzymes, primarily neutral proteinases (elastase, cathepsin G and collagenase), released from the lysosomes of decaying neutrophils. Neutrophil proteinases cause melting of the body's own tissues (histolysis), increase vascular permeability, promote the formation of chemotactic substances and enhance phagocytosis. Pus has bactericidal properties. Non-enzymatic cationic proteins contained in specific granules of neutrophils are adsorbed on the membrane bacterial cell, resulting in the death of the microorganism, which is then lysed by lysosomal proteinases.

The reasons. Purulent inflammation is caused by pyogenic bacteria: staphylococci, streptococci, gonococci, meningococci, Frenkel diplococcus, typhoid bacillus, etc. Aseptic purulent inflammation is possible when some chemical agents (turpentine, kerosene, toxic substances) enter the tissues ).

Morphological characteristic. Purulent inflammation can occur in any organs and tissues. Basic forms purulent inflammation are abscess, phlegmon, empyema.

Abscess - focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A rampart forms around the abscess granulation tissue, through the numerous capillaries of which leukocytes enter the abscess cavity and partially remove decay products. The abscess that produces pus is called pio-gene membrane. With a long course of inflammation, the granulation tissue that forms the pyogenic membrane matures, and two layers form in the membrane: the inner one, consisting of granulations, and the outer one, represented by mature fibrous connective tissue.

Phlegmon is a purulent diffuse inflammation in which purulent exudate diffusely spreads into tissues, exfoliating and lysing tissue elements. Usually, phlegmon develops in tissues where there are conditions for easy spread of pus - in fatty tissue, in the area of ​​\u200b\u200btendons, fascia, along the vascular-nerve bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. With the formation of phlegmon, except anatomical features, an important role is played by the pathogenicity of the pathogen and the state of the body's defense systems.

There are soft and hard phlegmon. Soft phlegmon characterized by the absence of visible foci of necrosis in the tissues, with hard cellulitis in the tissues, foci of coagulation necrosis are formed, which are not subjected to melting, but are gradually rejected. Phlegmon of adipose tissue is called goal-lulite, it has a limitless distribution.

Empyema is a purulent inflammation of hollow organs or body cavities with accumulation of pus in them. In body cavities, empyema can form if there are purulent foci in neighboring organs (for example, pleural empyema with lung abscess). Empyema of hollow organs develops when there is a violation of the outflow of pus during purulent inflammation (empyema of the gallbladder, appendix, joint, etc.). With a long course of empyema, the mucous, serous, or synovial membranes become necrotic, and granulation tissue develops in their place, as a result of which adhesions or obliteration of cavities are formed.

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

outcomes and complications. Both outcomes and complications of purulent inflammation depend on many factors: the virulence of microorganisms, the state of the body's defenses, the prevalence of inflammation. With spontaneous or surgical emptying of the abscess, its cavity collapses and fills with granulation tissue, which matures with the formation of a scar. Less commonly, the abscess becomes encapsulated, the pus thickens and may undergo petrification. With phlegmon, healing begins with the delimitation of the process, followed by the formation of a rough scar. With an unfavorable course, purulent inflammation can spread to the blood and lymphatic vessels, while bleeding and generalization of infection with the development of sepsis are possible. With thrombosis of the affected vessels, necrosis of the affected tissues may develop, in case of their contact with the external environment, they speak of secondary gangrene. Long-term chronic purulent inflammation often leads to the development of amyloidosis.

Meaning. The value of purulent inflammation is very great, since it lies in basis of many diseases and their complications. The value of purulent inflammation is determined mainly by the ability of pus to melt tissues, which makes it possible for the process to spread by contact, lymphogenous and hematogenous.

putrid inflammation. It develops when putrefactive microorganisms enter the focus of inflammation.

The reasons. Putrefactive inflammation is caused by a group of clos-ridia, causative agents of anaerobic infection - C.perfringens, C.novyi, C.septicum. Several types of Clostridium are usually involved in the development of inflammation in combination with aerobic bacteria(staphylococci, streptococci). Anaerobic bacteria form butyric and acetic acids, CO 2 , hydrogen sulfide and ammonia, which gives the exudate a characteristic putrid (ichorous) odor. Clostridium enters the human body, as a rule, with the earth, where there are a lot of bacteria themselves and their spores, therefore, most often putrefactive inflammation develops in wounds, especially with massive wounds and injuries (wars, disasters).

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

Exodus. Usually unfavorable, which is associated with the massiveness of the lesion and a decrease in the resistance of the macroorganism. Recovery is possible with active antibiotic therapy in combination with surgical treatment.

Meaning. It is determined by the predominance of anaerobic gangrene in case of mass wounds and the severity of intoxication. Putrid inflammation in the form of sporadic cases can develop, for example, in the uterus after a criminal abortion, in the colon in newborns (the so-called necrotizing colitis of newborns).

hemorrhagicinflammation. It is characterized by the predominance of erythrocytes in the exudate. In the development of this type of inflammation, the main importance belongs to a sharp increase in the permeability of microvessels, as well as negative neutrophil chemotaxis.

The reasons. Hemorrhagic inflammation is characteristic of some serious infectious diseases - plague, anthrax, smallpox. With these diseases, erythrocytes predominate in the exudate from the very beginning. Hemorrhagic inflammation in many infections can be a component of mixed inflammation.

Morphological characteristic. Macroscopically, the areas of hemorrhagic inflammation resemble hemorrhages. Microscopically, a large number of erythrocytes, single neutrophils and macrophages are determined in the focus of inflammation. Significant tissue damage is characteristic. Hemorrhagic inflammation can sometimes be difficult to distinguish from hemorrhage, for example, with hemorrhage into the abscess cavity from an arrozirovanny vessel.

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

Meaning. It is determined by the high pathogenicity of pathogens that usually cause hemorrhagic inflammation.

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

The reasons. A change in the composition of the exudate is naturally observed in the course of inflammation: for a start inflammatory process the formation of serous exudate is characteristic, later fibrin, leukocytes, erythrocytes appear in the exudate. There is also a change in the qualitative composition of leukocytes; neutrophils are the first to appear in the focus of inflammation, they are replaced by monocytes and later - lymphocytes. In addition, in the case of a new infection joining an already ongoing inflammation, the nature of the exudate often changes. For example, when a bacterial infection is attached to a viral respiratory infection, a mixed, more often mucopurulent exudate is formed on the mucous membranes. And, finally, the addition of hemorrhagic inflammation with the formation of serous-hemorrhagic, fibrinous-hemorrhagic exudate can occur when the body's reactivity changes and is a prognostically unfavorable sign.

Morphological characteristic. Determined by a combination of changes characteristic of various kinds exudative inflammation.

Outcomes, meaning mixed inflammation are different. In some cases, the development of mixed inflammation indicates a favorable course of the process. In other cases, the appearance of a mixed exudate indicates the addition of a secondary infection or a decrease in the body's resistance.

catarrhalinflammation. It develops on the mucous membranes and is characterized copious excretion exudate flowing from the surface of the mucosa, hence the name of this type of inflammation (Greek katarrheo - I drain). A distinctive feature of catarrhal inflammation is the admixture of mucus to any exudate (serous, purulent, hemorrhagic). It should be noted that mucus secretion is a physiological protective reaction, which is enhanced in conditions of inflammation.

The reasons. Extremely diverse: bacterial and viral infections, allergic reactions on infectious and non-infectious agents (allergic rhinitis), the action of chemical and thermal factors, endogenous toxins (uremic catarrhal colitis and gastritis).

Morphological characteristic. The mucous membrane is edematous, plethoric, exudate flows from its surface. The nature of the exudate can be different (serous, mucous, purulent), but its essential component is mucus, as a result of which the exudate takes the form of a viscous, viscous mass. At microscopic examination in the exudate, leukocytes, deflated cells of the integumentary epithelium and mucous glands are determined. The mucous membrane itself has signs of edema, hyperemia, is infiltrated with leukocytes, plasma cells, in epithelium with many goblet cells.

Flow catarrhal inflammation can be acute and chronic. Acute catarrh is characteristic of a number of infections, especially for acute respiratory viral infections, while there is a change in the types of catarrh; serous catarrh is usually replaced by mucous, then purulent, less often purulent hemorrhagic. Chronic catarrhal inflammation can occur both in infectious (chronic purulent catarrhal bronchitis) and in non-infectious (chronic catarrhal gastritis) diseases. Chronic inflammation in mucous membrane is often accompanied by a violation of the regeneration of epithelial cells with the development of atrophy or hypertrophy. In the first case, the shell becomes smooth and race, in the second it thickens, its surface becomes uneven, it can swell into the lumen of the organ in the form of polyps.

Exodus. Acute catarrhal inflammations proceed 2 — 3 weeks and usually come to an end with full recovery. Chronic catarrhal inflammation is dangerous by the development of atrophy or hypertrophy of the mucous membrane.

Meaning. It is ambiguous due to the variety of reasons that cause it.

Etiology.

Inflammation can be caused by various factors.

1. Biological (exogenous and endogenous):

a) microorganisms and their metabolic products;

b) immune factors: antibodies, immune complexes, sensitized lymphocytes, etc.

2. Physical: radiation, electricity, high and low temperatures, trauma.

3. Chemical: drugs, toxins, poisons.

Inflammation on the border between living and dead tissue is called demarcation, borderline. the inflammatory reaction in a given person under the action of a given stimulus is of a moderately pronounced nature, adequate to the strength of the etiological factor. This inflammatory reaction is called normergic. In cases, the body may have hypersensitivity - hyperergic, decreased sensitivity. hypoergic and anergic reactions.

In the focus of inflammation and in nearby lymph nodes inflammation causes changes. At the same time, nearby lymph nodes increase and form, together with the focus of inflammation, the so-called complex or primary inflammatory complex.

phases of the inflammatory response.

Inflammation consists of three phases: alteration exudation and proliferation.

Alteration or damage.

Alteration is represented by dystrophy and necrosis. This is the initial phase of inflammation leading to the release of mediators.

It occurs both as a result of a direct effect on the tissues of a harmful principle, and due to circulatory and innervation disorders.

mediators of inflammation.

plasma mediators.

Plasma mediators provide an increase in vascular permeability, activate chemotaxis of polymorphonuclear leukocytes for phagocytosis, intravascular coagulation in the vessels draining from the focus of inflammation to delimit the pathogen and the focus itself. They appear when factors circulating in the blood are activated.

1.kalikrein-kinin system. The main mediator is bradykinin, which is formed upon activation of the Hageman factor (factor XIIa - prekallikrein - kininogen - bradykinin).

2. Complement system. Consists of a group of plasma proteins, which, sequentially activated, are involved in the immune lysis of cells.

In inflammation, the most important role play the following complement components:

C3a and C5a - anaphylotoxins (cause degranulation of mast cells - mastocytes, expression of adhesive molecules, increase the release of lipoxygenase metabolites of arachidonic acid - leukotrienes);

C3b is an opsonin, enhances phagocytosis;

C3b is a 9-membrane attack complex that causes lysis of bacteria and other cells.

3. The blood coagulation system and the fibrinolytic system.

Main mediators: Hageman factor, plasmin, fibrin degradation products (formed during fibrinolysis).

The Hageman factor is a link between the complementary, kallikrein-kinin system and the coagulation - fibrinolytic systems. It activates the kinin system, "starts" the internal coagulation system and the fibrinolytic system, which in turn turns on the complementary system.

Cell mediators

Cellular mediators are produced various cells; are contained in the cell in finished form (histamine, serotonin, lysosomal enzymes) or are formed during the inflammatory reaction. They provide:

a) increased vascular permeability, chemotaxis, phagocytosis;

b) activation of the immune response to eliminate the damaging agent.

c) repair by proliferation and differentiation of cells in the focus of inflammation.

The following groups of cellular mediators are distinguished:

1. Vasoactive amines:

a) histamine (mast cells and platelets);

c) serotonin (platelets).

2. Metabolic products of arachidonic acid.

3. Lysosomal products(leukocytes, macrophages).

4. Platelet activating factor(leukocytes, endothelium).

5. Cytokines.

Cytokines are soluble proteins secreted by several types of cells (mainly macrophages and leukocytes), which, by specifically binding to receptors, change the behavior of cells.

6. Nitric oxide (NO).

Main effects of inflammatory mediators.

Vasodilation - prostaglandins, nitric oxide.

Increased vascular permeability - vasoactive amines, C3a, C5a, bradykinin, leukotrienes, FAT.

Chemotaxis, activation of leukocytes - C3b, leukotriene B4, Il8, bacterial products.

Fever - IL1, tumor necrosis factor (TNF), prostaglandins.

Pain - bradykinin, prostaglandins.

Tissue damage - lysosomal enzymes of leukocytes, macrophages, oxygen metabolites, nitric oxide.

Exudation.

Exudation is the release of the liquid part of the blood and shaped elements outside the vascular bed.

stages of exudation.

The reaction of the microvasculature in violation rheological properties blood:

short-term vasoconstriction;

vasodilation (arterioles, capillaries and postcapillaries) with the development of inflammatory hyperemia;

slowing down of blood flow and increase in blood viscosity, stasis.

Increasing the permeability of the microvasculature:

The appearance of pores between endothelial cells due to their contraction and vasodilation, as well as due to damage to the endothelium.

Output of fluid and plasma proteins:

Interendothelially through interendothelial pores;

Intraendothelial with increased pinocytosis of the endothelium.

Electron microscopic picture.

In the endothelium, accumulations of small pinocytic vesicles are visible on the side of the endothelial cell facing the lumen of the vessel.

cell emigration(exit of cells from vessels) occurs mainly in postcapillaries and venules. Polymorphonuclear leukocytes (PMNs) are the first to enter the field of view (after 10-15 minutes with medium-strength stimuli).

Stages of leukodiapedesis:

a) margination (marginal standing);

b) adhesion to the endothelium (using adhesive molecules expressed on the cell surface);

c) emigration - occurs interendothelially: leukocytes, with the help of pseudopodia, push apart interendothelial contacts and migrate between the endothelium and the basement membrane. The penetration of PMNs through the basement membrane of the endothelium is associated with the phenomenon of thixotropy (hypothesis!), which is based on the transition of the basement membrane from the gel state to the sol and vice versa. The movement of the PNL towards the site of damage is carried out with the help of chemotactic factors.

Phagocytosis

Phagocytosis can be:

a) completed;

b) incomplete (microorganisms are not digested by phagocytes and multiply in their cytoplasm; incomplete phagocytosis leads to chronic inflammation).

Formation of exudate and inflammatory cellular infiltrate.

Exudate is an inflammatory fluid containing protein (more than 2%) and cellular elements. When cells accumulate in tissues, they speak of an inflammatory cellular infiltrate.

The composition of the infiltrate cells is different:

In the first 6-24 hours, PMNs predominate in the exudate;

In the period of 24-48 hours, monocyte-macrophages begin to predominate;

For inflammation associated with hypersensitivity reactions immediate type, eosinophils predominate in the exudate.

inflammation manifests itself:

Redness - rubor reflects hyperemia, expansion of all working and reserve blood vessels as a result of irritation of the vasodilator nerves. Initially, the blood flow accelerates, and then slows down until the stasis and stasis.

Swelling of tissues - the release of blood plasma and leukocytes mixed with local tissue cells from the vessels into the tissue

Pain - associated with irritation of nerve endings in the area of ​​inflamed infiltrate

Local temperature increase is associated with the rapid course of metabolism and the synthesis of substances, blood flow.

Violation of the function - functio laesa - an understandable phenomenon - damaged tissue works weaker.

Proliferation.

Proliferation is the final phase of inflammation, which is characterized by:

1. Reproduction in the field of inflammation of cells capable of proliferation: macrophages, cambial mesenchymal cells, smooth muscle cells (SMC), epithelium.

2. Differentiation and transformation of cells:

A macrophage can transform into an epithelioid and giant cell;

B-lymphocyte - into a plasma cell;

The cambial mesenchymal cell develops into a fibroblast.

Cell proliferation in the field of inflammation with the appearance of a large number of fibroblasts serves to restore damaged tissues.

Proliferation and differentiation of cellular elements in the field of inflammation are carried out with the help of cytokines and numerous factors height:

a) platelet growth factor - proliferation of fibroblasts and GMC;

b) epidermal growth factor - proliferation of endothelium, fibroblasts, epithelium;

c) fibroblast growth factor - stimulates the synthesis of extracellular matrix components;

d) transforming growth factor alpha - acts similarly to epidermal growth factor;

e) interleukin-1 (IL1) and tumor necrosis factor (TNF) enhance the proliferation of fibroblasts, SMCs and endothelium.

Inflammation is regulated by hormonal, nervous and immune factors. It has been established that some hormones, such as somatotropic hormone (GH) of the pituitary gland, deoxycorticosterone, aldosterone, increase the inflammatory response (pro-inflammatory hormones), others - glucocorticoids and adrenocorticotropic hormone (ACTH) of the pituitary gland, on the contrary, reduce it (anti-inflammatory hormones). Cholinergic substances, stimulating the release of inflammatory mediators, act like pro-inflammatory hormones, adrenergic substances, inhibiting mediator activity, behave like anti-inflammatory hormones.

Biological entity proliferation is reduced to the process of rebirth of dead structures - regeneration.

classification of inflammation.

1. Depending on the nature of the course, inflammation can be acute, subacute and chronic.

2. According to the predominance of the inflammation phase, exudative inflammation (mainly acute) and productive (mainly chronic) are distinguished.

EXUDATIVE INFLAMMATION

It is characterized by the predominance of exudation and the formation of exudate in the tissues and body cavities.

Depending on the nature of the exudate,: serous, fibrinous, purulent, putrefactive, hemorrhagic and mixed inflammation; can develop on mucous membranes special kind inflammation is catarrhal.

serous inflammation characterized by the release of bloody exudate, with a low content of protein and cells.

Externally, this exudate is similar to congestive fluid transudate, which appears, for example, with cardiac edema.

Features the following:

In the serous exudate, the protein is up to 6-8%, the specific gravity is higher / 1018-1020 /, there are more cells. If acetic acid is added to the test tube with serous exudate, the proteins coagulate and a cloud forms, like smoke from a cigarette. Exudate accumulates rapidly over time, serous inflammation is acute. after serous inflammation, on the basis of the remaining proteins, connective tissue develops, adhesions. With inflammation, there is hyperemia, redness, pinpoint hemorrhages, some tarnishing from the imposition of proteins.

Causes of serous inflammation

chemical influences - mustard, turpentine, spanish flies

thermal and physical moments - burns and frostbite, ultraviolet rays, x-rays and radium rays,

infectious agents - Frenkel's diplococcus, tuberculosis bacillus, influenza virus, vibrio cholerae, streptococci, serous inflammation is a consequence of tissue sensitization and manifests itself in anaphylactic conditions. For example, the Artyus-Sakharov phenomenon

Serous Inflammation

Serous inflammation of the skin
Serous exudate accumulates between the collagen and elastic fibers of the skin under the epidermis and between the Malpighian and horny layers of the epidermis, serous exudate collects under the stratum corneum, exfoliates the epidermis and forms blisters, vesicles.

Serous inflammation in the serous sheets of the pleura, pericardium, peritoneum, joints is accompanied by the accumulation of serous exudate in the corresponding cavity.

serous inflammation can also develop on the mucous membranes.

If in the skin, serous sheets, mucous membranes serous inflammation is complicated by purulent inflammation, then this does not happen in the internal parenchymal organs.

With serous myocarditis, there is a picture of edema of the interstitial tissue of the myocardium. Serous fluid with a small amount of cells, accumulating in the interstitium of the organ, pushes the muscle fibers apart. In this case, hydropic swelling of the collagen and elastic fibers of the interstitial tissue is observed.

In the liver with this form of inflammation, serous exudate accumulates in the spaces of Disse along the course of the trabeculae, pushing the walls of the sinusoids away from the trabeculae. The interstitial tissue is also edematous. It is observed with Graves' disease, with sepsis.

In the kidneys, serous exudate accumulates in the cavity of the Shumlyansky-Bowman capsule - serous glomerulonephritis.

In the lungs - in the alveoli. Often with serous exudate that desquamated cells of the capsular and alveolar epithelium are mixed

Serous inflammation in the internal organs always develops in the interstitial tissue of the organ or, as it is also called, in the interstitium and always wears diffuse character covering the entire organ. It usually proceeds acutely, ending with the resorption of the serous fluid and recovery, or passes into a productive inflammation.

fibrinous inflammation . Fibrinous inflammation is characterized by the release of exudate containing a large amount of coarse proteins and fibrinogen, leukocytes and cells of necrotic tissue. Croupous inflammation - necrosis during fibrinous inflammation captures only the surface layers of the tissue, then the coagulated fibrin lies superficially, it is easily removed without damaging the tissue. diphtheritic inflammation - tissue necrosis is deep, then fibrinous exudate is secreted and coagulated in the depths of the tissue itself, often undergoes hyalinization with the formation of a dense film. When you try to remove the film, you get bleeding, an ulcer. This second subspecies of fibrinous inflammation is called diphtheritic inflammation.

On mucous membranes covered multilayer flat epithelium (oral cavity, pharynx, tonsils, epiglottis, esophagus, true vocal cords, cervix), films are usually associated with the epithelium. In mucous membranes covered prismatic epithelium (upper respiratory tract, gastrointestinal tract, etc.), the connection of the epithelium with the underlying tissue is loose.

Exodus diphtheritic inflammation: on the site of deep ulcers that occur when the film is rejected, scars appear.

Purulent inflammation .

The most common cause is pyogenic microorganisms

characteristic morphological feature is histolysis - tissue melting by proteolytic enzymes of leukocytes

Purulent inflammation can be limited (abscess) and diffuse (phlegmon), purulent inflammation in pre-existing cavities with accumulation of pus in them is called empyema.

Abscess- focal purulent inflammation, the formation of a cavity filled with pus. An abscess develops when tissue necrosis occurs in the focus of inflammation. The resulting abscess is delimited from the adjacent tissue by a shaft of granulation tissue. Outside, it consists of connective tissue fibers, and inside it is formed by granulation tissue and thickened pus. The abscess membrane that produces pus is called pyogenic membrane.

Abscesses may be single or multiple; the latter are often formed in organs with septicopyemia due to microbial embolism.

Abscess outcome: on the site of abscesses (histolysis) scars are formed; in some cases, the abscess takes a chronic course: a connective tissue capsule is formed around it, the inner layer of which is represented by granulation tissue (pyogenic membrane).

Phlegmon- diffuse (diffuse) purulent inflammation, in which purulent exudate spreads diffusely between tissue elements, impregnating and exfoliating tissues. Occurs in the subcutaneous tissue, in the area of ​​the fascia, along the neurovascular bundles, in the parenchymal organs, in the pia mater. Phlegmon of fibrous fat is called cellulite.

There are soft and hard phlegmon. Soft phlegmon is characterized by the absence of foci of necrosis in the tissue, hard phlegmon - the presence of such foci that are not subject to purulent fusion, as a result of which the tissue becomes very dense; dead tissue is gradually sloughed off.

Hemorrhagic inflammation. It is characterized by the presence of a large number of red blood cells in the exudate. In its development, the importance of vascular permeability is great. It occurs in severe infectious diseases: plague, anthrax, influenza, in the past - with smallpox.

Putrid inflammation. More often occurs in wounds with extensive crushing of tissues. It is associated more often with clostridial (anaerobic) infection in combination with pyogenic microorganisms. Extensive foci of necrosis are characteristic.

Catarrh. Occurs on mucous membranes. It is characterized by an abundance of exudate that drains from the surface.

The exudate always contains mucus. May be serous, purulent and mucous. It can occur with infectious diseases (catarrh of the upper respiratory tract with acute respiratory infections), allergic conditions, etc.

Exodus more often favorable - complete restoration of the mucous membrane; sometimes catarrh can take chronic course, which is accompanied by a restructuring of the mucous membrane and its atrophy or hypertrophy.

Topic 6. Inflammation

6.7. Classification of inflammation

6.7.2. Exudative inflammation

Exudative inflammation characterized by the predominance of the reaction of the vessels of the microvasculature with the formation of exudate, while the alterative and proliferative components are less pronounced.

Depending on the nature of the exudate, the following types of exudative inflammation are distinguished:

-serous;
- hemorrhagic;
- fibrinous;
-purulent;
- catarrhal;
- mixed.

Serous inflammation

Serous inflammation characterized by the formation of exudate containing 1.7-2.0 g/l of protein and a small number of cells. Flow serous inflammation is usually acute.

The reasons: thermal and chemical factors (burns and frostbite in the bullous stage), viruses (for example, herpes labialis, herpes zoster and many others), bacteria (for example, mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella), rickettsia, allergens of plant and animal origin, autointoxication (for example, with thyrotoxicosis, uremia), bee sting, wasp, caterpillar, etc.

Localization . It occurs most often in serous membranes, mucous membranes, skin, less often in internal organs: in the liver, exudate accumulates in perisinusoidal spaces, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule, in the stroma.

Morphology . Serous exudate is a slightly cloudy, straw-yellow, opalescent liquid. It contains mainly albumins, globulins, lymphocytes, single neutrophils, mesothelial or epithelial cells and looks like a transudate. In the serous cavities, macroscopically, exudate from transudate can be distinguished by the state of the serous membranes. When exuding, they will have everything morphological features inflammation, with transudation - manifestations of venous plethora.

Exodus serous inflammation is usually favorable. Even a significant amount of exudate can be absorbed. Sclerosis sometimes develops in the internal organs as a result of serous inflammation in its chronic course.

Meaning determined by the degree functional disorders. In the cavity of the heart shirt, the inflammatory effusion impedes the work of the heart; in the pleural cavity, it leads to compression of the lung.

Hemorrhagic inflammation

Hemorrhagic inflammation characterized by the formation of exudate, represented mainly by erythrocytes.

With the flow is acute inflammation. The mechanism of its development is associated with a sharp increase in the permeability of microvessels, pronounced erythrodiapedesis and reduced leukodiapedesis due to negative chemotaxis in relation to neutrophils. Sometimes the content of red blood cells is so high that the exudate resembles a hemorrhage, for example, with anthrax meningoencephalitis - “the red cap of the cardinal”.

The reasons: severe infectious diseases - influenza, plague, anthrax, sometimes hemorrhagic inflammation can join other types of inflammation, especially against the background of beriberi C, and in persons suffering from pathology of the hematopoietic organs.

Localization. Hemorrhagic inflammation occurs in the skin, in the mucosa of the upper respiratory tract, gastrointestinal tract, lungs, and lymph nodes.

Exodus hemorrhagic inflammation depends on the cause that caused it. With a favorable outcome, complete resorption of the exudate occurs.

Meaning. Hemorrhagic inflammation is a very severe inflammation, which often ends in death.

fibrinous inflammation

fibrinous inflammation characterized by the formation of exudate rich in fibrinogen, which in the affected (necrotic) tissue turns into fibrin. This process is facilitated by the release of a large amount of thromboplastin in the necrosis zone.

Flow fibrinous inflammation is usually acute. Sometimes, for example, with tuberculosis of the serous membranes, it has chronic.

The reasons. Fibrinous inflammation can be caused by pathogens of diphtheria and dysentery, Frenkel's diplococci, streptococci and staphylococci, mycobacterium tuberculosis, influenza viruses, endotoxins (with uremia), exotoxins (mercuric chloride poisoning).

Localized fibrinous inflammation on the mucous and serous membranes, in the lungs. A grayish-whitish film appears on their surface (“membraneous” inflammation). Depending on the depth of necrosis and the type of epithelium of the mucous membrane, the film can be connected with the underlying tissues either loosely and, therefore, easily separated, or firmly and, as a result, separated with difficulty. There are two types of fibrinous inflammation:

-croupous;
-diphtheritic.

Croupous inflammation(from scot. group- film) occurs with shallow necrosis in the mucous membranes of the upper respiratory tract, gastrointestinal tract, covered with prismatic epithelium, where the connection of the epithelium with the underlying tissue is loose, so the resulting films are easily separated along with the epithelium even when deeply impregnated with fibrin. Macroscopically, the mucous membrane is thickened, swollen, dull, as if sprinkled with sawdust, if the film is separated, a surface defect occurs. The serous membrane becomes rough, as if covered with hair - fibrin threads. With fibrinous pericarditis in such cases, they speak of a “hairy heart”. Among internal organs croupous inflammation develops in the lung with croupous pneumonia.

Diphtheritic inflammation(from Greek. diphtera- leathery film) develops with deep tissue necrosis and impregnation of necrotic masses with fibrin on mucous membranes covered with squamous epithelium (oral cavity, pharynx, tonsils, epiglottis, esophagus, true vocal cords, cervix). The fibrinous film is tightly soldered to the underlying tissue; when it is rejected, a deep defect occurs. This is due to the fact that squamous epithelial cells are closely related to each other and to the underlying tissue.

Exodus fibrinous inflammation of the mucous and serous membranes is not the same. With croupous inflammation, the resulting defects are superficial and complete regeneration of the epithelium is possible. With diphtheritic inflammation, deep ulcers form, which heal by scarring. In the serous membranes, fibrin masses undergo organization, which leads to the formation of adhesions between the visceral and parietal sheets of the pleura, peritoneum, pericardial shirt (adhesive pericarditis, pleurisy). In the outcome of fibrinous inflammation, complete infection of the serous cavity is possible. connective tissue- its obliteration. At the same time, calcium salts can be deposited in the exudate, an example is the “shell heart”.

Meaning fibrinous inflammation is very large, since it forms the morphological basis of diphtheria, dysentery, and is observed during intoxication (uremia). With the formation of films in the larynx, trachea, there is a danger of asphyxia; with rejection of films in the intestine, bleeding from the resulting ulcers is possible. Adhesive pericarditis and pleurisy are accompanied by the development of pulmonary heart failure.

Purulent inflammation

Purulent inflammation characterized by a predominance of neutrophils in the exudate, which, together with liquid part exudate form pus. The composition of pus also includes lymphocytes, macrophages, necrotic cells of local tissue. In pus, microbes called pyogenic are usually detected, which are located freely, or are contained inside pyocytes (dead polynuclear cells): it's septic pus capable of spreading infection. However, germ-free pus does exist, such as when turpentine is injected, which was once used to “stimulate defensive reactions in the body” in debilitated infectious patients: as a result, developed aseptic pus .

Macroscopically pus is a cloudy, creamy liquid of a yellowish-greenish color, the smell and consistency of which varies depending on the aggressive agent.

The reasons: pyogenic microbes (staphylococci, streptococci, gonococci, meningococci), less often Frenkel's diplococci, typhoid bacillus, mycobacterium tuberculosis, fungi, etc. It is possible to develop aseptic purulent inflammation when certain chemicals enter the tissue.

The mechanism of pus formation associated with adaptation polynuclear cells specially to antibacterial control.

Polynuclear cells or granulocytes actively penetrate into the focus of aggression, thanks to amoeboid movements as a result of positive chemotaxis. They are unable to divide because they are the final cell of the myeloid series. The duration of their normal life in the tissues is no more than 4-5 days, in the focus of inflammation it is even shorter. Physiological role they are similar to macrophages. However, they absorb smaller particles: this microphages. Neutrophilic, eosinophilic and basophilic intracytoplasmic granules are a morphological substrate, but they reflect different functional characteristics of granulocytes.

Neutrophil polynuclear cells contain specific, optically visible, very heterogeneous granules of a lysosomal nature, which can be divided into several types:

Small granules, elongated in the form of a bell, dark in the electron microscope, which contain alkaline and acid phosphatases;
-medium granules, rounded, moderate density, contain lactoferrin
- bulk granules are oval, less dense, contain proteases and beta-glucuronidase;
- large size granules, oval, very electron dense, contain peroxidase.

Due to the presence of various types of granules, the neutrophil polynuclear is able to carry out in a different way fight infection. Penetrating into the focus of inflammation, polynuclear cells release their lysosomal enzymes. Lysosomes, represented by aminosaccharides, contribute to the destruction of cell membranes and the lysis of some bacteria. Lactoferrin containing iron and copper enhances the action of lysozyme. The role of peroxidases is more important: by combining the actions of hydrogen peroxide and cofactors such as halide compounds (iodine, bromine, chlorine, thiocyanate), they enhance their antibacterial and antiviral actions. Hydrogen peroxide is necessary for polynuclear cells for efficient phagocytosis. They can additionally produce it at the expense of some bacteria, such as streptococcus, pneumococcus, lactobacillus, some mycoplasmas that produce it. The lack of hydrogen peroxide reduces the lysing effect of polynuclear cells. In chronic granulomatous disease (chronic familial granulomatosis), which is transmitted by a recessive type only to boys, bactericidal failure of granulocytes is observed and then macrophages are involved in the capture of bacteria. But they are not able to completely resorb the lipid membranes of microorganisms. The resulting products of antigenic material cause a local necrotic reaction of the Arthus type.

Eosinophilic polynuclear cells capable of phagocytosis, although to a lesser extent than macrophages, for 24 to 48 hours. They accumulate in allergic inflammation.

Basophilic polynuclear cells . They share many functional properties with tissue basophils ( mast cells). Unloading of their granules is caused by cold, hyperlipemia, thyroxin. Their role in inflammation is not well understood. In large numbers, they appear with ulcerative colitis, regional colitis (Crohn's disease), with various allergic skin reactions.

Thus, the dominant population in purulent inflammation is the population neutrophilic granulocytes. Neutrophil polynuclear cells carry out their destructive actions in relation to the aggressor with the help of an increased outpouring of hydrolases into the focus of inflammation as a result of the following four mechanisms:

At polynuclear destruction under the influence of an aggressor;
-auto-digestion of polynuclear cells as a result of a rupture of the lysosomal membrane inside the cytoplasm under the action of various substances, for example, silicon crystals or sodium urates;
-release of enzymes by granulocytes into the intercellular space;
-by inverted endocytosis, which is carried out with the help of invagination cell membrane without swallowing the aggressor, but by pouring enzymes into him.

The last two phenomena are most often observed during resorption of the antigen-antibody complex.

It must be emphasized that lysosomal enzymes, if released, exert their destructive effect not only on the aggressor, but also on the surrounding tissues. Therefore, purulent inflammation is always accompanied histolysis. The degree of cell death in various forms of purulent inflammation is different.

Localization. Purulent inflammation occurs in any organ, in any tissue.

Types of purulent inflammation depending on the prevalence and localization:

-furuncle;
-carbuncle;
-phlegmon;
-abscess;
- empyema.

Furuncle

Furuncle- this is an acute purulent-necrotic inflammation of the hair follicle (follicle) and associated sebaceous gland with the surrounding tissue.

The reasons: staphylococcus, streptococcus.

Terms conducive to the development of a boil: constant contamination of the skin and friction with clothing, irritation chemicals, abrasions, scratches and other microtraumas, as well as increased activity of sweat and sebaceous glands, beriberi, metabolic disorders (for example, diabetes mellitus), starvation, weakening of the body's defenses.

Localization: a single boil can occur on any part of the skin where there is hair, but most often on the back of the neck (in the back of the head), face, back, buttock, in the armpit and inguinal region.

The development of a boil begins with the appearance of a dense painful nodule with a diameter of 0.5-2.0 cm, bright red, rising above the skin in a small cone. On the 3-4th day, a softening area is formed in its center - a purulent “head”.

Macroscopically on the 6-7th day, the furuncle is a cone-shaped, towering above the surface of the skin, inflammatory infiltrate of purple-bluish color with a yellowish-greenish apex (“head” of the boil).

Then the boil breaks through with the release of pus. At the site of the breakthrough, a greenish area of ​​necrotic tissue is found - the core of the boil. Together with pus and blood, the rod is rejected.

Exodus. With an uncomplicated course of the process, the cycle of development of the boil lasts 8-10 days. The skin tissue defect is filled with granulation tissue, which then matures to form a scar.

Meaning. The process of development of a boil can be accompanied by a pronounced local inflammatory reaction and relatively quickly end in clinical recovery. But with reduced resistance, a necrotic rod may melt and an abscess, phlegmon, may occur. A furuncle on the face, even a small one, is usually accompanied by rapidly progressive inflammation and edema, and a severe general course. In an unfavorable course, the development of fatal complications is possible, such as septic thrombosis of the sinuses of the dura mater, purulent meningitis and sepsis. In debilitated patients, the development of multiple boils is possible - this is furunculosis.

Carbuncle

Carbuncle- this is an acute purulent inflammation of several adjacent hair follicles and sebaceous glands with necrosis of the skin and subcutaneous tissue the affected area.

A carbuncle occurs when pyogenic microbes enter the ducts of the sebaceous or sweat glands, as well as when they penetrate the skin through minor lesions, squeezing out a boil.

Terms development and localization the same as for the furuncle.

Macroscopically, the carbuncle is an extensive dense, red-purple infiltrate on the skin, in the center of which there are several purulent “heads”.

The most dangerous carbuncle of the nose and especially the lips, in which the purulent process can spread to the membranes of the brain, resulting in developing purulent meningitis. Treatment operational; at the first symptoms of the disease, it is necessary to consult a surgeon.

Meaning. A carbuncle is more dangerous than a boil, it is always accompanied by a pronounced intoxication. With carbuncle, there may be complications: purulent lymphadenitis, purulent thrombophlebitis, erysipelas, phlegmon, sepsis.

Phlegmon

Phlegmon- this is a diffuse purulent inflammation of the tissue (subcutaneous, intermuscular, retroperitoneal, etc.), or the walls of a hollow organ (stomach, appendix, gallbladder, intestines).

The reasons: pyogenic microbes (staphylococci, streptococci, gonococci, meningococci), less often Frenkel's diplococci, typhoid bacillus, fungi, etc. It is possible to develop aseptic purulent inflammation when certain chemicals enter the tissue.

Phlegmon examples:

Paronychius- acute purulent inflammation of the periungual tissue.

Felon- acute purulent inflammation of the subcutaneous tissue of the finger. The tendon and bone may be involved in the process, purulent tendovaginitis and purulent osteomyelitis occur. With a favorable outcome, scarring of the tendon occurs and contracture of the finger is formed. With an unfavorable outcome, phlegmon of the hand develops, which can be complicated by purulent lymphadenitis, sepsis.

Phlegmon of the neck- acute purulent inflammation of the tissue of the neck, develops as a complication of pyogenic infections of the tonsils, maxillofacial system. Distinguish soft and hard phlegmon. Soft phlegmon characterized by the absence of visible foci of tissue necrosis, in hard cellulitis there is a coagulative necrosis of the fiber, the tissue becomes very dense and does not undergo lysis. Dead tissue can be sloughed away, exposing the vascular bundle, which can lead to bleeding. The danger of neck phlegmon also lies in the fact that the purulent process can spread to the tissue of the mediastinum (purulent mediastinitis), pericardium (purulent pericarditis), pleura (purulent pleurisy). Phlegmon is always accompanied by severe intoxication and may be complicated by sepsis.

Mediastenitis- acute purulent inflammation of the tissue of the mediastinum. Distinguish front and rear purulent mediastinitis.

Anterior mediastinitis is a complication of purulent inflammatory processes of organs anterior mediastinum, pleura, phlegmon of the neck.

Posterior mediastinitis most often caused by the pathology of the esophagus: for example, traumatic injuries by foreign bodies (damage to the fish bone is especially dangerous), decaying cancer of the esophagus, purulent-necrotic esophagitis, etc.

Purulent mediastinitis is a very severe form of purulent inflammation, accompanied by pronounced intoxication, which often causes the death of the patient.

Paranephritis - purulent inflammation of the perirenal tissue. Paranephritis is a complication of purulent nephritis, septic kidney infarction, decaying kidney tumors. Meaning: intoxication, peritonitis, sepsis.

Parametritis- purulent inflammation of the uterine tissue. Occurs in septic abortions, infected childbirth, decay malignant tumors. First, purulent endometritis occurs, then parametritis. Meaning: peritonitis, sepsis.

paraproctitis- inflammation of the tissue surrounding the rectum. It can be caused by dysentery ulcers, ulcerative colitis, decaying tumors, anal fissures, hemorrhoids. Meaning: intoxication, the occurrence of pararectal fistulas, the development of peritonitis.

Abscess

Abscess(abscess) - focal purulent inflammation with tissue melting and the formation of a cavity filled with pus.

Abscesses are acute and chronic. The wall of an acute abscess is the tissue of the organ in which it develops. Macroscopically, it is uneven, rough, often with torn structureless edges. Over time, the abscess is delimited by a shaft of granulation tissue, rich in capillaries, through the walls of which there is an increased emigration of leukocytes. Formed as if the shell of the abscess. Outside, it consists of connective tissue fibers that are adjacent to the unchanged tissue, and inside - of granulation tissue and pus, which is continuously renewed due to the constant supply of leukocytes from granulations. The abscess that produces pus is called pyogenic membrane.

Abscesses can be localized in all organs and tissues, but are of the greatest practical importance abscesses of the brain, lungs, liver.

Abscesses of the brain are usually divided into:

Peacetime abscesses;
wartime abscesses.

wartime abscesses are most often a complication of shrapnel wounds, blind injuries of the skull, less often through bullet wounds. It is customary to distinguish between early abscesses that occur up to 3 months after injury and late abscesses that occur after 3 months. A feature of wartime brain abscesses is that they can occur 2-3 years after injuries, and also occur in the lobe of the brain opposite the wound zone.

Peacetime abscesses. The source of these abscesses are:

-purulent otitis media (purulent inflammation of the middle ear);
-purulent inflammation of the paranasal sinuses (purulent sinusitis, frontal sinusitis, pansinusitis);
-hematogenous metastatic abscesses from other organs, including furuncle, facial carbuncle, pneumonia.

Localization. Most often, abscesses are localized in the temporal lobe, less often - the occipital, parietal, frontal.

The most common in the practice of medical institutions are brain abscesses of otogenic origin. They are caused by scarlet fever, measles, influenza and other infections.

A middle ear infection can spread:

By continuation;
- lympho-hematogenous way;
- perineural.

From the middle ear, the infection continues to spread to the pyramid temporal bone and causes purulent inflammation (osteomyelitis of the temporal bone), then the process passes to the dura mater (purulent pachymeningitis), pia mater (purulent leptomeningitis), later, with the spread of purulent inflammation to the brain tissue, an abscess is formed. With lymphohematogenous occurrence of an abscess, it can be localized in any part of the brain.

Meaning brain abscess. An abscess is always accompanied by tissue death and therefore the function of the area of ​​the brain in which the abscess is localized completely falls out. Purulent inflammation toxins have a tropism for neurons, causing their irreversible dystrophic changes and death. An increase in the volume of an abscess can lead to its breakthrough into the ventricles of the brain and death of the patient. When inflammation spreads to the soft membranes of the brain, purulent leptomeningitis occurs. With an abscess, there is always a violation of blood circulation, accompanied by the development of edema. An increase in the volume of the lobe leads to dislocation of the brain, displacement of the trunk and infringement of it in the foramen magnum, which leads to death. Treatment of fresh abscesses is reduced to their drainage (according to the principle “ ubi pus ibi incisio et evacuo”), old abscesses are removed along with the pyogenic capsule.

lung abscess

lung abscess most often a complication various pathologies lungs, such as pneumonia, lung cancer, septic heart attacks, foreign bodies, less often it develops with hematogenous spread of infection.

The significance of lung abscess is that it is accompanied by severe intoxication. With the progression of the abscess, purulent pleurisy, pyopneumothorax, pleural empyema, and pulmonary bleeding may develop. In the chronic course of the process, the development of secondary systemic amyloidosis and exhaustion is possible.

liver abscess

liver abscess- occurs most often in diseases of the gastrointestinal tract, which are complicated by the development of the inflammatory process in portal vein. These are pylephlebitic liver abscesses. In addition, infection in the liver can penetrate the biliary tract - cholangitis abscesses. And, finally, it is possible to get an infection by the hematogenous route, with sepsis.

Causes of pylephlebitic abscesses liver are:

-intestinal amebiasis;
- bacterial dysentery;
-appendicitis;
- peptic ulcer of the stomach and duodenum.

Causes of cholangitis abscesses most often are:

-purulent cholecystitis;
-typhoid fever;
-purulent pancreatitis;
- disintegrating tumors of the liver, gallbladder, pancreas;
- phlegmon of the stomach.

Meaning process consists in severe intoxication, which leads to dystrophic changes in vital important organs, it is also possible the development of such formidable complications as subdiaphragmatic abscess, purulent peritonitis, sepsis.

empyema

empyema- purulent inflammation with accumulation of pus in closed or poorly drained pre-existing cavities. Examples are the accumulation of pus in the pleural, pericardial, abdominal, maxillary, frontal cavities, in the gallbladder, appendix, fallopian tube (pyosalpinx).

Empyema of the pericardium- occurs either by continuation from adjacent organs, or when an infection enters the hematogenous route, or with a septic heart attack. This is a dangerous, often fatal complication. With a long course, adhesions occur, calcium salts are deposited, the so-called armored heart develops.

Pleural empyema- occurs as a complication of pneumonia, lung cancer, pulmonary tuberculosis, bronchiectasis, septic pulmonary infarction. The value is in severe intoxication. The accumulation of a large amount of fluid causes a displacement, and sometimes - a rotation of the heart with the development of acute heart failure. Compression of the lung is accompanied by the development of compression atelectasis and the development of pulmonary heart failure.

empyema abdominal cavity , as an extreme morphological manifestation of purulent peritonitis is a complication of many diseases. To the development of purulent peritonitis lead:

-wired (perforated) ulcers of the stomach and duodenum;
- purulent appendicitis;
-purulent cholecystitis;
- intestinal obstruction of various origins;
- intestinal infarction;
- disintegrating tumors of the stomach and intestines;
-abscesses (septic heart attacks) of the abdominal organs;
-inflammatory processes of the pelvic organs.

Meaning. Purulent peritonitis is always accompanied by a pronounced intoxication and, without surgical intervention, usually leads to death. But even in the case of surgical intervention and successful antibiotic therapy possible development of adhesive disease, chronic, and sometimes acute intestinal obstruction, which, in turn, requires surgical intervention.

Catarrh(from Greek. catarrheo- flow down), or Qatar. It develops on the mucous membranes and is characterized by an abundant accumulation of mucous exudate on their surface due to hypersecretion of the mucous glands. The exudate can be serous, mucous, and desquamated cells of the integumentary epithelium are always mixed with it.

The reasons catarrh are different. Catarrhal inflammation develops with viral, bacterial infections, under the influence of physical and chemical agents, it can be of an infectious-allergic nature, the result of autointoxication (uremic catarrhal gastritis, colitis).

Catarrh may be acute and chronic. Acute catarrh is characteristic of a number of infections, for example, acute catarrh of the upper respiratory tract with acute respiratory infections. Chronic catarrh can occur both in infectious (chronic purulent catarrhal bronchitis) and noncommunicable diseases. Chronic catarrh may be accompanied by atrophy or hypertrophy of the mucosa.

Meaning catarrhal inflammation is determined by its localization, intensity, nature of the course. The most important are catarrhs ​​of the mucous membranes of the respiratory tract, often taking on a chronic character and having severe consequences (emphysema, pneumosclerosis).

Mixed inflammation. In those cases when another type of exudate joins, mixed inflammation is observed. Then they talk about serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic inflammation. Most often, a change in the type of exudative inflammation is observed with the addition of a new infection, a change in the reactivity of the body.