Causes of serous inflammation. Inflammation exudative type of inflammation

Definition.

Exudative inflammation is a form of inflammation in which phagocytosis is carried out by neutrophilic leukocytes.

Classification.

Depending on the nature of the exudate, there are following forms exudative inflammation:

1. Serous- a lot of fluid (with a protein content of about 3%) and few neutrophilic leukocytes.
2. Fibrinous- due to a sharp increase in capillary permeability, not only relatively small albumin molecules, but also large fibrinogen molecules, which turn into fibrin, leave their limits.
   On mucous membranes there are 2 types fibrinous inflammation:
   • lobar, when the films are easily rejected due to the single-layer nature of the epithelium covering the trachea, bronchi, etc. And
   • diphtheritic, when the films are difficult to reject due to the multilayered nature of the epithelium, for example, on the oral mucosa, or due to the peculiarities of the relief of the mucous membrane (in the intestines).
3. Purulent- liquid containing 8-10% protein and big amount leukocytes.
   There are 2 types of purulent inflammation:
   • phlegmon - with unclear boundaries and without the formation of destructive cavities,
   • abscess - a limited accumulation of pus in the cavity of tissue destruction.
4. On the mucous membranes, inflammation with serous or purulent exudate is called catarrhal. It is characterized by hypersecretion of mucus by glands located in the thickness of the membrane.

The so-called hemorrhagic inflammation- not a separate type of inflammation. This term only reflects the admixture of red blood cells with serous, fibrinous or purulent exudate.

Highlight as separate form putrefactive inflammation is impractical, since the nature of tissue damage is associated not with the characteristics of the exudate, but with their necrosis under conditions of vital activity of anaerobic microbes and weakly expressed neutrophilic infiltration of these tissues.

Occurrence.

Exudative inflammation occurs in most infectious diseases, for all surgical infectious complications and less often - with inflammation of a non-infectious nature, for example, with such artificial diseases in prisoners as turpentine or gasoline phlegmon.

Conditions of occurrence.

Penetration of bacteria, RNA viruses into tissue, denaturation of tissue proteins under the influence of external or internal factors.

Mechanisms of occurrence.

Macroscopic picture.

With the serous nature of the inflammation, the tissue is hyperemic, loose and edematous.

With fibrinous inflammation, the surface of the mucous or serous membranes is covered with dense grayish films of fibrin. With diphtheritic inflammation, their rejection is accompanied by the formation of erosions and ulcers. With fibrinous inflammation of the lungs, they become similar in density to liver tissue (hepatization).

With phlegmon, the tissue is diffusely saturated with pus. When an abscess is opened, a cavity filled with pus is revealed. In an acute abscess, the walls are the very tissue in which it formed. In a chronic abscess, its wall consists of granulation and fibrous tissue.

Catarrhal inflammation is characterized by hyperemia and swelling of the mucous membrane, covered with mucus or pus.

Microscopic picture.

With serous inflammation, the tissues are loosened, contain slightly eosinophilic fluid, and a few neutrophils.

With purulent inflammation, the liquid part of the exudate is intensely stained with eosin, neutrophils are numerous, sometimes forming entire fields, and cellular detritus is detected.

With fibrinous inflammation, fibrin threads are visible in the exudate, which are clearly visualized with special stains according to Weigert, chromotrope 2B, etc. The epithelium of the mucous membranes is usually necrotic and desquamated.

With catarrhal inflammation, desquamation of some epithelial cells, edema, congestion of blood vessels and neutrophilic infiltration of the mucous membrane are noted.

Clinical significance.

In the vast majority of cases, exudative inflammation is acute.

Serous and catarrhal inflammation usually results in complete restoration of the tissue structure.

Fibrinous inflammation except full recovery in the lungs may result in the organization of fibrin by carnification, which may affect lung function. Fibrinous inflammation on serous membranes often ends in the formation of adhesions, which is especially dangerous in abdominal cavity and in the pericardial cavity.

Phlegmon, if it is not opened in a timely manner, is fraught with the spread of pus to other tissues and corrosion large vessels. Abscesses are accompanied by tissue destruction, which can be far from indifferent if they are large in volume or in a certain location (for example, in the heart). Chronic abscesses are dangerous due to the possibility of developing secondary AA amyloidosis.

EXUDATIVE INFLAMMATION

ALTERNATIVE INFLAMMATION

TERMINOLOGY OF INFLAMMATION

The name of inflammation of a particular tissue (organ) is usually composed by adding the ending to the Latin and Greek name of the organ or tissue itis , and to Russian - it . For example, inflammation of the pleura is designated as pleuritis- pleurisy, kidney inflammation - nephritis- jade. However, inflammation of some organs has special names. For example, inflammation of the pharynx is called sore throat, inflammation of the lungs is called pneumonia.

CLASSIFICATION OF INFLAMMATION

Based on the predominance of one or another component of inflammation, the following are distinguished:

-alterative inflammation;
- exudative inflammation;
- proliferative inflammation.

According to the nature of the flow:

-acute - up to 2 months;
- subacute, or prolonged acute - up to 6 months;
-chronic, lasting for years.

By localization in the organ:

-parenchymal;
- interstitial (intermediate);
-mixed.

By type of tissue reaction:

-specific;
-nonspecific (banal).

Alterative inflammation- this is a type of inflammation in which damage in the form of dystrophy and necrosis predominates. Downstream it is acute inflammation . By localization - parenchymal . Examples of alterative inflammation include alterative myocarditis and alterative neuritis in diphtheria of the pharynx, viral encephalitis, poliomyelitis, acute hepatitis with Botkin's disease, acute ulcers in the stomach. Sometimes this type of inflammation can be a manifestation of an immediate hypersensitivity reaction.

Exodus depends on the depth and area of ​​tissue damage and usually ends with scarring.

Meaning Alterative inflammation is determined by the importance of the affected organ and the depth of its damage. Alterative inflammation in the myocardium and nervous system is especially dangerous.

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

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

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

Serous inflammation characterized by the formation of exudate containing 1.7-2.0 g/l protein and not a large number of cells. Flow serous inflammation is usually acute.

Causes: 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 sting, caterpillar sting, etc.

Localization. Occurs most often in serous membranes, mucous membranes, skin, less often in internal organs: in the liver, exudate accumulates in the 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 transudate. In serous cavities, exudate can be macroscopically distinguished from transudate by the state of the serous membranes. During exudation they will contain everything morphological characteristics inflammation, with transudation - manifestations of venous congestion.

Exodus serous inflammation is usually favorable. Even significant amount exudate may resolve. Sclerosis sometimes develops in internal organs as a result of serous inflammation during its chronic course.

Meaning determined by degree functional disorders. In the cavity of the cardiac membrane, inflammatory effusion complicates the work of the heart, in pleural cavity leads to compression of the lung.

. Exudative inflammation characterized by the predominance of the second, exudative, phase of inflammation. As is known, this phase occurs in different terms following damage to cells and tissues and is caused by 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. At slight damage vessels, only low-molecular-weight albumins leak into the site of inflammation; with more severe damage, large-molecular globulins appear in the exudate and, finally, the largest fibrinogen molecules, which are converted into fibrin in the tissue. 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, and mixed inflammation are distinguished (Diagram 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 (PMN) and deflated epithelial cells. Serous inflammation develops most often in serous cavities, mucous membranes, soft meninges, however, less often - in the internal organs.

Causes. 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 characteristic feature inflammation caused by viruses of the Herpesviridae family (herpes simplex, chicken pox).

Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel's 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.

When the serous membranes are inflamed, a cloudy fluid accumulates in the serous cavities, poor cellular elements, among which deflated mesothelial cells and single PMNs predominate. The same picture is observed in the soft meninges, which become thickened and 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, peeling it away from the dermis with the formation of large blisters (for example, in burns). With serous inflammation, vascular congestion is always observed. Serous exudate helps remove pathogens and toxins from affected tissues.

Exodus. Usually favorable. The exudate is well absorbed. 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 outflow obstruction cerebrospinal fluid(liquor) and cerebral edema, pericardial effusion complicates the work of the heart, and serous inflammation of the lung parenchyma can lead to acute respiratory failure.

Fibrinousinflammation. It is characterized by 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, PMNs and elements of necrotic tissue are also found in the exudate. Fibrinous inflammation is most often localized on the serous and mucous membranes.

Causes. The causes of fibrinous inflammation are varied - bacteria, viruses, chemical substances exogenous and endogenous origin. Among bacterial agents, the development of fibrinous inflammation is most promoted by diphtheria corynebacterium, Shigella, and Mycobacterium tuberculosis. Fibrinous inflammation can also be caused by Frenkel diplococci, pneumococci, streptococci and staphylococci, and some viruses. The development of fibrinous inflammation during autointoxication (uremia) is typical. The development of fibrinous inflammation is determined sharp increase permeability vascular wall, which may be due, on the one hand, to the characteristics of bacterial toxins (for example, the vaso-paralytic effect of the diphtheria corynebacterium exotoxin), on the other hand, to the hyperergic reaction of the body.

Morphological characteristics. A light gray film appears on the surface of the mucous or serous membrane. Depending on the type of epithelium and the depth of necrosis, the film can be loosely or firmly connected to the underlying tissues, and therefore two types of fibrinous inflammation are distinguished; croupous and diphtheritic.

Croupous inflammation most often develops on 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 removable. When such a film is separated, surface defects are formed. The mucous membrane is swollen, dull, sometimes it seems as if it is sprinkled with sawdust. The serous membrane is dull, covered with gray fibrin threads, resembling hairline. For example, fibrinous inflammation of the pericardium has long been figuratively called hairy heart. Fibrinous inflammation in the lung with the formation of blood clots. postural exudate in the alveoli of the lung lobes is called lobar pneumonia.

Diphtheritic inflammation flutters and organs covered with multilayer flat epithelium or single-layer epithelium with a loose connective tissue base, promoting 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 the mucous 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 in lobar inflammation and deep in diphtheria. Superficial ulcers usually regenerate completely; when deep ulcers heal, scars form. In the lung with lobar pneumonia the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils at the exu site. tsata appears connective tissue(exudate is organized), with excessive activity of neutrophils, an abscess may develop and lung gangrene. On serous membranes, fibrinous exudate can melt, but more often it is submerged. organization is destroyed with the formation of adhesions between the serous layers. Complete overgrowth of the serous cavity—obliteration—may occur.

Meaning. The significance of fibrinous inflammation is largely determined by its type. For example, with diphtheria of the pharynx, a fibrinous film containing pathogens is tightly bound to the underlying tissues (diphtheritic inflammation), and severe intoxication of the body with corynebacterium toxins and decay products of necrotic tissues develops. With diphtheria of the trachea, intoxication is mild, but easily torn off films cover the lumen of the upper respiratory tract, which leads to asphyxia (true croup).

Purulent inflammation. Develops when neutrophils predominate in the exudate. Pus is a thick, creamy mass of yellow-green color with characteristic odor. Purulent exudate is rich in proteins (mainly globulins). Shaped 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 inflammation site; 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 the 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 of the bacterial cell, resulting in the death of the microorganism, which is then lysed by lysosomal proteinases.

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

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

An abscess is a focal purulent inflammation, characterized by the melting of tissue with the formation of a cavity filled with pus. A shaft of granulation tissue is formed around the abscess, through numerous capillaries of which leukocytes enter the abscess cavity and decay products are partially removed. The membrane of an abscess that produces pus is called pio-gene membrane. At long term inflammation, the granulation tissue that forms the pyogenic membrane matures, and two layers are formed 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 the tissue, exfoliating and lysing tissue elements. Typically, phlegmon develops in tissues where there are conditions for easy distribution pus - in fatty tissue, in the area of ​​tendons, fascia, along the neurovascular bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, in addition to anatomical features, the pathogenicity of the pathogen and the state of the body’s defense systems play an important role.

There are soft and hard phlegmon. Soft cellulitis characterized by the absence of visible foci of necrosis in tissues, with hard cellulitis Foci of coagulation necrosis form in the tissues, which do not melt, but are gradually rejected. Cellulitis of fatty tissue is called whole-lulite, it is characterized by limitless distribution.

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

Flow. Purulent inflammation can be acute or chronic. Acute purulent inflammation tends to spread. The delineation of the abscess from the surrounding tissues is rarely good enough; progressive melting of the surrounding tissues may occur. The abscess usually ends with spontaneous emptying of pus during 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 canal lined with granulation tissue or epithelium, connecting the abscess cavity with hollow organ or body surface. In some cases, pus spreads under the influence of gravity along the muscle-tendon sheaths, neurovascular bundles, and fatty layers into the underlying sections and forms clusters there - leaks. 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 leaks of pus cause severe intoxication and lead to exhaustion of the body. With chronic purulent inflammation, the cellular composition exudation and inflammatory infiltrate. In the pus, along with neutrophilic leukocytes, a relatively large number of lymphocytes and macrophages appear; infiltration with lymphoid cells predominates in the surrounding tissue.

Outcomes and complications. Both the outcomes and complications of purulent inflammation depend on many factors: virulence of microorganisms, condition protective forces body, the prevalence of inflammation. When an abscess empties spontaneously or surgically, its cavity collapses and is filled with granulation tissue, which matures to form a scar. Less commonly, the abscess becomes encapsulated, the pus thickens and may undergo petrification. With phlegmon, healing begins with delimitation of the process, followed by the formation of a rough scar. If the course is unfavorable, purulent inflammation can spread to the blood and lymphatic vessels, and 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 significance of purulent inflammation is very great, since it lies V basis of many diseases and their complications. The significance of purulent inflammation is determined mainly by the ability of pus to melt tissue, which makes it possible for the process to spread by contact, lymphogenous and hematogenous routes.

Putrid inflammation. Develops when putrefactive microorganisms enter the focus of inflammation.

Causes. Putrefactive inflammation is caused by a group of clostridia, pathogens anaerobic infection— C.perfringens, C.novyi, C.septicum. Several types of clostridia are usually involved in the development of inflammation in combination with aerobic bacteria(staphylococci, streptococci). Anaerobic bacteria form oil and acetic acid, CO 2 , hydrogen sulfide and ammonia, which gives the exudate a characteristic putrefactive (ichorous) odor. Clostridia enter the human body, as a rule, from the ground, where there are a lot of bacteria themselves and their spores, so most often putrefactive inflammation develops in wounds, especially in cases of mass injuries and injuries (wars, disasters).

Morphological characteristics. Putrefactive inflammation develops most often in wounds with extensive crushing of tissue, with impaired blood supply conditions. The resulting inflammation is called anaerobic gangrene. A wound with anaerobic gangrene has characteristic appearance: its edges are bluish, gelatinous swelling of the tissue is observed. Fiber and pale, sometimes necrotic muscles protrude from the wound. When palpated, crepitus is detected in the tissues, and the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is initially determined, which is replaced by widespread necrotic changes. Neutrophils that enter the site of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign and 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 mass injuries and the severity of intoxication. Putrefactive inflammation in the form of sporadic cases can develop, for example, in the uterus after a criminal abortion, in the colon of newborns (the so-called necrotizing colitis of newborns).

Hemorrhagicinflammation. Characterized by a predominance of erythrocytes in the exudate. In the development of this type of inflammation, the main significance belongs to a sharp increase in microvascular permeability, as well as negative chemotaxis of neutrophils.

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

Morphological characteristics. Macroscopically areas hemorrhagic inflammation resemble hemorrhages. Microscopically, a large number of red blood cells, single neutrophils and macrophages are determined at the site of inflammation. Significant tissue damage is typical. Hemorrhagic inflammation can sometimes be difficult to distinguish from hemorrhage, for example, with hemorrhage into the abscess cavity from an arrosive 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, usually causing hemorrhagic inflammation.

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

Causes. A change in the composition of the exudate is naturally observed during inflammation: for starters inflammatory process The formation of serous exudate is characteristic; later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change quality composition leukocytes; Neutrophils are the first to appear at the site of inflammation; they are replaced by monocytes And later - lymphocytes. Moreover, in case of joining new infection In addition to ongoing inflammation, the nature of the exudate often changes. For example, when a bacterial infection joins a viral one respiratory infection mixed, 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 reactivity of the body changes and is a prognostically unfavorable sign.

Morphological characteristics. Determined by a combination of changes characteristic of various types 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 mixed exudate indicates the addition of a secondary infection or a decrease in the body’s resistance.

Catarrhalinflammation. Develops on mucous membranes and is characterized by copious discharge exudate, flowing from the surface of the mucosa, hence the name of this type of inflammation (Greek katarrheo - flowing). 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 physiological defensive reaction, which increases under conditions of inflammation.

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

Morphological characteristics. The mucous membrane is edematous, congested, exudate flows from its surface. The nature of the exudate can be different (serous, mucous, purulent), but mandatory component it 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, V epithelium contains many goblet cells.

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

Exodus. Acute catarrhal inflammations last 2-3 weeks and usually end with complete recovery. Chronic catarrhal inflammation is dangerous due to the development of atrophy or hypertrophy of the mucous membrane.

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

With this type of inflammation, a vascular-exudative reaction with the accumulation of serous exudate predominates in the focus; alteration and proliferation are less pronounced.

Causes- physical and chemical factors, frostbite, skin burns (solar, high temperature), infectious diseases: foot and mouth disease (phthisis), smallpox (vesicles), vesicular disease, pasteurellosis (edematous form), edematous disease of piglets.

Localization- in serous and mucous membranes, skin, subcutaneous tissue, parenchymal organs.

Flow- acute, chronic.

Classification:

Serous inflammatory edema,

Serous inflammatory dropsy,

· Bullous form.

Serous inflammatory edema. It is observed in the intestinal wall during poisoning, in the skin of pigs with erysipelas, in the subcutaneous tissue, the mesentery of the large intestine and the wall of the bottom of the stomach of piglets with edematous disease, in the subcutaneous tissue of the head of cattle with the edematous form of pasteurellosis; in the brain of horses with IEM (serous encephalitis), in the kidneys with erysipelas of pigs and with INAN of horses (serous glomerulonephritis), with serous lymphadenitis, serous pneumonia, serous myocarditis and dermatitis (erysipelas of pigs), serous dermatitis (allergy).

Serous inflammation can be:

· superficial and

· deep in the mucous membranes.

For superficial inflammation: the mucous membrane is swollen, focally or diffusely reddened, dull, without a characteristic shine, collected in folds. Often serous exudate is not detected. After 1-2 days, mucus is mixed with it, and serous inflammation turns into catarrhal inflammation.

For deep serous inflammation: the intestinal wall is sharply thickened due to the accumulation of serous exudate in the submucosa, loose. The mucous membrane is folded, dull, moist, focally reddened, and covered with mucus. The cut surface is wet.

Lymph nodes with serous inflammation are enlarged, focally or diffusely reddened on the incision, gray liquid flows from the surface of the incision. This is a serous exudate.

Serous inflammatory hydrops. It is characterized by the accumulation of serous exudate in the serous cavities (pleura, peritoneum, pericardium) with serous pericarditis (pasteurellosis), pleurisy, peritonitis (edematous disease of piglets).

Serous exudate is formed, which accumulates in the serous cavities. The serous membrane is spotty or diffusely reddened, matte due to desquamation of the mesothelium, rough, with hemorrhages, covered with fibrin threads or films.

It must be distinguished from dropsy not inflammatory in nature. If this is not inflammation, then the serous membrane remains unchanged - smooth, moist, shiny, gray in color.

Bullous form- accompanied by the formation in the skin, mucous membrane oral cavity blisters (blisters). With foot and mouth disease in cattle and pigs - aphthae in the skin of the crown of the hooves, udder, in the mucous membrane of the oral cavity, in pigs - in the skin of the limbs and snout. With smallpox - vesicles (bubbles) in the skin, with burns and frostbite - blisters in the skin.

Serous inflammation is characterized by the formation of exudate containing up to 2% proteins and a small amount of cellular elements. The course is usually acute. It occurs more often in the serous cavities, mucous membranes and meninges, less often in internal organs and skin. Morphological picture. In the serous cavities, serous exudate accumulates - a cloudy liquid, poor in cellular elements, among which desquamated mesothelial cells and single neutrophils predominate; the membranes become full-blooded. When the mucous membranes become inflamed, mucus and desquamated epithelial cells are mixed with the exudate, and serous catarrh occurs. The cause of serous inflammation is various infectious agents (mycobacterium tuberculosis, Frenkel diplococcus, meningococcus), exposure to thermal and chemical factors, autointoxication. The outcome of serous inflammation is usually favorable. Even a significant amount of exudate can be absorbed. In internal organs (liver, heart, kidneys) as a result of serous inflammation during its chronic course, sclerosis sometimes develops. The significance is determined by the degree of functional impairment. In the cavity of the heart sac, effusion makes it difficult the work of the heart, in the pleural cavity leads to lung collapse.

Fibrous inflammation characterized by the formation of exudate rich in fibrinogen, which turns into fibrin in the affected tissue. This process is facilitated by the release of a large amount of thromboplastin in the necrosis zone. Fibrinous inflammation is localized in the mucous and serous membranes, less often in the thickness of the organ. Morphological picture. A whitish-gray film appears on the surface of the mucous or serous membrane. Depending on the depth of necrosis and the type of epithelium, the film can be loosely connected to the underlying tissues and therefore easily separated, or firmly and therefore difficult to separate. In the first case they talk about lobar, and in the second - about diphtheritic inflammation.

Croupous inflammation occurs when there is shallow necrosis of tissue and impregnation of necrotic masses with fibrin. The film is loosely associated with the underlying tissue, making the mucous or serous membrane dull. The mucous membrane thickens and swells. The serous membrane becomes rough, as if covered with hairy fibrin threads. Diphtheritic inflammation develops with deep tissue necrosis and impregnation of necrotic masses with fibrin. It develops on the mucous membranes. The fibrinous film is tightly fused to the underlying tissue, and when it is rejected, it indicates a deep defect. The causes of fibrinous inflammation are different: it can be caused by diplococci Frankel, streptococci and staphylococci, pathogens of diphtheria and dysentery, mycobacterium tuberculosis. The outcome of fibrinous inflammation is not the same. Films remain on the mucous membranes after rejection different depths defects-ulcers, with lobar inflammation they are superficial, with diphtheritic inflammation they are deep and leave behind scar changes. Resorption of fibrous exudate is possible on serous membranes. Often fibrin masses undergo organization. As a result of fibrinous inflammation, complete overgrowing of the serous cavity with connective tissue—its obliteration—can occur.

Putrid hemorrhagic and catarrhal inflammation.

Putrefaction develops due to the entry of putrefactive bacteria into the site of inflammation, causing tissue decomposition with the formation of foul-smelling gases.

Hemorrhagic occurs when the exudate contains a large number of red blood cells. With this type of inflammation, microvascular permeability, blood flow, and negative chemotaxis towards neutrophils increase. Occurs when: anthrax, plague, flu, etc.. the outcome depends on the cause.

Catarrhal disease develops on the mucous membranes and is characterized by abundant release of exudate on their surface. The exudate can be serous, mucous, purulent, hemorrhagic, and it is always mixed with desquamated cells of the integumentary epithelium. Catarrhal inflammation can be acute and chronic. Acute - with inf.. chronic catarrh is accompanied by atrophy or hypertrophy of the mucous membrane. Reasons: inf., inf.-allergy. Reactions. The value is determined by its localization, intensity, and nature of the flow. Of greater importance is catarrh of the mucous respiratory tract, which acquires chronic nature and having complications - emphysema, pneumosclerosis.

Purulent inflammation.

A distinctive feature of the exudate is a large number of neutrophils. They develop fatty phonesis. Etiology: cocci. Chemical agents, typhoid bacillus. Purulent inflammation can occur in any organs and tissues. Types: limited (focal), boil, carbuncle, distributive phlegmon. Abscess - purulent inflammation characterized by melting of tissue to form a cavity filled with pus. Around the abscess, leukocytes enter from the granulation tissue through capillaries and partially remove decay products. It is called the pyogenic membrane. With prolonged granulation along the periphery they grow into mature fibrous fabric and stage abscess - a two-layer fusion is formed. Outcome: release of pus to the surface of the body or cavity. After a breakthrough, scarring of the cavity is possible. If there is no collapse of the walls, then a fistula forms.

Cellulitis is a differentiated purulent inflammation with penetration and melting of tissue, usually found in subcutaneous fatty tissue, in the intermuscular layers. It can be soft (if lysis predominates) and hard (if there is coagulation necrosis in the inflammation). Complications: arterial thrombosis, tissue necrosis, purulent thrombophlebitis. Histolysis at the site of inflammation leads to bleeding and intoxication. Outcome: favorable - petrification, organization, encapsulation.

Productive inflammation.

Hyperplastic growths - proliferation of the mucous membrane with pronounced histiocytic infiltration. Outgrowths of glandular epithelium are polyps. Outgrowths of multilayered epithelium - candyloma. Meaning: precancerous process.

Granulomatous inflammation.

Granulomatous inflammation (nodule) - occurs as a result of proliferation and transformation of cells capable of phagocytosis. Morphogenesis: accumulation of monocytes at the site of inflammation, maturation of monocytes into macrophages, transformation of macrophages into epithelioid cells, fusion of epithelioid cells into giant multinucleated cells. That. granulomas are divided into macrophage, epithelioid cell and giant cell. Depending on the level of metabolism, granulomas with a low level of metabolism (arising from the action of inert substances) are distinguished, mainly giant cell granulomas, and with high level exchange - most often epithelioid cells. Classification: by etiology - inf., non-inf., unknown etiology; with the flow: acute - abdominal typhus, rabies, encephalitis, polio, and chronic rheumatism, rheumatoid arthritis, brucelosis, mycoses; by origin: specific and nonspecific;