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

Causes. The causes of serous inflammation are diverse: infectious agents, thermal and physical factors, autointoxication. Serous inflammation in the skin with the formation of vesicles is a characteristic sign of inflammation caused by viruses of the Herpesviridae family (herpes simplex, chicken pox).

Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella) can also cause serous inflammation. Thermal, less often chemical burns are 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, vascular plethora is always observed. 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 (CSF) 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.

fibrinous inflammation. 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 composition of the exudate. Fibrinous inflammation is more often localized on the serous and mucous membranes.

Causes. The causes of fibrinous inflammation are diverse - bacteria, viruses, chemicals of exogenous and endogenous origin. Among bacterial agents, the development of fibrinous inflammation is most favored by diphtheria corynebacterium, shigella, mycobacterium tuberculosis. Fibrinous inflammation can also be caused by Frenkel's diplococci, pneumococci, streptococci and staphylococci, and some viruses. Typically, the development of fibrinous inflammation during autointoxication (uremia). Development of fibrinous

inflammation is determined by a sharp increase in the permeability of the 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 mucous 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 croupous exudate in the alveoli of the lobe of the lung is called croupous pneumonia.

Diphtheritic inflammation develops in organs covered with stratified squamous epithelium or a single-layer epithelium with a loose connective tissue base, which contributes to the development of deep tissue necrosis. In such cases, the fibrinous film is thick, difficult to remove, and when it is rejected, a deep tissue defect occurs. Diphtheritic inflammation occurs 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 with lobar inflammation and deep with diphtheria. Superficial ulcers usually regenerate completely, while deep ulcers heal with scarring. In the lung with croupous pneumonia, the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils, connective tissue appears at the site of the exudate (exudate is organized), with excessive activity of neutrophils, it is possible to develop an abscess and gangrene of the lung. On serous membranes Fibrinous exudate may melt, but more often it undergoes organization with the formation of adhesions between 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 tracheal diphtheria, 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 creamy 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 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 bacterial cell membrane, 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 is possible when certain chemical agents (turpentine, kerosene, toxic substances) enter the tissues.

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

Abscess - focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A granulation sac is formed around the abscess.

tissue, through the numerous capillaries of which leukocytes enter the abscess cavity and partially remove decay products. The abscess that produces pus is called pyogenic membrane. With a long course of 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 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 neurovascular bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, in addition to 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 cellulite, 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 in the presence of purulent foci in neighboring organs (for example, pleural empyema with lung abscess). Empyema of hollow organs develops when the outflow of pus is disturbed 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. 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 - swells. 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 exudate and inflammatory infiltrate changes. In pus, along with neutrophilic leukocytes, a relatively large number of lymphocytes and macrophages appear, and infiltration by lymphoid cells predominates in the surrounding tissue.

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 often, 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 high, as it underlies 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 to spread the process by contact, lymphogenous and hematogenous.

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

Causes. Putrefactive inflammation is caused by a group of clostridia, anaerobic infection pathogens - C.perfringens, C.novyi, C.septicum. In the development of inflammation, several types of clostridia are usually involved 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, so 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. Cellulose and pale, sometimes necrotic muscles bulge out of the wound. When feeling in the tissues, crepitus is determined, the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is first determined, which is replaced by widespread necrotic changes. Neutrophils that enter the focus of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign, indicating the attenuation of the process.

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 wounds 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 in newborns (the so-called necrotizing colitis of newborns).

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

Causes. 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, 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 arrosed 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.

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

Causes. A change in the composition of the exudate is naturally observed during inflammation: the formation of serous exudate is characteristic for the onset of the inflammatory process, later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change in the qualitative composition of leukocytes; neutrophils are the first to appear in the focus of inflammation, they are replaced by monocytes and later by lymphocytes. In addition, 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. It is determined by a combination of changes characteristic of various types of 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.

Catarrh. It develops on the mucous membranes and is characterized by an abundant release of exudate flowing down from the surface of the mucous membrane, hence the name of this type of inflammation (Greek katarrheo - I drain). A distinctive feature of catarrh 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.

Causes. Extremely diverse: bacterial and viral infections, allergic reactions to 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. Microscopic examination in the exudate determines leukocytes, desquamated cells of the integumentary epithelium and mucous glands. The mucous membrane itself has signs of edema, hyperemia, is infiltrated with leukocytes, plasma cells, there are many goblet cells in the epithelium.

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 the 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 thin, 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.

exudative inflammation is characterized by a pronounced stage of exudation, the remaining stages (alteration and proliferation) are slightly expressed.

By the nature of the exudate, exudative inflammation can be:

Serous, purulent, fibrinous, putrefactive, hemorrhagic, catarrhal, mixed.

SEROUS INFLAMMATION characterized by a light, cloudy, liquid exudate, in which there are few cells, and the protein content is more than 2%.

Etiology- infectious agents (microbes, viruses), toxins, burns, allergic reactions.

fibrinous inflammation characterized by the formation of exudate in the form of gray-yellow films (membraneous inflammation), which consist of fibrin filaments and other blood plasma proteins. Etiology- tuberculosis bacillus, diphtheria bacillus, influenza viruses, toxins in case of poisoning of the body (for example, with uremia). Localization- mucous membranes, serous membranes, less often - in the thickness of the organ (lungs). Pathomorphology. Types of fibrinous inflammation

5. lobar inflammation- the films are thin, loosely connected to the fabric, easily move away.

6. diphtheritic inflammation - the films are thick, firmly connected to the tissue and are difficult to separate.

G NOYAL INFLAMMATION. The exudate is cloudy, green, yellow or white. Pus contains a large number of neutrophils, elements of dead tissue, microbes and purulent bodies (dead white blood cells). Pus melts tissues (histolisis), which leads to the formation of cavities, ulcers and fistulas (purulent passages). Etiology- pyogenic microorganisms: staphylococci, streptococci, meningococci, Pseudomonas aeruginosa, etc.

abscess (abscess)- limited purulent inflammation with the formation of a cavity in the organ, which is filled with pus. A chronic abscess is delimited from the tissue of the organ by an outer shell of connective tissue, the inner shell that forms pus is a pyogenic membrane. Examples: abscess of the lung, liver, brain.

phlegmon- diffuse, unlimited purulent inflammation. It spreads diffusely between tissues, along the fiber, tendons, intermuscular layers.

empyema- accumulation of pus in the anatomical cavities. Empyema of the pleura, pericardium, gallbladder, bladder.

· pustule- an abscess on the skin.

· furuncle- purulent inflammation of the hair follicle and sebaceous gland.

· purulent catarrh- purulent inflammation of the mucous membranes.

· felon - purulent inflammation of the tissues of the finger.

· apostematosis- multiple, small pustules.

putrefactive inflammation(gangrenous) develops under the action of putrefactive bacteria, which leads to tissue necrosis.

HEMORRHAGIC INFLAMMATION occurs with high vascular permeability. Exudate resembles blood, because. is made up of erythrocytes. Often joins serous or catarrhal inflammation. This type of inflammation occurs with plague, scurvy, anthrax and influenza.

CATARRH occurs only on the mucous membranes and is characterized by increased formation of exudate, which can be serous, mucous, purulent, hemorrhagic.

Etiology- infectious agents, allergies, intoxication.

The mucous membrane in all types of catarrh is full-blooded, swollen, covered with exudate, which always contains an admixture of mucus.

MIXED INFLAMMATION- different types of exudate.

Lecture 14
EXUDATIVEINFLAMMATION
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 damage to the vessels, 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.
Scheme 20. Kindsexudativeinflammation

Serous inflammation. It is characterized by the formation of exudate containing up to 2% protein, single polymorphonuclear leukocytes (PMNs) and desquamated epithelial cells. Serous inflammation develops most often in the serous cavities, mucous membranes, pia mater, skin, less often in the internal organs.
Causes. The causes of serous inflammation are diverse: infectious agents, thermal and physical factors, autointoxication. Serous inflammation in the skin with the formation of vesicles is a characteristic sign of inflammation caused by viruses of the Herpesviridae family (herpes simplex, chicken pox).
Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella) can also cause serous inflammation. Thermal, less often chemical burns are 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, vascular plethora is always observed. 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 (CSF) 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.
fibrinous inflammation. 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 composition of the exudate. Fibrinous inflammation is more often localized on the serous and mucous membranes.
Causes. The causes of fibrinous inflammation are diverse - bacteria, viruses, chemicals of exogenous and endogenous origin. Among bacterial agents, the development of fibrinous inflammation is most favored by diphtheria corynebacterium, shigella, mycobacterium tuberculosis. Fibrinous inflammation can also be caused by Frenkel's diplococci, pneumococci, streptococci and staphylococci, and some viruses. Typically, the development of fibrinous inflammation during autointoxication (uremia). Development of fibrinous
inflammation is determined by a sharp increase in the permeability of the 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 mucous 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 croupous exudate in the alveoli of the lobe of the lung is called croupous pneumonia.
Diphtheritic inflammation develops in organs covered with stratified squamous epithelium or a single-layer epithelium with a loose connective tissue base, which contributes to the development of deep tissue necrosis. In such cases, the fibrinous film is thick, difficult to remove, and when it is rejected, a deep tissue defect occurs. Diphtheritic inflammation occurs 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 with lobar inflammation and deep with diphtheria. Superficial ulcers usually regenerate completely, while deep ulcers heal with scarring. In the lung with croupous pneumonia, the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils, connective tissue appears at the site of the exudate (exudate is organized), with excessive activity of neutrophils, it is possible to develop an abscess and gangrene of the lung. On serous membranes Fibrinous exudate may melt, but more often it undergoes organization with the formation of adhesions between 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 tracheal diphtheria, 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 creamy 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 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 bacterial cell membrane, 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 is possible when certain chemical agents (turpentine, kerosene, toxic substances) enter the tissues.
Morphological characteristic. Purulent inflammation can occur in any organs and tissues. The main forms of purulent inflammation are abscess, phlegmon, empyema.
Abscess - focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A granulation sac is formed around the abscess.
tissue, through the numerous capillaries of which leukocytes enter the abscess cavity and partially remove decay products. The abscess that produces pus is called pyogenic membrane. With a long course of 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 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 neurovascular bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, in addition to 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 cellulite, 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 in the presence of purulent foci in neighboring organs (for example, pleural empyema with lung abscess). Empyema of hollow organs develops when the outflow of pus is disturbed 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. 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 - swells. 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 exudate and inflammatory infiltrate changes. In pus, along with neutrophilic leukocytes, a relatively large number of lymphocytes and macrophages appear, and infiltration by lymphoid cells predominates in the surrounding tissue.
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 often, 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 high, as it underlies 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 to spread the process by contact, lymphogenous and hematogenous.
Putrid inflammation. It develops when putrefactive microorganisms enter the focus of inflammation.
Causes. Putrefactive inflammation is caused by a group of clostridia, anaerobic infection pathogens - C.perfringens, C.novyi, C.septicum. In the development of inflammation, several types of clostridia are usually involved 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, so 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. Cellulose and pale, sometimes necrotic muscles bulge out of the wound. When feeling in the tissues, crepitus is determined, the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is first determined, which is replaced by widespread necrotic changes. Neutrophils that enter the focus of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign, indicating the attenuation of the process.
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 wounds 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 in newborns (the so-called necrotizing colitis of newborns).
Hemorrhagic inflammation. It is characterized by the predominance of erythrocytes in the exudate. In the development of this type of inflammation, the main significance belongs to a sharp increase in the permeability of microvessels, as well as negative neutrophil chemotaxis.
Causes. 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, 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 arrosed 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.
Mixed inflammation. It is observed in cases when another type of exudate joins. As a result, serous-purulent, serous-fibrinous, purulent-hemorrhagic and other types of inflammation occur.
Causes. A change in the composition of the exudate is naturally observed during inflammation: the formation of serous exudate is characteristic for the onset of the inflammatory process, later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change in the qualitative composition of leukocytes; neutrophils are the first to appear in the focus of inflammation, they are replaced by monocytes and later by lymphocytes. In addition, 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. It is determined by a combination of changes characteristic of various types of 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.
Catarrh. It develops on the mucous membranes and is characterized by an abundant release of exudate flowing down from the surface of the mucous membrane, hence the name of this type of inflammation (Greek katarrheo - I drain). A distinctive feature of catarrh 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.
Causes. Extremely diverse: bacterial and viral infections, allergic reactions to 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. Microscopic examination in the exudate determines leukocytes, desquamated cells of the integumentary epithelium and mucous glands. The mucous membrane itself has signs of edema, hyperemia, is infiltrated with leukocytes, plasma cells, there are many goblet cells in the epithelium.
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 the 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 thin, 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.

It is characterized by the predominance of the exudation phase and the accumulation of exudate in the focus of inflammation. Depending on the nature of the exudate and the localization of the process, there are: 1) serous 2) fibrinous 3) purulent 4) putrefactive 5) hemorrhagic 6) mixed 7) catarrhal (feature of localization of the process on the mucous membranes).

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

Macroscopically - mucous membranes are full-blooded, edematous, exudate flows from the surface (in the form of a viscous, viscous mass). Microscopically - in the exudate there are leukocytes, desquamated epithelial cells, edema, hyperemia, infiltration of Le, plasma cells, there are many goblet cells in the epithelium. The change of serous catarrh is characteristic - mucous, then purulent, there is a gradual thickening of the exudate as inflammation develops.

Exodus. The acute course lasts 2-3 weeks and ends with complete recovery, often accompanied by acute respiratory viral infections. Chronic inflammation can lead to the development of atrophy or hypertrophy of the mucous membranes (Example: atrophy of the gastric mucosa in chronic gastritis).

Serous inflammation - develops on the serous membranes, mucous membranes, pia mater, skin, less often in the internal organs. The exudate contains at least 3-5% protein. If the protein is less than 2%, then this is not an exudate, but a transudate (for example, with ascites). The serous exudate contains single PMNs and single desquamated epitheliocytes. Turbid fluid accumulates in the serous membranes and serous cavities. The soft meninges become edematous. 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. In the skin, exudate accumulates under the epidermis, can exfoliate it from the dermis, with the formation of blisters (for example, with burns, or herpes).

Exodus. Usually favorable - resorption of exudate. A transition to purulent or fibrinous inflammation is possible. And tissue hypoxia in chronic course can stimulate the proliferation of fibroblasts and lead to the development of sclerosis. Perhaps the development of hyalinosis.

fibrinous inflammation. Occurs on the mucous membranes and serous membranes, less often in the interstitial tissue. In the exudate, a lot of fibrinogen is found, which turns into the affected tissue, under the action of tissue thromboplastin fibrin. In addition to fibrin, the composition of the exudate includes Le and elements of necrotic tissues. A grayish film appears on the surface of the mucous or serous membrane. There are croupous, diphtheritic and diphtheroid inflammation.

1. Croupous inflammation- develops on mucous membranes lined with multi-row - ciliated epithelium (trachea, bronchi), serous membranes (surfaces of the epicardium, pleura) and gives them a dull gray color. The films lie freely and can be easily removed. Only some cells of the mesothelium or epithelium are damaged. When the films are rejected, hyperemia is determined. Favorable outcome - resorption of exudate. Unfavorable - the formation of adhesions in the cavities, rarely complete overgrowth of the cavity with connective tissue - obliteration. With croupous pneumonia, carnification is possible (from the Latin caro - meat) - “meatification” of the lobe of the lung, as a result of the replacement of fibrin with connective tissue. Rejection of fibrin films in the form of casts from the trachea and bronchi in diphtheria leads to the development of asphyxia and is called true cereal. Fibrin films on the epicardium with fibrinous pericarditis resemble hair, the heart is figuratively called “hairy”.

2. Diphtheritic inflammation- usually observed on mucous membranes with glandular epithelium, and a loose connective tissue base, contributing to the development of deep necrosis (intestinal mucosa, endometrium). Necrotic masses are impregnated with fibrin. Fibrin films and necrosis extend deep beyond the epithelial layer. Thick films are tightly soldered to the underlying tissue, it is difficult to reject, when the films are rejected, a deep defect is formed - an ulcer that heals with the formation of a scar.

3.Diphtheroid (diphtheritic-like) inflammation- occurs on mucous membranes covered with stratified squamous non-keratinized epithelium (in the larynx, pharynx, tonsils, in the region of the epiglottis and true vocal cords). The epithelium becomes necrotic, impregnated with fibrin. Fibrin films can penetrate to the basal layer of the epithelium. When such a film is removed, a surface defect is formed - erosion, which heals by epithelization.

Purulent inflammation - is characterized by the predominance of Le in the exudate. Pus is a thick, creamy yellow-green liquid with a characteristic odor. Purulent exudate is rich in proteins (mainly globulins). Formed elements from 17 to 29%, these are living and dead leukocytes, single lymphocytes and macrophages. Neutrophils in the focus of inflammation die after 8-12 hours. Dead white blood cells are called purulent bodies. In addition, in the exudate you can see elements of destroyed tissues, colonies of microbes, it contains many enzymes, neutral proteases (ellastase, cathepsin G and collagenases) released from the lysosomes of decaying neutrophils. Proteases cause the melting of the body's own tissues (histolysis), increase vascular permeability, promote the formation of chemotactic substances and enhance phagocytosis. Non-enzymatic cationic proteins of specific granules of neutrophils have bactericidal properties.

Causes. The causes of the development of purulent inflammation can be various bacteria. Aseptic purulent inflammation is possible when certain chemicals enter the tissues (turpentine, kerosene, some toxic substances).

Purulent inflammation can develop in all tissues and organs. The main forms are abscess, phlegmon and empyema.

1. Abscess- focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A shaft of granulation tissue is formed around the abscess, with numerous capillaries through which Le enters the abscess cavity and partially removes decay products. The pus-producing membrane is called the pyogenic membrane (two-layer capsule). With a long course, the granulation tissue matures in the membrane, mature fibrous connective tissue is formed. Allocate spicy(two-layer capsule) and chronic abscess(the capsule has three layers).

2. Phlegmon- diffuse purulent inflammation, in which purulent exudate diffusely spreads into tissues, exfoliates and lyses tissue elements. Usually, phlegmon develops in tissues where there are conditions for easy spread of pus - in fatty tissue, in the area of ​​\u200b\u200btendons, fascia, along the neurovascular bundles, etc. Distinguish soft(absence of visible foci of necrosis in the tissues) and hard phlegmon(foci of coagulative necrosis, which do not melt, but are gradually rejected).

3. empyema- purulent inflammation in body cavities or hollow organs with accumulation of pus in them and preservation of the anatomical integrity of the organ. In body cavities, empyema can form in the presence of purulent foci in neighboring organs (for example: pleural empyema with lung abscess). Hollow organ empyema may develop in violation of the outflow of pus (for example: empyema of the gallbladder, appendix, joint). With a long course of empyema, the mucous, serous and synovial membranes become necrotic, and granulation tissue develops in their place, which leads to the development of adhesions and obliteration of the cavity.

Flow purulent inflammation can be acute and chronic. Acute purulent inflammation tends to spread. The demarcation of the abscess from the surrounding tissue is rarely good enough, and progressive tissue fusion may occur. Or the emptying of pus into the external environment or cavity. Possible education fistula- a channel lined with granulation tissue or epithelium, connecting the abscess with a hollow organ or body surface. If pus, under the influence of gravity, passively, along the muscular-tendon sheaths, neurovascular bundles, fatty layers, flows into the underlying sections and forms accumulations there - sills . Due to the absence of hyperemia, feelings of heat and pain - called cold leaks. Extensive streaks of pus cause severe intoxication and lead to depletion of the body.

Outcomes and complications- With spontaneous and surgical emptying of the abscess, its cavity collapses and fills with granulation tissue, which matures with the formation of a scar. Petrification is possible with thickening of pus. With phlegmon, rough scars form. With an unfavorable course, bleeding, generalization of infection with the development of sepsis is possible. With thrombosis of blood vessels in the focus of inflammation, the development of a heart attack or gangrene is possible. With a long chronic course, the development of amyloidosis is possible. The value of purulent inflammation is determined by the ability of pus to melt tissues, which makes it possible to spread the process by contact, lymphogenous and hematogenous. Purulent inflammation underlies many diseases.

Putrid inflammation - characterized by putrefactive decomposition of inflamed tissues. As a result of entering the focus of one or another type of inflammation of putrefactive bacteria (clostridia, anaerobic infection pathogens - C. perfringens, C. novyi, C septicum), a combination with other types of bacteria is possible, causing tissue decomposition and the formation of foul-smelling gases (ichorous smell - associated with the formation of butyric and acetic acid, CO 2, hydrogen sulfide and ammonia). Such inflammation occurs when the earth gets into the wounds, which is typical for mass wounds and injuries during wars and disasters. It has a severe course, accompanied by the development of gangrene.

Hemorrhagic inflammation - characterized by a predominance of red blood cells in the exudate. It often develops in severe infectious diseases (influenza, anthrax, plague, etc.) accompanied by a pronounced increase in microvascular permeability and negative chemotaxis. Runs hard and hard. Macroscopically, areas of hemorrhagic inflammation resemble hemorrhages. Microscopically in the focus of inflammation: a large number of erythrocytes, single neutrophils and macrophages. Significant tissue damage is characteristic. The outcome depends on the pathogenicity of the pathogen and the reactivity of the organism, often unfavorable.

Mixed inflammation - develops when another type of exudate joins. For example: Serous-purulent; Serous-fibrinous; Purulent-hemorrhagic and other possible combinations.

Inflammation is the reaction of the mesenchyme to damage.

Purpose of inflammation:

1) isolation of the damaging factor

2) destruction of the damaging factor

3) creation of optimal conditions for recovery.

Phylogenetically, inflammation is a younger reaction than damage and compensation, since many factors are involved in its implementation - cells, blood vessels, nervous and endocrine systems.

The etiology of inflammation coincides with the etiology of damage. That is, inflammation is caused by 7 groups of factors: physical, chemical, toxins, infection, discirculation, neurotrophic, metabolic.

Pathogenesis

It consists of 3 consecutive processes (phases).

Ι Alteration

ΙΙ Exudation

ΙΙΙ Proliferation

Ι PHASE OF ALTERATION

Plays a critical role in the development of inflammation. There is no inflammation without alteration (damage) of cells and tissues. Why?

Because when cells are damaged (dystrophy, necrosis), lysosomes containing proteolytic enzymes leave the cells. These enzymes, after the breakdown of lysosomes, cause the appearance of inflammatory mediators that trigger the exudation phase.

Inflammatory mediators are active biological products. A lot of mediators are currently known. But a special place is occupied by such mediators as - HISTAMINE and SEROTONIN.

Mediators secrete 5 cells - labrocytes, granulocytes, platelets, lymphocytes, macrophages. But a special place in this series is occupied by LABROCYTES (mast cells), which produce a large amount of histamine and serotonin.

Inflammatory mediators cause an increase in the permeability of the vessels of the microcirculatory bed - therefore, they initiate the 2nd phase of inflammation - exudation.

ΙΙ EXUDATION PHASE

The site of action is the microcirculatory bed.

Dynamics ---- 7 successive stages (processes):

1) the reaction of blood vessels and blood

2) increase in permeability

3) plasmorrhagia

4) emigration of blood cells

5) phagocytosis

6) pinocytosis

7) the formation of exudate and infiltrate

1) The reaction of blood vessels and blood -

Under the influence of mediators (histamine, serotonin), a short-term spasm of arterioles and precapillaries occurs first, followed by LONG-TERM paralytic expansion of arterioles and the development of arterial hyperemia, which is manifested by redness and warming of the inflammation focus. Arterial plethora contributes to the development of lymphostasis, lymphothrombosis and lymphatic edema - the exit of lymph into the area of ​​inflammation. Under the influence of mediators, there is an increase in blood viscosity and the formation of blood clots in the venules. This leads to venous plethora, which gives the site of inflammation a bluish tint and causes hypoxic damage.

2) Increased permeability.

Under the influence of mediators and hypoxia, the capillary wall becomes loose due to damage to the endothelium and loosening of the basement membrane. This causes an increase in the permeability of the capillary wall.

3) Plasmorrhagia

As a result of an increase in the permeability of the capillary walls, an increased outflow of plasma from the lumen of the capillaries into the zone of inflammation (plasmorrhagia) occurs.

4) Emigration of blood cells.

Movement to the area of ​​inflammation of granulocytes, lymphocytes, monocytes through the wall of the capillary (leukodiapedesis). The transition of these cells occurs in 2 ways - a) interendothelial and b) transendothelial (through the endothelium). Granulocytes and monocytes migrate interendothelially. Transendothelial - lymphocytes. The cause of migration is chemotaxis - the attraction of leukocytes by decay products that accumulate in the area of ​​inflammation. Chemotaxis can be carried out by proteins, nucleoproteins, kinins, plasmins, complementary factors and other substances that appear in the focus of inflammation.

5) Phagocytosis

Phagocytosis is the capture and consumption of microbes and foreign bodies. There are 2 types of phagocytes - a) microphages (neutrophils) - they are able to destroy only microbes, b) macrophages (monocytes) - they are able to capture small particles - (microbes) and large particles - foreign bodies. The phagocytic function of macrophages is provided by lysosomal enzymes, microphages - by cationic proteins (proteolytic enzymes) and atomic oxygen, which is formed in the process of peroxidation. Phagocytosis of microbes can be complete (complete destruction of microbes) and incomplete (the microbe is not destroyed and is carried by phagocytes throughout the body). Causes of incomplete phagocytosis: 1. immunodeficiency caused by many factors, including the immunodeficiency virus, 2. features of the microbe (phagocytes cannot destroy the tubercle bacillus because it has a thick waxy shell).

6) Pinocytosis

The capture of tissue fluid, which contains the antigen, by macrophages, in the cytoplasm of which an information complex is formed. Composition of the informational complex: transformed antigen + informational ribonucleic acid. The information complex is transmitted through cytoplasmic contacts to the B-lymphocyte. A B-lymphocyte turns into a plasma cell. The plasma cell produces antibodies specific for this antigen. Specific antibodies bind to this antigen, which increases the phagocytic reaction of destroying the antigen by 100 times.

7) Formation of exudate and infiltrate.

At the end of the exudation phase, exudate and infiltrate are formed. Exudate in its usual form is a liquid containing decay products of tissues and cells. It accumulates in the stroma, cavities. Its composition is complex, but unlike tissue fluid, it contains more than 2% proteins. Therefore, it is an opaque cloudy liquid. Whereas the transudate is a clear liquid. In cases where the cellular component prevails over the liquid, the exudate receives a special name - infiltrate. The infiltrate is more characteristic of chronic inflammation.

ΙΙΙ PROLIFERATION PHASE

Completion of the inflammatory process. There is a delimitation of the zone of inflammation from the surrounding tissue. The processes of proliferation predominate over the processes of alteration and exudation. Reproduce: 1) cambial cells of the mesenchyme, 2) adventitial cells, 3) endothelium, 4) reticular cells, 5) B- and T-lymphocytes, 6) monocytes.

During reproduction, differentiation and transformation of cells are carried out.

As a result

Mesenchymal cambial cells develop into epithelioid cells (resembling squamous cells), histiocytes, macrophages, fibroblasts, and fibrocytes;

B-lymphocytes - into plasma cells

Monocytes - into epithelioid cells and macrophages.

As a result, all these cells carry out the function of cleansing and restoring the activity of the microvasculature. And this allows you to start the recovery process in full.

The inflammatory response manifests itself differently in different age periods. It develops in full in adulthood. In other age groups, it has its own characteristics.

So, in fetuses and newborns, there is a predominance of alteration and proliferation over exudation, and there is also a tendency to generalization. This is due to the imperfection of protective and immune mechanisms during this period of life. In old age, there is a decrease in reactivity and protracted inflammatory processes due to a relative decrease in defense mechanisms.

regulation of inflammation.

Inflammation is regulated by the endocrine and nervous systems. Both systems can increase and decrease the strength of inflammation.

Endocrine system

There are 2 groups of hormones

1) pro-inflammatory

2) anti-inflammatory.

1) Pro-inflammatory (increase inflammation) - growth hormone, aldosterone.

Mechanism of action: increase the osmotic pressure of tissue fluid due to the accumulation of sodium in it. As a result, plasmorrhagia (exudation) increases.

2) Anti-inflammatory (reduce inflammation) - glucocorticoids, ACTH.

Mechanism of action: blocking the transition of lymphocytes into mast cells (mast cells), which produce inflammatory mediators. A logical chain of events arises: no mastocytes - no inflammatory mediators - no exudation - no inflammation.

Nervous system

Also, 2 groups of factors -

1) pro-inflammatory

2) anti-inflammatory

1) Pro-inflammatory - cholinergic substances.

Mechanism of action: an increase in cGMP (universal mediator), which activates the production of inflammatory mediators, which enhances the inflammatory process.

2) Anti-inflammatory - adrenergic factors.

Mechanism of action: increase the amount of cAMP (universal messenger), which blocks the production of inflammatory mediators, resulting in a weakening of the inflammatory process.

Clinical and morphological signs of inflammation.

Their-5: 1) redness - due to arterial plethora

2) an increase in temperature - due to arterial plethora

3) swelling - due to exudation

4) pain - due to the action of mediators on nerve endings

5) dysfunction is due to damage to structures, which triggers inflammation.

Types of inflammatory response .

1. Adequate(or normergic reaction) is characterized by

directly proportional relationship between the strength of the damaging factor and the strength of inflammation.

2. inadequate characterized by a discrepancy between the strength of the damaging factor and the severity of inflammation.

It could be a hypoergic reaction (weakened)

Hyperergic reaction (enhanced)

- Hypoergic reaction may be

1) the reaction of the strength of immunity - when a strong damaging factor is reflected with less losses with moderate inflammation.

2) immune weakness reaction - when a weak damaging factor leads to severe damage (dystrophy, necrosis), and the inflammatory reaction is almost absent (this is evidence of the defenselessness of the body, and it accompanies serious diseases, such as blood diseases).

- Hyperergic the reaction always reflects an increased sensitization of the body. It can be the result of impaired humoral and cellular immunity. And always accompanies immune inflammation.

There are 2 types of hyperergic reaction -

1) immediate hypersensitivity \ HNT \

2) delayed type hypersensitivity \ HRT \

1) Immediate type hypersensitivity occurs immediately after exposure to an antigen (drugs, plant pollen, food and other allergens). It is characterized by acute inflammation with the development of an alterative-exudative reaction. Inflammation is triggered by humoral factors - antibodies, immune complexes, antigens.

2\ Delayed type hypersensitivity - observed in violation of cellular immunity (aggressive action of T-lymphocytes and macrophages). The inflammatory reaction occurs one day after exposure to the antigen. Example: inflammation on the skin a day after the introduction of tuberculin.

Terminology. Classification .

Inflammation of an organ or tissue is indicated by the ending -it. It is added to the name of an organ or tissue. Examples: myocardium—myocarditis; endocardium - endocarditis, etc.

There are also special terms: pneumonia - inflammation of the lungs, empyema - purulent inflammation of the cavities, etc.

Classification. It is carried out according to 3 principles -

Current duration

By causative factors

According to pathomorphology

There are 3 types of inflammation downstream:

• Ø acute - up to 3 weeks
• Ø subacute - up to 3 months
• Ø chronic - longer than 3 months.

Causative factors are:

• banal (nonspecific) inflammation
• specific inflammation (inflammation in tuberculosis, syphilis, leprosy, rhinoscleroma, glanders).

According to pathomorphology (basic principle), 3 types of inflammation are distinguished depending on the predominance of one of the main components of inflammation -

1) alternative

2) exudative

3) proliferative (productive).

1) ALTERATIVE INFLAMMATION

In this type of inflammation, damage to the parenchyma of the organ predominates. Vascular reaction is weakly expressed. The degree of damage is very diverse and ranges from ordinary dystrophy (mild damage) to necrosis (necrotic damage). Pathomorphology depends on the degree of damage.

Outcome - small foci heal completely - scar tissue forms in place of large foci. Value - depends on the localization and severity of the process.

2) EXUDATIVE INFLAMMATION

It is characterized by the predominance of the exudation reaction during inflammation with the formation of an effusion, which determines the entire picture of inflammation.

According to the characteristics of the exudate, 7 types of exudative inflammation are distinguished -

A. Serous

B. Fibrinous

V. Purulent

G. putrid

D. Hemorrhagic

E. catarrhal

G. Mixed.

A. Serous inflammation

features of inflammation. Exudate is a liquid containing 3-8% albumin. There are few cells. The course of inflammation is acute. The hyperemia is well expressed. Porosity of capillaries is expressed moderately. Localization - serous cavities (cardiac, abdominal, pleural), meninges, stroma of the liver, myocardium, kidneys.

Appearance of the exudate: slightly hazy, straw-yellow liquid.

Causes - thermal, chemical, infections, etc.

The outcome is favorable: complete resorption. Rarely - sclerosis - more often in the liver, kidneys, myocardium.

B. Fibrinous inflammation

Exudate contains a lot of fibrin. Damage to the capillaries in this type of inflammation is significant. Serous and mucous membranes are affected more often, less often the stroma of organs.

There are 2 types of this inflammation:

1) croupous

2) diphtheria

1) Croupous inflammation. The word croup (crow-crow, croaking, wheezing like a crow) emphasizes the predominant localization of the process (for example, the mucosa of the trachea, bronchi). It is characterized by the formation of a fibrinous gray-yellow film. The film is loosely connected to the surface of the necrotic mucosa or serous membrane. When the film is separated, a surface defect is detected.

2) Diphtheritic inflammation. It is characterized by deep necrotic changes in the mucosal and submucosal layers. Fibrin prolapse occurs both in depth and on the surface. The fibrinous gray-yellow film is tightly soldered to the underlying tissues, and when it is rejected, a deep defect is formed.

Diphtheritic (meaning leathery) inflammatory process is noted not only in diphtheria (disease). This is a broader concept, since diphtheria inflammation occurs in various types of pathology.

Causes of fibrinous inflammation:

Bacteria: streptococci, staphylococci, bacilli - tuberculosis, diphtheria, etc.

Uremia (renal failure) - endogenous poisoning with the development of fibrinous pericarditis (hairy heart), fibrinous pleurisy, etc.

exogenous poisoning.

Course: 1) acute 2) chronic

Outcome: small defects on the mucous membranes heal, in place of large ones, scar tissue is formed with the possible development of stenosis, for example, of the trachea and bronchi; fibrous adhesions are always formed on the serous membranes, which can lead to adhesive disease when localized in the abdominal cavity and intestinal obstruction.

B. Purulent inflammation

Pus is a thick, viscous gray-green liquid. The purulent exudate contains a lot of globulins, fibrin and, most importantly, neutrophils.

Types of purulent inflammation.

1) Phlegmon - a spilled abscess. It is characterized by the spread of pus in the intermuscular spaces, in fatty tissue, fascia, tendons

2) Abscess - delimited purulent inflammation. There is pus in the abscess cavity, the abscess wall is formed by a pyogenic membrane.

Localization is different: skin, head, kidneys, liver, lungs and other internal organs.

3) Empyema - purulent inflammation of the cavities: pleural, abdominal, joints.

4) Furuncle - purulent inflammation of the hair follicle.

5) Carbuncle - purulent inflammation of a group of hair follicles.

6) Paronychia - purulent inflammation of the periungual bed.

7) Panaritium - purulent inflammation of the finger.

Causes: more often pyogenic microorganisms (all types of coccal infection), tuberculosis bacilli, fungi, chemical agents.

Current - 1) Acute 2) Chronic.

Acute proceeds in the form of diffuse or limited inflammation. In severe cases, the process spreads over large areas and can cause death from intoxication and multiple organ failure.

Chronic proceeds for a long time with the development of fibrosis around the purulent process. It gives such complications as - chronic fistulous passages, extensive streaks of pus, intoxication, wound depletion, amyloidosis.

D. putrefactive inflammation

It develops when an inflammation of a putrefactive infection enters the zone. It is characterized by an increase in necrobiotic processes, the formation of fetid gas.

D. Hemorrhagic inflammation

Occurs when erythrocytes penetrate into the exudate. This indicates severe damage to the microvasculature. It is noted in severe forms of influenza, natural black pox, anthrax, plague.

E. Catarrh.

This is an inflammation of the mucous membranes with the formation of mucus and its accumulation in the exudate. The composition of the exudate is different, but it always contains mucus.

Forms of catarrhal inflammation (catarrh) -

1) serous

2) slimy

3) purulent.

1) Serous. Muddy exudate is characteristic. The mucosa is swollen, full-blooded. It is noted with a viral respiratory infection in the respiratory organs and with cholera in the mucous membrane of the small intestine.

2) Slimy. Characterized by the presence of a large amount of mucus. The exudate is viscous, located on the hyperemic mucosa. Localization - respiratory and digestive organs.

3) Purulent. Severe purulent inflammation followed by erosive and ulcerative processes, as well as fibrosis and deformity.

The course of catarrh is acute and chronic.

The outcome of acute inflammation depends on the form of catarrh; with serous and mucous, complete recovery takes place, with purulent - cicatricial and ulcerative processes with stenosis and deformity.

Chronic catarrh proceeds according to the type

1) atrophic catarrh with the development of atrophy (decrease) in the thickness of the mucosa. 2) hypertrophic catarrh - with thickening of the mucosa due to the proliferation of parenchymal and mesenchymal structures.

In this case, there is a violation of the function of the organ with the development of chronic gastritis, enteritis, colitis, bronchitis, emphysema and pneumosclerosis.

G. Mixed inflammation.

Options: serous - purulent, serous - fibrinous, purulent - fibrinous and others.

It usually develops when a new infection joins in the course of inflammation, or the reactive, protective forces of the body change significantly.