Topic 6. Inflammation

6.7. Classification of inflammation

6.7.2. Exudative inflammation

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

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

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 . It occurs most often in the 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 a significant amount of exudate can be absorbed. In internal organs As a result of serous inflammation during its chronic course, sclerosis sometimes develops.

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.

Hemorrhagic inflammation

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

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

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

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

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

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

Fibrinous inflammation

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

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

Causes. Fibrinous inflammation can be caused by pathogens of diphtheria and dysentery, Frenkel diplococci, streptococci and staphylococci, Mycobacterium tuberculosis, influenza viruses, endotoxins (for uremia), exotoxins (sublimate poisoning).

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

-lobar;
-diphtheritic.

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

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

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

Meaning fibrinous inflammation is very high, since it forms the morphological basis of diphtheria, dysentery, and is observed during intoxication (uremia). When films form in the larynx and trachea, there is a risk of asphyxia; When films in the intestines are rejected, bleeding from the resulting ulcers is possible. Adhesive pericarditis and pleurisy are accompanied by the development of pulmonary heart failure.

Purulent inflammation

Purulent inflammation characterized by a predominance of neutrophils in the exudate, which, together with the liquid part of the exudate, form pus. The pus also includes lymphocytes, macrophages, and necrotic cells of local tissue. In pus, microbes called pyogenic are usually detected, which are located freely or are contained inside pyocytes (dead polynuclear cells): this is septic pus capable of spreading infection. Nevertheless, there is pus without germs, for example, with the introduction of turpentine, which was once used to “stimulate protective reactions in the body” in weakened infectious patients: as a result, aseptic pus .

Macroscopically pus is a cloudy, creamy, yellowish-greenish liquid whose odor and consistency varies depending on the offending agent.

Causes: pyogenic microbes (staphylococci, streptococci, gonococci, meningococci), less commonly Frenkel diplococci, typhoid bacillus, Mycobacterium tuberculosis, fungi, etc. It is possible to develop aseptic purulent inflammation when certain chemicals enter the tissue.

Mechanism of pus formation Connected with adaptation polynuclear cells specially to antibacterial fight.

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

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

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

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

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

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

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

At polynuclear destruction under the influence of an aggressor;
-autodigestion of polynuclear cells as a result of rupture of the lysosomal membrane inside the cytoplasm under the influence of various substances, for example, silicon crystals or sodium urates;
-release of enzymes by granulocytes into the intercellular space;
-by knockover endocytosis, which is carried out using intussusception cell membrane without absorbing the aggressor, but by pouring enzymes into it.

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

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

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

Types of purulent inflammation depending on the prevalence and location:

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

Furuncle

Furuncle is an acute purulent-necrotic inflammation of the hair follicle and associated sebaceous gland with the surrounding fiber.

Causes: staphylococcus, streptococcus.

Conditions contributing to the development of a boil: constant contamination of the skin and friction with clothing, irritation with chemicals, abrasions, scratching and other microtraumas, as well as increased activity of the sweat and sebaceous glands, vitamin deficiencies, metabolic disorders (for example, diabetes), starvation, weakening protective forces organism.

Localization: a single boil can occur on any area of ​​the skin where there is hair, but most often on the back of the neck (nape), face, back, buttock, armpit and groin area.

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

Macroscopically on the 6-7th day, the boil is a cone-shaped, rising above the surface of the skin, an inflammatory infiltrate of a purplish-bluish color with a yellowish-greenish tip (“head” of the boil).

The boil then bursts, releasing pus. At the site of the breakthrough, an area of ​​necrotic greenish tissue is found - the core of the boil. Together with pus and blood, the rod is rejected.

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

Meaning. The process of development of a boil can be accompanied by a pronounced local inflammatory reaction and relatively quickly result in clinical recovery. But with reduced resistance, melting of the necrotic core may occur and an abscess and phlegmon may occur. A boil on the face, even a small one, is usually accompanied by rapidly progressing inflammation and swelling, and a severe general course. If the course is unfavorable, fatal complications may develop, such as septic thrombosis of the dural sinuses, purulent menigitis and sepsis. In weakened patients, multiple boils may develop - this is furunculosis.

Carbuncle

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

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

Conditions development and localization the same as with a boil.

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

The most dangerous carbuncle is the nose and especially the lips, in which the purulent process can spread to the membranes of the brain, resulting in the development of purulent meningitis. Treatment is surgical; At the first symptoms of the disease, you should consult a surgeon.

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

Phlegmon

Phlegmon- this is a diffuse purulent inflammation of the tissue (subcutaneous, intermuscular, retroperitoneal, etc.) or the wall of a hollow organ (stomach, appendix, gall bladder, intestine).

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

Examples of phlegmon:

Paronychia- acute purulent inflammation of the periungual tissue.

Felon- acute purulent inflammation of the subcutaneous tissue of the finger. The process may involve tendon and bone, causing purulent tenosynovitis and purulent osteomyelitis. If the outcome is favorable, the tendon becomes scarred and a contracture of the finger is formed. If the outcome is unfavorable, phlegmon of the hand develops, which can become complicated purulent lymphadenitis, sepsis.

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

Mediastenitis- acute purulent inflammation of the mediastinal tissue. Distinguish front and back purulent mediastinitis.

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

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

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

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

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

Paraproctitis- inflammation of the tissue surrounding the rectum. Its causes may be dysenteric ulcers, ulcerative colitis, decaying tumors, anal fissures, hemorrhoids. Meaning: intoxication, the occurrence of perirectal fistulas, the development of peritonitis.

Abscess

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

Abscesses can be acute or chronic. The wall of an acute abscess is the tissue of the organ in which it develops. Macroscopically, it is uneven, rough, often with ragged, structureless edges. Over time, the abscess is delimited by a shaft of granulation tissue rich in capillaries, through the walls of which increased emigration of leukocytes occurs. A kind of abscess shell is formed. On the outside it consists of connective tissue fibers that are adjacent to unchanged tissue, and on the inside it consists of granulation tissue and pus, which is continuously renewed due to the constant supply of leukocytes from granulations. The membrane of an abscess that produces pus is called pyogenic membrane.

Abscesses can be localized in all organs and tissues, but most practical significance present abscesses of the brain, lungs, liver.

Brain abscesses are usually divided into:

Peacetime abscesses;
- wartime abscesses.

Wartime abscesses are most often a complication of shrapnel wounds, blind injuries to the skull, and less often penetrating bullet wounds. It is customary to distinguish between early abscesses, which occur up to 3 months after injury, and late abscesses, which occur after 3 months. The peculiarity of wartime brain abscesses is that they can occur 2-3 years after injury, and also occur in the lobe of the brain opposite the wounded area.

Peacetime abscesses. The source of these abscesses are:

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

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

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

A middle ear infection can spread:

To continue;
-lympho hematogenously;
- perineural.

From the middle ear, the infection continues to spread to the pyramid temporal bone and causes purulent inflammation (temporal bone osteomyelitis), then the process moves to the dura mater (purulent pachymeningitis), soft meninges (purulent leptomeningitis), and later, when purulent inflammation spreads to the brain tissue, an abscess is formed. When an abscess occurs lymphohematogenously, it can be localized in any part of the brain.

Meaning brain abscess. An abscess is always accompanied by tissue death and therefore the entire function of the area of ​​the brain in which the abscess is localized is lost. Toxins of purulent inflammation have a tropism for neurons, causing their irreversible dystrophic changes and death. An increase in the volume of the abscess can lead to its breakthrough into the ventricles of the brain and the death of the patient. When inflammation spreads to the soft membranes of the brain, purulent leptomeningitis occurs. With an abscess, there is always a circulatory disorder, accompanied by the development of edema. An increase in the volume of the lobe leads to dislocation of the brain, displacement of the brainstem and pinching of it in the foramen magnum, which leads to death. Treatment of fresh abscesses comes down to their drainage (according to the principle “ ubi pus ibi incisio et evacuo"), old abscesses are removed along with the pyogenic capsule.

Lung abscess

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

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

Liver abscess

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

Causes of pylephlebitic abscesses liver are:

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

Causes of cholangitis abscesses most often there are:

-purulent cholecystitis;
-typhoid fever;
- purulent pancreatitis;
- decaying tumors of the liver, gall bladder, pancreas;
- phlegmon of the stomach.

Meaning The process consists of severe intoxication, which leads to dystrophic changes in vital organs, and the development of such dangerous complications as subphrenic abscess, purulent peritonitis, sepsis.

Empyema

Empyema- purulent inflammation with accumulation of pus in closed or poorly drained pre-existing cavities. Examples include the accumulation of pus in the pleural, pericardial, abdominal, maxillary, frontal cavities, in the gall bladder, vermiform appendix, fallopian tube (pyosalpinx).

Pericardial empyema- occurs either as a continuation from nearby organs, or when an infection occurs through the hematogenous route, or during a septic heart attack. This is a dangerous, often fatal complication. At long term adhesions occur, calcium salts are deposited, and the so-called armored heart develops.

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

Empyema of the abdominal cavity, as an extreme morphological manifestation of purulent peritonitis is a complication of many diseases. The development of purulent peritonitis leads to:

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

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

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

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

Catarrhal inflammation may be acute and chronic. Acute catarrh is characteristic of a number of infections, for example, acute upper respiratory tract catarrh for acute respiratory infections. Chronic catarrh can occur both with infectious (chronic purulent catarrhal bronchitis) and non-communicable diseases. Chronic catarrhal inflammation may be accompanied by atrophy or hypertrophy of the mucous membrane.

Meaning catarrhal inflammation is determined by its localization, intensity, and nature of the course. Catarrh of the mucous membranes of the respiratory tract, often becoming chronic and having serious consequences (pulmonary emphysema, pneumosclerosis), acquires the greatest importance.

Mixed inflammation. In cases where one type of exudate is joined by another, mixed inflammation is observed. Then they talk about serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic inflammation. Most often, a change in the type of exudative inflammation is observed when new infection, changes in the body's reactivity.

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 alternative inflammation are alternative myocarditis and alternative neuritis in pharyngeal diphtheria, viral encephalitis, poliomyelitis, acute hepatitis with Botkin's disease, acute ulcers in the stomach. Sometimes this kind 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, the following types of exudative inflammation are distinguished:

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

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

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. It occurs most often in the 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. With exudation, they will have all the morphological signs of inflammation, with transudation - manifestations of venous congestion.

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

Meaning determined by the degree of functional impairment. In the cavity of the heart sac, inflammatory effusion complicates the work of the heart; in the pleural cavity it 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 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. At slight damage 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.

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

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 disruption of the outflow of cerebrospinal fluid (liquor) and cerebral edema, pericardial effusion impedes the work of the heart, and serous inflammation of the lung parenchyma can lead to acute respiratory failure.

Fibrinousinflammation. It is characterized by an exudate rich in fibrinogen, which is converted into fibrin in the affected tissue. This is facilitated by the release of tissue thromboplastin. In addition to fibrin, PMN and elements of necrotic tissues are also found in the exudate. Fibrinous inflammation is 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, diphtheria Corynebacterium, Shigella, Mycobacterium tuberculosis are the most conducive to the development of fibrinous inflammation. Fibrinous inflammation can also be caused by Frenkel diplococcus, pneumococcus, streptococcus and staphylococcus, and some viruses. The development of fibrinous inflammation during autointoxication (uremia) is typical. The 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), and on the other hand, to a 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 also occurs in organs covered with stratified squamous epithelium or 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 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 detached films close 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 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 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 is 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. With prolonged inflammation, the granulation tissue that forms the pyogenic membrane matures, and two layers are formed in the membrane: the inner layer, consisting of granulations, and the outer layer, 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. When phlegmon forms, except 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 goal-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 exudate 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: the virulence of microorganisms, the state of the body’s defenses, 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 vessels and lymphatic vessels, in this case 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 in combination with aerobic bacteria (staphylococci, streptococci) usually take part in the development of inflammation. Anaerobic bacteria produce butyric and acetic acids, 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. Wound at anaerobic gangrene It 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, the wound emits bad smell. 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 of 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: the onset of the inflammatory process is characterized by the formation of serous exudate, later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change quality composition leukocytes; Neutrophils are the first to appear at the site of inflammation; they are replaced by monocytes And later - lymphocytes. In addition, if a new infection joins an existing inflammation, the nature of the exudate often changes. For example, when a bacterial infection joins a viral respiratory infection, a 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. 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 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 is exacerbated by inflammation.

Causes. Extremely diverse: bacterial and viral infections, allergic reactions on 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 detected. 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 full 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.