65. Exudative inflammation: definition, causes, types. Pathological anatomical characteristics of serous inflammation, causes, localization, outcomes, clinical significance.

Exudative inflammation is characterized by the predominance of exudation, the formation of exudate in the tissues and cavities of the body. Depending on the nature of the exudate, serous, fibrinous, purulent, putrefactive, hemorrhagic, catarrhal and mixed inflammation are isolated. Serous inflammation With serous inflammation, an exudate is formed containing up to 2% protein and a small amount of cellular elements. It often occurs in serous cavities, mucous membranes and meninges, less often in internal organs, skin.

Morphological picture. Serous exudate accumulates in the serous cavities — a cloudy liquid, poor in cellular elements, among which exfoliated epithelial cells, mesothelium and a small number of neutrophils predominate; the shells are full-blooded. A similar pattern occurs with serous meningitis. Causes: various infectious agents (viruses, mycobacterium tuberculosis, Frenkel's diplococcus, meningococcus, shigella), thermal and chemical factors, auto-intoxication (thyrotoxicosis, uremia). The outcome of serous inflammation is usually favorable. Even a significant amount of exudate can be absorbed. In the chronic course of serous inflammation in the internal organs (liver, heart, kidneys), sclerosis sometimes develops in the outcome.

The value is determined by the degree of functional impairment. In the cavity of the cardiac shirt, effusion makes it difficult for the heart to work, in the pleural cavity it leads to collapse (compression) of the lung. Fibrinous inflammation

Fibrinous inflammation is the formation of exudate rich in fibrinogen, which turns into fibrin in the affected (necrotized) tissue. This is facilitated by the release of a large amount of thromboplastin in the necrosis zone. Fibrinous inflammation is localized in the mucous membranes and serous membranes, less often in the thickness of the organ. Morphological picture. A whitish-gray film appears on the surface of the mucous membrane or serous membrane. Depending on the depth of tissue necrosis and the type of epithelium of the mucous membrane, the film can be loosely connected to the underlying tissues and easily separated or firmly connected and separated with difficulty. In the first case, they talk about croup, and in the second — about the diphtheria variant of fibrinous inflammation. The causes of fibrinous inflammation are infectious agents: Frenkel's diplococcus, streptococci and staphylococci, pathogens of diphtheria and dysentery, mycobacterium tuberculosis, influenza viruses. In addition to infectious agents, fibrinous inflammation is caused by toxins and poisons of endogenous (uremia) or exogenous (sulema) origin.

The course of fibrinous inflammation is usually acute. Sometimes (for example, with tuberculosis of the serous membranes) it has a chronic character.

The outcome of fibrinous inflammation of the mucous membranes and serous membranes is different. After the rejection of the films, defects of varying depths remain on the mucous membranes — ulcers. Resorption of fibrinous exudate is possible on serous membranes. However, fibrin masses are often subjected to organization, which leads to the formation of adhesions between the serous sheets of the pleura, peritoneum, and pericardium. In the outcome of fibrinous inflammation, complete overgrowth of the serous cavity with connective tissue may occur — obliteration. Purulent inflammation

With purulent inflammation, neutrophils predominate in the exudate. Decaying neutrophils — purulent corpuscles — together with the liquid part of the exudate form pus, which also contains lymphocytes, macrophages, dead tissue cells, and microorganisms. Pus is a cloudy thick liquid having a yellow-green color. A characteristic feature of purulent inflammation is histolysis, due to the effect of proteolytic enzymes — neutrophils on tissues. Purulent inflammation occurs in any organ and tissue. Morphological picture. Purulent inflammation is an abscess or phlegmon, depending on the prevalence.

An abscess (abscess) is a focal purulent inflammation characterized by the formation of a cavity filled with pus. Phlegmon is a diffuse purulent inflammation in which purulent exudate spreads between tissue elements, impregnating, delaminating and lysing tissues. The causes of purulent inflammation are often pyogenic microbes (Staphylococcus, streptococcus, gonococcus, meningococcus), less often Frenkel's diplococcus, typhoid bacillus, Mycobacterium tuberculosis, fungi. Aseptic purulent inflammation is possible when chemicals enter the tissue.

The course of purulent inflammation is acute and chronic. Acute purulent inflammation, especially in the form of an abscess or phlegmon, tends to spread. Chronic purulent inflammation occurs when the abscess is encapsulated. Sclerosis develops in the surrounding tissues. If the pus finds a way out, a chronic fistula is formed, or a fistula, which opens through the skin to the outside. The outcome of purulent inflammation depends on its prevalence, the nature of the course, the virulence of the microbe and the reactivity of the body. An unfavorable outcome is the generalization of infection with the development of sepsis. Putrefactive inflammation

Putrefactive inflammation (gangrenous, ichorous, from the Greek ichor — sucrose) usually develops due to ingestion of putrefactive bacteria into the inflammation site, causing tissue decomposition with the formation of foul-smelling gases.

Hemorrhagic inflammation

Hemorrhagic inflammation occurs if red blood cells are mixed with the exudate. In its development, not only the sharply increased permeability of microvessels, but also the negative chemotaxis of neutrophils, plays a great role. Hemorrhagic inflammation occurs in severe infectious diseases — anthrax, plague, flu, etc. Sometimes there are so many red blood cells that the exudate resembles a hemorrhage (for example, with anthrax meningoencephalitis). Hemorrhagic inflammation often joins other types of exudative inflammation.

The outcome of hemorrhagic inflammation depends on the cause that caused it. Catarrhal inflammation

Catarrhal inflammation, or catarrh, develops on the mucous membranes and is characterized by an abundant release of exudate on their surface (Fig. 5-11). Exudate can be serous, mucous, purulent, hemorrhagic, and it is always mixed with exfoliated cells of the integumentary epithelium. Catarrhal inflammation can be acute and chronic. Acute catarrh is characteristic of a number of infections — acute catarrh of the upper respiratory tract in acute respiratory infection. At the same time, the change of one type of catarrh to another is characteristic — serous catarrh to mucous, and mucous — purulent or purulent hemorrhagic. Chronic catarrh occurs in both infectious (chronic purulent catarrhal bronchitis) and non-infectious (chronic catarrhal gastritis) diseases. Chronic catarrh is accompanied by atrophy (atrophic catarrh) or hypertrophy (hypertrophic catarrh) of the mucous membrane. The causes of catarrhal inflammation are different. Most often, catarrhs have an infectious or infectious-allergic nature. They can develop with auto-intoxication (uremic catarrhal gastritis and colitis) due to exposure to thermal and chemical agents. Mixed inflammation

If one type of exudate is joined by another, mixed inflammation develops — serous-purulent, serous-fibrinous, purulent hemorrhagic or fibrinous-hemorrhagic inflammation. Often, a change in the type of exudative inflammation is observed with the addition of a new infection, a change in the reactivity of the body.