Types of exudative inflammation. Exudative inflammation: causes, types, outcomes Types of exudative inflammation and their characteristics

Inflammation is a complex local vascular-tissue, protective and adaptive reaction of the body to the action of harmful factors, characterized by a complex of alterative, exudative and proliferative processes.

Causes of inflammation:
1. Physical - mechanical (wounds, bruises, blows), thermal (burns, frostbite), solar (burns) and radiation factors (energy of X-rays and radioactive substances).

2. Chemical – mineral (acids, alkalis, salts) and organic substances.

Sometimes inflammation occurs in the tissue system, then they talk about systemic inflammatory lesions (rheumatic diseases with systemic damage to connective tissue, systemic vasculitis, etc.).

Inflammation consists of the following sequentially developing phases: 1) alteration, 2) exudation, 3) proliferation hematogenous and histogenic cells and, less commonly, parenchymal cells (epithelium).

2 Phases of inflammation, their morphological characteristics

1. Alteration– tissue damage, manifested by dystrophic (granular, hyaline-droplet, vacuolar, fatty), necrotic and atrophic changes. Primary alteration is caused by the direct action of a damaging factor, secondary alteration is caused by the influence of decay products of cells and tissues after the primary alteration (in this case, mediators are released).

2. Exudation– a complex of vascular changes in the microcirculatory bed, increased vascular permeability, emigration of blood cells, phagocytosis, exudation.
3. Proliferation– cell proliferation with tissue and cell restoration or scar formation.

Clinical signs of inflammation: redness, swelling, pain , increased local temperature, dysfunction.

Morphology and pathogenesis of inflammation.

The development of inflammation begins with tissue damage - alteration(alteratio). It manifests itself in dystrophic, necrotic or atrophic changes.

There are:
1) primary alteration – damage arising from the direct influence of a harmful agent;
2) secondary alteration, manifested as a result of disturbances of innervation, blood circulation and exposure to tissue decay products after primary alteration.

Necrotic changes usually occur under the influence of strong and harsh factors (mechanical injuries, burns, acids, alkalis, etc.), as well as circulatory disorders (stasis, thrombosis), nervous trophism and hypertensive conditions.
Dystrophic changes occur with less intense exposure to pathogenic factors, mainly under the influence of toxic substances of various origins and in infectious diseases.
In inflammatory areas the following are found: granular, vacuolar and fatty degeneration of parenchymal cells, mucous degeneration of the epithelium, in the stroma of the organ - mucoid swelling and fibrinoid necrosis.

Exudation in the broad sense of the word, the entire complex of vascular changes observed during inflammation was designated. These changes boil down to inflammatory hyperemia, actual exudation and emigration.

Inflammatory hyperemia, i.e. overflow of blood vessels of the inflammatory focus. This is the initial point in exudative inflammation. Under the influence of a pathogenic factor, a very short-term vasospasm occurs first. Subsequently, their paralysis and stimulation of the vasodilator nerves determine the expansion of arterial vessels, increased arterial blood flow, increased temperature and redness in the inflammatory focus. Paralysis of the vasodilator nerves leads to a slowdown in blood flow in dilated vessels, to the occurrence of thrombosis and stasis, and a change in the colloidal state of the elements of the vascular wall. Similar changes occur in the lymphatic vessels.
Exudation in the narrow sense of the word is the process of sweating from the vessels of the constituent parts of blood plasma (ex - outside, sudor - sweat), and the effusion itself is exudate.
Exudation is a direct consequence of inflammatory hyperemia, since the dilation of blood vessels is determined by the thinning of their walls. This, together with changes in the colloidal state of the wall under the influence of toxic metabolic products, helps to increase vascular permeability.
The reproduction of local tissue elements is called

2. proliferation(Latin proles – ceiling, fero – carry, create). Connective tissue elements proliferate predominantly (reticular cells, vascular endothelium, histocytes, fibroblasts, fibrocytes). This is facilitated by the abundance of nutrients and biostimulants. Proliferating cells play a significant role both in the processes of destruction of pathogenic origin and resorption of tissue decay products, and in the development of healing processes (regeneration).

3 Classification of inflammation

By etiology: ordinary(banal) inflammation and specific inflammation.
By flow: acute, subacute, chronic.
By state of body reactivity and immunity: allergic, hyperergic (delayed and immediate type), hypoergic, immune.
By prevalence inflammatory reaction: focal, diffuse or diffuse.

By morphological signs:
1. Alternative(parenchymal): acute, chronic.
2. Exudative: serous (edema, dropsy, bullous form); fibrinous (lobar - superficial, diphtheritic - deep); purulent (abscess, phlegmon, empyema); hemorrhagic, catarrhal (serous, mucous, purulent, desquamative, atrophic and hypertrophic catarrh); putrefactive (gangrenous, ichorous); mixed (serous-purulent, etc.).
3.Proliferative(productive): interstitial (intermediate) – focal and diffuse; granulomatous – infectious, invasive granulomas and foreign body granulomas; hyperplastic.
4. Specific inflammation.

The name of the inflammation is determined by the Greek or Latin name of the affected organ and the ending “ it» ( itis). For example, bronchitis, pleurisy, etc. There are exceptions to the rule according to the tradition of ancient medicine: inflammation of the pharynx - “sore throat”, inflammation of the lungs - “pneumonia”.

The inflammatory condition of the organ’s own membrane or capsule is denoted by the prefix “ peri» – perihepatitis – inflammation of the liver capsule, pericarditis – inflammation of the outer membranes of the heart.

When there is inflammation of the connective tissue of the tissue surrounding the organ, the prefix “ steam" - parametritis, etc. To indicate inflammation of the inner lining of the cavity organ, the prefix "endo" is used - endocarditis, endometritis, endobronchitis.

The mechanism of the inflammatory process in the middle layer of the abdominal organs is indicated by the prefix “ meso» – mesoarthritis.

For full characteristics inflammation is recommended indicate the shape of its flow and type. For example, acute catarrhal gastritis, chronic fibrinous pericarditis.

A pathological condition that occurs as a result of a completed inflammatory process (adhesions, fusions) is denoted by adding the name of the ending organ to the Greek " pathy": mastopathy (a disease of the mammary gland in which tumor-like nodules are formed, often with a combination of ovarian dysfunction), pleuropathy, etc.

Dystrophic, necrotic and proliferative changes in the organ, occurring without exudative phenomena, cannot be considered inflammation and are designated by adding “to the Greek name of the end organ” oz"(nephrosis, lymphadenosis), and the proliferation of fibrous connective tissue in an organ is called "fibrosis" - (Latin fibra - fiber).

Examples of some designations for inflammation of the mucous membranes: conjunctiva - conjunctevitis,

cornea – keratitis,

all membranes of the eye - panophthalbitis,

nasal cavity – rhinitis,

oral cavity – stomatitis,

tonsils - tonselitis,

larynx - farengitis,

trachea - tracheitis,

lungs - pneumonia,

bronchial tubes - bronchitis,

pleura - pleurisy,

cardiac sac - pericarditis,

cardiac muscle tissue – myocarditis,

inner lining – endocarditis,

esophagus - oesophagitis,

stomach - gastritis,

scar - rumens,

mesh – reticulitis,

books will smear

rennet - abomasite,

duodenum - duodenitis,

jejunum - jejunitis,

ileum - ileitis,

cecum (cecum) – typhlitis,

colon – colitis,

rectum - practit,

bladder - cystitis,

kidney - nephritis,

inflammation of the kidney and pelvis - pyelonephritis, etc.

4 Morphological characteristics of alterative inflammation, outcomes and significance for the body

At alternative In inflammation, tissue alteration (damage) predominates: dystrophy, atrophy, necrosis, and exudative and proliferative processes are weakly expressed and are detected only during histological examination. This inflammation is called parenchymal, since parenchymal organs (liver, kidneys, skeletal muscles, etc.) are most often affected. Distinguish acute and chronic course of inflammation.
Alterative inflammation is caused by bacteria, viruses, helminth larvae, protozoa, chemicals, and occurs when immediate hypersensitivity occurs.

Examples of alterative inflammation: alternativemyocarditis(malignant form of foot and mouth disease), alternativemyositis and myocarditis(white muscle disease), toxic liver dystrophy in piglets, alterative inflammation (in the oral cavity and on the extremities with necrobacteriosis, in the mucous membrane of the large intestine in piglets with salmonellosis), caseous lymphadenitis(tuberculosis).
In acute cases, parenchymal organs (liver, kidneys, etc.) are enlarged, flabby, dull, and hyperemic; in chronic cases, the organs are reduced in volume, dense, with a wrinkled (shagreen) capsule.

Rice. 3.1 Appearance of the heart in alterative myocarditis (white muscle disease).

Rice. 3.2 Toxic liver degeneration of a piglet.

Rice. 3.3 Radiating caseosis of the lymph node.

Fig. 3.4 Necrotizing colitis in a piglet with salmonellosis of the mucous membrane and thickening of the wall of the cecum of a piglet with chronic salmonellosis.

Control questions:

1. Characterize inflammation:
a) definition of inflammation,
b) phases of the inflammatory reaction,
c) forms of inflammation depending on the predominance of one or another phase,
d) components of alteration.
2. Characterize alterative inflammation:
a) definition of inflammation,
b) what characterizes the phases of alteration;
c) give examples of alterative inflammation;
d) causes of alterative inflammation.
3. Characterize exudative inflammation:
a) what component of inflammation is present,
b) the mechanism of emigration through the endothelium of the lymphocyte vessel,
c) types of exudative inflammation depending on the nature of the exudate.

Lesson plan
1 Serous inflammation
2 Fibrinous inflammation
3 Hemorrhagic inflammation
4 Catarrhal inflammation
5 Purulent inflammation
6 Putrid inflammation

Exudative inflammation characterized by the predominance of the exudation process and the appearance of exudate of one type or another in the area of ​​inflammation. Depending on the nature of the exudate, the following types of exudative inflammation are distinguished: serous, fibrinous, purulent, putrefactive, hemorrhagic, catarrhal, mixed .

1 Serous inflammation

Serous inflammation– in the focus of inflammation, a vascular-exudative reaction predominates (serous exudate with a small amount of cellular elements).

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

Localization – in serous and mucous membranes, skin, parenchymal organs.
Flow – acute and chronic.

Exudate its composition is similar to blood serum, contains 2-5% proteins (albumin and globulins) and a small amount of leukocytes (neutrophils). It is a clear, slightly cloudy (opalescent), colorless or yellowish liquid.

Depending on the location of the exudate, three forms of serous inflammation are distinguished: serous-inflammatory edema, serous-inflammatory dropsy and bullous form .

Serous-inflammatory edema . It is observed in the intestinal wall during poisoning, in the skin of pigs with erysipelas, in the subcutaneous tissue, the mesentery of the large intestine and the wall of the bottom of the stomach of piglets with edematous disease, in the kidneys with erysipelas of pigs (serous glomerulonephritis), with serous lymphadenitis, serous pneumonia, serous myocarditis and dermatitis (erysipelas of pigs), serous dermatitis (allergy).

Rice. 4.1 Erysipelas on pig skin

Serous-inflammatory dropsy . It is characterized by the accumulation of serous exudate in the serous cavities during serous pericarditis (pasteurellosis), pleurisy, peritonitis (edematous disease of piglets).

Fig. 4.2 Chronic catarrhal gastritis in a pig.

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

Fig. 4.3 Aphthae and erosions on the pig’s snout

Lecture 9. Exudative inflammation

1. Definition, characteristics and classification

2. Types and forms of inflammation.

Vascular changes predominate, expressed in inflammatory hyperemia and the release of blood components from the vessels. Alterative and proliferative phenomena are insignificant.

The exudative type of inflammation is divided into types depending on the nature of the exudate, and each type is divided into various forms depending on the localization of the process and the acute and chronic course.

Serous inflammation is characterized by the formation of serous exudate, which in its composition is very close to blood serum. It is a watery, sometimes slightly cloudy (opalescent) liquid, colorless, yellowish or with a reddish tint due to the admixture of blood.

Serous exudate contains from 3 to 5% protein; in air it coagulates.

Depending on the location of the accumulation of exudate, three forms of serous inflammation are distinguished: serous-inflammatory edema, serous-inflammatory dropsy and bullous form.

Serous-inflammatory edema

Characteristic is the accumulation of serous exudate in the thickness of the organ, between the tissue elements. Most often, exudate is found in loose connective tissue: in subcutaneous tissue, intermuscular tissue, and in the stroma of various organs. The reasons are different: burns, chemical irritations, infections, injuries.

Macroscopically, swelling or thickening of the affected organ, its doughy consistency, and hyperemia of the inflamed area are noted. The cut surface has a gelatinous appearance, with copious discharge of watery exudate; along the vessels - pinpoint hemorrhages. Under a microscope, signs of hyperemia and accumulation of serous weakly oxyphilic fluid are visible between the separated cells and fibers. Alterative changes are manifested by cell necrosis, and proliferative changes are manifested by the proliferation of small cell elements mainly along the vessels.

Serous-inflammatory edema must be distinguished from ordinary edema, in which there are no macroscopically visible hemorrhages and plethora, and alterative and proliferative changes are not visible under microscopy.

The outcome of serous-inflammatory edema with rapid elimination of the cause is favorable. The exudate resolves and the changes may disappear without a trace. But often serous inflammation is a prestage of more severe forms of the inflammatory process: purulent, hemorrhagic.

With chronic inflammation, connective tissue develops.

Serous-inflammatory dropsy is characterized by the accumulation of exudate in closed cavities (pleural, abdominal, pericardial). At autopsy, there is an accumulation of serous exudate with fibrin threads in the cavity. Serous covers are swollen, dull, hyperemic, with hemorrhages.

With cadaveric transudation, the serous covers are shiny, smooth, without hemorrhages and tarnishing. A clear liquid the color of red grape wine is found in the cavity.

Causes of serous-inflammatory dropsy: cooling, the action of infectious pathogens, inflammation of organs located in the serous cavity.

In acute cases, the process does not leave lasting changes.

In chronic cases, the formation of adhesions (synechias) and complete closure of the cavity (obliteration) is possible.

The bullous form is characterized by the accumulation of serous exudate under any membrane, resulting in the formation of a blister. Causes: burns, frostbite, chemical irritations, infections (foot and mouth disease, smallpox), allergic reactions.

More or less large thin-walled bubbles with watery liquid appear.

When the contents of the blisters are aseptic, the exudate is reabsorbed, the blisters shrink and heal. When blisters rupture or pyogenic pathogens penetrate into their cavity, the serous-inflammatory process can turn purulent, and with smallpox it sometimes turns into hemorrhagic (“black” smallpox).

Fibrinous inflammation

This type of inflammation is characterized by the formation of exudate, which immediately clots upon exiting the vessels, causing fibrin to fall out. This coagulation of the exudate occurs due to the fibrinogen content in it, and also because necrosis of tissue elements occurs, promoting the enzymatic coagulation process.

Fibrinous inflammation, depending on the depth of the initially occurring changes, is divided into two forms - lobar and diphtheritic.

Croupous (superficial) inflammation

A fibrin film forms on the mucous, serous and articular surfaces, which is initially easily removed, revealing swollen, hyperemic, dull tissue. Subsequently, the fibrin layer thickens (in large animals up to several centimeters). In the intestine, casts of its inner surface can form. Fibrin thickens and grows with connective tissue. Examples: “hairy heart” with fibrinous pericarditis, fibrinous pleurisy, membranous inflammation of the intestine.

In the lungs, fibrin fills the cavities of the alveoli, giving the organ the consistency of liver (hepatization), the cut surface is dry. Fibrinous deposits in the lungs can resolve or grow into connective tissue (carnification). If, as a result of compression of blood vessels by fibrin, blood circulation is disrupted, necrosis of the affected areas of the lung occurs.

Croupous inflammation is caused by infectious pathogens (pasteurella, pneumococci, viruses, salmonella).

Diphtheritic (deep) inflammation

With this form of inflammation, fibrin is deposited between cellular elements deep in the tissue. This is observed in the mucous membranes and, as a rule, is the result of exposure to infectious factors (pathogens of swine paratyphoid, fungi, etc.).

When fibrin is deposited between the cellular elements, the latter always become dead, and the area of ​​the affected mucous membrane has the appearance of a dense, dryish film or pityriasis-like deposits of a grayish color.

Purulent inflammation

This type of exudative inflammation is characterized by the formation of exudate, in which polymorphonuclear leukocytes and their breakdown products predominate.

The liquid part formed from the plasma is called purulent serum. It contains leukocytes, partly preserved, partly subjected to degeneration and necrosis. Dead leukocytes are called purulent bodies.

Depending on the ratio of purulent bodies and purulent serum, benign and malignant pus are distinguished. Benign – thick, creamy due to the predominance of leukocytes and purulent bodies in it. Malignant has a more liquid consistency, watery, cloudy appearance. It contains less formed elements and more purulent serum.

The localization of purulent inflammation is very diverse. It can occur in any tissue and organ, as well as on serous and mucous membranes.

Depending on the location of the pus, several forms of the purulent-inflammatory process are distinguished, the most important of which are: abscess, empyema, and phlegmon.

Abscess- a closed, newly formed cavity filled with pus. Some types of abscesses have received special names. For example, purulent inflammation of the hair vagina - a boil. Boils sometimes merge into large foci of purulent inflammation called carbuncles. Accumulations of pus under the epidermis are called pustules.

The size of abscesses can range from barely noticeable to extensive (15–20 cm or more). On palpation, fluctuations or, conversely, tension are detected.

An autopsy reveals a cavity filled with pus, sometimes with tissue scraps. The area surrounding the abscess (pyogenic membrane) has the appearance of a dark red or red-yellow stripe 0.5 to 1–2 cm wide. Here, under a microscope, dystrophic changes or necrotic tissue local elements, leukocytes, purulent bodies, young cells of the connective tissue are visible. tissues and hyperemic vessels.

The outcome of an abscess can vary. When a spontaneous breakthrough or cutting occurs, the pus is removed, the abscess cavity collapses and becomes overgrown. In other cases, when the resorption of pus is delayed, they are converted into a dry mass enclosed in a fibrous capsule. Sometimes encystment is observed, when purulent exudate resolves faster than the connective tissue grows. At the site of the abscess, a bubble (cyst) is formed, filled with tissue fluid.

In some cases, from deep-lying abscesses, pus makes its way towards the least resistance, breaks through to the free surface, and after opening, the cavity of the abscess is connected to it by a narrow channel lined with granulation tissue, the so-called fistula, through which pus continues to be released.

If pus seeps through the interstitial connective tissue into the underlying parts of the body and accumulates in their interstitial tissue, for example in the subcutaneous tissue, in the form of a limited focus, then they speak of a septic, or cold, abscess.

Empyema– accumulation of pus in a naturally closed cavity of the body (pleural, pericardial, abdominal, articular). More often this process is referred to in relation to the affected part of the body (purulent pleurisy, purulent pericarditis, peritonitis, etc.). Empyema occurs due to trauma, hematogenous, lymphogenous spread, the transition of a purulent-inflammatory process from the affected organs (contact) or due to an abscess breaking into the cavity. At the same time, purulent exudate accumulates in the cavities, their integuments swell, become dull, and become hyperemic; there may be hemorrhages and erosions.

Phlegmon– diffuse (diffuse) purulent inflammation with separation of purulent exudate between tissue elements. Typically, this form of inflammation is observed in organs with loose connective tissue (subcutaneous tissue, intermuscular tissue, submucosa, organ stroma). The phlegmonous area swells, has a pasty consistency, bluish-red color, and a turbid, purulent liquid flows from the surface of the cut. Under a microscope, an accumulation of purulent exudate is noted between the separated tissue elements; the vessels are dilated and filled with blood.

Phlegmonous inflammation can undergo reverse development, sometimes ending in diffuse proliferation of connective tissue (tissue elephantiasis).

A phlegmonous focus that has developed in the mucous membrane and skin can open onto the free surface with one or more fistulous tracts. With purulent softening of significant areas of skin tissue and submucosal tissue, separation of the skin from the underlying tissues is observed, followed by necrosis and rejection. An extensive, deep, suppurating phlegmonous ulcer is formed.

Hemorrhagic inflammation

The main symptom is the formation of exudate with a predominance of red blood cells. In this case, severe changes occur in the vascular system with a sharp increase in their permeability. The causes may be microorganisms, toxins of plant and animal origin.

Macroscopic signs of hemorrhagic inflammation: tissue soaking in blood, accumulation of bloody exudate in cavities (intestines, pulmonary alveoli, etc.).

With hemorrhagic inflammation of the skin (for example, with anthrax), the affected area swells, becomes dark red in color, bloody exudate flows from the cut surface, and then necrosis occurs - the formation of an ulcer. In some cases, hemorrhagic exudate accumulates under the epidermis, resulting in the formation of thin-walled red-black blisters filled with bloody fluid (“black” pox). Swelling, blood-red staining followed by necrosis occurs in the lymph nodes and parenchymal organs.

In the lungs, the hemorrhagic exudate filling the alveoli coagulates. The pneumonic area becomes dark red in color and has a dense consistency. Bloody fluid drains from the cut surface.

During hemorrhagic inflammation, the mucous membranes become swollen, saturated with blood, and the surface is covered with a blood-red effusion, which in the intestine, due to the influence of digestive juices, acquires a dirty coffee color; the surface layers of the mucosa become necrotic.

Under a microscope, dilated and blood-filled vessels are visible, around which and between the separated tissue elements red blood cells are located. Cells of local tissue are in a state of degeneration and necrosis.

Hemorrhagic inflammation is one of the most severe inflammatory processes, often ending in death.

Catarrh

This type of inflammation develops only on the mucous membranes and is characterized by the accumulation of exudate, which can be different - serous, mucous, purulent, hemorrhagic.

Causes: mechanical influences (friction, pressure from stones, foreign bodies), irritation with chemicals, infections.

Mucous catarrh manifests itself in mucous degeneration and abundant desquamation of epithelial cells (desquamative catarrh). With a pronounced process, the epithelium may become partially necrotic. The number of goblet cells is sharply increased; they are abundantly filled with mucus and flake off. The mucous membrane is congested and edematous, it contains small cell infiltrates. Macroscopically, the mucous membrane is dull, swollen, full-blooded, sometimes with hemorrhages.

Serous catarrh is expressed in the formation of colorless or cloudy watery exudate. The mucous membrane is swollen, hyperemic, dull. Microscopy reveals mucous degeneration of epithelial cells, but less intense than with mucous catarrh. There is plethora and edema.

Purulent catarrh. The mucous membranes are swollen, dull, covered with purulent exudate. Erosion and hemorrhage are often observed.

Hemorrhagic catarrh. The mucous membranes are swollen, thick, saturated with blood, and there is a bloody exudate on the surface. In the intestines, the mucous membrane quickly acquires a slate, dirty-gray color, and the contents turn coffee-colored. Microscopy shows that erythrocytes predominate in the exudate. Exudate is located both on the surface and in the thickness of the mucous membrane. The vessels are full of blood. In the epithelium there are dystrophic changes and necrosis.

These forms of catarrhal inflammation in their pure form are relatively rare. Sometimes one form turns into another, more severe one (for example, serous into purulent).

Catarrhal inflammation is of a mixed nature.

In chronic catarrh, fibrous connective tissue grows in the mucous membrane. The mucous membrane thickens, becomes wrinkled, dull, pale, and grayish in color.

Putrefactive (gangrenous, ichorous) inflammation

This type usually develops as a result of complications of one or another type of exudative inflammation by the process of putrefactive decomposition of inflamed tissues. This occurs due to putrefactive bacteria entering the inflammation site, causing inflammation. Typically, in such foci of inflammation the following are found: Escherichia coli, Proteus, B. perfringens and other anaerobes. Putrefactive inflammation develops in parts of the body that are easily accessible to infection from the external environment (pneumonia, putrefactive bronchitis, etc.).

Tissues with gangrenous inflammation emit an unpleasant odor, have a dirty green color, and easily disintegrate, turning into a smearing mass.

This type of inflammation poses a great danger to the body.

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Inflammation is the response of the mesenchyme to damage.

Purpose of inflammation:

1) isolation of the damaging factor

2) destruction of the damaging factor

3) creating 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, dyscirculation, neurotrophic, metabolic.

Pathogenesis

Consists of 3 sequential processes (phases).

Ι Alteration

ΙΙ Exudation

ΙΙΙ Proliferation

Ι ALTERATION PHASE

Plays a decisive role in the development of inflammation. Without alteration (damage) to cells and tissues, inflammation does not occur. 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, which trigger the exudation phase.

Inflammatory mediators are active biological products. Currently, many mediators are known. But a special place is occupied by such mediators as HISTAMINE and SEROTONIN.

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

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

ΙΙ EXUDATION PHASE

The site of action is the microvasculature.

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

1) reaction of blood vessels and blood

2) increased permeability

3) plasmorrhagia

4) emigration of blood cells

5) phagocytosis

6) pinocytosis

7) formation of exudate and infiltrate

1) Reaction of blood vessels and blood -

Under the influence of mediators (histamine, serotonin), a short-term spasm of arterioles and precapillaries initially occurs, followed by LONG-TERM paralytic dilatation of arterioles and the development of arterial hyperemia, which is manifested by redness and warming of the inflammation. Arterial congestion contributes to the development of lymphostasis, lymphothrombosis and lymphatic edema - the release of lymph into the area of ​​inflammation. Under the influence of mediators, blood viscosity increases and blood clots form in the venules. This leads to venous congestion, which gives the inflammation site 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 increased permeability of the capillary walls, there is an increased outflow of plasma from the lumen of the capillaries into the area of ​​inflammation (plasmorrhagia).

4) Emigration of blood cells.

Movement of granulocytes, lymphocytes, monocytes into the zone of inflammation through the capillary wall (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 reason for 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 at the site 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 capable of destroying 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, of microphages - by cationic proteins (proteolytic enzymes) and atomic oxygen, which is formed during the process of peroxidation. Phagocytosis of microbes can be complete (complete destruction of microbes) or incomplete (the microbe is not destroyed and is carried by phagocytes throughout the body). Reasons for incomplete phagocytosis: 1. immunodeficiency, caused by many factors, including the immunodeficiency virus, 2. characteristics of the microbe (phagocytes cannot destroy the tuberculosis bacillus because it has a thick waxy shell).

6) Pinocytosis

Capture of tissue fluid that contains antigen by macrophages, in the cytoplasm of which an information complex is formed. Composition of the information complex: transformed antigen + information 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 to this antigen. Specific antibodies bind to this antigen, which increases the phagocytic reaction to destroy 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 and cavities. Its composition is complex, but unlike tissue fluid it contains more than 2% proteins. Therefore, it is an opaque, cloudy liquid. Whereas transudate is a clear liquid. In cases where the cellular component predominates over the liquid, the exudate receives a special name - infiltrate. Infiltrate is more typical of chronic inflammation.

ΙΙΙ PROLIFERATION PHASE

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

During reproduction, differentiation and transformation of cells occur.

As a result

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

B lymphocytes - into plasma cells

Monocytes - into epithelioid cells and macrophages.

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

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

Thus, in fetuses and newborns, alteration and proliferation predominate over exudation, and there is also a tendency to generalization. This is explained by the imperfection of protective and immune mechanisms during this period of life. In old age, there is a decrease in reactivity and prolonged 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 or decrease the severity of inflammation.

Endocrine system

There are 2 known groups of hormones:

1) pro-inflammatory

2) anti-inflammatory.

1) Pro-inflammatory (increase inflammation) - somatotropic 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 to mast cells (mast cells), which produce inflammatory mediators. A logical chain of events arises: no mast cells - no inflammatory mediators - no exudation - no inflammation.

Nervous system

There are also 2 groups of factors -

1) pro-inflammatory

2) anti-inflammatory

1) Pro-inflammatory - cholinergic substances.

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

2) Anti-inflammatory - adrenergic factors.

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

Clinical and morphological signs of inflammation.

There are 5 of them: 1) redness - caused by arterial plethora

2) increased temperature - due to arterial plethora

3) swelling - due to exudation

4) pain - caused by the action of mediators on nerve endings

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

Types of inflammatory response .

1. Adequate(or normergic reaction) is characterized

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.

This may be a hypoergic reaction (weakened)

Hyperergic reaction (intensified)

- Hypoergic the reaction may be

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

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

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

There are 2 types of hyperergic reaction -

1) immediate type hypersensitivity \GNT\

2) delayed-type hypersensitivity\HRT\

1) Immediate-type hypersensitivity occurs immediately after exposure to an antigen (drugs, pollen, foods 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 when cellular immunity is impaired (aggressive action of T-lymphocytes and macrophages). The inflammatory reaction occurs one day after exposure to the antigen. Example: inflammation of the skin one day after the administration of tuberculin.

Terminology. Classification .

Inflammation of an organ or tissue is indicated by the ending -it. It is added to the name of the 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 -

Duration of flow

By causal factors

According to pathomorphology

According to the flow, there are 3 types of inflammation -

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

According to the causative factors, there are:

• banal (nonspecific) inflammation
• specific inflammation (inflammation due to 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) ALTERNATIVE INFLAMMATION

With this type of inflammation, damage to the organ parenchyma predominates. The 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 lesions heal completely - scar tissue forms in place of large lesions. The meaning 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 effusion, which determines the entire picture of inflammation.

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

A. Seroznoe

B. Fibrinous

V. Purulent

G. Glinostnoe

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. Hyperemia is well expressed. The porosity of the capillaries is moderate. Localization - serous cavities (cardiac, abdominal, pleural), meninges, stroma of the liver, myocardium, kidneys.

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

Reasons: thermal, chemical, infections, etc.

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

B. Fibrinous inflammation

The exudate contains a lot of fibrin. Damage to capillaries with this type of inflammation is significant. Serous and mucous membranes are most often affected, less often the stroma of organs.

There are 2 types of this inflammation:

1) lobar

2) diphtheritic

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

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

Diphtheritic (meaning leathery) inflammatory process is observed not only with diphtheria (disease). This is a broader concept, since diphtheritic 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 forms with the possible development of stenosis, for example, of the trachea and bronchi; Fibrous adhesions always form 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 many globulins, fibrin and, most importantly, neutrophils.

Types of purulent inflammation.

1) Phlegmon is a diffuse abscess. Characterized by the spread of pus through the intermuscular spaces, fatty tissue, fascia, tendons

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

Localization varies: 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: most often pyogenic microorganisms (all types of coccal infections), tuberculosis bacilli, fungi, chemical agents.

Course - 1) Acute 2) Chronic.

Acute inflammation occurs 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 occurs over a long period of time with the development of fibrosis around the purulent process. It gives complications such as chronic fistula tracts, extensive leaks of pus, intoxication, wound exhaustion, amyloidosis.

G. Putrefactive inflammation

It develops when a putrefactive infection enters the area. It is characterized by increased necrobiotic processes and the formation of foul-smelling gas.

D. Hemorrhagic inflammation

Occurs when red blood cells penetrate into the exudate. This indicates severe damage to the microvasculature. It is observed in severe forms of influenza, smallpox, anthrax, and plague.

E. Catarrhal inflammation.

This is an inflammation of the mucous membranes with the formation of mucus and its accumulation in 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. A cloudy exudate is characteristic. The mucous membrane is swollen, full-blooded. It is observed with a viral respiratory infection in the respiratory system and with cholera in the mucous membrane of the small intestine.

2) Mucous. Characterized by the presence of a large amount of mucus. The exudate is viscous and is 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 deformation.

The course of catarrhal inflammation is acute and chronic.

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

Chronic catarrh occurs as follows:

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, organ function is impaired 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, in the course of inflammation, a new infection occurs, or the reactive, protective forces of the body change significantly.

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

According to 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 (germs, viruses), toxins, burns, allergic reactions.

FIBRINOUS INFLAMMATION characterized by the formation of exudate in the form of gray-yellow films (membranous inflammation), which consist of fibrin strands 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, not firmly attached to the fabric, and come off easily.

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

G SOURING 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 leukocytes). Pus melts the tissue (histolysis), which leads to the formation of cavities, ulcers and fistulas (purulent tracts). Etiology– pyogenic microorganisms: staphylococci, streptococci, meningococci, Pseudomonas aeruginosa, etc.

abscess (ulcer)- limited purulent inflammation with the formation of a cavity in the organ that is filled with pus. A chronic abscess is delimited from the organ tissue by an outer shell of connective tissue; the inner shell, which 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, and intermuscular layers.

empyema– accumulation of pus in 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 on the mucous membranes.

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

· apostematosis– multiple, small pustules.

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

HEMORRHAGIC INFLAMMATION occurs with high vascular permeability. The exudate resembles blood, because consists of red blood cells. Often associated with 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 of 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 caused by the release of inflammatory mediators. Depending on the degree of damage to the walls of capillaries and venules and the intensity of the action of mediators, the nature of the resulting exudate may be different. With mild damage to the vessels, only low-molecular-weight albumins leak into the site of inflammation; with more severe damage, large-molecular globulins appear in the exudate and, finally, the largest fibrinogen molecules, which are converted into fibrin in the tissue. The exudate also includes blood cells emigrating through the vascular wall and cellular elements of damaged tissue. Thus, the composition of the exudate may be different.
Classification. The classification of exudative inflammation takes into account two factors: the nature of the exudate and the localization of the process. Depending on the nature of the exudate, serous, fibrinous, purulent, putrefactive, hemorrhagic, and mixed inflammation are distinguished (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 (PMN) and desquamated epithelial cells. Serous inflammation develops most often in serous cavities, mucous membranes, soft meninges, skin, and less often in internal organs.
Causes. The causes of serous inflammation are varied: 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, chickenpox).
Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel's diplococcus, shigella) can also cause serous inflammation. Thermal, and less commonly, chemical burns are characterized by the formation of blisters in the skin filled with serous exudate.
When the serous membranes become inflamed, a cloudy fluid, poor in cellular elements, accumulates in the serous cavities, 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 off 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. 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 impedes the functioning of the heart, and serous inflammation of the lung parenchyma can lead to acute respiratory failure.
Fibrinous inflammation. It is characterized by exudate rich in fibrinogen, which is converted into fibrin in the affected tissue. This is facilitated by the release of tissue thromboplastin. In addition to fibrin, PMNs and elements of necrotic tissue are also found in the exudate. Fibrinous inflammation is most often localized on the serous and mucous membranes.
Causes. The causes of fibrinous inflammation are varied - bacteria, viruses, chemicals of exogenous and endogenous origin. Among bacterial agents, diphtheria corynebacterium, Shigella, and Mycobacterium tuberculosis most contribute to the development of fibrinous inflammation. Fibrinous inflammation can also be caused by Frenkel diplococci, pneumococci, streptococci and staphylococci, and some viruses. The development of fibrinous inflammation during autointoxication (uremia) is typical. 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, to the hyperergic reaction of the body.
Morphological characteristics. A light gray film appears on the surface of the mucous or serous membrane. Depending on the type of epithelium and the depth of necrosis, the film can be loosely or firmly connected to the underlying tissues, and therefore two types of fibrinous inflammation are distinguished: lobar 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 was sprinkled with sawdust. The serous membrane is dull, covered with gray fibrin threads resembling hair. For example, fibrinous inflammation of the pericardium has long been figuratively called hairy heart. Fibrinous inflammation in the lung with the formation of lobar exudate in the alveoli of the lung lobe is called lobar pneumonia.
Diphtheritic inflammation develops 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, and 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. If the proteolytic function of neutrophils is insufficient, connective tissue appears at the site of the exudate (exudate is organized); with excessive activity of neutrophils, the development of an abscess and gangrene of the lung is possible. On serous membranes, fibrinous exudate can melt, but more often it undergoes organization 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 site of inflammation; such decaying cells are called purulent bodies. In addition, elements of destroyed tissues, as well as colonies of microorganisms, can be seen in the exudate. 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 neutrophil granules 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 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 granulation shaft forms around the abscess.
tissue, through the 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 pyogenic 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 spread of pus - in fatty tissue, in the area of ​​tendons, fascia, along the neurovascular bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, in addition to anatomical features, the pathogenicity of the pathogen and the state of the body's defense systems play an important role.
There are soft and hard phlegmon. Soft cellulitis characterized by the absence of visible foci of necrosis in tissues, with hard cellulitis Foci of coagulative necrosis form in the tissues, which do not melt, but are gradually rejected. Cellulitis of fatty tissue is called cellulite, 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 impaired due to purulent inflammation (empyema of the gallbladder, appendix, joint, etc.). With a long course of empyema, the 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 tissue is rarely good enough, and progressive melting of the surrounding tissue 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 canal 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, 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 of the exudate and inflammatory infiltrate changes. 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 and lymphatic vessels, and bleeding and generalization of infection with the development of sepsis are possible. With thrombosis of the affected vessels, necrosis of the affected tissues may develop; if they come into 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 underlies 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.
Putrefactive inflammation. It develops when putrefactive microorganisms enter the source of inflammation.
Causes. Putrefactive inflammation is caused by a group of clostridia, causative agents of 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. A wound with anaerobic gangrene has a characteristic appearance: its edges are bluish, and gelatinous swelling of the tissue is observed. Fiber and pale, sometimes necrotic muscles protrude from the wound. When palpated, crepitus is detected in the tissues, and the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is initially determined, which is replaced by widespread necrotic changes. Neutrophils that enter the site of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign and indicates the attenuation of the process.
Exodus. Usually unfavorable, which is associated with the massiveness of the lesion and a decrease in the resistance of the macroorganism. Recovery is possible with active antibiotic therapy in combination with surgical treatment.
Meaning. It is determined by the predominance of anaerobic gangrene in mass injuries and the severity of intoxication. Putrefactive inflammation in the form of sporadic cases can develop, for example, in the uterus after a criminal abortion, in the colon of newborns (the so-called necrotizing colitis of newborns).
Hemorrhagic inflammation. 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, red blood cells 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.
Mixed inflammation. 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 in the qualitative composition of leukocytes; Neutrophils are the first to appear at the site of inflammation, they are replaced by monocytes and later by 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 body’s reactivity 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.
Catarrh. It develops on the mucous membranes and is characterized by an abundant release of exudate flowing from the surface of the mucosa, hence the name of this type of inflammation (Greek katarrheo - flowing down). A distinctive feature of catarrhal inflammation is the admixture of mucus to any exudate (serous, purulent, hemorrhagic). It should be noted that mucus secretion is a physiological protective reaction that increases under conditions of inflammation.
Causes. Extremely diverse: bacterial and viral infections, allergic reactions to infectious and non-infectious agents (allergic rhinitis), the effects 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 its obligatory component is mucus, as a result of which the exudate takes the form of a viscous, viscous mass. Microscopic examination reveals leukocytes, desquamated cells of the integumentary epithelium and mucous glands in the exudate. The mucous membrane itself has signs of edema, hyperemia, is infiltrated with leukocytes, plasma cells, and there are many goblet cells in the epithelium.
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 in the mucous membrane is often accompanied by impaired regeneration of epithelial cells with the development of atrophy or hypertrophy. In the first case, the membrane becomes smooth and thin, in the second it thickens, its surface becomes uneven, and can bulge into the lumen of the organ in the form of polyps.
Exodus. Acute catarrhal inflammations last 2-3 weeks and usually end with complete recovery. Chronic catarrhal inflammation is dangerous due to the development of atrophy or hypertrophy of the mucous membrane.
Meaning. It is ambiguous due to the variety of reasons that cause it.