Definition of "inflammation"

Inflammation - local reaction  blood vessels, connective tissue and nervous system damage.

The development of inflammation is closely related to the reactivity of the organism as a whole. The state of reactivity of the body affects inflammation. Reduced reactivity causes a slowdown and weakening of the development of inflammation. For example, in old people, in people with reduced nutrition, with beriberi inflammation develops very slowly, sluggishly and is not accompanied by the presence of all its signs. On the other hand, inflammation affects the reactivity of the whole organism. More or less extensive inflammation in humans causes fever, leukocytosis and other changes in the reactivity of the whole organism.

During inflammation, there are three groups of processes:

• 1) tissue damage (alteration);
• 2) circulatory disorders and microcirculation in the inflamed tissue;
• 3) the reproduction reaction (proliferation) of connective tissue elements.

Comparative pathology of inflammation

Comparative pathology of inflammation developed by the great Russian scientist D.I. Mechnikov.

Inflammation occurs in various forms in all members of the animal world. The increasing complexity of the organization of the animal is accompanied by a complication of the inflammatory response. Like other pathological processes, inflammation evolves with the evolution of animal species. In animals lacking blood vessels (sponges, intestinal cavities, echinoderms), inflammation is expressed in the accumulation of amoeboid connective tissue cells (amoebocytes) around the site of damage. I. I. Mechnikov injected a spike of rose into the transparent bell of the jellyfish and observed the accumulation of amoebocytes around the damaged area of ​​tissue. This reaction was inflammation. In higher invertebrates (crustaceans, insects) that have an open circulatory system, inflammation is also expressed in the accumulation of blood cells - lymphohematocytes - at the site of injury. Changes in blood circulation in the inflamed tissue, characteristic of vertebrates and humans, did not occur in invertebrates.

The development of the circulatory system and its nervous regulation in vertebrate animals and in humans has significantly complicated the inflammatory response. Circulatory disturbance in the inflamed tissue is the most important expression of inflammation. In addition, the nervous system has become essential in the development of inflammation. The involvement of connective tissue cells in inflammation in higher animals and in humans is manifested by the release of blood cells (leukocytes) into inflamed tissue and reproduction of local connective tissue cells (histiocytes, fibroblasts) in the inflamed tissue focus.

The main signs of inflammation in humans

The external manifestations of inflammation on the skin and mucous membranes in humans have been described in ancient times (Hippocrates, Celsus, Galen). Celsus wrote: “True signs of inflammation are the essence: redness ( rubor) and a tumor ( tumor) with heat ( calor) and bolyo ( dolor) ". Galen added to this definition of inflammation a fifth sign - “impaired function” ( functio laesa).

The development of inflammation in internal organs  not always accompanied by these signs. However, in various combinations they are often found in inflammation and are still considered to be classic signs of an inflammatory reaction.

To denote inflammation in a particular organ or tissue is taken by adding the end " itis"To the Latin name of this tissue or organ." For example, nerve inflammation is called neuritis, muscle inflammation - miositis, inflammation, kidneys - nephritis, liver inflammation - hepatitis etc. The inflammation of some organs has a special name: for example, pneumonia is called pneumonia (from Greek. pneuma  - air), inflammation of the subcutaneous tissue - cellulitis (from the Greek. phlegmone  - inflammation), etc.

Etiology of inflammatory processes

Inflammation is caused by a variety of damaging agents:

• 1) mechanical (scratch, wound);
• 2) physical:
  • a) thermal (burn),
  • b) barring (blood sucking jars),
  • c) radiation (ultraviolet rays, heat rays, ionizing radiation), etc .;
• 3) chemical (action of acids, alkalis, foreign proteins, various salt solutions  and other chemical irritants);
• 4) biological (pyogenic cocci, pathogenic fungi, protozoa, etc.);
• 5) mental and so forth.

The concept of "inflammation." Causes of inflammation. Local and common symptoms  inflammation. Types of inflammation.

Inflammation- complex local protective and adaptive response of the connective tissue, blood vessels and nervous system of the whole organism, in response to damage, is aimed at isolation, removal of the damaging agent and the elimination of damage consequences.

Causes of inflammation  exogenous and endogenous.

Endogenous factors that occur in the body as a result of another disease include tissue decay products, blood clots, heart attacks, hemorrhages, gallstones or urinary stones, salt deposits.

Local signs of inflammation: redness; swelling (edema); pain; temperature rise; dysfunction of the affected organs and tissues. Common signs of inflammation : fever; leukocytosis; ESR acceleration, etc.

Any inflammation includes 3 main components:

Alterations - damage to cells and tissues;

Microcirculation disorder with exudation and emigration;

Proliferation - cell multiplication and tissue integrity.

Respectively distinguish between:  alterative inflammation, exudative inflammation, proliferative (productive) inflammation and - as its separate variant - granulomatous inflammation.

The type of inflammation depends on the reactivity of the organism, the localization of the process, the type, strength and duration of the action of the phlogogen.

Alterative inflammationcharacterized by a special manifestation of the phenomena of dystrophy (up to necrobiosis and necrosis) and, thus, their predominance over exudative-infiltrative and proliferative. Most often, alterative inflammation develops in parenchymal organs and tissues (myocardium, liver, kidneys, skeletal muscle) with infections and intoxications, which is why it is also called parenchymatous. In case of pronounced necrobiotic changes, alterative inflammation is called necrotic, for example, immunocomplex allergic inflammation (an experimental phenomenon of Arthus and art-like reactions in humans).

Exudative-infiltrative inflammationcharacterized by a predominance of circulatory disorders with exudation and emigration over alteration and proliferation. Depending on the nature of the exudate, it can be serous, fibrinous, purulent, putrid, hemorrhagic and mixed.

Stage of inflammation. Circulatory disorders and microcirculation disorders during inflammation. Outcomes of inflammation. The value of the inflammatory reaction for the body. Inflammation as the cause of mental defects, hearing, vision, speech.

If this barrier is overcome, then there is a process of damage, which is the beginning of inflammation.

Inflammatory reactions  are the second protective barrier.

The last protective barrier is immune.

Any inflammation is a complex of three phases:

1) damage; 2) vascular reaction; 3) immunological reaction. In accordance with this, the following stages of inflammation are distinguished: 1) the stage of alteration (damage); a) primary; b) secondary.

Alteration - damage to the structure of cells, tissues and organs, accompanied by a violation of their vital functions.

2) Stage of exudation and emigration;

Exudation - the release of liquid blood from the lumen of blood vessels into the extravascular space.

3) Stage of proliferation and reparation: a) proliferation; b) completion of inflammation

Proliferation - cell multiplication and tissue integrity.

The outcome of inflammation  depends on its type and course, location and prevalence. The following outcomes of inflammation are possible:

1. Almost complete restoration of the structure and function (return to normal - restitutio ad integrum).Observed with minor damage, when the restoration of specific tissue elements.

2. Scar formation (return to normal with incomplete recovery). Observed with a significant defect at the site of inflammation and its replacement connective tissue. A scar may not affect functions or lead to dysfunctions as a result of: a) deformation of an organ or tissue (for example, cicatricial changes of heart valves); b) displacement of organs (for example, of the lungs as a result of the formation of adhesions in the chest cavity in the outcome of pleurisy).

3. The death of the organ and the whole body - with necrotic inflammation.

4. The death of the body with a certain localization of inflammation - for example, from asphyxiation due to the formation of diphtheria films on the mucous membrane of the larynx. Localization of inflammation in the vital organs is threatening.

5. The development of complications of the inflammatory process

6. Transition acute inflammation  in chronic.

In the clinical outcome of inflammation, the underlying disease is of great importance if the occurrence of a focus (lesions) of inflammation is associated with it.

Types of inflammation, depending on the causes, reactivity, course, prevalence of stages. Stage of inflammation. General and local signs of inflammation.

Inflammation  - a typical pathological process, a protective-adaptive reaction that develops in response to the action of the phlogogenic agent, aimed at eliminating and localizing this agent, and repairing the tissue, although it may lead to their damage.

Inflammation is a typical pathological process, evolutionarily developed and fixed, developing at the level of histohematogenous barriers with the participation of vascular-tissue structures (endothelium, macrophages, leukocytes), it is a universal, mainly protective and adaptive process aimed at restoring structural homeostasis (DN Mayansky ).

Inflammation is an evolutionarily fixed, predominantly locally appearing histo-vascular response of the whole organism in response to locally acting (exogenous and endogenous) damaging factors (V.А. Vorontsov).

Inflammatory diseases account for about 80% of all pathology in the practice of a doctor of any specialty, giving the greatest number of days of disability.

Classification of inflammation According to the etiology of inflammation (depending on the type of phlogogenic agent):

Exogenous factors:

Mechanical.

Physical (radial, electrical energy, heat, cold).

Chemicals (acids, alkalis).

Antigenic (allergic inflammation).

Endogenous factors:

Products of tissue decay - heart attack, necrosis, hemorrhage.

Thrombosis and embolism.

Products of impaired metabolism - toxic or biologically active substances (for example, in uremia, toxic substances formed in the body are secreted from the blood by mucous membranes, skin, kidneys and cause an inflammatory reaction in these tissues).

Salt deposition or loss of biological compounds in the form of crystals.

Neuro-dystrophic processes.

On the participation of microorganisms:

Infectious (septic).

Non-infectious (aseptic).

By reactivity:

Hyperergic.

Normergic.

Hypoergic.

With the flow:

• Subacute.

  Chronic.

According to the predominance of the stage:

Alterative arises in parenchymal organs (recently denied).

Exudative occurs in fiber and blood vessels (lobar, serous, fibrinous, purulent, putrid, hemorrhagic, catarrhal, mixed).

Proliferative (productive) occurs in bone tissue.

Stages of inflammation

The stage of alteration (damage) is:

primary,

secondary.

The stage of exudation includes:

vascular reactions

exudation itself,

marginalization and leukocyte emigration,

extravascular reactions (chemotaxis and phagocytosis).

Stage of proliferation (restoration of damaged tissues):

Autochthonous- this property of inflammation once started, to proceed through all stages to its logical conclusion, i.e. the cascade mechanism is activated when the preceding stage spawns the next.

Local signs inflammations were described by the Roman encyclopaedist Celsus. He called 4 signs of inflammation: redness  (rubor), swelling  (tumor) local heat  (color) pain  (dolor). The fifth sign called Galen is dysfunction  - functio laesa.

Redness    associated with the development of arterial hyperemia and "arterialization" of venous blood in the inflammation.

Heat    due to the increased influx of warm blood, activation of metabolism, separation of the processes of biological oxidation.

"Tumor" ("swelling")    occurs due to the development of exudation and edema, swelling of tissue elements, an increase in the total diameter of the vascular bed in the focus of inflammation.

Pain    develops as a result of irritation of the nerve endings with various biologically active substances (histamine, serotonin, bradykinin, etc.), a shift in the active response of the medium to the acidic side, the occurrence of disionium, an increase in osmotic pressure, and mechanical stretching or compression of tissues.

Dysfunction of the inflamed organ    associated with the disorder of its neuroendocrine regulation, the development of pain, structural damage.

Fig. 10.1. Caricature of P. Cull on Dr. A. A. Willoughby’s description of classic local signs of inflammation.

Inflammation is a process that is manifested not only by pronounced local signs, but also by very characteristic and often significant changes in the whole organism. Among the factors responsible for the interconnection of local and general changes in inflammation, along with autocoids formed and circulating in the blood (kinins, cytokines, components of the complement system, prostaglandins, interferons, etc.), so-called “acute phase” reactants are of great importance. These substances are not specific for inflammation, they appear after a variety of tissue damage, including after injury during inflammation. Of these, C-reactive protein,? 2-macroglobulin,? 1 - glycoprotein, haptoglobin, transferrin, appoferritin have the greatest value. Most of the "acute phase" reactants are synthesized by macrophages, hepatocytes and other cells.

The following changes at the level of the whole organism, so-called signs of a general nature, may indicate the development of inflammation:

I. Change in the number of leukocytes in peripheral blood.

The vast majority of inflammatory processes is accompanied by leukocytosis, much less often, with inflammation of viral origin - leukopenia. By its nature, leukocytosis is mainly redistributive, i.e. due to the redistribution of leukocytes in the body, their release into the bloodstream. A certain contribution to the increase in the number of leukocytes in peripheral blood is made by the activation of leukopoiesis. The main causes of the development of leukocytosis include the stimulation of the sympathoadrenal system, the effects of certain bacterial toxins, tissue breakdown products, and a number of inflammatory mediators (interleukin-I ?, an induction factor of monocytopoiesis, etc.).

2. Fever develops under the influence of pyrogenic factors coming from the inflammatory focus: primary pyrogens of exogenous and endogenous origin (endotoxins - lipopolysaccharide nature, structural elements of cell membranes of various bacteria, various antigens of microbial and nonmicrobial origin, alloantigens, various exotoxins, etc.) and secondary pyrogens (interleukin-I ?, interleukin-6, tumor necrosis factor).

3. Changes in the amount and quality of plasma proteins (dysproteinemia). In the acute inflammatory process, so-called “proteins of the acute phase” synthesized by hepatocytes, macrophages and other cells accumulate in the blood. The chronic course of inflammation is characterized by an increase in the blood content of? - and especially? -Globulin, an imbalance of albumin and globulins.

4. An increase in the erythrocyte sedimentation rate (ESR), which is especially the case for chronic inflammatory processesdue to an increase in blood viscosity, a decrease in the negative charge and agglomeration of red blood cells, changes in physicochemical constants, the composition of proteins (dysproteinaemia) of blood, temperature rise.

5. Changes in the content of hormones in the blood usually consist in increasing the concentration of catecholamines and corticosteroids.

Related topics Common signs of inflammation:

1. Inflammation. Definition, essence, mediators of inflammation. Local and general manifestations of exudative inflammation, morphological manifestations of exudative inflammation. The answer is the acute phase. Ulcer-necrotic reactions with inflammation.
2. INFLAMMATION: DEFINITION, ESSENCE, BIOLOGICAL SIGNIFICANCE. MEDIATORS OF INFLAMMATION. LOCAL AND GENERAL INFLAMMATION. ACUTE INFLAMMATION: ETIOLOGY, PATHOGENESIS. MORPHOLOGICAL MANIFESTATION OF EXUDENT INFLAMMATION. The outcome of acute inflammation