64. Inflammation: definition of the concept, etiology, classification, pathoanatomical characteristics of the phases of inflammation, outcomes, clinical significance.

Inflammation is a complex local vascular—mesenchymal reaction to tissue damage aimed at destroying the agent that caused this damage and restoring damaged tissue. Inflammation is a reaction developed during phylogeny, which has a protective nature. Etiology: Any damaging agent that exceeds the adaptive capabilities of the tissue in strength and duration can cause inflammation. All phlogogenic factors are usually divided into external and internal (endogenous). External ones include MO (bacteria, viruses, fungi); animal organisms (protozoa, worms, insects), chemicals (acids, alkalis), mechanical (foreign bodies, pressure, rupture) and thermal effects (cold, heat), radiation energy (X-rays, radioactive, ultraviolet rays).

Endogenous factors include those that occur in the body itself as a result of another disease. For example, inflammation may occur as a reaction to a tumor, gallstones or urinary stones, or a blood clot formed in the vessels. The cause of inflammation can be antigen—antibody complexes, if they are fixed in any organ.

STAGES OF INFLAMMATION

I. The stage of alteration (damage):

A. Primary alterations

B. Secondary alterations

II. The stage of exudation and emigration

III. The stage of proliferation and repair

I.The stage of alteration is complex and extensive physico-chemical and structural-functional changes in the focus of inflammation.:

1. Primary alteration is damage caused by the action of an inflammatory factor.

2. Secondary alteration is the release from cells and the formation of biologically active substances – inflammatory mediators and activation of lysosomal enzymes - and their effect on biological biomolecules. Inflammatory mediators are biologically active substances that are formed in the blood as a result of primary damage.

By origin:

1)Cellular: histamine, serotonin, lysosomal enzymes, prostaglandins, lymphokines.

2) Mediators formed in the body's liquid media (kallikrein-kinin system, blood coagulation system, complement-binding system). II Exudation – this component of inflammation includes a triad:

• Vascular reactions and inhibition of blood circulation in the focus of inflammation

• The exit of the liquid part of the blood from the vessels is actually exudation

Emigration is the release of leukocytes in the focus of inflammation from the developing phagocytic reaction III .Proliferation – elements of connective tissue origin mature in the focus of inflammation, which protect the damaged area. The final stage is the lysis of collagen structures, the involution of the scar. Proliferation is influenced by:

1. Fibroblasts that synthesize procollagen and collagenase.

2. Fibroblasts form fibronectin, which promotes the stimulation of migration, proliferation and adhesion of connective tissue cells.

3. Macrophages secrete PGE, which is able to activate the growth of regenerating tissue.

4. Neutrophils produce xylones, antixylones, which affect the proliferation process.

Corticosteroids – glucocorticoids inhibit regeneration and reduce collagen synthesis. Mineralocorticoids stimulate the regeneration process. With alternative inflammation, damage, dystrophy, and necrosis prevail. It is observed most often in parenchymal organs in infectious diseases that occur with severe intoxication (curdled breakdown of the adrenal glands or lungs in tuberculosis). Exudative inflammation is characterized by a pronounced circulatory disorder with the phenomena of exudation and emigration of leukocytes. By the nature of the exudate, serous, purulent, hemorrhagic, fibrinous, and mixed inflammation are distinguished. The spread of inflammation to the mucous membranes, such as the respiratory tract or the alimentary canal, and the high content of mucus in the exudate indicate catarrhal inflammation. Proliferative, or productive, inflammation is characterized by a dominant proliferation of cells of hematogenic and histogenic origin. Cellular infiltrates occur in the inflamed zone, which, depending on the nature of the accumulated cells, are divided into round-cell (lymphocytes, histiocytes), plasma cell, eosinophilic cell, epithelioid cell, macrophage infiltrates. With inflammation, cells with a complete development cycle (mature) die, while mesenchymal cells undergo transformation and differentiation, as a result of which young connective tissue is formed. Downstream: acute, subacute, chronic The outcome of inflammation varies depending on its etiology and the nature of the course, the state of the body and the structure of the inflamed organ. Tissue breakdown products undergo enzymatic cleavage and phagocytic resorption, and decomposition products are resorbed. Due to cellular proliferation, the focus of inflammation is gradually replaced by connective tissue cells. If the focus of inflammation is small, complete tissue recovery may occur. With a significant tissue defect, a scar forms at the site of the lesion.