Components and signs of inflammation

There are three components of inflammation — alteratiou, exudation and proliferatiou are closely related.
The initial alteration (LAT. alteratio-change) is the set of metabolic changes of physical and chemical properties, structure and function of cells and tissues under the influence of etiological factor of inflammation. The initial alteration as a result of interaction with organism etiological factor and causes inflammation persists after the termination of this interaction. Examples are nekrobioticheskie changes due to severe tissue injuries that cause inflammation after exposure to the ranâŝego projectile.

Secondary alteration is the accumulation of changes of cells and tissues as a result of the inflammation. One of the reasons is the changes of Microcirculation in the middle of inflammation and the surrounding tissues, causing a significant drop in oxygen tension in the center of inflammation. Hypoxia and associated gipoèrgoz cellular components is one of the causes cytolysis in the middle of inflammation. Cause cytolysis damaged primary cells and activate a alteration systems complement prior acute inflammatory reaction in her hearth. Also cause cytolysis free oxygen radicals and enzymes released in the middle of inflammation activated phagocytes. Cytolysis is the reason high content in the intercellular spaces of the inflammation, and gipoèrgoz increases potassium content of protons (lactate metabolic acidosis type a).

Colloid-osmotic pressure in interstitia hearth inflammation increases:
♦ accumulation in the plasma proteins;
♦ exit potassium cells and related anions because cytolysis macromolecular;
♦ pulmonary venules and lymphatic vessels, which prevents the removal of osmolej from home inflammation.

Cellular effectors of inflammation are established through the review of its functioning, which is alteratiou. Nekrobioticheskie changes of cells in the middle of inflammation lead to dysfunctions of characterizing them as primary and secondary alteratiou.
Articular exudation (LAT. exudatio-bleeding), exit the liquid part of blood plasma in interstitia and emigration from vessels in the intercellular space of cells as cellular effectors of inflammation. The result is filling the interstitial spaces of the exudation and hotbed of inflammation exudate. Transudate is a fluid that accumulates in the intercellular spaces as a result of the increased hydrostatic pressure in mikrososudah and (or) increasing their permeability, non-acute inflammatory reaction. At an inflammation of hydrostatic pressure on mikrososudah hearth is growing as a result of acute inflammation and thrombosis venules, lymph, arterioles and microvessels prekapillârnyh sphincters. Permeability in the middle of inflammation increases the number of mediators of inflammation. As a result of the liquid part of blood plasma is intersticij. Honors from transsoudata is a high fluid content of protein (not less than 30 g/l), proteolytic enzymes, antibodies, leukocytes and tissue residues.

Separately as an element emit growth response of permeability of exudation of microvessels in the middle of inflammation. It causes the local growth of flogogenov that increase the permeability of the wall of the microvessels in the middle of inflammation and cause the emigration of leukocytes. Early growth response of permeability causes a transient effect of histamine levels-4, CE-rotonina, bradykinin. Early transient reaction mainly affects venules with diameter not greater than 100 μm. Blood capillaries is not changed. In this phase the inflammatory response of permeability of èndote growth-liocity venules are reduced, leading to the formation of gaps between them, through which may occur out of the liquid part of blood plasma and the emigration of leukocytes in intersticij. The immediate and long-term growth response of permeability of its primary alteration is mainly as a result of exogenous etiological factors of mechanical (trauma, injury), thermal or chemical nature. As a result of the etiological factor occurs at the level of the endothelial cell necrosis of arterioles, small diameter capillaries and venules, which leads to a persistent increase its permeability. Delayed and persistent growth response of permeability of microvessels in the middle of inflammation develops over hours or days from its start. It is typical for the inflammation caused by Burns, the action of bacterial toxins, ultraviolet and ionizing radiation and allergic reactions delayed (retarded) type. One of the major mediators of this reaction is slow reacting substance of anaphylaxis, lakotriena and polyunsaturated fatty acids that are synthesized from arachidonic acid and platelet-activating factor. Slowly responsive substance formed in the middle of inflammation and release fat cells. Stable growth of microvessels in the middle of inflammation immediately reacting substance of anaphylaxis is conditioned by proteolysis of the basal membranes of microvessels.

The biological meaning of exudation as component of inflammation is not only to ensure the destruction of the alien through his attack of the complement system and activated phagocytes of circulating blood, but also in the boundary of inflammation through the squeeze of blood and lymph due to interstitial edema microvessels, as well as in breeding flogogenov and cytolysis in the middle of inflammation factors to prevent redundant secondary alteration.

Proliferation (LAT. proliferatio — reproduction) is a division of fibroblasts and intensification of education of the stroma of connective tissue (collagen) in the middle of inflammation to the tissue defects due to substitution of primary and secondary alteration. Proliferatiou completes the involution of the scar, the destruction and elimination of excess Collagenous structures. The main cellular effectors of cell proliferation is an activated phagocyte mononuklearnye fibroblasts and immune cells. Fibroblasts form in the middle of inflammation and release collagen and enzyme-kollagenzu, responsible for the formation of collagen stroma of connective tissue structures. In addition, they form a fibronectin that defines the migration, adhesion and proliferation of fibroblasts. Mononukleary and lymphocytes secrete cytokines as stimulating and inhibiting the function of fibroblasts. Neutrophils as cellular effectors inflammation affect proliferation, sekretiruâ stimulators of proliferation and antikejlony kejlony.

Redness and heat as local signs of inflammation are mostly associated with arterial hyperaemia and intense oxidation processes in the middle of inflammation in which almost does not capture the free energy of the cells. Swelling in the middle of inflammation is the result of arterial blood and interstitial edema as a result of exudation. Pain in the middle of inflammation is the result of direct and/or indirect action of flogogenov on a sensitive nerve. Pain in the middle of inflammation increases acidosis. It may cause mechanical irritation to the nerve endings as a result of increased pressure in the middle of inflammation. Disorders of functional systems whose bodies-effectors are amazed by inflammation, as signs of inflammation are mainly related to the destruction of their structural and functional units, preventing systemic regulatory influences and geeky in the effectors of functions of mass and energy shortages.

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