Inflammation is a typical pathological process characterized by alteration, exudation and proliferation. It developed during evolution in organisms having vascular system to destroy, dilute, or wall off the injurious agents as well as to induce healing and reconstituting the damaged tissue.
Acute inflammation is characterized by a short duration (from minutes to few weeks), exudation of fluid and plasma proteins and emigration of leukocytes, predominantly neutrophils.
Chronic inflammation is manifested by a prolonged duration, persistent necrosis, accumulation of cells, predominantly macrophages and their derivates, lymphocytes, fibroblasts and sclerosis.
Most common causes of inflammation are: microbial infections, hypersensitivie reactions and autoimmunity, physical agents, irritant and corrosive chemicals, tissue necrosis.
Alteration may be divided into primary and secondary. Primary alteration is caused by the action of initial stimuli. Secondary alteration results from the conditions that take place in the focus of inflammation. These conditions include: oxygen deficiency, metabolic acidosis, high osmotic pressure, ionic imbalance, toxic effect of cellular enzymes and inflammatory mediators.
INFLAMMATORY MEDIATORS
Inflammatory mediators are soluble, diffusible molecules that act locally at the site of tissue damage and infection, and at more distant sites, and they determine the course and signs of inflammation. Inflammatory mediators may be cellular (histamine, prostaglandins, interleukine-1, tumor necrosis factor and interferons and others) or plasma in origin (complement, kinin, and clotting system factors). The major source of cellular mediators is leukocytes.
In acute inflammation vascular changes have the following order: inconstant and transient ischemia (several seconds), arterial hyperemia, venous hyperemia and stasis.