INFLAMMATION AS A FUNDAMENTAL PATHOLOGICAL PROCESS: LECTURE 1 (ALTERATION, VASCULAR REACTIONS)

Abstract

Inflammation is the most widespread pathological process in medical practice. Inflammation is the basis of the vast majority of diseases. In this connection, the topic is actual for any medical student, as well as a doctor of any specialty. Local signs of inflammation (redness, swelling, heat, pain, dysfunction) were described more than two thousand years ago. Like any typical pathological process, inflammation includes protective and damaging reactions. Their knowledge is very important for understanding the pathogenesis of inflammatory diseases. The first part of the lecture describes the causes and mechanisms leading to the development of inflammation, as well as the consequences of tissue damage (acidosis, hyperonkia, hyperosmia, synthesis and release of inflammatory mediators). Inflammatory mediators are biologically active substances those regulate all reactions in the focus of inflammation. Various cells (neutrophils, macrophages, lymphocytes, endothelial cells, hepatocytes, etc.) can be sources of mediators. By origin, mediators are divided into cell-derived (biogenic amines, derivatives of arachidonic acid, lysosomal enzymes and reactive oxygen species, cytokines) and plasma-derived (components of the complement system, kinins and the hemostasis system). There are pro-inflammatory mediators (they increase inflammatory response) and anti-inflammatory ones. Under the influence of inflammatory mediators, changes in microcirculatory blood flow begin (vasospasm, arterial hyperemia, venous congestion, stasis) and exudation develops. Exudation is caused by an increase in the permeability of microvessels, its mechanisms are different. The composition of the exudate is determined by the cause of the inflammation and degree of tissue damage, the spectrum and amount of chemoattractants influence the type of exudate as well. The main types of exudates are serous, purulent, fibrinous, hemorrhagic, ichorous, catarrhal.