General characteristics of systemic inflammation as a typical pathological process. Inflammation is a universal and common type of pathological the process underlying most of the known human diseases. The essence of inflammation is the body's reaction to local damage, which is aimed at isolating and eliminating the damaging factor, and then tissue regeneration. The reaction develops mainly locally – in the focus of inflammation. The main functional role in the focus of inflammation is played by inflammatory infiltrate cells – various types of leukocytes and mobile macrophages. In turn, the reaction of microvessels, the hemostasis system, mastocytes and many other types of stromal cells ensures the migration of effector cells to the focus of inflammation, as well as the localization of damaging agents. The type of inflammatory process – exudative-destructive inflammation (purulent) or various variants of productive inflammation, as well as the final effectiveness of the inflammatory process as a whole depends on the composition of the inflammatory infiltrate cells and the nature of their relationship. The implementation of effector mechanisms in the focus of inflammation cannot be carried out without "resource support" from the whole organism. This task is mainly solved by a systemic inflammatory reaction, which includes a number of interrelated processes: stress response of the neuroendocrine system, primarily the hypothalamic-pituitary-adrenal complex; generalized manifestations of the immune response, acute phase response of the liver, increased leukocytopoiesis in the bone marrow. The main initiating mechanism for the development of a systemic inflammatory reaction is the entry of individual cytokines and some other inflammatory mediators into the systemic bloodstream from the focus of inflammation. The need for it does not arise with any, but only with a pronounced inflammatory process, with a high level of expenditure of metabolic and cellular resources. Manifestations of a systemic inflammatory reaction are diverse: fever, neuromuscular asthenia, an increase in blood glucose and other energy substrates, leukocytosis, an increase in acute phase proteins in the blood and other adaptive changes in homeostasis. Thus, the systemic inflammatory reaction has both common and different manifestations from other stress variants at the level of the whole organism. In general, the inflammatory process includes two complementary genetically determined programs in relation to the focus of inflammation: "internal" – at the local level and "external" – systemic inflammatory response. Like any other protective mechanism for the body, individual manifestations of inflammation can in certain cases have negative consequences, which, however, does not negate the expediency of inflammation as a protective process for the body as a whole. Knowledge of the general patterns of the inflammatory process allows us to understand the pathogenesis of a wide range of inflammatory diseases. Meanwhile, there are pathological processes directly related to the involvement of "inflammatory" mechanisms, the pathogenesis of which is difficult to describe, and in some cases impossible from the standpoint of traditional (classical) ideas about inflammation. This applies, first of all, to the most life–threatening forms of pathology - shock states, acute manifestations of multiple organ failure, the development of disseminated intravascular coagulation syndrome and some other critical human conditions. Very often, the role of the focus of inflammation in these conditions is insignificant, and in some cases it (the focus) is completely absent. Practitioners were the first to note the connection between the development of critical conditions in humans with "inflammatory" mechanisms in sepsis, and then non-infectious processes. At the same time, two out of four possible criteria are sufficient to verify a systemic inflammatory reaction. The use of criteria for systemic inflammatory response in clinical practice allowed us to identify a risk group for severe complications. "Inflammatory" mechanisms, which are characterized by signs of a systemic inflammatory reaction, are generally adaptive in nature and cannot directly determine the pathogenesis, for example, of a shock state. All this predetermined the need to describe the model of systemic inflammation as an independent typical pathological process, related, but not identical to classical inflammation, which requires the separation of the designated two alternative typical pathological processes. To this end, we will pay attention to the origins of the inflammatory reaction. Any cell is capable of responding to the effects of a damaging factor, this response can be referred to as cellular stress. Meanwhile, the damaging factors themselves are heterogeneous. Firstly, these are various micro defects of cellular structures and changes in vital environmental parameters, such as hypoxia, disturbances of acid-base balance and temperature regime; parasitization by viruses and other intracellular organisms. All these factors are capable of damaging the cell directly and are damaging agents by definition. Secondly, it is the effect on the cell, or rather on cellular receptors, of molecules carrying information about the possibility of damage. These molecules "warn" the cell about the presence of microorganisms or other factors that pose a potential danger.
So, the development of inflammatory reactivity can be considered from the perspective of cellular stress, which solves two main tasks
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