inflammation(redirected from diphtheritic inflammation)
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a complex defense reaction of the body for dealing with harmful agents developed in the course of evolution and manifested by various vascular and tissue changes. Inflammation is one of the processes underlying many diseases with different clinical symptoms. The biological role of inflammation is to limit the spread of pathogenic agents in the body; sometimes the inflammatory process helps to destroy them. Intensive study of the mechanisms of inflammation began after R. Virchow advanced his theory of cellular pathology. According to this theory, inflammation is a local tissue reaction morphologically manifesting itself in protein dystrophy of cells. The German scientist J. Konheim regarded disturbances in the flow of blood and lymph in the inflammatory focus as the primary factor in inflammation. The Russian biologist E. Metchnikoff developed a fundamentally new approach to the analysis of inflammation with his general biological theory (1892) based on the results of a comparative pathological study of the process. Metchnikoff demonstrated the decisive significance of evolutionary characteristics and perfection of the organism in the development of inflammation. He also described phagocytosis as an inseparable part of the inflammatory process and scientifically substantiated the relationship between a focus of inflammation and the body as a whole.
The causes of inflammation may be either exogenous (external), such as bacteria and their toxins, mechanical injury, effects of radiation or electrical energy, and chemical substances, or endogenous (arising within the organism itself), including products of tissue necrosis and decomposition, thrombi, infarcts, hematomas, and deposits of salts. Depending on the course, inflammation may be acute, subacute, or chronic. An acute inflammation of the skin, such as an abscess or burn, is manifested by redness, swelling, elevated temperature in the area of inflammation, soreness, and functional impairment of the affected organs and tissues. Not all of the above symptoms are present in chronic inflammation or in inflammation of the internal organs.
Inflammation consists of a vascular reaction, alteration, and proliferation. The vascular reaction is manifested first by a transient vascular spasm in the inflammatory focus followed by dilation of the arterioles and capillaries, which undergo an intensified filling with blood (arterial hyperemia). The external signs are elevated temperature in the focus, redness, and pulsation. These vascular changes are due to an accumulation in the inflammatory focus of substances that affect the tone of the vascular wall, such as acetylcholine, histamine, and adenine nucleotides. The next phase of the vascular changes involves dilation of the venous network and slowing of the blood flow. Because of an increased permeability of the vascular walls, plasma (the liquid part of the blood) and leukocytes (exudation) emerge into the surrounding tissues. The causative agent of the inflammation greatly affects the nature of the exudative process and composition of the exudate (inflammatory effusion). The exudate can be serous (from serum), fibrinous (with an increased amount of protein), leukocytic (with many leukocytes), purulent, or hemorrhagic (with many erythrocytes). The exudate causes the swelling of tissues in the focus of inflammation. It can accumulate in cavities, for example, in pleuritis. Pain is caused by compression of the edema and by irritation of the nerve endings in the inflammatory focus by the metabolic products. During the vascular changes the leukocytes approach the vascular wall (phenomenon of margination of leukocytes), after which they emerge from the vascular stream (diapedesis) and migrate to the focus of inflammation. Here they carry out phagocytosis. The migration of leukocytes to the focus is caused by chemotaxis (drawing of leukocytes from the blood by chemical agents accumulating in the inflammatory focus), by the appearance in the inflammatory focus of substances capable of decreasing the surface tension of leukocytes and of substances that convert leukocyte protoplasm from a sol to a gel, and by electrokinetic factors.
Circulatory disturbances in a focus of inflammation are accompanied by the development of thrombi and protein coagula (protein flakes) in the blood vessels and lymphatics, by the filling of their lumens with various cellular elements that enter the exudate in profusion, and by increased vascular tone and compression of the small vessels by edema. These processes eventually block the efferent blood vessels and lymphatics, thus making it difficult for bacteria and the toxic products formed by tissue breakdown to become absorbed and enter the bloodstream; that is, the focus of inflammation is separated from healthy tissue. The presence of a greater or lesser admixture of multiplying mesenchymal cells stimulates the subsequent regenerative processes in the injured tissues.
Alteration (lesion) of tissues in inflammation is reflected in structural and functional changes in the injured tissue. The tissue changes range from dystrophy (protein, fatty, and hyaline) to necrosis (death) of tissues, and they are the result of nutritional and metabolic disorders. All the metabolic processes (the “fire of metabolism”) are sharply intensified and qualitatively changed in a focus of inflammation. Glucose is excessively consumed in inflamed tissue at a time when the oxygen is relatively inadequate. Moreover, the respiratory coefficient decreases and anaerobic glycolysis intensifies. The accumulation of lactic acid and other incompletely oxidized metabolic products produces acidosis, fatty acids increase, and the content of ketone bodies increases in blood flowing from the focus. In the inflamed tissue protein decomposition also intensifies. The metabolic disturbances give rise to increased osmotic and oncotic pressure in the focus.
Proliferation (multiplication of cellular elements) takes place on the periphery of a focus of inflammation against a background of exudation and alteration processes, and it is most pronounced in the final stages of the process. Proliferation is followed by gradual regeneration (repair of tissues), which completes the inflammatory process. Inflammation may be exudative, alterative, or proliferative, depending on the particular component that is dominant. Inflammation always results in the death of tissues. The outcome of the inflammation depends on the condition of the body, the form of inflammation, and the size of the focus. Inflammation may be normergic (characteristic of a healthy body) or hyperergic, when the body is sensitized. The latter form is characterized by intensive alteration, for example, Pirquet’s reaction. Hypoergic inflammation occurs in the presence of immunity to the factor that caused the inflammation and when the body is exhausted. Development of the inflammatory process is also largely a function of age, nutrition, and metabolism. The nervous and endocrine systems play a major role in the development of inflammation. Excitation of the sympathetic nervous system decreases the inflammatory phenomena, while excitation of the parasympathetic nervous system intensifies them. Hormones also influence the course of inflammation in different ways. Thus, the adenocorticotropic hormone (ACTH) of the hypophysis and the glucocorticoids of the suprarenal gland inhibit the development of inflammation while the mineralocorticoids of the suprarenal gland activate it. Dysfunction of the pancreas (diabetes mellitus) causes a predisposition to stubborn pyoderma. Inflammation is severe with increased thyroid function (hyperthyroidism). Small thrombi and dead tissues are resorbed in the final stage of inflammation (enzymic splitting, phagocytosis). The large defects formed in the tissues as a result of fibrinous-necrotic inflammation are replaced by scar tissue, which impairs the function of organs (for example, cirrhosis of the liver after hepatitis) and deforms them (for example, deformity of the heart valves after endocarditis). Inflammation of the tubular organs (esophagus, uterine tubes, intestines) may result in their becoming constricted and their lumens closing completely (obliteration). When the exudate is resorbed from the body cavities (abdominal, pleural, and others), the fibrin remaining on the surface of the serous membranes forms adhesions.
Inflammation may provoke a greater or lesser reaction throughout the body, depending on where it originates and on the size of the focus. The body mobilizes its defensive forces and creates antibodies. Moreover, symptoms of intoxication (poisoning) may appear when the products of the vital activity of the causative agents and the products of tissue decomposition are resorbed. They include chiefly fever, an increased number of leukocytes in the peripheral blood (leukocytosis), and an accelerated erythrocyte sedimentation rate (ESR). When the bacteria are carried to parts of the body remote from the focus of inflammation, metastatic inflammatory foci may arise.
REFERENCESAl’pern, D. E. Vospalenie (Voprosy patologii). Moscow, 1959.
Metchnikoff, E. Lektsii o sravnitel’noi patologii vospaleniia. Moscow, 1947.
Menkin, V. Dynamics of Inflammation. New York, 1940.
V. A. FROLOV