69. Hemorrhagic inflammation: definition, causes, mechanisms. Pathological anatomical characteristics, complications, outcomes, clinical significance.

Hemorrhagic inflammation occurs if red blood cells are mixed with the exudate. In its development, not only the sharply increased permeability of microvessels, but also the negative chemotaxis of neutrophils, plays a great role. Hemorrhagic inflammation occurs in severe infectious diseases — anthrax, plague, flu, etc. Sometimes there are so many red blood cells that the exudate resembles a hemorrhage (for example, with anthrax meningoencephalitis). Hemorrhagic inflammation often joins other types of exudative inflammation.

The outcome of hemorrhagic inflammation depends on the cause that caused it. Catarrhal inflammation

70. Proliferative inflammation: definition, types, causes, mechanisms of development. Pathological anatomical characteristics, complications, outcomes, clinical significance.

Proliferative (productive) inflammation occurs in any organ and tissue. It is characterized by a predominance of proliferation of cellular and tissue elements. Alteration and exudation fade into the background. As a result of cell proliferation, focal or diffuse cellular infiltrates are formed. They can be polymorphic-cellular, lymphocytic-monocytic, macrophage, plasma cell, epithelioid cell, giant cell.

The causes of productive inflammation vary. It is caused by biological (microorganisms, animal parasites), physical (radiation) and chemical (medicines) factors or occurs as a manifestation of immunopathological processes (immune inflammation).

The course of productive inflammation can be acute, but more often chronic. The acute course of productive inflammation is characteristic of a number of infectious diseases (typhoid and typhoid fever, tularemia, acute rheumatism, acute glomerulitis), the chronic course is for most inter—daily productive processes in the myocardium, kidneys, liver, muscles, which end in sclerosis.

The importance of productive inflammation is very high. It is observed in many diseases, with a prolonged course it leads to sclerosis and cirrhosis of organs, which means that their functional insufficiency. Acute productive inflammation

Types of acute proliferative inflammation: interstitial (interstitial), granulomatous, inflammation around animal parasites and foreign bodies. The inflammatory hyperplastic growths sometimes mentioned — polyps and genital warts — are essentially a hyperregenerative reaction of the epithelium to chronic exudative (catarrhal or purulent) inflammation.

Interstitial inflammation is caused by various infectious agents or it is possible as a reaction of the body to pronounced toxic effects or microbial intoxication. It occurs in all parenchymal organs and is localized in their stroma, where inflammatory and immunocompetent cells accumulate. The infiltrate consists of histiocytes, monocytes, lymphocytes, plasma cells, labrocytes, single neutrophils, eosinophils. The features of this inflammation in the acute phase are a significant number of mononuclears (monocytes) in the infiltrate and dystrophic and necrobiotic changes in the parenchymal elements of the organ, since the functions of blood and lymphatic vessels and nerve endings passing through the stroma are impaired. At the same time, the organ does not change much externally. The progression of interstitial inflammation leads to the development of mature fibrous connective tissue — sclerosis. Granulomatous inflammation is characterized by the formation of granulomas (nodules) as a result of proliferation and transformation of cells capable of phagocytosis. Granulomatous inflammation as an independent form of inflammatory reaction occurs mainly in the chronic course of inflammation. However, it can also occur acutely, as a rule, in acute infectious diseases: typhoid fever, typhoid fever, rabies, epidemic encephalitis, acute anterior polio. In typhoid fever, granulomas occur in the lymphoid formations of the small intestine and are clusters of phagocytes transformed from reticular cells — "typhoid cells". Upon recovery, acute granulomas disappear either without a trace, as in typhoid fever, or leave glial scars, as in neuroinfections. In this case, the outcome of the disease depends on the location and volume of these scars. Productive inflammation around animal parasites and foreign bodies

It is aimed at separating them from the surrounding tissues by a connective tissue capsule, since they cannot be phagocytized and eliminated. Granulation tissue and infiltration from fibroblasts, macrophages and giant cells of foreign bodies are formed around foreign bodies (shell fragments, etc.). The outcome of productive inflammation varies depending on its type, the nature of the course and the structural and functional characteristics of the organ and tissue. Acute productive inflammation often ends with the formation of a scar in the area of inflammation.