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Necrosis can be activated by components of the immune system, such as the complement system; bacterial toxins; activated natural killer cells; and peritoneal macrophages. [1] Pathogen-induced necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation. [1]
Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass. [1] Often it is associated with focal bacterial or fungal infections, and can also manifest as one of the symptoms of an internal chemical burn . [ 2 ]
Acute inflammation of the lung (usually in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings. [15] Heat and redness are due to increased blood flow at body core temperature to the inflamed site. Swelling is caused by accumulation of fluid.
Fat necrosis may result from various injuries to adipose tissue, including: physical trauma, enzymatic digestion of adipocytes by lipases, [3] radiation therapy, [4] hypoxia, or inflammation of subcutaneous fat (panniculitis). The gross appearance of fat necrosis is as an irregular, chalky white area within otherwise normal adipose tissue. [1]
The lack of oxygen (hypoxia) causes cell death in a localized area which is perfused by blood vessels failing to deliver primarily oxygen, but also other important nutrients. While ischemia in most tissues of the body will cause coagulative necrosis, in the central nervous system ischemia causes liquefactive necrosis , as there is very little ...
Necrosis is indeed an unregulated form of cell death, unlike apoptosis, which is a more controlled, programmed process. When tissues undergo necrosis, they swell, rupture, and release their contents, which can trigger inflammation and further tissue damage. When a large area of tissue is affected by necrosis, it can lead to gangrene.
Histologically, early TEN shows scattered necrotic keratinocytes. In more advanced TEN, full thickness epidermal necrosis is visualized, with a subepidermal split, and scant inflammatory infiltrate in the papillary dermis. Epidermal necrosis found on histology is a sensitive but nonspecific finding for TEN. [7]
Fibrinoid necrosis is a pathological lesion that affects blood vessels, and is characterized by the occurrence of endothelial damage, followed by leakage of plasma proteins, including fibrinogen, from the vessel lumen; these proteins infiltrate and deposit within the vessel walls, where fibrin polymerization subsequently ensues.