Under a necrosis (also necrobiosis ) ( ancient Greek νέκρωσις nékrosis "killing", also "the death of individual limbs", to νεκρόω nekróō "I kill") is understood in biology and medicine the dying or death of single or multiple cells . The necrosis is pathological - that is, the process is pathological and is triggered by damaging influences on the cell: nutrient and oxygen deficiency, toxins, radioactivity and others. As a result, the cells in the tissue die and usually lead to an inflammatory reaction . Depending on the type of tissue and extent of damage, the necrosis heals completely through regrowth of surviving cells, or the dead tissue is replaced by a connective tissue scar (example: myocardium after a heart attack - with corresponding functional restrictions).
Necrosis is observed not only in humans and animals, but also in plants.
Forms of necrosis
This form of necrosis occurs when protein-rich tissues, such as muscles, die. A prime example is the heart muscles after a heart attack. First, the cells swell and become acidic. This leads to the precipitation and "coagulation" of the proteins and to increased eosinophilia of the cytoplasm. The histological tissue drawing becomes more indistinct and the cell nucleus dissolves in several steps: Initially, the nucleus shrinks ( pycnosis ) and then the nucleus breaks ( karyorrhexis ). Ultimately, the nucleus loses its chromatin and fades ( karyolysis ). Macroscopically (with the naked eye), the necrotic tissue appears clay-yellow and dry (after six hours at the earliest).
Inflammatory substances are released from the destroyed cells, so that granulocytes are attracted. These migrate into the tissue and, via the release of proteases, lead to the dissolution of the necrotic tissue. Cell and tissue residues are phagocytosed by macrophages . Macroscopically, there is a red border. However, the necrotic area loses its strength in the course of the process and can tear. For example, the heart wall can rupture after an extensive infarct. At the end there is the scarred healing of the tissue.
It is typical for tissues with a high percentage of fat and a low percentage of protein, for example in the brain with insufficient oxygen supply , or for tissues with a high percentage of proteases such as the pancreas . Chemical burns from the action of lye or abscess formation also lead to colliquation necrosis. The proteases of the body's own immune cells are decisive for abscesses. In contrast to coagulation necrosis, after initial cell swelling, the tissue liquefies ( colliquation ) and then an inflammatory reaction (except in the nervous system). Macroscopically, the tissue appears mushy, greasy and softened.
In tuberculosis , the peculiarities of the triggering bacteria cause a cheesy necrosis (also known as cheese formation ). Gangrene is a special form of necrosis that is black and looks like it has been burned. The gangrene is dry ( dry gangrene ), unless it is attacked by putrefactive bacteria and becomes inflamed ( wet gangrene ). When fat necrosis is the death of fat cells, for example, a calcified necrosis in the adipose tissue around the pancreas around. It arises traumatically or enzymatically as a result of lipases released from the pancreas in the context of pancreatitis . Other special forms are gummatous necrosis , which occurs in syphilis , and fibrinoid necrosis , which is typical of rheumatoid arthritis , polyarthritis nodosa or peptic gastric ulcers .
Under a Panzernekrose refers absterbendes tanks tissue in turtles , for example by wet or fungi.
So-called phosphorus necrosis occurred as an occupational disease among matchmakers in the 19th century .
In rare cases, necrosis occurs as an adverse drug reaction. Sub-therapeutic concentrations of antibiotics of the fluoroquinolone group can lead to necrosis of adult chondrocytes in healthy adult human cartilage . Histologically, necrosis has also been documented in connection with fluoroquinolone-related tendon and kidney damage. Necrosis of hepatocytes of the liver can with poisoning by paracetamol be associated. In 2011, about half of all acute liver failure cases in the US and UK were attributed to acetaminophen. Necroses are caused by reactive metabolites and the subsequent oxidative stress, the loss of the mitochondrial membrane potential and the loss of the ability of the mitochondria to synthesize ATP. Likewise, the broad spectrum anti-epileptic valproic acid can cause fatal liver dysfunction in which extensive confluent lytic necrosis of liver acini has been observed. Liver necrosis has also been documented with diclofenac , methyldopa , and halothane .
- Burn (medicine)
- Necrotizing fasciitis
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- Phosphorous necrosis
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