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In contrast to apoptosis, cleanup of cell debris by phagocytes of the immune system is generally more difficult, as the disorderly death generally does not send cell signals which tell nearby phagocytes to engulf the dying cell. This lack of signaling makes it harder for the immune system to locate and recycle dead cells which have died through necrosis than if the cell had undergone apoptosis.
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In contrast to apoptosis, cleanup of cell debris by phagocytes of the immune system is generally more difficult, as the disorderly death generally does not send cell signals which tell nearby phagocytes to engulf the dying cell. This lack of signaling makes it harder for the immune system to locate and recycle dead cells which have died through necrosis than if the cell had undergone apoptosis.
Causes
There are many causes of necrosis including prolonged exposure to injury, infection, cancer, infarction, poisons, and inflammation. Severe damage to one essential system in the cell leads to secondary damage to other systems, a so-called "cascade of effects." Necrosis can arise from lack of proper care to a wound site. Necrosis is accompanied by the release of special enzymes, that are stored by lysosomes, which are capable of digesting cell components or the entire cell itself. The injuries received by the cell may compromise the lysosome membrane, or may initiate a disorganised chain reaction which causes the release in enzymes. Unlike apoptosis, cells that die by necrosis may release harmful chemicals that damage other cells. In biopsy, necrosis is halted by fixation or freezing. Many species of viper (e.g. rattlesnakes or Bothrops) produce venom which causes severe necrosis in snake-bite victims. Additionally, some spiders (eg the brown recluse) contain venom which may cause significant cutaneous injuries with tissue loss and necrosis.
Morphologic patterns
There are seven distinctive morphologic patterns of necrosis:
- Coagulative necrosis is typically seen in hypoxic environments (e.g. myocardial infarction, infarct of the spleen). Cell outlines remain after cell death and can be observed by light microscopy.
- Liquefactive necrosis is usually associated with cellular destruction and pus formation (e.g. pneumonia). This is typical of bacterial or, sometimes, fungal infections because of their ability to stimulate an inflammatory reaction. Curiously, ischemia (restriction of blood supply) in the brain produces liquefactive rather than coagulative necrosis, this is due to the lack of any substantial supportive stroma.
- Gummatous necrosis is restricted to necrosis involving spirochaetal infections (e.g. syphilis).
- Haemorrhagic necrosis is due to blockage of the venous drainage of an organ or tissue (e.g. in testicular torsion).
- Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e.g. tuberculosis), fungi, and some foreign substances. It can be considered a combination of coagulative and liquefactive necroses.
- Fatty necrosis results from the action of lipases on fatty tissues (e.g. acute pancreatitis, breast tissue necrosis).
- Fibrinoid necrosis is caused by immune-mediated vascular damage. It is marked by deposition of fibrin-like proteinaceous material in arterial walls, which appears smudgy and eosinophilic on light microscopy.
























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