Cell Death (Necrosis

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Individual Cell Death
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Common event in some regenerating tissues: such as skin and gut epithelium and during embryogenesis Not a typical event in developed tissues such as brain becomes a serious occurrence when many cells are involved in such organs as the liver Programmed cell death: Apoptosis

What are the important factors on the outcome of injury on cells? Severity of injury and duration have a major effect on the outcome of injury

Etiology of Tissue Necrosis
1) Hypoxia 2) Physical injury a) Trauma b) Radiation ‑ U.V., Cosmic, X‑ray 3) Chemicals ‑ variable 4) Biological toxins ‑ endotoxins 5) Immunological reactions 6) Inborn genetic disorders 7) Nutritional

Mechanisms of Necrosis
Basic mechanisms: 1) Impaired oxidative phosphorylation 2) Membrane dissolution 3) Osmotic regulation

Major Signs of Necrosis Similar to Apoptosis
1) Nuclear degeneration ‑ Chromatin clumping ‑ Karyopyknosis (shrinking) ‑ Karyolysis (dissolution of chromatin) ‑ Karyorrhexis (fragmentation of chromatin) 2) Cytoplasmic changes

Types of Necrosis
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Liquefactive necrosis: Necrosis in brain, abscesses Coagulative necrosis: Necrosis of kidney, liver, or heart muscle Caseous necrosis: Infection with Mycobacterium tuberculosis Gangrene: Necrosis of an appendage, usually limbs Fat necrosis

Coagulative necrosis
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Caused by ischemia. Ischemia results in decreased ATP, increased cytosolic Ca++, and free radical formation, which each eventually cause membrane damage. Example: Infarct: localized area of ischemic necrosis as in myocardial infarct.

Liquefactive Necrosis
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Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes. The enzymes in the polys are released to fight the bacteria, but also dissolve the tissues nearby, causing an accumulation of pus, effectively liquefying the tissue (hence, the term liquefactive). Example: Abscess

Caseation Necrosis
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Caseous: A distinct form of coagulative necrosis seen in mycobacterial infections (e.g., tuberculosis), or in tumor necrosis, in which the coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris. Usually there is a giant cell and granulomatous reaction, sometimes with polys, making the appearance distinctive. Example: Tuberculosis.

Fat necrosis
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Fat Necrosis: A term for necrosis in fat, caused either by release of pancreatic enzymes from pancreas or gut (Enzymatic fat necrosis) or by trauma to fat, either by a physical blow or by surgery (Traumatic fat necrosis). The effect of the enzymes (lipases) is to release free fatty acids, which then can combine with calcium to produce detergents (soapy deposits in the tissues). Histologically, one sees shadowy outlines of fat cells (like coagulative necrosis), but with Ca++ deposits, foam cells, and a surrounding inflammatory reaction.

Consequences of Necrosis
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Healing vs. permanent damage Local vs. systemic effects. 1) Type of tissue

2) Size of lesion 3) Location of lesion

AUTOLYSIS
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Lysis of tissues by their own enzymes, following the death of the organism. Therefore, the key difference is that there is no vital reaction (i.e., no inflammation). Autolysis is essentially rotting of the tissue. Early autolysis is indistinguishable from early coagulative necrosis due to ischemia, unless the latter is focal.

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