Necrosis

From Wikipedia, the free encyclopedia

Part of a series on
Toxicology and poison
Toxicology (Forensic) - Toxinology
History of poison
(ICD-10 T36-T65, ICD-9 960-989)
Concepts
Poison - Venom - Toxicant - Antidote
Acceptable daily intake - Acute toxicity
Bioaccumulation - Biomagnification
Fixed Dose Procedure - LD50 - Lethal dose
Toxic capacity - Toxicity Class
Toxins and venoms
Neurotoxin - Necrotoxin - Hemotoxin
Mycotoxin - Aflatoxin - Phototoxin
List of fictional toxins
Incidents
Bradford - Minamata - Niigata
Alexander Litvinenko - Bhopal
2007 pet food recalls
List of poisonings
Poisoning types
Elements
Toxic metal (Lead - Mercury - Cadmium - Antimony - Arsenic - Beryllium - Iron - Thallium) - Fluoride - Oxygen
Seafood
Shellfish (Paralytic - Diarrheal - Neurologic
Amnesic)
- Ciguatera - Scombroid
Tetrodotoxin
Other substances
Pesticide - Organophosphate - Food
Nicotine - Theobromine - Carbon monoxide - Vitamin - Medicines
Living organisms
Mushrooms - Plants - Animals
Related topics
Hazard symbol - Carcinogen
Mutagen - List of Extremely Hazardous Substances - Biological warfare
This box: view  talk  edit

Necrosis (in Greek Νεκρός = Dead) is the name given to accidental death of cells and living tissue. It begins with cell swelling, chromatin digestion, and disruption of the plasma membrane and organelle membranes. Late necrosis is characterized by extensive DNA hydrolysis, vacuolation of the endoplasmic reticulum, organelle breakdown, and cell lysis. The release of intracellular content after plasma membrane rupture is the cause of inflammation in necrosis.

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.

Contents

[edit] 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 (eg 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.

Severe tissue necrosis following Bothrops asper envenomation. The victim was an 11-year old boy, bitten two weeks earlier in Ecuador, but treated only with antibiotics.
Severe tissue necrosis following Bothrops asper envenomation. The victim was an 11-year old boy, bitten two weeks earlier in Ecuador, but treated only with antibiotics.[1]

[edit] Morphologic patterns

There are seven distinctive morphologic patterns of necrosis:

[edit] Arachnogenic necrosis

Spider bites are cited as causing necrosis in some areas. These claims are widely disputed. In the US at least, only the bites of spiders in the genus Loxosceles or brown recluse have been proven to consistently cause necrosis.[2] Many other spider species are claimed to cause necrosis but in most cases firm evidence is lacking. Partially this is because the early bite is often painless and the spider species cannot be identified.

Several species of spiders possess toxins proven to cause necrosis:

Spiders suspected of, but not shown to cause necrosis:

[edit] See also

[edit] Footnotes

  1. ^ Norris R. 2004. Venom Poisoning in North American Reptiles. In Campbell JA, Lamar WW. 2004. The Venomous Reptiles of the Western Hemisphere. Comstock Publishing Associates, Ithaca and London. 870 pp. 1500 plates. ISBN 0-8014-4141-2.
  2. ^ Atkins J, Wingo C, Sodeman W (1957). "Probable cause of necrotic spider bite in the Midwest". Science 126 (3263): 73. doi:10.1126/science.126.3263.73. PMID 13442644. 
  3. ^ Isbister G, Gray M (2003). "White-tail spider bite: a prospective study of 130 definite bites by Lampona species.". Med J Aust 179 (4): 199-202. PMID 12914510. 
  4. ^ Vetter R, Isbister G (2004). "Do hobo spider bites cause dermonecrotic injuries?". Ann Emerg Med 44 (6): 605-7. doi:10.1016/j.annemergmed.2004.03.016. PMID 15573036. 
  5. ^ Vetter R, Isbister G, Bush S, Boutin L (2006). "Verified bites by yellow sac spiders (genus Cheiracanthium) in the United States and Australia: where is the necrosis?". Am J Trop Med Hyg 74 (6): 1043-8. PMID 16760517.