Necrosis is defined as a localised area of death of tissue followed by degradation of tissue by hydrolytic enzymes liberated from dead cells; it is invariably accompanied by inflammatory reaction.
Necrosis can be caused by various agents such as hypoxia, chemical and physical agents, microbial agents, immunological injury, etc.
Two essential changes characterise irreversible cell injury in necrosis of all types
i) Cell digestion by lytic enzymes.
ii) Denaturation of proteins |
Types of Necrosis
Morphologically, there are five types of necrosis
Coagulative,
Liquefaction (colliquative),
Caseous, Fat,
and Fibrinoid necrosis. |
COAGULATIVE NECROSIS.
- Most common type
- Caused by irreversible focal injury, mostly from sudden cessation of blood flow (ischaemia), and less often from bacterial and chemical agents.
- Commonly affected are the heart, kidney, and spleen.
Gross features |
Microscopic features |
- In the early stage are pale, firm, and slightly swollen.
- With progression, they become more yellowish, softer, and shrunken.
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- Hallmark of coagulative necrosis is the conversion of normal cells into their ‘tombstones’
- The necrosed cells are swollen and appear more eosinophilic than the normal,
- Eventually,the necrosed focus is infiltrated by inflammatory cells and the dead cells are phagocytosed leaving granular debris and fragments of cells
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LIQUEFACTION (COLLIQUATIVE) NECROSIS.
- Occurs commonly due to ischaemic injury and bacterial or fungal infections.
- It occurs due to degradation of tissue by the action of powerful hydrolytic enzymes.
- The common examples are infarct brain and abscess cavity.
Gross features |
Microscopic features |
- Affected area is soft with liquefied centre containing necrotic debris.
- A cyst wall is formed.
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- The cystic space contains necrotic cell debris and macrophages filled with phagocytosed material.
- The cyst wall is formed by proliferating capillaries, inflammatory cells, and gliosis (proliferating glial cells) in the case of brain and proliferating fibroblasts in the case of abscess cavity
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CASEOUS NECROSIS.
- Caseous necrosis is found in the centre of foci of tuberculous infections.
- It combines features of both coagulative and liquefactive necrosis.
Gross features |
Microscopic features |
- Resemble dry cheese and are soft, granular and yellowish.
- This appearance is partly attributed to the histotoxic effects of lipopolysaccharides present in the capsule of the tubercle bacilli, mycobacterium tuberculosis
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- The necrosed foci are structureless, eosinophilic, and contain granular debris
- The surrounding tissue shows characteristic granulomatous inflammatory reaction consisting of epithelioid cells with interspersed giant cells of langhans’ or foreign body type and peripheral mantle of lymphocytes.
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FAT NECROSIS.
- A special form of cell deathoccurring at two anatomically different locations but morphologically similar lesions.
- These are: following acute pancreatic necrosis, and traumatic fat necrosis commonly in breasts
- Fat necrosis hydrolyses neutral fat present in adipose cells into glycerol and free fatty acids.
- The damaged adipose cells assume cloudy appearance. The leaked out free fatty acids complex with calcium to form calcium soaps (saponification)
Gross features |
Microscopic features |
- Appears as yellowishwhite and firm deposits.
- Formation of calcium soaps imparts the necrosed foci firmer and chalky white appearance.
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- Cells have cloudy
- Appearance and are surrounded by an inflammatory reaction.
- Formation of calcium soaps is identified in the tissue sections as amorphous, granular and basophilic material
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FIBRINOID NECROSIS
Gross features |
Microscopic features |
- Characterised by deposition of fibrin-like material which has the staining properties of fibrin.
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- Fibrinoid necrosis is identified by brightly eosinophilic, hyaline-like deposition in the vessel wall.
- Necrotic focus is surrounded by nuclear debris of neutrophils (leucocytoclasis)
- Local haemorrhage may occur due to rupture of the blood vessel.
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