1. Necrosis is the localized death of cells and living tissue. It is caused by factors like hypoxia, chemicals, microbes, or immune reactions. There are two key changes in necrosis - irreversible cell injury and digestion of cells by lytic enzymes. 2. There are five main types of necrosis defined by their etiology and appearance: coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis is the most common type seen as pale, swollen areas that become yellow and shrunken over time. Liquefactive necrosis results in a soft, liquefied center containing debris. Caseous necrosis forms a cheese-like focus found in tuberculosis. Fat necrosis

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3. NECROSIS
 localised area of death of tissue
 degradation of tissue by hydrolytic enzymes
liberated from dead cells
 invariably accompanied by inflammatory reaction.
Causes :
 various agents such as hypoxia
 chemical and physical agents
 microbial agents
 Immunological injury, etc.
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4. CHARACTERISE
 2 Essential change characterize
 Irreversible cell injury in necrosis of all types
 1.cell digestion – Lytic enzymes
 2.Denaturation -Proteins
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6. TYPES OF NECROSIS
 Based on etiology and morphologic appearance
 5 types of necrosis
 Coagulative
 Liquefaction
 Caseous
 Fat &
 fibrinoid necrosis.
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7. 1.COAGULATIVE NECROSIS
 most common type of necrosis
 caused by irreversible focal injury
 Mostly from sudden cessation of blood flow -
(ischaemic necrosis)
 less often from bacterial and chemical agents
Grossly
 Early stage - pale, firm, slightly swollen - infarct.
(tissue death due to inadequate blood supply)
 With progression, the affected -more yellowish,
softer, and shrunken
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8. COAGULATIVE NECROSIS
Microscopically
 hallmark - conversion of normal cells into their ‘tomb stones’
 (outlines of the cells are retained and the cell type can still be
recognized but their cytoplasmic and nuclear details are lost. )
 necrosed cells are swollen , more eosinophilic cytoplasm than
the normal.
 nuclear changes of pyknosis, karyorrhexis and karyolysis
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9. COAGULATIVE NECROSIS
 Infiltrated by inflammatory cells
 the dead cells are phagocytosed leaving granular debris
and fragments of cells
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11. 2.LIQUEFACTIVE NECROSIS
 commonly due to ischemic injury
 bacterial or fungal infections
 But hydrolytic enzymes in tissue degradation have a
dominant role in causing semi-fluid material.
 common examples - infarct (tissue death )brain and
abscess cavity
Grossly
 affected area -soft with liquefied center containing necrotic
debris.
 Later - cyst wall is formed
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12. LIQUEFACTIVE NECROSIS
Microscopically
 the cystic space contains necrotic cell debris &
macrophages filled with phagocytosed material.
 cyst wall -proliferating capillaries,
inflammatory cells, and gliosis - case of brain
 proliferating fibroblasts( that synthesizes the extracellular
matrix & collagen) - case of abscess cavity
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14. 3.CASEOUS NECROSIS –CHEESE LIKE
 necrosis is found in the centre of foci of tuberculous
infections.
 combines features of both coagulative and
liquefactive necrosis.
Grossly
 resemble dry cheese and are soft, granular and
yellowish.
 present in the capsule of the tubercle bacilli,
Mycobacterium tuberculosis.
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15. CASEOUS NECROSIS –CHEESE LIKE
Microscopically
 centre of the necrosed focus contain structureless
 eosinophilic material having scattered granular
debris of disintegrated nuclei.
 surrounding tissue shows characteristic
granulomatous inflammatory reaction consisting of
epithelioid cells
 (modified macro phages having slipper-shaped
vesicular nuclei),
interspersed giant cells of Langhans’
 foreign body type
 peripheral mantle of lymphocytes
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18. CASEOUS NECROSIS –CHEESE LIKE
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19. 4.FAT NECROSIS
 special form of cell death occurring at mainly fat-
rich anatomic locations in the body.
 examples are: traumatic fat necrosis of the breast,
 especially in heavy and pendulous breasts,
 mesenteric ( wrapping around the circumference of
the intestine – creeping fat )fat necrosis due to
acute pancreatitis.
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20. FAT NECROSIS
 Acute pancreatitis -there is liberation of
pancreatic lipases from injured or inflamed tissue
 results in necrosis of the pancreas as well as of the
fat depots throughout the peritoneal cavity
 sometimes, even affecting the extraabdominal
adipose tissue.
 fat necrosis - there is hydrolysis and rupture of
adipocytes
 causing release of neutral fat which changes into
glycerol and free fatty acids.
 leaked out free fatty acids complex with calcium to
form calcium soaps (saponification) 20

21. FAT NECROSIS
 Grossly - appears as yellowish-white and firm
deposits.
 Formation of calcium soaps imparts the necrosed
foci firmer
 chalky white appearance.
 Microscopically -the necrosed fat cells have cloudy
appearance
 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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23. FAT NECROSIS
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24. 5.FIBRINOID NECROSIS
 characterised by deposition of fibrin-like material
 staining properties of fibrin such phosphotungistic acid
haematoxylin (PTAH) stain.
 examples - peptic ulcer etc
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25. 5.FIBRINOID NECROSIS
Microscopically
 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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