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Necrosis
Definition:
Causes:
Development of Necrosis(2 mechanisms)
irreversible damage to mitochondria(failure of ATP generation)
↓anaerobic respiration
↓lactic acid accumulation
↓↓ pH in intracellalar matrix (↑
acidity)↓
activation of lysosomal enzymes↓
proteolytic digestion of cell↓
dead tissue cleaned away
damage to cell membrane↓
loss of phospholipids & damage due to lipid breakdown material
↓cytoskeleton detached from cell
membrane↓
injury allows enzymes to escape into ECF↓
Influx of Ca2+ ions↓
Ca2+ causes permanent damage to mitochondria, inhibits cellular
enzyme action & denatures protein↓
characteristic cell changes(coagulative necrosis)
Cytoplasmic changes
1- Increased eosinophilia:
• Increased binding of eosin to the denatured protein
• Loss of basophilia of RNA
2- Glassy homogenous appearance: due to loss of glycogen particles.
3- Vacuolated cytoplasm: due to enzymatic degradation of the organelles.
Nuclear changes• Pyknosis – shrinking & condensation• Karyorrhexis – rupture of nuclear membrane• Karyolysis – basophilia gradually fades
Types of Necrosis
• Coagulative necrosis (Ischaemia Infarction)
• Colliquative necrosis (Liquefactive necrosis)
• Caseous necrosis• Fat necrosis
- Enzymatic fat necrosis- Traumatic fat necrosis
• Gangrenous necrosis (putrefactive infection)
• Coagulative necrosis
• Many nuclei have become pyknotic (shrunken and dark) and have then undergone karorrhexis (fragmentation) and karyolysis (dissolution). The cytoplasm and cell borders are not recognizable.
• Here is myocardium in which the cells are dying. The nuclei of the myocardial fibers are being lost. The cytoplasm is losing its structure, because no well-defined cross-striations are seen.
Liquefactive necrosis
• The necrotic tissue is rapidly liquefied.
• It occurs in:
1- Infarctions of the brain: due to high lipid and fluid content.
2- Pyogenic abscess: due to proteolytic enzymes released by pus cells
3- Amoebic abscess: due to liquefactive enzymes released by the parasite
Fat NecrosisEnzymatic Fat Necrosis Traumatic Fat Necrosis
acute pancreatitis
↓enzymes escape into surrounding
tissue↓
lipases hydrolyse true fat into glycerol & fatty acids
↓fatty acids saponify or form soaps (white opaque masses or plaques)
↓diagnostic of acute pancreatitis
↓calcification may occur later
rupture of cell membrane↓
release natural fat into tissues↓
phagocytosed by macrophages↓
foamy appearance↓
chronic inflammatory reaction↓
fibrosis & scarring(no enzymatic fat breakdown)
Acute pancreatitis
Fat necrosis
• Caseation necrosis
• Distinctive type of necrosis in which there is coagulative necrosis with slow liquefaction
• Caseation necrosis
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