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