Cell injury: Necrosis and Gangrene

Morphology of irreversible cell injury

• Autolysis• Necrosis• Apoptosis

Autolysis

• “self digestion”• Disintegration of the cell by its own

hydrolytic enzymes liberated from lysosomes

• Rate of autolysis depends on the hydrolytic enzymes

• Morphology – homogenous and eosinophilic cytoplasm with loss of cellular details

Necrosis

• Localised area of cell death followed by degradation of the tissue by the hydrolytic enzymes

• ALWAYS accompanied by inflammatory reaction

Causes

• Hypoxia• Chemical agents• Physical agents• Microbial agents• Immunological agents• ..

Mechanisms

1. Denaturation of the intracellular proteins2. Enzymatic digestion of the cell

Morphology

Increased eosinophilia of the cytoplasm due to

Loss of normal basophilia imparted by RNA

Binding of eosin to the denatured proteins

Cytoplasmic vacuolation

Dystrophic calcification

Nuclear changesDue to nonspecific changes of the DNA

Basophilia of the chromatin fades

Reflects DNase activity

Nuclear shrinkage and increased basophilia

Due to condensation of DNA into mass

Pyknotic nucleus gets fragmented

Nuclei dissapears

KARYOLYSIS PYKNOSIS KARYORRHEXIS

Types of necrosis

• Mass of necrosis has several morphological patterns– Coagulative– Liquefaction– Caseous– Fat– Fibrinoid

Coagulative necrosis

• Most common type of necrosis• Sudden cessation of the blood flow is the

most common cause• Any organ or tissue can be involved,

however heart, kidney spleen are most commonly affected

• Gross – Early stage – firm,pale and swollen– Late- yellowish, softer and shrunken

• Micro :– “Tombstone”- outline of the cells are maintained– Cells are swollen and appear more eosinophilic and

with nuclear changes as described– Infiltration by inflammatory cells.

LIQUEFACTION NECROSIS(COLLIQUATIVE NECROSIS)

• Due to ischemic injury and due to bacterial or fungal infections

• Occurs due to degradation of the tissue by the action of powerful enzymes.

• Examples – Infarct brain– Abscess cavity

CASEOUS NECROSIS

• Found in the centre of foci of tuberculous infections

• It combines features of coagulative and liquefactive necrosis

• gross – soft, cheesy, granular and yellowish

• Micro – – Amorphous, eosinophlic granular debris

surrounded by a granulomatous reaction– The tissue architecture is completely

obliterated.

Fat necrosis

• It is descriptive of focal areas of fat destruction.

• Seen in acute pancreatitis• Typically occuring as a result of release of

pancreatic lipases into the substance of pancreas and the peritoneal cavity

• The enzymes liquefy the fat cell membranes and

• the lipases split the triglyceride esters contained in the fat cells.

• The released fatty acids combine with calcium to produce grossly visible chalky white areas– Fat saponification

Identify the lesion with the clues below!

Fibrinoid necrosis• Commonly occurs in small vessels• Insudation & Deposition of fibrin like material(plasma

proteins) in the vesel wall.• Mainly in immunologic injuries• Fibrin is the result of polymerization of a pre-existing

soluble plasma protein (fibrinogen)

• Micro – – brightly eosinophilic , hyaline like deposition in the

vessel wall– Necrotic foci is surrounded by nuclear debris

CONT’D