Cell injury: Necrosis and Gangrene
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Transcript of 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