Cell Injury:

Cell Injury:

Necrosis:
◼ “Necrosis refers to a spectrum of
morphologic changes that follow cell death
in living tissue, largely resulting from
progressive degradative action of enzymes
on the lethally injured cells”.
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Why Inflammation around it???

◼ Necrotic cells are unable to maintain the
membrane integrity and their contents
often leak out. This will elicit inflammation
in the surrounding tissue.
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Pathogenesis:
◼ Autolysis: Due to enzymatic digestion of
the cell and denaturation of intracellular
proteins.
◼ Enzymes: released from lysosome of dead
cells themselves or from immigrant
leukocytes of inflammation.
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Morphology:
◼ Increased Eosinophilia: attributable to loss
of normal basophilia imparted by RNA in
the cytoplasm.
◼ More glassy homogeneous appearance.
◼ Cytoplasmic vacuolation: due to digestion
of cytoplasmic organelles –moth eaten
appearance.
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Morphology: ……
◼ Nuclear changes: 3 forms--
1. Pyknosis: Nuclear shrinkage and
increased basophilia
2. Karyorrhexis: Fragmentation of the
pyknotic nucleus.
3. Karyolysis: Dissolution of the nucleus
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Types of Necrosis:

1. Coagulative Necrosis
2. Liquefactive Necrosis
3. Caseous Necrosis
4. Enzymatic Fat Necrosis
5. Fibrinoid Necrosis
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1. Coagulative Necrosis:
◼ Implies preservation of basic outline of the
coagulated cell at least for some days.
◼ Example: Myocardial infarction—
acidophilic, coagulated, anucleate cells
persisting for few weeks.
◼ Ultimately it is removed by phagocytosis
by scavenger leukocytes.
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COAGULATIVE
NECROSIS -KIDNY
Cell Injury:

COAGULATIVE
NECROSIS -SPLEEN
Cell Injury:

Normal Myocardium Ischemic Myocardium

Cell Injury:
COAGULATIVE
NECROSIS -KIDNY
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INFARCTION CAUSING COAGULATIVE NECROSIS: ADRENAL CORTEX

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2. Liquefactive Necrosis:
◼ MC hypoxic death in CNS.
◼ Transformation of tissue into a liquid
viscous mass.
◼ Seen in fungal/ bacterial infections also.
◼ Pus: creamy yellow material containing
dead white cells.
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LIQUEFACTIVE NECROSIS—BRAIN
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LIQUEFACTIVE NECROSIS—BRAIN
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LIQUEFACTIVE NECROSIS—BRAIN
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LIQUEFACTIVE NECROSIS—BRAIN
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LIQUEFACTIVE NECROSIS—KIDNEY
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3. Caseous Necrosis:
◼ Most often seen in TUBERCULOSIS.
◼ Cheesy white- gross appearance of the
area of necrosis.
◼ Amorphous, granular debris enclosed
within a distinctive inflammatory border
known as Granulomatous inflammation.
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CASEOUS NECROSIS
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4. Fat Necrosis:
◼ Due to release of activated pancreatic
lipases—into pancreatic substances and
peritoneal cavity–destroying the fat.
◼ MC seen in acute pancreatits.
◼ Lipases split triglycerides into fatty acids
that combine with calcium to produce
grossly visible chalky white areas- FAT
SAPONIFICATION.
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FAT NECROSIS --PANCREAS

Cell Injury:

FAT NECROSIS
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Examples:
◼ Acute pancreatitis- release of pancreatic
lipase—liquefy the fat cell membranes.
◼ Fatty acids+ Ca++ Saponification
◼ Microscopy: foci of necrotic fat cells
surrounded by basophilic calcium deposits
and inflammatory reaction.
◼ Finally may end in dystrophic calcification.
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Conclusions:
◼ Cellular Injury - Various causes
◼ Reversible Injury - Adaptations
◼ Hypertrophy, Hyperplasia, Atrophy
◼ Accumulations - Hydropic, hyaline, fat..
◼ Irreversible Injury - Necrosis
◼ Coagulative, Liquifactive, Caseous, fat…
◼ Ageing - Lipofuscin
◼ Apoptosis - Programmed cell death.
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