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MORPHOLOGY OF CELL INJURY
By- Dipesh Gamare
MORPHOLOGY OF REVERSIBLE CELL INJURY
 Cellular swelling
 Fatty change
 Hyaline change
 Mucoid change
• CELLULAR SWELLING
1) commonest and earliest form of cell injury
2) common causes are- bacterial toxins, chemicals, poisons,
burns, high fever, intravenous administration of hypertonic
glucose or saline
3) also known as cloudy swelling (for gross appearance of
affected organ)
Hydropic change (accumulation of water within the cell)
FATTY CHANGE
Also known as steatosis or fatty metamorphosis, is
the intracellular accumulation of neutral fat within
parenchymal cells eg: fatty liver
•HYALINE CHANGE
•1) intracellular hyalinehyaline droplets, hyaline
degeneration, mallorys hyaline, hyaline inclusions,
russells bodies
•2) extracellular hyaline
•Hyaline degeneration in leiomyomas,
•Hyalinised old scar,
•Hyaline arteriolosclerosis
•Hyalinised glomeruli
•Corpora amylacea
• MUCOID CHANGE
• Disturbences of epithelial mucin1)catarrhal inflammation
• 2)obstruction of duct
• 3)cystic fibrosis
• 4)mucin secreting tumours
• Disturbances of connective tissue mucin
• 1)mucoid or myxoid degeneration
• 2)dissecting aneurysm
• 3)myxomatous change
• 4)myxoid change
•AUTOLYSIS
•1)self-digestion-is disintegration of the cell by its
own hydrolytic enzyme liberated from lysosomes
•2)autolysis can occur in the living body when it is
surrounded by inflammatory reaction
•3)autolysis is rapid in tissues rich in hydrolytic
enzyme eg: pancreas, gastric mucosa
NECROSIS
DEF: FOCAL DEATH ALONG WITH DEGRADATION OF TISSUE BY HYDROLYTIC ENZYME LIBERATED BY CELLS
1)CAUSED BY VARIOUS AGENTS LIKE HYPOXIA, CHEMICAL AND PHYSICAL AGENTS, MICROBIAL AGENTS AND
IMMUNOLOGICAL INJURY
2)TWO ESSENTIAL CHANGES BRING ABOUT IRREVERSIBLE CELL INJURY IN NECROSIS-CELL DIGESTION BY
LYTIC ENZYME AND DENATURATION
TYPES OF NECROSIS
1)COAGULATIVE
2)LIQUEFACTION
3) CASEOUS
4)FAT
5) FIBRINOID
•APOPTOSIS
•Coordinated and internally programmed cell death
•Morphologic changes
•1)shrinkage of cell
•2) apoptic bodies
•3)no acute inflammatory reaction
•4)chromatin condensation
•5)phagocytosis
•GANGRENE
• Necrosis of tissue with superadded putrefaction
• Types
• 1)dry-effected part is dry, shrunken and dark black resembling
foot of mummy, black is due to liberation of haemoglobin from
haemolysed rbc which is acted upon by h2s
• 2)wet-effected part is soft, swollen, putrified, rotten and dark.
• 3)gas-caused by gas forming clostridia , affected area is
swollen, oedematous, painful and crepitant due to
accumulation of gas bubbles
• PATHOLOGIC CALCIFICATION
• Deposition of ca other than bone/enamel
• 1) dystropic-
• Dead- caseous, liquefaction, fat
• Degenerated- atheromas, monckebergs sclerosis, cysts
• 2)metastatic-
• Mobilisation from bone-hyperthyroidism, bony
destructive lesion, prolonged immobilisation
• Absorption from gut-hypervitaminosis D, milk alkali
syndrome, hypercalcaemia of infancy
 cell injury morphology.pptx

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cell injury morphology.pptx

  • 1. MORPHOLOGY OF CELL INJURY By- Dipesh Gamare
  • 2. MORPHOLOGY OF REVERSIBLE CELL INJURY  Cellular swelling  Fatty change  Hyaline change  Mucoid change
  • 3. • CELLULAR SWELLING 1) commonest and earliest form of cell injury 2) common causes are- bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline 3) also known as cloudy swelling (for gross appearance of affected organ) Hydropic change (accumulation of water within the cell)
  • 4. FATTY CHANGE Also known as steatosis or fatty metamorphosis, is the intracellular accumulation of neutral fat within parenchymal cells eg: fatty liver
  • 5. •HYALINE CHANGE •1) intracellular hyalinehyaline droplets, hyaline degeneration, mallorys hyaline, hyaline inclusions, russells bodies •2) extracellular hyaline •Hyaline degeneration in leiomyomas, •Hyalinised old scar, •Hyaline arteriolosclerosis •Hyalinised glomeruli •Corpora amylacea
  • 6. • MUCOID CHANGE • Disturbences of epithelial mucin1)catarrhal inflammation • 2)obstruction of duct • 3)cystic fibrosis • 4)mucin secreting tumours • Disturbances of connective tissue mucin • 1)mucoid or myxoid degeneration • 2)dissecting aneurysm • 3)myxomatous change • 4)myxoid change
  • 7. •AUTOLYSIS •1)self-digestion-is disintegration of the cell by its own hydrolytic enzyme liberated from lysosomes •2)autolysis can occur in the living body when it is surrounded by inflammatory reaction •3)autolysis is rapid in tissues rich in hydrolytic enzyme eg: pancreas, gastric mucosa
  • 8. NECROSIS DEF: FOCAL DEATH ALONG WITH DEGRADATION OF TISSUE BY HYDROLYTIC ENZYME LIBERATED BY CELLS 1)CAUSED BY VARIOUS AGENTS LIKE HYPOXIA, CHEMICAL AND PHYSICAL AGENTS, MICROBIAL AGENTS AND IMMUNOLOGICAL INJURY 2)TWO ESSENTIAL CHANGES BRING ABOUT IRREVERSIBLE CELL INJURY IN NECROSIS-CELL DIGESTION BY LYTIC ENZYME AND DENATURATION TYPES OF NECROSIS 1)COAGULATIVE 2)LIQUEFACTION 3) CASEOUS 4)FAT 5) FIBRINOID
  • 9. •APOPTOSIS •Coordinated and internally programmed cell death •Morphologic changes •1)shrinkage of cell •2) apoptic bodies •3)no acute inflammatory reaction •4)chromatin condensation •5)phagocytosis
  • 10. •GANGRENE • Necrosis of tissue with superadded putrefaction • Types • 1)dry-effected part is dry, shrunken and dark black resembling foot of mummy, black is due to liberation of haemoglobin from haemolysed rbc which is acted upon by h2s • 2)wet-effected part is soft, swollen, putrified, rotten and dark. • 3)gas-caused by gas forming clostridia , affected area is swollen, oedematous, painful and crepitant due to accumulation of gas bubbles
  • 11. • PATHOLOGIC CALCIFICATION • Deposition of ca other than bone/enamel • 1) dystropic- • Dead- caseous, liquefaction, fat • Degenerated- atheromas, monckebergs sclerosis, cysts • 2)metastatic- • Mobilisation from bone-hyperthyroidism, bony destructive lesion, prolonged immobilisation • Absorption from gut-hypervitaminosis D, milk alkali syndrome, hypercalcaemia of infancy