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NECROSIS, INFARCT ,GANGRENE ,
OEDEMA AND CONGESTION
BY- Dr Tanya Agarwal
MODERATOR- Dr Vinita Paswan
NECROSIS
Def: It is defined as focal death along with degradation of tissue by hydrolytic
enzymes liberated by cells and is accompanied by inflammation.
Causative agents:
• Hypoxia
• Chemical and physical agents
• Microbial agents
• Immunological injury
MORPHOLOGY
Cytoplasm
• Increased eosinophilia due to loss of RNA
• Glassy homogenous appearance due to loss of glycogen particles
• Vacuolated or moth eaten appearance
• Myelin figures
• Electron microscopy- discontinuities in plasma & organelle membranes, marked dilation of
mitochondria ,amorphous densities
NUCLEUS
Pyknosis
• Nuclear shrinkage due to condensation of nuclear chromatin
Karyolysis
• Chromatin fades- loss of DNA due to enzymaticdegradation by
endonucleases
Karyorrhexis
• Pyknotic nucleus undergo fragmentation
COAGULATIVE NECROSIS
• Most common type due to ischaemia
• Organs- heart, kidney, spleen
• Grossly- foci of necrosis
• Early pale, firm & slightly swollen and shrunken
• Later yellowish softer & shrunken
• Microscopy- Conversion of normal cells into their tombstones i.e cell outline preserved but
nuclear details lostCells swollen, more eosinophilic with nuclear changes
LIQUEFACTIVE NECROSIS
• It is characterised by digestion of the dead cells, resulting in transformation of the tissues into
liquid viscous mass
• Seen in focal bacterial and fungal infections
• Examples- infarct brain, abscess cavity
• Grossly- affected area is soft with liquefied centre containing necrotic debris, cyst wall
• Microscopically- cystic space shows necrotic cell debris and macrophages
CASEOUS NECROSIS
Combines featues of coagulative and liquefactive necrosis
Example:
• tuberculosis lesions
• fungal infections
• Coccidioidomycosis
• Blastomycosis
• Histoplasmosis
Gross- Dry cheese, soft, granular and yellowish
Microscopy- necrosed foci are structureless eosinophilic with
granular debris surrounded inflammatory cells (granulomas)
FATTY NECROSIS
• Focal area of fat destruction, resulting from release of pancreatic
lipases.
• Traumatic fat necrosis
• Gross- fat necrosis seen as yellowish white and firm deposits, chalky
white appearance.
• Microscopy-Necrosed fat cells have cloudy appearance & are
surrounded by inflammatory reaction.
FIBRINOID NECROSIS
• It is characterised by depostion of fibrin like material
which has staining properties of fibrin•
• Seen in immunological tissue injury , immune
complex vasculitis, autoimmune diseases, arthus
reaction), Arterioles in hypertension and peptic ulcer
GANGRENE
• Gangrene is a form of necrosis of tissue with superadded
putrefaction
• Usually coagulative type due to ischaemia
Example-
• gangrene of bowel
• gangrene of limb
• Gangrenous or necrotising inflammation- gangrene lung, gangrenous
appendicitis
Types-
• Dry gangrene
• Wet gangrene
DRY GANGRENE
It begins in the distal part of a limb due to ischaemia.
Examples- dry gangrene in toes & feet of an old person due to arteriosclerosis
• Thromboangitis obliterans( Buerger's disease)
• Raynaud's disease
• Trauma
• Ergot poisoning
Line of separation is formed between gangrenous and viable part.
Gross
• Affected part is dry, shrunken and dark black (foot of mummy)
• black due to liberation of Hb from haemolysed RBC's which is acted upon by H2S
produced by bacteria resulting in formation of black iron sulphide
• Line of separation- separation with falling off the gangrenous tissue
Microscopy
• Necrosis with smudging off tissue. Line of separation consists of inflammatory
granulation tissue.
WET GANGRENE
• It occurs in moist tissues and organs such as mouth, bowel, lung, cervix, vulva,
etc
Examples:
• Diabetic foot
• Bed sores
Wet gangrene develops due to blockage of venous and less commonly arterial
Affected part is stuffed with blood- growth of putrefactive bacteria
No clear cut line of demarcation, may spread to peritoneal cavity causing
peritonitis.
Gross-
• Affected part is soft, swollen, putrid, rotten and dark.
Microscopy-
• Coagulative necrosis with stuffing of affected part with blood.
• No clear cut line of demarcation.
GAS GANGRENE
• It is form of wet gangrene caused by gas forming clostridia. ( gram positive anaerobic
bacteria)•
Gross
• Affected tissue swollen, oedematous, painful and crepitant due to accumulation of gas
bubbles within the tissues
• Later tissue becomes dark black and foul smelling.
Microscopy
• Muscle fibres show coagulative necrosis with liquefaction, edema and leucocytic infiltrate
CVC LIVER
CVC LUNG
CVC SPLEEN
RED IN INFARCT VS WHITE INFARCT

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necrosis.pptx

  • 1. NECROSIS, INFARCT ,GANGRENE , OEDEMA AND CONGESTION BY- Dr Tanya Agarwal MODERATOR- Dr Vinita Paswan
  • 2. NECROSIS Def: It is defined as focal death along with degradation of tissue by hydrolytic enzymes liberated by cells and is accompanied by inflammation. Causative agents: • Hypoxia • Chemical and physical agents • Microbial agents • Immunological injury
  • 3. MORPHOLOGY Cytoplasm • Increased eosinophilia due to loss of RNA • Glassy homogenous appearance due to loss of glycogen particles • Vacuolated or moth eaten appearance • Myelin figures • Electron microscopy- discontinuities in plasma & organelle membranes, marked dilation of mitochondria ,amorphous densities
  • 4. NUCLEUS Pyknosis • Nuclear shrinkage due to condensation of nuclear chromatin Karyolysis • Chromatin fades- loss of DNA due to enzymaticdegradation by endonucleases Karyorrhexis • Pyknotic nucleus undergo fragmentation
  • 5. COAGULATIVE NECROSIS • Most common type due to ischaemia • Organs- heart, kidney, spleen • Grossly- foci of necrosis • Early pale, firm & slightly swollen and shrunken • Later yellowish softer & shrunken • Microscopy- Conversion of normal cells into their tombstones i.e cell outline preserved but nuclear details lostCells swollen, more eosinophilic with nuclear changes
  • 6.
  • 7.
  • 8. LIQUEFACTIVE NECROSIS • It is characterised by digestion of the dead cells, resulting in transformation of the tissues into liquid viscous mass • Seen in focal bacterial and fungal infections • Examples- infarct brain, abscess cavity • Grossly- affected area is soft with liquefied centre containing necrotic debris, cyst wall • Microscopically- cystic space shows necrotic cell debris and macrophages
  • 9.
  • 10. CASEOUS NECROSIS Combines featues of coagulative and liquefactive necrosis Example: • tuberculosis lesions • fungal infections • Coccidioidomycosis • Blastomycosis • Histoplasmosis Gross- Dry cheese, soft, granular and yellowish Microscopy- necrosed foci are structureless eosinophilic with granular debris surrounded inflammatory cells (granulomas)
  • 11.
  • 12.
  • 13. FATTY NECROSIS • Focal area of fat destruction, resulting from release of pancreatic lipases. • Traumatic fat necrosis • Gross- fat necrosis seen as yellowish white and firm deposits, chalky white appearance. • Microscopy-Necrosed fat cells have cloudy appearance & are surrounded by inflammatory reaction.
  • 14.
  • 15. FIBRINOID NECROSIS • It is characterised by depostion of fibrin like material which has staining properties of fibrin• • Seen in immunological tissue injury , immune complex vasculitis, autoimmune diseases, arthus reaction), Arterioles in hypertension and peptic ulcer
  • 16.
  • 17.
  • 18. GANGRENE • Gangrene is a form of necrosis of tissue with superadded putrefaction • Usually coagulative type due to ischaemia Example- • gangrene of bowel • gangrene of limb • Gangrenous or necrotising inflammation- gangrene lung, gangrenous appendicitis Types- • Dry gangrene • Wet gangrene
  • 19. DRY GANGRENE It begins in the distal part of a limb due to ischaemia. Examples- dry gangrene in toes & feet of an old person due to arteriosclerosis • Thromboangitis obliterans( Buerger's disease) • Raynaud's disease • Trauma • Ergot poisoning Line of separation is formed between gangrenous and viable part.
  • 20. Gross • Affected part is dry, shrunken and dark black (foot of mummy) • black due to liberation of Hb from haemolysed RBC's which is acted upon by H2S produced by bacteria resulting in formation of black iron sulphide • Line of separation- separation with falling off the gangrenous tissue Microscopy • Necrosis with smudging off tissue. Line of separation consists of inflammatory granulation tissue.
  • 21.
  • 22. WET GANGRENE • It occurs in moist tissues and organs such as mouth, bowel, lung, cervix, vulva, etc Examples: • Diabetic foot • Bed sores Wet gangrene develops due to blockage of venous and less commonly arterial Affected part is stuffed with blood- growth of putrefactive bacteria No clear cut line of demarcation, may spread to peritoneal cavity causing peritonitis.
  • 23. Gross- • Affected part is soft, swollen, putrid, rotten and dark. Microscopy- • Coagulative necrosis with stuffing of affected part with blood. • No clear cut line of demarcation.
  • 24.
  • 25. GAS GANGRENE • It is form of wet gangrene caused by gas forming clostridia. ( gram positive anaerobic bacteria)• Gross • Affected tissue swollen, oedematous, painful and crepitant due to accumulation of gas bubbles within the tissues • Later tissue becomes dark black and foul smelling. Microscopy • Muscle fibres show coagulative necrosis with liquefaction, edema and leucocytic infiltrate
  • 26.
  • 30. RED IN INFARCT VS WHITE INFARCT