NECROSIS
DR PREETI AGRAWAL
DEFINITION :
it is defined as a localised area of death
of tissue followed later by degradation of tissue by
hydrolytic enzymes liberated from dead cells ;
accompanied by inflammatory reaction
Causes
Hypoxia
Chemical agents
Physical agents
Microbial agents
Immunological injury etc.
Types of necrosis : based on etiology and
morphological appearance , five types
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid necrosis
Coagulative necrosis
•Cells have died but the basic shape and
architecture of the tissue endures
•Most common manifestation of ischaemic
necrosis in tissues.
•Affected tissue maintains solid consistency.
•In most cases the necrotic cells are ultimately
removed by inflammatory cells.
•The dead cells may be replaced by regeneration
from neighboring cells, or by scar (fibrosis).
MORPHOLOGY
Grossly :
Early stage – area of necrosis is pale , firm ,
slightly swollen.
Late stage – area becomes yellowish , softer
, shrunken
Microscopically : Outlines of cells are
retained and cell type can still be recognised
but their cytoplasmic and nuclear details are
lost.
The necrosed cells are swollen and have
more eosinophilic cytoplasm than normal
Normal Necrosis
LIQUEFACTION ( COLLIQUATIVE ) NECROSIS
•Occurs commonly due to ischaemic injury and
bacterial or fungal infections
•Hydrolytic enzymes in tissue degradation have
dominent role in causing semifluid material
•Egs. infarct brain , abscess cavity
Grossly : affected area is soft with liquefied centre
containing necrotic debris later, cyst wall is formed
Microscopically : cystic space contains necrotic
debris and macrophages filled with phagocytosed
material.
The cyst wall is formed by proliferating capillaries ,
inflammatory cells , proliferating glial cells or
fibroblasts
LIQUIFACTION NECROSIS OF BRAIN
CASEOUS NECROSIS
•Accumulation of amorphous (no structure) debris
within an area of necrosis.
•Tissue architecture is abolished and viable cells
are no longer recognizable.
•Characteristically associated with the
granulomatous inflammation of tuberculosis. Also
seen in some fungal infections.
Grossly : foci of necrosis resemble dry cheese and
soft , granular and yellowish.
Microscopically : center of necrosed focus contain
structurless , eosinophilic material having
scattered granular debris of disintegrated nuclei .
The surrounding tissue shows granulomatous
inflammatory reactions consisting of epithelioid
cells , interspesed langhans’ and foreign body giant
cells and peripheral mantle of lymphocytes.
Caseous necrosis
FAT NECROSIS
•Results from the action of lipases released into
adipose tissue.
egs. pancreatitis, trauma.
•Free fatty acids accumulate and precipitate as
calcium soaps (saponification).
Grossly : it appears as yellowish white and firm
deposits. Formation of calcium soaps imparts
necrosed foci firmer and chalky white appearance.
Microscopically : Fat cells have cloudy appearance
and surrounded by inflammatory reaction .
formation of calcium soaps is identified as
amorphous , granular and basophilic material .
FAT NECROSIS
FIBRINOID NECROSIS
Fibrinoid necrosis is characterized by deposition of
fibrin like material.
Egs. Immunologic tissue injury (immune comlex
vasculitis , autoimmune diseases, arthus reaction )
, arterioles in hypertension , peptic ulcer etc.
Microscopically : it is identified by brightly
eosinophilic , hyaline like deposits in vessel wall
.surrounded by nuclear debris of neutrophils.
Necrosis

Necrosis

  • 1.
  • 2.
    DEFINITION : it isdefined as a localised area of death of tissue followed later by degradation of tissue by hydrolytic enzymes liberated from dead cells ; accompanied by inflammatory reaction
  • 3.
  • 4.
    Types of necrosis: based on etiology and morphological appearance , five types Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat necrosis Fibrinoid necrosis
  • 5.
    Coagulative necrosis •Cells havedied but the basic shape and architecture of the tissue endures •Most common manifestation of ischaemic necrosis in tissues. •Affected tissue maintains solid consistency. •In most cases the necrotic cells are ultimately removed by inflammatory cells. •The dead cells may be replaced by regeneration from neighboring cells, or by scar (fibrosis).
  • 6.
    MORPHOLOGY Grossly : Early stage– area of necrosis is pale , firm , slightly swollen. Late stage – area becomes yellowish , softer , shrunken Microscopically : Outlines of cells are retained and cell type can still be recognised but their cytoplasmic and nuclear details are lost. The necrosed cells are swollen and have more eosinophilic cytoplasm than normal
  • 7.
  • 8.
    LIQUEFACTION ( COLLIQUATIVE) NECROSIS •Occurs commonly due to ischaemic injury and bacterial or fungal infections •Hydrolytic enzymes in tissue degradation have dominent role in causing semifluid material •Egs. infarct brain , abscess cavity
  • 9.
    Grossly : affectedarea is soft with liquefied centre containing necrotic debris later, cyst wall is formed Microscopically : cystic space contains necrotic debris and macrophages filled with phagocytosed material. The cyst wall is formed by proliferating capillaries , inflammatory cells , proliferating glial cells or fibroblasts
  • 10.
  • 12.
    CASEOUS NECROSIS •Accumulation ofamorphous (no structure) debris within an area of necrosis. •Tissue architecture is abolished and viable cells are no longer recognizable. •Characteristically associated with the granulomatous inflammation of tuberculosis. Also seen in some fungal infections.
  • 13.
    Grossly : fociof necrosis resemble dry cheese and soft , granular and yellowish. Microscopically : center of necrosed focus contain structurless , eosinophilic material having scattered granular debris of disintegrated nuclei . The surrounding tissue shows granulomatous inflammatory reactions consisting of epithelioid cells , interspesed langhans’ and foreign body giant cells and peripheral mantle of lymphocytes.
  • 14.
  • 16.
    FAT NECROSIS •Results fromthe action of lipases released into adipose tissue. egs. pancreatitis, trauma. •Free fatty acids accumulate and precipitate as calcium soaps (saponification).
  • 17.
    Grossly : itappears as yellowish white and firm deposits. Formation of calcium soaps imparts necrosed foci firmer and chalky white appearance. Microscopically : Fat cells have cloudy appearance and surrounded by inflammatory reaction . formation of calcium soaps is identified as amorphous , granular and basophilic material .
  • 18.
  • 20.
    FIBRINOID NECROSIS Fibrinoid necrosisis characterized by deposition of fibrin like material. Egs. Immunologic tissue injury (immune comlex vasculitis , autoimmune diseases, arthus reaction ) , arterioles in hypertension , peptic ulcer etc. Microscopically : it is identified by brightly eosinophilic , hyaline like deposits in vessel wall .surrounded by nuclear debris of neutrophils.