Cell injury: Necrosis and Gangrene

morphology of irreversible cell injury

1. Morphology of irreversible cell
injury

2. •Autolysis
•Necrosis
•Apoptosis

3. 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

4. Necrosis
•Localised area of cell death followed by
degradation of the tissue by the hydrolytic
enzymes
•ALWAYS accompanied by inflammatory
reaction

5. Causes
•Hypoxia
•Chemical agents
•Physical agents
•Microbial agents
•Immunological agents
•..

6. Mechanisms
1.Denaturation of the intracellular proteins
2.Enzymatic digestion of the cell

7. 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

8. Nuclear changes
Due 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
KARYOLYSI
S
PYKNOSIS
KARYORRHEXIS

10. Types of necrosis
•Mass of necrosis has several
morphological patterns
–Coagulative
–Liquefaction
–Caseous
–Fat
–Fibrinoid

11. 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

12. •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.

15. 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

17. CASEOUS NECROSIS
•Found in the centre of foci of tuberculous
infections
•It combines features of coagulative and
liquefactive necrosis

18. •gross – soft, cheesy, granular and
yellowish
•Micro –
–Amorphous, eosinophlic granular debris
surrounded by a granulomatous reaction
–The tissue architecture is completely
obliterated.

23. 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

24. •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

26. Identify the lesion with the clues
below!

27. 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

32. CONT’D