Necrosis and gangrene

Concept of reversible injury
Concept of necrosis
Subcellular, cellular and gross features of necrosis
Morphological types of necrosis
Utility of tissue specific enzyme assay to detect necrosis

1. 21/07/2015 Dept of Pathology, AFMC 1
NECROSIS

2. Learning objectives
•Concept of reversible injury
•Concept of necrosis
•Subcellular, cellular and gross features of
necrosis
•Morphological types of necrosis
•Utility of tissue specific enzyme assay to
detect necrosis

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Mitochondrial
dysfunction
Membrane
Dysfunction

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Reversible injury
Cellular swelling Fatty changeCellular swelling Fatty change

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CELL DEATH
NECROSIS APOPTOSIS

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NECROSIS

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Enzymatic digestion
Enzymes
from
inflammatory
cell
Enzymes
from cellular
lyzosome

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Cytoplasmic changes
•Light microscopy
–Increased eosinophilia
–“moth-eaten”

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Cytoplasmic changes
•Electron microscopy
–Discontinuous
membrane
–Mitochondria –dilated,
amorphous densities
–Lyzosomes disrupted
–Myelin figures

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Nuclear changes
Normal
nucleus
Karyorrhexis
Pyknosis Karyolysis

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Cell
Completed
digested
Myelin figures
Phagocytosed Fatty acids
Calcified
Fate of
Necrosed
Cell

12. 1.Coagulative necrosis
2.Liquefactive necrosis
3.Gangrenous necrosis
4.Caseous necrosis
5.Fat necrosis
6.Fibrinoid necrosis
Morphological types
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Coagulative necrosis
•Tissue architecture is preserved
•Denatures the enzymes (proteins) –block
proteolysis
•‘Ghost’ cells persist for days –weeks
•Cleared by leucocytes
•Eg: infracts –all solid organs except brain

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Liquefactive necrosis
•Leucoytes enzymes –digest (liquefy)
•Eg
–bacterial / some fungal infections (PUS !)
–Brain –peculiar (? reduced supporting framework)

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Gangrenous
•‘Clinical’ term
Ischemia
Coagulative
Necrosis
Dry
Gangrene
Bacterial
infection
Liquefactive
necrosis
Wet
gangrene
Limb
Ischemia
Coagulative
Necrosis
Ischemia
Coagulative
Necrosis
Ischemia
Dry
Gangrene
Coagulative
Necrosis
Ischemia
Bacterial
infection
Bacterial
infection
Liquefactive
necrosis
Bacterial
infection
Wet
gangrene
Liquefactive
necrosis
Bacterial
infection

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Caseous necrosis
•Tuberculous infection
•‘Cheese-like’
•Amorphous granular pink on H&E
•? high lipid content in bacterial membrane

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Fat necrosis
•Release of pancreatic
enzymes
•‘chalky white’ areas
•Basophilic deposits
on H&E
Proteases liquefy
membranes
Lipases split
triglyceride esters
Fatty acids + Ca
= Saponification
Proteases liquefy
membranes

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Fibrinoid necrosis
•‘Special’ -Visible by
light microscopy
•Immune reactions
•Involves vessel wall
•Bright pink /
amorphous on H&E
•Eg: Polyarteritis
nodosa
Immune
complex
Leaked
fibrin
Deposited in
the vessel wall
Immune
complex
Leaked
fibrin
Immune
complex
Leaked
fibrin
Deposited in
the vessel wall

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Necrosis
damaged cell
Intracellular
proteins
leak
Proteins
reach
circulation

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•Eg:
–Heart –Myocardial infarction -↑ Troponin
–Liver –Jaundice -↑ Alkaline phosphatase

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Summary
•Reversible injury
–cellular swelling, fatty change
•Necrosis
–Cytoplasmic, Nuclear features
–Fate of necrosis
•Patterns –
–Coagulative, liquefactive, gangrenous,
caseous, fat, fibrinoid
•Applied aspect

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Questions ?

29. Questions
1.Liquefactive necrosis is typically seen in:
(a)Ischemic necrosis of the brain
(b)Ischemic necrosis of the heart
(c)Ischemic necrosis of the intestine
(d)Tuberculosis
Ans: (b) Ischemic necrosis of the brain

30. 2.ApatientSachinpresentstothehospitalwith
jaundice,rightupperquadrantpainand
fatigue.HetestspositiveforhepatitisBsurface
antigen.Theserumbilirubinlevelis4.8mg/dl
(directis0.8mg/dlandindirectis4.0mg/dl),
ASTlevelis300U/L,ALTis325U/Land
alkalinephosphataseiswithinnormallimits.
TheelevationinASTandALTcanbe
explainedbywhichofthefollowing?
(a)Bleb formation
(b)Cell membrane rupture
(c)Clumping of chromatin
(d)Swelling of endoplasmic reticulum
Ans: (b) Cell membrane rupture

31. 3.Which of the following is a manifestation
of reversible cell injury:
(a)Apoptosis
(b)Caseous necrosis
(c)Dystrophic calcification
(d)Fatty change
Ans: (d) Fatty Change

32. 4.A58yearoldman,MrDumakaytudevelopsa
thrombusinhisLeftanteriordescendingcoronary
artery.Theareaofmyocardiumsuppliedbythisvessel
isirreversiblyinjured.Thethrombusisdestroyedby
theinfusionofstreptokinase,whichisaplasminogen
activatorandtheinjuredareaisreperfused.The
patient,howeverdevelopsarrhythmiaanddies.An
electronmicroscopicpicturetakenoftheirreversibly
injuredmyocardiumrevealsthepresenceoflarge,
dark,irregularamorphousdensitieswithinthe
mitochondria.Whataretheseabnormalstructures?
(a)Apoptotic bodies
(b)Flocculent densities
(c)Myelin figures
(d)Psammoma bodies
(e)Russell bodies
Ans: (b) Flocculent densities

33. 5.In cell death myelin figures are derived
from
(a)Nucleus
(b)Cytoplasm
(c)Cell membrane
(d)Mitochondria
Ans: (c) Cell membrane

34. Thank You