This document defines and describes different types of necrosis. It begins by defining necrosis as focal death and degradation of tissue by hydrolitic enzymes, accompanied by inflammation. It then describes several types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis is the most common type caused by ischemia. Liquefactive necrosis occurs due to enzymatic degradation. Caseous necrosis is seen in tuberculosis. Fat necrosis occurs in the pancreas and breast. Fibrinoid necrosis involves fibrin deposition. The document also discusses pathologic changes seen in different types of necrosis both grossly and microscopically.

1. NECROSIS
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2. OBJECTIVES
• Highlight the basic concepts and principles
of necrosis (cell death)
• Differentiate between different types of
necrosis
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3. CONTENTS
4.1 Definition of necrosis
4.2 Different types of necrosis
4.3 Different types of necrosis base on pathologic
changes
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4. 4.1 Definition Of Necrosis
• Necrosis; defined as focal death along with degradation of tissue by
hydrolitic enzymes liberated by cells. It’s invariably accompanied
by inflammatory reaction.
• Causes; 1. Loss of blood supply - caused by blockage of a vessel by a
blood clot which produces immediate local
anoxia.
2. Bacterial toxins – inflammation is produced & if it’s strong the
result is necrosis.
3. Physical irritants – excessive heat, excessive cold, trauma &
radiation.
4. Chemical irritants – strong acid.
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5. 4.2 Types Of Necrosis
• Morphologically, 5 types of necrosis are identified:
i) Coagulative necrosis
ii) Liquefaction (Colliquative) necrosis
iii) Caseous necrosis
iv) Fat necrosis
v) Fibrinoid necrosis
• Gangrene is a form of necrosis of tissue with superadded
putrefaction; gangrene necrosis
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6. i) Coagulative necrosis
 Most common type of necrosis caused by irreversible
focal injury (mostly because ischaemia).
 Less often bacterial & chemical agents.
 The organs commonly affected are HEART, KIDNEY &
SPLEEN.
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7. Coagulative necrosis – Renal infarction
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8. Coagulative necrosis – Spleenic infarction
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9. ii) Liquefaction (Colliquative) necrosis
 Occurs commonly due to ischaemic injury & bacterial or
fungal infections.
 Occurs due to degradation of tissue by the action of
powerful hydrolytic enzymes.
 Examples are INFARCT BRAIN (stroke) & ABSCESS
CAVITY.
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10. Liquifactive necrosis - Stroke
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11. Liquifactive necrosis – Liver abscess
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12. iii) Caseous necrosis
 Found in the centre of foci of tuberculosis infections.
 It combines features of both coagulative & liquefactive
necrosis.
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13. Caseous necrosis
-Tuberculosis
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14. Caseous necrosis -Tuberculosis
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15. iv) Fat necrosis
 Special form of cell death occurring at two anatomically different
locations but morphologically similar lesions.
 These are ACUTE PANCREATIC NECROSIS & TRAUMATIC FAT
NECROSIS (breast).
 In the case of pancreas, there is liberation of pancreatic lipase from
injured or inflamed tissue that results in necrosis of the pancreas.
 Fat necrosis in either of the two instances results in hydrolysis of
neutral fat present in adipose cells into glycerol & free fatty acid.
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16. v) Fibrinoid necrosis
 Characterized by deposition of fibrin-like material which has the
staining properties of fibrin.
 It’s encountered in various examples of immunologic tissues injury,
arterioles in hypertension, peptic ulcer etc.
vi) Gangrene necrosis
 The type of necrosis is usually coagulative due to ischaemia.
 Is characterized by primarily inflammation provoked by virulent
bacteria.
 3 types; dry, wet & gas gangrene.
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17. 4.3 Types Of Necrosis Base On
Pathologic Changes
i) Coagulative necrosis
 Grossly: foci of coagulative necrosis in the early stage are PALE, FIRM
& SLIGHTLY SWOLLEN.
: with progression, they become more YELLOWISH, SOFTER
& SHRUNKEN.
Micro: the pattern of microscopic change results from 2 processes
which are DENATURATION OF PROTEINS & ENZYMATIC
DIGESTION OF THE CELL.
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18. ii) Liquefaction (Colliquative) necrosis
 Grossly: the affected area is soft with liquefied centre containing necrotic
debris.
: later, a cyst wall is formed.
Micro: the cystic space contains necrotic cell debris & macrophages filled
with phagocytosed material.
: the cyst wall is formed by proliferating cappilaries,
inflammatory cells & gliosis (proliferating glial cells) in the
case of brain & proliferating fibroblasts in the case of
abscess cavity.
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19. iii) Caseous necrosis
 Grossly: resemble dry cheese and are soft, granular & yellowish.
Micro: the necrosed foci are structureless, eosinophilic & contain granular
debris.
iv) Fat necrosis
 Grossly: appears as yellowish-white & firm deposits.
: formation of calcium soaps imparts the necrosed foci firmer &
chalky white appearance.
Micro: necrosed fat cells have cloudy appearance & are surrounded by an
inflammatory reaction.
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20. v) Fibrinoid necrosis
 Grossly: is identified by brightly eosinophilic, hyaline-like deposition in
the vessel wall or on the luminar surface of peptic ulcer.
: local haemorrhages may occur due to rupture of these blood
vessels.
vi) Dry gangrene
 Macro: the affected part is dry, shrunken & dark black, resembling the foot
: it’s black due to liberation of haemoglobin from haemolysed red
blood cells.
Histo: the separation consists of inflammatory granulation tissue.
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21. vii) Wet gangrene
 Macro; the affected part is soft, swollen, putrid, rotten & dark.
: the example is gangrene of bowel.
Histo: there is ulceration of the mucosa & intense inflammatory infiltration.
viii) Gas gangrene
 Grossly: the affected area is swollen, edematous, painful & crepitant due
to accumulation of gas bubbles within the tissues.
: the affected tissue becomes dark black & foul smelling.
Micro: at the periphery, a zone of leucocytic infiltration, edema &
congestion are found.
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22. THANK YOU
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