The term necrosis is derived from a greek word nekros which means dead body. Definition: Necrosis is defined as local or focal death of cells along with degradation of tissues by hydrolytic enzymes released from lysosome of the cell. It is often associated with surrounding inflammatory reaction. Necrosis is a series of morphological changes that follows cell death due to the irreversible cell injury/lethal cell injury/pathological cell injury.

1. Government Tibbi College & Hospital, Patna
NECROSIS
Dr Shabista Fatma Taiyabi
PG - Scholar
Dept. of Mahiyatul Amraz

2. CONTENTS
NCEROSIS
• Overview
• Definition
• Causes
• Mechanism
• Morphological changes
• Biomarkers
• Types
APOPTOSIS
• Definition
• Diff b/w necrosis and
apoptosis
• Physiological condition
• Pathological conditions

3. Overview
The term necrosis is derived from a greek word nekros which means dead body.
Definition: Necrosis is defined as local or focal death of cells along with
degradation of tissues by hydrolytic enzymes released from lysosome of the cell.
It is often associated with surrounding inflammatory reaction.
Necrosis is a series of morphological changes that follows cell death due to the
irreversible cell injury/lethal cell injury/pathological cell injury.
Notes: lethal injury means cell can not reverse its damage, then
histological changes occur in 4-12 hrs which is identified by light
microscope.

5. APOPTOSIS AND NECROSIS (A COMPARISON)
Apoptosis
i. Programmed cell death
ii. Death by suicide
iii. Death by shrinkage
iv. Death by karyorrhexis
v. Affects isolated cells
vi. Membrane budding
vii. Buds detach-Apoptotic bodies
viii.Phagocytosis of the apoptotic
bodies
ix. Physiological and Pathological
both
i. Induced cell death
ii. Death by homicide
iii. Death by swelling
iv. Death by karyolysis
v. Affects groups of cell
vi. Membrane bleb formation
vii. Blebs rapture out
viii.Inflammatory reaction occur
ix. Always pathological
Necrosis

6. APOPTOSIS IN PHYSIOLOGICAL
CONDITIONS:
Destruction of cells during embryogenesis- implantation, organogenesis.
Involution of hormone-dependent tissues upon hormone withdrawal- endometrial
Cell breakdown, ovarian follicular atresia in menopause, after withdrawal of breast
Feeding-regression of breast.
 Cell loss in proliferating cell populations- immature lymphocyte in bone marrow
And thymus.

7. APOPTOSIS IN PATHOLOGICAL
CONDITIONS:
 Death of cells in tumor after the chemotherapy.
 Cell death by toxic T cells in immune mechanisms.
 Some viral infection
Progressive depletion of CD4 and T cells in HIV
Councilman bodies in hepatitis
 Atrophy of kidney due to obstruction in ureter.
 Atrophy of prostate after orchiectomy.

8. CAUSES OF NECROSIS:

9. IRREVERSIBLE CELL INJURY

10. 1) Increased cytosolic Ca2+
cytosolic Ca2+conc.
Activation of ATPase
enzyme
Result
ATP DEPLETION
2)Hypoxia ( O2 level in cell )
Impairment of oxidative
phosphorylation in
mitochondria
ATP production
MITOCHONDRIAL DAMAGE
There are 3 causes:

11. ROS (Reactive Oxygen species)
free radicals having O2 molecules
molecules having unpaired electron on
outer orbit
highly reactive species
can cause damage to cell and its
components.

12. ACCUMULATION OF OXYGEN-DERIVED FREE RADICALS ( OXIDATIVE STRESS )

13. Influx of intracellular calcium and loss of calcium homeostasis
Ischemia causes an increase in cytosolic calcium conc……….Increased
ca2+ ……in turn activates a number of enzymes, eg.
ATPases (thereby hastening ATP depletion )
Phospholipases ( which cause membrane damage )
Proteases ( which break down both membrane and cytoskeleton proteins) and
Endonucleases ( which are responsible for DNA and chromatin fragmentation )

14. Defect in membrane permeability
1. Increased influx of calcium activate endogenous phospholipases
Break bilipid plasma membrane
2. ATPase also activated decreased synthesis of membrane phospholipid

15. MORPHOLOGICAL CHANGES IN NECROSIS

16. NUCLEAR CHANGES
 In 1 or 2 days, the nucleus of dead cell may completely disappear.

17. Cytoplasmic changes
 Eosinophilic appearance due to -loss of cytoplasmic RNA
-Denatured cytoplasmic proteins
 Formation of myelin figures- derived from damaged cell membrane.
 Calcifications- derived from phospholipid formation.
Electron microscopic finding
 Swollen mitochondria with large amorphous densities.
 Discontinuities in plasma and organellar membrane.

19. BIOMARKER OF NECROSIS
• Necrosis lead to cell membrane damage, so cell content ultimately goes in blood Circulation that
used as a biomarker of cell death.
Example:
MI - troponin
Bile duct damage - ALP (alkaline phosphatase) release
Liver cell damage – transaminase in blood esp. SGPT (Serum Glutamic Pyruvic Transaminases)

20. TYPES OF NECROSIS
1. COAGULATIVE NECROSIS
2. LIQUEFACTIVE NECROSIS
3. CASEOUS NECROSIS
4. FAT NECROSIS
5. FIBRINOID NECROSIS

21. 1-COAGULATIVE NECROSIS
• M/c type
• M/c cause ischemia except ischemia of
brain.
• Commonly occur in parenchymal cells…..
• M/c affected organs are the heart, kidney,
liver, spleen

22. Cont…
Grossly:
In early stage- organ become pale, firm, slightly swollen
In late stage- more yellowish, soften, shrunken
Microscopically:
 The hallmark of CN is ̔TOMBSTONE
̓ appearance
cell outline retained
cytoplasmic and nuclear details are lost
 cell cytoplasm become More eosinophilic and homogeneous
 Eventually, the necrosed tissue focus is infiltrated by inflammatory cells and the dead
cells are phagocytosed leaving granular debris and fragments of cells.
Pathological changes

24. COAGULATIVE NECROSIS
Tombstone appearance

26. 2-LIQUEFACTIVE NECROSIS
• Also k/s colliquative necrosis.
• M/c cause bacterial or fungal infection and ischemic injury.
• M/c examples are abscess cavity and infarct brain.
Grossly:
in early stage- soft and liquefied center
In late stage- a cyst wall is formed (proliferation of capillaries, fibroblast/ glial cells)
Microscopically:
 The cystic space contains necrotic cell debris and phagocytized material.
 In case of brain, the cyst wall is formed by gliosis.
 In case of abscess cavity, the cyst wall is formed by proliferating fibroblast.

28. LIQUEFACTIVE NECROSIS

29. 3-CASEOUS NECROSIS
• It has combining features of both coagulative and liquefactive necrosis.
• M/c in the tuberculous infections. Occurs in center of foci of tuberculosis.
• It is highly infectious.
Grossly:
Resemble dry cheese, soft, granular and yellowish
Microscopically:
 Granulomatous inflammation
 Epithelioid cells (activated macrophages resembling
epithelial cells)
 Giant cells of LANGHANS (aggregates of macrophages)
Form at center of granulomas

31. CASEOUS NECROSIS

32. Giant cells of langhans

34. 4-FAT NECROSIS
M/c in pancreas due to acute pancreatitis
In breasts due to trauma
In mesentery
Grossly:
 Formation of calcium soaps
 Firm and chalky white appearance
Microscopically:
 Necrosed fat cells have cloudy appearance and inflammatory cells
Amorphous calcium soaps

38. 5-FIBRINOID NECROSIS
• Characterized by deposition of fibrin or fibrin like material or protein material having
staining property of fibrin.
• Found in immune complex vasculitis (arterioles)
• Autoimmune disease
Grossly:
• fibrin like deposition
Microscopically:
Brightly eosinophilic area
LEUCOCYTOCLASIS (focal area will be surrounded by nuclear debris of nutrophils)
Local hemorrhages

40. UNANI CONCEPT OF NECROSIS
• According to Unani Medicine, There are three types
of disease:
1. Sue Mizaj
2. Sue Tarqeeb
3. Taffaruq e ittesal
These basic disease mainly affects Aza Mufrda.

41. Amraz e Mufrda and Amraz e Muraqba
If at one point of time only one of the disease affect
any organ then it called Amraz e Mufrda. and
If simultaneously any of the two or more types of
simple disease affects any organ then it is called
Amraz e Muraqba.
Example Awram
• Amraz e Mufrda affects Aza Mufrda and Amraz e
Muraqba affcts Aza Muraqba.

42. Aza Mufrda: 10 in number

43. ABU SAHAL MASIHI AND IBN ABBAS MAJOOSI

44. Mahiyat e Merz of Sue Mizaj
Due to improper supply of or stop of supply of
Rooh.
 Due to accumulation of fasid akhlat
Due to supply of fasid agzia (mal-nutrition) to aza
mufrda

45. NECROSIS
• Necrosis is caused by sue mijaz, which finally leads to tafaruq
ittesal. Results in local or focal death of aza mufrda.