Hi..! This presentation series is about 'Cell Injury'.. So, here is the 1st part- 'OVERVIEW OF CELLULAR NECROSIS' which I tried to explain in simplest way.. i hope that it will be helpful.. Plz like n do share... Thank You..!!

1. Cell Injury-I
Overview of
Cellular
Necrosis
DR. SHARAYU PATIL

5. Irreversible Cell Injury
Cell death – Irreversible cell injury
It may occur in living body as local or focal
change (Autolysis, Necrosis and Apoptosis)
and changes that follow it( Gangrene and
Pathologic Calcification) or result in end of
life ( Somatic death).
Types-
 Autolysis
 Necrosis
 Apoptosis
 Gangrene
 Pathologic Calcification

6. Necrosis
 Definition – it is defined as focal death along
with degradation of tissue by hydrolytic
enzymes liberated by cells.
 It is invariably accompanied Inflammatory
reaction.
 Focal cell death + Degradation of Tissue +
Inflammatory Reaction = Necrosis
 2 essential changes bring about irreversible cell
injury in Necrosis –
1. Cell digestion by lytic enzymes
2. Denaturation of proteins

9. NECROSIS
 CYTOPLASMIC CHANGES-
1. Homogenous and intensely eosinophilic,
2. Vacuolation or dystrophic calcification
occasionaly
 NUCLEAR CHANGES-
1. Pyknosis - condensation of N. chromatin
2. Karyolysis - dissolution, decreased basophilia
3. Karyorrhexis - fragmentation into granular
clumps.

10. Types of Necrosis
 1. Coagulative Necrosis
 2. Liquefactive Necrosis
 3. Caseous Necrosis
 4. Fat Necrosis
 5. Fibrinoid Necrosis

11. 1.Coagulative Necrosis
 Most common type
 Mostly from ischemia , less
often from bacteria and
chemical agents.
 Organs commonly affected-
heart, kidney, spleen.

12. Gross-
1. Foci of
coagulative
necrosis in
early stages
are pale,
firm,
slightly
swollen .
2. With
progression
, they
become
more
yellowish ,
softer ,
shrunken .
COAGULATIVE
NECROSIS-Kidney

13. Microscopy-
 Hallmark – Conversion of normal cells into
their Tomb stones
 i. e. outlines of the cells are retained so that
the cell type can still be recognised but their
cytoplasmic and nuclear details are lost.
 Necrosed cells- swollen and appear more
eosinophilic.
 Changes d/t 1. Denaturation of proteins
2. Enzymatic digestion of cells
Eventually, the necrosed focus is infiltrated by
inflammatory cells and the dead cells are
phagocytosed leaving granular debris and
fragments of the cells.

15. 2.Liquefactive Necrosis
 Due to ischaemic injury and
bacterial or fungal infection.
 d/t degradation of tissue by the
action of powerful hydrolytic
enzymes.
 E.g. Infarct Brain, Abscess
cavity.

16. Gross –
Affected
area is
soft with
liquefied
centre
containing
necrotic
debris.
Later,
cyst wall
is formed.
Liquefactive Necrosis-Brain

17. Microscopy-
 Cystic space contains necrotic cell
debris and macrophages filled
with phagocytosed material.
 The cyst wall is formed by
proliferating capillaries,
inflammatory cells.
 Gliosis (proliferating Glial cells) in
the case of brain abscess and
fibroblasts in the case of abscess
cavity.

18. Liquefactive Necrosis- Brain

19. 3.Caseous Necrosis
 Is found in centre of foci of
tuberculous infections. It combines
feature of both coagulative and
liquefactive necrosis.
 This appearance is partly attributed
to the histotoxic effects of
lipopolysaccharides present in the
capsule of tubercle bacilli ,
Mycobacterium tuberculosis.

20. Gross –
 Foci of
caseous
necrosis ,
resemble
dry
cheese
 Soft
granular
and
yellowish.
CASEOUS NECROSIS- LUNG

21. Microscopy -
 The necrosed foci are
structureless, eosinophilic and
contains granular debris.
 The surrounding tissue shows
characteristic granulomatous
inflammatory reaction consisting of
epitheloid cells with interspersed
‘Giant cells of Langhans’ or Foreign
body type and peripheral mantle of
lymphocytes.

22. Caseous Necrosis- Lymph Node

23. 4.Fat Necrosis-
 Is a special form of cell death
occuring at two anatomically
different locations but
morphologically similar lesions.
 These are following acute
pancreatic necrosis and traumatic
fat necrosis commonly in breasts.
 Fat necrosis in either of two
instances results in hydrolysis of
neutral fat present in adipose cells
into glycerol and FFA.

24.  The damaged adipose tissue assume
cloudy appearance when only FFA
remain behind, after glycerol leaks
out.
 The leaked out FFA complex with ca
to form calcium soaps
(saponification)- dystrophic
calcification.

25. GROSS-
1. Yellowish
white and
firm
deposits.
2. Formation
of calcium
soaps
imparts the
necrosed
foci firmer
and chalky
white
appearance.
Fat necrosis

26.  Microscopy –
1. The necrosed fat cells have
cloudy appearance and are
surrounded by an
inflammatory reactions.
2. Formations of calcium soaps is
identified in the tissue
sections as amorphous,
granular and basophilic
material.

27. Fat Necrosis- Pancreas

28. 5.Fibrinoid Necrosis
Deposition of fibrin like
material which has the
staining properties of fibrin.
E.g. seen in immunologic tissue
injury, arterioles in HTN,
Peptic ulcers.

29. Microscopy-
1. Brightly
eosinophilic ,
hyaline like
deposition
into vessel
wall or on
luminal
surface of
peptic ulcer.
2. Local
haemorrhage
may occur d/t
rupture of
rupture of
these blood
vessel.
Fibrinoid Necrosis