1. Necrosis is the pathological death of cells and living tissue. The main types are coagulative, liquefactive, and caseous necrosis. 2. Coagulative necrosis results in firm, dry tissue with cellular detail lost but architectural outline preserved. Liquefactive necrosis leads to tissue disintegration into a liquid mass where all details are lost. Caseous necrosis converts tissue into a cheese-like granular mass. 3. Necrosis can be caused by ischemia, toxins, infections, burns, and other injuries. It progresses from changes at the nuclear and cellular levels to loss of cell outlines and tissue disintegration. The outcome depends on the size and type of necrosis, ranging from removal

1. IRREVERSIBLE CELL INJURY

2. IRREVERSIBLE CELL INJURY
• Necrosis
The morphological changes that follow the cell
death in living tissue or organ.
Processes that induce necrosis
Degradation of cell contents by:
1)Autolysis (self digestion)—process of cell
death caused by lysosomal enzymes of dead
cells.
2) Heterolysis—process of cell death caused by
lysosomal enzymes of infiltrating leukocytes.

3. Etiology
1. Poisons
• Chemical poisons
• Poisons of pathogenic organisms
• Plant poisons
• Animal poisons ----- bee stings causes focal
necrosis of tissues.
2. Disturbances in circulation
Ischemia or loss of blood supply
Passive hyperemia
General anemia

4. 3. Mechanical injuries
4. Thermal changes
5. Electric current

5. Gross appearance
• Loss of color
-dead tissue is paler than normal.
Paleness is due to;
Hemolysis of RBC in necrotic area. diffusion of pigmented
substances from cytosol of necrotic cell.
If large amount of hemolyzed blood is present,it will impart
blackish-red color to affected area.
• Loss of strength
Necrotic tissue has less tensile strength due to enzymatic
digestion of cytoskeleton, cell membrane and intercellula
r connections.
A finger may easily thrust into a necrosed liver or lung.

6. • Loss of odour
Putrefactive odour from dead tissues is due
to foul smelling compounds (hydrogen
sulphide , ammonia) produced by bacterial
fermentation of organic tissues.
Necrotic changes first apparent at;
Then at histological level; 6-12 hrs.
And finally at gross level; 24-48 hrs.

7. Microscopic appearance
• Changes in the nucleus
1) Pyknosis
The nucleus is decreased in size ,round and
hyperchromatic
2) Karyorrhexis
It is the fragmentation of chromatin into tiny
basophillic granules because of rupture of the
nuclear membrane.
3) Karyolysis
it is the lysis of the chromatin by nucleases
released from leaking lysosomes of dead cells
4) Loss of the nucleus
pyknosis, karyorrhexis and karyolysis results in
the loss of nucleus

8. Changes in cytoplasm
.
1. Increased eosinophilia of cytoplasm
It is because of the enzymatic degradation of
cytoplasmic RNA ,which usually imparts a
degree of basophilia to the cytoplasm.
2. Cytoplasmolysis
when the changes of necrosis progress, the
cytoplasm tends to become less and less
dense and ultimately disappears completely.

9. Changes in the whole cell
1. Loss of cell outline nucleus or its cells remains
visible but the shape and nature of the cell are
quite unidentifiable.
2. Loss of differential staining nuclear and
cytoplasmic colors, characteristics of different
histologic tissues, cannot be distinguished
because of chromatolysis.
3. Loss of cell (desquamation)

10. Types of necrosis
• The classification of necrosis is based up
on the gross appearance of the tissues.
1. Coagulative necrosis
2. Liquifactive necrosis
3. Caseous necrosis
4. Fat necrosis

11. Coagulative necrosis
• This is the most common type of necrosis.
• Architectural detail of the area persists but
the cellular detail is lost.

12. Etiology
• Sudden severe ischemia-heart, liver, kidne
ys, adrenal gland
• Sphaerophorus necrophorus—liver of bovi
ne
• Vitamin E deficiency---muscular dystrophy
• Mercury, thiamine, or uranium salts poison
ing ---renal tubular epithelium
• Application of concentrated phenol---skin,
mucous membrane or wound .

13. Pathogenesis
• Cell injury
• Increased intracellular acidosis
• Denaturation of structural and enzymatic proteins
• Blockage of proteolysis/dissolution of the cell
• Loss of cellular detail and persistance of architectural det
ail

14. Gross appearance
1. Necrotic area is firm and dry.
2. It has homogeneous ,opaque or cooked
appearance.
3. Its color may be grey, white or tan.

15. Microscopic appearance
• Architecral outline of the tissue or organ is
maintained.
• Cellular detail of the tissue is lost.

16. Significance and result
1. Area of the coagulative necrosis has no g
reat attraction for neutrophils.
2. The dead materials remains in the area f
or a long period of time.
3. Necrotic cells are removed by fragmentat
ion and phagocytosis of cellular debris.

17. Liquifactive necrosis
• It is characterized by disintegration of necr
otic material into a liquid mass in which ce
llular and architectural detail is lost.

19. Etiology and pathogenesis
• Focal bacterial infection especially pyogenic bact
eria or chemicals e.g., turpentine or hypo
xic death of cells
• Powerful stimuli for accumulation of WBC
• Digestion by enzymes of bacterial and leukocytic
origin
• Liquefactive necrosis

20. • Hypoxic death of cells within CNS produces liq
uefactive necrosis due to following characteris
tics of normal nervous tissues;
I. Very soft
II. Little structural support
III. High lipid and water contents
• Hypoxic death of most cells (except nervous ti
ssues) of body followed by coagulative necrosi
s.

21. Gross appearance
1. Tissues are liquefied and may be watery,
tenacious or semisolid in consistency.
2. Color of tissues is white, yellow, green or
red.
In long standing necrosis, a wall of fibrous c
onnective tissues (FCT) may be formed a
round the necrotic mass.

22. Microscopic appearance
1. No architectural or cellular detail is visible in th
e area of necrosis.
2. The dead tissue is homogenous and stains pin
k with eosin.
3. Disintegration of neutrophils occurs if bacteria
are present.
4. Necrotic mass is surrounded by a zone of acut
e or chronic inflamation depending upon the le
ngth of time necrosis has been present.

23. Caseous necrosis
• It is characterized by the conversion of de
ad tissue into a homogeneous granular ma
ss resembling cheese, and by the absence
of both architectural and cellular detail.

24. Caseous Necrosis

25. Etiology
• Caseous necrosis is encountered principa
lly with;
1. Tuberculosis in animals
2. Caseous lymphadenitis in sheep

26. Pathogenesis
• It is mainly developed by;
1. Locally acting toxins of specific microorg
anisms.
2. Release of enzyme from the defensive ce
lls (leukocytes)

27. Gross appearance
1. Area of necrosis is granular amorphous material
resembling cheese.
2. Mass is dry but creamy in consistency.
3. Mass is soft ,friable and whitish grey in color
4. Deposition of calcium salts (dystrophic calcificati
on) in dead tissues.
5. The caseous mass is enclosed within a connectiv
e tissue capsule.
6. An older lesion(Chronic) as compared to coagula
tive necrosis, often associated with poorly degra
dable lipids of bacterial origin.

28. Microscopic appearance
1. The cells are not totally liquefied not their outli
ne is preserved.
2. Neither architectural nor cellular detail is prese
rved.
3. Calcification occurs in necrotic areas in sheep a
nd cattle.
4. Delayed degradation of bacterial cell wall; lead
s to development of caseous lesions
5. The caseous necrosis is enclosed within a gran
ulomatous inflammatory wall (encapsulation )

29. Fat necrosis
• It is the death of adipose tissue within th
e living individuals.
• There are three types of fat necrosis.
1. Pancreatic fat necrosis
2. Traumatic fat necrosis
3. Nutritional fat necrosis

30. Pancreatic fat necrosis
• It is the death of adipose tissues in the vic
inity of the pancrease due to action of lipa
ses.

31. Gross appearance
• Necrotic fat appears as white or yellowish
white chalky or opaque.
• A zone of acute or chronic inflamation app
ear around the necrotic area.
• Connective tissues may undergo metaplasi
a and produce bone.

32. Microscopic appearance
• Necrotic tissue takes the form of foci of sh
adow outlines of necrotic fat cells surroun
ded by an inflammatory reaction .
• The grossly visible chalky white areas, app
ear as amorphous,granular,basophilic dep
osits.

33. Traumatic fat necrosis
• It is the death of adipose tissues in an are
a of mechanical injury.
• Etiology ;
it commonly occurs in subcutaneous adip
ose tissue due to mechanical injuries recei
ved during working, fighting or exercising.

34. Gross appearance
• Necrotic fat appears as firm,opaque,chalky
mass in area of injury.
• A zone of acute or chronic inflamatory rea
ction surrounds necrotic area.

35. Nutritional fat necrosis
• It is the death of adipose tissue due to nutritio
nal deficiency.
• Etiology
• It occurs in;
1. Starving or debilitated animals (animals sufferi
ng from tuberculosis and Johne’s disease).
2. Necrosis may occur throughout the body fat bu
t is most common in abdominal fat (mesenteric
, omental and peritoneal)

36. Gross appearance
• The fat is opaque ,chalky ,white or unusua
lly firm.
• Calcification may occur.

37. Microscopic appearance
• Adipose cells contain a pale pink and slight
ly granular material in which numerous cle
fts and crystals are seen.
• When calcification occurs ,the small spheri
cal masses take blue stain with hematoxyli
n.
• A chronic inflammatory reaction occurs at
the junction of necrotic and living tissues.

38. Outcome of necrosis
When necrotic area is small---liquefaction
and removed by neutrophils, lymph and bl
ood
When necrotic area is large ---liquefaction
of tissues and formation of cyst.
Invasion of pyogenic bacteria ---liquefacti
on ,abscessation and discharge of necrotic
material.
Invasion of saprophytic bacteria----develo
pment of gangrene.

39. If coagulative and caseous necrosis---enca
psulation without liquefaction.
Necrosis of internal and external body surf
aces---sloughing and desqumation.
Healing by formation of scar tissue.
Atrophy of the organ with loss of its cells
Calcification -----converts the dead tissue i
nto gritty mass.
Regeneration (i.e. formation of new paren
chymal cells replacing the dead cells) may
occur

40. Necrosis vs. Autolysis
• How to differentiate between necrosis and autol
ysis;
• A sharp line of demarcation between necrotic an
d viable tissue by a zone of inflammation.
• Necrotic tissue is pale, soft and friable
• An exception to pale color occurs when blood oo
zes to necrotic tissue by damaged blood vessel i
n adjacent viable tissue as happens in renal infar
cts which is often surrounded by a narrow(1-3m
m) red rim (active hyperemia)