2.

Necrosis
Severe damage
Metabolism stop
Structure destroy
Function lose

Classification: necrosis &

apoptosis

(1) Definition: Localized death of

cell or tissue occurring in the living
body.

(2) Cell death is recognized

by:

Ultrastructural changes

Margination or progressive loss of

nuclear chromatin

Focal
rupture
membrane

Breakdown of the plasmalemma.

Development of flocculent densities in

mitochondria.

of

the

nuclear

 Changes in the nucleus.

Pyknosis: condensation of chromatin

of chromatin and shrinkage of the
nucleus.

Karyorrhexis: fragmentation of the

nucleus.

Karyolysis: dissolution of the nucleus.

Normal
Karyolysis

Pyknosis

Karyorrhexis

1979 )

 Changes in cytoplasm staining

Positive staining with vital dyes such as

Trepan blue which reflects abnormal
membrane permeability.

Opacification: denaturation of proteins

lead to aggregation with resultant
opacification of the cytoplasm.

Eosino0.philia: exposure of basic amino

groups results in increased affinity for
acidic dyes such as eosin.

 Biochemical changes

Release of K+ by dead cells.

Release of enzymes into the blood. e.

g. increased plasma levels of
creatine
kinases,
lactic
dehydrogenase
and
aspartate
aminotransferase.

Release of protein or protein

breakdown products into the blood.

Postmortem change: General of

normal tissues occurring dead
body, generally distinguished from
necrosis by being diffuse and not
associated
with
inflammatory
response.
Autolysis: Digestion of cell by
enzymes released from lysosome;
occurs after cell dies.

(3) Types:
Coagulative necrosis:
Gross features: The necrosis area is
swollen, firm and pale.
LM: cell detail is lost, but architecture
preserved. The dead cells retain their
outline but only indistinctly.
This type of necrosis is frequently
caused by lack of blood supply and is
exemplified well in infarcts of solid
organs, e. g. heart, spleen, kidney.

Coagulative necrosis of kidney

Coagulative necrosis of the left ventricular wall

From ROBBINS BASIC PATHOLOGY 2003

Special types of coagulative

necrosis
A. Caseous necrosis:
Gross features: soft, granular, and
friable a cream-cheesy appearance.
granular, eosinophilic.
LM: architecture completely
destroyed.
i. e. Tuberculosis, syphilis, some
sarcoma.

A tuberculous lung with a large area of caseous necrosis

From ROBBINS BASIC PATHOLOGY 2003

Caseous necrosis

Special types of coagulative necro

B. Gangrene
Definition: necrosis of big tissue with
superadded
putrefaction,
black,
fousmelling appearance.
Necrosis of big tissue
green

putrefactive

black,

Or organ or limb
organisms infection
appearance
(black or green due to breakdown of haemoglobin)

Types of gangrene :
a. Dry gangrene:
Conditions: only occurs on the skin
surface
following
arterial
obstruction. It is particularly liable to
affect the limbs, especially the toes.
Character: mummification

Dry gangrene
Offered by Prof.Orr

Types of gangrene :
b. Wet gangrene:
Conditions: Both arterial and venous
obstruction; wet in environment;
Character: wet swollen, foul-smelling,
black or green.
Commonly in small intestine,
appendix, lung, and uterus, also in
limbs.

Moist gangrene

Types of gangrene :
c. Gas gangrene:
Conditions: deep contaminated wounds in
which there is considerable muscle
damaged by gas formation bacteria.
Character: swollen obviously, gas bubbles
formation. The infection rapidly spreads
and there is associated severe toxaemia.
Only occasionally in civilian practice but
is a serious complication of war wounds.

 Liquefactive necrosis:
Soft and liquid grossly. Enzymes
digest the cell and convert it to a
formless proteinaceous mass.
Ultimately, discharge of the
contents forms a cystic space. i. e.
central nervous system after
ischemic injury; abscesses.

Special type:
Fat necrosis:
Grossly: Opaque and chalky
LM: outline of necrotic fat cells
filled with amorphous basophilic
material (calcium soaps).
i. e. Digestion of peritoneal fat by
pancreatic enzymes in pancreatic
inflammation.

 Fibrinoid necrosis:

Definition: This is not a true

degeneration
but
a
strongly
eosinophilic stain like fibrin.
Location: interstitial collagen and
blood vessels (small artery and
arteriole)
Nature: one kind of necrosis.
e. g. in allergic reactive diseases:
active
rheumatism,
polyarteritis
nodose.
in non-allergic reactive diseases:
malignant hypertension.

Fibrinoid change in blood vessel

(4)
Consequences
necrosis

of

Acute or chronic inflammation

Immunological reactions to sub
cellular components released
by dead tissue or self-antigens
altered by denaturation.

 lysis and absorption

Isolation
and
discharge:
ulceration and cavity formation
organization
encapsulation, calcification.