Transcript Tissue and Cellular Injury

2. Necrosis
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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:
① Ultrastructural changes
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Margination or progressive
nuclear chromatin
loss
of
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Focal rupture of the nuclear membrane
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Breakdown of the plasmalemma.
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Development of flocculent densities in
mitochondria.
② Changes in the nucleus.
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Pyknosis: condensation of chromatin of
chromatin and shrinkage of the nucleus.
Karyorrhexis:
nucleus.
fragmentation
of
the
Karyolysis: dissolution of the nucleus.
Normal
Pyknosis
Karyorrhexis
（参照武忠弼 病理学规划教材第一版 人民卫生出版社1979，修改)
Karyolysis
③ Changes in cytoplasm staining
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Positive staining with vital dyes such as
Trepan blue which reflects abnormal
membrane permeability.
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Opacification: denaturation of proteins
lead to aggregation with resultant
opacification of the cytoplasm.
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Eosino0.philia: exposure of basic amino
groups results in increased affinity for
acidic dyes such as eosin.
④ Biochemical changes
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Release of K+ by dead cells.
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Release of enzymes into the blood. e. g.
increased plasma levels of creatine
kinases, lactic dehydrogenase and
aspartate aminotransferase.
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Release of protein or protein breakdown
products into the blood.
⑤ Postmortem change: General of
normal tissues occurring dead body,
generally distinguished from necrosis by
being diffuse and not associated with
inflammatory response.
⑥Autolysis: Digestion of cell by
enzymes released from lysosome;
occurs after cell dies.
(3) Types:
① 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 necrosis
B. Gangrene
Definition:
necrosis of big tissue with
superadded putrefaction, black, fou-smelling
appearance.
Necrosis of big tissue
putrefactive
black, green
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.
② 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.
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Fibrinoid change in blood vessel
(4) Consequences of necrosis
① Acute or chronic inflammation
② Immunological reactions to sub
cellular components released by
dead tissue or self-antigens altered
by denaturation.
③ lysis and absorption
④ Isolation and discharge: ulceration
and cavity formation
⑤ organization
⑥ encapsulation, calcification.