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Necrosis:
Necrosis is the
cellular death
in living
cell or
tissue
and is characterized by swelling, denaturation and coagulation of
proteins, breakdown of cellular organelles and cell rupture.
Necrosis is
mainly caused by
extra-cellular enzymes, liberated from inflammatory cells.
Presence of inflammatory cells around the
necrotic area differentiates infarct from autolysis.
Cytoplasmic changes :
The cytoplasm shows a decrease
in basophilia ( indicating a loss of RNA protein) and an increased
infinity for acid dyes such as eosin. This increased eosinophilia is due
to denaturation of some of the cytoplasmic proteins with exposure of
basic groups which bind the eosin. When appropriate special stains such
as the periodic acid-Sciff method are used, loss of glycogen is noted
and there may be some fragmentation and clumping of the cytoplasmic
contents.
Nuclear changes :
-
Karyolysis
- There is a gradual fading away of the basophilic
nuclear material, presumably due to action of DNAses.
-
Karyorrhexis
- There is fragmentation of nucleus and the debris is either
phagocytosed by other cells or just disappears.
-
Pyknosis
- There is condensation of nucleus into a deep basophilic mass. This
stage is often followed by karyorrhexis.
1.
Coagulation
(Coagulative)
necrosis:
It is the most common pattern
of necrosis. It is characterized by denaturation of cytoplasmic proteins
with preservation of the framework of the coagulated cell.
Necrosed area becomes dry, homogeneous and opaque. Example: Infarct
kidney, heart.
Normal
architectural pattern is preserved but the cellular detail is lost.
2.
Caseative (Caseous)
necrosis:
Cellular death
with
complete
loss of architectural pattern.
Necrotic area is dry, cheesy and friable. Example: Tuberculosis.
3.
Liquefaction necrosis:
Occurs when autolysis and heterolysis prevail over
protein denaturation. The necrotic area is soft and filled with fluid
with obliteration of normal architecture. This type of necrosis is most
frequently seen in localized bacterial infection (abscesses) and in the
brain.
4.
Fat necrosis:
-
Traumatic fat necrosis
- mostly seen in female breast. Rupture of adipocytes causes release of
fat with lipolysis releasing fatty acids and glycerol.
Microscopically, there is fatty acid crystals, lipid filled macrophages
and foreign-body giant cells.
Fat necrosis is also seen in subcutaneous
fat -
Example:
thigh, abdomen etc.
-
Pancreatic fat necrosis
- In acute hemorrhagic pancreatitis (
Pancreatitis
;
Acute Pancreatitis
)
there is liberation of pancreatic
lipase, which acts on the adipose tissue liberating glycerol and fatty
acids. Glycerol combines with calcium forming soap, which appear as
small, opaque and intensely white patches on adipose tissues of
pancreas, omentum and other areas of peritoneum.
5.
Fibrinoid necrosis:
Necrotic area becomes homogeneous and
eosinophilic and involves mainly the small blood vessels in
Immune-complex-vasculitis and Malignant hypertension.

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