Necrosis

Dr. Farhat C.

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 Necrosis

“Sequence of morphological change that follow

cell death in living tissues”

Irreversible exogenous injury

 Necrosis is defined as focal death along with
degradation of tissue by hydrolytic enzymes
liberated by cells.
 It is invariably accompanied by inflamatory
reactions.

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 Causes

 Hypoxia
 Chemical and physical agents
 Microbial agents
 Immunological agents

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 Two Essential Changes Cause
Irreversible Cell Injury

ENZYMATIC DIGESTION DENATURATION OF

OF CELL PROTEIN

HYDROLYTIC ENZYMES
AUTOLYSIS
HETEROLYSIS

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 Morphologically App
Increase Eosinophilia
(binding of eosin + denatured
intra cytoplasmic proteins. )
Homogenous appearance
Nuclear changes – non-specific breakdown of DNA
PYKNOSIS
KARYOLYSIS
KARYORRHEXIS
DENATURATION occur as primary pathology in
the coagulative necrosis

dominant enzyme digestion –(liquefaction Necr)

Some other circumstances ---- caseous necrosis

---- fat necrosis

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 Coagulation necrosis

 Causes: ischaemia
bacterial agents
chemical agents
 Commonly affected: heart, kidney, spleen.

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 COAGULATIVE NECROSIS

Preserve basic structural outline ,

injury cause -- acidosis
--denaturation of structural &
enzymatic proteins–
blockage.
Myocardial infarction – acidophilic, anuclear,
coagulate leads- necrosis

Debris which remain after necrosis– fragmentation &

phagocytosis www.similima.com 9
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 Coagulative Necrosis

G/A– Early stage pale firm and later on

yellowish softer and shrunken.

M/E -- tombstones (ie)outline of cell retain but

there cytoplasmic and nuclear details are lost.
 Coagulative necrosis

ischemia and
infarction (loss of
blood supply and
resultant tissue
anoxia) there is a
wedge-shaped pale
area of coagulative
necrosis
(infarction) in the
renal cortex of the
kidney.

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 LIQUEFACTION NECROSIS
 Commonly due to ischemic injury and bacterial
or fungal infection,accumulation of WBC.
 Powerful hydrolytic enzymes
 Brain infarct and abscess
G/A—AREA is soft liquefied center containing
necrotic debris and wall is formed

M/E—Cyst Wall Is Formed by proliferative

capillaries, inflammatory cell and gliosis
(brain) and proliferating fibroblast in abscess.13
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 Caseous necrosis
 Centre of foci of tuberculous infections. Coagulative and
liquefactive.
 G/A – dry cheese like, soft granular, yellowish
 M/E
–Structreless, Eosinophilic, Granular debris,
 Surrounding tissue- characteristic granulomatous

inflammatory reaction
 (histotoxic effect of lipopolysccharides –present in the

capsule of tubercle bacilli)

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 Caseous necrosis
Caseous
necrosis, with
confluent
cheesy tan
granulomas in
the upper
portion of this
lung in a patient
with
tuberculosis.

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gross appearance
of caseous
necrosis in a hilar
lymph node
infected with
tuberculosis. The
node has a cheesy
tan to white
appearance

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 Fat necrosis

 Two location following acute pancreatic

necrosis or truamatic necrosis.
 Liberation of pancreatic lipase
 Hydrolysis of neutral fat in adipose tissue
into glycerol &free fatty acids. Combine to
calcium to form calcium soaps,
(saponification)

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 G/E – yellowish white and firm deposit.
 Formation of calcium soaps – chalky white
appearance.

 M/E– cloudy appearance & surrounded by an

inflammatory reaction , formation of calcium soaps is
identified in section as amorphous, granular,
&basophilic material.

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 Fat necrosis

fat
necrosis
of the
pancreas

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 Fibrinoid necrosis

 deposition of fibrin like material – which stain like

fibrin,
 E.g –immunologic tissue injury, immune complex
vasculitis, arterioles in HTN, peptic ulcer,
 M\e :brightly eosinophilic, hyaline like deposition
in vessels.
 Local haemorrhage.

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 Therapeutics

 Belladonna  Hepar sulp

 Arsenic album  Iod
 Fluoric Acid  Nat sil
 Bacillinum  Nit acid
 Aurum met  Phos
 Calc flur  Phos A
 Merc  Cal

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 BACILLINUM

 Has been employed successfully in the treatment of tuberculosis;

 its good effects seen in the change of the sputum, which becomes decreased and more
aerated and less purulent.
 Many formsof chronic non-tubercular disease are influenced favorably
by Bacillinum, especially when bronchorrhoea and dyspnoea are present. Respiratory
pyorrhoea.
 The patient expectorates less.

 Bacillinum is especially indicated for lungs of old people,

 with chronic catarrhal condition and enfeebled pulmonary circulation, attacks of
suffocation at night with difficult cough.
 Suffocative catarrh. Tubercular meningitis.
 Favors falling off of tartar of teeth. Constant disposition to take cold.

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 Fluoric Acid
 Syphilitic mercurial dyscrasias, abuse of mercury or silica
 CARIES of bones. Necrosis.
 Painful VARICOSE VEINS.
 Felon.
 Rheumatic pains.
 UNCOVERS FEET AT NIGHT IN BED (Med, Puls, Sulph).
 - Abscess. Fistulas.
 - Hard, horny skin and eruptions (Ant-c, Graph). Epithelioma.
 - Bedsores, < warmth.
 - Itching in spots; of orifices.
 - Itching, redness, painfulness of cicatrices which become red
around edges and threaten to become open ulcer.

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 Aurum Met

 Syphilitic and mercurial affections of bones.

 Caries with excessively foetid discharge.
 Pains < night, drive to despair. Extremities.-Pain as from
ulceration in finger tips. Shooting and
 tearing in tips of finger and toes. Ulcerative pain in heels.
 Neuralgic pain in amputated limbs. Offensive sweaty feet.
 Skin.-Itching, generally evenings. Blisters on various parts.
 Intense burning better cold applications.

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