Necrosis

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Necrosis

• Dr.
  Farhat C.

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Necrosis

• Sequence of morphological change that follow
• cell death in living tissues
• Irreversible exogenous injury

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• 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 OF CELL
DENATURATION OF 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

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• 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
proteinsblockage.
Myocardial infarction acidophilic, anuclear,
coagulate leads- necrosis Debris which remain
after necrosis fragmentation phagocytosis
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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.
  

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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/AAREA is soft liquefied center containing
  necrotic debris and wall is formed
• M/ECyst Wall Is Formed by proliferative
  capillaries, inflammatory cell and gliosis
  (brain) and proliferating fibroblast in abscess.

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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
• Arsenic album
• Fluoric Acid
• Bacillinum
• Aurum met
• Calc flur
• Merc

• Hepar sulp
• Iod
• Nat sil
• Nit acid
• Phos
• Phos A
• 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, lt 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 lt 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.