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2. Necrosis Severe damage

Metabolism stop Structure destroy

Function lose

Classification: necrosis & apoptosis

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(1) Definition: Localized death of cell ortissue occurring in the living body.

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Ultrastructural changes

Margination or progressive loss of

nuclear chromatin Focal rupture of the nuclear membrane

Breakdown of the plasmalemma.

Development of flocculent densities inmitochondria.

(2) Cell death is recognized by:

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Changes in the nucleus.

Pyknosis: condensation of chromatin ofchromatin and shrinkage of the nucleus.

Karyorrhexis: fragmentation of the

nucleus.

Karyolysis: dissolution of the nucleus.

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Normal Pyknosis Karyorrhexis Karyolysis

1979)

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Changes in cytoplasm staining

Positive staining with vital dyes such asTrepan blue which reflects abnormalmembrane permeability.

Opacification: denaturation of proteinslead to aggregation with resultantopacification of the cytoplasm.

Eosino0.philia: exposure of basic aminogroups results in increased affinity foracidic dyes such as eosin.

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Biochemical changes

Release of K+ by dead cells.

Release of enzymes into the blood. e. g.increased plasma levels of creatinekinases, lactic dehydrogenase and

aspartate aminotransferase. Release of protein or protein breakdown

products into the blood.

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Postmortem change: General ofnormal tissues occurring dead body,generally distinguished from necrosis by

being diffuse and not associated withinflammatory response.

Autolysis: Digestion of cell byenzymes released from lysosome;occurs after cell dies.

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(3) Types:

Coagulative necrosis:

Gross features: The necrosis area is swollen,firm and pale.

LM: cell detail is lost, but architecturepreserved. The dead cells retain their outlinebut only indistinctly.

This type of necrosis is frequently caused bylack of blood supply and is exemplified well ininfarcts of solid organs, e. g. heart, spleen,

kidney.

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Coagulative necrosis of kidney

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Coagulative necrosis of the left ventricular wall

From ROBBINS BASIC PATHOLOGY2003

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A. Caseous necrosis:

Gross features: soft, granular, and

friable a cream-cheesy appearance.granular, eosinophilic.

LM: architecture completely destroyed.

i. e. Tuberculosis, syphilis, somesarcoma.

Special types of coagulative necrosis

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From ROBBINS BASIC PATHOLOGY2003

A tuberculous lung with a large area of caseous necrosis

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a. Dry gangrene:

Conditions: only occurs on the skinsurface following arterial obstruction. It

is particularly liable to affect the limbs,especially the toes.

Character: mummification

Types ofgangrene:

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Dry gangrene

Offered by Prof.Orr

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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.

Types ofgangrene:

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Moist gangrene

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c. Gas gangrene:

Conditions: deep contaminated wounds in

which there is considerable muscle damagedby gas formation bacteria.

Character: swollen obviously, gas bubbles

formation. The infection rapidly spreads andthere is associated severe toxaemia.

Only occasionally in civilian practice but is a

serious complication of war wounds.

Types ofgangrene:

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Liquefactive necrosis:

Soft and liquid grossly. Enzymes digestthe cell and convert it to a formlessproteinaceous mass. Ultimately,discharge of the contents forms a cysticspace. i. e. central nervous system afterischemic injury; abscesses.

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Special type:Fat necrosis:

Grossly: Opaque and chalky

LM: outline of necrotic fat cells filledwith amorphous basophilic material(calcium soaps).

i. e. Digestion of peritoneal fat bypancreatic enzymes in pancreaticinflammation.

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Definition: This is not a truedegeneration but a strongly eosinophilicstain like fibrin.

Location: interstitial collagen and bloodvessels (small artery and arteriole)

Nature: one kind of necrosis.

e. g. in allergic reactive diseases: activerheumatism, polyarteritis nodose.

in non-allergic reactive diseases:malignant hypertension.

Fibrinoid necrosis:

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Fibrinoid change in blood vessel

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(4) Consequences of necrosis

Acute or chronic inflammation

Immunological reactions to subcellular components released by

dead tissue or self-antigens alteredby denaturation.

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lysis and absorption

Isolation and discharge: ulcerationand cavity formation

organization

encapsulation, calcification.