2.

Necrosis

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:

Ultrastructural changes

Margination or progressive nuclear chromatin

loss

of

Focal rupture of the nuclear membrane

Breakdown of the plasmalemma.

Development of flocculent densities in mitochondria.

 Changes in the nucleus.

Pyknosis: condensation of chromatin of chromatin and shrinkage of the nucleus. Karyorrhexis: nucleus. fragmentation of the

Karyolysis: dissolution of the nucleus.

Normal

Pyknosis

Karyorrhexis

Karyolysis

1979)

 Changes in cytoplasm staining

Positive staining with vital dyes such as Trepan blue which reflects abnormal membrane permeability. Opacification: denaturation of proteins lead to aggregation with resultant opacification of the cytoplasm.

Eosino0.philia: exposure of basic amino groups results in increased affinity for acidic dyes such as eosin.

 Biochemical changes

Release of K+ by dead cells.

Release of enzymes into the blood. e. g. increased plasma levels of creatine kinases, lactic dehydrogenase and aspartate aminotransferase. Release of protein or protein breakdown products into the blood.

 Postmortem change: General of normal tissues occurring dead body, generally distinguished from necrosis by being diffuse and not associated with inflammatory response. Autolysis: Digestion of cell by enzymes released from lysosome; occurs after cell dies.

(3) Types:
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 PATHOLOGY2003

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 PATHOLOGY2003

Caseous necrosis

Special types of coagulative necrosis B. Gangrene

Definition:
necrosis of big tissue with superadded putrefaction, black, fou-smelling appearance.
putrefactive black, green

Necrosis of big tissue

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.

 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.

Fibrinoid change in blood vessel

(4) Consequences of necrosis

Acute or chronic inflammation Immunological reactions to sub cellular components released by dead tissue or self-antigens altered by denaturation.

 lysis and absorption

Isolation and discharge: ulceration and cavity formation organization

encapsulation, calcification.