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David, Kathlyn Ann C.

Gen path- assignment

august 8,2016

1. Types of necrosis
Necrosis may be coagulative, liquifactive, caseous, fat necrosis, gummatous necrosis or fibrinoid
Coagulative Necrosis
Coagulative necrosis is the commonest type and is ischemic. It may occur in heart, kidney, or adrenal
glands and is firm in texture.
In coagulative necrosis, architecture of dead tissue is preserved for some days. It may occur due to
denaturation of proteins including enzymes.
Ischemia results in coagulative necrosis, except in brain. An infarct is localized area of coagulative
Gross features:
The necrosis area is swollen, firm and pale.
Light Microscopy:
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.
Liquefactive Necrosis
Necrosis of big tissue with super added putrefaction, with black, foul-smelling appearance is known as
liquefactive necrosis (black or green color is due to breakdown of haemoglobin).
In liquefactive necrosis, digestion of dead cells leads to liquid mass (infections & hypoxic death in CNS).
Autolysis predominates resulting in liquified mass. Examples include cerebral infarction and abscess.
Brain cells secrete increased hydrolases. These make neural tissue soft & liquid. Abscess hyrolases from
neutrophils liquefy tissue.
Soft and liquid
Enzymes digest the cell and convert it to a formless proteinaceous mass. Ultimately, discharge of the
contents forms a cystic space
Gangrenous Necrosis
It is the clinical term for ischemic necrosis of lower limb involving multiple tissue planes with super added
bacterial infections.
Necrosis and putrifaction by saprophytes takes place.

Wet gangrene
Coagulative necrosis by ischemia + liquifactive necrosis by superimposed infection.
Conditions: Both arterial and venous obstruction; wet in environment;
Character: wet, swollen, foul-smelling, black or green.
Common in small intestine, appendix, lung, and uterus, also in limbs.
Dry gangrene
Drying of dead tissue associated with peripheral vascular diseases. Necrosis is separated from viable
tissue by line of demarcation.
Conditions: only occurs on the skin surface following arterial obstruction. It is particularly liable to affect
the limbs, especially the toes.
Character: mummification
Gas gangrene
Gas is produced in necrotic tissue by anaerobic bacteria, clostridium perfringes.
Conditions: deep contaminated wounds in which there is considerable muscle damage by gas forming
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.
Caseous Necrosis
It is cheese-like, as in tuberculosis.
Granuloma is formed with central cheesy material rimmed by epitheloid cells & giant cells (foreign body
giant cells/Langhan giant cells). Tuberculosis coagulative necrosis is modified by capsule of
lipopolysaccharide of Tb bacilli.
Gross features: soft, granular, and friable as cream -cheesy appearance.
Light Microscopy: Granular and eosinophilic. Architecture is completely destroyed.
Examples: Tuberculosis, syphilis, some fungal infections.
Fat necrosis
In fat necrosis, there is focal area of fat destruction (pancreatic lipase digest cell membrane & form fatty
acid + calcium white deposits).
Gross: Opaque and chalky
Light Microscopy: outline of necrotic fat cells filled with amorphous basophilic material (calcium soaps).
i.e. digestion of peritoneal fat by pancreatic enzymes in pancreatic inflammation.

Truamatic fat necrosis Foreign body giant cell + foamy histiocytes form calcifications producing hard



Acute pancreatits -released enzymes digest fat

c. Adipose tissue -TG + FFA lead to saponification + calcification.

Fibrinoid necrosis
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.
Examples include:

in allergic reactive diseases: active rheumatism, polyarteritis nodose


in non-allergic reactive diseases: malignant hypertension.

Deposition of immune complexes & fibrin in arterial wall results in fibrinoid necrosis. Arterial wall shows
amorphous pink circumferential necrosis with inflammation.
Haemorrhagic Necrosis
Ischemic tissue necrosis in organs with dual blood supply like, portal & systemic. One patent vascular
channel results in haemorrhagic morphology. Examples include:




Lung is supplied by bronchial & pulmonary artery

2. Tissue repair (primary & secondary)

Wound healing is a natural restorative response to tissue injury. Healing is the interaction of a
complex cascade of cellular events that generates resurfacing, reconstitution, and restoration of the
tensile strength of injured skin.
Healing is a systematic process, traditionally explained in terms of 4 overlapping classic phases:
hemostasis, inflammation, proliferation, and maturation. While platelets play a crucial role in clot formation
during hemostasis, inflammatory cells dbride injured tissue during the inflammatory phase.
Epithelialization, fibroplasia, and angiogenesis occur during the proliferative phase. Meanwhile,
granulation tissue forms and the wound begins to contract. Finally, during the maturation phase, collagen
forms tight cross-links to other collagen and with protein molecules, increasing the tensile strength of the