Necrosis.docx

Necrosis AP DR MIE MIE SEIN Learning outcomes: 1. Define necrosis. (C1) 2. Correlate the various types of necrosis with their clinical examples. (C4) a) Coagulative necrosis. b) Liquefactive necrosis. c) Caseous necrosis. d) Fat necrosis. e) Fibrinoid necrosis. 3. Define gangrene and differentiate b...

Necrosis AP DR MIE MIE SEIN Learning outcomes: 1. Define necrosis. (C1) 2. Correlate the various types of necrosis with their clinical examples. (C4) a) Coagulative necrosis. b) Liquefactive necrosis. c) Caseous necrosis. d) Fat necrosis. e) Fibrinoid necrosis. 3. Define gangrene and differentiate between dry gangrene and wet gangrene. (C4) 1. Define necrosis. (C1) Necrosis is a pathologic process that is the consequence of severe injury. 2. Correlate the various types of necrosis with their clinical examples. (C4) a. Coagulative necrosis. Most commonly seen in hypoxic death of all tissues except the brain i.e.- kidney, heart and adrenal glands. Pathogenesis: The injury denatures structural proteins and enzymes- - blocking the cellular proteolysis- - preservation of basic structural outline. Ultimately, necrotic cells are removed by fragmentation and phagocytosis by infiltrating leucocytes. Morphology: Gross: Affected area is pale and firm. Demarcated from uninvolved tissues by rim of hyperemia. Histology: Affected cells are acidophilic, opaque mass with loss of nucleus. Basic cellular outline and tissue architecture are preserved. b. Liquefactive necrosis. Hypoxic death of brain tissue. Focal bacterial/fungal lesions Characterized by digestion of dead cells –transformation of tissue into a liquid viscous mass. Pathogenesis: Microbes stimulate the accumulation of leucocytes and liberation of enzymes from these cells. Morphology: Gross: Affected area is soft, liquid, viscous mass. If associated with acute inflammation, material is creamy yellow due to dead white cells (pus) Histology. Amorphous acidophilic fluid with complete destruction of cells. c. Gangrenous necrosis. Coagulative necrosis modified by liquefactive necrosis caused by bacteria and the attracted leucocytes. Dry gangrene - coagulative necrosis is predominant. Wet gangrene - liquefactive necrosis is predominant. Sites: lower leg, appendix, intestine. d. Caseous necrosis. Seen in foci of tuberculous infection. Pathogenesis: Result from hypersensitivity reaction to the lipopolysaccharide present in the cell wall of tubercle bacilli. Morphology: Gross: affected area appears soft, friable white cheesy material. Histology: pink amorphous granular debris enclosed within granulomatous reaction. (soft tubercle) e. Fat necrosis. Focal area of fat destruction seen in acute haemorrhagic pancreatitis. Pathogenesis: Resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. Pancreatic enzymes leak out of acinar cells and liquefy the membrane of fat cells in the peritoneum Lipases split the triglyceride esters combined within fat cells. The fatty acids combine with calcium to produce visible chalky white areas. (fat saponification) Morphology: Gross: Variegated appearance. Gray white necrotic area in the pancreas. Black haemorrhage areas. Amorphous opaque chalky white deposits in the pancreas. Fat globules floating in the ascitic fluid. (Chicken broth) Histology: Amorphous granular deposits on the shadowy outline of necrotic fat cells surrounded by inflammatory reaction. Areas of haemorrhage. Eosinophilic necrotic areas in pancreatic acini. e2. Traumatic fat necrosis Due to trauma to superficial adipose tissue. (Breast) Gross: Early: sharply localized lesion. Late: ill defined indurations. Histology: Focal area of necrotic fat cells surrounded by neutrophils and lipid filled macrophages. enclosed by fibrous tissue and mononuclear inflammatory cells. f. Fibrinoid necrosis. Special form of necrosis usually seen in immune reaction involving blood vessels. (Immunologically mediated vasculitis) Pathogenesis: Complexes of antigens and antibodies are deposited in the wall of arteries. Immune complexes together with fibrin leaked out of vessels. Histology: Bright pink and amorphous (fibrinoid) appearances in H&E stains. 3. Define gangrene and differentiate between dry gangrene and wet gangrene. Features. Dry gangrene. Wet gangrene. Cause. Mainly arterial occlusion (coagulative necrosis) More in venous occlusion followed by secondary bacterial infection (liquefactive necrosis. Distribution. Limbs. Limbs and bowel. Gross appearances. Organ is dry, shrunken and black. Moist, soft, swollen. Line of demarcation. Present at junction between healthy and gangrenous parts. Not clear. Putrefaction. Limited. Marked. Presence of bacteria. Absent, little or no septicaemia. Overwhelming septicaemia present.