Ans. a (Brain). (Ref. Robbins, Pathologic Basis of Disease, 8th/pg.7-13)NECROSIS# Enzymatic degradation of a cell resulting from exogenous injury.# Characterized by enzymatic digestion and protein denaturation, with release of intracellular components.# Morphologically occurs as coagulative (heart, liver, kidney), liquefactive (brain), caseous (tuberculosis), fat (pancreas), fibrinoid (blood vessels), or gangrenous (limbs, GI tract).# Kidney infarct exhibiting coagulative necrosis will be seen with loss of nuclei and clumping of cytoplasm but with preservation of basic outlines of glomerular and tubular architecture.# Liquefactive necrosis in the kidney can be caused by fungal infection, which will be seen filled with white cells and cellular debris, creating a renal abscess that obliterates the normal architecture.IRREVERSIBLE INJURY AND CELL DEATHMORPHOLOGIC PATTERNCHARACTERSTICSCOAGULATIVE NECROSISMost common type (e.g. Heart, liver, kidney)LIQUEFACTIVE NECROSISAbscesses, brain infarcts, pancreatic necrosisCellular destruction by hydrolytic enzymesCASEOUS NECROSISSeen in tuberculosisCombination of coagulation and liquefaction necrosis soft, friable, and "cottage-cheese-like" appearanceFAT NECROSISCaused by the action of lipases on fatty tissue (e.g. with pancreatic damage)Chalky white appearanceFIBRINOID NECROSISEosinophilic homogenous appearance - resembles fibrinGANGRENOUS NECROSISCommon sites: lower limbs, gallbladder, Gl tract and testesDry gangrene - coagulative necrosisWet gangrene - liquefactive necrosisAPOPTOSISA specialized form of programmed cell death, an active process under genetic control.Executed in mitochondria.Mediated by a cascade of caspases (digest nuclear and cytoskeletal proteins and active endonucleases).