Irreversible injury Severe injury or persistent injury causes irreversible damage. Extensive damage to cell membrane Vacuolisation of mitochondria Reduced capacity to generate ATP Necrosis Morphogical changes are : Nuclear changes and cytoplasmic changes
Nuclear changes: Are pathognomonic of necrosis and are of 3 types: Pyknosis – shrunken,small and hyperchromatic nuclei. Karyorrhexis – pyknotic nucleus breaks up into fragments Karyolysis – with time the nuclear fragments slowly fade and ultimately disappear( enzymatic degradation by endonucleases )
Cytoplasmic changes: Dense pink cytoplasm ( eosinophilic cytoplasm ) Glassy and homogeneous Becomes vacuolated and motheaten in appearance Dead cells may be replaced by large, whorled phospholipid masses called myelin figures
Necrosis Is the result of denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell unable to maintain membrane integrity their contents often leak out , a process that may elicit inflammation in the surrounding tissue.
Coagulative necrosis the architecture of dead tissues is preserved for a span of at least some days the injury denatures enzymes also and so blocks the proteolysis of the dead cells as a result, eosinophilic , anucleate cells may persist for days or weeks E.g Renal infarction, Myocardial infarction Caused by obstruction of blood supply A localized area of coagulative necrosis is called an infarct
Coagulative necrosis
Coagulative necrosis
Coagulative necrosis
Liquefactive necrosis is characterized by digestion of the dead cells, resulting in transformation of the tissue into a liquid viscous mass. No structural detail can be made out The necrotic material is frequently creamy yellow because of the presence of dead leukocytes and is called pus CNS often manifests as liquefactive necrosis E.g., Bacterial, fungal and ischemic injury of CNS
Liquefactive necrosis
Liquefactive necrosis
Gangrenous necrosis not a specific pattern of cell death usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone necrosis (typically coagulative necrosis) involving multiple tissue planes.
Caseous necrosis Most often in foci of tuberculous infection The term “ caseous ” ( cheeselike ) is derived from the friable white appearance of the area of necrosis microscopic examination, the necrotic area appears as a collection of fragmented or lysed cells and amorphous granular debris
Caseous necrosis
Caseous necrosis
Fat necrosis The focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity The fatty acids, so derived, combine with calcium to produce grossly visible chalky-white areas ( fat saponification )
Fat necrosis
Fat necrosis
Fibrinoid necrosis Special form of necrosis usually seen in immune reactions involving blood vessels Deposits of these “immune complexes,” together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “ fibrinoid ” (fibrin-like) by pathologists