TissueandCellularInjury-汕头大学医学院病理学.pptVIP

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. ① Ultrastructural changes Margination or progressive loss of nuclear chromatin Focal rupture of the nuclear membrane Breakdown of the plasmalemma. Development of flocculent densities in mitochondria. ② Changes in the nucleus. Pyknosis: condensation of chromatin of chromatin and shrinkage of the nucleus. Karyorrhexis: fragmentation of the nucleus. Karyolysis: dissolution of the nucleus. ③ 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. ④ 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. ⑤Postmortem change: General of normal tissues occurring dead body, generally distinguished from necrosis by being diffuse and not associated with inflammatory response. ⑥Autolysis: Digestion of cell by enzymes released from lysosome; occurs after cell dies. (3) Types: ① 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. A. Caseous necrosis: Gross features: soft, granular, and friable a cream-cheesy appearance. granular, eosinophilic. LM: architecture completely destroyed.