Cell Death: Necrosis and Apoptosis
Start with the big picture
Necrosis follows severe cellular injury and involves membrane damage, ATP depletion, calcium influx, and leakage of lysosomal enzymes. Its nuclear changes progress through pyknosis, karyorrhexis, and karyolysis; the resulting inflammation contrasts with the generally non-inflammatory clearance of apoptotic bodies. Necrosis has several morphologic patterns, including coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous forms, each associated with characteristic settings or tissue changes. Apoptosis is regulated and energy-dependent, with cell shrinkage, chromatin condensation, membrane blebs, and apoptotic bodies. Caspases carry out the process through intrinsic mitochondrial and extrinsic receptor-mediated pathways. Physiological and pathological contexts help explain when apoptosis occurs.
What you'll learn
- Distinguish necrosis from apoptosis by mechanism, morphology, and inflammatory response.
- Describe the major cellular and nuclear changes associated with necrosis.
- Relate morphologic patterns of necrosis to their characteristic settings.
- Outline the intrinsic and extrinsic pathways that activate apoptosis.
- Identify physiological and pathological contexts in which apoptosis occurs.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
