APOPTOSIS

• Necrosis


  Not planned, always inflammatory, always pathological
• Apoptosis


  Programmed cell death, not inflammatory, usually not pathological but can become pathological if out of control
• Types of necrosis


  • Coagulative
  • Liquefactive
  • Caseous
  • Fat
  • Fibrinoid
  • Gangrenous
• Intrinsic pathway of apoptosis

  1. Bax and Bak activate mitochondria to release cytochrome C

  2. Cytochrome C activates caspases, causing cell death

  3. Bcl-2 and Bcl-xL inhibit apoptosis by preventing cytochrome C release
• Extrinsic pathway of apoptosis

  1. Fas ligand or TNF-alpha bind to receptors, activating initiator caspases

  2. Cytotoxic T cells release granzyme B, which perforates membranes and activates caspases
• Coagulative necrosis


  Seen in ischemia, histology shows eosinophilia
• Liquefactive necrosis


  Seen in abscesses, histology shows neutrophilic debris
• Caseous necrosis


  Seen in tuberculosis and fungal infections, histology shows granulomas
• Fat necrosis


  Seen in pancreatitis and breast trauma, histology shows saponification and calcium complexing
• Fibrinoid necrosis


  Seen in vasculitis, histology shows fibrin thickening of vessels
• Gangrenous necrosis


  Seen in distal extremity ulcers, histology shows coagulative and liquefactive changes