Lecture on Necrosis

Introduction to Necrosis

• Necrosis is a pathway of cell death due to irreversible injury.
• Differentiated from apoptosis, which is also a result of irreversible cell injury.

Understanding Necrosis

• Necrosis occurs when a cell is severely damaged and cannot adapt or recover.
• Necrosis involves a series of morphological changes in the cell's cytoplasm, nucleus, and organelles.
• These changes are visible histologically after 4 to 12 hours.
• Key Causes: Trauma, severe ischemia, toxins, radiation.

Mechanisms of Necrosis

• Protein Denaturation: Structural and functional proteins denature, disrupting cell structure and function.
• Enzymatic Digestion: Enzymes digest the cell, leading to morphological changes.
• Loss of Membrane Integrity: Plasma membrane rupture leads to leakage of intracellular contents, causing inflammation.

Differences Between Necrosis and Apoptosis

• Necrosis is always pathological; apoptosis can be physiological or pathological.
• Necrosis involves inflammation, unlike apoptosis.

Cellular Changes in Necrosis

• Cytoplasmic Changes:

  • Increased eosinophilia due to protein denaturation.
  • Loss of glycogen granules, leading to a glassy appearance.
  • Moth-eaten appearance due to organelle digestion.

• Nuclear Changes:

  • Karyolysis: Fading of the nucleus.
  • Pyknosis: Condensation of the nucleus.
  • Karyorrhexis: Fragmentation of the nucleus.

Types of Necrosis

Coagulative Necrosis

• Seen in myocardial infarction.
• Characteristics:
  • Preservation of cellular architecture for days.
  • Denaturation of structural and enzymatic proteins halts autolysis initially.
• Repair: Inflammatory response leads to formation of scar tissue over time.

Liquefactive Necrosis

• Occurs in brain infarctions and abscesses.
• Characteristics:
  • Intense enzymatic digestion leads to tissue liquefaction.
  • Involves pyogenic bacteria, leading to pus formation.

Abscess

• Localized pus in deep tissues or confined spaces.
• Structure:
  • Central core of dead neutrophils and microbes.
  • Active neutrophil zone around the core.
  • Inflammatory response with dilated blood vessels.
  • Peripheral repair attempts by local cells.

Cellular and Molecular Considerations

• Necrotic cells release inflammatory mediators causing surrounding cell injury.
• Auto- vs. Heterolysis:
  • Autolysis: Digestion by cell's own enzymes.
  • Heterolysis: Digestion by enzymes from leucocytes or microbes.

Conclusion

• Necrosis is a complex process with significant implications for tissue inflammation and repair.
• Understanding the progression and characteristics of necrosis is essential for diagnosing and treating various diseases.

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Note: This summary captures the main points of a lecture on necrosis, detailing the process, types, and cellular changes involved.

Extra:

When a cell is irreversibly damaged, either it undergoes necrosis or apoptosis. Necrosis always follows pathological cell injury by toxins, radiations, trauma, hypoxia. Apoptosis may be physiological (during embryogenesis) or pathological. NECROSIS: Necrosis is a series of morphological changes in a lethally and irreversibly injured cell. These changes may be recognized by light microscope only after a few hours. When cell is lethally injured, it cannot produce ATPs. Reserve of ATPs run out. In case of hypoxia, pyruvic acid produced from glucose cannot enter Krebs cycle. So they get converted into lactic acid. So intracellular environment becomes acidic. And structural and functional proteins get denatured. This will translate into morphological changes in cell. There is also enzymatic digestion of severely injured cell.

A.These enzymes are from burst lysosomes.