1 / 39

Necrosis: Causes, Morphology, and Types

Learn from Dr. Kiran H.S., Assistant Professor of Pathology, about necrosis - unregulated cell death from damage, morphology, and its various types like coagulative, liquefactive, gangrenous, caseous, fat, and fibrinoid necrosis.

cmcneill
Download Presentation

Necrosis: Causes, Morphology, and Types

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. IRREVERSIBLE CELL INJURY- NECROSIS Dr. Kiran H S AssisstantProffessor Pathology,YMC

  2. OVERVIEW • Definition • Morphology & mechanism • Types of necrosis

  3. Necrosis Definition • Unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis. • Morphological changes of cell death in a living tissue as a result of irreversible injury. • Necrotic cells loose membrane integrity  leakage of cell contents  inflammatory reaction. CELL INJURY

  4. Necrosis • Mechanism:Denaturation of intracellular proteins or enzymatic digestion of lethally injured cell. • Ischemia, exposure to toxins, various infections & trauma. • Autolysis: Enzymatic digestion by cells’ own enzymes stored in lysosomes. • Heterolysis: Enzymatic digestion by enzymes released by inflammatory cells. CELL INJURY

  5. Necrosis Morphology • Cytoplasmic changes. • Nuclear changes. CELL INJURY

  6. Necrosis • Cytoplasmic changes. • Increased eosinophilia: Loss of RNA; bright pink in H/E stain. • Homogenous appearance: Loss of glycogen. • Moth-eaten appearance of cytoplasm: Enzymatic digestion. CELL INJURY

  7. Necrosis • Nuclear changes: • Breakdown of DNA by DNA lysing enzymes. • Three patterns. • Karyolysis: Loss of basophilia; appear pale in H/E. • Pyknosis: Nuclear shrinkage and appear dark (increased basophilia). • Karyorrhexis: Nuclear fragmentation. CELL INJURY

  8. CELL INJURY

  9. CELL INJURY

  10. Necrosis Myelin Figures • End result of cell death. • Laminated structures derived form damaged cell membrane. • Both in reversible and irreversible cell injury; more pronounced in irreversible cell injury. • Intracellular and extracellular. • Phagocytosed or degraded into fatty acids. CELL INJURY

  11. Necrosis Types of Necrosis • Coagulative necrosis. • Liquefactive necrosis. • Gangrenous necrosis. • Caseous necrosis. • Fat necrosis. • Fibrinoid necrosis CELL INJURY

  12. Necrosis 1. Coagulative Necrosis • Intracellular acidosis  denaturation structural and enzymatic proteins  blocking proteolysis  coagulation of cells. • Hypoxic death of all tissues except brain. • Gross: Localized area of coagulative necrosis is called infarct. Affected tissue is firm. • Microscopy: Preservation of basic cell outline. CELL INJURY

  13. CELL INJURY

  14. CELL INJURY

  15. Necrosis 2. Liquefactive Necrosis • Complete digestion of dead cells liquid viscous mass ; creamy yellow pus  abscess. • Bacterial infection, and hypoxic cell death of brain. • Bacterial infection  accumulation of inflammatory cells  release enzymes  cell digestion. • Gross: Affected tissue is soft. • Microscopy: Amorphous debris, no cell outline, inflammatory cells. CELL INJURY

  16. CELL INJURY

  17. Necrosis 3. Gangrenous necrosis • Gross feature of extensive necrosis. • Dry gangrene: Ischemia  loss of blood supply  coagulative necrosis. • Wet gangrene: Superimposed bacterial infection on dry gangrene  degradative enzymes released by bacteria and WBCs  liquefactive necrosis. CELL INJURY

  18. CELL INJURY

  19. CELL INJURY

  20. CELL INJURY

  21. CELL INJURY

  22. CELL INJURY

  23. Necrosis 4. Caseous Necrosis • Type of coagulative necrosis. • Seen in tuberculosis. • Caseous = Cheesy (gross). • Amorphous granular debris of coagulated cells and granulomatous reaction. CELL INJURY

  24. CELL INJURY

  25. CELL INJURY

  26. CELL INJURY

  27. Necrosis 4. Fat Necrosis • Localized area of fat destruction. • Acute pancreatitis and breast trauma. • Acute pancreatitis: Acute inflammation of pancreas  release of activated pancreatic lipase into peritoneum  liquefaction of fat cells  release of fatty acids  combine with calcium. • Gross: Chalky white areas of calcification. • Microscopy: Necrotic fat cells, calcium deposits, inflammatory infiltration. CELL INJURY

  28. CELL INJURY

  29. 5. Fibrinoid necrosis • Special form of necrosis, usually seen in immune reactions involving blood vessels. • Due to antigen antibody complex deposition on the walls of arteries. • Vasculitis syndromes.

More Related