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  1. The necrotic cells show increased eosinophilia and cell have more glassy appearance as a result of loss of glycogen particles.
  2. The cytoplasm become vacuolated and appears moth – eaten.Q
  3. Finally calcification may appear.
  4. Nuclear changes are seen as –
    1. Pyknosis                        
    2. Karyorrhexis                    
    3. Karyolysis
Morphological types of necrosis
  1. Coagulative Necrosis
    It implies the preservation of the basic outline of the coagulated cell for a span of some time.
    The affected tissue exhibit a firm texture.
    1. Most common form of necrosisQ   Due to denaturing by hydrolytic enzymes
    2. Micro Loss of nucleus but cellular outline is preserved
    3. Common in organs like HeartQ, liver, KidneyQ
    4. The process of coagulative necrosis with preservation of the general tissue architecture, and it is characterstic of hypoxic death of cells in all the tissues except the brain. Q
  2. Liquefactive Necrosis
  1. It is characterstic of focal bacterial or occasionally fungal infections.
  2. These agents constitute powerful stimuli to the accumulation of inflammatory cells.
  3. It completely digests the dead cells.
  4. The end result is the formation of liquid viscous mass; occurs in brain. Q
  1. Caseous necrosis
  1. Combination of caseous and coagulative necrosis
  2. Gross-friable, soft and Cottage - cheese like appearance
  3. Characteristic feature of tuberculosis Q
  4. Unlike coagulative necrosis, the tissue architecture is completely obliterated Q.
  1. Fat necrosis
  1. Caused by action of Lipases on fatty tissue
  2. Grossly: Chalky white in appearance
  3. Seen in breast and pancreas Q
  1. Fibrinoid Necrosis
  1. Fibrinoid necrosis is special form of necrosis usually seen in immune reactions involving blood vessels.
  2. This pattern of necrosis typically occurs when complexes of antigen and antibodies are deposited in the walls of arteries.
  3. Deposits of these "immune complexes", together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H & E stains, called "fibrinoid" (fibrin like) by pathologists.
  4. It is seen in :
    1. Immune complex vasculitis            
    2. Malignant hypertension. 
  5. Deposition of immune complexes, together with fibrin, results in bright pink and amorphous appearance in H & E stain, called fibrinoid (fibrin like). 
  6. Diseases with fibrinoid necrosis.
  1. Malignant hypertension                                                    
  2. SLE                                                              
  3. HBV
  4. PAN                                                                                       
  5. Henoch – Schönlein purpura                 
  6. Near peptic ulcer
  7. Acute rheumatic fever (Aschoff's nodule)                     
  8. SABE                                                           
  9. Malignancy
  10. Rheumatoid arthritis
  1. Gangrenous necrosis                                                                
    1. Gross term used to describe dead tissue
    2. Common sites: lower limbs, GI tract, testes
    3. Dry gangrene: microscopic pattern is coagulative necrosisQ
    4. Wet gangrene: Microscopic pattern is liquefactive necrosisQ
  2. Subcellular Responses to Injury
  1. Autophagy refers to lysosomal digestion of the cell's own components and is contrasted with heterophagy, in which a cell (usually a macrophage) ingests substances from the outside for intracellular destruction.
  2. Autophagy is thought to be a survival mechanism in times of nutrient deprivation, such that the starved cell lives by eating its own contents.
  3. In this process, intracellular organelles and portions of cytosol are first sequestered from the cytoplasm in an autophagic vacuole formed from ribosome-free regions of the rough ER (RER).
  1. Ischemia-Reperfusion Injury (New Concept)
  1. If cells are reversibly injured, the restoration of blood flow can result in cell recovery. However, under certain circumstances, the restoration of blood flow to ischemic but otherwise viable tissues results, paradoxically, in exacerbated and accelerated injury.
  2. As a result, tissues sustain the loss of cells in addition to those that are irreversibly damaged at the end of the ischemic episode.
  3. This so-called ischemia-reperfusion injury is a clinically important process that may contribute significantly to tissue damage in myocardial and cerebral infarctions.Q
  4. New damage may be initiated during reoxygenation by increased generation of ROS from parenchymal and endothelial cells and from infiltrating leukocytes

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