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Necrosis:

Necrosis is the cellular death in living cell or tissue and is characterized by swelling, denaturation and coagulation of proteins, breakdown of cellular organelles and cell rupture.

Necrosis is mainly caused by extra-cellular enzymes, liberated from inflammatory cells.

Presence of inflammatory cells around the necrotic area differentiates infarct from autolysis.

Cytoplasmic changes :

The cytoplasm shows a decrease in basophilia ( indicating a loss of RNA protein) and an increased infinity for acid dyes such as eosin. This increased eosinophilia is due to denaturation of some of the cytoplasmic proteins with exposure of basic groups which bind the eosin. When appropriate special stains such as the periodic acid-Sciff method are used, loss of glycogen is noted and there may be some fragmentation and clumping of the cytoplasmic contents.

Nuclear changes :

- Karyolysis - There is a gradual fading away of the basophilic nuclear material, presumably due to action of DNAses.

- Karyorrhexis - There is fragmentation of nucleus and the debris is either phagocytosed by other cells or just disappears.

- Pyknosis - There is condensation of nucleus into a deep basophilic mass. This stage is often followed by karyorrhexis.

1. Coagulation (Coagulative) necrosis:

It is the most common pattern of necrosis. It is characterized by denaturation of cytoplasmic proteins with preservation of the framework of the coagulated cell.  Necrosed area becomes dry, homogeneous and opaque. Example: Infarct kidney, heart. Normal architectural pattern is preserved but the cellular detail is lost.

2. Caseative (Caseous) necrosis:

Cellular death with complete loss of architectural pattern. Necrotic area is dry, cheesy and friable.  Example: Tuberculosis.

3. Liquefaction necrosis:

Occurs when autolysis and heterolysis prevail over protein denaturation. The necrotic area is soft and filled with fluid with obliteration of normal architecture. This type of necrosis is most frequently seen in localized bacterial infection (abscesses) and in the brain.

4. Fat necrosis:

  - Traumatic fat necrosis - mostly seen in female breast. Rupture of adipocytes causes release of fat with lipolysis releasing fatty acids and glycerol.                                                                                                                    Microscopically, there is fatty acid crystals, lipid filled macrophages and foreign-body giant cells.

Fat necrosis is also seen in subcutaneous fat - Example: thigh, abdomen etc.

  - Pancreatic fat necrosis - In acute hemorrhagic pancreatitis ( Pancreatitis ; Acute Pancreatitis ) there is liberation of pancreatic lipase, which acts on the adipose tissue liberating glycerol and fatty acids. Glycerol combines with calcium forming soap, which appear as small, opaque and intensely white patches on adipose tissues of pancreas, omentum and other areas of peritoneum.

5. Fibrinoid necrosis:

Necrotic area becomes homogeneous and eosinophilic and involves mainly the small blood vessels in Immune-complex-vasculitis and  Malignant hypertension.

                  

 

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