Necrosis

Introduction:
– Defined as localized area of death of tissue, followed by degeneration of tissue, by hydrolytic enzymes, liberated by dead cells, accomplnied by inflammatory reaction..
– Caused by various agents like hypoxia, chemical agents, physical agents, microbial agents, immunological injury..

Types:
1. Coagulative Necrosis:
– common type.
– focal irreversible injury.
             – mostly by ischaemic necrosis. 
              (sudden cessation of blood flow)
             – rarely bacterial and chemical
                agents.
– organs effected are heart, kidney, spleen.
– Microscopically it is the hallmark for conversion of normal cells into ‘tombstones’. (the cytoplasm and other material disappears but cell wall remains)

2. Liquefaction (colliquative)  Necrosis:
-ischaemic injury or bacterial infection.
-hydrolytic enzymes causes the material to become semi-fluid.

3. Caseous Necrosis:
– shows features of both Coagulative and Liquefaction necrosis.
– found in centers of foci of tuberculous infection.

4. Fat Necrosis:
– usually seen in breast and acute pancreatitis.

5. Fibrenoid Necrosis:
– immunological tissue injury.

Others:
1. Avascular Necrosis:
– of bones….. resulting from ischaemia.
– common condition.
Etiopathogenisis:
     i) common cause:
             – fracture/dislocation.
             – sickle cell disease.
             – corticosteroid administration.
             – radiation therapy.
             – chronic alcoholism.
             – idiopathic.
    ii) mechanism : interruption of blood supply to bones due to – trauma
                                          – compression 
                                          – thromboembolic
                                            obstruction. 

2. Lever cell Necrosis:
i)  Diffused (submassive to massive)
ii) Zonal
         – Centrilobular
         – Midzone
         – Periportal (peripheral)
iii) Focal.

Refrence: Harsh Mohan textbook of Pathology (seventh edition).
            

ThePhoenixRevival

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