Necrosis Pathology PDF

## Necrosis - Morphological changes indicative of cell death in a living tissue following harmful injury. - **Necrosis** is an "accidental" and unregulated form of cell death. - It results from damage to cell membranes and loss of ion homeostasis. - Necrotic cells cannot maintain integrity of memb...

## Necrosis - Morphological changes indicative of cell death in a living tissue following harmful injury. - **Necrosis** is an "accidental" and unregulated form of cell death. - It results from damage to cell membranes and loss of ion homeostasis. - Necrotic cells cannot maintain integrity of membrane and their contents leak out. - This brings out acute inflammatory reaction in surrounding tissue. ### Patterns/Types of Tissue Necrosis *** * **Coagulative Necrosis** - Common type, outline of dead tissues is preserved (at least for few days). - Infarct is a localized area of coagulative necrosis. - **Causes**: Ischemia caused by obstruction in a vessel. - **Mechanism**: Ischemia denatures and coagulates structural proteins and enzyme - **Gross**: - **Organs affected**: All organs except brain. - More frequent in heart, kidney, spleen Limb (dry gangrene). - **Appearance**: Involved region appear dry, pale, yellow and firm. - It is wedge-shaped in organs like kidney and spleen. - **Microscopy**: - Indistinct outline of dead tissue. - Nucleus may be either absent or show karyolysis. * **Liquefactive Necrosis (Colliquative Necrosis)** - Dead cells are transformed into a liquid viscous mass due to enzymes released from leukocytes accumulated at site of necrosis. - Dead tissue rapidly undergoes softening and transforms into a liquid viscous mass. - **Causes**: - Ischemic injury to central nervous system (CNS) - Suppurative infections: Infections by bacteria which stimulate accumulation of leukocytes. - **Mechanism**: Liquefaction is due to digestive action of hydrolytic enzymes released from dead cells (autolysis) and leukocytes (heterolysis). - **Gross**: - **Organs affected are**: Brain: Necrotic area is soft and center show liquefaction. - **Abscess anywhere**: Localized collection of pus. - **Microscopy**: - Pus consists of liquefied necrotic cell debris, dead leukocytes and macrophages (scavenger cells) * **Caseous Necrosis** - Distinctive type of necrosis which shows combined features of both coagulative and liquefactive necrosis. - **Cause**: Characteristic of tuberculosis and is due to hypersensitivity reaction. - **Gross**: - **Organs affected**: Tuberculosis may involve any organ, most common in lung and lymph node. - **Appearance**: Necrotic area appears yellowish-white, soft, granular and resembles dry, clumpy cheese, hence the name caseous (cheese-like) necrosis - **Microscopy**: - Focal lesion of tuberculosis is a granuloma which may be caseating (soft granuloma) or noncaseating (hard granuloma). - Caseous necrosis appears as eosinophilic, coarsely granular material. - It is surrounded by epithelioid cells → Langhans type giant cells (nuclei arranged in a horseshoe pattern), lymphocytes and fibroblasts. - Caseous necrotic material may undergo dystrophic calcification. * **Fat Necrosis** - It refers to focal areas of fat destruction which affects adipose tissue - **Types**: * **Enzymatic Fat Necrosis**: - Occurs in adipose tissue around acutely inflamed pancreas (in acute pancreatitis). - **Mechanism**: - In pancreatitis, enzymes (one of them is lipase) leak from acinar cells and causes tissue damage. - Lipase destroys fat cells and liberates free fatty acids which combine with calcium and form calcium soaps (fat saponification). - **Gross**: Appears as chalky-white areas - **Microscopy**: Necrotic fat cells appear pale with shadowy outlines surrounded by an inflammatory reaction. * **Traumatic Fat Necrosis**: - Occurs in tissues with high fat content (like in breast and thigh) following severe trauma. * **Fibrinoid Necrosis** - Characterized by deposition of pink-staining (fibrin-like) proteinaceous material in tissue matrix with a staining pattern reminiscent of fibrin - It obscures → underlying cellular detail. - **Causes**: Usually seen in immune-mediated (deposition of antigen-antibody complexes in the wall of vessels) vascular injury/vasculitis (e.g. polyarteritis nodosa), malignant hypertension, Aschoff bodies in rheumatic heart disease, placenta in preeclampsia, or hyperacute transplant rejection.