• Necrosis is a pathologic process that is the consequence of severe injury.
• It is characterized by denaturation of cellular protiens and also by the leakage of contents through the damaged membranes
• And also further it is characterized by local inflammation and moreover by the enzymatic digestion of the lethally injured cell.

Causes :

• Loss of oxygen supply
• Ischemia
• Exposure to microbial toxins
• Burns
• Other forms of physical and chemical injury
• Moreover unusual situations in which the proteases get released out of the cells
• And also Pancreatitis

Features :

• Whenever the damage to the membranes of the cell remains lethal, lysozymes enter the cytoplasm and digest the cell.
• And moreover, the cellular contents also starts getting released to the extracellular space, where they elicit the host immune response.
• Some specific substances that are released from the cells are called Damage associated molecular protiens.
• Examples for damage associated molecular protiens are ATP, Uric acid and also some other molecular substances.
• And thus their release indicates the lethal cell injury.
• Necrosis associated with the leakage of intracellular protiens through the damaged plasma membranes is the basis for blood tests.
• It helps to detect tissue specific cellular injury.
• For example, cardiac muscle cells – during cardiac tissue necrosis, release the cardiac specific protiens.
• The cardiac specific protiens are Troponin-I, Troponin-T and moreover CK-MB.
• Whereas, the bile duct epithelium expresses a specific isoforms of the enzyme.
• And they are the Alkaline phosphatase.
• Most importantly the hepatocytes expresses transaminases.
• Cardiac specific troponins can be detected in the blood as early as 2 hours after the myocardial cell necrosis.
• And therefore the necrosis of any of these cells types leads to release of specific biomarkers of the particular cell line.
• Because of their specificity and sensitivity, serial measurement of cardiac troponins has a central role in the diagnosis and management of the Myocardial infaction.

Morphology :

• Necrotic cells shows increases eosinophilia in H & E stains.
• This eosinophilic appearance is due to the loss of the Cytoplasmic RNA.
• And also leads to the accumulation of the degraded cytoplasmic protiens.
• The necrotic cell may have a homogenous glassy appearance.
• And this is mainly due to the loss of glycogen particles.
• When enzymes have digested the cell’s organelles, the cytoplasm becomes vacuolated.
• And this gives a Moth-eaten appearance.
• Dead cells are replaced by large phospholipid precipitates called the Myelin figures.
• Further these Myelin figures are phagocytosed by other cells of degraded into fatty acids.
• And also these degraded fatty acids gets calcified.
• Nuclears changes that takes place in the necrotic cells are Karyolysis, Pyknosis and also Karyorrhexis.
• Karyolysis – Loss of DNA that leads to loss of basophilia.

Types :

• Coagulative necrosis
• Liquefactive necrosis
• Gangrenous necriosis
• Caseous necrosis
• Fat necrosis and also
• Fibrinoid necrosis

Coagulative type :

• In coagulative necrosis, the architecture of the dead tissue is preserved.
• Injury not only damages the structural protiens but also the functional protiens like the enzymes.
• And hence the proteolysis of the dead cells is also blocked and that results in the intensively eosinophilic cells with indistinct or reddish nuclei that may persist for years or days.
• Ischemia caused by decreased blood supply due to obstruction of the blood vessels results in coagulative necrosis.
• That is except in the central nervous system where it leads to liquefactive necrosis.
• Moreover the localized area of liquefactive necrosis is called Infarct.

 

Liquefactive type :

• In contrast to coagulative necrosis, liquefactive necrosis is characterized by the digestion of dead cells .
• It results in the transformation of the tissue into a viscous liquid.
• Moreover it is bacterial and also fungal infections.
• The necrotic tissues are more often creamy yellow because of the presence of leukocytes and is called the pus.
• And also the necrosis taking place in the central nervous system often manifests as Liquefactive necrosis.

 

Gangrenous type:

• Gangrenous necrosis is not a specific pattern of cell death.
• It takes place usually in the lower extermities.
• When bacterial infection is superimposed, there is more liquefactive necrosis.
• Moreover it is because of degradative enzymes in the bacteria and attracted leukocytes – Wet gangrene.

Caseous type :

• Most encountered often in the foci of tuberculosis infection.
• The term caseous is derived from the friable white appearance of the area of necrosis.
• On microscopic examination, the necrotic area appears as a structureless collection of fragmented or lysed cells.
• And moreover the amorphous granular debris is enclosed within a distinctive inflammatory border.
• This appearance is the characteristic of a focus of inflammation known as a Granuloma.

 

Fat necrosis :

• Fat necrosis refers to the destruction of fat in the particular focal.
• It typically results due to the release of pancreatic lipases into the substance of the pancreas and the peritoneal cavity.
• Moreover this condition occurs in the emergency condition called Acute pancreatitis.
• In this disorder, pancreatic enzymes leak out of the damaged acinar cells.
• These liquify the membranes of fat cells in the peritoneum,
• This leads to release of triglyceride esters that are split by the pancreatic lipases.
• Fatty acids generated combines with the calcium to produce grossly visible chalky-white areas (fat saponification).
• It enables the surgeon and pathologist to identify the underlying disorder.
• Histologic examnination reveals necrotic areas that contains the shadowy outlines of necrotic fat cells, basophilic calcium deposits and also an inflammatory reaction.

 

Fibrinoid type :

• Fibrinoid necrosis is a special form of vascular damage.
• It is usually seen in the immune reactions involving the blood vessels.
• It typically occurs when complexes of antigens and also antibodies are deposited in the walls of the arteries.
• Deposits of these immune complexes together with plasma protiens that has leaked out of vessels – results in a bright pink and amorphous appearance in H & E stains.
• Moreover it is called “Fibrinoid”.