Types of Necrosis
Dry Gangrene
Coagulative necrotic tissue can take on a "MUMMIFIED" appearance Typically seen in limbs
Caseous necrosis
Considered a combination of coagulative and liquefactive necrosis Typically caused by MYCOBACTERIUM (TB) and FUNGI, and occurs most often in foci of tuberculous infections Necrotic tissue takes on a whitish "cheese-like" appearance Dead cells are disintegrated but not completely digested, leaving behind granular, cheese-like particles On microscopy particles appear as structureless collections of lysed cells and amorphous granular debris, enclosed within a distinctive inflammatory border Results in a characteristic focus of inflammation known as a GRANULOMA
Gas Gangrene
Feels like rice krispies - snap crackle pop - subcutaneous __________ Typically seen after amputations
Wet Gangrene
If a bacterial infection is superimposed on this tissue, liquefactive necrosis may develop from the decaying actions of the bacteria and develop this type of gangrene
Gangrenous necrosis
Not a true "pattern" of cell death, but a CLINICAL OBSERVATION Term used in clinical practice to describe additional changes seen in tissue that has lost its blood supply and underwent coagulative necrosis Effected tissue can progress to either dry or wet
Fat necrosis
Occurs with focal areas destruction to fatty tissue Secondary to digestive enzymes or after injury to fatty tissue Commonly seen in the pancreas, abdomen, breasts, and subcutaneous tissue
Pancreatitis
Pancreatic enzymes are released into the parenchyma of the pancreas and the peritoneal cavity Pancreatic enzymes liquefy the membranes of fat cells Released lipases also break down triglycerides into fatty acids Fatty acids that are released combines with calcium to produce grossly visible chalky white areas, a process known as fat saponification
Coagulative necrosis
Pattern typically seen in HYPOXIA related to INFARCTION Characterized by formation of a gel-like substance within necrotic tissue, in which underlying tissue architecture is preserved for several days to weeks Injury not only denatures structural proteins, but also enzymes, which blocks proteolysis of the dead cells Microscopically, dead cells retain their outline and appear as anucleated masses of homogeneous cytoplasm Occurs in all solid organs except the brain, and the affected tissues take on a firm texture
Liquefactive necrosis
Seen in focal BACTERIAL INFECTIONS, and sometimes fungal infections, in which microbes stimulate an acute inflammatory reaction Influx of lysosomal and proteolytic enzymes digest the dead cells, forming a liquefied mass of tissue In bacterial infections the necrotic debris forms a creamy yellow-type material, called "PUS" Also typical of hypoxic brain injury related to infarcts, where there is little connective tissue but high amounts of digestive enzymes and lipids
Fibrinoid necrosis
Typically seen with autoimmune diseases causing immune-mediated vascular damage Ag-Ab complexes deposited in vessel walls combine with fibrin that leaks out of affected blood vessels Complexes adhere to the vessel wall, attracting inflammatory cells and compliment that ultimately causes further tissue damage and necrosis to the vessel wall On histologic examination, the wall of the affected artery shows a circumferential bright pink area (fibrin) of necrosis with protein deposition and inflammation Seen in autoimmune disease like RA, SLE, polyarteritis nodosa