Structural signs that indicate irreversible cell injury and the progression of<unk>  include dense clumping and progressive disruption of genetic material, and disruption to membranes of cells and organelles. Morphological patterns There are six distinctive morphological patterns of<unk> : # Coagulative<unk>  is characterized by the formation of a gelatinous (gel-like) substance in dead tissues in which the architecture of the tissue is maintained, and can be observed by light microscopy. Coagulation occurs as a result of protein denaturation, causing albumin to transform into a firm and opaque state. This pattern of<unk>  is typically seen in hypoxic (low-oxygen) environments, such as infarction. Coagulative<unk>  occurs primarily in tissues such as the kidney, heart and adrenal glands. Severe ischemia most commonly causes<unk>  of this form. # Liquefactive<unk>  (or colliquative<unk> , in contrast to coagulative<unk> , is characterized by the digestion of dead cells to form a viscous liquid mass. This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response. The<unk> otic liquid mass is frequently creamy yellow due to the presence of dead leukocytes and is commonly known as pus. Hypoxic infarcts in the brain presents as this type of<unk> , because the brain contains little connective tissue but high amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their own enzymes. # Gangrenous<unk>  can be considered a type of coagulative<unk>  that resembles mummified tissue. It is characteristic of ischemia of lower limb and the gastrointestinal tracts. If superimposed infection of dead tissues occurs, then liquefactive<unk>  ensues (wet gangrene). # Caseous<unk>  can be considered a combination of coagulative and liquefactive<unk> , typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign substances. The<unk> otic tissue appears as white and friable, like clumped cheese. Dead cells disintegrate but are not completely digested, leaving granular particles. Microscopic examination shows amorphous granular debris enclosed within a distinctive inflammatory border. Some granulomas contain this pattern of<unk> . # Fat<unk>  is specialized<unk>  of fat tissue, resulting from the action of activated lipases on fatty tissues such as the pancreas. In the pancreas it leads to acute pancreatitis, a condition where the pancreatic enzymes leak out into the peritoneal cavity, and liquefy the membrane by splitting the triglyceride esters into fatty acids through fat saponification. Calcium, magnesium or sodium may bind to these lesions to produce a chalky-white substance. The calcium deposits are microscopically distinctive and may be large enough to be visible on radiographic examinations. To the naked eye, calcium deposits appear as gritty white flecks. # Fibrinoid<unk>  is a special form of<unk>  usually caused by immune-mediated vascular damage. It is marked by complexes of antigen and antibodies, referred to as immune complexes deposited within arterial walls together with fibrin. Other clinical classifications of<unk>  # There are also very specific forms of<unk>  such as gangrene (term used in clinical practices for limbs which have suffered severe hypoxia), gummatous<unk>  (due to spirochaetal infections) and hemorrhagic<unk>  (due to the blockage of venous drainage of an organ or tissue). # Some spider bites may lead to<unk> . In the United States, only spider bites from the brown recluse spider (genus Loxosceles) reliably progress to<unk> . In other countries, spiders of the same genus, such as the Chilean recluse in South America, are also known to cause<unk> . Claims that yellow sac spiders and hobo spiders possess<unk> otic venom have not been substantiated. # In blind mole rats (genus Spalax), the process of<unk>  replaces the role of the systematic apoptosis normally used in many organisms. Low oxygen conditions, such as those common in blind mole rats' burrows, usually cause cells to undergo apoptosis. In adaptation to higher tendency of cell death, blind mole rats evolved a mutation in the tumor suppressor protein p53 (which is also used in humans) to prevent cells from undergoing apoptosis. Human cancer patients have similar mutations, and blind mole rats were thought to be more susceptible to cancer because their cells cannot undergo apoptosis. However, after a specific amount of time (within 3 days according to a study conducted at the University of Rochester), the cells in blind mole rats release interferon-beta (which the immune system normally uses to counter viruses) in response to over-proliferation of cells caused by the suppression of apoptosis. In this case, the interferon-beta triggers cells to undergo<unk> , and this mechanism also kills cancer cells in blind mole rats. Because of tumor suppression mechanisms such as this, blind mole rats and other spalacids are resistant to cancer.
Necrosis
Demineralization 
Desquamation
Degeneration 
Tissue expansion
Remyelination
Granulation
Cell death