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Hypoxic Cell Injury
This Sqadia video states the most important events taking place during cellular reactions. Hypoxic cell injury results from cellular anoxia or hypoxia, which in turn results from various mechanisms, including ischemia (obstruction of arterial blood flow), which is the most common cause of anaemia. Hypoxic cell injury first affects the mitochondria, with resultant decreased oxidative phosphorylation and adenosine triphosphate (ATP) synthesis. Consequences of decreased ATP availability. Cellular swelling, or hydropic change, is characterized by the presence of large vacuoles in the cytoplasm. Swelling of the endoplasmic reticulum is one of the first ultrastructural changes evident in reversible injury. Hypoxic cell injury eventually results in membrane damage to plasma and to lysosomal and other organelle membranes, with loss of membrane phospholipids. Finally, cell death is caused by severe or prolonged injury.
Adaptation to Environmental Stresses
These molecules have a single unpaired electron in the outer orbital. Examples include the activated products of oxygen reduction, such as the superoxide and the hydroxyl (OH) radicals. Oxygen toxicity, such as in the alveolar damage that can cause adult respiratory distress syndrome or as in retrolental fibroplasia (retinopathy of prematurity), an ocular disorder of premature infants that leads to blindness. Intracellular enzymes, such as glutathione peroxidase, catalase, or superoxide dismutase. Exogenous and endogenous antioxidants, such as vitamin A, vitamin C, vitamin E, cysteine, glutathione, selenium, ceruloplasmin, or transferrin. Metaplasia is the replacement of one differentiated tissue by another. Squamous metaplasia is exemplified by the replacement of columnar epithelium at the squamocolumnar junction of the cervix by squamous epithelium. It can also occur in the respiratory epithelium of the bronchus, in the endometrium, and in the pancreatic ducts.
Apoptosis is a pathway of cell death that is induced by a tightly regulated suicide program in which cells destined to die activate enzymes capable of degrading the cells’ own nuclear DNA and nuclear and cytoplasmic proteins. Fragments of the apoptotic cells then break off, giving the appearance that is responsible for the name (apoptosis, “falling off”). Apoptosis occurs normally in many situations and serves to eliminate potentially harmful cells and cells that have outlived their usefulness. It is also a pathologic event when cells are damaged beyond repair, especially when the damage affects the cell’s DNA or proteins; in these situations, the irreparably damaged cell is eliminated.
The term necrosis was first used by morphologists to refer to a series of changes that accompany cell death, largely resulting from the degradative action of enzymes on lethally injured cells. Coagulative necrosis is a form of tissue necrosis in which the component cells are dead, but the basic tissue architecture is preserved for at least several days. Liquefactive necrosis is seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest (“liquefy”) the tissues. Caseous necrosis is encountered most often in foci of tuberculous infection. Fat necrosis, a term that is well fixed in medical parlance, refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. Fibrinoid Necrosis is a special form of necrosis usually seen in immune reactions involving blood vessels.
Reversible Cellular Changes and Abnormalities of Protein Folding
Fatty change is characterized by the accumulation of intracellular parenchymal triglycerides and is observed most frequently in the liver, heart and kidney. For example, in the liver, fatty change may be secondary to alcoholism, diabetes mellitus, malnutrition, obesity, or poisonings. Hyaline change denotes a characteristic (homogeneous, glassy, eosinophilic) appearance in haematoxylin and eosin sections. Disorders of protein folding involve failure of protein structural stabilization or degradation by specialized proteins known as chaperones. Important chaperones include heat shock proteins induced by stress, one of which is ubiquitin, which marks abnormal proteins for degradation. Abnormal protein aggregation, which is characteristic of amyloidosis; a number of neurodegenerative diseases, such as Alzheimer disease, Huntington disease, and Parkinson disease; and perhaps prion diseases, such as "mad cow" disease. Normal protein transport and secretion, which is characteristic of cystic fibrosis and α1-antitrypsin deficiency.