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necrosis[nĕ-kro´sis, ne-kro´sis] (Gr.)
the morphological changes indicative of cell death caused by enzymatic degradation.
aseptic necrosis necrosis without infection or inflammation.
acute tubular necrosis acute renal failure with mild to severe damage or necrosis of tubule cells, usually secondary to either nephrotoxicity, ischemia after major surgery, trauma (see crush syndrome), severe hypovolemia, sepsis, or burns. See also lower nephron nephrosis.
Balser's fatty necrosis gangrenous pancreatitis with omental bursitis and disseminated patches of necrosis of fatty tissues.
bridging necrosis septa of confluent necrosis bridging adjacent central veins of hepatic lobules and portal triads characteristic of subacute hepatic necrosis.
caseous necrosis caseation (def. 2).
central necrosis necrosis affecting the central portion of an affected bone, cell, or lobule of the liver.
cheesy necrosis caseation (def. 2).
coagulation necrosis death of cells, the protoplasm of the cells becoming fixed and opaque by coagulation of the protein elements, the cellular outline persisting for a long time.
colliquative necrosis liquefactive necrosis.
fat necrosis necrosis in which fat is broken down into fatty acids and glycerol, usually occurring in subcutaneous tissue as a result of trauma.
liquefactive necrosis necrosis in which the necrotic material becomes softened and liquefied.
massive hepatic necrosis massive, usually fatal, necrosis of the liver, a rare complication of viral hepatitis (fulminant hepatitis) that may also result from exposure to hepatotoxins or from drug hypersensitivity.
moist necrosis necrosis in which the dead tissue is wet and soft.
postpartum pituitary necrosis see postpartum pituitary necrosis.
selective myocardial cell necrosis myofibrillar degeneration.
subcutaneous fat necrosis of newborn a benign, self-limited disease affecting term newborns and young infants, characterized by circumscribed, indurated, nodular areas of fat necrosis. It is thought to be related to trauma on bony prominences during delivery, hypothermia, asphyxia, or maternal diabetes; it usually resolves spontaneously by 2 to 4 weeks with no scarring. Called also adiponecrosis neonatorum or subcutanea.
a type of necrosis in which the affected cells or tissue are converted into a dry, dull, fairly homogeneous eosinophilic mass without nuclear staining, as a result of the coagulation of protein as occurs in an infarct; microscopically, the necrotic process involves chiefly the cells, and remnants of histologic elements (for example, elastin, collagen, muscle fibers) may be recognizable, as well as "ghosts" of cells and portions of cell membranes; may be caused by heat, ischemia, and other agents that destroy tissue, including enzymes that would continue to alter the devitalized cellular substance.
coagulation necrosisA type of necrosis caused by denaturation of intracellular proteins in response to severe injury—e.g., hypoxia, infection, ischaemia, toxins and trauma.
co·ag·u·la·tion ne·cro·sis(kō-ag'yū-lā'shŭn nĕ-krō'sis)
A type of cell death in which the affected cells or tissue are converted into a dry, dull, homogeneous eosinophilic mass without nuclei, as a result of the coagulation of protein as occurs in an infarct.
1. formation of a clot.
2. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation.
activated coagulation time (ACT)
a test of the intrinsic or common pathway of coagulation, using diatomaceous earth as an activating agent to hasten coagulation of whole blood, the time being measured. More sensitive than Lee-White or capillary tube tests. See also clotting time.
see monopolar electrocoagulation.
the sequence of enzymatic reactions leading to the formation of a blood clot. Each is initiated by the preceding and, in turn, produces the enzyme that catalyzes the next with an amplification of the process as it progresses.
normal CSF does not coagulate. Inflammation of the meninges or contamination of the fluid by blood, possibly during collection, can cause coagulation in a sample.
disseminated intravascular coagulation (DIC)
widespread formation of thromboses in the microcirculation, mainly within the capillaries. It is a secondary complication of a wide variety of disorders all of which activate in some way the intrinsic coagulation sequence. Paradoxically, the intravascular clotting ultimately produces hemorrhage because of rapid consumption of fibrinogen, platelets, prothrombin, and clotting factors V, VIII and X. Because of this pathology, DIC is sometimes called defibrination syndrome or consumption coagulopathy. Called also diffuse intravascular coagulation. Called also consumption coagulopathy, defibrination syndrome, defibrinogenation syndrome.
these systems prevent widescale intravascular coagulation as a result of minor injury. The important systems are c1-inactivator, antithrombin III, alpha1-antitrypsin, α2-macroglobulin, factor XIa inhibitor, lipoprotein factor Xa inhibitor.
see coagulative necrosis.
the coagulation cascade can follow alternative routes depending on the initiating factor. The extrinsic pathway is initiated by tissue thromboplastin (factor III) and involves calcium ions and factor VII. In the intrinsic pathway, factors XII, XI, IX and VIII are activated by exposure to subendothelial collagen or foreign surfaces. Both pathways lead to the activation of factor X and proceed along the common pathway, involving factors V, II, I and XIII, to the formation of a fibrin clot.
see clotting factors.
normal synovial fluid does not clot, but gels on standing (thixotropism). It contains no fibrinogen, nor any of the coagulation factors. Clotting is an indication of damage to the synovial membrane.
are used to determine the integrity of the coagulation pathways, and platelet function. In general, the common tests for the intrinsic or common pathways are the activated partial thromboplastin time (APTT) and activated coagulation time (ACT). One-stage prothrombin time (OSPT) is usually used to evaluate the extrinsic or common pathways, and platelet count, clot retraction, bleeding time and activated coagulation time reflect platelet numbers and function.
see clotting time.
see bipolar electrocoagulation.
pl. necroses [Gr.] the morphological changes indicative of cell death caused by enzymatic degradation.
necrosis without infection or inflammation.
necrosis in which the tissue is soft, dry and cheesy, occurring typically in tuberculosis.
necrosis affecting the central portion of an affected bone, cell or lobule of the liver.
that in which the tissue resembles cottage cheese; most often seen in tuberculosis.
death of cells, the protoplasm of the cells becoming fixed and opaque by coagulation of the protein elements, the cellular outline persisting for a long time.
see liquefactive necrosis (below).
necrosis in which the necrotic material becomes softened and liquefied.
necrosis in which the dead tissue is wet and soft.
hyaline degeneration and necrosis of striated muscle; called also Zenker's degeneration.