coagulation necrosis

necrosis /ne·cro·sis/ (nĕ-kro´sis) pl. necro´ses   [Gr.] the morphological changes indicative of cell death caused by progressive enzymatic degradation; it may affect groups of cells or part of a structure or an organ.

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aseptic necrosis  necrosis without infection, usually in the head of the femur after traumatic hip dislocation.

Balser's fatty necrosis  gangrenous pancreatitis with omental bursitis and disseminated patches of necrosis of fatty tissues.

caseous necrosis  cheesy n.

central necrosis  that affecting the central portion of an affected bone, cell, or lobule of the liver.

cheesy necrosis  that in which the tissue is soft, dry, and cottage cheese–like; most often seen in tuberculosis and syphilis.

coagulation necrosis  necrosis of a portion of some organ or tissue, with formation of fibrous infarcts, 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  that in which the necrotic material becomes softened and liquefied.

contraction band necrosis  a cardiac lesion characterized by hypercontracted myofibrils and contraction bands and mitochondrial damage, caused by calcium influx into dying cells resulting in arrest of the cells in the contracted state.

fat necrosis  that in which the neutral fats in adipose tissue are split into fatty acids and glycerol, usually affecting the pancreas and peripancreatic fat in acute hemorrhagic pancreatitis.

liquefaction necrosis  colliquative n.

phosphorus necrosis  necrosis of the jaw bone due to exposure to phosphorus.

postpartum pituitary necrosis  necrosis of the pituitary during the postpartum period, often associated with shock and excessive uterine bleeding during delivery, and leading to variable patterns of hypopituitarism.

subcutaneous fat necrosis  induration of the subcutaneous fat in newborn and young infants.

necrosis ustilagi´nea  dry gangrene due to ergotism.

Zenker's necrosis  see under degeneration.

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coagulation necrosis

n.

Necrosis in which the affected cells or tissue are converted into a dry, dull, fairly homogeneous eosinophilic mass as a result of the coagulation of protein.

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coagulation necrosis,

necrosis in which tissue becomes a dry, opaque, eosinophilic mass containing outlines of anucleated cells. It results from the denaturation of proteins following hypoxic injury, such as that caused by ischemia in infarction. Also called avascular necrosis, ischemic necrosis.

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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.

Zenker's necrosis hyaline degeneration and necrosis of striated muscle; called also Zenker's degeneration.

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coagulation

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.

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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.

biterminal coagulation

see monopolar electrocoagulation.

coagulation cascade

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.

cerebrospinal coagulation

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.

coagulation defects

see coagulopathy.

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.

coagulation factors

see clotting factors. platelet factors also play a role in coagulation. They are designated by Arabic numerals from 1 to 4.

coagulation inhibitors

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.

coagulation necrosis

see coagulative necrosis.

coagulation pathways

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.

coagulation proteins

see clotting factors.

synovial coagulation

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.

coagulation tests

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.

coagulation time

see clotting time.

unipolar coagulation

see bipolar electrocoagulation.

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necrosis

pl. necroses [Gr.] the morphological changes indicative of cell death caused by enzymatic degradation.

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aseptic necrosis

necrosis without infection or inflammation.

caseous necrosis

necrosis in which the tissue is soft, dry and cheesy, occurring typically in tuberculosis.

central necrosis

necrosis affecting the central portion of an affected bone, cell or lobule of the liver.

cheesy necrosis

that in which the tissue resembles cottage cheese; most often seen in tuberculosis.

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

see liquefactive necrosis (below).

liquefactive necrosis

necrosis in which the necrotic material becomes softened and liquefied.

moist necrosis

necrosis in which the dead tissue is wet and soft.

Zenker's necrosis

hyaline degeneration and necrosis of striated muscle; called also Zenker's degeneration.