Akademik

diabetes
Either d. insipidus or d. mellitus, diseases having in common the symptom polyuria; when used without qualification, refers to d. mellitus. [G. d., a compass, a siphon, d.]
- adult-onset d. non-insulin-dependent d. mellitus.
- alimentary d. SYN: alimentary glycosuria.
- alloxan d. experimental d. mellitus produced in animals by the administration of alloxan, which damages the insulin-producing islet cells of the pancreas.
- brittle d. d. mellitus in which there are marked fluctuations in blood glucose concentrations that are difficult to control.
- bronze d. d. mellitus associated with hemochromatosis, with iron deposits in the skin, liver, pancreas, and other viscera, often with severe liver damage and glycosuria. SEE ALSO: hemochromatosis. SYN: bronzed d., bronzed disease.
- bronzed d. SYN: bronze d..
- calcinuric d. SYN: hypercalciuria.
- chemical d. SYN: latent d..
- galactose d. SYN: galactosemia.
- gestational d. carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.Gestational d. occurs in 3–6% of all pregnancies, and although it typically resolves after delivery, as many as 60% of women with this disorder eventually develop type 2 d.. D. occurring during pregnancy increases the risk of maternal pyelonephritis and of certain congenital anomalies, and is often associated with polyhydramnios and fetal macrosomia, with resultant dystocia. It is recommended that all pregnant women be screened for gestational d. between the 24th and 28th week of pregnancy by determination of the plasma glucose level 1 hour after a 50 g oral glucose load. A level above 140 mg/dL (7.8 mmol/L) is an indication for a 3-hour glucose tolerance test. Gestational d. can usually be managed by diet alone, but insulin is sometimes required.
- growth-onset d. SYN: insulin-dependent d. mellitus.
- d. innocens obsolete term for renal glycosuria.
- d. insipidus chronic excretion of very large amounts of pale urine of low specific gravity, causing dehydration and extreme thirst; ordinarily results from inadequate output of pituitary antidiuretic hormone; the urine abnormalities may be mimicked as a result of excessive fluid intake, as in psychogenic polydipsia. Several types exist: central, neurohypophyseal, and nephrogenic. Autosomal dominant [MIM*125700, *125800, *192340], X-linked [MIM*304800 and *304900], and even autosomal recessive forms [MIM*222000] have been described. SEE ALSO: nephrogenic d. insipidus.
- insulin-dependent d. mellitus (IDDM) severe d. mellitus, often brittle, usually of abrupt onset during the first two decades of life but can develop at any age; characterized by polydipsia, polyuria, increased appetite, weight loss, low plasma insulin levels, and susceptibility to ketoacidosis; immune-mediated destruction of pancreatic B cells; insulin therapy and dietary regulation are necessary. Term declared obsolete by American D. Association. SYN: growth-onset d., juvenile-onset d., type I d..
- insulinopenic d. any form of d. mellitus resulting from inadequate secretion of insulin.
- d. intermittens d. mellitus in which there are periods of relatively normal carbohydrate metabolism followed by relapses to the previous diabetic state.
- juvenile d. d. mellitus appearing in a child or adolescent; often fatal before the discovery of insulin, usually of abrupt onset during first or second decades of life; characterized by polyuria, polydipsia, weight loss; usually severe, insulin dependent, and prone to periods of ketoacidosis; can be familial, follow a viral infection such as mumps; thought to be due to virus-induced or immune destruction of pancreatic islets. SYN: type I d. mellitus.
- juvenile-onset d. SYN: insulin-dependent d. mellitus.
- ketosis-prone d. type I or juvenile d. mellitus, in which inadequate treatment leads to development of ketoacidosis.
- ketosis-resistant d. type II or adult onset d. mellitus, in which episodes of ketoacidosis rarely occur.
- latent d. a mild form of d. mellitus in which the patient displays no overt symptoms, but displays certain abnormal responses to diagnostic procedures, such as an elevated fasting blood glucose concentration or reduced glucose tolerance. Term declared obsolete by American D. Association. SYN: chemical d..
- lipoatrophic d. SYN: lipoatrophy.
- lipogenous d. d. and obesity combined.
- maturity-onset d. non-insulin-dependent d. mellitus.
- maturity onset d. of youth a relatively mild, non-insulin requiring form of d. mellitus beginning at a younger age than usual.
- d. mellitus (DM) a chronic metabolic disorder in which utilization of carbohydrate is impaired and that of lipid and protein enhanced; it is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma; long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessel s, and increased susceptibility to infection. [L. sweetened with honey] D. mellitus affects at least 16 million Americans, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. About 95% of persons with DM have type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have type 1, in which exogenous insulin is required for long-term survival. In type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acid s from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in d. mellitus is an impairment of glucose tolerance of such a degree as to threaten or impair health. Revised diagnostic criteria for DM were published by the American D. Association in June 1997. All criteria depend on the glucose concentration of venous plasma. The diagnosis is confirmed when any 2 tests performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7.0 mmol/L); 2 hours postprandially (after a 75-g glucose load), or at random, 200 mg/dL (11.1 mmol/L). Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism, obesity, hypertension, and impairment of renal function. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications (retinopathy, neuropathy, and nephropathy). Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in type 1 DM), drugs that stimulate endogenous insulin production (in type 2 DM), or both. Some studies suggest that the risk of cardiovascular disease may be increased in some patients by intensive treatment of DM because of elevation of body weight, blood pressure, triglycerides, and total and low-density cholesterol. Pharmaceutical agents developed during the 1990s have improved control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. See Also insulin resistance; alpha-reductase inhibitor.
- metahypophysial d. 1. d. mellitus caused by large quantities of endogenous or exogenous pituitary growth hormone; 2. term used to designate the irreversible phase of d. mellitus in acromegaly.
- Mosler d. inosituria with excretion of large quantities of water.
- nephrogenic d. insipidus [MIM*304800] d. insipidus due to inability of the kidney tubules to respond to antidiuretic hormone; X-linked inheritance, caused by mutation in the vasopressin V2 receptor gene (AVPR2) on Xq. There is also an autosomal dominant form [MIM*125800], caused by mutation in the aquaphorin 2 gene (AQP2) on 12q. SYN: vasopressin-resistant d..
- non-insulin-dependent d. mellitus (NIDDM) an often mild form of d. mellitus of gradual onset, usually in obese individuals over age 35; absolute plasma insulin levels are normal to high, but relatively low in relation to plasma glucose levels; ketoacidosis is rare, but hyperosmolar coma can occur; responds well to dietary regulation and/or oral hypoglycemic agents, but diabetic complications and degenerative changes can develop. Term declared obsolete by American D. Association.
- pancreatic d. 1. d. mellitus demonstrably dependent upon a pancreatic lesion; 2. d. following removal of the pancreas in an animal.
- phlorizin d. (flo-rid′zin) SYN: phlorizin glycosuria.
- phosphate d. excessive secretion of phosphate in the urine due to a defect in tubular reabsorption; usually part of a more generalized abnormality, such as Fanconi syndrome.
- piqûre d. SYN: puncture d.. [Fr.]
- pregnancy d. subclinical d..
- puncture d. experimental d. produced in animals by puncture of the floor of the fourth ventricle of the brain. SYN: piqûre d..
- renal d. SYN: renal glycosuria.
- starvation d. after prolonged fasting, glycosuria following the ingestion of carbohydrate or glucose because of reduced output of insulin and/or reduced rate of glucose metabolism with a reduced ability to form glycogen.
- steroid d. d. mellitus produced by pharmacological doses of steroid hormones, particularly glucocorticoids or estrogens; characterized by one or more of the typical manifestations of d. mellitus.
- steroidogenic d. abnormal glucose tolerance, often frank d. mellitus, induced by the metabolic effects of adrenocortical steroid hormones such as cortisone or therapeutic analogues such as prednisone. The effect may be temporary, resolving when the steroid therapy is discontinued, or d. mellitus may persist.
- subclinical d. a form of d. mellitus that is clinically evident only under certain circumstances, such as pregnancy or extreme stress; persons so afflicted may, in time, manifest more severe forms of the disease. Term declared obsolete by American D. Association.
- thiazide d. impaired carbohydrate metabolism associated with the use of thiazide diuretic drugs; severe manifestations are seen in persons having d. mellitus, but impairment is mild or absent in nondiabetic individuals.
- type I d. SYN: insulin-dependent d. mellitus.
- type II d. non-insulin-dependent d. mellitus.
- type I d. mellitus SYN: juvenile d..
- vasopressin-resistant d. SYN: nephrogenic d. insipidus.

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di·a·be·tes .dī-ə-'bēt-ēz, -'bēt-əs n, pl diabetes any of various abnormal conditions characterized by the secretion and excretion of excessive amounts of urine esp DIABETES MELLITUS

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n.
any disorder of metabolism causing excessive thirst and the production of large volumes of urine. Used alone, the term most commonly refers to diabetes mellitus. See also diabetes insipidus, haemochromatosis.
diabetic adj. n.

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di·a·be·tes (di″ə-beґtēz) [Gr. diabētēs a siphon, from dia through + bainein to go] 1. any of various disorders characterized by polyuria. 2. d. mellitus.

Medical dictionary. 2011.