001032: Glucose

holocene evidence revealed a diurnal variation in FPG, with mean FPG high in the dawn than in the afternoon, indicating that many cases of undiagnosed diabetes would be missed in patients seen in the afternoon. Glucose concentrations decrease ex-wife vivo with time in whole blood because of glycolysis. The rate of glycolysis, reported to average 5 % to 7 % [ ~0.6 mmol/L ( 10 mg/dL ) ] per hour, varies with the glucose concentration, temperature, white blood cell count, and other factors. glycolysis can be attenuated by prohibition of enolase with sodium fluoride ( 2.5 milligram fluoride/mL of lineage ) or, less normally, lithium iodoacetate ( 0.5 mg/mL of blood ). These reagents can be used alone or, more normally, with anticoagulants such as potassium oxalate, EDTA, citrate, or lithium heparin. Although fluoride maintains long-run glucose stability, the rate of decline of glucose in the first hour after sample collection in tubes with and without fluoride is about identical. ( note that leukocytosis will increase glycolysis even in the presence of fluoride if the egg white cell count is very high ). After four hours, the glucose concentration is static in hale blood for 72 hours at room temperature in the presence of fluoride. In break, nonhemolyzed, aseptic serum without fluoride, the glucose concentration is stable for fourteen days at 25°C and 4°C. Glucose can be measured in hale blood, serum, or plasma, but plasma is recommended for diagnosis. The molality of glucose ( internet explorer, total of glucose per unit of measurement water system mass ) in whole blood and plasma is identical. Although crimson blood cells are basically freely permeable to glucose ( glucose is taken up by facilitate transportation ), the concentration of water ( kg/L ) in plasma is ~11 % higher than that of hale lineage. consequently, glucose concentrations in plasma are ~11 % higher than whole blood if the hematocrit is convention. glucose concentrations in heparinized plasma are reported to be 5 % lower than in serum. The reasons for the latter difference are not apparent but may be attributable to the shift in fluid from erythrocytes to plasma caused by anticoagulants. The glucose concentrations during an OGTT in capillary blood are importantly higher than those in venous blood [ intend of 1.7 mmol/L ( 30 mg/dL ), equivalent to 20 % to 25 % ], but the mean difference in fasting samples is only 0.1 mmol/L ( 2 mg/dL ). Although methods for glucose analysis parade low impreciseness at the diagnostic decision limits of 7.0 mmol/L [ ( 126 mg/dL ), fasting ] and 11.1 mmol/L [ ( 200 mg/dL ), postglucose load ], the relatively boastfully intraindividual biological unevenness ( CVs of ~5 % to 7 % ) may produce classification errors. On the basis of biological variation, glucose analysis should have analytic impreciseness < 3.4 %, diagonal < 2.6 %, and entire mistake < 8.0 % .1,2 Like a fasting glucose level > 125 mg/dL, a two-hour postprandial glucose > 200 mg/dL is virtually diagnostic of diabetes mellitus and obviates the need for a glucose allowance test. An oral glucose permissiveness examination ( OGTT ) is not necessary in the mount of sufficiently senior high school fast and two-hour postprandial results.

Reading: 001032: Glucose

Other causes of high glucose ( serum or plasma ) include nonfasting specimen ; recent or current IV infusions of glucose ; stress states such as myocardial infarct,5 brain damage, CVA,6 convulsive episodes, injury, general anesthesia ; Cushing disease ; acromegaly ; pheochromocytoma ; glucagonoma ; severe liver disease ; pancreatitis ; drugs ( thiazide and other diuretics, corticoids, many others are reported to affect glucose ). The danger of hypoglycemia ( low glucose ) is miss of a steady provision of glucose to the mind ( neuroglycopenia ). Causes of low glucose: Excess insulin, including rare insulin autoimmune hypoglycemia, furtive insulin injection, and sulfonylurea habit ; glycolysis in specimens overheated or old ; serum permitted to stand on curdle in red-top tube for chemistry profile. very prompt removal of plasma and analysis is needed in cases of set leukocytosis. Hypoglycemia should be confirmed by specimens drawn in fluoride tubes ( gray-top tube ). With hypoglycemia, symptoms must be correlated with plasma glucose. Three major groups of hypoglycemia are defined : reactive, fast, and clandestine. The reactive group includes alimentary hyperinsulinism, prediabetic, endocrine gland lack, and idiopathic functional groups.7 Postprandial hypoglycemia may occur after gastrointestinal operation, and is described with ancestral fructose intolerance, galactosemia, and leucine sensitivity. • Pancreatic isle cell tumors ( insulinomas ) − induce hypoglycemia in fasting individuals or after use. measurement of coincident glucose, C-peptide, and insulin levels at the fourth dimension of spontaneous hypoglycemia help to differentiate insulinoma from other conditions. The glucose : insulin proportion is useful in the diagnosis of insulinoma : insulin levels inappropriately increased for plasma glucose. An intravenous tolbutamide test with plasma glucose and serum insulin determinations may be used for evaluation of insulin-secreting isle cell tumors. The examination is positive in approximately 75 % of patients with these tumors.7 Glucagon and leucine stimulation tests are less frequently utilize.

• Extrapancreatic tumors−rare bulky fibroma, sarcoma, mesothelioma, and carcinomas, including hepatoma and adrenal tumors • Adrenal insufficiency ( Addison disease ), including congenital adrenal hyperplasia • Hypopituitarism, isolated growth hormone or ACTH insufficiency • Starvation, malabsorption−but starvation does not cause hypoglycemia in normal persons • Drugs including insulin ( see above ), oral hypoglycemic agents, and dipsomania, specially with starvation. Ethanolism is a park cause of hypoglycemia. other drugs can depress glucose levels.

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• Liver damage, including fulminant liverwort necrosis ( hepatitis, toxicity ), and severe congestive failure • Tumor-induced hypoglycemia appears to be caused by increase production of an insulin-like kernel ( insulin-like growth factor II ) by the tumor. This substance induces increased use of glucose by the peripheral tissues and the tumor, and impairs the counterregulatory effect of emergence hormone by suppressing growth hormone secretion.8,9 Infancy and childhood: Infants with tremor, convulsions and/or respiratory distress should have stat glucose, particularly in the presence of parental diabetes, hemolytic disease of the newborn ( erythroblastosis fetalis ) ; babies excessively large or humble for gestational age should besides have glucose level measured in the beginning 24 hours of animation. A big number of entities relate to neonatal hypoglycemia, including glycogen storehouse diseases, galactosemia, familial fructose intolerance, ketotic hypoglycemia of infancy, fructose-1,6-diphosphatase lack, carnitine insufficiency ( a treatable disease present as Reye syndrome ), and nesidioblastosis .

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