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Serum glucose concentrations

Hyperglycemic hyperosmolar nonketotic syndrome Severe increase in serum glucose concentration without the production of ketones, leading to an increase in serum osmolality and symptoms... [Pg.1568]

Glucosuria (which may be indicative of proximal tubular damage if the serum glucose concentration is within the normal physiological range)... [Pg.266]

Gatifloxacin was well tolerated in patients with non-insu-lin-dependent diabetes mellitus maintained with diet and exercise (432). It had no significant effect on glucose homeostasis, beta cell function, or long-term fasting serum glucose concentrations, but it caused a brief increase in serum insulin concentrations. [Pg.603]

A non-obese 51-year-old man without a history of diabetes mellitus had a serum glucose concentration of 89 mmol/1 and was non-ketotic. Treatment with olanzapine had been started less than 6 months before about 2 months before the event, his blood glucose concentration was 6.0 mmol/1, and 8 days after withdrawal the glucose concentration returned to normal he no longer required insulin nor any other hypoglycemic drug. [Pg.633]

Clinical signs and symptoms of hypoglycemia are reported occasionally most cases are subclinical, but severe cases have been described (SEDA-13, 815). A study of the effect of quinidine on glucose homeostasis in Thai patients with malaria showed a near doubling of plasma insulin concentrations and a corresponding fall in serum glucose concentrations. An additional factor may have been impaired nutritional status and the effects of parenteral quinine in severely ill patients not taking food (SEDA-13, 815 SEDA-14, 240 SEDA-18, 288). [Pg.643]

Apart from the fact that a linear calibration can be performed, bracketing offers excellent precision and accuracy. With the determination of serum cholesterol as an example, Cohen et al. (1980) showed that the replication error on five different serum pools was characterized by a CV of 0.17% with a set-to-set variability of 0.32%. For each serum average, a standard error (considering all causes of variability combined) of 0.16% CV was obtained. The undetected systematic error (bias) in this study was estimated to be smaller than 0.5%, while White et al. (1982), using two different IDMS methods, found serum glucose concentrations to agree within 1%. [Pg.140]

Eventually, the infant s need for hydrocortisone began to decrease so that by the ninth day of life she no longer required steroids, and she maintained serum glucose concentrations above 2.8 mmol/L with a glucose infusion of less than 7 mg/kg per minute. Subsequently, glucose control was no longer difficult, and no further medications were given for this problem. [Pg.108]

FIGURE 9 Effect of (a) concentrations, (b) osmolarity, and (c) medium of chitosan solution on mean serum glucose concentrations after nasal administration of lOIU/kg insulin to rats. Bars represent the standard deviation (SD) of five experiment. (Reproduced from ref. 73 with permission of Elsevier.)... [Pg.611]

In the liver glycogen metabolism is largely regulated by glucose concentrations, which in turn reflect serum glucose concentrations. [Pg.307]

A 28-year-old woman took an overdose of oral salbutamol (100 mg of salbutamol BP solution) (30). She developed diabetic ketoacidosis, with a serum glucose concentration of 17 mmol/1 (308 mg/dl). Diabetic ketoacidosis induced by salbutamol overdose is uncommon in patients without diabetes however, this patient had a family history of diabetes. [Pg.3096]

The CSF normally is clear, with a protein content of less than 50 mg/dL, a glucose concentration of approximately 50% to 66% of the simultaneous peripheral serum glucose concentration, and a pH of approximately 7.4 also, it typically contains fewer than five white blood cells (WBCs) per cubic millimeter, all of which should be lymphocytes (Table 105-1). As meninges become inflamed, the constituency of the CSF will change, and these changes can be used diagnostically as markers of infection. [Pg.1924]

The short- and long-term monitoring plan for the ESKD patient receiving PN or EN needs to be carefuUy tailored. Special attention should be paid to maintenance of fluid and electrolyte homeostasis. This can be achieved via frequent (daily) monitoring of serum electrolyte concentrations (e.g., sodium, potassium, phosphorus, magnesium, and calcium) and fluid balance. Serum glucose concentrations should be followed frequently (four times daily) in the ESKD patient who develops persistent hyperglycemia. [Pg.2642]

Insulin is produced by pancreatic islet beta cells and is released in response to elevated serum glucose concentrations. The principle actions of insulin are presented in Table 10.9. Each of these actions reduces the plasma glucose concentration. [Pg.154]

B. Oral hypoglycemic overdose, when serum glucose concentrations cannot be adequately maintained by intravenous 5% dextrose Infusions and the preferred agent, octreotide, is unavailable or intolerable to the patient (known hypersensitivity). [Pg.434]


See other pages where Serum glucose concentrations is mentioned: [Pg.548]    [Pg.451]    [Pg.166]    [Pg.1505]    [Pg.557]    [Pg.763]    [Pg.598]    [Pg.633]    [Pg.110]    [Pg.117]    [Pg.702]    [Pg.314]    [Pg.548]    [Pg.352]    [Pg.171]    [Pg.1146]    [Pg.2605]    [Pg.175]    [Pg.140]    [Pg.519]    [Pg.939]    [Pg.946]    [Pg.1052]    [Pg.1052]    [Pg.1335]    [Pg.2601]    [Pg.177]    [Pg.112]    [Pg.95]    [Pg.95]    [Pg.449]    [Pg.480]   
See also in sourсe #XX -- [ Pg.171 ]




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