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Insulin - continued

Insulin For patients stabilized on insulin, continue the insulin dose upon initiation of rosiglitazone therapy. Dose rosiglitazone at 4 mg daily. Doses greater than 4 mg daily in combination with insulin are not currently indicated. It is recommended that the insulin dose be decreased 10% to 25% if the patient reports hypoglycemia or if fasting plasma glucose concentrations decrease to less than 100 mg/dL. [Pg.326]

Insulin delivery by a pump may be superior to glargine insulin. Continuous subcutaneous insulin infusion was compared with intensive therapy with insulin glargine plus insulin lispro in 19 patients (224). The patients who received insulin glargine were exposed to glucose concentrations under 3.9 mmol/1 overnight for three times as long as those who used continuous subcutaneous insulin infusion. [Pg.407]

Antibodies to inhaled insulin continue to be a concern, although there has been no correlation with antibody titer and insulin dosage or the development of hypoglycemia. Presensitization may be important. Patients with type 2 diabetes who had not used insulin before starting to use inhaled insulin had a lower antibody response, despite the addition of subcutaneous insulin in 32% of participants by the end of the study (278). [Pg.411]

Preprinted order set design Hypokalemia Sliding scale insulin Continuous renal replacement therapy... [Pg.208]

An estimated five million people in North America and 30 million in the world are diabetic. Almost half of these people require repeated, often daily, injections of insulin to maintain approximately normal glucose levels. While gross metabolic control is achieved, diabetics are still subject to unavoidable complications. Conventional insulin therapy is inadequate for the restoration of normoglycemia sufficient to prevent these degenerative sequelae of diabetes (1). Hence, artificial pancreata have been designed and developed to deliver insulin continuously in direct response to the physiological need to provide the finer control of glycemia necessary for homeostasis in insulin-dependent diabetes. [Pg.501]

Thyroid hormone, like insulin, continues to present a puzzle in terms of its mechanism of action. Since thyroid hormones increase the activity of a number of enzymes, as well as protein synthesis in general, an effect on protein synthesis either at the level of transcription or translation has been sought (Rail, 1978). Nuclear binding of T4 has been demonstrated, apparently to nonhistone proteins. It appears that it is free T4 which binds to the nucleus and not the T4 already bound to the cytoplasmic receptor. In fact, it appears that cytoplasmic receptors compete for T4 bound to nuclear sites. Nonetheless, there is strong inferential evidence for a role of T4 on transcription of mRNA (Rall,1978), but this does not represent the only means of explaining the pleiotropic effects of the hormone (Sterling, 1979). [Pg.211]

The number and amount of daily insulin doses, times of administration, and diet and exercise requirements require continual assessment. Dosage adjustments may be necessary when changing types of insulin, particularly when changing from the single-peak to the more pure Humulin insulins. [Pg.491]

Continue Combination Therapy HbA C q 6 months Add intermediate bedtime insulin or add third oral agent or switch to insulin... [Pg.502]

For the preparation of nanoparticles based on two aqueous phases at room temperature one phase contains chitosan and poly(ethylene oxide) and the other contains sodium tripolyphosphate. The particle size (200-1000 nm) and zeta potential (between -i- 20 mV and -l- 60 mV) could be modulated by varying the ratio chitosan/PEO-PPO. These nanoparticles have great proteinloading capacity and provide continuous release of the entrapped protein (particularly insulin) for up to one week [100,101]. [Pg.161]

The rate of mitochondrial oxidations and ATP synthesis is continually adjusted to the needs of the cell (see reviews by Brand and Murphy 1987 Brown, 1992). Physical activity and the nutritional and endocrine states determine which substrates are oxidized by skeletal muscle. Insulin increases the utilization of glucose by promoting its uptake by muscle and by decreasing the availability of free long-chain fatty acids, and of acetoacetate and 3-hydroxybutyrate formed by fatty acid oxidation in the liver, secondary to decreased lipolysis in adipose tissue. Product inhibition of pyruvate dehydrogenase by NADH and acetyl-CoA formed by fatty acid oxidation decreases glucose oxidation in muscle. [Pg.135]

Much of the insulin is released over the first 1-2 days, but significant amounts continue to be released for 4-5 days. [Pg.57]

Kasicka, V., Pruslk, Z., Sazelova, P., Jiracek, J. and Barth, T., Theory of the correlation between capillary and free-flow zone electrophoresis and its use for the conversion of analytical capillary separations to continuous free-flow preparative processes. Application to analysis and preparation of fragments of insulin, ]. Chromatogr. A, 796, 211, 1998. [Pg.441]

Use a continuous IV infusion of insulin based on an institution-specific protocol... [Pg.70]

Prepare 100 units of insulin in 100 mL normal saline ° 10 units or 0.1 units/kg IV bolus, then 0.05-0.1 units/kg/h continuous IV infusion... [Pg.104]

When plasma glucose drops to 250 mg/dL, decrease insulin infusion rate and continue until acidosis is corrected (i.e., anion gap closes)... [Pg.104]

If hypoglycemia develops in the setting of continued ketoacidosis, lower the insulin infusion and administer glucose infusions to maintain euglycemia. Do not stop the insulin infusion... [Pg.104]

Intensive insulin therapy, the administration of insulin three or more times daily to maintain preprandial blood glucose levels between 70 and 120 g/dL and postprandial blood glucose levels less than 180 g/dL, has been shown to decrease the incidence of proteinuria and albuminuria in patients with diabetes, both with and without documented nephropathy. The development and progression of nephropathy is also delayed in patients with type 1 DM receiving intensive insulin therapy. Continued benefits of intensive insulin therapy have been demonstrated up to 8 years after the study.16... [Pg.378]

Monitor electrocardiogram continuously in patients with cardiac abnormalities until serum potassium levels drop below 5 mEq/L (5 mmol/L) or cardiac abnormalities resolve. Evaluate serum potassium and glucose levels within 1 hour in patients who receive insulin and dextrose therapy. Evaluate serum potassium levels within 2 to 4 hours after treatment with SPS or diuretics. Repeat doses of diuretics or SPS if necessary until serum potassium levels fall below 5 mEq/L (5 mmol/L). Monitor blood pressure and serum potassium levels in 1 week in patients who receive fludrocortisone. [Pg.382]

Dextrose and insulin (with or without sodium bicarbonate) are typically given at the time of calcium therapy in order to redistribute potassium into the intracellular space. Dextrose 50% (25 g in 50 mL) can be given by slow IV push over 5 minutes or dextrose 10% with 20 units of regular insulin can be given by continuous TV infusion over 1 to 2 hours. The onset of action for this combination is 30 minutes and the duration of clinical effects... [Pg.412]

Currently, the most advanced form of insulin therapy is the insulin pump, also referred to as continuous subcutaneous insulin infusion (CSII). Using the short- or rapid-acting insulins only, these pumps are programmed to provide a slow release of small amounts of insulin as the basal portion of therapy, and then larger bolus doses are injected by the patient to account for the consumption of food. [Pg.651]

Monotherapy with sulfonylureas generally produce a 1.5% to 2% decline in HbAlc concentrations and a 60 to 70 mg/dL (3.33-3.89 mmol/L) reduction in FBG levels. Secondary failure with these drugs occurs at a rate of 5% to 7% per year as a result of continued pancreatic p-cell destruction. One limitation of sulfonylurea therapy is the inability of these products to stimulate insulin release from (1-cells at extremely high glucose levels, a phenomenon called glucose toxicity. [Pg.656]

Administer regular insulin IV (0.1 units/kg) or IM (0.4 units/kg), then 0.1 units/kg per hour by continuous IV infusion increase 2- to 10-fold if no response by 2-4 hours. If initial serum potassium is less than 3.3 mmol/L (3.3 mEq/L), do not administer insulin until the potassium is corrected to greater than... [Pg.663]

Continue above until patient is stable, glucose goal is 150-250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05-0.1 units/kg per hour. [Pg.663]


See other pages where Insulin - continued is mentioned: [Pg.46]    [Pg.43]    [Pg.161]    [Pg.71]    [Pg.46]    [Pg.43]    [Pg.161]    [Pg.71]    [Pg.46]    [Pg.46]    [Pg.142]    [Pg.117]    [Pg.124]    [Pg.125]    [Pg.240]    [Pg.625]    [Pg.945]    [Pg.498]    [Pg.178]    [Pg.454]    [Pg.166]    [Pg.420]    [Pg.60]    [Pg.646]    [Pg.662]   


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Continuous basal insulin infusion

Continuous subcutaneous insulin

Continuous subcutaneous insulin hypoglycaemia

Continuous subcutaneous insulin infusion

Continuous subcutaneous insulin infusion CSII)

Insulin - continued secretion

Insulin administration continuous subcutaneous

Insulin therapy continuous subcutaneous infusion

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