A group of diseases characterized by hyperglycemia (fasting plasma glucose level >100 mg/dL) and abnormalities in fat, carbohydrate, and protein metabolism that lead to microvascular, macrovascular, and neuropathic complications
Classification of diabetes mellitus by pathologic cause
Type 1 diabetes (beta cell destruction, usually leading to absolute insulin deficiency)
Type 2 diabetes (The pancreas still maintains some capacity to produce and secrete insulin)
Other specific types (Genetic defects of beta cell function, Genetic defects in insulin action, Disease of the exocrine pancreas, Endocrinopathies)
Gestational Diabetes Mellitus
Signs and symptoms of diabetes mellitus
weight gain or loss, Blurred vision/diabetic retinopathy, numbness or tingling of the extremities (paresthesia), loss of sensation, orthostatic hypotension, impotence, vaginal yeast (candidiasis) infections, difficulty in controlling urination (neurogenic bladder), Nonhealing ulcers of the lower extremities may indicate chronic vascular disease
Treatmentofdiabetesmellitus
Balanced diet, Medical Nutrition Therapy (MNT), Insulin or oral antidiabetic therapy, Routine exercise, Good hygiene, Maintenance of an ideal body weight, Reduction of lipids and cholesterol, smoking cessation [including e-cigarettes], blood pressure control, influenza and pneumococcal vaccinations
Nursingimplications for patients with diabetes mellitus
Diet, Activity level, Blood or urine testing, Medication, Self-injection techniques, Prevention of complications, Illness management, Effective management of hypoglycemia or hyperglycemia
A hormone produced in the beta cells of the pancreas, is a key regulator of metabolism. Insulin is required for the entryofglucose into skeletal and heart muscle and fat. It also plays a significant role in protein and lipid metabolism. It is not required for glucose transport into the brain, kidney, gastrointestinal, or liver tissue.
The time required for the medication to have an initial effect or action
Peak
When the insulin will have the maximum effect
Duration
How long the agent remainsactive in the body
Storage of insulin
Refrigerator (not the freezer) until opened, Roomtemperature (68° to 75°F) until gone, Gently rolled in the palms of the hands (not shaken) to warm and resuspend the insulin, Discarded within 30 days after opening
Premedicationassessment for insulin
Confirm that a blood glucose level was recently measured and was acceptable for the individual patient, Confirm that the patient has had a level of activity reasonable for that patient and that the anticipated level of activity planned for the next several hours is balanced with the insulin dose, Confirm that the prescribed diet is being consumed as planned and that no changes in diet are anticipated in relation to insulin dosage over the next several hours
Common and serious adverse effects of insulin
Metabolic: Hyperglycemia, Hypoglycemia, Immune system: Allergic reactions (Itching, Redness, swelling at the site of injection, Acute rashes/anaphylactic are rare symptoms), Lipodystrophies
Treatment for adverse effects of insulin
Antihistamines, Epinephrine, Steroids
Metformin
A class of oral antihyperglycemic agents known as the biguanides. It reduces absorption of glucose from the small intestine, and increases insulin sensitivity, improving glucose uptake in peripheral muscle and adipose cells. Insulin must be present for metformin to be active, and therefore metformin is not effective in type 1 diabetes.
Dosage and administration of metformin
PO: Immediate-release tablet or solution: Initial: 500 mg twice daily or 850 mg once daily; titrate in increments of 500 mg weekly or 850 mg every other week; may also titrate from 500 mg twice a day to 850 mg twice a day after 2 weeks, PO: Extended-release tablet: Initial: 500 to 1000 mg once daily; dosage may be increased by 500 mg weekly up to a maximum of 2500 mg/day
Therapeutic Outcomes of Metformin
1. Fewer long-term complications associated with poorly controlled type 2 diabetes mellitus
Actions of Sulfonylurea Oral Hypoglycemic Agents
The sulfonylureas lower blood glucose levels by stimulating the release of insulin from the beta cells of the pancreas. The sulfonylureas also diminish glucose production and metabolism of insulin by the liver
Actions of Meglitinide Oral Hypoglycemic Agents
They lower blood glucose levels by stimulating the release of insulin from the beta cells of the pancreas
Actions of Thiazolidinedione Oral Antidiabetic Agents
The TZDs lower blood glucose levels by increasing the sensitivity of muscle and fat tissue to insulin, allowing more glucose to enter the cells in the presence of insulin for metabolism. Unlike sulfonylureas or meglitinides, TZDs do not stimulate the release of insulin from the beta cells of the pancreas, but insulin must be present for these agents to work
Drug interactions that may enhance hypoglycemic effects of Thiazolidinediones
Drug interactions with Beta-adrenergic blocking agents
Beta blockers (e.g., propranolol, nadolol, metoprolol, carvedilol) may induce hypoglycemia but may also mask many of the symptoms of hypoglycemia
Actions of Alpha-GlucosidaseInhibitor Agents
Acarbose and miglitol are classified as an antihyperglycemic agents. They are enzyme inhibitors that inhibit pancreatic alpha-amylase and gastrointestinal alpha-glucoside hydrolase enzymes used in the digestion of sugars. In patients with diabetes, this enzyme inhibition results in delayed glucose absorption and a lowering of postprandial hyperglycemia
Alpha-Glucosidase Inhibitor Agents
Acarbose, Precose, miglitol, Glyset
Sodium-glucosecotransporter2inhibitors
Block the secretion of the SGLT2 protein, dropping glucose reabsorption from 90% to less than 10%, causing the glucose to be excreted in the urine
Glucagon
A hormone secreted by the alpha cells of the pancreas that breaks down stored glycogen to glucose, resulting in elevated blood glucose levels