The following definition was extracted and abridged from

diabetes

    brittle diabetes Diabetes mellitus that is exceptionally difficult to control.The disease is marked by alternating episodes of hypoglycemia and hyperglycemia. Frequent adjustments of dietary intake and insulin dosage are required.

    ETIOLOGY: Diabetes may be brittle when 1. insulin is not well-absorbed; 2. insulin requirements vary rapidly; 3. insulin is improperly prepared or administered; 4. the Somogyi phenomenon is present; 5. the patient has coexisting anorexia or bulimia; 6. the patient's daily exercise routine, diet, or medication schedule varies; or 7. physiological or psychological stress is persistent.

    bronze diabetes Hemochromatosis.

    chemical diabetes 1. Asymptomatic diabetes mellitus; that is, a stage of diabetes mellitus (DM) in which no obvious clinical signs and symptoms of the disease are present, but blood sugar measurements are abnormal. 2. Type 2 DM occurring in an obese child or adolescent. The syndrome is sometimes referred to as “mature onset diabetes of youth” (MODY).

    endocrine diabetes Diabetes mellitus that results from diseases of the pituitary, thyroid, or adrenal glands or from the ovaries.

    gestational diabetes Diabetes mellitus that begins during pregnancy, typically in the second or third trimester.It occurs in 1% to 4% of pregnancies and requires careful treatment to prevent fetal anomalies (e.g., macrosomia) and maternal complications (e.g., pregnancy-induced hypertension, eclampsia, and the need for cesarean delivery). Although gestational diabetes usually subsides after delivery, more than one third of women with gestational diabetes will eventually develop type 2 diabetes mellitus during their lifetimes.

    iatrogenic diabetes Diabetes mellitus brought on by administration of drugs such as corticosteroids, certain diuretics, or birth control pills.

    immune-mediated diabetes mellitus Type 1 diabetes.

    diabetes insipidus ABBR: DI. Excessive urination caused either by inadequate amounts of antidiuretic hormone in the body (hypothalamic DI) or by failure of the kidney to respond to antidiuretic hormone (nephrogenic DI).Urinary output is often massive (e.g., 5 to 10 L/day), which may result in dehydration, esp. in patients who cannot drink enough liquid to replace urinary losses (e.g., those with impaired consciousness). The urine is dilute (specific gravity is often below 1.005), and typically the patient's serum sodium level and osmolality rise as free water is dumped into the urine. If water deficits are not matched or the urinary losses are not prevented, death will result from dehydration.

    ETIOLOGY: DI usually results from hypothalamic injury (e.g., brain trauma or neurosurgery) or from the effects of certain drugs (e.g., lithium or demeclocycline) on the renal resorption of water. Other representative causes include sickle cell anemia (in which renal infarcts damage the kidney's ability to retain water), hypothyroidism, adrenal insufficiency, inherited disorders of antidiuretic hormone production, and sarcoidosis.

    SYMPTOMS: The primary symptoms are urinary frequency, thirst, and dehydration.

    TREATMENT: When DI is a side effect of drug therapy, the offending drug is withheld. DI caused by failure of the hypothalamus to secrete antidiuretic hormone is treated with synthetic vasopressin.

    PROGNOSIS: The prognosis is usually good when the disease is recognized and appropriately managed.

    NURSING-IMP: Fluid balance is monitored. Fluid intake and output, urine specific gravity, and weight are assessed for evidence of dehydration and hypovolemic hypotension. Serum electrolyte and blood urea nitrogen levels are monitored.

    The patient is instructed in nasal insufflation of vasopressin or administration of subcutaneous or intramuscular hormones. The length of the therapy and the importance of taking medications as prescribed and not discontinuing them abruptly are stressed. Meticulous skin and oral care are provided; use of a soft toothbrush is recommended, and petroleum jelly is applied to the lips and an emollient lotion to the skin to reduce dryness. Adequate fluid intake should be maintained.

    Both the patient and family are taught to identify signs of dehydration and to report signs of severe dehydration and impending hypovolemia. The patient is taught to measure intake and output, to monitor weight daily, and to use a hydrometer to measure urine specific gravity. The patient should wear or carry a medical identification tag and keep a supply of medication with him or her at all times.

    insulin-dependent diabetes mellitus ABBR: IDDM. Type 1 diabetes.

    juvenile-onset diabetes Type 1 diabetes.

    latent diabetes Diabetes mellitus that manifests itself during times of stress such as pregnancy, infectious disease, weight gain, or trauma.Previous to the stress, no clinical or laboratory findings of diabetes are present. There is a very strong chance that such individuals will eventually develop overt type 2 diabetes mellitus.

    mature-onset diabetes of youth ABBR: MODY. Type 2 DM that presents during childhood or adolescence, typically as an autosomal dominant trait in which there is diminished, but not absent, insulin production by the pancreas.Children with this form of diabetes mellitus are not prone to diabetic ketoacidosis.

    diabetes mellitus A chronic metabolic disorder marked by hyperglycemia.Diabetes mellitus (DM) results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and in pregnancy, the developing fetus. Type 1, or insulin-dependent, DM has a prevalence of just 0.3% to 0.4%. Type 2 DM (previously known as “adult-onset” DM) has a prevalence in the general population of 6.6%. In some populations (e.g., elderly persons, Native Americans, blacks, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM (formerly called “juvenile-onset” DM) occurs usually in children, most of whom are active and thin. SEE: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon. Type 1 DM usually presents as an acute illness with dehydration and often diabetic ketoacidosis. Type 2 DM is often asymptomatic in its early years and therefore occult. The American Diabetes Association (1-800-DIABETES) estimates that more than 5 million Americans have type 2 DM without knowing it. Diagnosis is based on a fasting plasma glucose level greater than 126 mg/dl on more than one occasion or a glucose level exceeding 200 mg/dl in a patient with excessive urinary volume (polyuria), excessive thirst (polydipsia), and weight loss.

    ETIOLOGY: Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.

    SYMPTOMS: Classic symptoms of DM are polyuria, polydipsia, and weight loss. In addition, patients with hyperglycemia often have blurred vision, increased food consumption (polyphagia), and generalized weakness. When a patient with type 1 DM loses metabolic control (e.g., during infections or periods of noncompliance with therapy), symptoms of diabetic ketoacidosis occur. These may include nausea, vomiting, dizziness on arising, intoxication, delirium, coma, or death. Chronic complications of hyperglycemia include retinopathy and blindness, peripheral and autonomic neuropathies, glomerulosclerosis of the kidneys (with proteinuria, nephrotic syndrome, or end-stage renal failure), coronary and peripheral vascular disease, and reduced resistance to infections. Patients with DM often also sustain ulcerations of the feet, which may result in osteomyelitis and the need for amputation.

    TREATMENT: DM types 1 and 2 are both treated with specialized diets, regular exercise, intensive foot and eye care, and medications.

    Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels (i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides, and a fall in HDL cholesterol). Participation in an intensive therapy program requires a motivated patient.

    Some patients with type 2 DM can control their disease with a calorically restricted diet (e.g., 1600 to 1800 cal/day) and regular aerobic exercise. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (e.g., tolazamide, tolbutamide, glyburide, or glipizide), which typically increase pancreatic secretion of insulin; biguanides or thiazolidinediones (e.g., metformin or troglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (e.g., acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. When combinations of these agents fail to normalize blood sugar levels, insulin injections are added.

    PREVENTION OF COMPLICATIONS: Patients with DM should avoid using tobacco products, actively manage their serum lipid levels, and keep hypertension under optimal control because failure to do so may result in a risk of atherosclerosis much higher than that of the general public. Other elements in good diabetic care include receiving regular vaccinations (e.g., to prevent influenza and pneumococcal pneumonia).

    PROGNOSIS: Diabetes is a chronic, incurable disease, but symptoms can be ameliorated and life prolonged by proper therapy. The isolation and eventual production of insulin in 1922 by Canadian physicians Banting and Best made it possible to allow persons with the disease to lead a normal life.

    NURSING-IMP: The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) as well as those of high blood sugar, such as polyuria and polydipsia. When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and ketone levels are evaluated. The effects of diabetes on other body systems, such as cerebrovascular, coronary artery, and peripheral vascular impairment; visual impairment; and peripheral and autonomic nervous system impairment are assessed. The patient is observed for signs and symptoms of diabetic neuropathy, such as numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy.

    Insulin or oral hypoglycemic agents are administered as prescribed and their action and use explained. With help from a dietitian, a diet is planned based on the recommended amount of calories, protein, carbohydrates, and fats. The patient learns how to choose food exchanges and how to read food container labels. A steady, consistent level of daily exercise is prescribed, and participation in a supervised exercise program is recommended.

    Hypoglycemic reactions are promptly treated by giving carbohydrates (oral orange juice, hard candy, honey, or any sugar-containing food); as necessary, SC or IM glucagon or IV dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin, and later, with potassium replacement based on laboratory values.

    Skin care, esp. to the feet and legs, is provided, and the patient is instructed in these techniques. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, bed linens, and walking barefoot. The patient is referred to a podiatrist for ongoing foot care and is warned that decreased sensation can mask injuries. Regular ophthalmological examinations are recommended for early detection of diabetic retinopathy.

    The patient is educated about diabetes, its possible complications and their management, and the importance of strict adherence to the prescribed therapy. Emotional support and a realistic assessment of the patient's condition are offered; this assessment should stress that, with proper treatment, the patient can have a near-normal lifestyle and life expectancy. Assistance is offered to help the patient to develop positive coping strategies. The patient and family may be referred for counseling and to local and national support and information groups. SEE: Nursing Diagnoses Appendix.

    non–insulin-dependent diabetes mellitus ABBR: NIDDM. Type 2 diabetes. SEE: type 1 diabetes for table.

    pancreatic diabetes Diabetes associated with disease of the pancreas, such as chronic or recurrent pancreatitis.

    phlorhizin diabetes Glycosuria caused by administration of phlorhizin.

    renal diabetes Renal glycosuria; this condition is marked by a low renal threshold for glucose.Glucose tolerance is normal and diabetic symptoms are lacking.

    secondary diabetes mellitus DM that results from damage to the pancreas (e.g., after frequent episodes of pancreatitis), or from drugs such as corticosteroids (which increase resistance to the effects of insulin).

    strict control of diabetes Regulation of blood sugars to normal, or nearly normal levels, both before and after meals.Tight control has been shown to prevent microvascular complications of diabetes mellitus (DM), such as blindness, nerve damage, and kidney failure. Patients with meticulously controlled DM typically have a hemoglobin A1c level of about 7%; fasting blood sugars that are less than 110 mg/dl; and postprandial blood sugars that are less than 180 mg/dl. Strategies to attain these levels including paying careful attention to dietary regimens, exercising regularly, and monitoring blood sugars, oral medications, and insulin doses frequently throughout the day. SYN: tight control of diabetes.

    tight control of diabetes Strict control of diabetes.

    true diabetes Diabetes mellitus.

    type 1 diabetes Diabetes mellitus that usually has its onset before the age of 25 years, in which the essential abnormality is related to absolute insulin deficiency. SYN: juvenile-onset diabetes. SEE: table.

    type 2 diabetes A group of forms of diabetes mellitus that occur predominantly in adults.The insulin produced is sufficient to prevent ketoacidosis but insufficient to meet the total needs of the body. This form of diabetes in nonobese patients can usually be controlled by diet and oral hypoglycemic agents, such as sulfonylurea drugs or metformin, a nonsulfonylurea drug. Occasionally insulin therapy is required. In some patients the condition can be controlled by careful diet and regular exercise. SYN: non–insulin-dependent diabetes mellitus. SEE: type 1 diabetes for table..

"Taber's Cyclopedic Medical Dictionary," Copyright © 2001 by F. A. Davis Co., Phil., PA