Diabetes mellitus (DM) is a chronic disease of absolute or relative insulin deficiency or resistance characterized by disturbances in carbohydrate, protein, and fat metabolism. A leading cause of death by disease in the United States, this syndrome is a contributing factor in about 50% of myocardial infarctions and about 75% of strokes as well as in renal failure and peripheral vascular disease. It’s also the leading cause of new blindness.
DM occurs in four forms classified by etiology: type 1, type 2, other specific types, and gestational diabetes mellitus (GDM). Type 1 is further subdivided into immune-mediated diabetes and idiopathic diabetes. Those who were previously in the type 1 diabetes group fall into this group.Children and adolescents with type 1 immune-mediated diabetes rapidly develop ketoacidosis, but most adults with this type experience only modest fasting hyperglycemia unless they develop an infection or experience another stressor. Patients with type 1 idiopathic diabetes are prone to ketoacidosis.
Most patients with type 2 diabetes are obese. The “other specific types” category includes people who have diabetes as a result of a genetic defect, endocrinopathies, or exposure to certain drugs or chemicals. GDM occurs during pregnancy. In this type of diabetes, glucose tolerance levels usually return to normal after delivery.
DM affects an estimated 6% of the population of the United States, about half of whom are undiagnosed. Incidence is greater in females and rises with age. Type 2 accounts for 90% of cases.
In type 1 diabetes, pancreatic beta-cell destruction or a primary defect in beta-cell function results in failure to release insulin and ineffective glucose transport. Type 1 immune-mediated diabetes is caused by cell-mediated destruction of pancreatic beta cells. The rate of beta-cell destruction is usually higher in children than in adults. The idiopathic form of type 1 diabetes has no known cause. Patients with this form have no evidence of autoimmunity and don’t produce insulin.
In type 2 diabetes, beta cells release insulin, but receptors are insulin-resistant and glucose transport is variable and ineffective. Risk factors for type 2 diabetes include:
❑ obesity (even an increased percentage of body fat primarily in the abdominal region); risk decreases with weight and drug therapy
❑ lack of physical activity
❑ history of GDM
❑ hypertension
❑ Black, Hispanic, Pacific Islander, Asian American, Native American origin
❑ strong family history of diabetes
❑ older than age 45
❑ high-density lipoprotein cholesterol of less than 35 or triglyceride of greater than 250
❑ Seriously impaired glucose tolerance (IGT) test.
The “other specific types” of DM result from various conditions (such as a genetic defect of the beta cells or endocrinopathies) or from use of or exposure to certain drugs or chemicals. GDM is considered present whenever a patient has any degree of abnormal glucose during pregnancy. This form may result from weight gain and increased levels of estrogen and placental hormones, which antagonize insulin.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage in the fat deposits. Insulin deficiency compromises the body tissues’access to essential nutrients for fuel and storage.
Diabetes may begin dramatically with ketoacidosis or insidiously. Its most common symptom is fatigue from energy deficiency and a catabolic state. Insulin deficiency causes hyperglycemia, which pulls fluid from body tissues, causing osmotic diuresis, polyuria, dehydration, polydipsia, dry mucous membranes, poor skin turgor and, in most patients, unexplained weight loss.
In ketoacidosis and hyperosmolar hyperglycemic nonketotic syndrome, dehydration may cause hypovolemia and shock. Wasting of glucose in the urine usually produces weight loss and hunger in type 1 diabetes, even if the patient eats voraciously.
Long-term effects of diabetes may include retinopathy, nephropathy, atherosclerosis, and peripheral and autonomic neuropathy. Peripheral neuropathy usually affects the hands and feet and may cause numbness or pain. Autonomic neuropathy may manifest itself in several ways, including gastroparesis (leading to delayed gastric emptying and a feeling of nausea and fullness after meals), nocturnal diarrhea, impotence, and orthostatic hypotension.
Because hyperglycemia impairs the patient’s resistance to infection, diabetes may result in skin and urinary tract infections (UTIs) and vaginitis. Glucose content of the epidermis and urine encourages bacterial growth.
According to the American Diabetes Association (ADA), DM can be diagnosed if any of the following exist:
❑ symptoms of diabetes (polyuria, polydipsia, and unexplained weight loss) plus a random (non-fasting) blood glucose level greater than or equal to 200 mg/dl accompanied by symptoms of diabetes.
❑ a fasting blood glucose level (no caloric intake for at least 8 hours) greater than or equal to 126 mg/dl.
❑ a plasma glucose value in the 2-hour sample of the oral glucose tolerance test greater than or equal to 200 mg/dl. This test should be performed after a glucose load dose of 75 g of anhydrous glucose.
If results are questionable, the diagnosis should be confirmed by a repeat test on a different day. The ADA also recommends the following testing guidelines:
❑ Test every 3 years: people age 45 or older without symptoms
❑ Test immediately: people with the classic symptoms
❑ High-risk groups should be tested frequently: Individuals with impaired glucose tolerance usually have normal blood levels unless challenged by a glucose load, such as a piece of pie or glass of orange juice. Two hours after a glucose load, the glucose level ranges from 140 to 199 mg/dl. These individuals have an abnormal fasting glucose level between 110 and 125 mg/dl. Because the fasting plasma glucose test is sufficient to make the diagnosis of diabetes, it replaces the oral glucose tolerance test. (See Classifying blood glucose levels.)
An ophthalmologic examination may show diabetic retinopathy. Other diagnostic and monitoring tests include urinalysis for acetone and blood testing for glycosylated hemoglobin (Hb A1C), which reflects recent glucose cortisol.
Effective treatment normalizes blood glucose and decreases complications using insulin replacement, diet, and exercise. Current forms of insulin replacement include single-dose, mixed-dose, split-mixed dose, and multiple-dose regimens. The multiple-dose regimens may use an insulin pump. Insulin may be rapid acting, intermediate acting, long acting, or a combination of rapid acting and intermediate acting; it may be standard or purified, and it may be derived from beef, pork, or human sources. Purified human insulin is used commonly today. Pancreas transplantation is experimental and requires chronic immunosuppression.
Successful treatment requires an extensive dietary education. The patient’s diet is specifically tailored to include the right amount and combination of foods. Almost all foods may be eaten occasionally. The diet should address dietary prescriptions as well as personal and cultural preferences to improve adherence and control. For the obese patient with type 2 diabetes, weight reduction is a goal. In type 1 diabetes, the calorie allotment may be high, depending on growth stage and activity level.
Type 2 diabetes may require oral antidiabetic drugs to stimulate endogenous insulin production, increase insulin sensitivity at the cellular level, and suppress hepatic gluconeogenesis.
Five types of drugs have been used to treat diabetes. Sulfonylureas stimulate pancreatic insulin release, increase tissue sensitivity to insulin, and require insulin’s presence to work. Meglitinides cause immediate, brief release of insulin and are taken immediately before meals. Biguanides decrease hepatic glucose production and increase tissue sensitivity to insulin. Alpha-glucosidase inhibitors slow the breakdown of glucose and decrease postprandial glucose peaks. The thiazolidinediones enhance the action of insulin; however, insulin must be present for them to work. These drugs also reduce insulin resistance by decreasing hepatic glucose production and increasing glucose uptake. They have also been shown to lower blood pressure in diabetic hypertensive patients. Cholesterol and triglyceride levels may also be reduced.
Treatment of long-term diabetic complications may include transplantation or dialysis for renal failure, photocoagulation for retinopathy, and vascular surgery for large-vessel disease. Meticulous blood glucose control is essential.
Keeping glucose at near-normal levels for 5 years or more reduces both the onset and progression of retinopathy, nephropathy, and neuropathy. In type 2 diabetes, blood pressure control as well as smoking cessation reduces the onset and progression of complications, including cardiovascular disease.
Stress the importance of complying with the prescribed treatment program. Tailor your teaching to the patient’s needs, abilities, and developmental stage. Include diet; purpose, administration, and possible adverse effects of medication; exercise; monitoring; hygiene; and the prevention and recognition of hypoglycemia and hyperglycemia. Stress the effect of blood glucose control on long-term health.
❑ Monitor diabetes control by obtaining blood glucose, glycohemoglobulin, lipid levels, and blood pressure measurements regularly.
❑ Watch for diabetic effects on the cardiovascular system, such as cerebrovascular, coronary artery, and peripheral vascular impairment, and on the peripheral and autonomic nervous systems. Treat all injuries, cuts, and blisters (particularly on the legs or feet) meticulously. Be alert for signs of UTI and renal disease.
❑ Urge regular ophthalmologic examinations to detect diabetic retinopathy.
❑ Assess for signs of diabetic neuropathy (numbness or pain in hands and feet, footdrop, neurogenic bladder). Stress the need for personal safety precautions because decreased sensation can mask injuries. Minimize complications by maintaining strict blood glucose control.
❑ Teach the patient to care for his feet by washing them daily, drying carefully between toes, and inspecting for corns, calluses, redness, swelling, bruises, and breaks in the skin. Urge him to report changes to the physician. Advise him to wear nonconstricting shoes and to avoid walking barefoot. Instruct him to use over-the-counter athlete’s foot remedies and seek professional care should athlete’s foot not improve.
❑ Teach the patient how to manage his diabetes when he has a minor illness, such as a cold, flu, or upset stomach.
❑ To delay the clinical onset of diabetes, teach people at high risk to avoid risk factors. Advise genetic counseling for young adult diabetics who are planning families.
❑ Further information may be obtained from the Juvenile Diabetes Foundation, the ADA, and the American Association of Diabetes Educators.
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Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
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