A chronic disease of absolute or relative insulin deficiency or resistance, diabetes mellitus is characterized by disturbances in carbohydrate, protein, and fat metabolism.
This condition occurs in two forms: type 1, characterized by absolute insulin insufficiency, and type 2, characterized by insulin resistance with varying degrees of insulin secretory defects.
Onset of type 1 usually occurs before age 30 (although it may occur at any age); the patient is usually thin and requires exogenous insulin and dietary management to achieve control. Conversely, type 2 usually occurs in obese adults after age 40, although it’s commonly seen in North American youths. It’s most commonly treated with diet and exercise (in combination with antidiabetic drugs), although treatment may include insulin therapy.
Diabetes mellitus is estimated to affect nearly 8% of the population of the United States (16 million people), about one-third of whom are undiagnosed. Incidence is equal in men and women and rises with age.
The effects of diabetes mellitus result from insulin deficiency. Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the body tissues’ access to essential nutrients for fuel and storage.
Type 1A results from autoimmune beta-cell destruction, resulting in insulin deficiency. Type 1B leaves these immunologic markers but results in insulin deficiency and kerosis.
Other risk factors include the following:
Obesity contributes to the resistance to endogenous insulin.
Physiologic or emotional stress can cause prolonged elevation of stress hormone levels (cortisol, epinephrine, glucagon, and growth hormone). This raises blood glucose levels, which, in turn, places increased demands on the pancreas.
Pregnancy causes weight gain and increases levels of estrogen and placental hormones, which antagonize insulin.
Some medications can antagonize the effects of insulin, including thiazide diuretics, adrenal corticosteroids, and hormonal contraceptives.
Signs and symptoms
Diabetes may begin dramatically with ketoacidosis in type 1 or insidiously. Its most common symptom is fatigue, from energy deficiency and a catabolic state. However, many patients with type 2 diabetes may be asymptomatic.
Insulin deficiency or resistance causes hyperglycemia, which pulls fluid from body tissues, causing osmotic diuresis, polyuria, dehydration, polydipsia, dry mucous membranes, and poor skin turgor. In ketoacidosis and hyperglycemic hyperosmolar nonketotic state, dehydration may cause hypovolemia and shock. Wasting of glucose in the urine usually produces weight loss and hunger in uncontrolled type 1 diabetes, even if the patient eats voraciously.
In diabetes, long-term effects 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 postural hypotension.
Because hyperglycemia impairs the patient’s resistance to infection, diabetes may result in skin and urinary tract infections and vaginitis. Glucose content of the epidermis and urine encourages bacterial growth.
In nonpregnant adults, diabetes mellitus is diagnosed with:
at least two occasions of a fasting plasma glucose level greater than or equal to 126 mg/dl
typical symptoms of uncontrolled diabetes and a random blood glucose level greater than or equal to 200 mg/dl
a blood glucose level greater than or equal to 200 mg/dl at 2 hours after ingestion of 75 grams of oral dextrose.
Two tests are required for diagnosis; they can be the same two tests or any combination and may be separated by more than 24 hours.