Diabetes mellitus is a chronic multisystem disease characterized by alterations in carbohydrate, fat, and protein metabolism resulting from abnormal insulin production, impaired insulin utilization, or both. The hallmark of this metabolic disorder is hyperglycemia.
Diabetes* is often complicated by structural and functional abnormalities in the blood vessels and nerves. The atherosclerotic changes that frequently occur in the large vessels (macroangiopathy) affect the cardiac, cerebral, and peripheral circulation. Thickening of the basement membrane of the capillaries (microangiopathy) can also occur and is especially significant when it involves the vessels in the eyes and kidneys. The neurological involvement can be manifested in a wide variety of ways and is referred to as diabetic neuropathy. There are several different mechanisms that are thought to contribute to the development of diabetic neuropathy. These include reduced blood flow to the nerves as a result of angiopathies and a metabolic defect in the polyol pathway resulting in accumulation of sorbitol in the nerves, which subsequently alters nerve function. The most common neuropathy is peripheral sensorimotor polyneuropathy, which has a gradual onset of sensory manifestations such as numbness and tingling, burning or shooting pain sensations, and/or hyperesthesia. Neuropathy of the autonomic nervous system is also common. Parasympathetic involvement often occurs earlier and is more profound than sympathetic nervous system involvement and manifestations vary depending on the system involved.
The two major types of diabetes are type 1 and type 2. Type 1 diabetics have an absolute insulin deficiency and are dependent on insulin replacement. The insulin deficiency is usually due to an immune-mediated destruction of the pancreatic B-cells in a person with a genetic predisposition and a triggering environmental insult (e.g., viral infection). Type 2 diabetics have a relative deficiency of insulin caused by decreased tissue responsiveness to insulin (insulin resistance), a defect in insulin secretion, and inappropriate hepatic glucose production. Heredity plays a role in development of type 2 diabetes. Additional risk factors for type 2 diabetes include a history of gestational diabetes mellitus or impaired glucose tolerance, increasing age, obesity, and a sedentary lifestyle.
A sequence of pathophysiological events occurs in diabetes. When an insulin deficiency exists, glucose cannot be transported into the cells for energy metabolism. As a result, glucose accumulates in the blood and starts to spill into the urine once the level exceeds the renal threshold (180 mg/dl or greater). The high blood glucose acts as an osmotic diuretic, which leads to excessive diuresis and subsequent deficient fluid volume. Because the glucose cannot be utilized as an energy source by many cells, fat and protein are broken down to provide a source of energy for the starving cells. The free fatty acids that are mobilized from adipose tissue are converted by the liver to ketones to be used as an energy source. The ketones are strong acids and eventually deplete the body’s buffer system and respiratory compensatory ability, leading to a state of metabolic acidosis. The simultaneous increase in glucagon and epinephrine release that occurs with an insulin deficiency exacerbates the hyperglycemia and ketogenesis. Continuation of these metabolic derangements leads to life-threatening imbalances.
Ineffective tissue perfusion
Risk for deficient fluid volume
Imbalanced nutrition: less than body requirements
Altered comfort: burning, aching, cramping, hyperesthesia, numbness, and/or tingling (particularly in lower extremities)
Altered comfort: gastric discomfort
Disturbed sensory perception: visual
Risk for impaired tissue integrity
Risk for infection
Potential acute metabolic complications
diabetic ketoacidosis (DKA)
hyperglycemic hyperosmolar nonketotic coma
Ineffective therapeutic regimen management
Deficient knowledge or Ineffective health maintenance
Risk for injury
Ineffective coping or Impaired adjustment