Diabetes mellitus is a group of metabolic diseases characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both (American Diabetes Association [ADA], 2004r). Normally, a certain amount of glucose circulates in the blood. The major sources of this glu-cose are absorption of ingested food in the gastrointestinal tract and formation of glucose by the liver from food substances.

Insulin, a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose. In diabetes, the cells may stop responding to insulin or the pancreas may stop producing insulin entirely. This leads to hyperglycemia, which may result in acute metabolic complications such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Long-term effects of hyperglycemia contribute to macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral vascular disease), chronic microvascular complications (kidney and eye disease), and neuropathic complications (diseases of the nerves).

Type 1 Diabetes

Type 1 diabetes is characterized by destruction of the pancreatic beta cells. Combined genetic, immunologic, and possibly environmental (eg, viral) factors are thought to contribute to beta cell destruction. Although the events that lead to beta cell destruction are not fully understood, it is generally accepted that a genetic susceptibility is a common underlying factor in the development of type 1 diabetes. People do not inherit type 1 diabetes itself but rather a genetic predisposition, or tendency, toward development of type 1 diabetes. This genetic tendency has been found in people with certain human leukocyte antigen (HLA) types. HLA refers to a cluster of genes responsible for transplantation antigens and other immune processes; a cluster is referred to as a haplotype. About 95% of Caucasians with type 1 diabetes exhibit specific HLA-DR3 or HLA-DR4. The risk of developing type 1 diabetes is increased three to five times in people who have one of these two HLA types. Compared with the general population, this risk is increased 10 to 20 times in people who have both DR3 and DR4 HLA haplotypes. Immune-mediated diabetes commonly develops during childhood and adolescence, but it can occur at any age (ADA, 2004r).

There is also evidence of an autoimmune response in type 1 diabetes. This is an abnormal response in which antibodies are directed against normal tissues of the body, responding to these tissues as if they were foreign. Autoantibodies against islet cells and against endogenous (internal) insulin have been detected in people at the time of diagnosis and even several years before the development of clinical signs of type 1 diabetes. In addition to genetic and immunologic components, environmental factors, such as viruses or toxins, that may initiate destruction of the beta cell are being investigated.

Regardless of the specific cause, the destruction of the beta cells results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may not reabsorb all of the filtered glucose; the glucose then appears in the urine (glycosuria). When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. This is called osmotic diuresis.

Because insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production of new glucose from amino acids and other substrates), these processes occur in an unrestrained fashion in people with insulin deficiency and contribute further to hyperglycemia. In addition, fat breakdown occurs, resulting in an increased production of ketone bodies, which are the byproducts of fat breakdown.


REFERENCE: Brunner and Suddarth (2006). Medical-Surgical Nursing, 11th edition