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Diabetes Mellitus Type 2 Pathophysiology & Schematic Diagram

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Diabetes Mellitus is a complex, chronic syndrome characterized by the impairment in the ability to metabolize carbohydrates, fats, proteins generally.

Type II Diabetes Mellitus, also known as adult-onset diabetes, maturity-onset diabetes, or noninsulin dependent diabetes mellitus is a condition where one of these factors or both are at play: defective insulin secretion and insulin resistance or reduced insulin sensitivity. Since insulin is needed for transport of glucose into the cell, this condition leads to hyperglycemia.

In 2006, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes. This incidence is increasing rapidly, and it is estimated that by the year 2030, this number will double. DM occurs throughout the world, but, common, especially Type II in more developed countries. The greatest prevalence, however, is expected to occur in Asia and Africa. The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps, most importantly, a “western-style diet.”

Pathophysiology

Insulin is secreted by beta cells, which is one of four types of cells in the islets of Langerhans in the pancreas. Insulin is an anabolic, or storage hormone. When a person eats meal, insulin secretion increases and moves glucose from the blood into muscle, liver and fat cells. In those cells, insulin transports and metabolizes glucose for energy, stimulates storage of glucose in the liver and muscle, signals the liver to stop release of glucose, enhances storage of dietary fat in adipose tissues, and accelerates transport of amino acids into cells. Insulin also inhibits the breakdown of stored glucose, protein and fat.

During fasting periods, the pancreas continuously releases a small amount of insulin; another pancreatic hormone called glucagon is released when blood glucose levels decrease and stimulates the liver to release stored glucose. The insulin and the glucagon in the blood by stimulating the release of glucose from the liver.

Initially, the liver produces glucose through the breakdown of glycogen. After 8-12 hours without food, the liver forms glucose from the breakdown of non-carbohydrate substances, including amino acids.

In type II diabetes, the two main problems are insulin resistance and impaired insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type II diabetes, these intracellular reactions are diminished, making insulin less effective at stimulating glucose uptake by the liver. The exact mechanisms that lead to insulin resistance and impaired insulin secretion in type II diabetes are unknown, although genetic factors are ought to play a role.

To overcome insulin resistance and prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level at a normal or slightly elevated level. However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rises and type II diabetes develops.

Despite the impaired secretion of insulin that is a characteristic of type II diabetes, there is enough insulin present to prevent the breakdown of fat the accompanying production of ketone bodies. Therefore, DKA does not typically occur in type II diabetes. However, uncontrolled type II diabetes may lead to another acute problem.

Because type II diabetes is associated with a slow, progressive glucose intolerance, its onset may go undetected for many years. If the patient experiences symptoms, they are frequently mild and may include fatigue, irritability, polyuria, polydipsia, poor healing skin wounds, vaginal infections or blurred vision if glucose levels are very high.

Schematic Diagram

Nursing Care Plans

For nursing care plans, please read Diabetes Mellitus Nursing Care Plans.