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Diabetes mellitus is a group of metabolic diseases characterized by elevated levels of glucose in the blood

(hyperglycemia) resulting from defects in insulin secretion, insulin action, or both (American
Diabetes Association [ADA], Expert Committee on the Diagnosis and Classification of Diabetes
Mellitus, 2003)
Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not
responding properly to the insulin produced.

INSULIN - a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the
production and storage of glucose. In the diabetic state, 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).
TYPES:
Type 1 DM
results from the pancreas's failure to produce enough insulin. This form was previously referred to
as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes". The cause is unknown.

Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly. As the
disease progresses a lack of insulin may also develop. This form was previously referred to as "non
insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes". The primary cause is
excessive body weight and not enough exercise.

Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes
develop high blood-sugar levels.
ETIOLOGY/RISK FACTORS:

TYPE 1 DM

Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to
insulin deficiency.

This type can be further classified as immune-mediated or idiopathic.

The majority of type 1 diabetes is of the immune-mediated nature, in which a T-cell-mediated autoimmune attack leads to the loss of
beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe.

Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are
usually normal, especially in the early stages.

Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases
were in children.

TYPE 2 DM Type 2 DM is characterized by insulin resistance, which may be combined with relatively reduced
insulin secretion.

The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor.
However, the specific defects are not known. Diabetes mellitus cases due to a known defect are
classified separately. Type 2 DM is the most common type of diabetes mellitus.

Type 2 DM is due primarily to lifestyle factors and genetics.

RISK FACTORS Dietary factors also influence the risk of developing type 2 DM. Consumption of sugar-sweetened drinks in excess is
associated with an increased risk. The type of fats in the diet is also important, with saturated fats and trans fatty acids increasing the risk
and polyunsaturated and monounsaturated fat decreasing the risk.Eating lots of white rice also may increase the risk of diabetes. A lack
of exercise is believed to cause 7% of cases.\

type 2 DM, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and
urbanization.Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 6080% of cases in those of
European and African descent, and 100% of Pima Indians and Pacific Islanders.Even those who are not obese often have a high waist
hip ratio.
PATHOPHYSIOLOGY
Insulin is secreted by beta cells, which are 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 a 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 (in the form of glycogen)
*Signals the liver to stop the release of glucose
*Enhances storage of dietary fat in adipose tissue
*Accelerates transport of amino acids (derived from dietary protein) into cells
Insulin inhibits the breakdown of stored glucose, protein, and fat. During fasting periods (between meals
and overnight), the pancreas continuously releases a small amount of insulin (basal insulin); another
pancreatic hormone called glucagon (secreted by the alpha cells of the islets of Langerhans) is
released when blood glucose levels decrease and stimulate the liver to release
stored glucose. The insulin and the glucagon together maintain a constant level of glucose in the
blood by stimulating the release of glucose from the liver.
TYPE 1 DIABETES
Type 1 diabetes is characterized by destruction of the pancreatic beta cells.

RISK FACTORS
It is thought that combined genetic, immunologic, and possibly environmental (eg, viral) factors contribute to beta cell destruction.
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; rather, they inherit a genetic predisposition, or tendency, toward developing 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
are 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 etiology, 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 (glucosuria). 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), in people with insulin deficiency, these processes occur in an unrestrained fashion 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.
TYPE 2 DIABETES

The two main problems related to insulin in type 2 diabetes 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 2 diabetes, these intracellular reactions are diminished, thus rendering insulin less effective at stimulating glucose uptake by the
tissues and at regulating glucose release by the liver

RISK FACTORS
Type 2 diabetes occurs most commonly in people older than 30 years
who are obese, although its incidence is increasing in younger

If symptoms are experienced, they are frequently mild and may include fatigue, irritability, polyuria, polydipsia, skin wounds that heal
poorly, vaginal infections, or blurred vision (if glucose levels are very high).

GESTATIONAL DIABETES
Gestational diabetes is any degree of glucose intolerance with its onset during pregnancy. Hyperglycemia develops during pregnancy
because of the secretion of placental hormones, which causes insulin resistance.
RISK FACTORS:
Between the 24th and 28th weeks of gestation:
age 25 years or older; age 25 years or younger obese; family history of diabetes in first-degree relatives; or member of an ethnic/racial
group with a high prevalence of diabetes (eg, Hispanic American, Native American, Asian American, African American, or Pacific
Islander). hypertensive
MANAGEMENT

If hyperglycemia persists, insulin is prescribed. Oral antidiabetic agents should not be used during pregnancy.
Goals for blood glucose levels during pregnancy are 105 mg/dL (5.8 mmol/L) or less before meals and 120 mg/dL (6.7 mmol/L) or less
2 hours after meals (ADA, Gestational Diabetes Mellitus, 2003).
After delivery of the infant, blood glucose levels in the woman with gestational diabetes return to normal. However, many women who
have had gestational diabetes develop type 2 diabetes later in life.
Therefore, all women who have had gestational diabetes should be counseled to maintain their ideal body weight and to exercise
regularly to reduce their risk for type 2 diabetes

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