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DIABETES MELLITUS

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. A number of lifestyle factors are known to be
important to the development of
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 waisthip 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 also 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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