Sabtu, 29 Juni 2013

Diabetes milletus Dalam bahasa Inggris

Diabetes Mellitus

By :

1.Dwi Lestari

2.Ghina rahmi

3.Mutohirin

4.Nopiyah

5.Triana Dewi

Guidance Counselor :

Surya Darma,SE,SPd,M.Si

STIK Siti Khadijah Palembang

Tahun Ajaran 2012 - 2013

Preface

Thank God we prayed to Allah SWT who has given grace and His gift to us so we managed to finish the
paper on time alhamdulillah titled Nursing care of diabetes mellitus
This paper contains information about milletus diabetes, complications, pahtofisiologi, how to cope and
ways of treatment. Expected that this paper can give us all the information about this hereditary disease.

We realize that this paper is far from perfect, therefore criticism and suggestions from all stakeholders
that are built for the perfection we always hoped this paper.

Finally, we say thank you to all those who have participated in the preparation of this paper from
beginning to end. May Allah always be pleased with all our efforts. amen

Table of Contents

Preface.........................................................................................i

Table of Contents........................................................................ii

Causes for Diabetes Mellitus............................................................1

PATHOPHYSIOLOGY OF DIABETES...................................2

Type 1 Diabetes & Type 2 Diabetes Mellitus............................3

Diabetes Associated with Other Conditions...............................4

Diabetes Management................................................................5

Five Components of Diabetes Management..............................6

Nursing care plans for Diabetes Mellitus

Diabetes mellitus is a disorder in which the level of blood glucose is persistently raised above the normal
range. Diabetes mellitus is a syndrome with disordered metabolism and inappropriate hyperglycemia
due to either a deficiency of insulin secretion or to a combination of insulin resistance and inadequate
insulin secretion to compensate. Diabetes mellitus occurs in two primary forms:

type 1, characterized by absolute insufficiency, and the more prevalent

type 2, characterized by insulin resistance with varying degrees of insulin secretory

defects.

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 (ADA], Expert
Committee on the Diagnosis and Classification of Diabetes Mellitus, 2003.

Causes for Diabetes Mellitus

The cause of both type 1 and type 2 diabetes remains unknown, although genetic factors may play a
role. Diabetes mellitus results from insulin deficiency or resistance. Insulin transports glucose into the
cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid
storage. Insulin deficiency or resistance compromises the body tissues access to essential nutrients for
fuel and storage. The resulting hyperglycemia can damage many of the bodys organs and tissues.

Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an autoimmune process,
and these patients are prone to ketoacidosis.

Type 2 diabetes is the more prevalent form and results from insulin resistance with a defect in
compensatory insulin secretion

Insulin, a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the
production and storage of glucose.

Risk Factors For Diabetes Mellitus Include:

Obesity.

Physiologic or emotional stress, which can cause prolonged elevation of stress hormone levels.

pregnancy, which causes weight gain and increases levels of estrogen and placental hormones, which
antagonize insulin

metabolic syndrome, which is considered a precursor to the development of type 2 diabetes mellitus

some medications that can antagonize the effects of insulin, including thiazide diuretics, adrenal
corticosteroids, and hormonal contraceptives

Classification of Diabetes Mellitus

There are several different types of diabetes mellitus; they may differ in cause, clinical course, and
treatment. The major classifications of diabetes are:

Type 1 diabetes (insulin dependent diabetes mellitus) is caused by B-cell destruction, usually leading to
absolute insulin deficiency

a)Immune mediated

b)Idiopathic

Type 2 diabetes (previously referred to as non insulin dependent diabetes mellitus) ranges from those
with predominant insulin resistance associated with relative insulin deficiency, to those with a
predominantly insulin secretory defect with insulin resistance

PATHOPHYSIOLOGY OF DIABETES
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. Initially, the liver produces glucose through the breakdown of glycogen
(glycogenolysis). After 8 to 12 hours without food, the liver forms glucose from the breakdown of
noncarbohydrate substances, including amino acids (gluconeogenesis).

Type 1 Diabetes

This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less than 10%. The rate
of pancreatic B cell destruction is quite variable, being rapid in some individuals and slow in others. Type
1 diabetes is usually associated with ketosis in its untreated state. It occurs at any age but most
commonly arises in children and young adults with a peak incidence before school age and again at
around puberty. It is a catabolic disorder in which circulating insulin is virtually absent, plasma glucagon
is elevated, and the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is
therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and
reduce blood glucose.

Immune-mediated type 1 diabetes mellitus (type 1A)

Most patients with type 1 diabetes mellitus have circulating antibodies to islet cells (ICA), insulin (IAA),
glutamic acid decarboxylase (GAD65), and tyrosine phosphatases (IA-2 and IA2-) at the time the
diagnosis is made. These antibodies facilitate screening for an autoimmune cause of diabetes,
particularly screening siblings of affected children, as well as adults with atypical features of type 2
Diabetes). Antibody levels decline with increasing duration of disease. Also, low levels of anti-insulin
antibodies develop in almost all patients once they are treated with insulin.
This theory is referred to as the hygiene hypothesis. None of these factors has so far been confirmed as
the culprit. Part of the difficulty is that autoimmune injury undoubtedly starts many years before clinical
diabetes mellitus develops.

Idiopathic type 1 diabetes mellitus (type 1B)

Less than 10% of subjects have no evidence of pancreatic B cell autoimmunity to explain their
insulinopenia and ketoacidosis. This subgroup has been classified as idiopathic type 1 diabetes and
designated as type 1B. Although only a minority of patients with type 1 diabetes fall into this group,
most of these are of Asian or African origin.

Type 2 Diabetes Mellitus

Circulating endogenous insulin is sufficient to prevent ketoacidosis but is inadequate to prevent

hyperglycemia in the face of increased needs owing to tissue insensitivity (insulin resistance).

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.

The exact mechanisms that lead to insulin resistance and impaired insulin secretion in type 2 diabetes
are unknown, although genetic factors are thought to play a role. Despite the impaired insulin secretion
that is characteristic of type 2 diabetes, there is enough insulin present to prevent the breakdown of fat
and the accompanying production of ketone bodies. Therefore, DKA does not typically occur in type 2
diabetes.

Prediabetes

Prediabetes is an abnormality in glucose values intermediate between normal and overt diabetes.

Impaired Fasting Glucose

A new category adopted by the American Diabetes Association in 1997 and redefined in 2004.

Occurs when fasting blood glucose is greater than or equal to 100 but less than 126 mg/dL.

Impaired Glucose Tolerance

Defined as blood glucose measurement on a glucose tolerance test greater than or equal to 140 mg/dl
but less than 200 in the 2-hour sample.

Asymptomatic; it can progress to type 2 diabetes or remain unchanged.

May be a risk factor for the development of hypertension, coronary heart disease, and hyperlipidemias.
Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance occurring during pregnancy.

Occurs in approximately 4% of pregnancies and usually disappears after delivery.

Women with GDM are at higher risk for diabetes at a later date.

GDM is associated with increased risk of fetal morbidity.

Screening for GDM for all pregnant women other than those at lowest risk (under age 25, of normal
body weight, have no family history of diabetes, are not a member of an ethnic group with high
prevalence of diabetes) should occur between the 24th and 28th weeks of gestation.

Diabetes Associated with Other Conditions

Certain drugs can decrease insulin activity resulting in hyperglycemia corticosteroids, thiazide diuretics,
estrogen, phenytoin.

Disease states affecting the pancreas or insulin receptors pancreatitis, cancer of the pancreas, Cushings
disease or syndrome, acromegaly, pheochromocytoma, muscular dystrophy, Huntingtons chorea.

CLINICAL MANIFESTATIONS

Clinical manifestations of all types of diabetes include the three Ps: polyuria, polydipsia, and
polyphagia. Polyuria (increased urination) and polydipsia (increased thirst) occur as a result of the excess
loss of fluid associated with osmotic diuresis. The patient also experiences polyphagia (increased
appetite) resulting from the catabolic state induced by insulin deficiency and the breakdown of proteins
and fats. Other symptoms include fatigue and weakness, sudden vision changes, tingling or numbness in
hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections. The onset
of type 1 Diabetes may also be associated with sudden weight loss or nausea, vomiting, or abdominal
pains, if DKA has developed.

DIABETES MANAGEMENT

The main goal of diabetes treatment is to normalize insulin activity and blood glucose levels to reduce
the development of vascular and neuropathic complications.

Drugs for Treating Hyperglycemia

The drugs for treating type 2 diabetes fall into several categories:

1) Drugs that primarily stimulate insulin secretion by binding to the sulfonylurea receptor. Sulfonylureas
remain the most widely prescribed drugs for treating hyperglycemia. The meglitinide analog repaglinide
and the D-phenylalanine derivative nateglinide also bind the sulfonylurea receptor and stimulate insulin
secretion.
2) Drugs that alter insulin action: Metformin works in the liver. The thiazolidinediones appear to have
their main effect on skeletal muscle and adipose tissue.

3) Drugs that principally affect absorption of glucose: The glucosidase inhibitors acarbose and miglitol
are such currently available drugs.

4) Drugs that mimic incretin effect or prolong incretin action: Exenatide and DPP 1V inhibitors fall into
this category.

5) Other: Pramlintide lowers glucose by suppressing glucagon and slowing gastric emptying.

Insulin

Insulin is indicated for type 1 diabetes as well as for type 2 diabetic patients with insulinopenia whose
hyperglycemia does not respond to diet therapy either alone or combined with other hypoglycemic
drugs.

Therefore, the therapeutic goal for diabetes management is to achieve normal blood glucose levels
(euglycemia) without hypoglycemia and without seriously disrupting the patients usual lifestyle and
activity.

There are five components of diabetes management

Nutritional management

Exercise

Monitoring

Pharmacologic therapy

Education