Ghina Rahmi

Sabtu, 29 Juni 2013

Diabetes milletus Dalam bahasa

Inggris
Diabetes Mellitus
C
O
M
P
L
I
D
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

i
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 body’s 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,
Cushing’s disease or syndrome, acromegaly, pheochromocytoma, muscular dystrophy,
Huntington’s 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
patient’s usual lifestyle and activity.

There are five components of diabetes management

• Nutritional management
• Exercise
• Monitoring
• Pharmacologic therapy
• Education

Diposting oleh Ghina Rahmi di 04.51

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1 komentar:
1.

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Talk soon.
Balas

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