Diabetes
Mellitus
C
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M
P
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D
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M
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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
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
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