College
of Nursing
Continuing
Nursing Education |
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Understanding Diabetes Mellitus
"This activity has been
approved by the Continuing Nursing Education Network, which is an Approved
Provider of continuing education by CNE-Net, the education division of the
North Dakota Nurses Association, an accredited approver by the American Nurses
Credentialing Center’s Commission on Accreditation. "
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Kari Lane, MSN, RN
Instructor
South Dakota State University
College of Nursing
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Introduction
Diabetes
Mellitus (DM) is a disease related to energy
metabolism, dealing primarily with how our bodies use glucose
(our major source of energy). DM is a growing concern not only among healthcare
providers in the United States, but worldwide. It's incidenceis
quickly reaching epidemic proportions.
Diabetes Mellitus affects
17 million individuals in the US and 5.9 million individuals are believed
to have DM, but have not yet been diagnosed. It is the 4th
leading cause of death in the US, and is the cause of severe
and debilitating disability in many individuals.
Diabetes also generates
a great deal of health care cost, which is bound to increase with time
and inflation. Understanding Diabetes Mellitus
will assist the health care provider to provide up-to-date, clear, and
concise information to the consumer. In today's fast paced, technology
oriented world, it is essential to be knowledgeable regarding the most
current information (CDC
Diabetes Public Health Resource, 2000) and (Sommers and Johnson, 2002).
Objectives
Upon completion of the course,
you will be able to:
-
Discuss the physiology of energy
metabolism.
-
Discuss the pathophysiology of
Diabetes Mellitus.
-
Differentiate between Type 1
and Type 2 Diabetes Mellitus.
-
Discuss the use of medication
to treat Diabetes Mellitus.
Table
of Contents
Physiology
of Energy Metabolism
Pathophysiology
of Diabetes Mellitus
Clinical
Presentation
Diagnostic
Criteria
Classification
Complications
Treatment
Conclusion
Post-Test
Evaluation
References
Physiology
of Energy Metabolism
It is important to understand
the physiology of energy metabolism in order to understand Diabetes Mellitus.
All body cells use glucose for energy, the brain requires the majority
of this energy, and also requires a constant source, as it cannot store
glucose. To maintain this constant source of energy, blood glucose levels
must be kept between 60-120 mg/dL. There are several mechanisms normally
present in our bodies to maintain this level (Quinn 2001 and Hart 2001).
Several hormones are required
to maintain the blood sugar between 60-120 mg/dL. First, the pancreas secretes
insulin from the beta cells, glucagon from the alpha-2 cells, and somatostatin
from the alpha-1 cells. These hormones are secreted based on changes in
our body's blood glucose levels, amino acid levels, ketone levels, and
fatty acid levels (Hart 2001).
For additional information about the Pancreas, surf
to Encyclopedia.com
Diabetes is a disease which
deals with insulin . Insulin is made in stages by the beta cells. A healthy
pancreas can release 40-50 units of insulin daily, still keeping several
hundred units available in storage to be released if the blood glucose
levels rise enough. When insulin enters the bloodstream, it binds to insulin
receptors on the membranes of the liver, muscle, and fat cells. This is
where insulin is able to promote the intake of glucose, encourage energy
storage, and prevent the breakdown of stored energy (Hart 2001).
The liver has several functions
as well. Increased insulin secretion inhibits the breakdown of stored glycogen,
suppresses the formation of new glucose, and increases the synthesis of
glycogen. Insulin also stimulates glycolysis which provides the precursors
for the formation of fatty acids. Insulin also discourages the production
of ketone bodies (Hart 2001).
The muscle and fat cells
also have a role. In these cells, insulin encourages glucose uptake by
causing a shift of another insulin sensitive glucose transporter, GLUT
4, to the surface of cells. It also encourages the storage of glucose and
promotes protein synthesis. Uptake of glucose by muscle accounts for around
85% of glucose deposits. Glucagon, somatostatin, catecholamines,
and glucocorticoid hormones all have an affect of insulin production, storage,
and release (Hart 2001).
Pathophysiology
of Diabetes Mellitus
Hart (2001, p. 207) described
the pathophysiology of Diabetes Mellitus best
in her text.
"Diabetes mellitus
is not a single disease but instead is a complex
syndrome characterized by hyperglycemia resulting from altered
carbohydrate, fat, and protein metabolism. This altered metabolism is secondary
to insulin insufficiency, insufficient insulin activity, or both, and to
increases in the counter-regulatory hormones that oppose the action of
insulin. Because of the sequelae of altered fuel metabolism, diabetes is
characterized by vascular and neurologic changes throughout the body.
Absence of insulin or ineffective insulin activity
prevents glucose from entering muscle and fat cells. As the blood glucose
level approaches 180 mg/dL, the ability of the kidney to reabsorb glucose
is surpassed, and glucose is excreted into the urine. Because it is an
osmotic diuretic, glucose causes the osmosis of large amounts of water
into the tubules, causing frequent urination in large quantities (polyuria),
notably at night (nocturia). Dehydration, hunger, and fatigue follow. The
classic symptoms of diabetes mellitus ensue: polyuria, polydipsia, and
polyphagia.
To overcome the lack of glucose, the body begins
breaking down protein stores, leading to a negative nitrogen balance. In
the continued absolute absence or ineffectiveness of insulin, fat stores
are mobilized into free fatty acids (FFAs). In the liver excess amounts
of fatty acids cannot enter into the Krebs cycle and instead condense into
acetoacetic acid and beta hydroxybutyrate, called ketone bodies, which
are acidic. To buffer these acids, the body excretes acidic urine and buffers
the blood acidity with bicarbonate and buffer bases reserves. However,
continued production and buffering of ketones causes a drop in plasma pH,
acidosis, and eventually death if left untreated."
Pictures regarding the pathophysiology of Diabetes
Mellitus can be found at:
Clinical
Presentation
Polyuria,
polydipsia,
and polyphagia are the most common
signs and symptoms that clients present with. Other possible signs and
symptoms include: weight loss (even when eating well), blurred vision,
and signs of infection.
Diagnostic
Criteria
The American
Diabetes Association (2002) has established three
criteria for diagnosing Diabetes Mellitus.
If any one of these three criteria are present in a client, they need to
be confirmed by one of the three methods on a separate day. If then the
criteria still exist, the client is diagnosed with DM.
The criteria are:
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A fasting plasma glucose level of 126 mg/dL or greater.
Fasting means no caloric intake for at least 8 hours.
-
A casual plasma glucose level of 200 mg/dL or greater
combined with the classic signs and symptoms of DM. Casual means this level
is taken at any time of day without regards to when the last meal was ingested.
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An oral glucose tolerance test of 200 mg/dL or greater
in the 2 hour sample.
The
American
Diabetes Association (Diabetes Care, 2002) does recommend the use of
the fasting plasma glucose level for universal testing as it is easy to
administer and is a low cost tool. The ADA has also established criteria
for being at high risk for DM they include:
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Impaired fasting glucose, where the FPG is > or equal
to 110 mg/dL but under 126 mg/d l.
-
Impaired glucose tolerance, where the result is greater
than or equal to 140 mg/dL but under 200 mg/dL with the 2 hour sample.
Classification
There are several types
of DM they include:
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Type 1
-
Type 2
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Gestational
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Other
This continuing education presentation will address
only Type 1 and Type
2.
Quinn (2001) & Hart
(2001) described Type 1 Diabetes Mellitus
as having two different etiologies (autoimmune and idiopathic). Type 1
DM, autoimmune disease, occurs when the beta cells of the pancreas are
destroyed. There are several markers found in the blood to determine if
a client has Type 1 DM or not.
They include:
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Islet cell autoantibodies (ICAs)
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Autoantibodies to insulin (IAAs)
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Autoantibodies to glutamic acid decarboxylase (GAD65)
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Autoantibodies to tyrosin phosphatase (IA-Z and IA-ZB)
There must be at least one of these present (although
there are usually more than one present) to determine autoimmunity and
Type 1 DM.
It has been determined
that the rate of beta cell destruction is quite variable. Unlike the information
which had been known in the past. Currently scientists have found that
usually, but not always, the rate of beta cell destruction is rapid in
infants and children and slow in adults. In fact, some clients may experience
such rapid beta cell destruction that ketoacidosis is the first presenting
symptom(s). Type 1 DM is common in childhood and the teen years, but in
fact can occur at any age. These clients are rarely obese, and are
prone to many other autoimmune disorders such as: Graves disease, Hashimoto's
thyroiditis, Pernicious anemia, Addison's disease, and/or Vitiligo (Quinn
2001 & Hart 2001).
Type
1, idiopathic DM, has no
known etiology and no evidence of autoimmunity. This form of DM has a varying
degree of insulin deficiencies, is strongly inherited, and the requirements
for insulin may come and go. Only a few clients suffer from this form of
Type 1 DM, and are most of Asian or African descent (Quinn 2001& Hart
2001).
Type
2 DM is a form of insulin resistance with a varying degree of
insulin deficiency. Usually clients do not require insulin when they are
first diagnosed, and often will never require insulin. The etiology of
Type 2 DM is unknown.
Although the etiology is
unknown three stages of Type 2 DM development have been confirmed. The
stages are described by Quinn(2001):
-
Hyperinsulinemia.
beta cells can overcome insulin resistance and maintain normal glucose
tolerance. A defect in insulin secretion causes the beta cells to increase
insulin production. The client's body can maintain normal glucose homeostasis
by compensating with Hyperinsulinemia.
-
Insulin Resistance.
The compensatory mechanisms of the body become insufficient, and the fasting
plasma glucose continues to be normal, but the postprandial glucose levels
rise.
-
Increased Insulin Resistance.
As insulin resistance continues the body attempts to compensate by changing
the hepatic glucose production. Postprandial glucose levels continue to
rise and insulin secretion decreases. This will change the fasting glucose
levels and signs and symptoms of elevated glucose levels begin to be present.
Quinn (2001) described clients
diagnosed with Type 2 DM as being obese, have an increased percentage of
body fat distributed in the abdominal area of the body. This form of DM
can go undiagnosed for years as ketoacidosis is very rare, and the progression
of the disorder is slow. These clients, as Type 1 clients, are at risk
for microvascular and macrovascular changes that can be quite severe in
nature. Studies have also shown that insulin resistance may improve with
weight loss or pharmacological treatment of high glucose levels, but rarely
will return to normal.
Clients who are at risk
for Type 2 DM include those with advanced age, obesity, sedentary lifestyle,
history of gestational diabetes, birth weight over 10 pounds, hypertension,
ethnic background, and/or genetic predisposition. Certain ethnic groups
have a higher incidence as do those in lower socioeconomic backgrounds
(Hart 2001).
The breakdown of ethnic groups with Type 2 DM includes:
-
Non-Hispanic White 7.8%
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Non-Hispanic Black 13%
-
Hispanic/Latino 10.2%
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American Indian 15.1%
-
Asian 3.8 %
*CDC
Diabetes Public Health Resource
Complications
For both Type 1 and Type
2 Diabetes Mellitus there are several known complications that occur with
higher incidence. Some of the complications can occur in an acute manner
or on a regular basis. These acute complications require some form of treatment,
either by the client themselves or by medical personnel. According to Sommers
& Johnson (2002) These acute complications include:
• Hyperglycemia
• Hypoglycemia
• Lipodystrophy
• Electrolyte Imbalances
• Diabetic Ketoacidosis (DKA)
• Hyperglycemic hyperosmoler nonketotic syndrome
(HNNK)
Hyperglycemia and Hypoglycemia are the most common
complications for the
diabetic client. Sommers & Johnson (2002) described
the signs and symptoms of both in the table below.
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Hyperglycemia
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Hypoglycemia
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Nausea, vomiting, anorexia
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Thirst, lethargy, cramping
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Flushed or dry skin, dry mucous membranes
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Confusion, irritability, fatigue
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Weakness, numbness, tachycardia
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Hypotension, decreased level of consciousness
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Coma, fruity breath
Treatment: Retore fluid balance, administer
regular insulin, monitor vital signs and respirations. |
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Nervousness, diaphoresis, weakness
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Fatigue, palpitations, tremors
-
Blurred vision, headache, confusion, seizures
-
Irritability, hunger, tachycardia, hypotension, pallor
-
Incoherent speech, numbness of tongue and lips
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Coma
Treatment: Provide rapidly absorbed source of
glucouse (fruit juice or cola, graham crackers). |
Other complications are
considered to be chronic, taking months to years, perhaps even decades
to develop, they include microvascular and macrovascular changes that put
clients at higher risk for serious and life threatening disease processes.
These complications are summarized by Diabetes Care (2002):
• Retinopathy with the possibility of blindness
• Nephropathy with the possibility of renal failure
• Peripheral neuropathy with the possibility of
amputation of extremities
• Autonomic neuropathy
• Hypertension
• Atherosclerotic disease
• Cardiovascular
• Peripheral vascular
• Cerebrovascular
• Periodontal disease
Additional information regarding the complications
of DM can be found at:
Treatment
Treatment options for
Type
1 and Type 2 DM differ depending on the degree of insulin deficiency
or resistance. They also differ depending on the client's ability to follow
a lifestyle altering treatment plan. This treatment plan begins with exercise
and diet changes, which is no simple task.
Each client must learn
how to exercise in a manner that will assist their body in maintaining
a proper or nearly proper blood sugar level. Exercise alone could achieve
this, but many times it is a combination of exercise, diet, and medication
which must be balanced.
Exercise plans for the diabetic client are further
described at:
Diet plans today are usually
focused on carbohydrate counting, or counting the amount and type of sugar
which is ingested over a 24 hour period of time. The concept is that if
you limit the amount of carbohydrate you ingest, your blood sugar should
be affected.
Carbohydrate counting is described in more detail
at:
Medication can be a form of
treatment for the diabetic client. Medication can include insulin or oral
antidiabetic agents. Insulin is produced by drug companies in two manners.
Insulin is either taken from a pig or synthetically made in a laboratory.
Most commonly today, the synthetic version of insulin is prescribed. Insulin
must be prescribed by a physician. Insulin is injected under the skin into
the fatty or subcutaneous layer of tissue. Currently this is the only way
insulin can be administered.
There are many different
forms of insulin and each of these have different way of working. It is
important for the client, nurse, and physician to understand how each of
the different types of insulin work in order to care for the client appropriately.
Wilson, Shannon & Stang (2003) described insulin affects as follows:
• Subcutaneous administration only
• Check the type of insulin to know when to inject
in relation to meals as each type of insulin varies tremendously
• Store insulin at room temperature unless the
vial in unopened. All unopened vials can be kept in the refrigerator
• Write the date when the vial was opened on the
vial and discard after one month
• Do not expose to sunlight or freeze
• Common side effects of insulin include: lipodystrophy,
rash, pruritus, hypoglycemia, hypokalemia
• Onset, Peak and Duration vary depending on the
type of insulin, check the package insert for this information
• Regular insulin is the only insulin type that
can be administered intravenously
• Some types of insulin can be mixed, check the
package insert for additional information
For additional information about injection
sites, surf to
LillyDiabetes.com
For additional information about types
of insulin, surf to:
Oral Antidiabetic Agents are
hormone replacement therapy for the diabetic client. These are administered
in a pill form and work in a variety of ways. There are four classifications
of oral antidiabetic agents: sulfonyureas, alph-glucosidase inhibitors,
biguanides, and thiazonlinediones. Currently research is under way to develop
other classifications and drugs. All of these drugs work very differently
as well. Healthcare providers and clients need to be familiar with these
agents in order to care for the clients appropriately. The client must
also be aware that other drugs/agents can affect how these drugs work and
they should ask their healthcare provider about possible side effects when
beginning any new drug.
For additional information about oral
antidiabetic agents, surf to:
There are currently two other
treatment options available for the diabetic client, a pancreas transplant
and islet cell transplant. The pancreas transplant is described in Diabetes
Care (2002) as being able to eliminate the need for exogenous insulin in
certain types of clients. Thus far transplants have been successfully performed
in clients with Type 1 DM with severe complications both acute and chronic.
This procedure has usually been performed on clients who have had DM for
20 years or more and do require long term immunosuppression to prevent
rejection. The ADA (2002) described a pancreas transplant being appropriate
for clients who:
• Have imminent or established end-stage
renal disease
• Have had or plan to have a kidney transplant
• If these clients do not have renal disease then
they should have:
• A history of frequent severe metabolic complications
• Clinical and or emotional problems with insulin
regimens
• Consistent failure of insulin based management
Click on the following link for a
pictural
diagram of a pancreas transplant.
Diabetes
Care (2002) also described islet cell transplantation being
performed in clinical research trials at this time. This procedure continues
to be in the research stages, but does offer hope to those patients with
Type 1 DM. Thus far several patients have received islet cell transplantation
from cadavers one or more times in order to reverse the effects of DM.
The research results are promising at this time, but further research must
be completed prior to approval for other Type 1 DM clients to receive this
type of treatment.
Conclusion
As described in this continuing
education article, Diabetes Mellitus is a long-term disorder that affects
the energy metabolism components of the human body. Diabetes affects millions
of people and its incidence in increasing by drastic measures. Due to the
widespread incidence, the cost of caring for those with DM, and the multisystem
complications that occur in these clients, DM must be identified quickly.
It is essential that these individuals control their blood sugars to the
best of their ability in order to minimize these life and limb threatening
complications.
Post-Test
Evaluation
References
CDC Diabetes public health
resource. (2002).
Found at
http://www.cdc.gov/diabetes/pubs/estimates.htm
DiabetesCare. (2002). Position
statement. Pancreas transplantation for patients with type 1 diabetes.
American Diabetes Association. 25(S111).
Found online at:
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s111.
DiabetesCare. (2002). Committee
report. Report of the expert committee on the diagnosis and classification
of diabetes mellitus. American Diabetes Association. 25(S5-S20).
Found online at:
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s5
DiabetesCare. (2002). Position
statement. Insulin administration. American Diabetes Association.
25(S112).
Found online at:
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s112.
DiabetesCare. (2002). Position
statement. Diabetes mellitus and exercise. American Diabetes Association.
25(S64).
Found online at:
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s64.
Hart, R. (2001). Diabetes.
In advanced pathophysiology: Application to clinical practice. By M. Groer.
Lippincott Williams & Wilkins: Philadelphia. Pp. 204-229.
Quinn, L. (2001). Type
2 diabetes epidemiology, pathophysiology, and diagnosis. Nursing clinics
of north america 36(2), p. 175-191.
Sommers, M.S., Johnson,
S.A. (2002). Diseases and disorders: A nursing therapeutics manual. F.A.
Davis Company: Philadelphia.
Wilson, B.A., Shannon,
M., Stang, C. ((2003). Nurse's drug guide 2003. Pearson Education, Inc.:
Upper Saddle River, NJ.
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