Diabetes Mellitus:
“Not So Sweet”
Prutha Dave, RN, BSN
davep@alverno.edu
MSN 621 Spring 2009
Alverno College
Let’s Learn About Type II
Diabetes: Home Page
Tutorial Objectives
Click Below For Instructions
On Navigating the Tutorial:
Quick Facts
Navigation
Patho & Genetics
Mini Quiz
Signs & Symptoms
Mini Quiz
Click Below To Take
The Pre-Test:
Pre - Test
Tests & Diagnosis
Mini Quiz
Treatment & Medications
Mini Quiz
Click Below To Start
The Tutorial:
Patient Education
Mini Quiz
Tutorial
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Navigation
•
•
•
•
•
•
Click on
to go to next slide.
Click on
to go back to previous slide.
Click on
to go to the home page.
Click on
to return back to where you were.
Click on
to learn more about the topic.
Role the mouse over or click underlined words to
learn more about them.
• Click on Mini Quiz to take a quick quiz after each
section.
Note: An incorrect answer page will ONLY allow
you to return BACK to the QUESTION.
Objectives of this Tutorial
• After completion of this tutorial the participant
will gain a better understanding of Diabetes
Mellitus, also known as Type II Diabetes.
• Also the participant will be able to care for a
patient with the disease more effectively.
• Topics Covered include:
– Pathology & Causes.
– Symptoms & Treatment.
– Labs/Diagnosis & Patient Education.
Quick Facts
•
•
•
•
•
•
•
In type 2 diabetes, either the body does not
produce enough insulin or the cells ignore
the insulin.
There are 23.6 million children and adults
in the United States, or 7.8% of the
population, who have diabetes.
Significant risk factor for coronary heart
disease and stroke.
Leading cause of blindness and end stage
renal disease.
Major contributor to lower extremity
amputations.
Can be successfully managed with the
right patient education.
Usually affects older adults but becoming
common in obese adolescents.
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1. How is Diabetes
diagnosed?
a. Two separate fasting glucose measurements of 126 mg/dL or higher
b. Using symptoms such as polydypsia, polyphagia, and polyuria
c. A hemoglobin A1C level of 6.5%
Correct! Yay! Great Job!
Two measurements are required to ensure reproducibility and therefore
decrease false positives and increase specificity.
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Oops! Try Again!
Click On The Question To Return To It:
Question 1
Question 2
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Question 3
Question 4
Question 5
2. A deficiency in which of the
following results in hyperglycemia?
a. Glucagon
b. Insulin
c. Ketones
d. Cortisol
Correct! Yay!
INSULIN helps to LOWER blood glucose concentration by
MOVING GLUCOSE into BODY TISSUES for energy
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3. What is the Metabolic
Syndrome?
a. Seen in patients with very slow metabolism
b. Seen in patients who lack growth hormone, insulin, and cortisol
c. Seen in patients with the following cluster of abnormalities:
obesity, hyperlipidemia, hypertension, and glucose intolerance
Correct! Yay!
Metabolic syndrome is a combination of abnormalities including high
triglycerides, low HDL’s, HTN, and inflammation.
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4. Which of the following class of
oral hypoglycemic medications can
cause excessive hypoglycemia?
a. Biguanides (Metformin)
b. ACE inhibitors (Lisinopril, Captopril)
c. Sulfonylureas (Glyburide, Glipizide)
d. Statins (Lipitor, Crestor)
Correct! Yay!
Sulfonylureas increase insulin levels and the rate at which glucose is removed from
the blood, it is important to know that they can cause hypoglycemic reactions.
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5. What are the most common
signs of Type II Diabetes?
a. Palpitations, restlessness, and diarrhea
b. Dehydration, hypotension, and fatigue
c. Excessive laughter, bad body odor, and hair loss
d. Weight gain, blurred vision, and excessive thirst
Correct! Yay!
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Pathophysiology
• Can be due to absolute insulin
deficiency or insulin resistance
• A metabolic disorder which is
characterized by disturbances in
carbohydrate, lipid, and protein
metabolism caused by an
imbalance between insulin
availability and insulin need
• Results in an inability to transport glucose into the cells of the body,
thus causing a breakdown of fat and muscle protein
(Porth, 2005)
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Video: What Happens in
Type II Diabetes?
Click On
Video To
View
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http://professional.diabetes.org/ResourcesForProfessionals.aspx?typ=17&cid=60425
Insulin
• A polypeptide which has a direct effect in
lowering blood glucose level
• Three actions:
– Promotes glucose uptake by target cells and
provides for storage as glycogen
– Prevents fat and glycogen breakdown
– Increases protein synthesis by inhibiting
gluconeogenesis
Insulin Production
• Made by the beta cells of the pancreas (islets
of Langerhans)
• Composed of two polypeptide chains: A and B
• Initially made as a larger molecule: proinsulin
and then cleaved to the active form of insulin
• Other cleavage product is the inactive Cpeptide
Insulin Release
1.
2.
3.
4.
5.
Glucose enters cell
Glycolysis makes
ATP
ATP production
causes K+ channel
to close and
depolarize the cell
Depolarization
opens voltage
sensitive Ca2+
channels (Ca2+
enters cell)
Ca2+ influx causes
insulin release by
exocytosis
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Insulin Action
• Travels through the
portal circulation to the
liver
• Binds to membrane
receptor
• Activates intracellular
enzymes to increase
protein, glycogen, and
fat synthesis, as well as
increasing glucose
transporters
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http://upload.wikimedia.org/wikipedia/commons/thumb/8/8c/Insulin_glucose_metabolism.jpg/400px-Insulin_glucose_metabolism.jpg
Glucagon: Another
Polypeptide
• Antagonist of Insulin
• Released during periods of fasting
to maintain blood glucose
• Released by pancreatic alpha cells
• Causes glycogen breakdown,
gluconeogenesis, protein
degradation, all resulting in
elevation of blood glucose
• In diabetes, can have a negative
effect as glucagon production
goes unchecked as cells are
starved of glucose resulting in
exacerbation of hyperglycemia
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Pathogenesis
• Genetic and
Environmental factors
can lead to insulin
resistance & decreased
release.
• This causes decreased
glucose uptake and
increased glucose output
resulting in
hyperglycemia and
Type II Diabetes.
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Beta Cell Dysfuntion:
Another Sign
• Initial decrease in beta cell
mass.
• Increased apoptosis of cell
and decreased regeneration.
• Long standing insulin
resistance – causing the beta
cells to get TIRED.
• Glucotoxicity, Lipotoxicity.
• Amyloid disposition causing
dysfuction. (Porth, 2005)
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Genetics and Diabetes Mellitus
• There is a strong inheritance pattern for Type
II Diabetes and it is a heterogeneous condition.
• Two major sets of factors play a role in the
development of Diabetes Mellitus:
Genetic Factors
Environmental Factors
Genetic Factors
•Research shows that Diabetes Mellitus is polygenic 
Meaning that it has different combinations of gene defects.
•Multiple “diabetogenic genes” or polymorphisms, each
insufficient in themselves, must be present in order to cause
diabetes.
Click to Learn about
Specific Candidate
Genes
Associated with
DM
•These genetic polymorphisms can affect the
utilization of blood glucose.
(Radha et al, 2003)
Polymorphic Genes :
Defects to Diabetes
Mutations in the following “candidate” genes are
seen in persons with Type II Diabetes and may
directly contribute to the onset of the disease:
*Click To Learn About Specific Genes
Genes Related to Insulin Secretion
Genes Related to Insulin Resistance
Genes Related to Obesity
Insulin Secretion Genes
Human Insulin Gene (INS) –
transcription of the insulin gene
is the restricting step for insulin
synthesis and secretion.
Beta Cell Genes (SUR/KIR 6.2) – these
genes encode components of the B-Cell
K ATP channel which mediate glucose
metabolism and membrane
depolaration to cause insulin realease.
Pancreatic Duodenal
Homedomain Gene (PDX 1) – a
transcription factor gene which
regulates pancreatic
devleopment and islet cell
function.
Images retrieved from: Microsoft Word Clipart 2003
(Radha et al, 2003)
Insulin Resistance Genes
Glucose Transporter Gene (GLUT) –
acts as a sensor to the B-cell
and as a major signaling molecule.
Peroxisome Proliferator Activated
Receptor Gene y (PPAR-y) –
a transcription factor gene
associated in the regulation of adipocyte gene
expression and glucose metabolism.
Insulin Receptor Substrate Gene (IRS) –
this gene is shown to be associated
with decreased insulin sensitivity.
(Radha et al, 2003)
Images retrieved from: Microsoft Word Clipart 2003
Obesity Related Genes
• Research has shown that variations in obesity genes have
resulted in insulin resistance followed with the onset of
Diabetes Mellitus. (Radha et al, 2003)
Single nucleotide
polymorphisms
within this
gene have been
Adiponectin
Genes
associated
with
risk for TypeMORE
II Diabetes.
CLICK
TOa DISCOVER
Mutations of this gene
have beenLeptin
associated
with hyperglycemia.
Receptor
Genes
CLICK TO DISCOVER MORE
Studies with these genes have shown to be
associated with obesity and DM.
Uncoupling
2 Genes
Mutations
may Protein
also cause
interference
CLICK
TOglucose
DISCOVER
MORE
with
homeostasis.
Environmental Factors
• The complex interactions between genes and the
environment make it difficult to identify a single factor
that leads to Diabetes Mellitus. (Radha et all, 2003)
• Environmental Factors Include:
Central Obesity
Lack of Activity
Uncontrolled Diet
Viruses
Toxins (Smoking)
MINI QUIZ: TEST YOUR KNOWLEDGE
What is one function of insulin?
a. Promote weight loss
b. Causes glycogen breakdown
c. Increases protein synthesis
d. Elevate blood glucose
Correct! Great Job!
INSULIN promotes glucose uptake, prevents fat and glycogen breakdown, and
Increases Protein Synthesis! Good Reading!
Oops! Try Again!
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The release of Glucagon has a positive
effect on patients with Type II Diabetes:
True or False?
TRUE
FALSE
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Correct! Great Job!
Glucagon production can have a NEGATIVE effect if it goes unchecked as cells are starved of
glucose resulting in exacerbation of hyperglycemia
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Sorry! Try Again!
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Signs & Symptoms
• Sneaky onset
• Most common signs: The “Polys”
– Polyuria
– Polydipsia
•
•
•
•
•
Blurred Vision
Fatigue
Skin Infections
Paresthesias
Weight loss at first
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MINI QUIZ: TEST YOUR KNOWLEDGE
Which symptom is the patient speaking of when
she says she is having an abnormal touch
sensation?
Polyuria
Gas
Presyncope
Paresthesias
Correct! Great Job!
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Uh-oh! Try Again!
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Tests and Diagnosis
TESTS TO KNOW:
• Fasting Plasma Glucose:
– A blood test that measure the blood glucose level after a person has
FASTING PLASMA GLUCOSE : CLICK TO LEARN MORE
been
fasting for at least eight hours. This is the fastest, most
reproducible, and cheapest method to make the diagnosis.
• Oral Glucose Tolerance Test:
– A test in which a 75g dose of a sugary solution is given and then 2
ORAL GLUCOSE TOLERANCE TEST : CLICK TO LEARN MORE
hours later the blood glucose level is measured. This test is slightly
more sensitive than the plasma glucose.
• Glycosylated Hemoglobin (HbA1c):
– Measures the percentage of red blood cells that have glucose bound to
HbA1c
CLICK TOglycemic
LEARN MORE
them and is useful
in :monitoring
control. Not recommended
for routine diagnosis.
How The Diagnosis is Made
Normal Response
Fasting Plasma Glucose (FPG)
• A fasting blood glucose level less than or equal to 110
mg/dl. This must be confirmed on a separate occasion.
Oral Glucose Tolerance Test (OGTT)
• 2 hour postload glucose level of less than 140 mg/dl.
Impaired Fasting Glucose
&
Impaired Glucose Tolerance
In essence, impaired fasting glucose and impaired glucose
tolerance are the same thing, just measured differently.
Impaired Fasting Glucose:
– A fasting glucose > 110 and < 126 mg/dl. This is considered a risk
factor diabetes, but by itself, does not make the diagnosis of diabetes.
The patient will require close monitoring.
Impaired Glucose Tolerance:
– 2-hour glucose results from the OGTT that are > 140 and < 200
mg/dl. This is also considered a risk factor for future diabetes.
Diabetes
A DIAGNOSIS OF DIABETES IS MADE WHEN:
1. Fasting Plasma Glucose level greater than 126 mg/dl on
separate occasions.
2. Random blood glucose > 200 with classic symptoms.
3. Oral glucose tolerance tests show that the blood glucose
level at 2 hours is > 200 mg/dl. This must be confirmed
by a second test on another day.
MINI QUIZ: TEST YOUR KNOWLEDGE
Which of the following tests is not used for
a routine diagnosis of Type 2 Diabetes?
Fasting Glucose
Oral Glucose
HbA1c
Finger Stick
Correct! Great Job!
Good Job. The HbA1C test is a measurement of glycosylated hemoglobin and is a useful
tool for monitoring glycemic control but is not recommended for diagnostic purposes.
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Almost! Try Again!
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True or False: For a diagnosis for Diabetes to be
made a person must have a Fasting Plasma
Glucose level greater than 126 mg/dl on only one
occasion.
True
False
Correct! Yaayy!
Must have a Fasting Plasma Glucose of 126 mg/dl or higher on TWO occasions. Great Job!
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Oops! Try Again!
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Treatments
• Aim to control blood glucose levels
Oral medications which lower blood glucose by a
variety of mechanisms
Injectable Insulin which directly lowers blood
glucose
• Prevention and reversal of diabetes can be
achieved by a strict diet, exercise, and weight
loss.
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Oral Medications
• Drugs that cause increased insulin release
– Sulfonylureas (Glyburide, Glipizide)
TO REVEAL
MEDICATIONS
– SitagliptinCLICK
(Januvia)
*newer
drug
– Exanatide (Byetta) *newer drug
• Drugs that sensitize cells to insulin
– Biguanides (Metformin)
CLICK TO REVEAL MEDICATIONS
– Thiazolidinediones (Rosiglitazone, Pioglitazone)
• Drugs that block carbohydrate absorption
– Acarbose
CLICK TO REVEAL MEDICATIONS
Sulfonylureas
• Drugs such as Glipizide and Glyburide
• Mechanism: Stimulate insulin secretion by closing
the Beta cell’s
K+TOchannel
causing
depolarization and
CLICK
LEARN THE
MECHANISM
calcium influx. See prior slide
• Side Effects:
–
–
–
–
Hypoglycemia
Rashes
GI upset
Hyponatremia
Biguanides
• Major drug in this class is Metformin
• Mechanism: Makes liver more sensitive to
insulin CLICK TO LEARN MECHANISM
– Great at inducing weight loss
• Side Effects:
– Diarrhea, abdominal pain
– Lactic Acidosis- serious and potentially fatal
• Thus avoid in patients with renal insufficiency, liver
dysfunction or CHF
Thiazolidinediones
• Major drugs in this class are Rosiglitazone
(Avandia) and Pioglitazone (Actos)
• Mechanism:CLICK
Makes
peripheral tissues such as
TO LEARN MECHANISM
fat and muscle more sensitive to insulin
• Side Effects:
–
–
–
–
Weight gain
Liver toxicity
Fluid retention and edema
Contradicted in CHF
Acarbose
• Mechanism: Inhibits enteric enzymes that
CLICK
TO LEARNcarbohydrates,
THE MECHANISM resulting
break down
complex
in partial malabsorption of carbohydrates.
• Side Effects:
–
–
–
–
Bloating
Abdominal discomfort
Diarrhea
Flatulence
Insulin Formulations
• Regular Insulin(Clear solution) Short
acting insulin and the
only form given IV.
• Lente and Ultralente(Cloudy solutions)
Intermediate and
Long acting versions
of insulin.
•NPH- (Cloudy
solution) Intermediate
acting insulin. Usually
given Subcutaneously
(SubQ).
Synthetic Insulin
Modified to have either very short or long half
lives.
Insulin Lispro (Humalog) and Insulin Aspart
(Novolog) have a quicker onset and shorter
duration than Regular Insulin.
Insulin Glargine (Lantus) is a very long acting
form of insulin.
All are administered subcutaneously.
Characteristics of Insulin
Type
Regular
Onset (hr)
0.5
Lispro/Aspart 0.2
NPH
2-4
Lente
1-3
Ultralente 4-6
Glargine
4-6
Peak (hr)
Duration (hr)
2-5
0.7
6-10
6-15
8-30
None
6-8
2
14-18
18-26
24-36
24-36
(Andreoli, 2004)
Profile of Action
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Dosing Regimens
Intermediate and long acting insulin's are
given to mimic the body’s natural 24 hour
basal insulin secretion.
Short acting insulin's are given preprandially to mimic nutrient stimulated
insulin secretion.
Sample Regimens
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Side Effects of Insulin
• Hypoglycemia – too much Insulin can cause
an abnormal decrease in blood glucose
resulting in hypoglycemia.
• Lipohypertrophy at injection site
• Edema
• Weight Gain
• Promotes atherosclerosis at high doses
Image retrieved with permission from: Microsoft Clipart 2003
MINI QUIZ: TEST YOUR KNOWLEDGE
Which of the following patients would you
want to avoid giving a Biguanide to?
Patients with hypothyroidism
Patients with pneumonia
Patients with renal insufficiency and
CHF
Patients with overactive bladders
Correct! Great Job!
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Sorry! Try Again!
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Fill In The Blank:
________ insulin is the only form of
insulin given intravenously.
NPH
Regular
Lantus
Aspart
Correct! Yay!
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Almost! Try Again!
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Patient Education
• Patient education will be the single most
important factor on helping a newly diagnosed
patient manage their Diabetes.
• CLICK ON THE STAR to learn about
outcomes and guidelines for Registered
Nurses who are initiating Diabetes Self
management education:
IMPORTANT !!
Patient Education
IMPORTANT !!
Patient Education
• Describing the diabetes disease process and
treatment options
Click Here To Learn More!!
• Incorporating nutritional management into lifestyle
Click Here To Learn More!!
• Incorporating physical activity into lifestyle
Click here to Learn More!!
• Using medication(s) safely and for maximum
therapeutic effectiveness
Click Here To Learn More!!
(Funnell et al, 2009)
Patient Education
• Monitoring blood glucose and other parameters and
interpreting and using the results for self-management decision
making
Click Here To Learn More!!
• Preventing, detecting, and treating acute and chronic
complications
Click Here To Learn More!!
• Developing personal strategies to address psychosocial issues
and concerns
Click Here To Learn More!!
• Developing personal strategies to promote health and behavior
change
Click Here To Learn More!!
(Funnell et al, 2009)
How To Educate Self
Management
Describing the
Teaching Nutritional
Disease
Physical Activity:
Management: first
Process: before
always, always
learn
beginning
promote
about the
education about the
any physical activity.
patients
disease process,
Help the patients
current diet
perform a
transition
and any
patient
into
cultural
assessment to gain
incorporating
influences that may
a better
an
affect diet.
understanding of the
exercise
Not every
Patient’s
regimen which is
patient
background such as
appropriate
will eat the
cultural beliefs
for them. Again,
same or like
as well as
know
the same food
readiness
that each patient is
that is recommended.
to learn.
exercise.
Safe Medication Use:
make sure the
patient understands
the medication and
why and how it will
help manage the
disease. Speak clearly
and use simple terms.
Also, recommending
The use of a
medication box may
be of great help for
the newly diagnosed
Diabetic.
How To Educate Self
Management
Blood Glucose
Preventing
Monitoring:
Complications:
help the
teach patients
patient understand
to watch out for
the need for blood
any changes in
glucose monitoring.
health status, and
Make sure they know
what specific
how to use their
symptoms to be
specific device
aware of. Examples
and have them do
are eye sight
a repeat
changes or
demonstration
numbness and
for you.
tingling.
Psychosocial Issues:
Promote discussing
any thoughts or
feelings associated
with the new
Diabetes diagnosis.
Provide resources
for patients to
use when dealing
with difficult
psychosocial issues
or concerns.
Promoting Health:
Always promote
healthy lifestyle
behaviors such
as quitting smoking,
eating healthy,
exercising, and
using a family or
personal support
system to
incorporate these
behaviors.
MINI QUIZ: TEST YOUR KNOWLEDGE
What is one of the most important
nursing practices before beginning
patient education for new onset Diabetes?
Making sure that
the patient
has all their
medications in hand.
Making sure that they
exercise everyday for
2 hours
Assessing the
patients background
and readiness to
learn.
Correct! Yay!
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Sorry! Try Again!
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Name a way that patients can remember
to safely take their medications?
Keep all their
medication in one
bottle.Slide 82
Obtain a medication pill
box with the days listed
and with separate
compartments for each
day.
Just double up on
medications the next day
if they forget.
Correct! Great Job!
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Oops! Try Again!
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The End : Credits
*Thank you to my dear husband who put up with me through this crazy
semester and for all his medical and technical expertise.
*Thank you to my mom who motivated me to pursue my knowledge in
Diabetes.
Image retrieved with permission from:http://www.fredscorner.nl/animations.html
References
•
•
•
•
•
•
•
•
American Diabetes Association, www.diabetes.org.
Andreoli, T.E., & Carpenter, C.J., & Griggs, R.C., & Loscalzo, J. (2004) Cecil Essentials of
Medicine. Philadelphia: Saunders.
Funnell, M. et al. (2009) National Standards for Diabetes Self-Management Education,
American Diabetes Association Diabetes Care, 32, S87-S94 DOI: 10.2337/dc09-S087
Hansen, L. (2003). Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility
genes or common polymorphisms? [Electronic Version]. Dan Med Bull, 50(4), 320-46.
Jochen, A.L. (2005) Pharmacology of Insulin and Oral Sulfonylureas. Medical Pharmacology.
Porth, C.M. (2005) Pathophysiology: Concepts of Altered Health States. Philadelphia:
Lippincott Williams & Wilkins.
Radha, V., & Vimaleswaran K.S., & Deepa R., & Mohan, V. (2003). The genetics of diabetes
mellitus. Indian J Med Res, 117, 225-238.
Rossini, A.A., & Mordes, J.P., & Handler, E.S. (1988). Perspectives in Diabetes: Speculations
on Etiology of Diabetes Mellitus: Tumbler Hypothesis [Electronic Version]. Diabetes, 37,
257-61.