1

Corinne Smith
KNH 411
Case Study #22
Type 1 Diabetes Mellitus
I.
Understanding the Disease and Pathophysiology
1. Define insulin. Describe its major functions within normal metabolism.
Insulin is a hormone produced by the beta cells of the islets of Langerhans in
the pancreas to regulate blood glucose; it promotes uptake, utilization, and
storage of nutrients (Nelms 476). Insulin is an anabolic hormone that controls
the metabolism of carbohydrates, lipids, and proteins. Insulin promotes the
uptake of glucose into hepatic, muscle, and adipose cells as well as the
stimulation of glycogen, triglycerides, and protein synthesis. It is stimulated
by an increased blood level of glucose. Tissues in the body rely on insulin for
transportation of glucose in the bloodstream to the cells. The GLUT-4
transporter, present in the skeletal and cardiac muscle and in adipocytes, is
insulin dependent and insulin allows it to travel into the cell membrane,
where it transports glucose into the cell. The net effect of insulin is to
promote glucose oxidation, glycogen storage, and triglyceride storage. In
protein metabolism, insulin promotes active transport of amino acids from
the blood into muscle and other tissues, allowing for protein synthesis within
cells. This anabolic effect of insulin on protein metabolism produces a
positive nitrogen balance (Nelms 476-477).
2. What are the current opinions regarding the etiology of type 1
diabetes mellitus (DM)?
Type 1 diabetes is an immune-mediated disease that results from a cellmediated autoimmune response that kills the beta cells in predisposed
individuals. There is a primary gene in the HLA region on chromosome 6
responsible for T1DM, but more than 20 gene associations have been linked
to the T1DM. The environmental agent that initiates the autoimmune
response is more difficult to pin point due to the lapse in time between the
exposure and the development of DM. Research shows that possible triggers
include viruses, gluten, vitamin D levels, and infant feeding practices.
Ongoing perspective studies will hopefully provide more information on these
triggers. Also, some forms of T1DM have absolutely no known cause and are
referred to as fulminant T1DM. This form has a more immediate and
complete destruction of beta cells with no evidence of an autoimmune
response. These individuals are more susceptible to ketoacidosis and
represent a very small minority consisting mostly of individuals with African
or Asian ancestry (Nelms 481).

3. What genes have been identified that indicate susceptibility to

type 1 diabetes mellitus?
The primary gene for type 1 DM is located in the HLA region on chromosome
6. Polymorphisms in the HLA complex account for 40-50% of the genetic risk
for developing type 1 DM, however there are greater than 20 different genes
that have been linked to risk for type 1 DM. The genetic component of T1DM
supports increased risk of relatives with T1DM, but this is relatively low.
Determining the environmental agents that stimulated the autoimmune
response has been difficult to pin point because of the time lapse between
exposure and disease onset. Research suggests that interaction of several
environmental factors plus predisposed genes contribute to the onset of
T1DM. Some examples of environmental triggers include viruses, gluten,
vitamin D levels, and infant feeding practices (Nelms 481).
4. After examining Susans medical history, can you identify any risk
factors for type 1 DM?
After examining Susans medical history, I was able to identify some risk
factors for type 1 DM. The risk factors include: family history of maternal
grandmother DM, suspected weight loss, irregular meal schedule containing
high carbohydrate and sugar intake, hemoglobin A1C levels at 7.95%
compared to the normal 3.9-5.2%, glucose levels of 250 mg/dL compared to
the normal 70-110 mg/dL, increased blood osmolality of 304 mmol/kg/H2O
(probably due to diabetic ketoacidosis), and high levels of blood urea
nitrogen of 20 mg/dL. Some of Susans resulting symptoms include
polydipsia, polyuria, polyphagia, weight loss, and fatigue.
5. What are the established diagnostic criteria for type 1 DM? How
can the physicians distinguish between type 1 and type 2 DM?
Criteria for diagnosis of Diabetes Mellitus:
A1c > or equal to 6.5% using standardized laboratory measures or fasting
plasma glucose^2 > OR equal to 126 mg/dL (7.0 mmol/L) OR symptoms of
diabetes (unexplained weight loss, polydipsia, polyuria) plus random glucose
concentration > or equal to 200 mg/dL (11.1 mmol/L) OR 2-hour postprandial glucose > or equal to 200 mg/dL (11.1 mmol/L) during an oral
glucose tolerance test (Nelms 481).
Physicians can distinguish between type 1 DM and type 2 DM by determining
whether the person is insulin resistant (type 2 DM) or if there is complete

3
destruction of beta cells in the pancreas making the person insulin
dependent (type 1 DM) (Nelms 481-484).
6. Describe metabolic events that lead to Susans symptoms
(polyuria, polydipsia, polyphagia, weight loss and fatigue) and
intergrate these with the pathophysiology of the disease.
Type 1 DM is characterized by destruction of beta cells causing a deficiency
of insulin, resulting in the inability of cells to use glucose for energy. When
glucose cannot enter the cells plasma glucose levels rise causing
hyperglycemia and cells starve. This signals an increase in gluconeogenesis
in the liver and stimulation of glycogenolysis, further exacerbating the
hyperglycemic state. To counterbalance this state, excess glucose is lost in
the urine because the kidneys can only filter so much glucose from the
blood. As a result, glycosuria and polyuria (frequent urination) occur. Loss of
so much fluid stimulates thirst, causing polydipsia. And since cells have no
glucose for energy, the body is fatigued and stimulates hunger to try and get
more glucose, causing polyphagia. As insulin deficiency persists, production
of additional hormones, such as catechlolamines, cortisol, glucagon, and
growth hormone, increases leading to lipolysis. As the body breaks down fat
stored in adipose tissue, the resulting fatty acids are made into keto acids in
the liver. This makes pH fall from 7.3 to 6.8 and ketone bodies are excreted
in the urine. Metabolic acidosis develops as bicarbonate concentration is
reduced and ketoacidosis occurs. The body tries to offset metabolic acidosis
through deep, labored respirations, known as Kussmaul respirations. As total
body water decreased from polyuria, potassium, sodium, magnesium,
phosphorus, and weight are lost. Serum levels of these ions may be normal
or elevated due to decreased fluid loss in the body causing hypovolemia.
This accounts for the increased hemocrit, hemoglobin, protein, WBC count,
creatinine, and serum osmolality. Hypovolemia and muscle catabolism are
causes for weight loss (Nelms 505).
7. List the microvascular and neurologic complications associated
with type 1 diabetes.
Microvascular complications associates with type 1 diabetes include
neuropathy and retinopathy. The risk factors for nephropathy and retinopathy
include hypertension, hyperglycemia, Native American, Hispanic American,
or African American descent and duration of DM (Nelms 489). Approximately
of people with diabetes have some form of peripheral neuropathy (PN).
This half of individuals either has polydiabetic, monodiabetic, or autoimmune
neuropathy. Autoimmune neuropathy includes cardiovascular autonomic

4
dysfunction, manifested as abnormal heart rate and vascular control.
Diabetes PN can be detected when there is loss of sensation in lower
extremities, this combined with abnormal vascular control results in lowerextremity ulceration. Diabetic neuropathy (DN) is a serious complication and
progression of T1DM and T2DM. It first begins with microalbuminuria, then to
albuminuria (increased albumin levels in the urine), and lastly kidney failure.
Diabetic retinopathy (DR) is a microvascular complication that impairs the
retina, macula, and can cause blindness in individuals with diabetes. The risk
for DR increases with the duration of diabetes (Cade, W. T. 2008).
8. When Susans blood glucose is tested at 2 AM, she is
hypoglycemic. In addition, her plasma ketones are elevated. When
she is tested early in the morning before breakfast, she is
hyperglycemic. Describe the dawn phenomenon. Is Susan likely to
be experiencing this? How might this be prevented?
The dawn phenomenon is an increase in blood glucose in the early morning,
most likely due to increased glucose production in the liver after overnight
fasting. It results from the effect of hormones involved in controlling
circadian rhythms. Cortisol and growth hormone stimulate gluconeogenesis,
this causes hyperglycemia between 5 AM and 9 AM, also known as dawn. To
correct this, bedtime snacks or insulin regimens should be adjusted. It is
possible Susan is experiencing this, but it may also be rebound effect. The
rebound effect refers to an elevation in blood glucose as a reaction to
previous low blood glucose levels during the night. Susan should adjust her
insulin to account for this dawn rise and eat a snack before bedtime (Nelms
470, 505).
9. What predicting factors may lead to the complication of diabetic
ketoacidosis? List these factors and describe the metabolic events
that result in the signs and symptoms associated with DKA.
Risk for DKA increases with acute illness (cerebrovascular accident,
alcohol/drug abuse, pancreatitis, pulmonary embolism, myocardial infraction,
trauma), infection, emotional stress, drug abuse, increased insulin needs
with growth spurts, pregnancy and omission of insulin (pump malfunction or
on purpose). Omission of insulin may occur when individuals feel too sick to
eat or when they are afraid of developing hypoglycemia. When sufficient
insulin is not available, glucose production by gluconeogenesis and lipolysis
are stimulated in effort to prevent starvation. Lipolysis generates ketones
and as these and glucose accumulate in the bloodstream, osmotic diuresis
occurs causing dehydrations and electrolyte imbalances. As the fluid is lost,

5
the individuals blood will become concentrated further contributing to
hyperglycemia. They resulting symptoms of DKA are nausea and/or vomiting,
stomach pain, fruity or acetone breath, Kussmaul respirations, polyuria,
polydipsia, dehydration, lethargy, cerebral edema (can lead to coma) and
metal status change (Nelms 505-506).
II.
Nutrition Assessment
A. Evaluation of weight/body composition
10. Determine Susan stature for age and weight for age percentile.
Susan weighs 45.45 kg and is 62 inches tall (157.48 cm).
Her BMI is 18.29 kg/m2
According to the CDC Susans weight for age is in the 20th percentile, her
stature for age is in the 25th percentile, and her BMI for age is in the 26th
percentile (CDC 2015).
11. Interpret these values using the appropriate growth chart.
According to the CDC, Susan is at a healthy weight and stature for age. Being
in the 20th percentile for weight for age means that 80% of children her age
and sex are larger than her and 20% are smaller. The same goes for her
stature for age, 74% are taller than her and 26% are shorter (CDC 2015).
B. Calculations of Nutrient Requirements
12. Estimate Susans daily energy and protein needs. Be sure to
consider Susans age.
EER for females 9-18 years old: 135.3- (30.8*age) + PA * (10.0*weight + 934
* height) +25
= 135.3- (30.8*15) + 1.44 * (10.0*45.45 kg + 934 *1.5748 m) +25=2470
Kcal
I chose the physical activity coefficient 1.44 since Susan reported being on a
volleyball team practicing 4 evenings a week and two games per week.
Estimate energy needs: 2400-2500 Kcal/day
Protein Needs: 45.45 kg * 0.8= 36.36; 36 grams protein/day
Or based on EER= 24002500 kcal x 0.15=360375 kcal/4=9093.75
grams
(Nelms)
13. What should the clinician monitor in order to determine whether
or not the prescribed energy level is adequate?

6
The clinician should monitor her biochemistry data such as prealbumin
levels, her lipid profile, blood glucose, the presence of ketones in her urine
and any weight loss or weight gain (Nelms).
C. Intake Domain
14. Using a computer dietary analysis or food composition table,
calculate the kcalories, protein, fat (saturated, polyunsaturated,
and monounsaturated), CHO, fiber, and cholesterol content of
Susans typical diet.
Kcalories
Protein
Fat
- Saturated
- Polyunsaturated
- Monounsaturated
CHO
Fiber
Cholesterol
(SuperTracker 2015)

3340 kcal
105 g x 4= 420 kcal; 13 %
113.8 g x 9= 1024 kcal; 32%
13%
7%
10%
474 g x 4= 1896 kcal; 57%
22 g
240 mg

15. What Dietary assessment tools can Susan use to coordinate her
eating patterns with her insulin and physical activity?
There are many dietary assessment tools Susan can use to coordinate her
eating patterns with her insulin and physical activity. She can start by
keeping a food log that contains what she ate, how many carbohydrates it
contained, how much insulin was required, and any blood glucose levels she
tests. She can estimate the number of CHO in her food either by using the
diabetic exchange system or carbohydrate counting. The exchange system
categorizes food intake into exchange amounts based on portion and foods
consumed. Carbohydrate counting converts 15 g of carbohydrates into one
carbohydrate choice. The amount of insulin needed to correct is then based
on the exchange or carbohydrate choice. Either method is effective, Susan
can chose which one works best for her, than I can educate her more in
depth about the method. After daily practice, it will be come second nature
(Nelms 501-502). With all the physical activity Susan does, she should record
her blood glucose before, during, and after practice/games and record it.
That way over time she could get a good idea about how her blood glucose
reacts to physical activity and plan accordingly with snacks and water
available.

7
16. Dieticians must obtain and use information from all components
of a nutrition assessment to develop appropriate interventions and
goals that are achievable for the patient. This assessment is
ongoing and continuously modified and updated throughout the
nutrition therapy process. For each of the following components of
an initial nutrition assessment, list at least three assessments you
would perform for each component.
Component
Clinical data

Nutrition History

Weight History
Physical activity history
Monitoring
Psychological/economic
Knowledge and skill level
Expectation and readiness to
change

Assessments you would perform

Visceral protein assessment,
Hematological assessment, lipid
assessment, renal assessment,
Endocrine-specific biochemical data,
medical tests & procedures, and MD
referral of patient chart
Ability to chew,
constipation/diarrhea, 24-hour recall,
previous nutrition education, ethnic
or religious influence
Usual body weight, highest adult
weight, current weight, BMI
Type of activities, frequency of
activities, length of activity, daily
chores and activity
Journaling daily diet-specifically
CHO, how frequent blood glucose is
checked, weight monitoring
Socioeconomic status of family,
health insurance availability,
attendance to support groups
Highest education level, ability to
check own blood sugar, knowledge
of CHO counting
Readiness to change visual (such as
thermometer or ruler), adherance to
new diabetic diet, willingness to
check blood glucose and administer
insulin shots

(Nelms 495-496)
D. Clinical Domain
17. Does Susan have any laboratory results that support her
diagnosis?

8
Susan has multiple lab results that support her diagnosis of T1DM. They
include increased osmolality of 304 mmom/kg/h20, glucose of 250 mg/dL,
BUN (blood urea nitrogen) of 20 mg/dL, and hemoglobin A1c of 7.95%. These
values meet the criteria for diagnosis of DM of A1c >6.5%, fasting plasna
glucose > 126 mg/dL. The table below outlines the reasons for abnormality
and comparison of normal values (Nelms 481).
18. Why did Dr. Green order a lipid profile?
Dr. Green ordered a lipid profile to assess Susans total cholesterol, her HDL
and LDL levels and triglyceride levels. These numbers are important because
they asses the her risk factors for cardiovascular disease. Total cholesterol
should be between 120-199 mg/dL, LDL should be less than 130 mg/dL, HDL
should be greater than 55 mg/dL for women and triglycerides should be
between 35-135 mg/dL for women, all of which Susan is within the normal
range. Cardiovascular disease is a macrovascular complication of diabetes
and its greatest risk factors are T2DM, hypertension, and dyslipidemia
(Nelms 489).
19. Evaluate Susans laboratory values
Chemistry
Normal
Susans
Values
Values
Prealbumin
16-35 mg/dL
40 mg/dL
Osmolality

285-295
mmol/kg/H20

304
mmol/kg/h20

Glucose

70-110 mg/dL 250 mg/dL

BUN

8-18 mg/dL

20 mg/dL

HbA1c

3.9-5.2 %

7.95%

Reason for
abnormality
Decreased
fluid volume
Hyperglycemi
a, decreased
fluid volume
Hyperglycemi
a
Decreased
kidney
function due
to excess
blood glucose
in the
bloodstream
Increased
blood glucose
over a 3
month period

Nutritional
Implications
Dehydration
Dehydration,
weightloss
Increased
hunger
Possible
kidney failure
and GI tract
complications

Polyuria,
polydipsia,
complications
associated
with T1DM

20. Compare the pharmacological differences in insulins:

Type of
Brand Name Onset of
Peak of
Duration of

9
Insulin
Lispro
Aspart
Glulisine
NPH

Action

action
(hours)
30-90
30-90
30-90
4-10

action
(hours)
3-5
3-5
3-5
10-18

Humalog
5-15 min
Novolog
5-15 min
Apidra
5-15 min
Humulin N,
2-4 hrs
ReliOn
Glargine
Lantus
2-4 hrs
Peakless
20-40
Detemir
Levemir
1-3 hours
6-8
18-22
70/30 premix Humulin
30-60 min
Dual
10-16
70/30,
Novolin 70/30
50/50 premix Humalog
10-15 min
Varies
10-16
50/50
60/40 premix Novolin 60/40 30-60 min
2-8
18-24
Insulins used in the United States. Diabetes Forecast 2015 Consumer Guide.
Alexandria, VA: American diabetes Association.
21. Once Susans blood glucose levels were under control, Dr. green
prescribes the following insulin regimen: 24 units of glargine in the
PM with the other 24 units as lispro divided between meals and
snacks. How did Dr. Greene arrive at this dosage?
Insulin dosages are determines based on the individuals type of diabetes,
age, body size, insulin sensitivity, and hepatic function, and the physicians
clinical judgment. A starting insulin dose is determined by dividing an
individuals weight in pounds by the number 4 or by multiplying the weight in
kg by 0.55. Dr. Greene used the following equation to determine Susans
insulin dosage: (100 lbs/2.2) x 0.55= 25 units (Nelsm 491).
E. Behavioral-Environmental Domain
22. Identify at least three specific potential nutrition problems
within the domain that will need to be addressed for Susan and her
family.
Common nutrition diagnoses associated with diabetes and within the domain
are inadequate energy intake, inappropriate intake of carbohydrates,
inadequate fiber intake, not ready for lifestyle change, and many others.
Susan and her family will have to learn about proper care and management
of type 1 diabetes, a diabetic diet, carbohydrate counting, and insulin
regimens to reduce her risk for complications (Nelms 495).
23. Just before Susan is discharged, her mother asks you, My
friend who owns a health food store told me that Susan should use

10
stevia instead of artificial sweeteners or sugar. What do you think?
What will you tell Susan and her mother?
According to the American Diabetes Association low-calorie sweeteners,
sometimes called artificial sweeteners, sugar substitutes or non-nutritive
sweeteners, are a good way to curb sweet cravings without the added
carbohydrates. There are six artificial sweeteners that have been tested and
approved by the U.S. Food and Drug Administration: acesulfame potassium,
aspartame, saccharin, sucralose, neotame, advantame. Stevia is generally
recognized as safe (GRAS) by the FDA (ADA 2015). This means that experts
have agreed that is safe for use by the public in appropriate amounts (AAD.
As a result I would recommend that Susan stick to the sweeteners approved
by the FDA. She can find them in stores under names such as Nutrasweet,
Splenda, PurVia and in diet drinks, baked goods, frozen desserts, candy. Light
yogurt and chewing gum.
F. Nutrition Diagnosis
24. Select two high-priority nutrition problems and complete PES
statement for each.
Unintended weight loss (NC-3.2) related to MD diagnosis of type 1 diabetes
as evidenced by parents concern of weight loss, physical exam showing a
tired-appearing adolescent female and 24-hour recall showing sufficient
calorie intake.
Food and nutrition related knowledge deficit (NB-1.1) related to new clinical
diagnosis of type 1 diabetes as evidenced by inappropriate carbohydrate
intake in diet history and HbA1c of 7.95%.
(eNCPT 2015)
III. Nutrition Intervention
25. For each of the PES statements that you have written, establish
an ideal goal (based on the signs and symptoms) and an appropriate
intervention (based on etiology).
Unintended weight loss intervention will include:
1. Education on how to properly receive the insulin the MD prescribed so
that her body can absorb the extra glucose in her blood
2. Education on the national guidelines:
a. 45% kcals from carbohydrates, <30% of total kcals from fat and
simple sugar <10% of total kcals, 10-15% total kcals from
protein

11
3. Increase of dietary fiber and begin to vary diet more
a. I will go over her 24 hour recall with her
Food- and nutrition- related knowledge deficit intervention would include:
1. Series of 3-4 encounter with an RD lasting from 45-90 minutes
a. Should be completed within 3-6 months
b. At least one follow-up encounter annually to reinforce lifestyle
changes and to evaluate and monitor outcomes that indicated
need for changes in MNT or medications.
2. Learning how to count carbohydrates so that meal time insulin can
match carbohydrates consumed
a. Eating consistent carbohydrates at every meal
b. The amount of food containing 15 g carbohydrates counts as one
carbohydrate choice
3. Choose nutrient dense, high fiber foods over processed foods
whenever possible
4. Create a meal planning method such as the Mediterranean diet, the
DASH diet, or low fat low carbohydrate diet will tailor it to Susan
based on her needs and preferences
5. Signs and symptoms of hypo/hyper- glycemia
a. Hypo= confusion, heart palpitations, shakiness, and anxiety
b. Hyper= polyuria, polydipsia, presence of glucose in the urine,
headache, blurred vision, fatigue
6. Monitoring instructions (SBGM, urine ketones, and use of record
system)
7. Importance of exercise for diabetes management
a. Improved glycemic control
b. Improved blood lipids and blood pressure
c. Improved coping and stress management and reduced feelings
of depression
d. Encouraged to engage in at least 60 min of PA per day
26. Does the current diet order meet Susans overall nutritional
needs? If yes, explain why it is appropriate. If no, what would you
recommend? Justify your answer.
I think that the diet order is sufficient for Susan and the goal to regain the
weight she lost. I estimated that her needs were 2400-2500 kcalday and the
diet order of 2400 kcal meets these needs. And since there is no real specific
diet order for diabetes, the national guidelines should be followed when it
comes to macronutrient distribution. The diet order calls for 300g CHO (50%
of total kcals), 55-65 g protein (9.2-10.8% of total kcals) that is in the range I

12
calculated above, and 80 g lipids (30% of kcals); all within the nation
guidelines (Nelms495-495).
III.

Nutrition Monitoring and Evaluation

27. Susan is discharged Friday morning. She and her family have
received information on insulin administration, SMBG, urine
ketones, record keeping, exercise, signs, symptoms, and Tx of
hypo-/hyperglycemia, meal planning (CHO counting), and
contraception. Susan and her parents verbalize understanding of
the instructions and have no further questions at this time. They are
instructed to return in 2 weeks for appointments with the
outpatient dietitian and CDE. When you come in to work Monday
morning, you see that Susan was admitted through the ER Saturday
night after her discharge on Friday. She tested her blood glucose
before going to the party, and it measured 95 mg/dL. She took 2
units of insulin and knew she needed to have a snack that contained
approximately 15 grams of CHO, so she drank one beer when she
arrived at the party. She remembers getting lightheaded and then
woke up in the ER. What happened to Susan physiologically?
In this situation Susan substituted her 15 grams of CHO snack for alcohol,
which is not recommended. The alcohol caused delayed hypoglycemia since
she missed her snack and the 95 mg/dL dosage was not properly
compensated for with glucose, therefore she had low blood sugar causing
hypoglycemia with symptoms such as feeling lightheaded and shaky which
led her to become unconscious since she did not recognize the symptoms or
seek help.
28. What kind of educational information will you give her before
this discharge? Keep in mind that she is underage for legal
consumption of alcohol.
Before this discharge I would remind her that since she is underage she is
not legally allowed to drink alcohol. I would also educate her on the
importance of her meal plan method and that meals and snacks should
always be consumed as planned, and if a meal is going to be late to have a
snack so that her insulin dosages will meet her CHO intake. I would also
provide her with more materials on the signs and symptoms of
hypoglycemia/hyperglycemia and what to do in those cases. Lastly I would
remind her that she is not old enough to drink, but if she does have a drink
to plan it in her meal plan and adjust her insulin accordingly and to NEVER

13
replace a meal/snack with alcohol and alcohol should be consumed with food
(Nelms 500).

References
American Diabetes Association. (n.d.). Retrieved November 15, 2015.
Cade, W. T. (2008). Diabetes-Related Microvascular and Macrovascular
Diseases in the Physical
Therapy Setting. Physical Therapy, 88(11), 13221335.
http://doi.org/10.2522/ptj.20080008
Center for Disease Control (2015, October 28). Retrieved November 15,
2015.
ENCPT Web Publication. Academy of Nutrition and Dietetics, 2014. Web.
Sept.2015.
<https%3A%2F%2Fncpt.webauthor.com>.
Nelms, M. (n.d.). Nutrition therapy and pathophysiology (Third ed.).

14
"SuperTracker: My Foods. My Fitness. My Health." SuperTracker Home.
USDA,n.d. Web. 02
Sept. 2015. <https://www.supertracker.usda.gov/>.