Case

Study 22: Type 1 Diabetes Mellitus

Sam Ballard
KNH 411
11.19.2015
I.

Understanding the Diagnosis and Pathophysiology

1. Define insulin. Describe its major functions within normal metabolism.
Nelms, Sucher, and Lacey define insulin as a hormone produced by the beta cells of
the islets of Langerhans in the pancreas to regulate blood glucose. Insulin is an
anabolic hormone that promotes the uptake, utilization, and storage of nutrients.
When blood glucose levels are increased, insulin secretion is stimulated. Insulin
allows glucose to be transported from the bloodstream into the cells to be used as
energy. Without adequate insulin, glucose will remain in the bloodstream and the
body will begin to breakdown other substances, such as fat, as fuel. This can lead
have dangerous consequences, such as the development of diabetic ketoacidosis.
Insulin promotes the uptake of glucose into hepatic, muscle, and adipose cells as
well as the stimulation of glycogen, triglyceride, and protein synthesis (Nelms,
Sucher, & Lacey, 476). In protein metabolism, amino acids are actively transported
from the blood into muscles and other tissues. This promotes protein synthesis
within cells and insulins anabolic effect in protein metabolism produces a positive
nitrogen balance.
2. What are the current opinions regarding the etiology of type 1 diabetes mellitus
(DM)?
The cause of type 1 diabetes mellitus is still unknown. One opinion is that the
development of type 1 diabetes mellitus is influenced by genetics. According to
Nelms, Sucher, and Lacey, immune-mediated type 1 diabetes mellitus results from
a cell-mediated autoimmune response causing a gradual decline in beta cell mass
within genetically susceptible individuals (481). There have more than 20 different
genes thought to be linked to this disease. This means that individuals with relative
who have T1DM may have an increased risk of developing the disease themselves.
Environmental agents have also been thought to initiate the autoimmune response
thought to be a factor in developing T1DM. Some potential environmental agents
thought to trigger this response include viruses, gluten, vitamin D levels, and infant
feeding practices including exposure to the proteins found in cows milk and the
length of breastfeeding. In T1DM cases that have no evidence of autoimmunity and
have no apparent cause, individuals have a more immediate and complete

destruction of beta cells, do not produce insulin, and are prone to ketoacidosis.
These cases are referred to as fulminant T1DM (Nelms, Sucher, & Lacey, 481).
3. What genes have been identified that indicate susceptibility to type 1 diabetes
mellitus?
Multiple genes have been identified that indicate susceptibility to type 1 diabetes
mellitus. Nelms, Sucher, and Lacey identify the primary gene for type 1 DM to be
located in the HLA region on chromosome 6. They also indicate that
polymorphisms in the HLA complex account for 40%-50% of the genetic risk of
developing type 1 DM, but more than 20 different gene associations have been
linked to risk for this disease (481). Van Belle, Coppieters, and Von Herrath refer to
this gene as IDDM1, for insulin-dependent diabetes mellitus locus. They also
identify a lesser predisposition to the insulin gene. This gene is referred to as
IDDM2 on chromosome 11 containing the insulin gene region. In addition, they
identify a relatively new member of the T1D susceptibility gene set is PTPN22,
which encodes the lymphoid protein tyrosine phosphatase (LYP), Allelic variation
in the interleukin (IL)-2 receptor- gene (IL2RA) region, which is an essential
molecule expressed on T cells upon activation and on natural Tregs at baseline, and
lastly the gene encoding cytotoxic T lymphocyte-associated protein 4 (CTLA-4) in
the IDDM12 region, which is by all accounts a vital molecule for proper negative
regulation of immune responses (Van Belle, Coppieters, and Von Herrath, 2011).
4. After examining Susans medical history, can you identify any risk factors for type 1
DM?
Susan has had an uneventful medical history with no significant illness until the past
several weeks, but there is a history of diabetes in the family from her maternal
grandmother. Her young age may also increase her risk for developing type 1 DM.
5. What are the established diagnostic criteria for type 1 DM? How can the physicians
distinguish between type 1 and type 2 DM?
There are four main criteria for the diagnosis of diabetes mellitus. An individual can
be diagnosed for diabetes if they meet any one of the four criteria. These include a
hemoglobin A1c of greater than or equal to 6.5% using standardized laboratory
measures, or a fasting plasma glucose level of greater than or equal to 126 mg/dL
(7.0 mmol/L), or symptoms of diabetes plus a random plasma glucose concentration
of greater than or equal to 200 mg/dL (11.1 mmol/L), or a 2-hour post-prandial
glucose level of greater than or equal to 200 mg/dL (11.1 mmol/L) during an oral

glucose tolerance test (OGTT) (Nelms, Sucher, & Lacey, Box 17.2, 481). Physicians
distinguish between type 1 and type 2 DM based on the individuals insulin status.
Beta cell destruction with absolute insulin deficiency indicates type 1 DM while
progressive defective insulin secretion with insulin resistance indicates type 2 DM
(Nelms, Sucher, & Lacey, Box 17.1, 480). Key indicators of type 1 DM may include
the presence of autoantibodies in the blood that are common in type 1 DM (Islet cell
autoantibodies, Glutamic Acid Decarboxylase autoantibodies, and Insulin
autoantibodies) or the presence of ketones in the urine that indicate the bodys
breakdown of fat (Mayo Clinic, 2014).
6. Describe the metabolic events that led to Susans symptoms (polyuria, polydipsia,
polyphagia, weight loss, and fatigue) and integrate these with the pathophysiology of
the disease.
When the bodys pancreatic beta cells are destroyed and insulin production ceases,
glucose cannot enter the cells. This causes hyperglycemia and cells begin to starve.
As a result of this, gluconeogenesis is increased in the liver and glycogenolysis is
stimulated and further contributes to the hyperglycemic state. Because the kidneys
can only filter so much glucose from the blood, excess glucose is lost in the urine,
resulting in glycosuria and polyuria. Glycosuria is the presence of glucose in the
urine while polyuria is frequent urination. This loss of fluid leads to polydipsia,
which describes excessive thirst. Polyphagia, or excessive hunger, is then initiated
due to the cells lack of glucose to use as energy. The body then begins to break
down fat stored in adipose tissue to use as energy. This results in weight loss and
the production of ketone bodies that are secreted in the urine. The ketoacidosis that
results from the breakdown of fat will cause the body to have deep, labored
respirations, called Kussmaul respirations, in an effort to offset this metabolic
acidosis. This, along with the many other symptoms previously listed, may
contribute to Susans fatigue. (Nelms, Sucher, & Lacey, 481)
7. List the microvascular and neurologic complications associated with type 1
diabetes.
Cardiovascular Disease (Nelms, Sucher, & Lacey, 507)
Hyperglycemia makes blood vessels prone to endothelial damage,
causing thickening and decreased flexibility of the vessels and
increased high blood pressure.
Hypertension is a risk factor for cardiovascular disease as well as a
complication for microvascular complications such as retinopathy and
nephropathy.

 Nephropathy (Nelms, Sucher, & Lacey, 507)

Leading cause of chronic kidney disease (CKD)--kidney failure that
must be treated with dialysis or transplantation
Hyperglycemia changes the structure of the blood vessels of the
glomerulus. Changes in capillary structure result in increased
permeability and decreased filtering ability.
Early stage of nephropathy is persistent albuminuria (albumin in the
urine).
Retinopathy (Nelms, Sucher, & Lacey, 507)
Most frequent cause of new cases of blindness in adults.
Prevalence is strongly associated with duration of DM.
Eye damage directly related to hyperglycemic damage to its blood
vessels.
Other eye ailments include glaucoma and cataracts.
Hypertension is also associated with retinopathy.
Neuropathy (Nelms, Sucher, & Lacey, 507)
Nervous system damage (due to hyperglycemia) causes impaired
sensation of pain in the feet or hands, slowed digestion of food in the
stomach, carpal tunnel syndrome, impaired wound healing, motor
dysfunction, and/or bone fracture.
Accumulation of abnormal substances, such as sorbitol and glycated
proteins, results in cellular damage, which disrupts normal nervous
system pathways.
Peripheral neuropathy--pain and loss of sensation in feet and hands,
which leads injuries to limbs to go unrecognized and cause
ulcerations, infection, and the need for amputation.
Autonomic neuropathy--affects many organ systems, such as the
gastrointestinal tract, genitourinary tract, and the cardiovascular
system.
Gastrointestinal: damage to vagus nerve causes delayed gastric
emptying and can cause anorexia, nausea, vomiting, early
satiety, post-prandial bloating, and erratic glycemic control;
constipation and diarrhea.
Genitourinary: bladder and/or sexual dysfunction that may
manifest as recurrent urinary tract infections, pyelonephritis,
or incontinence.
Cardiovascular: may manifest through resting tachycardia,
orthostatic hypotension, or increased risk of silent heart
disease.

8. When Susans blood glucose level 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?
Nelms, Sucher, and Lacey define the dawn phenomenon as an increase in blood
glucose in the early morning, most likely due to increased glucose production in the
liver after an overnight fast (470). If Susan is hypoglycemic at 2 AM, but
hyperglycemic before breakfast, she is likely experiencing the dawn phenomenon as
a result of her overnight fast. The dawn phenomenon is a result of hormones
involved in controlling circadian rhythms. Gluconeogenesis is stimulated by cortisol
and growth hormone, which causes hyperglycemia between 5 AM and 9 AM (Nelms,
Sucher, & Lacey, 505). This may be prevented by having bedtime snacks or
adjusting insulin regimens.
9. What precipitating 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.

II.

Risk factors:
Risk for DKA is highest during illness, infection, and emotional stress.
Omission of insulin, due to illness or infection and fear of
hypoglycemia, is a frequent cause of DKA. (Nelms, Sucher, & Lacey,
505)
Pathophysiology:
When insulin is not available for the cells to take in glucose, glucose is
produced via gluconeogenesis and lipolysis. Lipolysis, or the
breakdown of fat for energy, generates ketones that accumulate in the
bloodstream causing osmotic diuresis, dehydration, and electrolyte
imbalances. The blood becomes concentrated as fluid is lost, further
contributing to hyperglycemia. (Nelms, Sucher, & Lacey, 505)
Symptoms:
Nausea and/or vomiting
Stomach pain
Fruity or acetone breath
Kussmaul respirations
Mental status changes

(Nelms, Sucher, & Lacey, 505)

Nutrition Assessment

A. Evaluation of Weight/Body Composition

10. Determine Susans stature for age and weight for age percentiles.

Susans weight-for-age percentile: 10th - 25th percentile
Susans stature-for-age: 25th percentile
BMI:
wt (kg) / ht (m)2
45.5 / 1.572 = 18.5 kg/m2
Susans BMI-for-age percentile: 25th - 50th percentile (closer to 25th)
(Centers for Disease Control and Prevention, 2009)
11. Interpret these values using the appropriate growth chart.
According to these values, particularly Susans BMI-for-age percentile, Susan is
considered to be of normal or healthy weight. Normal or healthy weight for
adolescents is considered to be between the BMI-for-age 5th and 85th percentiles.
Susans BMI-for-age percentile is slightly above the 25th percentile. (Centers for
Disease Control and Prevention, 2015)
B. Calculation of Nutrient Requirements
12. Estimate Susans daily energy and protein needs. Be sure to consider Susans age.
Mifflin-St. Jeor (EER):
[10 x wt (kg) + 6.25 x ht (cm) - 5 x age (yrs) - 161] x PAL
[10 x 45.5 kg + 6.25 x 157.5 cm - 5 x 15 - 161] x 2.0
[455 + 984.4 - 75 - 161] x 2.0
1,203 x 2.0 = 2,407 kcal/day
Protein:
1.2 g/kg x wt (kg)
1.2 g/kg x 45.5 kg = 54.6 g protein/day
It is estimated that Susans daily energy needs are about 2,400 kcal/day. This is
consistent with her current diet order of 2,400 kcal/day. Her physical activity level
was chosen to be 2.0 to account for her involvement in volleyball practice four
evenings per week and volleyball games two days per week. Susans estimated
protein needs were calculated to be about 55 grams of protein per day. As an
athlete, Susan requires slightly more grams of protein per kilogram of body weight,

which is why she was estimated to need 1.2 grams of protein per kilogram of body
weight rather than the usual 0.8 grams of protein per kilogram of body weight.
13. What would the clinician monitor in order to determine whether or not the
prescribed energy level is adequate?
The clinician would need to monitor her weight to ensure she is maintaining her
currently healthy weight and discontinuing her weight loss. If Susan feels she is
continuing to lose weight, an increase in calories may be necessary. It would also be
beneficial to monitor any changes in Susans activity level, for example when
volleyball is in season versus out of season. Susans estimated energy and protein
requirements were calculated to take into account her participation in sports, but if
that changes, her energy and protein needs would need to be recalculated to reflect
her decrease in daily physical activity. Failure to take this into account could result
in excess calorie and protein intake and ultimately, weight gain.
C. Intake Domain
14. Using a computer dietary analysis program or food composition table, calculate
the kcalories, protein, fat (saturated, polyunsaturated, and monounsaturated), CHO,
fiber, and cholesterol content of Susans typical diet.
Meal
AM

Food Item

kcal

Pro
(g)

Fat
(g)

CHO
(g)

Fiber
(g)

Chol
(mg)

1 c dry cereal
(Frosted flakes)

232

3.06

2.1
S- 1.56
M- 0.36
P- 0.12

51.06

0.8

1 c 2% milk

137

9.68

4.85
S- 3.1
M- 1.38
P- 0.18

13.45

20

1 c orange juice

117

1.69

0.37
S- 0.05
M- 0.06
P- 0.08

27.41

0.7

1 c hot chocolate
(made with water)

80

0.6

3
S- 2
M- 0
P- 0

15

0.8

Lunch

Snack

PM

6 in pepperoni pizza

1,042

47.84

42.33
S- 19.2
M- 14.9
P- 7.57

117.37

6.3

97

1 c mixed salad

0.58

0.14
S- 0.02
M- 0.01
P- 0.08

1.55

c Thousand Island
dressing

119

0.51

6.93
S- 0.46
M- 3.96
P- 1.65

14.74

0.7

1 can Coke

155

0.92
S- 0
M- 0
P- 0

38.33

1 Snickers candy bar

280

4.29

13.59
S- 5.17
M- 4.49
P- 1.72

35.06

1.3

2 slices white bread

252

0.01

4.59
S- 1.17
M- 1.17
P- 1.17

45.18

1.4

1 tbsp grape jelly

56

0.03

0
S- 0
M- 0
P- 0

14.69

0.2

3 tbsp crunchy peanut

butter

283

11.55

23.97
S- 3.65
M- 11.1
P- 6.69

10.35

3.8

12 oz can of Coke

155

0.92
S- 0
M- 0
P- 0

38.33

2 c spaghetti noodles

477

17.52

2.81
S- 0.53

93.2

5.4

M- 0.40
P- 0.99

HS snack

Totals:

c spaghetti sauce

66

1.83

2.13
S- 0.29
M- 0.39
P- 0.89

9.81

2.4

1 oz ground beef

71

7.35

4.37
S- 1.63
M- 2.13
P- 0.18

25

3 stalks steamed
broccoli w/ cheese
sauce

299

17.08

10.58
S- 3.98
M- 2.49
P- 2.21

43.07

18.1

18

16 oz 2% milk

274

19.36

9.7
S- 6.18
M- 2.76
P- 0.36

26.9

39

2 c ice cream

558

9.64

29.04
S- 17.9
M- 8.16
P- 1.14

68.37

2.5

103

12 oz Coke

155

0.92
S- 0
M- 0
P- 0

38.33

4,816

152.62

163.26
S- 66.89
M- 53.76
P- 25.03

702.2

45.4

320

15. What dietary assessment tools can Susan use to coordinate her eating patterns
with her insulin and physical activity?
Susan can monitor her progress using self-monitoring records and laboratory tests.
These will assess whether or not she is effectively coordinating her eating patterns
with her insulin and physical activity. Self-monitoring blood glucose (SMBG) can

assist in adjusting daily eating patterns and medications as necessary to maintain

glycemic control and is also useful in identifying patterns and the ways in which
food, exercise, or other factors affect glycemic control (Nelms, Sucher, & Lacey,
504). Susan may also benefit from the use of an insulin pump. This will more
efficiently help her monitor her glucose levels and the amount of glucose to use for
each meal or activity. She will need to monitor her blood glucose before meals, 1-
and 2-hours after meals, before she goes to bed, during the night, and when she
wakes up in the morning. Monitoring these values will allow her to know if she
needs to make adjustments in her delivery of insulin for meals and activities. There
are also many apps that could be useful in estimating carbohydrate content of foods
if that becomes an issue for her. (Nelms, Sucher, & Lacey, 503-504)
16. Dietitians 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

Assessments You Would Perform

Clinical data

1. Blood glucose levels

2. Lipid profile
3. Ketones in urine

Nutrition history

1. 24-hour recall
2. Dietary intake journal
3. Food preferences, allergies, or
intolerances

Weight history

1. Current weight
2. % Usual body weight
3. BMI (BMI-for-age percentile)

Physical activity history

1. Physical activity journal

2. CHO and insulin intake before and
after exercise
3. Adjustment of nutrient
recommendations along with change
in physical activity status

Monitoring

1. Glucose self-monitoring records

2. Hydration status

3. Physical sensations (i.e. peripheral

nerve damage, bodily injuries)
Psychosocial/economic

1. Assess insurance coverage for

medical visits/medications
2. Assess mental/emotional state of
Susan and family in dealing with DM
3. Social/familial support

Knowledge and skill level

1. Assess/re-assess skills and safety

related to administering insulin via
pump and/or injection
2. Carbohydrate counting
3. Dealing with DM in special situations
(i.e. volleyball tournaments, on
vacation, emergencies)

Expectations and readiness to change

1. Progress with meal planning

2. Attitudes towards lifestyle change
3. Barriers to change

D. Clinical Domain
17. Does Susan have any laboratory results that support her diagnosis?
Susan has four abnormal laboratory values that support her diagnosis. Her
osmolality levels were high both at admit (304 mmol/kg/H20) and at d/c (297
mmol/kg/H20). This indicates that Susan was dehydrated, most likely as a result of
her hyperglycemia and related polyuria. Susans glucose levels were extremely high
at admit (250 mg/dL) and moderately high at d/c (120 mg/dL). This is the most
obvious indicator of her type 1 DM. If glucose is building up in her blood, this means
it isnt being used by her cells. Her cells need insulin to use glucose so if they arent
using the glucose, she is lacking insulin. Her BUN levels were slightly high at admit
(20 mg/dL) and in the upper range of normal at d/c (18 mg/dL). The presence of
increased nitrogen in her urine indicates that her kidneys are not working properly.
Diabetes can cause nephropathy, which describes damaged nerves and blood
vessels in the kidneys that cause them to work less efficiently. Lastly, Susans HbA1c
was high at admit (7.95%). This indicates that over the past three months, Susans
blood glucose levels were high (about 183 mg/dL on average). This constant
hyperglycemia supports her diagnosis of type 1 DM. Susan also had a slightly high
prealbumin level at admit (40 mg/dL) and d/c (39 mg/dL). This could simply be due
to her diet and shouldnt be of serious concern until her prealbumin levels fall below

normal levels. This could, however, indicate that there is decreased kidney function,
which would be supported by her high BUN levels.
18. Why did Dr. Green order a lipid profile?
Dr. Green ordered a lipid profile to evaluate Susans LDL cholesterol, HDL
cholesterol, and triglyceride levels. An abnormal lipid profile could indicate diabetic
dyslipidemia. Several factors are likely to be responsible for diabetic dyslipidemia:
insulin effects on liver apoprotein production, regulation of lipoprotein lipase (LpL),
actions of cholesteryl ester transfer protein (CETP), and peripheral actions of insulin
on adipose and muscle (Endocrine Society, 2013). Along with blood pressure
monitoring, Susans lipid profile should be monitored annually, or as frequently as
needed, and the accuracy of these tests are dependent on an overnight fast. Susans
goal values are an LDL cholesterol level of <100 mg/dL, an HDL cholesterol level of
>50 mg/dL, and a triglyceride level of <150 mg/dL (Nelms, Sucher, & Lacey, 504).
Abnormal lipid levels could also indicate that Susan needs to make lifestyle
adjustments, such as her diet, physical activity, or use of insulin for glucose
monitoring. Dr. Green may also be looking to see if Susan is using glucose as energy
or if she is burning fat.
19. Evaluate Susans laboratory values:
Chemistry

Prealbumin
(mg/dL)

Osmolality
(mmol/kg/H20)

Normal
Value

Susans Susans Reason for Abnormality

Value
Value
Admit
d/c

Nutritional
Implications

16-35

40

39

Slightly high, but may

just be due to dietary
protein intake. Could
possibly indicate
decreased kidney
function, which is also
evidenced by her BUN.

Susan is receiving
adequate calories and
protein and is not
experiencing
malnutrition.

285-295

304

297

Indicates that Susan was

dehydrated, most likely
as a result of her
hyperglycemia and
related polyuria.

May require
increased fluid needs
until returned to
normal range, but
will adjust once
hyperglycemia is
controlled.

Glucose (mg/dL)

BUN (mg/dL)

HbA1c (%)

70-110

250

120

Glucose is building up in
her blood because there
is insufficient insulin to
allow the cells to use
glucose as energy.

Use of insulin to
adjust alterations in
glucose levels caused
by carbohydrate
intake, exercise,
stress, etc. Requires
carbohydrate
counting and close
diet monitoring.

8-18

20

18

Diabetes can cause

nephropathy (damage to
nerves and blood vessels
in the kidneys), which
causes the kidneys to
filter less efficiently and
allows nitrogen to be
excreted in the urine.

Requires adequate
fluids and
electrolytes. May also
require reduced
protein intake until
diabetes is controlled
to give the kidneys
time to do less work
and repair.

3.9-5.2

7.95

Hyperglycemia due to
lack of insulin consistent
with type 1 DM. Over the
past three months,
Susans blood glucose
levels were high (about
183 mg/dL on average).

Same as nutritional
implications for
glucose. Once daily
glucose is controlled,
so will mean glucose
over 2-3 months.

20. Compare the pharmacological differences in insulins:

Type of Insulin

Brand Name

Onset of
Action

Peak of Action

Duration of
Action

lispro

Humalog

5-15 minutes

30-90 minutes

3-5 hours

aspart

Novolog

5-15 minutes

30-90 minutes

3-5 hours

glulisine

Apidra

5-15 minutes

30-90 minutes

3-5 hours

NPH

Humulin N
Novolin N

2-4 hours

4-10 hours

10-18 hours

glargine

Lantus

2-4 hours

Peakless

20-24 hours

detemir

Levemir

1-3 hours

6-8 hours

18-22 hours

70/30 premix

Humulin 70/30
Novolin 70/30

30-60 minutes

Dual

10-16 hours

Novolog Mix 70/30

5-15 minutes

Dual

10-16 hours

50/50 premix

Humalog Mix 50/50

10-15 minutes

Varies

10-16 hours

60/40 premix

Mixtard 40

30 minutes

2-8 hours

24 hours

(Nelms, Sucher, & Lacey, Table 17.6, 491)

(National Institutes of Diabetes and Digestive and Kidney Diseases, n.d.)
21. Once Susans blood glucose levels were under control, Dr. Green prescribed the
following insulin regimen: 24 units of glargine in PM with the other 24 units as lispro
divided between meals and snacks. How did Dr. Green arrive at this dosage?
Dr. Green chose glargine for use in the evening because it is a long-acting insulin.
This will sustain Susan for her overnight fast. He chose lispro to be divided between
meals and snacks because it is a rapid-acting insulin. This will quickly correct for
her food intake and because it is rapid-acting, each dose will only affect each meal
individually.
E. Behavioral-Environmental Domain
22. Identify at least three specific potential nutrition problems within this domain that
will need to be addressed for Susan and her family.
Self-Monitoring Deficit (NB-1.4): Now that Susan has been newly diagnosed
with type 1 DM, she will need to be educated in the self-monitoring of her
blood glucose levels. If she continues to have a self-monitoring deficit, her
diabetes could go unmonitored and cause severe nutrition and health issues.
Food- and Nutrition-Related Knowledge Deficit (NB-1.1): Due to lack of prior
diabetes-related education, Susan may have incomplete or inaccurate
knowledge about key information for controlling type 1 DM, such as
carbohydrate counting, reading food labels, what influences blood glucose
levels, etc.
Not Ready for Diet/Lifestyle Change (NB-1.3): Susan and her parents may not
be financially prepared to deal with Susans type 1 DM diagnosis. Expenses
may be due to medical visits, insulin supplies, self-monitoring equipment, etc.
Susan also may not be ready to mentally commit to the time and attention to
detail that are required to successfully monitor type 1 DM.

23. Just before Susan is discharged, her mother asks you, My friend who owns a health
food store told me that Susan should use stevia instead of artificial sweeteners or
sugar. What do you think? What will you tell Susan and her mother?
Stevia, also known as Rebaudioside A or rebiana, is generally recognized as safe by
the Food and Drug Administration as a food additive and a table-top sweetener.
Stevia is a non-caloric plant-based sweetener that is hundreds of times sweeter than
sugar. This allows individuals to use much less sweetener, but Stevia may affect
different individuals in various ways. There are many different opinions on the
effect Stevia may have on individuals with diabetes, so the only way to decide if
Stevia is right for you is to try it out! When trying Stevia, it is important to
constantly monitor your blood glucose levels to ensure that it does not negatively
affect these values. It is also important to note any physical changes, such as
lightheadedness, nausea, or any other symptoms that may indicate a change in
blood sugar. This may mean you have to adjust the amount of Stevia you are using,
or that you should discontinue the use of Stevia altogether. Artificial sweeteners
have more research on their safety and side effects so it may be easier to decide to
use these products.
F. Nutrition Diagnosis
24. Select two high-priority nutrition problems and complete the PES statement for
each.
Self-monitoring deficit (NB-1.4) related to food- and nutrition-related
knowledge deficit concerning self-monitoring as evidenced by a new medical
diagnosis of type 1 diabetes mellitus, no self-management equipment, a
blood glucose level of 250 mg/dL at admit, and a hemoglobin A1c of 7.95%.
Excessive carbohydrate intake (NI-5.8.2) related to physiological causes
requiring moderate carbohydrate intake (type 1 diabetes mellitus) as
evidenced by a blood glucose level of 250 mg/dL at admit, a hemoglobin A1c
of 7.95%, and a usual diet recall indicating an intake of 702 grams of
carbohydrate.
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 the
etiology).

 The ideal goal for Susans self-monitoring of her blood glucose would be to
lower her blood glucose levels to the normal range of 70-110 mg/dL. This
will also reduce her hemoglobin A1c to the normal range of 3.9-5.2%. In
order to achieve this goal, an appropriate intervention would be to educate
Susan on self-monitoring techniques common with type 1 diabetes mellitus.
This would include carbohydrate counting, insulin injections, insulin pumps,
and the effect of diet, physical activity, stress, and other lifestyle factors on
blood glucose levels and the need for insulin. In addition to these education
sessions, it would be useful for Susan to keep a self-monitoring/diet/physical
activity journal that would be reviewed in follow-up counseling sessions.
These sessions would continue two to three times per month until Susan felt
comfortable enough with her diabetes regimen to space out her sessions over
longer periods of time. She would also need frequent laboratory tests and
meetings with her physician to ensure her laboratory values are within their
normal ranges.
Susan is not necessarily at fault for her excess carbohydrate intake because
she had no knowledge of her type 1 diabetes mellitus diagnosis up until this
hospital visit. Now that she is aware of her diagnosis, the ideal goal for her
excessive carbohydrate intake would be to reduce her intake to about 300
grams per day. This value is reflected in her current diet order, which is
consistent with the values I have calculated. Her usual diet recall indicates
that she is consuming about 702 grams of carbohydrate per day and this is
resulting in a consistently elevated blood glucose level, reflected in her
hemoglobin A1c of 7.95%. In order for Susan to consciously reduce or control
her intake of carbohydrates, she must be educated on the carbohydrate
content of food items, the types of carbohydrates, and how they affect her
blood glucose levels. As long as Susan learns to administer the proper
amount of insulin to compensate for her carbohydrate consumption every
time she eats, she should be able to easily control her dietary blood glucose
levels.
26. Does the current diet order meet Susans overall nutrition needs? If yes, explain
why it is appropriate. If no, what would you recommend? Justify your answer.
The current diet order does meet Susans overall nutrition needs. The current diet
order suggests that Susan intake 2,400 kilocalories per day, 300 grams of
carbohydrate per day, 55-65 grams of protein per day, and 80 grams of lipid per
day. Susans estimated energy requirements were calculated in question #12 to be
about 2,407 kilocalories per day, using a physical activity factor of 2.0 to account for
her being a volleyball player. Susan should be getting about 45% of her kilocalories

from carbohydrates, which is calculated to be 270 grams of carbohydrate per day

(2,407 kcal x .45 = 1,083kcal / 4 kcal/g = 270 g CHO). Susans estimated protein
intake was also calculated in question #12 to be 54.6 grams of protein per day using
a factor of 1.2 grams per kilogram. Lastly, Susan should be getting about 30% or less
of her total kilocalories from lipids, which is calculated to be 80 grams of lipid per
day (2,407 kcal x .30 = 722 kcal / 9 kcal/g = 80 g lipid).
IV.

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
with a BG of 50 mg/dL. You see her when you make rounds and review her chart.
During an interview, Susan tells you she was invited to a party 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?
Physiologically, Susan suffered from hypoglycemia, or low blood sugar, due to the
effect alcohol has on insulin. Acute alcohol consumption increases insulin secretion,
which results in low blood glucose levels. Alcohol consumption may cause delayed
hypoglycemia in those individuals taking insulin or insulin secretagogues (Nelms,
Sucher & Lacey, 497). Alcohol can also impair the effectiveness of hypoglycemic
medications used to correct low blood sugar. Susan should not have substituted
food with a beer. Alcohol kilocalories should be considered an addition to regular
food or meals, and alcohol should not be substituted for food (Nelms, Sucher, &
Lacey, 497). Susan should have eaten a complex carbohydrate food item with 15
grams of CHO instead of drinking a beer. Since she decided to have a beer, she
should have also continued to check her blood glucose after consuming the beer so
that she could have corrected her low blood glucose sooner.
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.

I would simply explain to Susan the negative consequences that alcohol

consumption can have on individuals with diabetes and hopefully, this will
discourage her from drinking alcohol in addition to the fact that she is underage.
Alcohol consumption may place people with diabetes at increased risk for delayed
hypoglycemia, especially if taking insulin or insulin secretagogues (Nelms, Sucher,
& Lacey, 499). I would of course advise Susan to refrain from consuming alcohol
until she turns 21, for both legal and health reasons. When she becomes of age, she
should keep in mind that alcohol should be consumed in moderation, which means
one drink per day or less for adult women.

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