Meghan Ames

Mrs. Matuszak

KNH 406

March 18, 2010

Diabetes Case Study #4

Understanding the Disease and Pathophysiology

1) Define insulin. Describe its major functions within normal metabolism.

Insulin is a hormone produced in the β cells of the pancreas. It is responsible for

facilitating the movement of glucose from the blood into the body’s muscle and fat cells.

It is secreted in response to an increase in blood glucose.

2) What are the current opinions regarding the etiology of type 1 diabetes mellitus (DM)?

Type 1 DM results from the autoimmune destruction of pancreatic cells preventing the

synthesis and secretion of insulin. The trigger for autoimmune destruction is debated and

hypotheses include environmental toxins or infections

3) What genes have been identified that indicate susceptibility to type 1 diabetes mellitus?

Genes that influence the function of pancreatic β cells have been examined for possible

links to T1DM. Additionally, genes related to functions influencing metabolic syndrome

are being reviewed for a link to T2DM. For example, PPARγ is being reviewed for its

possible role in insulin resistance.

4) After examining Susan’s medical history, can you identify any risk factors for type 1

DM?

Susan has a family hx of DM which is a risk factor in her development of the disease

consider the potential genetic links of the disease.

5) What are the established diagnostic criteria for type 1 DM? How can the physicians

distinguish between type 1 and type 2 DM?

DM is usually diagnosed through an oral glucose tolerance test. T1DM can be diagnosed

in individuals with a plasma glucose ≥ 200 mg/dL or a fasting plasma glucose ≥ 126

mg/dL when presented with additional symptoms, such as unexplained weight loss,

pollydipsia, or polyuria. One distinction helpful in the diagnosis of DM is that T1DM is

illustrated by sudden onset of symptoms, where T2DM is more gradual. Additionally,

T2DM is almost always seen in conjunction with symptoms of metabolic syndrome.

6) Describe the metabolic events that led to Susan’s symptoms (polyuria, polydipsia,

polyphagia, weight loss, and fatigue) and integrate these with the pathophysiology of the

disease.

Glycosuria and polyuria result from the excretion of excess blood glucose that has built

up because of a lack of insulin in the body. This polyuria results in an excessive water

loss, leading to polydipsia, polyphagia, and weight loss. Fatigue is a symptom of muscle

and fat cells that are starved for energy due to inadequate insulin levels.

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7) List the microvascular and neurologic complications associated with type 1 diabetes.

Some of the long-term complications associated with T2DM include cardiovascular

disease, nephropathy, retinopathy, peripheral neuropathy, and autonomic neuropathy.

8) When Susan’s 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?

The dawn phenomenon is an increased blood glucose in the early morning resulting from

increased glucose production in the liver throughout an overnight fast. This can be

mediated by administration of a combination of short- and intermediate-acting insulins

before breakfast, short-acting insulin before evening meals, and intermediate-acting

insulin at bedtime.

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.

Omission or improper practice of insulin delivery, or general lack of blood glucose self

monitoring can lead to DKA because blood glucose levels can sky-rocket, resulting in

generation of ketones. Severe illness or infection can also impact a person’s blood

glucose and the amount of insulin needed. In addition, illness or emotional distress can

vary an individual’s eating patterns and throw off the balance between intake and insulin

delivery.

Nutrition Assessment

Evaluation of Weight/Body Composition

10) Determine Susan’s stature for age and weight for age percentiles.

62‖ = 1.65 m → 25th

percentile—CDC Stature-for-age percentiles: Girls, 2 to 20 years

100 # = 45.5 kg → 20th percentile—CDC Weight-for-age percentiles: Girls, 2 to 20 years

11) Interpret these values using the appropriate growth chart.

Stature and weight for age percentiles between the 10th and 85

th percentile are considered

normal. Considering this, Susan falls in a normal range according to the stature for age

(25th

percentile) and weight for age (20th percentile) growth curves. There is slight

concern that Susan’s weight may be a bit low for her stature considering the difference in

these two percentiles.

Calculation of Nutrient Requirements

12) Estimate Susan’s daily energy and protein needs. Be sure to consider Susan’s age.

EER for Females 9 through 18 Years

EER = 135.3 – 30.8 (15) + 1.31 [10.0 (45.5) + 934 (1.65)] + 25 = 2313 kcal

PA = active

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13) What would the clinician monitor in order to determine whether or not the prescribed

energy level is adequate?

To monitor whether or not Susan is receiving adequate energy, her weight should be

measured daily. Additional measures of her nutritional adequacy would include a lipid

panel, albumin, and nitrogen balance.

Intake Domain

14) Using a computer dietary analysis program or food composition table, calculate the

kilocalories, protein, fat (saturated, polyunsaturated, and monounsaturated),

carbohydrate, fiber, and cholesterol content of Susan’s typical diet.

4,435 kcal

134 g. protein

167 g. fat (66 g. saturated, 32 g. polyunsaturated, 56 g. monounsaturated)

617 g. carbohydrate

25 g. fiber

324 mg. cholesterol

*See attached FitDay nutrient analysis.

15) What dietary assessment tools can Susan use to coordinate her eating patterns with her

insulin and physical activity?

A diabetic exchange list is a relatively easy way to track the amount of carbohydrate

Susan takes in and determine the appropriate amount of insulin to deliver. She can

confirm this estimate by self-monitoring of blood glucose (SMBG) using a typical SMBG

test such as a pin-prick and a reagent strip. Physical activity is an important aspect of

Susan’s T1DM treatment, and must be carefully monitored. Blood glucose levels should

be taken both before and after exercise, and at times maybe during breaks in exercise to

ensure that hyperglycemia and hypoglycemia to not develop as a result of the increased

energy needs of Susan’s skeletal muscles.

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 Fasting plasma glucose

Plasma lipid profile

Glycated hemoglobin assays

Nutrition history Typical intakes of sugar

Overall energy intake

Profile of lipids consumed

Weight history Current anthropometrics

Acute changes in weight

Weight for age percentile

Physical activity history Typical daily activities

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Preferences of physical activity (ex: sports)

Any cardiovascular risks of physical activity

Monitoring Monthly anthropometrics

SMBG ≥ 3 times daily

HbA1C every 3 months

Psychosocial/economic Access to diabetic, low-sugar foods

Access to diabetic testing materials

Familial/social support of SMBG routine

Knowledge and skills level Knowledge of balanced diet

Understanding of T1DM

Ability to complete regular SMBG

Expectations and readiness to change Attitude towards diagnosis

Personal short- and long-term goals

Desire to remain in compliance

Clinical Domain

17) Does Susan have any laboratory results that support her diagnosis?

One criteria for diagnosis of DM is a causal plasma glucose ≥ 200 mg/dL. Susan’s

glucose is 250 mg/dL, which supports this diagnosis. Additionally, Susan’s glycated

hemoglobin is also high (normal is 3.9-5.2% and recommendations for glycemic control

are < 7.0%), which supports a diagnosis of DM.

18) Why did Dr. Green order a lipid profile?

Although Susan does not exhibit typical risk factors for CVD, her diabetes can increase

her risk for both macro- and microvascular complications that can be further exacerbated

by dyslipidemia. Regular monitoring of plasma lipids is an important preventative

approach for patients with DM.

19) Evaluate Susan’s laboratory values:

Chemistry Normal

Value

Susan’s

Value

Reason for

Abnormality

Nutritional

Implications

Prealbumin

(mg/dL)

16-35 40 Hypovolemia resulting

from polyuria

Rehydration and

prevention of polyuria

Osmolality

(mmol/kg/H2O)

285-295 304 Hypovolemia resulting

from polyuria

Rehydration and

prevention of polyuria

Glucose

(mg/dL)

70-110 250 Inadequate insulin

production

Regulation of glucose

intake and insulin

delivery

BUN (mg/dL) 8-18 20 Catabolism of protein

due to cell starvation

Make energy available

to cells

HbA1C (%) 3.9-5.2 7.95 Inadequate insulin

production

Chronic

hyperglycemia

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20) Compare the pharmacological differences in insulins:

Type of Insulin Brand Name Onset of

Action

Peak of Action Duration of

Action

Lispro Humalog 10-20 min 1-3 hr 3-5 hr

Aspart NovoLog 10-20 min 1-3 hr 3-5 hr

Glulisine Apidra 10-20 min 1-3 hr 3-5 hr

NPH Humulin N,

Novlin N

1-3 hr 8 hr 20 hr

Glargine Lantus 1 hr None 24 hr

Detemir Levemir 1 hr None 24 hr

70/30 premix Mixtard,

Humulin 70/30

30-60 min Dual 10-16 hr

50/50 premix Humulin 50/50 30-60 min Dual 10-16 hr

60/40 premix Mixtard 40 30 min 2-8 hr 24 hr

21) Once Susan’s 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’s insulin prescription is a flexible insulin therapy comprised of basal insulin

once daily and multiple daily injections (MDIs) of bolus insulin before meals. Susan’s

daily basal insulin dose can be determined by multiplying her weight in kilograms by 0.6

units of insulin, yielding 27.3 units. Dr. Green suggested 24 units of basal insulin and

approximately 24 units of bolus insulin depending on food intake. He selected a long-

acting basal insulin (glargine) to be delivered before bed and last through the night and a

faster acting insulin (lispro) to be delivered throughout the day and as needed.

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.

Excessive energy intake (NI-1.5) RT polyphagia AEB dietary recall of 4,435 kcal (EER

is 2313).

Undesirable food choices (NB-1.7) RT inadequate knowledge of and/or disregard for

nutritional guidelines AEB diet high in refined sugars and fats and low in nutrients.

Irregular eating patterns (NB-1.5) RT busy volleyball schedule AEB pt. self-report.

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 is a natural sweetener that can be used in place of sugar and other artificial

sweeteners. Sweeteners alternative to sugar can be helpful tools for individuals with

diabetes who are trying to manage their carbohydrate intake. Additional benefits of stevia

(such as the delayed development of insulin resistance) are debated within the scientific

community (Cheng, et. al., 2005). There also exist some support for detrimental impacts

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of artificial sweeteners, but these adverse health effects are only seen in unreasonably

high intakes of the products. In conclusion, there are a variety of sweetening alternatives,

including stevia, acesulfame-K, sucarlose, etc., that are all safe for Susan to use

depending on her personal preference.

Nutritional Diagnosis

24) Select two high-priority nutrition problems and complete the PES statement for each.

Impaired glucose utilization (NC-2.1) RT inadequate insulin synthesis by pancreas AEB

hyperglycemia, FBG of 250 mg/dL and HbA1C of 7.95%.

Involuntary weight loss (NC-3.2) RT impaired glucose utilization AEB pt. self-report.

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).

FBG < 200 mg/dL and HbA1C < 7.0% to be achieved by SMBG and delivery of

synthesized insulin.

Return to UBW (as determined by pt.) to be achieved by improved glucose utilization by

SMBG and delivery of synthesized insulin.

26) Does the current diet order meet Susan’s overall nutritional needs? If yes, explain why it

is appropriate. If no, what would you recommend? Justify your answer.

Nutrient Grams Kilocalories % Intake AMDR

Total energy NA 2,400 100% 100%

Carbohydrate 300 1,200 50% 45-65%

Protein 55-65 220-260 9-11% 10-35%

Lipid 80 720 30% 20-35%

Susan’s current diet order (2,400 kcal, 300 g CHO, 55-65 g protein, 80g lipid) does meet

all of her overall nutritional needs. Her total energy intake is within an acceptable range

of her EER (2,313) and all of her macronutrients also fall with the AMDR.

Nutrition Monitoring and Evaluation

27) Susan is discharged Friday morning. She and her family have received information on

insulin administration, SMBG, urine ketones, recordkeeping, 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 dietitan 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

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she drank one bee when she arrived at the party. She remembers getting lightheaded and

then woke up in the ER. What happened to Susan physiologically?

Susan suffered from acute severe hypoglycemia, resulting from her insulin injection.

While Susan was correct in selecting one beer as an appropriate delivery of 15 g. of

CHO, she was incorrect in selecting 15 g. of CHO as an appropriate delivery for 2 units

of insulin. One unit of insulin should be delivered for each carbohydrate exchange (15 g.

of CHO). Thus, Susan should have had a snack containing 30 g. of carbohydrate rather

than 15 g. Her insulin dose was twice what she needed to take in her 15 g. of

carbohydrate, sending her into a state of sever hypoglycemia, which resulted in her loss

of consciousness.

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.

At this point I would talk to Susan about her responsibility as a 15-year old to managing

her own health. I would reiterate the exchange system and how it correlates with insulin

doses and go over a few exercises with Susan to ensure that she understands the correct

calculations.

Secondly I would address with Susan some of the physiological effects of alcohol,

discussing the importance of her abstaining from alcohol until her brain is fully

developed (around age 21) as well as some of the legal ramifications that can result from

underage drinking.

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References

Chang, J.-C., Wu, M. C., Liu, I.-M., & Cheng, J.-T. (2005, April). Increase of insulin sensitivity

by stevioside in fructose-rich chow-fed rats. Hormone and Metabolic Research, 37(10),

610-616. Retrieved March 28, 2010 from http://web.ebscohost.com.proxy.lip.muohio.edu

Nelms, M., Sucher, K., & Long, S. (2007). Nutrition and pathophysiology. Belmont, CA:

Wadsworth.

Rolfes, S. R., Pinna, K., & Whitney, E. (2009). Understanding normal and clinical nutrition (8th

ed.). Belmont, CA: Wadsworth.