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Running head: CLINICAL CASE STUDY 1

Clinical Case Study: Type 2 Diabetes Mellitus

Kacy Shaffer

Fontbonne University
CLINICAL CASE STUDY 2

Literature Review

Epidemiology, Etiology, and Pathophysiology

Type 2 diabetes mellitus (T2DM) is a progressive disease that is characterized by high

blood glucose concentrations caused by a combination of insulin resistance and pancreatic -cell

failure. The -cells of the pancreas produce insulin, which helps store glucose in the cells. With

T2DM, the pancreas is unable to produce enough insulin and the cells are resistant to insulin,

causing a high amount of glucose in the blood stream known as hyperglycemia. In the beginning

stages of the disease, there is an increase in insulin secretion which keeps blood glucose

concentrations in a normal or prediabetic range, so T2DM is often present long before it is

diagnosed. First, hyperglycemia presents as post-prandial blood glucose elevation, then fasting

glucose concentrations rise. There is also an inadequate suppression of glucagon which results in

increased hepatic glucose production (Franz, 2012). The exact pathophysiology for -cell

dysfunction and insulin resistance are not well defined in T2DM, but is associated with

inflammation, metabolic stress, and the other contributors mentioned (Cefalu, 2017).

The Centers for Disease Control and Prevention (CDC) estimate that 30.3 million or

9.4% of Americans have diabetes. The majority of people with T2DM are overweight or obese

(CDC, 2017). Although anyone can get T2DM, it is more common in people ages 45 and older,

those who are overweight or obese, increased percentage of body fat in the abdominal region

those who have a family history of T2DM, and those who are African American,

Hispanic/Latino, American Indian, Asian American, or Pacific Islander. Other factors that can

increase risk for developing T2DM, include physical inactivity, high blood pressure, history of

cardiovascular disease (CVD) or stroke, low HDL cholesterol, high triglycerides, history of
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gestational diabetes, having depression, having PCOS, or having acanthosis nigricans. Other

possible causes of T2DM include genetic mutations, damage to the pancreas, certain hormonal

diseases, and certain medications (Cefalu, 2017; National Institute of Diabetes and Digestive and

Kidney Diseases, 2017).

How Other Body Systems are Affected

As the secretion of insulin decreases, the liver increases the production of glucose The

adipocytes are insulin resistant, which leads to lipolysis and elevation of free fatty acids in

circulation (Franz, 2012). Weight loss of greater than 5% is shown to have beneficial effects on

HbA1c, lipids, and blood pressure (Marincic et al., 2017). T2DM, especially uncontrolled, can

cause long term complications to other body systems. Macrovascular diseases can occur,

including dyslipidemia and hypertension. Microvascular diseases can occur, including

neuropathy, retinopathy, renal disease, and gastroparesis (Franz, 2012).

Clinical Symptoms and Features

The symptoms of diabetes include increased thirst (polydipsia) and urination (polyuria),

increased hunger, feeling tired, numbness or tingling in the feet or hands, sores that do not heal,

and unexplained weight loss. The symptoms of T2DM generally develop over the course of

several years and can be mild enough that a person does not notice them. It is important for

people with risk factors to be tested, because earlier interventions lead to better health outcomes.

Some people develop complications from diabetes such as blurred vision or CVD before they

even find out they have the disease (National Institute of Diabetes and Digestive and Kidney

Diseases, 2017). Diabetic ketoacidosis occurs when blood glucose is too high and there is

inadequate insulin for glucose use. The body relies on fat for energy, which produces ketones
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and leads to acidosis that can be life threatening Franz, 2012). Ketoacidosis rarely occurs

spontaneously, but often arises with the stress of illness or infection (Cefalu, 2017).

Diagnosis and Treatment

To test for and diagnose diabetes, healthcare professionals use the A1C test or fasting

plasma glucose (FPG) test most often. Sometimes a random plasma glucose (RPG) test is used.

The A1C provides the average blood glucose levels over the past three months because it shows

the glucose attached to hemoglobin, which occurs slowly. An A1C below 5.7% is considered

normal, between 5.7 and 6.4% is considered prediabetes, and 6.5% or above indicates a

diagnosis of diabetes (National Institute of Diabetes and Digestive and Kidney Diseases, 2017).

For people with conditions such as pregnancy or anemia, that cause abnormal red blood cell

turnover, glucose criteria must be used exclusively for diabetes diagnosis. A diabetes diagnosis

level for FPG is > 126 mg/dL (Franz 2012). A second test is recommended to confirm the

diagnosis (Cefalu, 2017).

Treatment must be individualized, depending on the persons preferences, values, goals,

age, ability, schedule, support systems, culture, health beliefs, and finances.

Relevance of Nutrition

The American Diabetes Association (ADA) Standards of Medical Care in

Diabetes includes the provision of diabetes self-management education (DSME) and support and

referral to a registered dietitian nutritionist (RDN) for medical nutrition therapy (MNT). These

have shown to improve clinical outcomes, behaviors, quality of life, and produce cost savings

(Marincic et al., 2017). Nutrition related MNT interventions that are recommended include

energy balance, macronutrient distribution and timing, alcohol consumption, and sodium intake.
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These all can play a role in improving health outcomes in those with T2DM by controlling intake

(Cefalu, 2017).
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Medical Management

Managing T2DM involves controlling blood glucose, blood pressure, and cholesterol,

quitting smoking for smokers, achieving and maintaining a healthy weight, being physically

active, and taking prescribed medications. Healthy food choices and physical activity with

diabetes medications can help manage T2DM. These medications include sulfonylureas,

thiazolidinediones, DPP-4 inhibitors, SGLT2 inhibitors, GLP-1 receptor agonists, and insulin.

Other options for management of T2DM include bariatric surgery for certain people. (Cefalu,

2017; National Institute of Diabetes and Digestive and Kidney Diseases, 2017).

Metformin is the preferred initial medicine to treat T2DM. Insulin should be considered

in newly diagnosed patients with an A1C > 10% or blood glucose of > 300 mg/dL (Cefalu,

2017). For glycemic targets, A1C is a common tool. For patients who can achieve it without

complications, an A1C of <6.5% is a reasonable goal. For those with a history of hypoglycemia,

diabetes complications, or a limited life expectancy, less stringent goals such as <8% may be

appropriate (Cefalu, 2017).

Nutrition Assessment Parameters and Medical Nutrition Therapy (MNT)

Nutrition assessment and MNT are essential for management of T2DM. The RD should

assess for glycemic control, lipid profiles, blood pressure, kidney disease and stage, use of

medications and supplements, height, weight, BMI, waist circumference, demographic

information, medical history, social history, cultural preferences, health literacy, education,

occupation, health beliefs, physical activity, previous nutrition care, and food and nutrition

history. For MNT, the RD should assess knowledge and educate patient on carbohydrate

counting, insulin-to-carbohydrate ratio, plate method, or food lists depending on patients


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abilities and type of medications used. Physical activity should be encouraged if medically safe.

Weight loss should be encouraged for those who are overweight or obese and weight

maintenance for those at a healthy weight (Academy of Nutrition and Dietetics, 2015). For those

who are overweight or obese, a sustained 5% weight loss of initial body weight can improve

glycemic control (Cefalu, 2017).

Prognosis

The prognosis for T2DM varies greatly depending on age of onset, glycemic control, and

diabetes-related complications. People with diabetes have a shorter life expectancy than those

without diabetes, largely due to complications, especially cardiovascular causes. Cardiovascular

disease is the cause of about 70% of mortality among people with T2DM. A table with estimated

life expectancy for men and women with T2DM was given in this article that takes smoking,

A1C, cholesterol and other factors into consideration. The prognosis is modifiable by gaining

glycemic control and reducing complications (Leal, Gray, & Clarke, 2009).

Nutrition Care Process for Mr. B

Nutrition Assessment Data

Mr. B is a 67-year-old white male who presented to the emergency room (ER), after a

transfer from his nursing home, with complaints of (c/o) increased upper epigastric pain getting

progressively worse for several days prior to admission (PTA). In the ER, patient (pt) was found

to be in ventricular tachycardia. The pt was shocked and converted to normal sinus rhythm. Pt

potassium level was markedly elevated. Pt required emergency hemodialysis. Pt admitted to ICU

for further evaluation and management.


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Pt has a history (Hx) of type 2 diabetes mellitus (T2DM), diagnosed about 21 years ago,

and blood glucose was running high on admission. Pt was unsure of most recent insulin regimen

and how his glucose was running at the nursing home. Pt has a Hx of diabetic neuropathy and

retinopathy. Pt also has Hx of obstructive sleep apnea (OSA), pulmonary embolism (PE),

coronary artery disease (CAD), non-ST-elevation myocardial infarction (NSTEMI), hypertension

(HTN), hyperlipidemia, deep vein thrombosis (DVT), peptic ulcer disease, acute kidney injury

(AKI), and benign prostatic hyperplasia (BPH).

Upon admission to the ICU unit, pt was evaluated by the critical care MD. It was noted

that on his last admission, Mr. B had acute kidney injury in the setting of sepsis. The

nephrologist was consulted and noted that Mr. B had HD at the last admission, he had HD on

3/23. His Cr was 2.5 and K was 3.5 and he did not need further HD on discharge. He is now

status post emergent HD. The endocrinologist was also consulted, who noted that the pt has

uncontrolled T2DM.

The RD was consulted for diabetic diet education and the dietetic intern did a thorough

nutrition assessment of Mr. B. His current diet order is noted to be consistent carb, renal. He was

awake and able to talk, but tired. He is 107.9 kg and 62 (187.96 cm) with a BMI of 30.5

indicating obesity. This is his usual body weight. His calculated kcal needs are 2,500 with 30

kcal per kg of IBW. His protein needs are 104 g/day with 1.2 g/kg IBW for HD. His fluid needs

are 1,000 mL plus urine output while on HD.

During interview with pt, he noted that his appetite is currently poor. His charted intakes

for meals are 0% for some and bites/sips for most meals. He says that he usually eats more, but is

not feeling well. He usually eats convenience foods, fast food, and snacks throughout the day on
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packaged foods. A few nights per week, his wife will make a dinner that includes a chicken or

burgers, green beans, corn, potatoes, and sometimes a salad. He also indicated that he has had

some education on carbohydrate counting, but does not remember much or count his carbs at

home.

Table 1:
Review of Medications
Medication Reason for Medication Side Effects/Interactions
Sodium bicarb Metabolic acidosis N/V, loss of appetite
Lantus Long acting insulin Nausea, hypoglycemia
Humalog Fast acting insulin Nausea, hypoglycemia

Table 2:
Review of Labs
Lab Test (date) Lab Value (high/normal/low) Possible Etiology
Potassium 7.7 (critically high) Acute kidney injury
Creatinine High Acute kidney injury
Blood glucose 243 (high) Uncontrolled diabetes, stress
C02 6.0 (low) Metabolic acidosis

Nutrition Diagnosis

The patients most important nutrition problem is lack of education about his consistent

carb diet. His current nutrition problem is his decreased appetite and intake.

PES 1: Knowledge deficit related to lack of education as evidenced by pt interview stating he

does not know much about counting carbs or how many he should have.

PES 2: Inadequate oral intake related to lack of appetite as evidenced by pt interview stating he

does not have an appetite and documentation of less than 25% of meals eaten.

Nutrition Intervention
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Provided diet education for consistent carb diet. Provided education materials to bring

with him on discharge. I assessed his readiness for change and he is in contemplation, saying he

will try it but it worried it will be difficult. I recommended he make an appointment with the

outpatient dietitian to address barriers and explained that it is a free service. I also ordered Nepro

BID for his inadequate oral intake as he is currently on HD. I documented him as high so that I

could follow up in 48 hours.

Monitoring and Evaluation

I reassessed his knowledge two days later and he was able to teach back the material. He

was drinking about half the Nepro provided. His current hospitalization and health status are

hampering his intakes. After discharge, if the pt makes the appointment with the outpatient RD,

his intakes can be assessed to ensure he is following consistent carb, eating adequately, and

determine what his barriers are. The barriers can be addressed in the outpatient session.

Health Care Team Members

The MDs included a critical care doctor, nephrologist, and endocrinologist. These doctors

explore and figure out the patients medical problems and appropriate interventions. The

pharmacist makes sure that the prescribed meds are appropriate. The nurse is the first line of care

for the patient, monitoring his vitals, intervening, and getting help from other healthcare team

members when needed. The RD provides MNT for patients with nutrition-related problems. The

social worker works to determine the patients needs upon discharge, contacting his nursing

home and making sure everything is ready for him.


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References

Academy of Nutrition and Dietetics. (2015). Diabetes (DM) guideline (2015). Retrieved from

https://www.andeal.org/topic.cfm?menu=5305&cat=5595

American Diabetes Association. (2017). 14. Diabetes care in the hospital. Diabetes Care,

40(S120-S127). doi:10.2337/dc17-S017

Cefalu, W. T. (2017). American Diabetes Association: Standards of medical care in diabetes

2017. The Journal of Clinical and Applied Research and Educaiton, 40(1), S1-S135.

Retrieved from

https://professional.diabetes.org/sites/professional.diabetes.org/files/media/dc_40_s1_fina

l.pdf

Centers for Disease Control and Prevention (CDC). (2017). Diabetes home. Retrieved from

https://www.cdc.gov/diabetes/home/index.html

Franz, M. J. (2012). Medical nutrition therapy for diabetes mellitus and hypoglycemia of

nondiabetic origin. In K. Mahan, S. Escott-Stump, & J. Raymond (Eds.), Krauses food

and the nutrition care process (pp. 33-128). Elsevier Saunders: St. Louis.

Marincic, P. Z., Hardin, A., Salazar, M. V., Scott, S., Fan, S. X., & Gaillard, P. R. (2017).

Diabetes self-management education and medical nutrition therapy improve patient

outcomes: A pilot study documenting the efficacy of registered dietitian nutritionist

interventions through retrospective chart review. Journal of the Academy of Nutrition and

Dietetics, 117(8), 1254-1264. http://dx.doi.org/10.1016/j.jand.2017.01.023

National Institute of Diabetes and Digestive and Kidney Diseases. (2017). Type 2 diabetes.

Retrieved from
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https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/type-2

-diabetes

Leal, J., Gray, A. M., & Clarke, P. M. (2009). Development of life-expectancy tables for people

with type 2 diabetes. European Heart Journal, 30(7). doi: 10.1093/eurheartj/ehn567

Powers, M. A., Bardsley, J., Cypress, M., Duker, P., Funnell, M. M., Fischl, A. H., Maryniuk, M.

D., Siminerio, L., & Vivian, E. (2015). Diabetes self-management education and support

in type 2 diabetes: A joint position statement of the American Diabetes Association, the

American Association of Diabetes Educators, and the Academy of Nutrition and

Dietetics. Journal of the Academy of Nutrition and Dietetics, 115(8), 1323 1334.

http://dx.doi.org/10.1016/j.jand.2015.05.012

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