Group 4B Case Study 2 Type 2 Diabetes New Onset
Nathan Harnois, Briana Santaniello, Sagar Shah, Derek Wilson
Chief Complaint: "My vision has been blurred lately and it seems to be getting worse."
HPI: Alfonso Giuliani is a 68-year-old man who presents to his family physician's office complaining of periodic blurred vision
for the past month. He further complains of fatigue and lack of energy that prohibits him from working in his garden.
PMH: HTN x 18 years Dyslipidemia x 8 years Gouty arthritis x 16 years with complicated course of uric acid urolithiasis
Hypothyroidism x 15 years Obesity x 25 years
FH: Diabetes present in mother. A.G. immigrated to the United States with his mother and sister after their father died
suddenly for unknown reasons at age 45. One younger sibling died of breast cancer at age 48.
SH: Retired candy salesman, married x 46 years with three children. No tobacco use. Drinks one to two glasses of
homemade wine with meals. He reports compliance with his medications.
Meds: Lisinopril 20 mg by mouth once daily, Allopurinol 300 mg by mouth daily, Levothyroxine 0.088 mg by mouth once
daily
All: NKDA
ROS: Occasional polydipsia, polyphagia, fatigue, weakness, and blurred vision. Denies chest pain, dyspnea, tachycardia,
dizziness or lightheadedness on standing, tingling or numbness in extremities, leg cramps, peripheral edema, changes in
bowel movements, GI bloating or pain, nausea or vomiting, urinary incontinence, or presence of skin lesions.
Physical Examination
GEN: The patient is a centrally obese, Caucasian man who appears to be restless and in mild distress.
VS: BP 124/76 without orthostasis; P 80; RR 18; T 37.2°C; Wt 77 kg; Ht 66″; BMI 27.4 kg/m 2
SKIN: Dry with poor skin turgor; no ulcers or rash
HEENT: PERRLA; EOMI; TMs intact; no hemorrhages or exudates on funduscopic examination; mucous membranes normal;
nose and throat clear w/o exudates or lesions
NECK/LN: Supple; without lymphadenopathy, thyromegaly, or JVD
CV: RRR; normal S1 and S2; no S3, S4, rubs, murmurs, or bruits
LUNGS: CTA
ABD: Soft, NT, central obesity; normal BS; no organomegaly or distention
GU/RECT: Normal external male genitalia
EXT: Normal ROM and sensation; peripheral pulses 2+ throughout; no lesions, ulcers, or edema
NEURO: A & O x 3, CN II–XII intact; DTRs 2+ throughout; feet with normal vibratory and pinprick sensation (5.07/10 g
monofilament)
Labs:
Na 141 mEq/L
Ca 9.9 mg/dL
A1C 7.8%
K 4.0 mEq/L
Phos 3.2 mg/dL
Fasting lipid profile
Cl 96 mEq/L
AST 21 IU/L
T. chol 280 mg/dL
CO2 22 mEq/L
ALT 15 IU/L
HDL 27 mg/dL
BUN 24 mg/dL
Alk phos 45 IU/L
LDL 193 mg/dL
SCr 1.1 mg/dL
T. bili 0.9 mg/dL
Trig 302 mg/dL
Random Glu 202 mg/dL
Creatinine clearance: 58 mL/min
UA: (–) Ketones, (–) protein, (–) microalbuminuria
Problem List:
 Type 2 Diabetes New Onset*
 Dyslipidemia*
 Obesity*
 Hypertension
 Gouty Arthritis
 Hypothyroidism
Group 4B Case Study 2 Type 2 Diabetes New Onset
Nathan Harnois, Briana Santaniello, Sagar Shah, Derek Wilson
A: AG is a 68-year-old man who presents to his family physician's office. His chief compliant is “My vision has been blurred
lately and it seems to be getting worse." AG also complains of lethargy and lack of energy that prohibits him from his daily
activities. AG’s chief complaints, past medical history, and current laboratory values are indicative of the presence of new
onset of diabetes. AG’s risk factors of new onset of diabetes, based on the American Diabetes Association (ADA) and
American Association of Clinical Endocrinologists (AACE), are his age which is greater than or equal to 45, a first degree
relative with diabetes, his central obesity is greater or equal to 25kg/m2, diagnosis of hypertension, and either HDL
cholesterol level less than 35 mg/dL or triglycerides greater than 250mg/dL. 2 Uncontrolled diabetes leads to hyperglycemia.
AG presents with symptoms of hyperglycemia including thirst, increased appetite, fatigue, blurred vision, polyphagia, and
polydipsia. Diabetes mellitus (DM) is a metabolic condition characterized by high glucose levels and can result in chronic
complications, including microvascular and macrovascular disorders. T2DM is also characterized by insulin resistance and a
relative lack of insulin secretion, with progressively lower insulin secretion over time. 3 Most individuals with type 2 diabetes
exhibit abdominal obesity, hypertension, dyslipidemia, and insulin resistance. Insulin resistance is based on NCEP ATP III,
which has five components: abdominal obesity, triglycerides, HDL, blood pressure, and fasting glucose. AG shows
characteristics of insulin resistance as seen by his past medical history of hypertension, gouty arthritis, dyslipidemia, central
obesity, and his glucose intolerance.4 Furthermore, environmental factors such as physical inactivity and his age are
contributors to his insulin resistance. The desired goals for AG’s type 2 diabetes, based upon AACE goals, are to increase
AG’s knowledge of diabetes to aid in the ability to make educated decisions regarding therapy and health care, implement
lifestyle modifications to improve overall health, initiate a treatment regimen that minimizes adverse effects (specifically
hypoglycemia) and drug interactions, prevent or delay the progression of chronic microvascular and macrovascular
complications, improve quality of life and decrease morbidity and mortality, and reduce or eliminate modifiable risk factors.
The ADA targets for glycemic controls are preprandial capillary plasma glucose 70–130 mg/dL, peak postprandial capillary
plasma glucose <180 mg/dL, and A1C ≤ 7%.1 The AACE has adopted the following glycemic controls which are: FPG
concentration <110 mg/dL, two-hour postprandial glucose concentration <140 mg/dL, and A1C ≤6.5%.2
Nonpharmacological recommendations for AG’s type 2 diabetes new-onset based on ADA and AACE guidelines include
medical nutritional therapy (which should be based upon AG’s lifestyle such as, reduced energy intake, reduced saturated
and trans-fatty acids, reduced cholesterol intake, educed sodium intake) and increased energy expenditure of 30 minutes of
aerobic exercise three to four times a week. AG should also consult a dietician for weight reduction therapy which is
important for insulin resistant overweight and obese individuals.1, 2 AG should monitor his metabolic parameters, including
blood glucose levels, A1C, blood pressure, and body weight. Pharmacological therapy for AG includes sulfonylureas,
meglitinides, biguanides, alpha-glucosidase inhibitors, thiazolidinediones, insulin therapy, incretin mimetics, dipeptidyl
peptidase-4 inhibitors, bile-acid sequestrants, and dopamine agonists. Metformin, a biguanide, is designated as the preferred
first-line choice in both monotherapy and dual therapy regimens 2. The initial treatment of type 2 diabetes is metformin due
to its high efficacy of a 1%-2% reduction in A1C, low risk of hypoglycemia, reduction in weight, occasional side effects of
mostly gastrointestinal and low cost.3 Additionally the UKPDS demonstrated that metformin use resulted in a reduction in allcause mortality in obese patients by one third.1,2 If metformin monotherapy has not reached individualized A1C goal after
three months, a two drug combination with metformin plus a sulfonylurea, thiazolidinedione, DPP-4 inhibitor, incretin, or
insulin may be used. If metformin dual therapy has not reached individualized A1C goal after three months, a triple drug
combination with metformin dual therapy plus sulfonylurea, thiazolidinedione, DPP-4 inhibitor, incretin, or insulin may be
used.3 Metformin’s primary mechanism of action is to decrease hepatic glucose production and secondary mechanism of
action is to improve insulin sensitivity and decrease intestinal absorption of glucose.3 Modest weight loss may occur in
patients taking metformin.1, 2 Metformin is also associated with modest decrease in total cholesterol, LDL, and triglycerides.
Metformin contraindications include renal disease or impairment (Scr >1.5mg/dL in males and Scr>1.4mg/dL in females),
acute or chronic metabolic acidosis, iodinated contrast for radiologic studies, patients >80 year olds and hepatic disease.
Metformin side effects include diarrhea, nausea, vomiting, rash, photosensitivity, urticaria, decreased vitamin B12
absorption, and lactic acidosis.3 The starting dose of metformin for AG should be between 500 and 1000mg (maximum daily
dose of 2550mg).3 Patient education is a major contributor to quality of life. AG should be educated about the causes of
diabetes, non- pharmacological and pharmacological treatments, short-term and long-term complications, and the
importance of adherence. Dyslipidemia can be directly related to T2DM and is one of the major risk factors for developing
cardiovascular disease in patients with diabetes. AG’s labs reveal increased TGs, low HDL, and increased LDL, which are
hallmarks of dyslipidemia in patients with diabetes. If not treated properly, these lab values will accelerate atherosclerosis
leading to severe cardiovascular events. HDL levels are decreased due to VLDL-transport triglycerides being exchanged for
HDL-transported cholesteryl ester, which results in increased amount of cholesterol-rich VLDL remnant particles and
triglyceride-rich, cholesterol-depleted HDL particles. Increase LDL levels increase due to CETP promoting the transfer of
triglyceride into LDL in the exchange for LDL-transported cholesteryl ester.5 The triglyceride-rich LDL undergoes hydrolysis
and results in lipid-depleted small dense LDL. Lifestyle modifications implicated for obesity, including exercise and proper
diet, should also help improve lipid levels. Since AG is 68 years old and his dyslipidemia is uncontrolled, statin therapy
should be initiated to prevent atherosclerosis. Atorvastatin 20mg daily would decrease his LDL levels 35-39%.5 This, in
combination with diet proper diet and exercise, should decrease his LDL levels to a target goal <100. A repeat lipid panel
test should be performed in a month to determine if the dose needs to be increased. Furthermore, AG’s Framingham risk
score is calculated at 30% which means AG has a 30% chance of a heart attack in 10 years.4 There is a strong link between
obesity and diabetes. About 80-90% of patients diagnosed with T2DM are currently obese. Being overweight puts a stress on
the body’s ability to maintain proper blood glucose levels. In addition, obesity can cause insulin resistance in non-diabetic
patients. When insulin is not working properly, more glucose will be converted to fat, especially glucose stored in adipose
tissue. In addition, when insulin is not working properly the patient may experience an increase in appetite leading to even
more weight gain. When the patient is placed on insulin therapy, appetite should decrease due to proper nutrient intake. A
decrease in weight can improve efficacy of insulin. A weight loss plan including exercise and diet should be initiated before
attempting pharmacotherapy of orlistat. If orlistat is initiated, adherence to a diet evenly divided between fats,
carbohydrates, and proteins is critical for efficacy and the prevention of adverse effects. Finally, low dose aspirin (75 to
Group 4B Case Study 2 Type 2 Diabetes New Onset
Nathan Harnois, Briana Santaniello, Sagar Shah, Derek Wilson
162mg/day) should be initiated as a primary prevention for AG as he has hypertension, BMI> 27.3, and dyslipidemia. Patient
education and monitoring of all parameters are critical for the enhancement of quality of life.3
P:
1. Educate patient on T2DM.
2. Initiate metformin 500 mg by mouth once daily with breakfast, then increase after 1 week to 500 mg by mouth twice
daily with breakfast and dinner.
a. Educate patient on the adverse effects of metformin.
i. Diarrhea, headaches, bloating, nausea, or general muscle aches
ii. Potential for lactic acidosis with decreased renal function and concomitant consumption of alcohol
iii. Check SCr at baseline and yearly.
1. Discontinue metformin if SCr is >1.5 mg/dL
iv. Check liver enzymes (AST, ALT) prior to initiation of therapy, then check annually.
v. Monitor vitamin B12 and folic acid levels every 2 years.
b. Ask patient for signs and symptoms of hypoglycemia (dizziness, hunger, sweating, tachycardia, confusion,
weakness, blurred vision) as may be a sign of possible toxicity.
c. Advise patient to have an A1C drawn every 3 months until glycemic goals are met (<7%) and then once
every 6 months.
3. Initiate self-monitoring of blood glucose (SMBG)
a. Use Accu-Chek Aviva Diabetes Monitoring Kit as directed twice a day before meals to check blood glucose
levels.
b. Use Accu-Chek Multiclix lancets and Accu-Chek Aviva test strips twice daily to check blood glucose levels
i. Advise patient to keep a journal of twice daily blood glucose readings before meals by utilizing SMBG
results and review every 2-4 weeks until glycemic goals are met, and then review quarterly
thereafter, with a goal of 90–130 mg/dL.
ii. Provide training on proper meter use, care, and maintenance.
iii. Provide patient with necessary information and education to assist in making therapeutic decisions
about self-care delivered over a series of visits.
4. Perform a psychosocial screening regarding T2DM and follow-up based on patient’s responses.
5. Start aspirin 81mg by mouth once daily.
6. Continue lisinopril 20 mg by mouth once daily.
a. Advise patient to monitor blood pressure the same time each day and record daily readings
b. Advise patient to report adverse effects such as dry cough and symptoms of hypotension (dizziness,
lightheaded, fatigue)
7. Initiate atorvastatin 20 mg by mouth every day at bedtime.
a. If LDL goals (reduction of 30-40% from baseline) are not achieved after 6-8 weeks increase dose to 40 mg
by mouth every day at bedtime.
b. Once LDL goals are met, obtain a fasting lipid profile annually.
c. Advise patient of the interaction between atorvastatin and grapefruit juice (causes increased risk of
myopathy and rhabdomyolysis).
d. Advise patient to report any signs of muscle aches or pain (Rhabdomyolysis) and Inform patient of common
side effects of atorvastatin (nausea, flatulence, diarrhea).
8. Begin Orlistat 120 mg by mouth three times a day with meals.
a. Weight loss is indicative of efficacy.
b. Educate patient on gastrointestinal side effects (abdominal pain and discomfort).
c. Use in combination with a diet in which no more than 30% of the total calories come from fat.
9. Initiate aquADEK vitamin supplement by mouth 2 hours before or after orlistat dose.
10. Initiate lifestyle changes consisting of weight loss of 2 kg/month until reach a normal BMI of 18.5 to 24.9.
a. Advise patient to buy a scale, unless already owns one and have him record his weight every morning and
before bed.
11. Advise patient to seek medical nutritional therapy preferably through a registered dietitian familiar with the
components of diabetes.
a. Advise patient to follow Dietary Approaches to Stop Hypertension (DASH)-style dietary pattern.
b. Decrease salt consumption to <2.4 g of sodium per day.
c. Saturated fat intake should be <7% of total calories and reduce intake of trans fats and cholesterol/Increase
of n-3 fatty acids, viscous fiber and plant stanols/sterols.
12. Advise patient to perform at least 150 min/week of moderate-intensity aerobic physical activity (50–70% of
maximum heart rate), spread over at least 3 days/week with no more than 2 consecutive days without exercise.
13. Advise patient to annually screen with random spot collection of urine albumin-to-creatinine ratio.
14. Advise patient to inspect feet daily for any abnormalities and report to physician.
15. Advise patient to see ophthalmologist, and then have annual appointment.
16. Advise patient to get influenza vaccination annually.
17. Recommend patient to be vaccinated against pneumococcal infections (unless already immunized).
18. Educate the patient to keep alcohol intake to less than two eight ounces glasses of 7% alcohol a day.
Group 4B Case Study 2 Type 2 Diabetes New Onset
Nathan Harnois, Briana Santaniello, Sagar Shah, Derek Wilson
References:
1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2013; 36(suppl 1):S67S74.
2. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical
Endocrinologists/American College of Endocrinology Consensus Panel on type 2 diabetes mellitus: an algorithm for
glycemic control. Endocr Pract. 2009;15(6):540-559. Erratum in: Endocr Pract. 2009;15(7):768-77
3. Triplitt C.L., Reasner C.A. (2011). Chapter 83. Diabetes Mellitus. In J.T. DiPiro, R.L. Talbert, G.C. Yee, G.R. Matzke, B.G.
Wells, L.M. Posey (Eds), Pharmacotherapy: A Pathophysiologic Approach, 8e. Retrieved October 17, 2013 from http://0www.accesspharmacy.com.wildpac.wne.edu/content.aspx?aID=7990956.
4. National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert
Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report.
Circulation 2002; 106:3143.
5. Talbert R.L. (2011). Chapter 28. Dyslipidemia. In J.T. DiPiro, R.L. Talbert, G.C. Yee, G.R. Matzke, B.G. Wells, L.M. Posey
6.
(Eds), Pharmacotherapy: A Pathophysiologic Approach, 8e. Retrieved October 17, 2013 from http://0www.accesspharmacy.com.wildpac.wne.edu/content.aspx?aID=7974214.
CHessman K.H., Kumpf V.J. (2011). Chapter 149. Assessment of Nutrition Status and Nutrition Requirements. In J.T.
DiPiro, R.L. Talbert, G.C. Yee, G.R. Matzke, B.G. Wells, L.M. Posey (Eds), Pharmacotherapy: A Pathophysiologic
Approach, 8e. Retrieved October 17, 2013.