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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 yearsFH: 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 dailyAll: NKDAROS: 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 ExaminationGen: 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/m2Skin: Dry with poor skin turgor; no ulcers or rashHEENT: PERRLA; EOMI; TMs intact; no hemorrhages or exudates on funduscopic examination; mucous membranes normal; nose and throat clear w/o exudates or lesionsNeck/LN: Supple; without lymphadenopathy, thyromegaly, or JVDCV: RRR; normal S1 and S2; no S3, S4, rubs, murmurs, or bruitsLungs: CTAAbd: Soft, NT, central obesity; normal BS; no organomegaly or distentionGU/Rect: Normal external male genitaliaExt: Normal ROM and sensation; peripheral pulses 2+ throughout; no lesions, ulcers, or edemaNeuro: 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/LCa 9.9 mg/dLA1C 7.8%K 4.0 mEq/LPhos 3.2 mg/dLFasting lipid profile?Cl 96 mEq/LAST 21 IU/L??T. chol 280 mg/dLCO2 22 mEq/L?ALT 15 IU/L??HDL 27 mg/dLBUN 24 mg/dLAlk phos 45 IU/L??LDL 193 mg/dLSCr 1.1 mg/dLT. bili 0.9 mg/dL??Trig 302 mg/dLRandom Glu 202 mg/dL??Creatinine clearance: 58 mL/minUA: (–) Ketones, (–) protein, (–) microalbuminuriaProblem List:Type 2 Diabetes New Onset*Dyslipidemia*Obesity*HypertensionGouty ArthritisHypothyroidismA: 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 regimens2. 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 all-cause 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 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: Educate patient on T2DM.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.Educate patient on the adverse effects of metformin.Diarrhea, headaches, bloating, nausea, or general muscle achesPotential for lactic acidosis with decreased renal function and concomitant consumption of alcoholCheck SCr at baseline and yearly.Discontinue metformin if SCr is >1.5 mg/dLCheck liver enzymes (AST, ALT) prior to initiation of therapy, then check annually.Monitor vitamin B12 and folic acid levels every 2 years.Ask patient for signs and symptoms of hypoglycemia (dizziness, hunger, sweating, tachycardia, confusion, weakness, blurred vision) as may be a sign of possible toxicity.Advise patient to have an A1C drawn every 3 months until glycemic goals are met (<7%) and then once every 6 months. Initiate self-monitoring of blood glucose (SMBG)Use Accu-Chek Aviva Diabetes Monitoring Kit as directed twice a day before meals to check blood glucose levels.Use Accu-Chek Multiclix lancets and Accu-Chek Aviva test strips twice daily to check blood glucose levelsAdvise 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.Provide training on proper meter use, care, and maintenance.Provide patient with necessary information and education to assist in making therapeutic decisions about self-care delivered over a series of visits.Perform a psychosocial screening regarding T2DM and follow-up based on patient’s responses.Start aspirin 81mg by mouth once daily.Continue lisinopril 20 mg by mouth once daily.Advise patient to monitor blood pressure the same time each day and record daily readingsAdvise patient to report adverse effects such as dry cough and symptoms of hypotension (dizziness, lightheaded, fatigue)Initiate atorvastatin 20 mg by mouth every day at bedtime.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.Once LDL goals are met, obtain a fasting lipid profile annually.Advise patient of the interaction between atorvastatin and grapefruit juice (causes increased risk of myopathy and rhabdomyolysis).Advise patient to report any signs of muscle aches or pain (Rhabdomyolysis) and Inform patient of common side effects of atorvastatin (nausea, flatulence, diarrhea).Begin Orlistat 120 mg by mouth three times a day with meals. Weight loss is indicative of efficacy.Educate patient on gastrointestinal side effects (abdominal pain and discomfort).Use in combination with a diet in which no more than 30% of the total calories come from fat.Initiate aquADEK vitamin supplement by mouth 2 hours before or after orlistat dose.Initiate lifestyle changes consisting of weight loss of 2 kg/month until reach a normal BMI of 18.5 to 24.9.Advise patient to buy a scale, unless already owns one and have him record his weight every morning and before bed.Advise patient to seek medical nutritional therapy preferably through a registered dietitian familiar with the components of diabetes.Advise patient to follow Dietary Approaches to Stop Hypertension (DASH)-style dietary pattern.Decrease salt consumption to <2.4 g of sodium per day.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.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.Advise patient to annually screen with random spot collection of urine albumin-to-creatinine ratio.Advise patient to inspect feet daily for any abnormalities and report to physician.Advise patient to see ophthalmologist, and then have annual appointment.Advise patient to get influenza vaccination annually.Recommend patient to be vaccinated against pneumococcal infections (unless already immunized).Educate the patient to keep alcohol intake to less than two eight ounces glasses of 7% alcohol a day.References: American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2013; 36(suppl 1):S67-S74. 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 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 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.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 (Eds), Pharmacotherapy: A Pathophysiologic Approach, 8e. Retrieved October 17, 2013 from 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. ................
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