Diabetes Case Study Yelena Tkachenko Farin Farahzadi Lilyan vosghanian Qundeel “q” Khattak Tatiana Kiesewetter
1.) Mrs. R’s IBW and % IBW :2.) Calculate Mrs. R’s BMI and Interpret the results: Hamwi Method for Females: 100lb for 5ft + lb/inch over or under 5ft. a.) IBW:100 lbs + ( 5 lb /inch x 6 inch= 30) → 100lb + 30 lb= IBW is 130 lbs b.)% IBW= Current Weight/ Ideal Body Weight x 100% 210 lb/130 lb = 1.62 x 100% = % IBW is 161.5 BMI = weight (kg) / height in (m)2 95.4 kg/ 167.64 cm → 95.5 kg /( 1.68 m)₂ → BMI = 33.82 Her BMI of 34 is an indicator that she is morbidly obese
3.) Calculate Mrs. R’s LDL in Table 3: Mrs. R Lab Results: Formula for LDL (mg/dl) = TC- (HDL + 0.2 TG) 300 mg/dl – (30mEq/L + 0.2 x 350 mg/dl) → 300mg/dl– ( 30mEq/L + 70 mg/dl)→ • 300 mg/dl–(100 mg/dl) = LDL is200 mg/dl
4.) is the HbA1c and how is it used in diabetes? HbA1c is a form of hemoglobin that has been gylcated. It is used to measure how much glucose is circulating in the bloodstream because of how HbA1c and glucose interact. If glucose levels are high, the glucose will slowly and irreversibly attach to proteins in plasma. It is a valuable long term indicator to investigate the last 2-3 months of an individual’s average blood glucose level. It is particularly valuable because short term factors such as food intake, exercise or stress will not affect the level of glycated HbA1. American Diabetes Association. Symptoms. Retrievedfrom http://www.diabetes.org/diabetes-basics/symptoms/
5.) List the Symptoms of Type 2 Diabetes that are manifested in Mrs. R: Polyphagia Polyuria Polydipsia Fatigue Vision has become blurred Frequent bladder infections
6.) Explain the pathophysiology of these symptoms: Polyuria:Occurs due to high amounts of solutes within the renal tubule cause a passive osmotic diuresis (solute diuresis) and thus an increase in urine volume. An example of this process is the glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, when high urinary glucose levels (> 250 mg/dL) exceed tubular reabsorption capacity, leading to high glucose levels in the renal tubules; water follows passively, resulting in glucosuria and increased urine volume. (Merks Manual for Health Care Professional, 2012) Polydipsia:Dehydration results from osmotic diuresis then leads to decreased circulation blood volume and decreased blood pressure. The fall in blood pressure triggers homeostatic mechanisms for maintaining blood pressure , including secretion of ADH, thirst that causes constant drinking (polydipsia) and cardiovascular compensations. Sillverthorn U., Dee.(2009) Human Physiology: Metabolism and Energy Balance(4th ed.) San Francisco: CA Person Benjamin Cummings. pg 736 Polyphagia: The metabolism of the brain is not insulin dependent , however, neurons in the brains’ satiety center are insulin sensitive . Thus, the absence of insulin , the satiety center is unable to take up plasma glucose. The center unable to take up glucose perceives itself as experiencing starvation and allows the feeding center to increase food intake. Sillverthorn U., Dee.(2009) Human Physiology: Metabolism and Energy Balance(4th ed.) San Francisco: CA Person Benjamin Cummings. pg 736
6.) Continued Fatigue: Many factors can contribute to this. They include dehydration from increased urination and body's insulin resistance and inability to function properly and perform metabolism and lowered plasma volume produces weakness and fatigue. Sillverthorn U., Dee.(2009) Human Physiology: Metabolism and Energy Balance(4th ed.) San Francisco: CA Person Benjamin Cummings. pg 737 Blurred Vision : Blurred vision develops as the lens and retina are exposed to higher osmolar fluids. Lowered plasma volume produces weakness and fatigue. Mattson, Carol .Essentials of Pathophysiology: Concepts of Altered Health States: 3rd ed. Wolters Kluwer Company Philadelphia: PA pg 811 Frequent Bladder Infections: Incomplete bladder emptying caused by autonomic neuropathy permits urinary colonization of some microorganisms in the presence of high glucose concentration. Aubert, Ronald. (1995) Diabetes in America 2nd ed. Diane Publishing Company pg 485-487
7.) Define these terms: Polydipsia: Excessive thirst Cohen, Barbara (2011) Medical Terminology 6thed. Wolters Kluwer Health Philadelphia: PA pg287 Polyphagia: Excessive or voracious eating Cohen, Barbara (2011) Medical Terminology 6thed. Wolters Kluwer Health. Philadelphia: PA pg 287 Polyuria: Elimination of large amounts of urine, as in diabetes mellitus Cohen, Barbara (2011) Medical Terminology 6thed. Wolters Kluwer Health. Philadelphia: PA pg 287
8.) What evidence did the MD have that suggested that Mrs. R was dehydrated? • Increased values for serum sodium, albumin, blood urea nitrogen (BUN), and creatinine are good indications of dehydration. • Increased output of urine can lead to dehydration.
9.) What labs may be elevated due to dehydration? • Dehydration causes everything in the body to rise superficially. • Other labs that may be elevated are serum protein, Hgb, Albumin, Hct, Mg, and Na.
10.) On what basis did the MD decide that Mrs. R was anemic? • Anemia is characterized by Hgb values below 95% of total blood volume • Hydration problems can mask nutritional anemia • Hgb levels are mid range • MCV, MCH, and MCHC values are below conventional levels • We can determine that Mrs. R has microcytic anemia, associated with Fe deficiency. (Table 1.14)
11.) After Mrs. R’s BS is corrected, what changes in other blood values would you expect? Explain. • A1c values ↓ • Total cholesterol, LDL, and TG and B.P. ↓ • HDL values will ↑ • When blood sugar is maintained in the system, then carbohydrate, protein and fat metabolism will be restored. • When insulin is sufficient,” it activates the transport system of glucose into muscle and adipose tissue; lowers blood amino acids in parallel with blood glucose levels; activates lipoprotein lipase, facilitating transport of triglycerides into adipose tissue.” (Mahan, 2012) • “Promotes storage and facilitates conversion of glucose to glycogen for storage in muscle and liver; stimulates protein synthesis; facilitates conversion of pyruvate to FFA, stimulating lipogenesis.” (Mahan, 2012) • “Insulin prevents the breakdown and release of glycogen from liver; inhibits protein degradation, diminishes gluconeogenesis; inhibits lipolysis, prevents excessive production of ketones and ketoacidosis.” (Mahan, 2012)
12.) What is considered to be good control for BS for someone with diabetes and what is considered poor control? • Good control is fasting blood glucose at 70-130 mg/dL; post meal <180 mg/dL. • Anything below the fasting blood glucose means hypoglycemic, and anything above post meal means hyperglycemic.
13.) Why should the physician be concerned about the abnormal lipid profile of a person with diabetes who is out of control like Mrs. R? • Long-term complications associated with diabetes are macrovascular disease (disease of large blood vessels), ex: CHD, and microvascular disease (disease of small blood vessels), which includes nephropathy, retinopathy, and diabetic neuropathy which is a nerve damage. • People with type II DM typically have smaller, denser LDL particles, which increase athrogenicity (clogged arteries). • Combination of these diseases will lead to metabolic syndrome: obesity, dyslipedimia, hypertension, and glucose intolerance.
14.) Describe the function of glipizide and list any nutritional complications? • Glipizide (Glucotrol) is in a class of medications called sulfonylureas. • This medication promotes insulin secretion by the beta cells of the pancreas. • Disadvantages may include weight gain, and potential to cause hypoglycemia. • No nutritional complications found.
15.)Describe the function of pravastatin sodium and list any nutritional complications. Why did the physician tell Mrs. R to take it at bedtime? Medication prescribed for lowering high cholesterol and triglycerides • Inhibits production of cholesterol by liver by inhibiting enzyme HMG-CoAreductase Drug/Drug Interactions • Colchicine: The risk of myopathy/rhabdomyolysis is increased with simultaneous administration of colchicine • Fibrates: Because it is known that the risk of myopathy during treatment with HMG-CoAreductase inhibitors is increased with concurrent administration of other fibrates, • Niacin: The risk of skeletal muscle effects may be enhanced when pravastatin is used in combination with niacin; a reduction in Pravachol dosage should be considered in this setting Alcohol • Alcohol can interact with certain medicines. • In the case of Pravastatin sodium: • There are no known interactions between alcohol and Pravastatin sodium Diet • Medicines can interact with certain foods. • In the case of Pravastatin sodium: • There are no specific foods that you must exclude from your diet when taking Pravastatin sodium (C. Song, personal communication, October 12, 2012) confirmed information above.
15.) Continued • Study: • Increased toxicity when fibrates and statins are administered in combination--a metabolomics approach with rats. • fatal side-effects like rhabdomyolysis followed by acute renal necrosis sometimes occur • doses of 100 mg/kg fenofibrate, 50mg/kg clofibrate, 70 mg/kg atorvastatin and 200 mg/kg pravastatin as well as combinations thereof were administered to rats for 4 weeks • Plasma metabolome profile was measured on study days 7, 14 and 28 • Upon study termination, clinical pathology parameters were measured • Lowering of blood lipid levels as well as toxicological effects, like liver cell degradation (statins) and anemia (fibrates) and distinct blood metabolite level alterations were observed in monotherapy • When fibrates and statins were co-administered metabolite profile interactions were generally under additive – fibrates and statins did not act on the body in the same way • However, more metabolite levels were significantly altered during combination therapy. • New effects on the antioxidant status and the cardiovascular system were found which may be related to a development of rhabdomyolysis
16.) Mrs. R’s BP was 150/88. What is the current recommended BP for Mrs. R? • 150/180 = Stage I Hypertension • Recommended BP for Mrs. R would be the normal recommendation => 120/80
17.) What is metabolic syndrome and what symptoms of metabolic syndrome does Mrs. R demonstrate? • Metabolic syndrome is a combination of metabolic risk factors such as: • Central or abdominal obesity (measured by waist circumference): • Men - Greater than 40 inches • Women - Greater than 35 inches • Fasting blood triglycerides greater than or equal to 150 milligrams per deciliter of blood (mg/dL) • Blood HDL cholesterol: • Men - Less than 40 mg/dL • Women - Less than 50 mg/dL • Blood pressure greater than or equal to 130/85 millimeters of mercury (mmHg) • Fasting glucose greater than or equal to 100 mg/dL meaning there’s insulin resistance or intolerance • Mrs. R demonstrates all!
18.) Describe the relationship between obesity, diabetes, and metabolic syndrome. Metabolic syndrome is a combination of metabolic risk factors, which includes obesity, high LDL levels, low HDL levels, high blood pressure, and insulin resistance or intolerance. A patient is said to have metabolic syndrome, if they demonstrate two or more of these risk factors. In the case of Mrs. R, she demonstrates all complications mentioned above; therefore, if she loses weight, she will reduce her total cholesterol thus increasing her HDL, and maximize her insulin efficiency ultimately ridding her of metabolic syndrome.
19.) Prepare a NCP note and write PES statement for Mrs. R up to this point. Obesity with Type II Diabetes (P) is related to family history, physical inactivity, and consumption of low-nutrient dense foods (E) as evidenced by high intake of processed foods, sweets, foods high in saturated fats and sodium, as well as little to no dairy intake (S).
20.) Approximate Mrs. R’s energy needs for weight reduction. • Female • Height = 5’6” = 167.64cm • Age = 48 years • IBW = 100 + 5(6) = 130lbs/2.2= 59.1kg • Harris Benedict (Women) 655 + (9.6 x wt in kg) + (1.8 x ht in cm) – (4.7 x age in yrs) x AF 655 + (9.6 x 59.1kg) + (1.8 x 167.64 cm) – (4.7 x 48yrs) x 1.4 655 + 567.36 + 301.75 – 225.6 x 1.4 1,817.9kcal = TEE
21.) Would you prescribe a 1000 kcal diet? Why or why not? • No, prescribe an 1,800 kcal diet instead (based on the HB formula). • Mrs. R’s condition is serious; she continues to gain weight – needs to make a drastic change in terms of weight loss and caloric intake to help control her blood sugar; however, 1,000 would be too drastic. • 1,800 kcal will also benefit her as she becomes more physically active.
22.) What recommendations for dietary intervention would you give Mrs. R? Carbohydrate Counting method or the standard Exchange Lists for Meal Planning? • Encourage Mrs. R to implement lifestyle modifications that reduce intakes of energy, saturated fats, cholesterol, and sodium and to increase physical activity • Plasma glucose monitoring can be used to determine whether adjustments in foods and meals will be sufficient to achieve blood glucose goals or if medication(s) needs to be combined with MNT • Implement a dietary pattern that includes carbohydrate from fruits, vegetables, whole grains, legumes, and low-fat milk • Monitor carbohydrate, whether by carbohydrate counting or exchanges • Limit intake of saturated fats and cholesterol • Increase consumption of protein – will aid in weight loss
22.) Continued • Recommendstandard Exchange Lists for Meal Planning: • Advantages • Offers variety and versatility to the person with diabetes • It provides a framework to group foods with similar carbohydrate, protein, fat, and calorie contents • It emphasizes important management concepts, such as carbohydrate amounts, fat modification, calorie control, and awareness of high-sodium foods • By making food choices from each of the different lists a variety of healthful food choices can be assured • It provides a system that allows individuals to be accountable for what they eat • Accurate and convenient
23.) The guidelines for meal plans for people with diabetes allows for a limited amount of sugar to be incorporated into the meal plan. Think about how you would persuade Mrs. R to limit her sugar intake and describe how you would teach her to use sugar in her meal plan. Include in your discussion any possible pitfalls of allowing sugar in the meal plan.
24.)Describe the Native-American foods, fry bread and wojapi. • Fry bread is flat dough fried or deep fried in oil, shortening, or lard. It is leavened by yeast or baking powder, and can be eaten alone, or with toppings such as honey, or ground beef, tomatoes, cheese, onions, and lettuce. • Wojapi is a thick berry dish, with a consistency of pudding. It is made with flour or cornstarch, sugar, and berries.
25.)What nutritional deficiencies are likely to result from following the diet Mrs. R described? Explain. • Deficiency in B Vitamins, especially B12, due to lack of meat consumption. • Deficiency in Vitamin A, Vitamin D and Calcium due to lack of milk consumption. • Iron, Folate, Potassium, Vitamin A, Vitamin C and Fiber deficiencies due to limited variety of fresh vegetables and fruits.
26.)What behavioral changes would you recommend to Mrs. R to help her keep her dietary and treatment goals? • Keep a daily food log to track her caloric and carbohydrate intake • Visualize her plate • Follow a special meal plan that includes a variety of foods containing a mixture of carbohydrate, protein and fat. • Monitor her BP on a weekly basis and BS levels on daily basis. • Eat snacks that will 1) keep her full and 2) blunt the effects of certain foods on blood glucose. Ex: adding a tablespoon of peanut butter to an apple will tame the apple’s effect on blood glucose level. • Strongly encourage her to loose weight – begin a walking/jogging program, 4 to 5 times a week. • Lower her blood pressure • Lower her intake of sodium • Continue to work in the garden but incorporate yoga/meditation in her routine • Stay consistent with her medications to insure stable lab results and controlled BS and BP levels. • Be compliant and visit the CDE dietitian, nurse and physician on a weekly basis.
27.) Prepare a Meal Plan using Exchange Method and Carbohydrate Counting Type II DM Exchange List MNT for Type II DM: Step II Diet is recommended Based on a 1800 Kcal/day Meal Plan CHO = 55% Total Calories= 990 kcal/4 kcal = 248grams PRO = 15% Total Calories, (20% for Mrs. R) = 360 kcal/4kcal = 90 grams FAT= <30% total Calories, (25% for Mrs. R) = 450kcal/ 9kcal= 50grams
27.) Continued Breakfast: 1 tortilla (6 inch) = 15 grams 1 banana (small) = 15 grams 1 peach (small) = 15 grams ½ cup cooked squash = 5 grams Total CHO: 50 grams Morning Snack: 1 apple = 15 grams 1 cup raw carrot = 5 grams 1 cup raw celery = 5 gram Total CHO: 25 grams Lunch: 1/3 cup brown rice = 15 grams 1/2 cup beans = 15 grams 1/2 cup mashed potato = 15 grams 1 cup of green = 5 grams I cup peppers = 5 grams 1 tbsp salad dressing, fat-free = 5 grams Total CHO: 60 grams • Afternoon Snack: • 2-5 whole wheat crackers= 15 grams • 1 small orange= 5 grams • I cup sugar snap peas = 5 grams • Total CHO: 25 grams Dinner: 1/2 cup corn = 15 grams 1/2 cup cooked lentils = 15 grams 1/2 cup cooked pasta = 15 grams 1 ¼ cup watermelon, cubes= 15 grams 1/2 cup red peppers = 5 grams 1/2 cup cooked spinach= 5 grams Total CHO: 70 grams • Midnight Snack: • Sugar-Free Candy = 5 grams • 3 medium prunes = 15 grams • Total CHO = 20 grams Total CHO count for the entire day: 250 grams
28.) Determine Mrs. R’s LDL levels in Tables 4 and 5 LDL (mg/dl )= TC-(HDL+ 0.2 TG) Table 4: Results after 3 months 224 mg/dl – (*35 mg/dl + 0.2 x 185 mg/dl) = 152 mg/dl Table 5: Results after 6 months 200 mg/dl – (**38 mg/dl + 0.2 x 150 mg/dl) = 132 mg/dl *1) 35mEq/L x (1.0mmol per L/40 mEq per L) = 0.9mmol/L 2) 0.9 mmol/L x (130 mg per dl/3.4 mmol per L) = 34.4 or 35 mg/dl ** 1) 40 mEq/L x(1.0 mmol per L/40 mEq per L) =1.0 mmol/L 2) 1.0 mmol x(130 mg per L/3.4 mmol per L) = 38.2 or 38 mg/dl
29.) Define Humulin N and R Insulin • Humulin(insulin human recombinant) is synthesized in a special non-disease-producing laboratory strain of E. coli bacteria that has been genetically altered to produce human insulin. The concentration is 100 units/mL (U-100). • Humulin N: crystalline suspension of human insulin with protamine and zinc, provides an intermediate-acting insulin with a slower onset of action (2-4 hrs), peak action (4 -10 hrs) and a longer duration of activity (up to 16-24 hrs). Very individualized. Only SQ (subcutaneous). • Humulin R: sterile, clear, aqueous, and colorless solution that contains human insulin (rDNA origin) 100 units/mL, glycerin 16 mg/mL and metacresol 2.5 mg/mL, endogenous zinc (approximately 0.015 mg/100 units) and water for injection. Short-acting insulin with fast onset (0.5-1 hr), peak action (2-4 hrs) and shorter duration (3-6 hrs). Requires to be injected 30 to 60 min before meals. May be used in combination with oral antihyperglycemic agents or longer-acting insulin products. SQ/IV. • Drug/food interactions: alcohol (causes hypoglycemia/hyperglycemia)
30.) Research the insulin Lantus and describe how it may help Mrs. R. • Study:Lantus by Sanofi-Aventis U.S. LLC • Controlled clinical trials in adults (n=3890) and in pediatric patients (n=349) • Production organism is E. Coli. Insulin glargine differs from human insulin in that the amino acid asparagine at position A21 is replaced by glycine and two argininesare added to the C-terminus of the B-chain.
30.) Continued • Insulin glargine is a human insulin analog that has been designed to have low aqueous solubility at neutral pH. At pH 4, as in the LANTUS injection solution, it is completely soluble. After injection into the subcutaneous tissue, the acidic solution is neutralized, leading to formation of microprecipitates from which small amounts of insulin glargine are slowly released, resulting in a constant concentration/time profile over 24 hours with no pronounced peak.
30.) Continued • Mrs. R’s worsening overtime condition was due to her refusal to follow specialized meal plans and not taking her medications in a timely and proper manner plus her low economic status. Mrs. R and benefits of Lantus: • Once a day dose, SQ only, usually HS (at bedtime). • Recommended (DM type 2) 10 units, with monitoring and adjustments • Slow dissolution at the injection site with a constant and peakless delivery over 24 hrs
31.)What is the action of Precose and what are its side effects? Precose(acarbose tablets): oral alpha-glucosidase inhibitor for use in the management of type 2 diabetes mellitus. Acarbose is an oligosaccharide which is obtained from fermentation processes of a microorganism, Actinoplanesutahensis. • Mechanism of action: works in the small intestine as a competitive inhibitor of intestinal brush-border alpha-glucosides required for breakdown of carbohydrates, thereby delaying carbohydrate absorption and lowering postprandial (after a meal) glycemia. • Side effects: Flatulence, diarrhea, cramping, abdominal pain • Interactions: drug/drug (activated charcoal, digestive enzyme products: amylase, pancreatin), metoprolol. No food interaction.
32.) Describe fully the process of insulin resistance. Insulin resistance (or metabolic syndrome) is a condition in which the cells of the body become resistant to the effects of insulin.One of insulin's responsibility is to get body cells to "open up" to take in glucose (or to store the glucose as fat). When cells don’t open, the body puts out more insulin to stabilize blood glucose. Overtime cells become insulin resistant due to their trying to protect themselves from the toxic effects of high insulin. They down-regulate their receptor activity and number of receptors so that they don't have to be subjected to all that stimuli all the time. Since the pancreas can't always keep up that high level of insulin production forever, the production of insulin starts slowing down, or the resistance goes up, then blood sugar goes up and the person becomes a diabetic.
33.) List the aspects of Mrs. R’s case that indicate insulin resistance. • Waist circumference 42” (normal <35”) • Genetics (Native American) • High-fat diet (fried bread, wojapi, potato chips, etc.) • Obesity (BMI 35) • Elevated BP (150/88) • Glucose intolerance (353 mg/d : 3 times more than normal)
34.) What is the action of Glucophage and what are its side effects? Mechanism of action: • Metformin activates AMPK, the cellular energy sensor. Activation of AMPK leads to suppression of many of the processes highly dependent on ATP, such as gluconeogenesis(formation of glucose, especially by the liver, from non-carbohydrate sources, such as amino acids by pathways mainly involving the citric acid cycle and glycolysis), protein, fatty acid, and cholesterol biosynthesis. • It inhibits transcription of gluconeogenesis genes in the liver and ↑ glucose uptake in skeletal muscle. Thus ↓ the levels of circulating glucose, ↑ insulin sensitivity and ↑ peripheral glucose uptake, and ↓ the hyperinsulinemia associated with insulin resistance. It also improves lipid levels. Side effects: GI distress (nausea, abdominal pain, & diarrhea) and Lactic acidosis (low pH, lactate buildup, fatal) Food/drug interactions:↓ Vitamin B12 , Ca, Folic Acid, Cr. Metformin: antihyperglycemic agent, class biguanides (insulin sensitizer), molecular formula of C4H11N5 • HCl , requires the presence of insulin, Unlike sulfonylureas, metformin does not produce hypoglycemia.
35.) This has been a long ordeal for Mrs. R. with many opportunities for her to become discouraged. Try to imagine what it would be like to be her dietician and to be counseling her through this ordeal. What advice would you give Mrs. R? • Nutrition assessment, diagnosis, monitoring and evaluation: • 1st) Theoretical Basis/ transtheoretical model • Precontemplation: reflection on patients attitude (be understanding) • Contemplation: no intention for change for next 6 months (discuss barriers) • Preparation: intends to take an action in next 6 months (set specific goals) • Action: intends to take action within next 30 days (eliminate triggers, use self-help) • Maintenance: changes for more than 6 months (encouragement, reinforcement) • 2nd) Health Belief model • Intervention, education, motivation and reinforcement to take health-related actions • Detailed explanation of food-planning approaches: • Diabetes nutrition guidelines • Carbohydrate counting • Exchange lists • Healthcare programs information (Medical, Medicare, Food stamps) • Family/friends support
Final PES Statement Mrs. R has excessive caloric intake of nutrient lack food and reduced intake of nutrient dense food as related to her high fat, carbohydrate, high sodium in processed food convenience foods and absence of dairy, fruit, and low protein as evidenced by her high BMI (obese) and fasting GLU levels of 353 mg/dl and lack of physical exercise.
References American Diabetes Association. (2012). Baking with sugar substitutes: Tips and recipes.Retrieved fromhttp://forecast.diabetes.org/baking-oct2012?loc=footer1_forecast-baking-sugar-substitutes_oct2012 American Diabetes Association. (2012). Symptoms. Retrievedfrom http://www.diabetes.org/diabetes-basics/symptoms/ American Heart Association. (2011, August 24). Metabolic Syndrome. Retrieved from http://www.heart.org/HEARTORG/Conditions/More/MetabolicSyndrome/Symptoms-and-Diagnosis-of-Metabolic-Syndrome_UCM_301925_Article.jsp Cohen, Barbara (2011) Medical Terminology 6thed. (PP 287) . WoltersKluwer Health. Philadelphia: PA Franz, M. (2008) MNT from Diabetes Mellitus and hypoglycemia of nondiabetic origin. In Mahan, K., Escott-Stump, S. Krause’s Food and Nutrition Therapy (pp.764- 800). St. Louis: Saunders Elsevier Press. Insulin Glargine (n.d.). Retrieved October 10, 2012 from US National Library of Medicine website: http://www.nlm.nih.gov/medlineplus/druginfo/meds/a600027.html Insulin Injection (n.d.) Retrieved October 10, 2012 from US National Library of Medicine website: http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682611.html Mahan, L.K., Escott-Stump, S. (2012). Krause’s Food and the Nutrition Care Process. Philadelphia, PA: W.B. Saunders Company. Mattson, Carol .Essentials of Pathophysiology: Concepts of Altered Health States: 3rd ed. WoltersKluwer Company Philadelphia: PA pg 811 Metformin. (n.d.). Retrieved October 10, 2012 from US National Library of Medicine website: http://www.nlm.nih.gov/medlineplus/druginfo/meds/a696005.html
References Metformin. (n.d.). Retrieved October 10, 2012 from US National Library of Medicine website: http://www.nlm.nih.gov/medlineplus/druginfo/meds/a696005.html Mihesuah, D.A. (2012). Traditional Indigenous recipes. Retrieved from http://www.aihd.ku.edu/recipes/wojapi.html Polyuria (n.d). Retrieved October 9, 2012. from the Merk Manual for Health Care Professionals website: http://www.merckmanuals.com/professional/genitourinary_disorders/symptoms_of_genitourinary_disorders/polyuria.html Pub med Health. (July 15, 2011). Glipizide. Retrieved from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000834/ Sanofi-Aventis U.S. LLC (2007). Lantus (insulin glargine) injection. (2007). Retrieved October 10, 2012 from Sanofi- Aventis Archived Drug-Label website: http://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=3517#section-4 Sillverthorn U., Dee. (2009) Human Physiology: Metabolism and Energy Balance(4th Ed.).(PP 736). San Francisco: CA Person Benjamin Cummings. Strauss, V., Mellert, W., Wiemer, J., Leibold, E., Kamp, H., Walk, T., . . . van Ravenzwaay, B. (2012). Increased toxicity when fibrates and statins are administered in combination--a metabolomics approach with rats.Experimental Toxicology and Ecology, 211(2), 187-200. Theoretical Basis. (2012). In Academy of Nutrition and Dietetics (4th Ed.), Pocket guide for international dietetics and nutrition terminology (IDNT) reference manual. (PP.316-328). Chicago: Academy of Nutrition and Dietetics Press. U.S. Food and Drug Administration. (2012, February). Safety - Pravachol (pravastatin sodium) Tablets. Retrieved from http://www.fda.gov/Safety/MedWatch/SafetyInformation/ucm295627.htm