Yajie Zhang KNH 411 Oct. 29, 2012 Case 22 Type 1 Diabetes Mellitus i. Understanding the Diesease and Pathophysiology 1. Define insulin. Describe its major functions within normal metabolism. Insulin is a hormone produced by the β cells of the Islets of Langerhans in the pancreas to regulate blood glucose; it promotes uptake, utilization, and storage of nutrients (472). The major functions of insulin within normal metabolism are regulating glucose metabolism, stimulating lipogenesis, diminishing lipolysis, and increasing amino acid transport into cells (473). 2. What are the current opinions regarding the etiology of type 1 diabetes mellitus (DM)? One current opinion regarding the etiology of type 1 diabetes mellitus is that it results from a cellular-medicated autoimmune destruction of β-cells of the pancreas. Also, multiple genetic predispositions and unidentified environmental factors appear to contribute to T1DM. Moreover, research has identified the coxsackie virus, cow’s milk proteins, and rubella as potential triggers (482-483). 3. What genes have been identified that indicate susceptibility to type 1 diabetes mellitus? IDDM2: the insulin gene HLA-DR/DQ: encode immune response proteins CTLA4: plays a regulatory role in immune response (“Genetics of Diabetes”) 4. After examining Susan’s medical history, can you identify any risk factors for type 1 DM? The main risk factor for Susan to develop T1DM is that her grandmother on her mother’s side had diabetes so that she has a chance of carrying the gene of DM. 5. What are the established diagnostic criteria for type 1 DM? How can the physicians distinguish between type 1 and type 2 DM? Established diagnostic criteria for T1DM: Symptoms of diabetes plus casual plasma glucose concentration ≥ 200 mg/dL (11.1 mmol/L) in addition to certain symptoms (unexplained weight loss, polydipsia, polyuria), OR Fasting plasma glucose ≥ 126 mg/dL (7.0 mmol/L) (483) Distinguishes between T1 and T2 DM: T1: complete lack of insulin, beta cells cannot produce insulin the pancreas T2: insufficient amount of insulin produced by beta cells, or weaker ability of the insulin to regulate glucose level 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. Susan’s insulin deficiency is caused by increase hepatic glucose output, decreased glucose uptake by cells, deceased triglyceride synthesis, increased lipolysis, decreased amino acid uptake by cells, and increased protein degradation. The increase hepatic glucose output and decreased glucose uptake by cells, caused hyperglycemia. The hyperglycemia caused glycosuria, which caused osmotic diuresis causing her symptom of polyuria. The polyuria caused dehydration, which caused her next symptom of polydipsia. Decreased triglyceride synthesis and increased lipolysis caused increased blood fatty acids. This caused the body to use fat as an alternative energy source, which produce ketones, and caused her symptoms of fatigue, polydipsia, polyuria, and polyphagia. Decreased amino acid uptake by cells and increased protein degradation cause the increased blood amino acids. Increased blood amino acids increased the activity of gluconeogenesis, which caused an aggravation of hyperglycemia. This leads back to all the symptoms caused by hyperglycemia. Increased protein degradation also caused muscle wasting which lead to her weight loss (483). 7. List the microvascular and neurologic complications associated with type 1 diabetes. Microvascular complications Retinopathy Nephropathy Neurological complications Peripheral neuropathy Cardiovascular autonomic neuropathy Genitourinary autonomic neuropathy Gastro paresis autonomic neuropathy (487) 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 hyperglycemia that occurs early in the morning between 4 and 8 am, most likely due to increased glucose production in the liver after fasting overnight. Since Susan is hyperglycemic early in the morning before eating anything, she might experience the dawn phenomenon. Conventional therapies can be used to control dawn phenomenon. Option one would be that short- or rapid-acting insulin mixed with intermediate-acting insulins given before breakfast and before evening meal. In the other way, combine short- and intermediate-acting insulins before breakfast, short-acting insulin before evening meals, and intermediate-acting insulin at bedtime (487-489). 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. Factors: illness, infection, emotional stress, and omission of insulin. When adequate insulin is not available, glucose production via gluconeogenesis and lipolysis is stimulated by counter-regulatory hormones in an effort to avoid starvation. One of the by-products of lipolysis is the generation of ketones. As glucose and ketones accumulate in the bloodstream, osmotic diuresis occurs, resulting in dehydration and electrolyte imbalances. As fluid is lost, the blood becomes concentrated, resulting in hyperglycemia (496). ii. Nutrition Assessment A. Evaluation of Weight/Body Composition 10. Determine Susan’s stature for age and weight for age percentiles. Stature for age: 23th percentile Weight for age: 17th percentile (Center for Disease Control) 11. Interpret these values using the appropriate growth chart. Both of Susan’s values are above 5th and below 95th, which indicates that Susan is in a normal and healthy condition. B. Calculation of Nutrient Requirements 12. Estimate Susan’s daily energy and protein needs. Be sure to consider Susan’s age. Ht = 5 feet 2 inch = 157 cm Age = 15 Wt = 100lb = 45.5 kg PAL = 1.9 (in volleyball team) REE (Harris Benedict Method) = 655 + (9.56 x 45.5) + (1.85 x 157) – (4.68 x 15) = 1310.23 kcal TEE = REE x PAL = 1310.23 kcal x 1.9 = 2489. 44 kcal EER for Female (9-18) = 135.3-30.8 x age (15) + PA (1.56) x (10.0 x wt-45.5 + 934 x ht-1.57) +25 = 2695 kcal 20% calories from protein = 20% x 2695 kcal = 539 kcal Gram of protein needs = 539 kcal / (4kcal/gram) = 134.8 g 13. What would the clinician monitor in order to determine whether or not the prescribed energy level is adequate? The clinician would monitor Susan’s weight to determine whether or not the prescribed energy level is adequate. Since she has lost weight the first goal will be to gain back what she has lost in order to get her to a healthy weight, then the clinician will monitor this weight to make sure she does not lose or gain too much weight. C. Intake Domain 14. Using a computer dietary analysis program or food composition table, calculate the kcalories, protein, fat (saturated, polyunsaturated, and monounsaturated), CHO, fiber, and cholesterol content of Susan’s typical diet. (FitDay.com) Total Kcal: 4,003 Kcal from protein: 491 (124.2 g) Kcal from fat: 1,317 (148.7 g) - Saturated: 531 (59.4 g) - Polyunsaturated: 260 (29.6 g) - Monounsaturated: 417 (47.2 g) Kcal from CHO: 2,247 (564.7 g) Fiber: 28.4 g Cholesterol: 393 mg 15. What dietary assessment tools can Susan use to coordinate her eating patterns with her insulin and physical activity? a. Susan could do a self-monitoring of blood glucose (SMBG) which indicates a person’s blood glucose the very moment the measurement is taken. This test includes a drop of blood obtained via a finger prick that is applied to a chemically treated reagent strip (493). b. A continuous glucose monitoring devise could be placed under the skin and would allow for constant reading of blood glucose levels every five minutes. This is not meant to replace SMBG but to provide a more detailed picture of blood glucose fluctuations (494). c. Susan can also test for ketones in her urine which should be done regularly during periods of illness or stressful situations when glucose levels are likely to be elevated (495). 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 Clinical data Nutrition history Weight history Assessment You Would Perform - Lipid assessment: total cholesterol, HDL, LDL, & TG - Renal assessment: BUN, creatine, creatine clearance, spot urinalysis for albumin: creatine ratio, & GFR - Hematological assessment: hemoglobin, hematocrit, MCV, MCHC, MCH, & TIBC - Nausea, vomiting - Food allergies, preferences, or intolerances - Ethnic, cultural and religious influences - Highest adolescent weight - Usual body weight - Recent weight changes Physical history Monitoring Psychosocial/economic Knowledge and skills level Expectations and readiness to change - Determine activity type - Determine activity frequency - Consider the length of the activity - Blood sugar - Weight - Blood pressure - Health insurance - Ensure parents are able to afford medical care for their child - Learn if Susan has any friends with diabetes to help her cope - Check what previous nutrition education she has received - Check how comfortable she is with sticking herself - Check knowledge gained after session with the RD - Willingness to learn about disease state - Cooperation with clinical team - Check labs on a regular basis to ensure she is taking her insulin shots (491) D. Clinical Domain 17. Does Susan have any laboratory results that support her diagnosis? Yes, her Prealbumin was 40 mg/dL when admitted and then dropped to 39 mg/dL; this is high since the normal range is between 16-35 mg/dL. Her osmolality was 304 mmol/kg/H2O when admitted and now 297 mmol/kg/H2O which is high because normal ranges are between 285-295 mmol/kg/H2O. Her glucose levels are also high since the normal ranges are between 70-110 mg/dL and when admitted she was at 250mg/dL and now is at 120 mg/dL. Finally, her HbA1C was 7.95% when admitted and it should be between 3.9-5.2%. 18. Why did Dr. Green order a lipid profile? To check Susan’s cholesterol, triglyceride, HDL and LDL levels 19. Evaluate Susan’s laboratory values: Chemistry Osmolality mmol/kg/H2O Normal Value Susan’s Value 285-295 Admit 304 d/c 297 Glucose mg/dL 70-110 Admit 250 d/c 120 BUN mg/dL 8-18 Admit 20 d/c 18 HbA1c % 3.9-5.2 Admit 7.95 Reason for Abnormality High levels of glucose due to dehydration Glucose is not being absorbed into the cells from the blood stream because she is not producing insulin Excessive protein breakdown and impaired kidney function Nutritional Implications Suggests a fluid imbalance. Patient needs proper amounts of carbohydrates and added insulin. CHO-consistent meal plan to control glucose levels with correct amount of insulin Due to dehydration from excessive urination. Proper intake of CHO and insulin needed to correct Long-term High blood glucose in blood glucose levels stream is elevated over several to about 200 months. Proper mg/dL intake of CHO and insulin needed to control blood glucose level (494) 20. Compare the pharmacological differences in insulins: Type of Insulins Lispro Aspart Glulisine NPH Glargine Detemir 70/30 premix Brand Name Humalog Novolog Apidra Isophane Lantus Levemir Humulin Onset of Action 5 – 15 min 5 – 15 min 5 – 15 min 2 – 4 hr 2 – 4 hr 2 – 4 hr 30 – 60 min Peak of Action 30 – 90 30 – 90 30 – 90 4 – 10 Peakless 6 – 14 Dual Duration of Action 3–5 3–5 3–5 10 – 16 20 – 24 16 – 20 10 – 16 50/50 premix 60/40 premix (488) Humulin Novolin 30 – 60 min 30 – 60 min Dual 2–8 10 – 16 18 – 24 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? As diagnosed, Susan has T1DM that she needs to receive a daily dose of insulin that is 0.6 units per kilogram of her actual body weight. 0.6 units/kg actual body wt 45.45 x 0.6 = 27.3 So, with concerns of other factor, Dr. Green slightly adjusted the dose from 27 units to 24 units for Susan. E. 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. Food- and nutrition-related knowledge deficit (NB-1.1) Not ready for diet/lifestyle change (NB-1.3) Undesirable food choices (NB-1.7) 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? Though there had been some debates on this topic, stevia is now generally recognized as safe by the U.S. Food and Drug Administration (FDA). This means this product is proved to sweeten food items or beverages as artificial sweeteners or sugar. Truvia (stevia-based sweetener) is a no-calorie sweetener and will not have an effect on your blood glucose levels. This can be useful for people who have diabetes. When used in excessive amounts, the carbs and calories in Truvia can add up quickly. As with anything, do not go overboard when you use it. It is new on the market, so hopefully more research will be available in the future about its effects on blood glucose in people with diabetes. (ADA) 24. Select two high-priority nutrition problems and complete the PES statement for each. Excessive energy intake related to high calorie intake as evidence by daily calorie intake 60% in excess of estimated needs Involuntary weight loss related to impaired nutrient utilization as evidence by lab results of 304 mmol/kg/H2O osmolality level, 250 mg/dL glucose level, 20 mg/dL BUN level and 7.95% HbA1c. 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). Goals: Average daily caloric intake will be no more than 110% of estimated needs about 2700 kcal, a reduction of about 1300 kcal/day. Blood glucose levels will be controlled as HbA1c below 7%, osmolality levels between 285-295 mg/dL, glucose levels between 70-110 mg/dL, and BUN levels between 8-18 mg/dL. Interventions: Though the client is losing weight, she still needs to follow the EER to avoid excessive energy intake which might affect her blood glucose level. Instruct client on 2700 kcal diet and educate client with basic T1DM knowledge and better food choices knowledge Educate client how to achieve glycemic control and monitor glucose levels; how to self-manage insulin administration; how to count carbohydrates and follow a CHO-consistent meal plan. 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. No, I do not believe this diet order meets her nutritional needs. She should be getting 15-20% of her kcal from protein which if she was following a 2695 kcal diet recommended here she should be getting anywhere from 101-135 g of protein a day. Her carbohydrate recommendations will be calculated specifically to her based on her eating habit, blood glucose goals, and lipid goals but at least 130 g/day are recommended. Her total fat will be the same as someone without diabetes which would mean that 30% of her kcal should come from fat. This would mean she should get 91 g/day from fat (491-492). iv. 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 dietitian and DCE. 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 she drank one beer when she arrived at the party. She remembers getting lightheaded and then woke up in the ER. What happened to Susan physiologically? Susan went into a severe fasting hypoglycemic state. She took her insulin which caused her blood glucose levels to drop because she did not consume any carbohydrates to keep her blood glucose levels in check. When blood glucose levels fall too low, glucagon releases stored hepatic glucose to raise blood glucose levels. Epinephrine is also releases, causing the symptoms of weakness, fatigue, sweating, and tachycardia. (507) 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. I would like to tell her the risks of alcohol in general and that it is illegal at her age. I will also explain to her that alcohol can produce hypoglycemia in a fasting state because the gluconeogenesis is blocked that it cannot be converted to glucose. I may tell her that it also interferes with counter regulatory responses and should be consumed with food. Insulin is not required when drinking alcohol unless it is mixed with other carbohydrates such as a mixed shot. I might also tell her that if her glucose is in good control, alcohol in moderation is ok. But since she is underage, I would strongly advise her not to drink at all. At last, I would go over her meal plan to make sure she understands what she needs to be eating and what she’d better not to eat. Reference: Nelms, M., Sucher, K, P., Lacey, K., Roth, S. L. (2011). Nutrition Therapy & Pathophysiology. (2 ed.). Belmont, CA: Wadsworth, Cengage Learning. Genetics of Diabetes. (2012, May 13). Retrieved from http://www.diabetes.org/diabetesbasics/geneticcs-of-diabetes.html Center for Disease Control. (2011, Sept. 22). Retrieved from http://www.cdc.gov/growthcharts/data/set1clinical/Cj41cs022c.pdf ADA. (2012, Mar. 24). Retrieved from http://www.diabetes.org/living-withdiabetes/treatment-and-care/ask-the-expert/ask-thedietitian/archives/index.jsp?page=6#is-the-sweetener-truvia-safe.html