Ruchi Patel, Vaishali Keshani, Casey Flowers, Punam Patel Nutrition 420-Clinical Nutrition I, section 001 21 October 2011

Case 23: Type 2 Diabetes Mellitus 1. What is the difference between type 1 diabetes mellitus and type 2 diabetes mellitus? Type 1 diabetes mellitus is an autoimmune disorder where the body stops producing insulin because the pancreass beta cells are destroyed, and patients require insulin. Type 2 diabetes mellitus is a metabolic disorder where the body becomes resistant to insulin. Insulin may be available within the body, but it is not properly utilized. Risk factors for type 1 diabetes mellitus are genetics, and environmental contributions are unclear (may be triggered by viral infection or dietary factors) and is typically diagnosed in childhood. Risk factors for type 2 diabetes mellitus include ethnicity, obesity, family history, gestational diabetes, and physical inactivity, to name a few. Onset is typically during middle age or later life. 2. How would you clinically distinguish between type 1 and type 2 diabetes mellitus? One could distinguish between type 1 diabetes mellitus and type 2 diabetes mellitus by looking at the age of diagnosis, the levels of insulin in the blood, and the level on beta cell destruction at onset. C-peptide levels can be looked at as well. Typically, onset type 1 diabetes mellitus is during childhood, and onset of type 2 diabetes mellitus is during middle age or later life. 3. What are the risk factors for development of type 2 diabetes mellitus? What risk factors does Mrs. Douglas present with? Risk factors for developing type 2 diabetes mellitus are overweight/obesity, inactivity, fat distribution, race, ethnicity, HDL cholesterol under 35mg/dL, high blood glucose levels, high levels of triglycerides, family history, age above 45 years, blood pressure above 140/90 mmHg, and having gestational diabetes, prediabetes, and/or metabolic syndrome. From what can be seen from the case study, Mrs. Douglas is at risk of type 2 diabetes mellitus due to her weight, inactivity, ethnicity, age, high glucose levels, high triglyceride levels, high blood pressure and family history. 4. What are the common complications associated with diabetes mellitus? Describe the pathophysiology associated with these complications, specifically addressing the role of chronic hyperglycemia. Tissue insulin resistance in type 2 diabetes mellitus is recognized as a major pathophysiologic determinant of this disease, and with this, the inability of the pancreas to compensate for peripheral insulin resistance that leads to hyperglycemia and the onset of diabetes. Hyperglycemia occurs when glucose cannot enter cells and plasma glucose rises. Other complications of chronic hyperglycemia include frequent hunger, frequent thirst, frequent

urination, blurred vision, weight loss, poor wound healing, dry mouth, dry skin, recurrent infections, cardiac arrhythmia, stupor, and coma. If left untreated, it can lead to ketoacidosis (confusion, dehydration, acute hunger/thirst, fruity breath, impairment in cognitive function, anxiety). Ketoacidosis, which is more commonly seen in type 1 diabetes mellitus, is a buildup of ketones when the body uses fat for energy when it cannot use glucose and cannot get rid of all the fat broken down (ketones). This can lead to death. Hyperglycemic hyperosmololar nonketotic syndrome (HHNS), which is more commonly seen in type 1 diabetes mellitus, is also caused by prolonged hyperglycemia, excessive fluid loss, and dehydration, and is very common among the older population. Unlike ketoacidosis, HHNS is not associated with ketones. Overcorrection of hyperglycemia can lead to mild to severe hypoglycemia. Individuals with hypoglycemia will typically experience trembling, nervousness, anxiety, and nausea. Prolonged hyperglycemia leads to nephropathy and the uncontrolled blood glucose puts an immense strain on the kidneys and can contribute to hypertension. Retinopathy is where small blood vessels of the eye are vulnerable to the effect of poor glucose control and become weakened due to chronic hyperglycemia, causing potential blindness. Hyperglycemia causes a non-enzymatic covalent bond with proteins that alters their function, leading to peripheral neuropathy (pain or tingling in feet or legs). Autonomic neuropathy is also due to nerve damage caused by hyperglycemia, and affects gastric emptying, sexual dysfunction, and postural hypotension. 5. Does Mrs. Douglas present with any complications of diabetes mellitus? If yes, which ones? Yes, Mrs. Douglas does present with complications of diabetes mellitus. She presents with a wound that will not heal, frequent bladder infections, tingling and numbness in her feet, and blurred vision. 6. Identify at least four features of the physicians physical examination as well as her presenting signs and symptoms that are consistent with her admitting diagnosis. Describe the pathophysiology that might be responsible for each physical finding. Physical Findings Physiological Change/Etiology Overweight High cholesterol, BMI Mild Retinopathy Hyperglycemia, small vessel damage Poor wound healing Hyperglycemia Diminished sensation in feet Hyperglycemia, nerve damage 7. Prior to admission, Mrs. Douglas had not been diagnosed with diabetes mellitus. How could she present with complications? A patient can have diabetes and develop complications without having a diagnosis, as well as being asymptomatic for a long period of time. It is possible Mrs. Douglas has not been to a doctor since she developed the diabetes, and therefore has had complications develop in this time.

8. Briefly describe hyperglycemic hyperosmolar nonketotic syndrome (HHNS). How is this syndrome different from ketoacidosis? Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) occurs most often in patients with type 2 diabetes mellitus, who have blood glucose greater than 600 mg/dL, serum osmolality greater than 320 mOsm/kg of water, and the absence of severe ketoacidosis. It typically occurs after dehydration and infection. Ketoacidosis is primarily related to insulin deficiency and leads to the accumulation of ketones in the body. Ketoacidosis is typically seen in type 1 diabetes mellitus patients. 9. What are the symptoms of HHNS? The symptoms of HHNS are polyuria (increased urination), polydipsia (increased thirst), polyphagia (increased hunger), general weakness, drowsiness, and weight loss. Symptoms gradually worsen over several days or dehydration increases. 10. What factors may lead to HHNS? Is Mrs. Douglas at risk? Not monitoring blood glucose levels frequently or taking insulin at the appropriate times could lead to HHNS. Also, infection, illness, and dehydration are factors that lead to HHNS as well. Mrs. Douglas had improper wound healing and this could lead to infection and in turn illness. According to her 24-hour recall, she seems to not be receiving enough fluids, which contributes to dehydration. 11. What is the immediate aim for treatment for HHNS? If HHNS is not treated, how would you expect the condition of HHNS to progress? Slow rehydration must be utilized in treatment, and insulin may or may not be required to correct hyperglycemia. It is important to monitor fluid intake, and address factors that are associated with dehydration, including electrolyte imbalance. Blood glucose should be monitored regularly as well. If left untreated, HHNS can lead to comas, seizures, and even death. 12. Calculate Mrs. Douglass body mass index (BMI). Mrs. Douglass Body Mass Index (BMI) is 30.34 kg/m2. 13. What are the health implications for a BMI in this range? A BMI of 30.34 puts Mrs. Douglas in class I obesity. Health implications for a BMI in this range are reduction of life expectancy and increases in risks of type 2 diabetes mellitus, stroke, diseases of the gallbladder, heart, and liver, breathing issues, arthritis, deep vein thrombosis, as well as many more complications. 14. Calculate Mrs. Douglass energy needs using the Mifflin-St. Jeor equeation. Should Mrs. Douglass weight be adjusted for obesity?

According to the Mifflin-St. Jeor equation, Mrs. Douglass energy needs are 1,367 calories/day for her sedentary lifestyle. Her weight should not be adjusted for obesity because the equation has been determined to be the most accurate with overweight/obese individuals. 15. Calculate Mrs. Douglass protein needs. (0.8g)(155/2.2=70kg) = 56.36g Mrs. Douglass protein needs are 56.36 grams/day. 16. Is the diet order of 1,200 kcal appropriate? Yes, a diet order of 1,200 kcal is appropriate. 17. If yes, explain why it is appropriate. If no, what would you recommend? Justify your answer. The 1,200 kcal diet order is appropriate because based on her nutrition assessment she needs to lose weight to decrease her BMI and this will allow her to lose weight. 18. Does Mrs. Douglass usual dietary intake meet the USDA Food Guide/MyPyramid guidelines? Is she deficient in any food group? If so, which ones? No, Mrs. Douglass usual dietary intake does not meet USDA Food Guide/My Pyramid guidelines. She is deficient in many food groups, especially in the dairy, vegetables, and fruits groups. In addition, she is deficient in whole grains. 19. Using a computer dietary analysis program or food composition table, calculate the kcalories, protein, fat, CHO, fiber, cholesterol, and Na content of Mrs. Douglass diet. Kcalories 1490 kcal Protein 54.770 grams Fat 72.191 grams Carbohydrates 159.704 grams Fiber 24.893 grams Cholesterol 307 milligrams Sodium 3822 milligrams 20. How would you compare Mrs. Douglass usual dietary intake to her current nutritional needs? Her current dietary intake does not meet all of her nutritional needs. She is greatly lacking in a multitude of food groups, so many essential vitamins and minerals are lacking in her diet. The current foods she eats are too also too high in fats, and sodium. 21. Compare the patients laboratory values that were out of range on admission with normal values. How would you interpret the patients labs? Make sure explanations are pertinent to this situation.

Parameter Glucose (mg/dL)

Normal Value 70-110

Patients Value 325

Reason for Abnormality Hyperglycemia

HbA1c(%)

3.9-5.2

8.5

Cholesterol (mg/dL)

120-199

300

LDL-Cholesterol (mg/dL)

<130

140

Poor neural function, and slow building of cells High intake of Increased risk of Triglycerides 35-135 400 fatty foods CVD As evidenced in Mrs. Douglass labs, it can be said that she has type 2 diabetes mellitus. She has high glucose, high HbA1C, high cholesterol, low HDL, and high triglycerides. This could possibly indicate a high fat diet and type 2 diabetes mellitus. HDL-Cholesterol >55 35 22. Identify two lab values that should be monitored regularly. Lab values to be monitored regularly are cholesterol and glucose. However, HbA1C should be monitored regularly over the long term. 23. Why wasnt HbA1C measured at discharge? HbA1c was not measured at discharge because it cannot be significantly affected by manipulating a diet for one week. It is only a valuable tool for measuring glycemic control for a longer period of time. 24. Why is regular insulin used to correct hyperglycemia in patients with HHNS? Regular insulin is used to correct hyperglycemia in patients with HHNS because they are not responding to or not producing enough insulin to maintain their blood glucose levels in a healthy range. The body is trying to correct the increase of glucose in the blood by passing it through the urine; the increase in fluid output accelerates dehydration. Regular insulin would control the uptake of glucose into the tissues, preventing the blood glucose from rising too high. Regular insulin will produce a slower decrease in the high level of glucose in the blood. When glucose is extremely elevated, as in HHNS, it is dangerous to drop glucose levels too rapidly, as this can

High concentration of glucose in the blood, so more hemoglobin is glycated High intake of fatty foods, weight status, poorly-controlled DM High intake of saturated fats, cholesterol, and trans fats Not significant amounts of longchain fatty acids

Nutritional Implications Blurred vision, delayed wound healing, polyuria Blurred vision, delayed wound healing, polyuria

Increased risk for CVD

Increased risk for CVD

lead to severe hypoglycemia and even comas. This is why it is helpful to use regular insulin to bring glucose levels down in a controlled manner.

25. When HHNS is treated, the initial target serum glucose level is typically set at the 250 mg/dL range instead of a normal blood glucose level. Why? When HHNS is treated, the target serum glucose level is set at 250 mg/dL instead of normal blood glucose range because you do not want the patient to go from hyperglycemia to hypoglycemia. It would also be dangerous to drop glucose levels too rapidly because this could lead to the body going into shock. It is also crucial to monitor electrolyte levels as blood glucose levels are decreasing. 26. Compare the pharmacological differences among the oral hypoglycemic agents.

Glucosid ase inhibitors

Precose Glyset Volix Acarbose Miglitol Voglibose

Delays intesti nal absorp tion of glucos e

Good Non for e T2DM, less efficacy with frequen t dosing Effectiv e for type 1 and 2 diabete s

Biguanid es

Decrea ses Metformin hepati c glucos e produc tion, while increas ing insulin uptake in muscle s Meglitini Prandin Stimul des Starlix ates insulin Repaglinide secreti Nateglinide on in presen ce of glucos e Sulfonylu Dymelor Stimul reas (first Diabinese ates generatio Tolinase insulin n) Orinase secreti Glucotrol on by Glucotrol XL bind to ATPAcetohexami ase K de depen Chlorpropam dent of ide pancre

Glucophage

Effectiv e but short acting

Effectiv e for T2DM but complet ely ineffect ive for T1DM

Non Flatulence e and diarrhea. Contraindicat ions: Individuals with intestinal disease must take with meals Lactic acidosis, transient diarrhea, nausea, bloating, anorexia, and flatulence. Contrandicati ons: Patients with renal insufficiency, liver failure, or treated for congestive heart failure Non Hypoglycemi e a and weight gain. Contraindicat ions: May have hyper sensitivity to the drug if T1DM Non Side effects: e increased risk of hypoglycemi a and weight gain. Contraindicat ions: May have hypersensitiv ity to the

50-100 3 mg (with meals)

500850 mg

1203 180mg (with meals)

500Most 3000m patient g s just need one dose daily

Adult Daily Maintenanc e Dose (mg) Number of Daily Doses 2

Effect on Plasma Insulinon Effect Levels Body Weight Effect on Plasma LipidEffects Side and Contraindic ations

Mechanism of Action

Brand Name (s) (& Generic Name)

Efficacy

Class

Tolazamide Tolbutamide

2nd generatio n

Thiazolid inediones

atic beta cells , depola rizatio n opens Calciu m channe ls Glucotrol Stimul Glucotrol XL ates DiabBeta insulin Micronase secreti PresTab on by Glynase bindin Amaryl g to ATPGlipizide ase K Glipizidedepen GITS dent of Glyburide pancre Glimepiride atic beta cells , depola rizatio n opens Calciu m channe ls Actos Activa Avandia te PPAR Pioglitazone s to Rosiglitazon decrea se e it has a black insulin resista box warning nce. for CVD and Death. not used as

drug if T1DM. Dont take if pregnant or wanting to get pregnant. Also if have renal insufficiencie s. Effectiv e for T2DM but complet ely ineffect ive for T1DM Non Same as with 75-250 1-2 e first generation, except increased risk of CVD compared to first generation, and safer for individuals with insufficiencie s.

Very effectiv e for treating highly insulin resistan t individ uals

Weight gain, 15-45 edema, and mg increases risk for Coronary heart failure. Contraindicat ions for liver disease, could lead to liver failure

Daily

the first line therapy

27. Avandia is often used to help control blood glucose levels. Describe the (medication) actions of Avandia. Avandia works by increasing insulin sensitivity in the body. It binds to peroxisome proliferatoractivated receptors, located inside the cell nucleus, and activates specific genes that help decrease insulin resistance. 28. The goal of healthy elderly patients with diabetes should be near-normal, fasting plasma glucose levels without hypoglycemia. Although acceptable glucose control must be carefully individualized, the elderly tend to be predisposed to hypoglycemia. List five factors that predispose elderly patients to hypoglycemia. Factors that predispose elderly patients to hypoglycemia are that they tend to eat less, their bodies have an altered metabolism of carbohydrates, they have more sedentary lifestyles, they may have other drug interactions to be concerned with, and they are more sensitive to insulin due to. Declining liver and kidney function (metabolism/excretion). 29. Identity at least three factors that may interfere with Mrs. Douglass compliance and success with her diabetes treatment. Factors that may interfere with Mrs. Douglass compliance and success with her diabetes treatment are her age, education level, and income. 30. Select two high-priority nutrition problems and complete the PES statement for each. Two high-priority nutrition problems are having a high fat intake and an improper knowledge of what sugars are considered to be. PES 1: Excessive fat intake related to frequent consumption of high fat meals as evidenced by average daily intake of 48.2 grams of fat, HDL of 35 mg/dL, and LDL of 140 mg/dL. PES 2: Food and nutrition related knowledge deficit related to excessive carbohydrate intake as evidenced by average daily intake of 159.7 grams of carbohydrate and blood glucose of 325 mg/dL. LDL= recommended at 100 (for healthy person it could be higher) HDL= 45 women and 40 men

31. What was the most important nutritional concern when the patient was originally admitted to the hospital (time of Dx)?

The most important nutritional concern was Mrs. Douglass blood glucose level and trying to maintain it within a normal range while also taking into account a non-healing wound. 32. What additional information does the dietitian need to collect before he or she can mutually develop clinical and behavioral outcomes with the patient and health care team? Additional information that needs to be collected would deal with getting information about her lifestyle and motivation for change. A food diary for a week would be helpful, as well as physical activity log. It would be useful to know how often Mrs. Douglas checks her blood glucose, good to figure out whether to put her on medication or insulin, and to determine allergies and food aversions as well.

33. 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). PES 1: Goal is to get within recommended ranges of fat, HDL > 55 mg/dL, and LDL <130 mg/dL. To do this, she must eat less high fat foods and eat more nutrient dense foods. PES 2: Goal is to maintain her blood glucose to the normal range of 70-110 mg/dL by checking glucose frequently and decreasing carbohydrate intake. This can be done by eating less simple carbohydrates and more complex carbohydrates and nutrient dense foods. Overall, bringing her BMI into normal range between 18.5-24.9 will help nutritional problems as well. 34. Mrs. Douglas was d/c with instructions for a non-kilocaloric-restricted, low-fat (less than or equal to 30% total kcal), high-CHO (greater than or equal to 50% total kcal) diet, in combination with a walking program, and a prescription for captopril to control her HTN. Glucose levels were well controlled for 6 months, but she became unable to afford the necessary supplies to check her BG or urine acetone levels. After 6 months, she was readmitted with a BG of 905 mg/dL, a slight temperature, BP of 68/100 mm Hg, tachycardia, and shallow, tachypneic breathing (Kussmal respirations). She was Dx with pneumonia, dehydration, and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). What is the MNT for patients with HHNS? The medical nutrition therapy for patients with HHNS is correcting high glucose levels via insulin therapy, replacing electrolytes and resolving dehydration through fluid therapy, and monitoring lab results frequently.