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NTRI 5020 Anemia Cases Mary Frances Hasty Lauren Antle Brittany Baerlocher Case Study: DKA Presentation in T1DM HPI: Kelly is an 18-year-old-female, who is brought to the ED in a small town (over 1 hour from her home) by her father. Her father reports that she does not feel well, has complained of some abdominal pain, and that she has appeared to be hyperventilating for the past several hours, which prompted the trip to the ED. ROS: General- 3# weight loss over the past month HEENT – negative Lungs – hyperventilation as noted above CV – feels heart is racing most of the day; denies chest pain Abd – mild abdominal pain as noted above, vomited once on trip in to ED, very thirsty GU – increased urination past several weeks, decreased past 24 hours Neuro – dizzy Skin – dry Medications – none Allergies – NKA PMH - Her past medical history is unremarkable except usual childhood illnesses and recent URI, which is resolved. UTD on immunizations. FH – unremarkable SH – deferred Physical Exam: WDWNF Ht 5’3”, Wt. 103#, R 35, P 101, T 97.4, BP 86/52 Eyes-EOM, PERRLA Neck – non-tender, no adenopathy Lungs – CTA, Kussmual respirations CV – tachycardia, as above; no murmur, gallop, or rub, no edema Abd – non-tender, nl BS X4, no HSM or masses Neuro – negative Skin – warm, dry, flushed; no rashes Lab Results: Glucose 650mg/dL BUN 45mg/dL Creatinine 1.1mg/dL TG 200mg/dL Sodium 143 Potassium 6.2 mmol/L Chloride 103 Phos 3.4 mg/dL Bicarbonate 12mEq/L Betahydroxybuterate 6.7 mg/dL ABGs: CO2 23; pH 7.0 Plasma OSM 304 mOsm/kg Urine Ketones: positive QUESTIONS: 1. Define the acid-base abnormality. Is it compensated? What data did you use to make this assessment? Acid-base abnormality is metabolic acidosis. This conclusion is supported by the low laboratory values of bicarbonate and CO2. Respiratory acidosis was ruled out because the CO2 levels would have been high, since they are directly related to [H+]. Additionally, it was apparent that the abnormality was acidosis and not alkalosis because of the below physiological blood pH level. The patient is partially compensating for the metabolic acidosis. Bicarbonate plays a role in compensating for the metabolic acidosis by functioning as an extracellular buffer for the increased acid load (ketones). The patient is hyperventilating to partially compensate for the abnormality. Hyperventilation results in a decrease in the PCO2 in the blood. This is in an effort to reestablish the PCO2:bicarbonate ratio. In addition to the data mentioned above, the presence of ketones in the urine also supports the diagnosis of DKA. The initial treatment for this patient is 2 liters of IV normal saline (0.9%) and insulin (usually a drip). She will be monitored closely over the first several hours. 2. Identify the normal range for each of the following labs. At the 2-hour point with fluid and insulin administration her labs were rechecked. Give the expected direction of change, and a brief explanation of why the lab would change in that direction. Give some detail. What is happening physiologically/pathologically and metabolically? You will likely need to expand the explanation box. Laboratory Normal Change Explanation Decrease Glucose 650mg/dL 70-100 mg/dL Insulin will initiate removal of glucose from the bloodstream; turn off hepatic glucose production 10-20 mg/dL Decrease The pt is currently dehydrated; kidney cannot get rid of waste products so with hydration the pt will be able to eliminate BUN 0.6-1.2 mg/dL Decrease The pt is receiving fluids and this will increase the excretion of creatinine Decrease Serum K levels are high d/t the transcellular shift of K out of the cell. However, there is a total body potassium loss d/t osmotic diuresis, so potassium levels will decrease, possibly to the level of hypokalemia. Decrease t Serum Phosphate levels are within normal limits because of the transcellular shift that occurred with the acidosis. BUN 45mg/dL Creatinine 1.1mg/dL Potassium 6.2 3.5 to 5.5 mmol/L mEq/L Phos 3.4 mg/dL 3-4.5 mg/dL increase Bicarbonate 12mEq/L 22-28 mEq/L Bicarbonate levels are low because the body is in acidosis. Most of the free bicarbonate would have been utilized for extracellular buffering to try and compensate for the low pH. increase CO2 23 33-45 mm Hg Low CO2 levels. This provides evidence that it is a metabolic acidosis by the fact this is still low. If it were higher, we would see she had a pulmonary acidosis and the CO2 would be compensating more. 7.35-7.45 increase Patient is in acidosis presently and treatment will resolve it. Decrease The osmolarity will decrease because the pt is getting hydrated and their electrolytes are being balanced. Decrease Beta-hydroxybuterate levels are high because it is a product of ketosis. Once ketosis is resolved pH 7.0 Osm 304 mOSM/kg 275-295 mosm/kg 0.4 mmol/L Beta-hydroxybuterate (6.7 mg/dL) (via treatment) beta-hydroxybuterate will also drop. Additionally, insulin will turn off lipolysis. Negative Ketones in urine (positive) Become negative The pt will no longer being in ketosis because of the treatment and therefore will no longer be excreting ketones. Kelly has a new diagnosis of T1DM. Current weight following rehydration and resolution of DKA = 110#s. Kelly has been transferred to the general medicine unit and stabilized over the past three days. She has been started on the following insulin regimen and an initial diet of 45 grams of CHO at each of three meals. There are plans for discharge tomorrow following initial diabetic teaching. STANDARD FORMULA OF HOW ONE ARRIVES AT INITIAL INSULIN DOSE (reference): Weight 50kg Initial starting dose = 25-30 units per day 0.5 units X 50 kg = 25units/day 0.6 units X 50 kg = 30 units/day 50% basal, 50% prandial Pre-breakfast Pre-lunch Pre-dinner 12 units Long-acting 4 units Rapid Acting Insulin 4 units Rapid Acting Insulin (Detemir or Glargine) + SQ SQ 6 units Rapid Acting Insulin SQ (Aspart) (dose could be 5 units) 3. Explain the rationale behind an insulin regimen that is 50% basal and 50% prandial. By giving a regimen that is 50% basal and 50% prandial, there is variation in the diet. Basal will allow for steady state blood glucose, whereas prandial will account for the glycemic response from a meal. Basal insulin will prevent blood glucose from rising too high throughout the day/night. Prandial insulin allows Kelly to adjust her insulin dosage to the amount of carbohydrates she is going to eat with her meal. 4. What is meant by sliding-scale insulin? Sliding-scale insulin is used in response to blood glucose levels. The dose is dependent on the patient’s blood sugar before a meal and predefined blood glucose ranges individualized for the patient. SSI is used in hospitals and healthcare facilities because it is easy to monitor. 5. Calculate the estimated insulin to CHO ratio of the initial prescribed regimen? 2 units of insulin 9 g CHO Total insulin for the day basal & bolus and total carbohydrate for the day. 6. Calculate the initial estimated insulin sensitivity factor for the proscribed regimen?(Define) Insulin Sensitivity Factor is the drop in blood glucose seen per unit of insulin. Insulin Sensitivity Factor is used to calculate the correction factor for preprandial blood glucose levels. You have been consulted to initiate diabetic teaching regarding Kelly’s diet. Please address the key points that you would cover under each of the following topics. CHO distribution based on prescribed insulin regimen? Carbohydrates should be distributed evenly throughout the day. Frequency of blood glucose monitoring. Blood glucose should be monitored before meals and snacks, before and after exercise, before bed and occasionally throughout the night. Intensive insulin therapy has many benefits, such as decreasing the pt’s A1C values which in turn decreases risk for After two weeks at home for Kelly you and microvascular disease. However, since the pt is so active in sports she must be aware the physician address the benefits of of the risk of hypoglycemia. With the pt on intensive insulin therapy for Kelly. What recommendations would you make to intensive therapy the pt should consume 15 Kelly regarding diet and intensive therapy? g CHO with every 30-60 minutes of exercise. With intense exercise pt may Be thorough and specific. need to decrease insulin and add a 6% glucose beverage for exercise lasting more than 60 mins. Kelly is a typical busy teenager on the run. She is active in sports. Recognition, prevention, and treatment of Symptoms of hypoglycemia: diapheresis, hypoglycemia. tachycardia, tremors, hunger, nausea, pallor, irritability, headache dizziness, paralysis, blurred vision, lethargy, confusion, seizures, poor judgement, brain damage, coma, and death Prevention: monitor blood glucose Treatment: Glucose (15-20g) from a source such as glucose tablets, juice; (avoid high fat and high protein foods) or glucagon Kelly is on the soccer team. What advice would you give Kelly to help manage her blood sugar during practice and games. (Hint: There are 3 key areas you need to address) Benefits of physical activity for T1 patients are enhancement of physical fitness and reduction in CVD risk. Negative effects: There is increased risk of exercise induced hypoglycemia and aggravation of hyperglycemia and ketosis. Team sports such as soccer, however only require short bursts of high power output and rely on ATP-PC for energy in muscle contractions. Kelly should not play until she is sure her insulin levels are adequate. She should also not play if glucose levels are >250 mg/dl or if ketones are present. There is also a risk of hypoglycemia. So she should ensure she is only using insulin she needs. During exercise, T1 are unable to reduce circulating insulin, This leads to hypoglycemia bc of increased glucose uptake by skeletal muscles and inadequate hepatic glucose release are imbalanced. Kelly should consume 15 g CHO for every 30-60 mins of exercise and add a 6% glucose beverage for exercise over 60 minutes What to do if she gets the bad case of gastroenteritis that is going around? Continue insulin even if not eating. Check blood glucose every 4 hours. Check ketone levels if blood glucose > 240. Also check for ketone levels if vomiting or symptoms of hyperglycemia or ketoacidosis. Call healthcare if ketones are high. Get 10-15 g of carbohydrates from liquid if you cannot eat. Case Study: Gestational Diabetes Mellitus Introduction DR is a 17-year-old Caucasian, female who presents at 24 weeks gestation for her first prenatal visit. She complains of heartburn and constipation. She admits to one previous pregnancy at age 15 that was terminated by abortion. History DR has no significant/serious PMH. She has a positive family history for obesity, T2DM, and HTN. DR smokes about ½ pack of cigarettes per day. Social History DR admits to occasional alcohol consumption, but states that it is not enough to hurt the baby. She takes no medications or vitamin supplements. DR is out of school for the summer and plans not to return to school in the fall. The baby is due in late October. She lives with her mother and older brother age 22. Clinical Chemistry Hgb 12.5 g/dL Glucose 155mg/dL BUN 18 mg/dL Creat 0.9 mg/dL Chol 201 mg/dL TG 125 mg/dL BP 120/82 mm/hg Assessment of Weight Gain DR is 5’5” tall and her current weight is 198#s. She estimates her pre-pregnancy weight at 182#s. 1. What is DR’s pre-pregnancy BMI? Plot her weight gain on the chart below. BMI: 30.3 2. What are your recommendations for weight gain for DR at this time? Looking at the recommendations for weight gain, we see that it is ideal for most of the weight gain to occur in the third trimester. Considering that DR is already overweight, she does not need to gain as much during pregnancy. This being said, it looks as though she already gained as much as she needs for an optimal pregnancy for her BMI. We recommend that she gain another 5-10 lbs throughout her pregnancy, while following a well balanced diet for a pregnant woman. Diabetes in Pregnancy Incidence-impacts 7% of all pregnancies; tripled since 1994. 3. What is the etiology of gestational diabetes (GDM)? Human chorionic gonadotropin and human placental lactogen are associated with strong anti- insulin as well as lypolytic characteristics. Hepatic glucose is also 30% higher even in situations with higher insulin. Pregnant women who cannot keep up with the increased need of insulin result in GDM. Do not confuse GDM with pre-gestational-diabetes · T1DM is high risk pregnancy- generally not managed in primary care · T2DM also high risk; seeing more due to obesity, may diagnosis at prenatal visit 4. Identify three of DR’s specific risk factors for GDM? Overweight prior to pregnancy. Quick weight gain during pregnancy. Family history of type 2 diabetes. Assessment of DR for GDM DR’s Random (casual) Blood Glucose = 155mg/dL 5. Is this diagnostic for GDM? How would this change if it was a FPG? What test would be performed to further evaluate her hyperglycemia? Yes. A normal casual should result in a blood glucose level of < 140mg/dL. DR falls in the range of a pre-diabetic person with her casual blood glucose level. Further tests, preferably fasting blood glucose or oral glucose tolerance test, should be performed. If this were her FPG, then DR would meet the criteria for diabetes, which is an FPG > 126 mg/dL. 6. Fill in the following table identifying 3 potential complications of GDM for the mother and three for the infant. Mother Infant Greater chances of pre-eclampsia Hypoglycemia Greater chance of GDM with other pregnancies Risk of pre-term birth Greater chance of diabetes later in life Excessive birth weight DR has been diagnosed with GDM. She has been referred to you for nutrition counseling. At this time, the plan is to give a two-week trial to control DRs diabetes with diet alone. DR has been sent home with a glucometer to check her glucose. Dietary Assessment DR DR’s 24-hour recall: o Breakfast (home) – 2 fried eggs, 4-slices of bacon, 2 slices of toast w/ butter, 2 cups coffee w/ 2 TBSP sugar o Lunch (work-free) – double cheeseburger, large fries, 32 oz. Coke, apple pie (McDonalds) o Snack – cinnamon rolls with butter o Dinner (home) – fried chicken, macaroni and cheese, corn, Coke o Ice-cream and Oreos (Provides: 3000 kcals, 13% protein, 40% carbohydrates, 47% fat) 8. What food groups/nutrients are missing from DR’s diet? What foods/food groups are contributing to DRs high blood glucose? Excessive weight gain? Fruits, vegetables, dairy, and water are all missing from DR’s diet. DR is taking in a large amount of carbohydrates on a regular basis, which may be contributing to her high blood glucose. 9. Provide 5 specific recommended changes to address problem areas. Consider DRs social situation/limitations when making recommendations. Talk food. Adding skim milk Cut back on portion sizes (two slices of bacon instead of three) Switch sugar to sweetener Diet coke instead of coke Adding fruit and vegetables for fiber 9. DR was started on prenatal multivitamin by her OBGYN. What are the three nutrients of greatest concern for pregnant women that are difficult to meet with diet alone? Iron Folic Acid Calcium DR returns to clinic in 3 weeks for follow-up. She has made some of the dietary changes that you have suggested, but her SBGM records show pre-prandial blood glucose averaging above 140mg/dL and post-prandial exceeding 200mg/dL at least 5 times per week. Her OBGYN has started her on Metformin, 250mg BID. 10. Metformin and glyburide are used in pregnancy, but they are not without risk. Look up current information of how these are classified by risk. Note here. Glyburide is in the class C for drugs, which means that adverse effect on fetus in animal reproduction studies have been found, however, there have been no well-controlled studies in humans. Metformin is categorized into class B according to the US FDA pregnancy categories. Class B states that animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate, well-controlled studies in pregnant women. CASE STUDY: COMPLICATED T2DM JD is a 59-year-old man is referred to you because of uncontrolled diabetes. Fourteen years ago the patient was found to have a blood glucose level of 300 mg/dL on a routine examination. At that time he received patient education for a program of diabetic exchange diet, exercise, and glipizide. With this regimen his glucose level fell to the 110 to 140 mg/dL range and his A1C fell to 7.5%. JD presents to clinic today after referral from his new primary care provider who he saw two weeks ago after urging from his now adult daughter. The patient relates that for the last eight years he has not focused on his diabetes, "I avoided it all," following no regimen and taking no medication for diabetes. In fact, he mentioned that he had not seen a physician for over 5 years. He had separated from his wife, now divorced, and moved from Florida to Houston. He works as a busy account executive, having the 2-martini lunch with clients, works late in his office, and gets little exercise. Brief diet history reveals that the patient eats three meals per day, breakfast a large Moo Latte at Starbucks and slice of banana bread or 2 scones; lunch out off the menu or lunch buffet, supper frozen entrée or fast food. His A1C today is 13%. He has had significant deterioration of his vision, is scheduled to see an ophthalmologist for evaluation of diabetic retinopathy later today. Additional lab today shows a BUN of 34 mg/dL, a serum creatinine of 1.4 mg/dL, and 2 + proteinuria, BP 130/85, TG 235. He has aching pain in his legs, mostly at night, from his feet to the level of the mid-calf. Light touch sensation is diminished to the thighs. Deep tendon reflexes are absent at the ankles and the knees. He has had nausea, reflux, abdominal pain, and intermittent constipation in the last year. He notes that on some occasions he feels that the food is just sitting/souring in his stomach. Pt is 5’9” and weighs 210 lbs. He admits to 10 pound weight loss over the past three months, which he attributes to the above symptoms. 1. An A1C of 13% would suggest what range of blood glucose? An A1C of 13% would suggest a mean blood glucose range of over 300 mg/dL. 2. Discuss the general metabolic etiology of microvascular disease? Some detail here please. Chronically high blood glucose levels can cause irreversible damage to cells, especially those in the capillaries and end organs. Through a process called glycosylation, glucose becomes irreversibly bound to proteins in the red blood cells, blood vessel walls and interstitial tissues. Glycosylation produces AGEs or Advanced Glycosylation End products that cause the basement membrane of the epithelium to thicken, increases the permeability of blood vessels and nerves, stimulates the release of cytokines (inflammation), growth factors and cellular proliferation in glomeruli in the kidney and smooth muscle in the vascular system resulting in fibrosis, and increases platelet adhesion in the blood vessels increase the formations of clots. In addition to all of these changes caused by the AGEs the body is also experiencing hyperglycemia. The glucose, trying to leave the bloodstream, is shunted into insulin-independent tissue. Tissues such as the nerves, eyes, kidneys, and blood vessels become flooded with glucose. This intake of glucose stimulates the Polyol Pathway which results in the accumulation of fructose in the cell; leading to cellular damage. 3. Complete the table to describe the common signs/symptoms of each of the following conditions and laboratory/diagnostic evaluation/screening. Complication Signs/Symptoms Diagnosis/Screening Diabetic Neuropathy Decreased sensation and vascular supply; gangrene (ischemia of limbs, poor healing of wounds and infections) Physical Exams are utilized for early screening of neuropathy, this largely depends on the patient letting the physician know about areas of concern. Physical exam should pay special attention to patient’s feet (complete foot exam) and any trouble walking. Electromyogram (EMG) and nerve conduction study to confirm diagnosis. Diabetic Retinopathy Stage 1 (nonproliferative):increased capillary permeability, vein dilation, microaneurysms, superficial/deep hemorrhages Visual acuity testing (measures ability to see at various distances); tonometry (measures pressure inside eye)checking for glaucoma; Pupil dilation (allows doctor to examine retina and optic nerve)- Doctor looks for swelling, blood or fatty deposits in the retina; growth of new blood vessels and scar tissue; bleeding in the vitreous; retinal detachment; abnormalities in optic nerve; Optical coherence tomography (uses light Stage 2 (pre-prolifeative): increased retinal ischemia with infarcts (cotton-wool spots) Stage 3 (proliferative): neovascularization; fibrous tissue formation waves to capture images of tissues)-to check for fluid leaking in to retinal tissue. Fluorescein angiography is used to identify the blood vessels that are closed, broken down or leaking fluid. Diabetic Nephropathy Albuminuria, proteinuria Screen for albuminuria by taking timed urine collection over a 24 hour period or taking a random “spot-urine” test. 30-300 mg of albumin in a 24 hour sample suggest nephropathy 30:300 albumin to creatinine ratio in spot urine test Gastroparesis Decreased motility, N/V, Blood tests (Electrolyte GERD, unintentional weight check & Chemical check), loss Upper GI series screening, Barium Beefsteak Meal (being aware of the amount of time it takes to digest), Radioisotope screening, Gastric Manometry, Esophagogastroduodenosco py, Scintigraphic gastric accommodation. The majority of these tests are ways to see the amount of time it takes for patient to digest foods. 4. Assuming that JD has early signs of diabetic gastroparesis, what dietary modifications might help to alleviate his symptoms? Gastroparesis shows as a decrease in gastric emptying therefore, small meals with lots of liquids will help alleviate the symptoms and possible increase gastric motility. Additionally, JD should be on a low fiber diet to prevent the motility from being further decreased. Having not seen a dietitian in over 10 years, JD is excited to learn that the approach to dietary management has been simplified and he does not need to follow a strict calorie level. Despite being disappointed that he has had to start on insulin, he is highly motivated since the physician explained that many of the medical issues he has largely been ignoring are the result of poor glucose control and that better control may delay further complications. INSULIN: Novolog 70/30 AM and 70/30 before supper 5. What is the number one priority/goal for this patient’s management at this time? For JD’s blood glucose to be as close to normal as possible.These issues he is experiencing should certainly be addressed but first and foremost, insulin should be regulated properly and a better diet followed. 6. What are your recommendations at this time for CHO intake and distribution? JD should evenly distribute his CHO intake throughout the day, limiting himself to 60 g of CHO per meal. JD should attempt to lose weight because he is obese and strive for glycemic control. 7. Identify five important/essential nutrition strategies at this time to help JD achieve his goal. Try to target specific patient-centered problem areas from history. Target/Focus/Key Points Rationale for Recommendations Increase liquids in diet. In order to treat gastroparesis, liquids and foods that are easier to digest is easier. This will also help with renal function. Decrease fiber in diet This will be effective for alleviating the symptoms of gastroparesis. Fiber slows down gastric motility. When gastroparesis is resolved, increase fiber Reduce Alcohol intake Consuming alcohol and carbohydrates together raises blood glucose levels. Additionally, alcohol consumption elevates triglyceride levels. Increase Exercise to 150 minutes of moderate intensity a week Exercise increases glycemic control and insulin sensitivity. Contributes to weight management. Reduce risk of cardiovascular disease. Carbohydrate Counting The patient needs to monitor his carbohydrate consumption. This is extremely important in the selfmanagement of blood glucose levels. Controlling level of CHO intake will work to lower blood glucose levels and A1C levels. CHO counting and distribution across the day is important for balance with the insulin the patient is taking.