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Type 1 Diabetes at School: Behind the Treatment Plan

Type 1 Diabetes at School: Behind the Treatment Plan. Laura Parker RN, CDE. Workshop Objectives. Describe how basal/bolus insulin therapy compares to normal physiology Normal insulin production Action and duration of basal and bolus insulin Dosing strategy using carb counting

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Type 1 Diabetes at School: Behind the Treatment Plan

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  1. Type 1 Diabetes at School: Behind the Treatment Plan Laura Parker RN, CDE

  2. Workshop Objectives • Describe how basal/bolus insulin therapy compares to normal physiology • Normal insulin production • Action and duration of basal and bolus insulin • Dosing strategy using carb counting • Discuss caused of BG variation • Causes of high blood glucose • Causes of low blood glucose • Preventing highs and lows • Discuss sick day management • Ketone production • Insulin, fuel and fluid needs

  3. Normal Metabolism Primary fuel source from carbohydrates Rapid Increase in blood glucose Insulin secretion stimulated Moves glucose into cells Stored in liver as glycogen Stored as fat Energy

  4. Normal Metabolism cont… As blood glucose levels drop (in a fasting state – no eating) Glucagon (ANOTHER HORMONE MADE IN THE PANCREAS) Releases the store of glucose from the liver (glycogenolysis) When adequate glucose is available Insulin turns off Glucagon (and release of glucose)

  5. Other Hormones • Incretins – GIP, GLP1, Amylin • Cortisol • Thyroid hormone • Growth hormone • Epinephrine

  6. Normal Daily Plasma Insulin Profile 100 B L D 80 Insulin Levels 60 40 20 8am 12 noon 6 pm 12 mid 0600 6am Time of day B=breakfast; L=lunch; D=dinner Polonsky KS et al. N Engl J Med. 1988;318:1231-1239

  7. Incidence of Type 1 Diabetes • Incidence increasing by 3.4% per year • 50% of patients diagnosed before age 20 years • 50% of patients diagnosed after age 20 years • Often mistaken for type 2 diabetes—may make up 10% to 30% of individuals diagnosed with type 2 diabetes • Oral agents ineffective; insulin therapy required • Autoimmune process slower and possibly different • Can usually be confirmed by islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA), insulin antibodies (IAA), and/or insulinoma-2–associated antibodies (IA-2A) EURODIAB ACE Study Group. Lancet. 2000;355:873-876; Naik RG, Palmer JP. Curr Opin Endocrinol Diabetes. 1997;4:308-315

  8. No muscle/fat insulin effect No hepatic insulin effect Pathogenesis of Type 1 DiabetesOne Defect Absent insulin secretion Hyperglycemia Unrestrained glucose production Impaired glucoseclearance Less glucose entersperipheral tissues More glucose entersthe blood Glycosuria 13

  9. Natural History Of “Pre”–Type 1 Diabetes Putative trigger -Cell mass 100% Cellular autoimmunity Circulating autoantibodies (ICA, GAD65) Loss of first-phase insulin response (IVGTT) Clinical onset— only 10% of-cells remain Glucose intolerance (OGTT) Genetic predisposition Insulitis-Cell injury “Pre”-diabetes Diabetes Time Eisenbarth GS. N Engl J Med. 1986;314:1360-1368 14

  10. Insulin Humalog, Novolog, Apidra Regular NPH Lantus, Levemir Novolin 70/30, Novolog mix 70/30 , 75/25 Humalog mix • It works! • Onset, peak and duration of action - depends on type of insulin or combination used • Side effects • Hypoglycemia • Weight gain • Lipohypertophy

  11. Action Profiles of Insulins 2 3 4 5 6 7 8 9 12 13 14 15 16 17 18 19 20 21 22 23 24 0 1 10 11 Novolog, Apidra, Humalog 4–5 hours (mostly 3 hrs) Regular 6–8 hours NPH 12–18 hours Detemir 12-24 hours Glucose infusion rates in clamp studies Glargine >24 hours Hours Lepore M. Diabetes. 2000;49:2142-48; Porcellati F. Diabetes Care. 2007;30:2447-52; Plank J. Diabetes Care. 2005;28: 1107-12; Mudaliar SR. Diabetes Care 1999;22:1501-06; Becker RHA. Exp Clin Endocrinol Diab 2005;113:435-443

  12. 12noon 12mid 6pm 8am 0600 6am Split-Mixed RegimenHuman Insulins NPH Regular Regular NPH 100 B L D Insulin Levels 80 Normal pattern 60 40 20 Time of Day B=breakfast; L=lunch; D=dinner

  13. 1800 0800 0600 1200 2400 Basal-Bolus Insulin TreatmentNPH + Rapid-Acting Insulin Analogues Novolog, Humalog, Apidra with each meal U/mL NPH NPH at bedtime 100 L D 80 B 60 Normal pattern 40 20 Time of day B=breakfast; L=lunch; D=dinner

  14. The Basal-Bolus Insulin Concept • Basal insulin • Controls glucose production between meals and overnight • Nearly constant levels • Approximately 40 - 50% of daily needs • Bolus insulin (mealtime or prandial) • Limits hyperglycemia after meals • Immediate rise and sharp peak at 1 hour postmeal • Duration of action is 3 hours (mostly) • 10% to 20% of total daily insulin requirement at each meal • More work, but allows for more flexibility in timing of meals and carbohydrate amount.

  15. Adjusting Bolus and Correction Doses Carbohydrate-to-Insulin RatioCorrection factor Based on four questions before meals: • What is my pre-meal blood sugar? • How much carbohydrate am I going to eat? (or did I eat?) • Should I lower the dose because I plan to be very active or have recently been active? • Is there any remaining insulin from my last “Bolus”?

  16. 0600 1800 0800 0600 1200 2400 Basal-Bolus Insulin TreatmentWith Insulin Analogues Humalog, Novolog, Apidra 100 Glargine Insulin Levels B L D 80 60 Normal pattern 40 20 Time of day B=breakfast; L=lunch; D=dinner

  17. Insulin pens Faster and easier than syringes Improve patient attitude and adherence Have accurate dosing mechanisms Appropriate technique is critical! (air shot and 6 second hold time) Insulin Injection Devices

  18. Continuous Subcutaneous Insulin Infusion (CSII)Benefits and Disadvantages Benefits • Programmability • Adjustable basal pattern • Temp basal • Extended bolus • Pharmacokinetic advantage • Reproducible insulin absorption • No subcutaneous depot, so less exercise-related hypoglycemia • Greater flexibility of lifestyle • Fewer injections • Dose calculator assists with more accurate dosing • Disadvantages • Risk of ketosis and DKA from interruption – only short acting insulin • Complexity—additional patient education required • Patients need to be motivated

  19. WHY IS IT SO HARD TO ACHIEVE GOOD CONTROL?????

  20. What effects insulin needs? • Food • Activity levels • Stress • Illness • Growth • Hormones of puberty • Thyroid hormone • Cortisol levels • Body weight • Fitness levels

  21. Limitations of insulin replacement therapy • Lack of normal counter regulatory mechanisms • Once you give the dose – you cannot stop the action • Carb counting is an estimation at best • Individual variations

  22. Pharmacokinetic Barriers to Intensive Therapy • Differences between insulin formulations and regimens • Mixing insulins—crystallization slows absorption of short-acting insulin • Timing of insulin (pre or post meal) • Insulin absorption variability from site to site • Injection sites - overuse and hypertrophy

  23. Basal Insulin Needs Vary Throughout the Day age 3-10 age 11-20 age 21-60 age > 60 1 0.9 0.8 0.7 Units/Hour 0.6 0.5 0.4 0.3 9:00 AM 7:00 AM 5:00 PM 5:00 AM 3:00 PM 3:00 AM 9:00 PM 7:00 PM 1:00 PM 1:00 AM 11:00 AM 11:00 PM Hour Scheiner G, Boyer BA. Diabetes Research and Clinical Practice. 2005; 69:14-21. 23

  24. What do we have some degree of control over? • Evaluation of food intake • Evaluation of level of activity or exercise • React to high or low blood glucose levels. • Evaluating patterns and trends that may indicate changing insulin needs. (Growth, weight gain or loss, increased fitness, puberty)

  25. USING BLOOD GLUCOSE MONITORING AS A TOOL • Evaluate blood glucose patterns • Identify hyperglycemia and hypoglycemia • Evaluate effect of meal plan • Monitor the effect of exercise • Monitor the effect of illness and stress • Helps with dose adjustments and therapy decisions • Can help motivate patients to adhere to treatment plan

  26. What foods effect blood glucose levels? Carbohydrates - Primary source of fuel, has the most significant on blood glucose levels, causing rapid increase Proteins - 40% converts to glucose, but it takes 4-6 hours and does not rapidly increase blood glucose. Recent studies also suggest that protein does not slow the absorption of glucose. Increases satiety. Fats - do not increase blood glucose and may delay the absorption of carbohydrates. May prolong post meal hyperglycemia. Increases satiety.

  27. A Carb is a Carb ADA Stand Starches and sugars have similar effects on blood glucose levels - based on total carbohydrate amount vs. type of carbohydrate = =

  28. Carb is a Carb …. well sort of…. • Glycemic index – rate of glucose availability • High glycemic index foods raise BG quickly and can increase free fatty acids • Low glycemic index foods digest more slowly and create a slower rise in BG and insulin levels – less hunger, improved weight management, better lipid levels Hard to use because there is more than one glycemic index scale and in fact, the amount of carb in the food item has an effect on the overall blood glucose response. Carb load – Carrots vs. pasta

  29. To simplify: • Encourage use of healthier carbs more often • higher in fiber • more vitamins and minerals • lower in saturated fats Whole grains - fruits – vegetables - low fat dairy products - legumes

  30. Carbohydrate Consistency = eating a similar amount of carbohydrate at each meal, every day. Goal of a certain amount of carb for breakfast, lunch and dinner – and try to meet that goal as often as possible. Safe approach for NPH/fast acting combo Carbohydrate Counting = strategy to match the amount of insulin to cover the amount of carbohydrate eaten. Allows for more variation in meal size and timing of meals. Typically appropriate with basal/bolus insulin regimen.

  31. Benefits of Meal Balancing Carbohydrate, eaten alone, will digest quickly and cause a short, high blood glucose spike. Breakfast Lunch This can cause hunger before the next meal and compel snacking, or potentially a low blood glucose reaction

  32. Meal Balancing The addition of fat, protein (maybe) and/ or fiber to each meal will slow down the digestion of the carbohydrate and create a smoother blood glucose curve. Breakfast Lunch This can help improve satiety and reduce risk of low blood glucose reactions

  33. Benefits of Exercise: • Improved lipid profile - LDL, HDL • Help control blood pressure • Weight loss • Improved glycemic control • Decrease insulin resistance • Reduce stress, reduce depression, feel better

  34. Glycemic effects of Exercise Short term : Immediate lowering of Blood glucose (exercising muscle uses glucose for fuel without insulin!). May see a post exercise spike with excitement or stress of competition. Can see delayed nocturnal hypoglycemia. Long term: Blood glucose improved even on the days not exercising – increased fitness may lower insulin needs Important to communicate with family – what is the child’s specific response to increased activity?

  35. Strategies to Manage Effects of Exercise • Blood glucose testing as appropriate to evaluate what is the child’s pattern and how the intervention is working. • Identify a “safe” BG level to commence activity • If adjacent to meal, may decrease insulin at that meal (ie: subtract 10 – 15 gms of carb from carb count). • Provide “uncovered” carb snack (ie: 10 – 15 gm) • Caution with correction of post exercise high – may need to reduce correctiondose by 50%

  36. HYPERGLYCEMIA Causes • Underestimating carbohydrate intake • High fat meal • Missed or inadequate medication doses • Ineffective insulin (exposed to high temperature) • Poor technique with insulin administration • Overuse of injection site (decreased absorption) • Less than usual activity (road trips!) • Influence from medications: ie: steroids, albuterol, decongestants • Illness, pain or stress (glucocorticoids, catecholamines, glucagon) • Menstrual cycle

  37. HYPERGLYCEMIA (high blood glucose) • Signs and Symptoms: • fatigue • frequent urination • thirsty • hungry • blurred vision • numbness or tingling of fingers and toes • dizziness • Symptoms may be subtle or absent until blood sugar is fairly high!

  38. HYPERGLYCEMIA - short term issues • Dehydration • Increased risk of infection • Impaired wound healing (BG > 200) • increased host susceptibility • decreased antibody function • decreased polymorphonuclear function • Ketoacidosis

  39. Ketoacidosis • A high blood glucose without ketones is not an emergency (not desirable for long term health). • Any blood sugar with high ketones is an emergency (Moderate/large urine; > 1.5 blood ketones)

  40. Diabetic Ketoacidosis • Nausea, vomiting, abdominal pain • Kussmaul respirations • Rapid pulse • Ketonuria • Acetone (fruity) breath • Dehydration • Electrolyte depletion • Acidosis (pH < 7.30, Bicarb < 15 meq/L)

  41. What causes ketones? • Starvation vs. insulin deficiency • How do we get rid of them? • Adequate fuel • Adequate insulin • Push fluids

  42. Hypoglycemia Causes • Irregular timing of medications • “Stacking” of insulin doses • Incorrect dosing of medication • Overestimation carbohydrate intake • Skipping or delaying meals • More than usual activity level • Decreased insulin needs ie: due to weight loss, increased fitness levels, hypothyroidism, adrenal insufficiency • Gastroparesis (probably underdiagnosed)

  43. Hypoglycemia = Blood glucose < 70 Symptoms Neuroglycopenic: Blurred vision Dizziness Decreased co-ordination Sleepiness Decreased ability to think Combativeness Headache Irritability Adrenergic: Sweating Shaking Tachycardia Anxiety Perioral numbness Hunger May harm the developing brain

  44. Hypoglycemia - < 70/80 or with symptoms • Test blood glucose • 10 - 30 gm fast acting (depending on child and typical response) • Usually 15 gm carbohydrate • 1/2 cup juice • 1/2 cup regular soda • 1 cup milk • 3-4glucose tablets • Retest in 15 min • If still < 80, repeat treatment

  45. Hypoglycemia • If low at premeal test – don’t just feed lunch! (even if you cut the insulin dose). Treat the low and ensure the BG is above 80. Then feed lunch and cover all the carb in the meal. • If low occurs away from mealtime, may need a snack to prevent recurrent low if “active” insulin on board from previous rapid acting insulin or if exercise is planned. • Glucose gel or glucagon for moderate to severe hypoglycemia.

  46. HYPOGLYCEMIA = LOW BLOOD SUGAR < 70-80 or with symptoms! Causes: Too Much Insulin Too Little Food Extra Exercise RECHECK BLOOD SUGAR AFTER 10 TO 15 MINUTES, REPEAT TREATMENT TO KEEP BLOOD SUGAR ABOVE 80. May need to follow with carbohydrate and protein snack (sandwich or peanut butter & crackers).

  47. Hypoglycemia Unawareness • Blunting of epinephrine and early warning signs. • Can be an indicator of too many hypoglycemic events (may miss lows). • Epinephrine response is also blunted during sleep – sleeping through lows is very common!

  48. Hypoglycemia • Increased risk with tight control • Increased symptoms if dropping rapidly • False hypoglycemia – Normal BG may not feel normal if running high

  49. Hypoglycemia Prevention • Appropriate timing and dosing of medications • Prevent “stacking of doses” – Is there active insulin on board? • Appropriate estimation of carbohydrate portion size • Appropriate response to increase in activity (increased carb or decreased insulin) • Identifying risk factors and educating patient and family re: signs, symptoms and treatment • Blood glucose monitoring!!

  50. Managing Diabetes During Illness Effect of illness on blood glucose • We require extra energy to cope with illness, infection, pain and stress • Extra energy requires increased fuel (supplied via hepatic glucose production) and extra insulin to use the fuel • This will usually cause and increase in blood glucose, even if the patient is not eating! Increased risk of ketosis and ketoacidosis

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