1. GOOD MORNING!! July 9, 2012

2. Phone message from mom:  “JS (well known to you, healthy 7 yr old Caucasian male) has a stomach ache that started yesterday and has vomited twice today. He has also been wetting the bed for the past 5 nights – which he hasn’t done in over 3 years!”  Activity level ok, a little tired  Emesis is non-bloody, non-bilious  No recent life changes/stressors  Hasn’t taken his temp; doesn’t think he has a fever

3. Symptoms Acute /subacuteChronic LocalizedDiffuse SingleMultiple StaticProgressive ConstantIntermittent Single EpisodeRecurrent AbruptGradual SevereMild PainfulNonpainful BiliousNonbilious Sharp/StabbingDull/Vague Problem Characteristics Ill-appearing/ Toxic Well-appearing/ Non-toxic Localized problemSystemic problem AcquiredCongenital New problem Recurrence of old problem Semantic Qualifiers

4. Illness Script  Predisposing Conditions  Age, gender, preceding events (trauma, viral illness, etc), medication use, past medical history (diagnoses, surgeries, etc)  Pathophysiological Insult  What is physically happening in the body  Clinical Manifestations  Signs and symptoms that result from the pathophysiological insult

5. Type 1 vs Type 2 DM**  Type 1  Absolute insulin deficiency  Antibodies against beta-cell antigens  Still the most common form in children  Type 2  Peripheral insulin resistance  hyperinsulinemia  beta-cell failure  relative insulin deficiency  Strongly related to obesity/metabolic syndrome  Strong family history  Becoming more common in young children

6. Type 1 DM Illness Script Predisposing Conditions  Onset typically in childhood  Peaks: 2y, 4-6y, 10-14y  Highest prevalence in the US: Caucasians  More cases present in cooler months  Genetic predisposition  Complex mode of inheritance  HLA region on chromosome 6 provides strongest determinant of susceptibility  Direct family member: 3-6% risk  Identical twin: 30-50% risk

7. Type 1 DM Illness Script Pathophysiology  Autoimmune destruction of the beta cells (islets) of the pancreas (T-cell mediated)  Environmental trigger in a genetically susceptible individual  Destruction is over months to years >80% of beta cells must be lost before glycemic control affected  Permanent insulin deficiency  Insulin deficiency  poor peripheral glucose uptake and increased hepatic and renal glucose production  hyperglycemia  Increase in fatty acid oxidation; protein breakdown for alternative fuel sources  ketones

8. Type 1 DM Illness Script Clinical Manifestations**  Classic Symptoms  Polyuria Serum glucose > 180mg/dL  glycosuria  osmotic diuresis  dehydration  Polydipsia Stimulated by polyuria to maintain euvolemia  Hyperphagia and Weight loss Persistent catabolic state Loss of calories through ketonuria and glucosuria  DKA: nausea, vomiting, dehydration, lethargy

9. Type 1 DM Diagnosis  Plasma glucose >200mg/dL (2-hr postprandial)  Fasting glucose ≥126mg/dL  2 separate occasions, or with classic symptoms  DKA  Arterial pH < 7.25  Serum bicarb < 15mEq/L  Elevated ketones in serum or urine

10. Treatment** Multi-faceted  Insulin  Multiple dosing regimens  Goals: Maintain normal glucose concentrations Prevent complications Watch for hypoglycemia

11. Treatment**  Nutrition  50-60% Carbohydrate  15-20% Protein  <30% Fat  Nutritionist support is always encouraged  Exercise  Pscyhologic support

12. “Honeymoon” Period**  Some beta cells recover with removal of the toxic effect of hyperglycemia  Insulin requirements decrease 1 to 3 months after diagnosis  Usually lasts several months May be >12 months

13. Self-management **  Hypoglycemia (<60mg/dL)  Symptoms: headache, vision changes, confusion, irritability, seizures, tremor, tachycardia, diaphoresis)  Mild-moderate: Ingestion of 10-15g of glucose (4oz of juice)  Severe: 1mg IM or SubQ glucagon  Patients should always carry a source of glucose

14. Self-management **  Sick days  Check for ketones when Persistent hyperglycemia >250mg/dL Illness (especially N/V)  Check ketones and blood glucose every 2-4 hrs  Do not stop insulin – even if uncertain oral intake Continue basal insulin May need rapid-acting at dose10-20% of daily requirement every 2-4 hours until ketones are cleared  Persistent vomiting or refusal/inability to take fluids or food orally REQUIRES an ER or office visit

15. Long-term Complications**  Microvascular damage  Retinopathy: >5-10y duration of disease First ophtho exam at 10y or 3-5y of disease Yearly thereafter  Nephropathy Annual urine microalbumin after age 10; or DM for 5yrs Nephrologist for HTN, proteinuria, elevated BUN/Cr  Neuropathy  Macrovascular damage  Atherosclerotic vascular disease at an earlier age Check fasting lipid panel at 12y or at diagnosis if +FHx

16. Prevention of Complications**  Strict glucose control will prevent long term complications  More frequent monitoring = improved glycemic control Before meals, at bedtime, overnight  HgA1C: Goal 7.5% to 8.5% Improvement of1% (mean glucose concentration of 30- 35mg/dL) decreases the risk of long-term complications by 20-50%

17. Comorbidities of Type 1 DM**  Autoimmune disorders  Thyroid dysfunction Check TSH every 1-2y  Adrenal hypofunction  Celiac disease Screened at least once and any time poor growth or GI symptoms occur  Growth Disturbance  Poor diabetic control can lead to decreased growth velocity, delayed skeletal and sexual maturation

18. Noon Conference: Growth (Chalew)