GOOD MORNING!!July 9, 2012

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

SymptomsAcute /subacute Chronic

Localized DiffuseSingle MultipleStatic Progressive

Constant IntermittentSingle Episode Recurrent

Abrupt GradualSevere MildPainful NonpainfulBilious Nonbilious

Sharp/Stabbing Dull/Vague

Problem CharacteristicsIll-appearing/

ToxicWell-appearing/

Non-toxicLocalized problem

Systemic problem

Acquired Congenital

New problem Recurrence of old problem

Semantic Qualifiers

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

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

Type 1 DM Illness ScriptPredisposing 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

Type 1 DM Illness ScriptPathophysiology 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

Type 1 DM Illness ScriptClinical 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

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

Treatment**Multi-faceted Insulin

Multiple dosing regimens

Goals: Maintain normal

glucose concentrations

Prevent complications

Watch for hypoglycemia

Treatment** Nutrition

50-60% Carbohydrate

15-20% Protein <30% Fat Nutritionist support

is always encouraged

Exercise Pscyhologic support

“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

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

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

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

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%

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

Noon Conference: Growth (Chalew)