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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!”

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Good morning

Good Morning!!

July 9, 2012


Phone message from mom

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


Semantic qualifiers

Semantic Qualifiers


Illness script

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 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 script

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


Type 1 dm illness script1

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


Type 1 dm illness script2

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


Type 1 dm diagnosis

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

Treatment**

Multi-faceted

  • Insulin

    • Multiple dosing regimens

    • Goals:

      • Maintain normal glucose concentrations

      • Prevent complications

      • Watch for hypoglycemia


Treatment1

Treatment**

  • Nutrition

    • 50-60% Carbohydrate

    • 15-20% Protein

    • <30% Fat

    • Nutritionist support is always encouraged

  • Exercise

  • Pscyhologic support


Honeymoon period

“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

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 management1

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

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

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

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

Noon Conference: Growth (Chalew)


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