good morning!! july 9, 2012. phone message from mom: “js (well known to you, healthy 7 yr old...
TRANSCRIPT
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
Symptoms
Acute /subacute Chronic
Localized Diffuse
Single Multiple
Static Progressive
Constant Intermittent
Single Episode Recurrent
Abrupt Gradual
Severe Mild
Painful Nonpainful
Bilious Nonbilious
Sharp/Stabbing Dull/Vague
Problem Characteristics
Ill-appearing/Toxic
Well-appearing/Non-toxic
Localized 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 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 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 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
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