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Diabetes Mellitus Type 1

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Presentation on theme: "Diabetes Mellitus Type 1"— Presentation transcript:

1 Diabetes Mellitus Type 1

2 Epidemiology Incidence – increase with age through puberty then declines Prevalence – 1.2 to 1.9/1000 Geography – common in northern and southern areas of the world, such as Scandinavia and new Zealand

3 Underlying pathogenesis?
Insulin deficiency

4 Combination of genetics and environment
Causes? Combination of genetics and environment

5 Genetic causes 30-50% concordant in identical twins
1/40-80 or 1/20-40 chance of developing diabetes if mom or dad has diabetes, respectively HLA DR3 or DR 4 3.5-fold increase with either one 10-fold increase with both 95% of type 1 have both Associated with other autoimmune diseases such Graves’ disease, hypothyroidism, alopecia

6 Environmental cause Viral infection, such as parvovirus B19 and mumps, trigger islet cell destruction, which accounts for frequent occurrence of type 1 in spring and fall

7 Rare causes Pancreatitis - not common in children except those with familial triglyceride Defective beta cell genes

8 Clinical symptoms Subacute or acute

9 Subacute presentations?
Malaise Weight loss – breaking down of proteins and fats to produce energy for the cells, because glucose could not be transported into the cells without insulin Polyuria Polydipsia Polyphagia Noctural enuresis

10 Acute presentations? Associated with diabetic ketoacidosis
Nausea and vomiting Abdominal pain due to DKA or appendicitis Dehydration or shock from osmotic diuresis Breathing Fruity smell Kussmaul’s breathing Altered mental status

11 Tests for diagnosis of diabetes mellitus type 1?
Fasting plasma glucose  126 mg/dL on two occasions Random plasma glucose  200 mg/dL with symptoms Two hours glucose tolerance test with plasma glucose  200 mg/dL at 2 hour

12 Distinctions from diabetes mellitus type 2
Thin Weight loss Insulin:serum glucose High in type 2 Low in type 1

13 Tests for work-up? Urinalysis Hemoglobin A1c Fasting lipid panel
Proteinuria – should get urine microalbumin Glucose does not confirm or rule out diagnosis of diabetes mellitus Ketones does not confirm or rule out diagnosis of DKA Hemoglobin A1c Fasting lipid panel

14 Diagnosis of DKA? Hyperglycemia Ketones – β-hydroxybutyrate
Metabolic acidosis

15 Work-up of DKA? Chemistry ABG Serum β-hydroxybutyrate Glucose Sodium
Potassium Magnesium Phosphorus BUN and creatinine ABG Serum β-hydroxybutyrate Sodium - – high from dehydration, low from dilutional hyperglycemia Potassium – high because K+ moves into the cell, as bicarbonate moves out of the cell to compensate for the acidosis

16 Management Hydration Correct ketoacidosis Monitor electrolytes
Start insulin regimen

17 Hydration Deficits 6-8 liters in DKA and 8-10 liters in NKH 5-10% in children Rate of replacement depends on the severity of shock – ½ fluid deficit + 40% of maintenance + urine loss + other losses (mL/hour) Start with normal saline solution and switch to ½ normal saline when patient is hemodynamically stable and potassium is added into IV fluid, because potassium is an osmotic solute Add dextrose to IV fluid once serum glucose drops < 300 mg/dL to prevent rapid decrease in osmolality leading to cerebral edema

18 Correct ketoacidosis? Regular insulin bolus Insulin infusion
After IV fluid bolus to prevent precipitating drop in glucose unit per kg Insulin infusion 0.1 unit per kg/hour Adjust insulin rate or IV fluid rate to maintain serum glucose mg/dL

19 Monitor electrolytes Glucose
Drop after hydration due to increased renal filtration and decreased insulin resistance due to decreased glucacon, corticoticoids, and catecholamines Not to lower faster to than 100mg/dL per hour or below 200 – 250 mg/dL acutely because of the risk of cerebral edema Potassium - drops very quickly after hydration Potassium moves back into the cells due to insulin and decreased acidosis 0.1 change in pH = 0.6 mEq/L change in potassium in opposite direction Replace as soon as patient has urine output and no more hyperkalemia Magnesium and phosphorus – supplement as necessary

20 Monitor metabolic acidosis
Follow serum bicarbonate and anion gap Not need to do serial ABG Bicarbonate for acidosis Not routine because CO2 moves into CSF and worsens cerebral pH Indication pH < 7.1 because of decreased cardiac contractility and vasodilation impairing tissue perfusion Life-threatening kyperkalemia

21 Insulin Start SQ regular insulin 1 hour or NPH 4 hours prior to stopping insulin infusion Insulin regimen Total 0.5 units/kg/day 2/3 in AM and 1/3 in PM 2/3 NPH and 1/3 regular in AM & 1/2 NPH and 1/2 regular in PM

22 The End

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