acute effects of diabetes mellitus

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    Acute Effects of Diabetes

    Mellitus

    Hao Xie

    01/08/2010

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    Causes of Diabetes Mellitus

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    Causes of Diabetes Mellitus

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    Causes of Diabetes Mellitus

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    Acute Effects: Fatty Liver

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    Acute Effects: Acidosis/Coma

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    Late Complications of Prolonged Hyperglycemia

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    DKA

    A collection of severe and potentially life-threatening metabolic disturbances:

    Hyperglycemia Osmotic diuresis

    Urinary loss of fluids & electrolytes

    Extracellular fluid volume contraction

    Depletion of total body K+ stores

    (even though may be hyperkalemic 2 to cell shift)

    Ketone productionMetabolic acidosis

    Compensatory Respiratory alkalosis (hopefully!)

    Uncontrolled lipolysis severe TG

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    DKA: Pathophysiology

    Glucose

    Pyruvate

    Acetyl-CoA

    Ketoacids

    Krebs

    + PFKInsulin

    fat cell

    TG

    FFA

    HSL

    Liver Cell

    Fatty

    Acyl-CoA

    Insulin -

    VLDL (TG)

    Glucagon

    Insulin

    +

    +

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    DKA: Pathophysiology

    Glucose

    Pyruvate

    Acetyl-CoA

    Ketoacids

    Krebs

    + PFKInsulin

    fat cell

    TG

    FFA

    HSL

    Liver Cell

    Fatty

    Acyl-CoA

    Insulin -

    VLDL (TG)

    Glucagon

    Insulin

    +

    +

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    DKA: Potassium

    K+ defecit: 3-5 mEq/Kg (350 mEq for 70Kg)

    Normal to high serum K+

    K+

    K+

    H+ H+

    Ketoacidosis

    Insulin

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    DKA: Potassium K+ deficit 3-5 mEq/kg (350 mEq 70kg)

    Need K+ with initial IV fluid & insulin Rxunless: (normal serum K+: 3.5-5.0 mEq/L)

    Anuric

    K+

    > 5.5 mEq/L or hyperkalemic ECG changes

    Initial [K] Replacement

    > 5.5 mEq/L nil (initially)

    5.2-5.5 mEq/L 10 mEq/h4-5.2 mEq/L 20 mEq/h

    3-4 mEq/L 30 mEq/h

    < 3 mEq/L 40 mEq/h

    > 20 mEq/h:

    Cardiac monitor

    > 60 mEq/L:Central line

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    HONCHyperosmolar Non-Ketotic Coma

    T2DM, elderly (mean age 60-73), F > M

    Pathogenesis poorly understood

    Mild extracellular fluid volume instigatingfactor

    Insulin/Glucagon ratio sufficient to limit DKA

    Diminished thirst or access to water Vicious cycle develops

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    Hyperglycemia

    Osmotic Diuresis

    Volume Contraction

    Pre-renal azotemia

    HONC

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    HONC: Insulin?

    Patients can be treated successfully without insulin

    If IV fluids inadequate, blood sugar and serum OSM

    will not drop despite insulin

    Majority of studies used insulin

    Hi-dose Insulin: severe hypokalemia, shock

    Therefore if going to use insulin, use low doses:

    Bolus 0.1 U/kg, Rate 1-2 U/h (or 0.1 U/kg/h)

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    Pathogenesis of DKA & HONC

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    References

    Silbernagl and Lang, Color Atlas of

    Pathophysiology 2000

    Kumar, Abbas et al. Robbins and Cotran

    Pathologic Basis of Disease

    William Harper, M.D. Endocrinology &

    Metabolism, McMaster University

    Kitabchi et al. Endocrinol Metab Clin N Am 35

    (2006) 725751