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19 Cards in this Set
- Front
- Back
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Effect of low insulin, high counterregulatory hormones on:
Muscle Liver Adipose |
Muscle: Decreased glucose utilization-->Hyperglycemia
Liver: Increased glucneo-->hyperglycemia Increased ketogenesis-->Ketoacidosis Adipose Tissue: Increased lipolysis-->increased ketogenesis |
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How does osmotic diuresis arise? What metabolites are lost because of this?
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Hyperglycemia-->glucosuria (spill glucose in urine)
-->Osmotic Diuresis (Water Loss) Spill Na+ and K+ too |
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What is the effect of dehydration on serum osmolality?
Effect on intracellular fluid? |
Dehydration (osmotic diuresis) increases osmolality
Leads to intracellular water depletion (flow of water out of cell into intracellular space) , cells then become hyperosmolar |
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What is the effect of osmotic diuresis on kidney function and glucose levels? Be specific.
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Decreased extracellular fluid volume--> Decreased GFR
THUS decreased glucose excretion (HIGHER GLUCOSE IN BLOOD) |
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What ketone body are prevalent in serum in diabetic ketoacidosis?
Effect on bicarbonate ions? |
beta-hydroxybutyric acid (not really a ketone)
acetoacetic acid acetone (not an acid, but it's volatile so it's breathed out: fruity, pear scent) Deplete bicarbonate ANIONS (base) |
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Symptoms of diabetic ketoacidosis?
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Polyuria (nocturia)
Thirst, polydipsia Recent weight loss Anorexia, nausea, vomiting MENTAL STATUS CHANGE (somnolence to coma) Volume depletion (skin turgor, hypotension, tachycardia) Hyeprventilation (KUSSMAUL respirations, fruity breath--acetone) |
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Laboratory findings that define DKA.
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Hyperglycemia (~600)
Ketonemia ANION GAP METABOLIC ACIDOSIS pH<7.3, bicarb <15 (Na)-(Cl+HCO3)>12 Unmeasured anion = ketones (beta-hydroxybutyrate is main one--it's an acid) |
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Describe potassium shifts in DKA. How will patient present?
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K+ shifts from ICF to ECF, lost in urine
When patient presents, K+ can be high, normal, or low, but ALWAYS has total body potassium depletion!! |
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What are common causes of DKA?
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Known insulin-dependent DM (most common):
Stop taking insulin Intercurrent stressful illness Previously undiagnosed DM (presenting finding): Common in TYPE 1 DM |
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DKA Treatment
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1)Insulin IV (bolus followed by continuous infusion)--must follow plasma glucose hourly!
(Initial rapid fall in glucose) 2) IV fluid administration--NORMAL SALINE initally (to replace sodium), then half-normal saline (extra water, half the volume of saline to correct free water deficit) 3) K replacement (unless patient is not putting out urine) 4) Glucose Administration (high sugar is not main problem, it's metabolic abnormalities!)--glucose drops faster than metabolites will normalize. Don't stop giving insulin! Need to continue insulin drip while still administering glucose. (Enables insulin suppression of lipolysis and clearance of ketone bodies)!!! |
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When should biacarbonate administration be considered in DKA?
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NEVER a good idea to give bicarb bc usually not necessary (can promote hypokalemia)
If pH<7.0 or bicarb <5.0 can consider. Solution is not to give base, but to give insulin. |
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What defines a hyperosmolar hyperglycemic state?
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Hyperglycemia (>600)
Hyporosmolar (>320) Absence of significant ketosis (not complete absence of ketosis) Predominantly older pts with DM II. |
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Presentation of HHS?
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Prominent neurological abnormalities (somnolence and obtundation to coma)
All due to predisposing underlying disorders similar to DKA, in addition to profound water and Na losses |
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Why aren't HHS patient ketoacidotic?
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Higher level of insulin in portal circulation sufficient to suppress ketogenesis but NOT gluconeogenesis
Hyperosmolarity may suppress ketogenesis DKA CAN occur in DM II |
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Why aren't DKA patients more hyperosmolar?
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Ketosis makes patients feel awful so seek medical attention before more severe volume depletion
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Treatment of HHS?
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Normal saline to restore saline (initial)
1/2 Normal saline to restore free water in addition to volume Then D5 1/2 Normal Saline (contains sugar to don't drop sugar too quickly-->might induce cerebral edema) |
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Why is cerebral edema a complicating treatment for HHS?
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Neurons protect themselved from intracell volume loss by forming idiogenic osmols
Idiogenic osmols draw water back into cell to maintain volume If hyperosmolarity treated too quickly, too much water drawn into neurons and results in cerebral swelling (cerebral edema) |
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Avoid insulin without fluids because ___________.
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Water shifts into cells (follows glucose)-->decreased vascular volume-->decreased tissue perfusion
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DKA vs HHS
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DKA:
Glucose >250 pH <7.3 HCO3 <15 Anion Gap HIGH Ketones +++ HHS: >600 pH >7.3 HCO3 >18 NORMAL anion gap Osmolality >330 Ketones +/- |
