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18 Cards in this Set
- Front
- Back
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DKA
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body cannot use sugar as a source of energy due to there not being enough insulin
fat is used for fuel instead-byproducts of this (ketones) buildup |
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insulin
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hormone that allows glucose to move from bloodstream into individual cells to be used for energy; produced by the pancreas
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Diagnosing DKA
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insulin >300
HCO3 less then 18 pH less then 7.3 |
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Clinical manifestations of DKA
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polydipsea
polyphagia polyuria dehydration electrolyte imbalance hypotension and increased heart rate GI effects CNS effects- lethargic kussmaul respirations- rapid/deep long expiration fruity breath smell |
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treatment of DKA
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administration of insulin (can't go from blood sugar 1200 to 200 in 8 hrs)
-loading dose of 25-50 units then 5-10 units/hr in NS replacement of fluids to correct hypovolemia |
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Which electrolyte imbalance occurs with initial DKA
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hypokalemia
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What is the most common precipitating factor in a patient with DKA?
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hyperglycemia and concurrent illness or injury
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How does HHNK differ from DKA
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HHNK has a slower onset much higher blood sugars and more profound dehydration
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HHNK mortality rate is..
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greater than 50%
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HHNK diagnosis
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BGL >600
serum osmalarity greater than 350 pH and HCO3 close to normal |
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adequate insulin to prevent ketogenesis occurs so that
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there is not enough to still cover BGL
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clinical manifestation of HHNK
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dehydration 15-25% of normal water
2 ps -polydipsia -polyuria hypotension increased HR vascular occlusions because they are so dehydrated |
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treatment for HHNK and DKA is similar except...
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HHNK requires greater fluid replacement
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How many liters in first 24-48 hrs for HHNK
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6-20L either .9 or .45 NS is used (volume expanders)
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insulin infusion for HHNK
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.1 units/kg/hr
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normal serum osmalality
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285-295
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hypoglycemia s&s
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cold sweats
weakness nervousness trembling irritability pallor increased HR confusion fatigue headache |
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trtmt
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10-15 g carbs recheck in 10 follow with another 10-15
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