Editing Anatomy and Physiology – RN Practice Questions (section)

==Question 15==
A patient with diabetic ketoacidosis is receiving a continuous intravenous insulin infusion and normal saline. The serum potassium on admission was 5.4 mEq/L and is now 3.4 mEq/L after 4 hours of therapy. What is the '''best''' explanation for this change, and what should the nurse anticipate?
# The insulin has caused potassium to move from the extracellular fluid into the cells; anticipate a prescription for potassium replacement.
# The saline has diluted the serum potassium; anticipate slowing the fluid rate with no other change.
# The correction of acidosis has increased renal potassium reabsorption; anticipate holding all potassium.
# The insulin has increased potassium excretion by the kidney; anticipate a potassium-sparing diuretic.

'''Answer:''' 1 (A). Insulin has shifted potassium intracellularly; anticipate potassium replacement.

''Rationale:'' In diabetic ketoacidosis, acidosis and insulin deficiency drive potassium out of the cells, so the measured serum potassium is often normal or high even though total body potassium is depleted by osmotic diuresis. When insulin therapy begins, potassium moves back into cells along with glucose, and the serum level can fall rapidly and dangerously. Standard practice is to monitor potassium frequently and add replacement to the intravenous fluids, and insulin is generally withheld until potassium is above roughly 3.3 mEq/L. Option 2 underestimates a physiologically important shift. Option 3 misstates the mechanism and would allow a dangerous fall. Option 4 is incorrect because insulin causes a transcellular shift rather than renal potassium wasting, and a potassium-sparing diuretic is not the treatment for hypokalemia in this setting.

[[Category:Anatomy and Physiology]]
[[Category:Registered Nurse (NCLEX-RN)]]
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