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How Does Use Of Insulin Lead To Hypokalemia?

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Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patient With Diabetes Mellitus?

Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium atpase located in cell plasma membranes. the insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. insulin deficiency allows a mild rise in plasma k+ chronically and makes the subject to severe hyperkalemia if a potassium load is given. conversely, potassium deficiency may cause decreased insulin release. thus plasma potassium and insulin participate in a feedback control mechanism. Continue reading >>

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Popular Questions

  1. standout22

    1 Speaking in terms of relationships, I understand that insulin effects K+. I also understand that with increased insulin production or administration you can have a state of hypokalemia. I just don't understand why, on an intracellular level why and how does insulin production or administration decreased serum K+?
    I appreciate any insight and help!

  2. medicrn16

    Hey Standout...we JUST had a test on this two weeks ago, lol. Hardest dang test I ever took.
    Basically, insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the famous sodium-potassium pump. However, this is only a temporary fix and monitoring for the hypokalemic/hypoglycemic effects would be necessary. You would have to give glucose with the insulin as part of the regimen. It depends on whether the person has an actual total body excess of K+ or the K+ has moved from ICF to ECF as to how well this will work and for how long.
    Causes of movement from ICF to ECF would be tissue damage, acidosis, hyperuricemia, and uncontrolled DM.
    Causes of excess total body K+ would be too much potassium foods, salt substitutes, transfusions of whole blood or PRBCs, and decreased K+ excretion from the kidneys due to K+ sparing diuretics, renal failure, or Addison's disease.
    Hope this helps. For me to pass this test (fluids and electrolytes) I made a chart with similarities/differences. Thank God for this. I escaped the doom of much of the class with a B. Hoo-ray. :wink2:

  3. Daytonite

    potassium levels are decreased by insulin. hypokalemia suppresses insulin release leading to glucose intolerance. this was the best explanation of why it happens that i could find and seems to be tied to atp activity:
    http://www.uhmc.sunysb.edu/internalm...ges/part_d.htm - insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium atpase located in cell plasma membranes. the insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. insulin deficiency allows a mild rise in plasma k+ chronically and makes the subject liabel to severe hyperkalemia if a potassium load is given. conversely, potassium deficiency may cause decreased insulin release. thus plasma potassium and insulin participate in a feedback control mechanism.

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