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How Does Use Of Insulin Lead To Hypokalemia?

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Hypokalemia (low Potassium)

What Is Hypokalemia? Hypokalemia is an electrolyte imbalance and is indicated by a low level of potassium in the blood. The normal adult value for potassium is 3.5-5.3 mEq/L. Potassium is one of many electrolytes in your body. It is found inside of cells. Normal levels of potassium are important for the maintenance of heart, and nervous system function. What Causes Hypokalemia? One way your body regulates blood potassium levels is by shifting potassium into and out of cells. When there is a breakdown or destruction of cells, the electrolyte potassium moves from inside of the cell to outside of the cell wall. This shift of potassium into the cells causes hypokalemia. Trauma or insulin excess, especially if diabetic, can cause a shift of potassium into cells (hypokalemia). Potassium is excreted (or "flushed out" of your system) by your kidneys. Certain drugs or conditions may cause your kidneys to excrete excess potassium. This is the most common cause of hypokalemia. Other causes of hypokalemia include: Increased excretion (or loss) of potassium from your body. Some medications may cause potassium loss which can lead to hypokalemia. Common medications include loop diuretics (such as 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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