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How Does Insulin Cause Hypokalemia

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What is HYPOKALEMIA? What does HYPOKALEMIA mean? HYPOKALEMIA meaning - HYPOKALEMIA pronunciation - HYPOKALEMIA definition - HYPOKALEMIA explanation - How to pronounce HYPOKALEMIA? Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. Hypokalemia, also spelled hypokalaemia, is a low level of potassium (K+) in the blood serum. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia. Mildly low levels do not typically cause symptoms. Symptoms may include feeling tired, leg cramps, weakness, and constipation. It increases the risk of an abnormal heart rhythm such as bradycardia and cardiac arrest. Causes of hypokalemia include diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet. It is classified as severe when levels are less than 2.5 mmol/L. Low levels can also be detected on an electrocardiogram (ECG). Hyperkalemia refers to a high level of potassium in the blood serum. The speed at which potassium should be replaced depends on whether or not there are symptoms or ECG changes

Hypokalemia

What is Hypokalemia? Hypokalemia is defined as low potassium level in the blood. Potassium is an electrolyte whose concentration within the cells is higher than outside the cells i.e. in the blood. The potassium levels as measured in the laboratory indicate the blood levels of potassium, and not the levels within the cells. Normal potassium levels in the blood serum range from 3.5 to 5.0 mEq /l. Low blood potassium levels is referred to as hypokalemia, while high blood potassium levels are referred to as hyperkalemia. Hypokalemia can range from mild to severe. Mild - serum potassium level ranges from 3-3.5 mEq /L. Moderate - serum potassium level ranges between 2.5-3 mEq /L. Severe – serum potassium level is below 2.5 mEq /L Serum refers to the liquid portion of the blood that does not clot, which is used for measuring potassium levels. How are Potassium Levels Maintained at Normal Levels? Potassium is obtained from the diet and excreted through the kidneys. It is essential that potassium levels are tightly regulated by physiological mechanisms. The adrenal glands and the pancreas play an important role in maintaining blood potassium levels. The adrenal glands secrete a hormone c Continue reading >>

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  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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Hypokalemia And Cardiac Disease

In health, serum potassium concentration is maintained within the approximate range of 3.5-5.2 mmol/L. Disturbance of potassium homeostasis is a common electrolyte disorder that is clinically manifest through its adverse effect on both skeletal and cardiac muscle cell function. Although often asymptomatic, both reduced serum potassium (hypokalemia) and increased serum potassium (hyperkalemia) can cause muscle weakness/paralysis and cardiac arrhythmias. A recently published short review focuses on hypokalemia occurring in patients with cardiovascular disease, in particular the contribution that hypokalemia can make to sudden cardiac death in this patient group. The article includes a brief consideration of the physiological mechanisms involved in maintaining normal serum potassium, and the prevalence of hypokalemia among patients with cardiovascular disease (7-17 %). Also included is a summary of the accumulating epidemiological evidence that hypokalemia increases the risk of cardiac arrhythmias and reduces survival among patients suffering myocardial infarction and heart failure. Common causes of hypokalemia in patients with cardiovascular disease are highlighted; these include the Continue reading >>

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  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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Take Dr. Berg's Advanced Evaluation Quiz: http://bit.ly/EvalQuiz Your report will then be sent via email analyzing 104 potential symptoms, giving you a much deeper insight into the cause-effect relationship of your body issues. It's free and very enlightening. Dr. Berg explains what hypokalemia is in this video. This is when you don't have enough potassium in your body. This can cause various problems such as tiredness, leg cramps, weak, constipation, arrhythmias, high blood pressure. There are various causes for this condition. The body need 7 to 10 cups of vegetables a day which would give the body enough potassium. This is generally never part of a person's diet. Find out how you can learn to handle this condition to a better degree. Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional and natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government and the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the auth

Hypokalemia (low Level Of Potassium In The Blood)

In hypokalemia, the level of potassium in blood is too low. A low potassium level has many causes but usually results from vomiting, diarrhea, adrenal gland disorders, or use of diuretics. A low potassium level can make muscles feel weak, cramp, twitch, or even become paralyzed, and abnormal heart rhythms may develop. Usually, eating foods rich in potassium or taking potassium supplements by mouth is all that is needed. Potassium is one of the body's electrolytes, which are minerals that carry an electric charge when dissolved in body fluids such as blood. Potassium is needed for cells, muscles, and nerves to function correctly. Causes of Hypokalemia Typically, the potassium level becomes low because too much is lost from the digestive tract due to vomiting, diarrhea, or excessive laxative use. Sometimes too much potassium is excreted in urine, usually because of drugs that cause the kidneys to excrete excess sodium, water, and potassium (diuretics). In many adrenal disorders, such as Cushing syndrome, the adrenal glands produce too much aldosterone, a hormone that causes the kidneys to excrete large amounts of potassium. Certain drugs (such as insulin, albuterol, and terbutaline) Continue reading >>

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  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

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