hypokalemia prolongs paralytic ileus - USMLE Forums
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Old 05-13-2011
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GIT hypokalemia prolongs paralytic ileus

Can someone pls explain HOW does hypokalemia prolong paralytic ileus? does it by any chance cause atony of the intestine? if yes, how does it work?

My internet is slow today n i cant find the answer that im looking for.
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Old 05-13-2011
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Yes! hypokalemia causes atony of intestinal muscles. this is because k has an imp role in nerve signal transmission and also for excitability of all muscle cell. therefore if paralytic ileus is already there then, decrease k level will prolong the recovery of paralytic ileus.
this what i have read for step 1 some where in acid base balance or initial chapters.

Please confirm this and correct if i am wrong.

best luck for studies.
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Old 05-14-2011
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Default Pseudo-obstruction

Paralytic ileus, also called pseudo-obstruction is a condition in which the bowel doesn't work correctly but there is no structural problem. Causes of paralytic ileus may include:
  • Chemical, electrolyte, or mineral disturbances (such as decreased potassium levels)
  • Complications of intra-abdominal surgery
  • Decreased blood supply to the abdominal area (mesenteric artery ischemia)
  • Injury to the abdominal blood supply
  • Intra-abdominal infection
  • Kidney or lung disease
  • Use of certain medications, especially narcotics
(http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001306/)
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Old 05-14-2011
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Default thx guys

think i got it.

severe hypokalemia causes an increased intracellular potassium shift, which then causes changes in membrane potentials on neural and muscle function, which causes worsening of paralytic ileus tht may have occurred after an abdominal surgery. so after surgery, checking serum electrolytes levels again and noticing a low potassium level, and subsequently replacing those levels will avoid this problem. hypokalemia also causes decrease in resting membrane potential of the cardiac muscles causing prolongation of PR interval and eventually leading to cardiac arrhythmia. potassium should be replaced at a rate NOT exceeding 10mEq/h (IV) because it can increase the risk of overload potassium which then leads to cardiac arrest.

anyone wants to add on or correct me perhaps?
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Old 05-14-2011
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Default just adding on some information

Hypokalemia can be caused by decreased intake of K but is usually caused by excessive losses of K in the urine or from the GI tract.

Insulin moves K into cells; high concentrations of insulin thus lower serum K concentration. Low insulin concentrations, as in diabetic ketoacidosis, cause K to move out of cells, thus raising serum K, sometimes even in the presence of total body K deficiency.


β-Adrenergic agonists, especially selective β2-agonists, move K into cells, whereas β-blockade and α-agonists promote movement of K out of cells.

Acute metabolic acidosis causes K to move out of cells, whereas acute metabolic alkalosis causes K to move into cells. However, changes in serum HCO3 concentration may be more important than changes in pH; acidosis caused by accumulation of mineral acids (nonanion gap, hyperchloremic acidosis) is more likely to elevate serum K. In contrast, metabolic acidosis due to accumulation of organic acids (increased anion gap acidosis) is not associated with hyperkalemia. Thus, the hyperkalemia common in diabetic ketoacidosis results more from insulin deficiency than from acidosis. Acute respiratory acidosis and alkalosis affect serum K concentration less than metabolic acidosis and alkalosis. Nonetheless, serum K concentration should always be interpreted in the context of the serum pH (and HCO3 concentration).
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