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Medical Forum / General / General / April 2007Question for any doctor
I am reading a book entitled, "Acid-Base, Fluids and Electrolytes" by Richard A. Preston, M.D. On page 116, Dr. Preston states: "Metabolic Alkalosis is a process that causes a primary increase in the plasma BICARBONATE concentration." On page 81, Dr. Preston states: "Potassium citrate (citrate is converted into BICARBONATE in the liver." On page 121, Dr. Preston states: The treatment for Bartter's Syndrome [a metabolic alkalosis disorder] is Potassium Citrate and [various medications]. My question is: Since Metabolic Alkalosis is a process that causes a primary increase in the plasma Bicarbonate concentration, why would Dr. Preston use Potassium Citrate to treat Bartter's Snyndrome? In other words, would Potassium Citrate cause the bicarbonate concentration to rise to dangerous levels since it is converted to Bicarbonate in the liver? Thanks in advance, Jason Probably because its broken down to citric acid , which is acid > Probably because its broken down to citric acid , which is > acid Citric acid is metabolized to bicarbonate, which is a base. I think the answer the question is that Preston doesn't know what he is talking about. Jeff > I am reading a book entitled, "Acid-Base, Fluids and Electrolytes" by > Richard A. Preston, M.D. [quoted text clipped - 19 lines] > Thanks in advance, > Jason http://www.emedicine.com/med/topic213.htm Relevant portion.... "High levels of aldosterone also enhance potassium and hydrogen exchange for sodium. Excessive intracellular hydrogen ion accumulation is associated with hypokalemia and intracellular renal tubule potassium depletion. This is because hydrogen is exchanged for potassium to maintain electrical neutrality. It may lead to intracellular citrate depletion because the alkali salt is used to buffer the intracellular acid and then lowers urinary citrate excretion. Hypocitraturia is an independent risk factor for renal stone formation. Excessive distal sodium delivery increases distal tubular sodium reabsorption and exchange with the electrically equivalent potassium or hydrogen ion. This, in turn, promotes hypokalemia, while lack of chloride reabsorption promotes inadequate exchange of bicarbonate for chloride, and the combined hypokalemia and excessive bicarbonate retention lead to metabolic alkalosis. " Hope this helps.... Seems its due to pottasium depletion . Replace the pottasium and the body cells wake up and excrete the alkalosis even if its made slightly worse by the citrate bits > Seems its due to pottasium depletion . Replace the pottasium > and the body cells wake up and excrete the alkalosis even if its made > slightly worse by the citrate bits ~~~~~~~~~~~~~~~~~~~ Good point. Do you believe that Potassium Gluconate would be a better solution than Potassium Citrate since citrate is converted into bicarbonate in the liver? As you know, metabolic alkalosios is a primary increase in serum bicarbonate concentration. > In article <46141885.5226...@news.clara.net>, hab...@anony.com (habshi) wrote: > > Seems its due to pottasium depletion . Replace the pottasium [quoted text clipped - 7 lines] > bicarbonate in the liver? As you know, metabolic alkalosios is a primary > increase in serum bicarbonate concentration. Didn't you read the portion I sent you? Bartter's Syndrome is juxtaglomerular hyperplasia with secondary aldosteronism. This causes hypokalemic metabolic alkalosis. The high levels of Aldesterone in the body cause H+ ions to replace K+ ions in the cells (Because K+ ions are urinated out, and the electrical balance needs to be maintained). If the H+ ions in the blood are lowered, then you have alkalosis without raising HCO3-. The extra H+ ions in the cells cause them to get acidic, so the intracellular citrate is used up by the cells to buffer themselves. This causes a lack of citrate(citrate is required for the Krebs cycle). Therefore potassium citrate would be used to bring up the K+ ion levels and restore the citrate that was used for the buffering. Does that make sense to you? > > In article <46141885.5226...@news.clara.net>, hab...@anony.com (habshi) wrote: > > > Seems its due to pottasium depletion . Replace the pottasium [quoted text clipped - 26 lines] > > Does that make sense to you? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Thanks for your post. I downloaded a 20 page report related to Metabolic Alkalosis and read it yesterday. I do not understand this subject as well as you understand this subject. If a patient had regular Metabolic Alkalosis and normal levels of aldosterone--would the bicarbonate concentration go up or down if that patient took high levels of Potassium Citrate? If that same patient had taken high levels of Potassium Chloride instead of Potassium Citrate would the bicarbonate concentration have gone up or down? Thanks in advance, Jason ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ > In article <1175745566.608170.3...@q75g2000hsh.googlegroups.com>, > [quoted text clipped - 46 lines] > > - Show quoted text - "If a patient had regular Metabolic Alkalosis and normal levels of aldosterone--would the bicarbonate concentration go up or down if that patient took high levels of Potassium Citrate?" Metabolic alkalosis is maintained by either a lack of K+ ions or a lack of Cl- ions. A patient wouldn't receive potassium citrate for chloride related metabolic alkalosis. The patient receiving the potassium citrate had Bartter's Syndrome. Which enhances alkalosis by a loss of potassium, caused by excessive aldesterone. The patient has an adequate level of Cl- in the blood and more Cl- would affect his bodies electroneutrality. IF, a patient received potassium citrate for Metabolic alkalosis AND that patient had normal levels of aldesterone and K+, then yes it would cause an increase in HCO3- concentrations. Potassium chloride would be give to a patient that had chloride related metabolic alkalosis. As a defiency in Cl- ions would maintain the alkalosis. Try looking here and here http://www.anaesthesiamcq.com/AcidBaseBook/ab7_2.php http://www.anaesthesiamcq.com/AcidBaseBook/ab7_6.php > > In article <1175745566.608170.3...@q75g2000hsh.googlegroups.com>, > > [quoted text clipped - 73 lines] > > http://www.anaesthesiamcq.com/AcidBaseBook/ab7_6.php ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Thanks for your post and thanks for informing me about those two web sites. You appear to have an excellent understanding of this subject. I downloaded a report from this site and most of what you wrote in your post agrees with what I read in this report: http://www.emedicine.com/MED/topic1459.htm |
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