Hey guys, help needed for UW question!

bt9099

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Mar 30, 2008
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    Hi I was hoping someone could please answer this:

    in primary hyperaldosteronism, you obviously lose Na and retain K. But you stay eunatremic because of aldoserone escape.

    THe question says you get metabolic alkalosis b/c of the H+ loss as well, but the answer states that HCO3- is increased. Why is the HCO3- increased, wouldn't there be a compensatory loss of bicarbonate to compensate for the loss of H+ (so to balance out pH)?

    Thanks!!
     

    TerpMD

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      Hi I was hoping someone could please answer this:

      in primary hyperaldosteronism, you obviously lose Na and retain K. But you stay eunatremic because of aldoserone escape.

      THe question says you get metabolic alkalosis b/c of the H+ loss as well, but the answer states that HCO3- is increased. Why is the HCO3- increased, wouldn't there be a compensatory loss of bicarbonate to compensate for the loss of H+ (so to balance out pH)?

      Thanks!!

      In a metabolic alkalosis the primary defect is the increased bicarb (in this case, from a loss of H+) so the compensation is respiratory. Even though the kidney isn't exactly keeping extra bicarb (it just not keeping H+), the kidney is the source of the problem so the lungs have to step in. Hope this helps :)
       

      DMBFan

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        I am not sure if I am right, but I thought that if you are losing H+ in your urine, you are automatically increasing HCO3- in the body. this is bec. when H+ is in the urine it undergoes that carbonic anhydrase reaction to get HCO3-, which is reabsorbed. That's what happens initially at least. Not sure if the question was asking what would happen post-compensation.

        Also, in primary hyperaldo, you are reabsorbing more Na+, and losing more K+ and H+ in the distal tubules - hence met. alkalosis. I hope this helps!
         
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        bt9099

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        Mar 30, 2008
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          Hi I was hoping someone could please answer this:

          in primary hyperaldosteronism, you obviously lose Na and retain K. But you stay eunatremic because of aldoserone escape.

          THe question says you get metabolic alkalosis b/c of the H+ loss as well, but the answer states that HCO3- is increased. Why is the HCO3- increased, wouldn't there be a compensatory loss of bicarbonate to compensate for the loss of H+ (so to balance out pH)?

          Thanks!!

          Sorry I'm going crazy. I meant hyperaldosteronism, but you I should have said you retain Na and lose K and lose H. You stay eunatremic b/c of aldosterone escape.

          THe question says you get metabolic alkalosis b/c of the H+ loss as well, but the answer states that HCO3- is increased. Why is the HCO3- increased, wouldn't there be a compensatory loss of bicarbonate to compensate for the loss of H+ (so to balance out pH)?
           

          bt9099

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          Mar 30, 2008
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            Can someone please answer this??

            Patient has primary hyperaldosteronism, so you retain Na and lose K and lose H. You stay eunatremic b/c of aldosterone escape.

            THe question says you get metabolic alkalosis b/c of the H+ loss as well, but the answer states that HCO3- is increased. Why is the HCO3- increased, wouldn't there be a compensatory loss of bicarbonate to compensate for the loss of H+ (so to balance out pH)?
             

            cyclohexanol

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              Can someone please answer this??

              It's actually been answered already, see below.

              In a metabolic alkalosis the primary defect is the increased bicarb (in this case, from a loss of H+) so the compensation is respiratory. Even though the kidney isn't exactly keeping extra bicarb (it just not keeping H+), the kidney is the source of the problem so the lungs have to step in. Hope this helps :)

              Hyperaldosteronism forces reabsorption of Na+ at the expense of K+ OR H+ in the DCT and CD, so you get both hypokalemia and metabolic alkalosis (via loss of H+). Dumping H+ in the tubule as NH4+ decreases H+ in the blood. Less H+ in the blood means a RELATIVE increase in HCO3 (again due to loss of H+ as NH4+, not due to kidneys reabsorbing HCO3).

              I think where you're getting hung up is why the kidney doesn't just dump HCO3 to compensate for the increased HCO3 in blood. So here is my attempt at why:

              Remember that HCO3- is filtered through the glomerulus where it can combine with H+ in the PCT. Brush border carbonic anhydrase splits it into H2O and CO2, which can freely diffuse through the tubular cells where intracellular carbonic anhydrase acts on it to produce H2CO3. The carbonic acid then gets split back into HCO3- and H+. The HCO3- is reabsorbed (no matter what, even if the plasma HCO3 concentration is high) resulting in no absolute loss or gain of HCO3-. This process can be inhibited by inhibiting carbonic anhydrase, and trapping HCO3- in the lumen (think acetazolamide - self-limited HCO3- diuresis).

              So as you can see, by dumping H+ into the lumen, you just potentiate the problem by allowing more HCO3- to combine with H+ to form H2O and CO2, which is readily reabsorbed. The only [easy] way to stop the process is by inhibiting carbonic anhydrase (even though the treatment for hyperaldosteronism is spironolactone, since it antagonizes aldosterone and removes the underlying cause of the metabolic alkalosis).

              Hope that helps.
               

              bt9099

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              Mar 30, 2008
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                It's actually been answered already, see below.



                Hyperaldosteronism forces reabsorption of Na+ at the expense of K+ OR H+ in the DCT and CD, so you get both hypokalemia and metabolic alkalosis (via loss of H+). Dumping H+ in the tubule as NH4+ decreases H+ in the blood. Less H+ in the blood means a RELATIVE increase in HCO3 (again due to loss of H+ as NH4+, not due to kidneys reabsorbing HCO3).

                I think where you're getting hung up is why the kidney doesn't just dump HCO3 to compensate for the increased HCO3 in blood. So here is my attempt at why:

                Remember that HCO3- is filtered through the glomerulus where it can combine with H+ in the PCT. Brush border carbonic anhydrase splits it into H2O and CO2, which can freely diffuse through the tubular cells where intracellular carbonic anhydrase acts on it to produce H2CO3. The carbonic acid then gets split back into HCO3- and H+. The HCO3- is reabsorbed (no matter what, even if the plasma HCO3 concentration is high) resulting in no absolute loss or gain of HCO3-. This process can be inhibited by inhibiting carbonic anhydrase, and trapping HCO3- in the lumen (think acetazolamide - self-limited HCO3- diuresis).

                So as you can see, by dumping H+ into the lumen, you just potentiate the problem by allowing more HCO3- to combine with H+ to form H2O and CO2, which is readily reabsorbed. The only [easy] way to stop the process is by inhibiting carbonic anhydrase (even though the treatment for hyperaldosteronism is spironolactone, since it antagonizes aldosterone and removes the underlying cause of the metabolic alkalosis).

                Hope that helps.

                THanks so much I appreciate it!
                 
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