frankiesunshine
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Can someone help me understand the relationship between these? I am constantly getting messed up. We have Na+/K+ which is affected by aldo to increase Na retention and increase K secretion. I know about the H/K pump, but why do we see hypokalemic alkalosis with Conn's? Since we have so much K in the urine due to the excess aldo, does that inhibit the H/K pump...so much K in urine that H/K doesn't work and H can't come in from forming urine leading to alkalosis?
I always get confused about kidney/alkalosis/acidosis.
Thx!
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| amitjosh
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In Conn's syndrome there is hyperaldosteronism, which causes retention of sodium by increasing reabsorptioin in the distal tubule and so we also have hypokalemia.
Whenever there is hypokalemia, remember the potassium levels in the blood are low. So intracellular potassium tends to come out of the cells.
Whenever 1K+ comes out of the cell 1H+ goes in (there is exchange of potassium and hydrogen ions)
Since H+ is removed from the blood and sent into the cells, there is alkalosis.
If in some other situation, like Addison's, there is hyperkalemia, the opposite would occur i.e. potassium moves into cells and hydrogen goes out into the blood. This would cause acidosis.
Hence whenever there is hypokalemia there is alkalosis.
Whenever there is hyperkalemia there is acidosis.
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| frankiesunshine
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thanks for the great explanation!
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| carmenburana
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An interesting aside
This interchange of K+/H+ is the reason why one treatment for hyperkalemia is to give Dextrose and insulin. The insulin helps guide the glucose into the cell and the glucose interchanges with the K+, increasing the extracelular K+. This also decreases the extracelular H+ and helps out with concurrent acidosis.
I think it's something like that?
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| hiwa
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except in renal tubular acidosis where u have hypokalemic acidosis.
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| bluedusk
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the other factor beside the general H+/K+ interchange resides in the collecting tubules. Hyperaldosteronism drives K+ into the urine (as noted above). The high K+ in the ducts then drives K+ re-entry and H+ ion explusion at the H+/K+ pump, furthering alkalosis.
Goljan's Saunders text is pretty good for this stuff.
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| H.of.Troy
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oups..little late 2 :?
but I was triggered by hiwa'sanswer!
I'd like some more exceptions to d rule of ALKALOSIS RELATED TO HYPOK..EMIA.
in ASA toxicity(3-4grams of aspirin)
+
in carbonic anhydrase(acetazolamide)use
we also observe ACIDOSIS NOT HYPERK..emic BUT HYPOK..emic :shock:
I don't know if it triggers U but I had a major probl in underst.totally acid/alkal. and their relationship to K/Na imbalance.. :icon_shake:
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| krishie
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Could u please clarify this for me-if ,in hyperkelemia,giving dextrose and insulin drives k out of the cell wont hyperkelemia increase?
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krish
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| krishie
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When we use acetazolamide,it inhibits carbonic anhydrase and causes bicarbonaturia.This causes loss of bicarb and hence acidosis.Due to the inhibition of na-h pump,decreased reabsorption of na and there is increased na load downstream.This causes k loss as well and causes hypokelemia
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krish
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| H.of.Troy
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as far as I'm concerned glucose entry in d cell is coupled with an Na-K ATPase-so glucose enhances d entry of K IN d cell..that's why d Rx of HYPERK..emia is:insulin+glucose!!...NaHCO3 only if there's metabolic acidosis-..b2agonists to promote Na-K ATPase function too..
:wink:
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