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Thread: Osmolarity Q

  1. #1
    GFLIP's Avatar
    GFLIP is offline Senior Member 510 points
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    Osmolarity Q

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    50 yo male patient with hyponatremia and hyperkalemia was ordered by his nephrologist to follow a fluid restriction. After 12 hours of fluid restriction, urine became concentrated until urine osmolarity of 900 mOsm/L was reached. Hyponatremia got worse. Hyponatremia due to:

    a. SIADH
    b. central diabetes insipidus
    c. nephrogenic diabetes insipidus
    d. psychogenic polydipsia





    PS: I know the answer but i won't post just yet.
    PSS: Someone who knows the answer too.... why is there hyperkalemia???

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    unknownunknown is offline Member 510 points
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    I think the answer would be nephro diabetes inspidis. There is hyperkalemia because there is no excretion of potassium, just as there is hyponatremia because of no reabsorption of sodium.

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    Anisha2939 is offline Junior Member 510 points
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    I think the answer wud b (A) - SIADH
    b/c in SIADH u produce low amounts of concentrated urine, thus causing hyponatremia....and since there's no reabsorption of sodium, potassium is not secreted bak in the collecting ducts, thus causing hyperkalemia.

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    navpreet is offline Member 510 points
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    it is SIADH,
    GFLIP can u please explain hyperkalemia.?

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    GFLIP's Avatar
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    the answer is A, but I can't explain the hyperkalmia... that's kinda why I asked someone else to explain.

    this is a question that I don't get...
    Last edited by GFLIP; 02-14-2007 at 12:43 AM.

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    Papermate's Avatar
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    I am going to try to explain, but this may be a misconception because I have read many in many books before about SIADH and this is the first time I see a case in which hyperkalemia is present, but again you should read my analysis and only that, because I am not sure about this, maybe I don't undestand the whole process and I am just working from a part of the process or maybe the question is wrong and we are just analysing a misconception of the author.
    Well, the only explanation I can see for the hyperkalemia is that SIADH by causing water retention(which is the cause of the hyponatremia) expands the ECF Vokume, as a regulatory mechanism this suppresses the renin-angiotensin-aldosterone system and increases ANP secretion, this maintains the normal volume in SIADH so this patients have euvolemic hyponatremia. Now, as a side effect of this regulatory mechanisms hype kalemia may occur since aldosterone normally causes secretion of K+, and due to the suppssion the the renin-ang-ald system the patient may retain the potassium.
    Another possible mechanism I think could be a shift from the intracellular to the exacellular compart as may occur in patients with cerebral edema in SIADH, the hyponatremia causes initially movement of fluid from the ECF to the ICF this cases brain edema and the characteristic neurologic manifestations of SIADH, now, as a compensatory mechanysm there is movement of osmoles from the ICF to the ECF causin depletion of intracellular osmoles including potassium, this in turn may cause hyperkalemia.

    These are my explanations, I looked over several books includig pathophysiology books and none of them mentioned hyperkalemia as a clinical manifestation of SIADH so as I said, maybe we are just analysing a misconception stated in the question. Ot would be helpful if someone confirm that SIADH may present with high K+ levels, if so please post the url (if is in a website) or book name with pages.

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    Papermate's Avatar
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    I just read in Harrison's that potassium level is normal in SIADH. I wanted to add that a hypoosmolality state may lead to hypokalemia because potassium goes with water in the initial osmotic movement of water from EFC to ICF compartment, so this may compensate for the potassium retention that is caused by suppression of renin caused by volume expanssion. And I also want to be clear in that the movement of osmoles from ICF to EFC that I mentioned above occurs basically in the brain as the only compensatory mechanism for the brain edema, this in fact PART of the postulated mechanism for the so famous central pontine myelinolysis that occurs when you try to correct the hyponatremia to fast.
    So, in conclusion, K+ is normal in SIADH, just as bicarbonate and H+ are also normal (in fact hyponatremia+hyperkalemia+metabolic acidosis may suggest an adrenal origin problem). Although there may be K+ retention by the kidney, I suppose that the hypoosmolality corrects that hyperkalemia by inducing hypokalemia so at the end K+ levels are normal. This may be a mistake or a MISCONCEPTION of the person that created the question. Be careful, I have found many questions, especially in physiology, with this kind of mistakes that may give you bad information.

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    MDiva's Avatar
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    GFLIP, where is this question from? To address both hyponatremia and hyperkalemia, I would consider adrenal gland insufficiency. Also, potassium-sparing diuretics would cause the clinical picture, wouldn't it?

    Thanks for the explanations, Papermate, good stuff.

    Of all the given choices, A makes the most sense, ignoring the hyperkalemia. Is this what Kaplan refers to as a "distractor"? Focusing on the part where even with fluid restriction, the pt remained hyponatremic points to SIADH.
    Last edited by MDiva; 03-06-2007 at 01:24 PM. Reason: i no spell good
    I used to pray and pray for a bike and never got one. Later I learned that God doesn't work that way... so I went out and stole a bike and asked God for forgiveness.

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