JustSomePreMed

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I'm having a brain fart here combined with conflicting information.

Do loop diuretics result in a loss of hyperosmotic or hypoosomtic loss of fluid? Our lecture notes say that loop diuretics cause hypovolemic hypernatremia by way of losing more water than sodium.

Goljan RR Path p. 57 says you'd lose more sodium than water and thus be losing a hypertonic solution.

I don't know why I can't seem to sort this out correctly in my head, but the differing info isn't helping.
 

devilpup

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I'm having a brain fart here combined with conflicting information.

Do loop diuretics result in a loss of hyperosmotic or hypoosomtic loss of fluid? Our lecture notes say that loop diuretics cause hypovolemic hypernatremia by way of losing more water than sodium.

Goljan RR Path p. 57 says you'd lose more sodium than water and thus be losing a hypertonic solution.

I don't know why I can't seem to sort this out correctly in my head, but the differing info isn't helping.
The loop diuretic would cause hypovolemic hyponatremia, the mechanism involves a decrease in both TBW and sodium, but with a relatively greater decrease in sodium. Goljan is correct because you're loosing more sodium relative to water --> hence, hyperosmotic loss if you wanna call it that.

Normally when you are hyponatremic due to fluid loss (by causes such as sweat/renal/GI/ pulmonary/blood loss or third spacing) the body attempts to minimize sodium loss by increasing Na reabsorption in the proximal and distal tubules, hence Urinary Na< 20 mmol/L, but when the hypovolemia is due to diuretics (specifically) the Urinary Na>20mmol/L because its diuretic induced. By the way, in addition to diuretics, mineralocorticoid insufficiency and cerebral salt wasting would also cause hypovolemic hyponatremia with a Urinary Na>20mol/L. Hence, "hyperosmotic loss."


The main point to remember is that diuretics can cause hypovolemic hyponatremia. Tx- discontinue diuretic and give normal saline.

Hope i didn't confuse you more...
 

ChubbyChaser

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Loop diuretics act on the Na+-K+-2Cl- symporter (cotransporter) in the thick ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption. This is achieved by competing for the Cl- binding site. Because magnesium and calcium reabsorption in the thick ascending limb is dependent on sodium and chloride concentrations (primarily on the recycling of the potassium due to the lack of the electropositive gradient generation), loop diuretics also inhibit their reabsorption. By disrupting the reabsorption of these ions, loop diuretics prevent the urine from becoming concentrated and disrupt the generation of a hypertonic renal medulla. Without such a concentrated medulla, water has less of an osmotic driving force to leave the collecting duct system, ultimately resulting in increased urine production. Loop diuretics cause an increase in the renal blood flow by this mechanism. This diuresis leaves less water to be reabsorbed into the blood, resulting in a decrease in blood volume.


Wiki says^
 

JustSomePreMed

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The loop diuretic would cause hypovolemic hyponatremia, the mechanism involves a decrease in both TBW and sodium, but with a relatively greater decrease in sodium. Goljan is correct because you're loosing more sodium relative to water --> hence, hyperosmotic loss if you wanna call it that.

Normally when you are hyponatremic due to fluid loss (by causes such as sweat/renal/GI/ pulmonary/blood loss or third spacing) the body attempts to minimize sodium loss by increasing Na reabsorption in the proximal and distal tubules, hence Urinary Na< 20 mmol/L, but when the hypovolemia is due to diuretics (specifically) the Urinary Na>20mmol/L because its diuretic induced. By the way, in addition to diuretics, mineralocorticoid insufficiency and cerebral salt wasting would also cause hypovolemic hyponatremia with a Urinary Na>20mol/L. Hence, "hyperosmotic loss."


The main point to remember is that diuretics can cause hypovolemic hyponatremia. Tx- discontinue diuretic and give normal saline.

Hope i didn't confuse you more...


Thanks for the reply. To confuse things even more, another of our lecturers made a big point of saying that Loop Diuretics = Isothenuria due to a loss of concentrating ability (loss of osmotic gradient in the medulla because you're not shuttling solutes through NaK2Cl).

Then we've got a clinician telling us the TAL is the only place where free water is generated, and a pathologist telling us the DCT is the only place where free water is generated (due to the impermeability of water and "high" solute permeability of both segments normally).

God I love med school.

Edit: Also, isn't sweating inducing hypERnatremia? (you're losing more water than salt). Hyponatremia would ensue if you only replaced the volume loss with pure water, correct?
 
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turkeyjerky

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Loop diuretics cause a diuresis of approximately 1/2 normal saline (thiazide diuretics uniquely cause excretion of hypertonic fluid). This is why they can be employed as ancillary treatment of euvolemic hyponatremia due to SIADH.

I don't think hypernatremia is a s/e of loop diuretics. They can cause hypOnatremia, though. How do they do this? Volume depletion leads to a non-osmotic stimulation of ADH release, causing reabsorption of whatever free water is possible. Hyponatremia is more prominent with thiazides, though, because the countercurrent exchange system in the medulla isn't f~cked up (thiazides induce hyponatremia both via direct excretion of hypertonic urine and volume depletion).

You're correct about sweating.