why do we give Loop diuretics for the management of SIADH/ hyponatremia and give Thiazide for Nephrogenic DI/hypernatremia?
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Diuretics
- Thread starter zenna
- Start date
why do we give Loop diuretics for the management of SIADH/ hyponatremia and give Thiazide for Nephrogenic DI/hypernatremia?
Yes, why would anyone give diuretics to a hyponatremic patient? They themselves cause hyponatremia after all! Loop diuretics are used in hypervolemic hyponatremia patients, where the problem is the excess of H2O (rather than a lack of Na+). Loop diuretics promote loss of H20 in excess of Na+, therefore there's a net loss of free water (cH2O).
In hypernatremia, the problem is water loss. Therefore, one of the goals of the treatment is to minimize the loss of water in urine. It seems contradictory that an agent that is -by definition- causes water loss (diuretic) can be used in a situation where the main objective is the gain of water. Thiazides are used in DI, because they they reduce plasma volume (their main effect) > which caused GFR to decrease > reabsorption of Na and H20 from proximal tubule is increased > less fluid arrives to diluting distal segments (where the pathology is), which decreases the amount of H20 lost in the urine.
Thank you so much, you are the same person who replied for my "Na" escape ?Do you also know why there is increased obstruction in HOCM when digitalis is given or when we increase contractility why is it bad for HOCM( hypertrophic obstructive cardiomyopathy)?
Thank you so much, you are the same person who replied for my "Na" escape ?Do you also know why there is increased obstruction in HOCM when digitalis is given or when we increase contractility why is it bad for HOCM( hypertrophic obstructive cardiomyopathy)?
Yes, I am the same person 🙂
In HOCM, the problem lies within the hypertrophied septum closing down the left ventricle outflow tract. This narrowing creates a pressure gradient. Think of it like a water hose: if you were to put your thumb over the end of the hose, water would come out with more pressure. However, this alone is not what produces the obstruction. Due to this pressure gradient, mitral valve moves towards the left ventricular outflow tract and closes it during systole ("systolic anterior movement of mitral valve"). This movement of the mitral valve is what produces the obstruction.
Therefore, anything that increases the gradient would cause obstruction to increase and vice versa. So what would happen to the pressure gradient if contractility of the heart were to increase. Or think of it this way: what would happen if you were to push the end of the water hose with more force? Water would come out with even more pressure. Therefore, contractility will increase the pressure gradient, which will increase the obstruction.
So giving digoxin to a patient with HOCM will increase the obstruction.
I don't know how many times I will be thanking you but thank you once again🙂.
Do you know why NSAIDs are given for nephrogenic DI, do NSAIDs have any relationship with ADH? Or is it inhibition of PGs that is utilized for treating NI if so how😕?
Do you know why NSAIDs are given for nephrogenic DI, do NSAIDs have any relationship with ADH? Or is it inhibition of PGs that is utilized for treating NI if so how😕?
I don't know how many times I will be thanking you but thank you once again🙂.
Do you know why NSAIDs are given for nephrogenic DI, do NSAIDs have any relationship with ADH? Or is it inhibition of PGs that is utilized for treating NI if so how😕?
Like you've written above, NSAIDs inhibit synthesis of PGs. Normally, PGE2 produces vasodilation of afferent arterioles. Because PGE2 synthesis is inhibited by NSAIDs, vasolation of afferent arterioles is decreased, which in turn is manifested as decreased GFR. The rest is similar to thiazides: A decrease in GFR will increase proximal tubule Na+ and H2O absorption and ultimately there will be less water to lose.
NSAIDs have no direct relationship with ADH.
Fuzuli, I am confused again about the Thiazides for hypernatremia. Thiazides are supposed to act on the distal tubule and how do they reduce the plama volume so the more H2o and Na is reabsorbed in the proximal tubule?
Fuzuli, I am confused again about the Thiazides for hypernatremia. Thiazides are supposed to act on the distal tubule and how do they reduce the plama volume so the more H2o and Na is reabsorbed in the proximal tubule?
Yes, that's true. Like I've written above, when plasma volume is reduced, GFR is reduced as well. Imagine the proximal tubule as a man with a standard-size bucket trying to take out the water in his basement, which comes from a broken pipe. Normally, he would have been able to flush all the water down his drain, but the drain is clogged and he can't access the drain. But some water can flow down the drain. If I were to increase the water flow to his house, what would happen (apart from an angry man)? He would be less able to remove water from his basement and water would continue to build up in his basement.
But if I were to lower the water flow to his house, then he would be able to carry out more water. Since there would be less water in the basement, the clogged drain can handle it better, compared to the scenario above.
However, the best way to solve his problem is still to patch the broken pipe 🙂
Hope this analogy helps.
