USMLE Cystic Fibrosis: Transepithelial Potential Difference

[justadream]

FA says that "increased Na+ reabsorption causes more negative transepithelial potential difference".

Can someone explain this (or have a good diagram/figure to show this)?

I believe there is an important distinction between transepithelital potential difference and transmembrane potential difference. I think that in CF, transmembrane potential difference would be more positive.


But how does this translate to the transepithelial potential difference being more negative?

---

Members don't see this ad.

 

[justadream]

Bump.

 

[BurghStudent]

Seems like less Na+ in the lumen as compared to the interstitial fluid causes a more negative potential. This might be helpful:

https://forums.studentdoctor.net/threads/transepithelial-potential-difference-in-cf.916227/

 

[justadream]

Seems like less Na+ in the lumen as compared to the interstitial fluid causes a more negative potential. This might be helpful:

https://forums.studentdoctor.net/threads/transepithelial-potential-difference-in-cf.916227/

Thanks for the reply!

I actually read that before I posted this thread but I'm not sure if I understand what is being said.

They key answer was:

The NPD test is measuring the charge on the luminal surface. The increase in sodium resorption results in a loss of positive valences in the bronchial lumen and thus a more negative difference. In patients with normally functioning CFTR channels, the sodium ions stay on the luminal surface, increasing the positive charge and thus decreasing the potential difference.

After some research, I believe the transepithelial potential difference is the difference between the lumen and blood (see setup below):

Lumen || Cell || Blood (or interstitial fluid? not sure)


So it's basically saying that if the cell reabsorbs more Na+, less Na+ is in the lumen. Thus, lumen becomes more negative relative to the blood (transepithelial potential difference becomes more negative).

However, if we were looking at transmembrane potential difference (between lumen and cell), in cystic fibrosis the greater reabsorption of Na+ would lead to a more positive transmembrane potential?

Am I understanding this correctly?

 

[PumpkinKing]

Not sure about your question but I had a similar one about CF.

Incr [Cl-]i.c. leads to incr [Na+]i.c. and [H20]i.c.

How does this eventually translate to contraction alkalosis? I'd think it had to do with aldosterone, but i couldn't find a concrete answer anywhere.

 

[justadream]

Not sure about your question but I had a similar one about CF.

Incr [Cl-]i.c. leads to incr [Na+]i.c. and [H20]i.c.

How does this eventually translate to contraction alkalosis? I'd think it had to do with aldosterone, but i couldn't find a concrete answer anywhere.

I might be wrong but I think it's something like this:
Excessive loss of fluid because Cl- in sweat cannot be reabsorbed (so H2O and Na+ follow it) ==> renin ==> angiotensin II ==> increased Na+/H+ exchange at PCT which leads to increased bicarbonate reabsorption* ==> alkalosis

*"Increases in angiotensin II cause increased Na+-H+ exchange in the proximal tubule and increased HCO3− (bicarbonate) reabsorption in the proximal tubule due to increased luminal H+" from Wikipedia - https://en.wikipedia.org/wiki/Contraction_alkalosis

I'm not sure why increased luminal H+ leads to increased bicarbonate reabsorption though.