Free 150 question--answer clarification

[ChessMaster3000]

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I had an issue with one of the Free 150 items. Basically, increase renal efferent constriction with a drug. Afferent tone remains the same, cardiac output remains the same...what happens to GFR, FF, and renal blood flow?

The answer given is gfr down, ff up, RBF down. I would be all over this question normally, seems easy enough. EXCEPT--if NBME is considering that the total RBF to go down, wouldn't GFR go down overall? I get that because the efferent is selectively constricted, FF goes up. But I dont see how RBF could go down without the GFR going down. Does anyone agree?

 

[alicealicealice]

But I dont see how RBF could go down without the GFR going down. Does anyone agree?​

FF=GFR/RPF
Think of FF as being dependent on GFR and RPF instead of the other way around. Increase renal efferent arteriole constriction is the same thing that an ATII does.
What I don't get is why they said that the GFR goes down if CO is the same.
My prediction would be
RPF Down-->GFR Up (increased hydrostatic pressure into bowmans capsule due to decreased flow through efferent arteriole)-->FF Up

Unless this patient was already very hypovolemic. In which case Both RPF and GFR go down, but RPF goes down more, so FF goes Up. End result:
RPF Double Down-->GFR down-->FF Up​

 

[alicealicealice]

Check out UW Qid 1017:

It explains how you get an increase in GFR and FF with efferent arteriolar constriction due to increase hydrostatic pressure up to a certain point, at which point the oncotic pressure from the unfilterable plasma proteins begins to dominate over the hydrostatic pressure. Therefore, GFR starts to drop but you still get an overall increase in FF because RBF is decreased even more.
And just as a side note, afferent constriction = equal decrease in GFR and RPF = No change in FF. Which is why for me at least thinking of FF as the most dependent variable and setting up the equation that way is helpful

 

[ChessMaster3000]

Check out UW Qid 1017:

It explains how you get an increase in GFR and FF with efferent arteriolar constriction due to increase hydrostatic pressure up to a certain point, at which point the oncotic pressure from the unfilterable plasma proteins begins to dominate over the hydrostatic pressure. Therefore, GFR starts to drop but you still get an overall increase in FF because RBF is decreased even more.
And just as a side note, afferent constriction = equal decrease in GFR and RPF = No change in FF. Which is why for me at least thinking of FF as the most dependent variable and setting up the equation that way is helpful

wow that was the perfect UW question for my question. it's a stretch to know how much the efferent constriction affected the gfr--that's an unfair question

 

[acciddropping]

What would be the Hct level in this pt? up or down?

 

[acciddropping]

Also, what do you expect for GFR, RPF and FF when there's a very severe constriction of efferent arteriole?

 

[ChessMaster3000]

Also, what do you expect for GFR, RPF and FF when there's a very severe constriction of efferent arteriole?

thats what we were discussing--a VERY SEVERE constriction would have the gfr go down. but a moderate constriction would have it go up. RPF is always down and FF is always up w efferent constriction. As for the hematocrit, its hard to evaluate that because its volume dependent. if their gfr is going up, then they would be getting dehydrated so their hct is going up, and vice versa.

 

[acciddropping]

thats what we were discussing--a VERY SEVERE constriction would have the gfr go down. but a moderate constriction would have it go up. RPF is always down and FF is always up w efferent constriction. As for the hematocrit, its hard to evaluate that because its volume dependent. if their gfr is going up, then they would be getting dehydrated so their hct is going up, and vice versa.

Thanks! I was thinking if Hct has an effect on FF but not relevant for step1.

But still I am not clear on why FF is up - how low is GFR relative to RPF?

 

[alicealicealice]

FF= GFR/RPF
FF is always up because the RPF is always decreased more relative to the GFR
This makes sense intuitively because the GFR goes up in the beginning when you reduce RPF due to increased hydrostatic pressure.
It is only when you are slowing the blood down so much that almost everything that can be physically filtered into Bowmans capsule is. Then you are left with a very lower plasma volume with lots of non filterable molecules in the glomerular capillary, and the resultant ONCOTIC pressure starts to dominate, drawing some fo teh filtrate back into the capillary side.
As an aside Hct is related in terms of step 1 in the sense that RPF = RBF(1-Hct)

 

[acciddropping]

FF= GFR/RPF
FF is always up because the RPF is always decreased more relative to the GFR
This makes sense intuitively because the GFR goes up in the beginning when you reduce RPF due to increased hydrostatic pressure.
It is only when you are slowing the blood down so much that almost everything that can be physically filtered into Bowmans capsule is. Then you are left with a very lower plasma volume with lots of non filterable molecules in the glomerular capillary, and the resultant ONCOTIC pressure starts to dominate, drawing some fo teh filtrate back into the capillary side.
As an aside Hct is related in terms of step 1 in the sense that RPF = RBF(1-Hct)

Can you explain how increased oncotic pressure results in increased FF? I can see how oncotic pressure starts to dominate. The way I understand oncotic pressure is that it keeps the blood together, so losing that pressure seen in proteinuria, water will leave blood into interstitium and cause swelling/ pitting edema.

So, increased oncotic pressure decreases GFR, right? but I cannot figure out why FF is increased. Thanks.