GMS 6401 ACTUAL FINALS ANSWERS AND
QUESTIONS SET A+
✔✔Moderate constriction of the afferent arteriole will lower RPF and increase
glomerular blood pressure (PGC) and there will be little change in GF. T/F - ✔✔F.
Constriction of the afferent arteriole lowers both RPF and PGC so GFR will definitely
fall. Constriction of the efferent arteriole does increase PGC (as well as lowering RPF)
and if the fall in RPF is small, there will be little net change in GFR because the
changes in RPF and PGC are offsetting
✔✔Renal vasoconstriction in response to an increase in renal perfusion pressure
(autoregulation) occurs exclusively at the efferent arteriole - ✔✔F. The afferent arteriole
constricts in response to an abrupt rise in BP, not the efferent. This allows both RPF
and PGC to be maintained constant, which leads to constancy of GFR
✔✔The peritubular capillaries have a high colloid osmotic (oncotic) pressure and a
lowhydrostatic (blood) pressure which favors tubular reabsorption. - ✔✔T. Due to the
protein concentration effect of filtration at the glomerulus and the fall in blood pressure
due to the efferent arteriole
✔✔An increase in renal metabolism is always accompanied by an increase in renal
oxygenextraction across the kidney (ie. An increased arterial - venous (A-V) oxygen
difference) - ✔✔F . Renal metabolism is linked to renal sodium reabsorption. An
increase in renal sodium reabsorption will occur when more sodium is filtered, due most
often to an increased RPF (and renal blood flow, RBF). Because an increased RBF
delivers more oxygen to the kidney there is no need to increase oxygen extraction, so
usually renal A-Voxygen difference doesn't change although absolute oxygen utilization
increases
✔✔Acute kidney injury involves a rapid loss of function (fall in GFR) due to falls in both
RPFand PGC - ✔✔True
, ✔✔During the development of chronic kidney disease the plasmas creatinine falls. -
✔✔F.Creatinine is removed from the body by glomerular filtration and excretion in the
urine. As GFR falls, plasma creatinine increases
✔✔Everywhere in the renal tubule, the Na-K ATPase is located on the luminal
membrane. - ✔✔F. It is only on the peritubular (outside) membrane because Na has to
be able to enter the luminal membrane for reabsorption
✔✔Less than 5% of the filtered Na is reabsorbed in the proximal tubule. - ✔✔F. ~65%
of the Nais reabsorbed proximally; this is the site of "bulk" reabsorption
✔✔The Na K 2Cl co-transporter (NKCC2) is the major Na transporter in the thick
ascending limb of the loop of Henle (TALH) - ✔✔T. The NHE3 (Na-H exchanger) plays
a minor role inTALH
✔✔Aldosterone stimulates proximal Na reabsorption. - ✔✔F. Aldosterone regulates
NCC and ENaC in the distal tubule and collecting duct
✔✔The diuretic Amiloride causes potassium wasting. - ✔✔F. Amiloride inhibits the
ENaC in collecting duct, which prevents K wasting. The upstream diuretics (lasix/TALH
and thiazide (distal tubule) cause K wasting by stimulating ENaC activity which indirectly
promotes K excretion.
✔✔When excess Na is retained in the body it leads to large increases in plasma Na and
nochange in blood volume - ✔✔F. Plasma Na does not change much (except under
pathological conditions) but the retained Na also causes expansion of the water in the
ECF to ECFV and plasma volume increase
✔✔The only regulation of total body sodium content is by the kidney which regulates
Naoutput - ✔✔True
✔✔Most people eat just enough Na each day to remain in balance. - ✔✔F. We all eat
Na that isgreatly in excess of our needs
✔✔We filter and reabsorb large amounts of Na each day. - ✔✔True
✔✔Most of the filtered Na (>90%) is reabsorbed in the distal tubule and collecting duct.
- ✔✔F.Together the proximal tubule (65%) and the TALH (25%) reabsorb ~ 90% of the
filtered Na.~ 9-9.5% of the filtered Na is reabsorbed in the distal tubule and collecting
duct
✔✔An increase in GFR leads to increase filtration and excretion of Na. - ✔✔True
QUESTIONS SET A+
✔✔Moderate constriction of the afferent arteriole will lower RPF and increase
glomerular blood pressure (PGC) and there will be little change in GF. T/F - ✔✔F.
Constriction of the afferent arteriole lowers both RPF and PGC so GFR will definitely
fall. Constriction of the efferent arteriole does increase PGC (as well as lowering RPF)
and if the fall in RPF is small, there will be little net change in GFR because the
changes in RPF and PGC are offsetting
✔✔Renal vasoconstriction in response to an increase in renal perfusion pressure
(autoregulation) occurs exclusively at the efferent arteriole - ✔✔F. The afferent arteriole
constricts in response to an abrupt rise in BP, not the efferent. This allows both RPF
and PGC to be maintained constant, which leads to constancy of GFR
✔✔The peritubular capillaries have a high colloid osmotic (oncotic) pressure and a
lowhydrostatic (blood) pressure which favors tubular reabsorption. - ✔✔T. Due to the
protein concentration effect of filtration at the glomerulus and the fall in blood pressure
due to the efferent arteriole
✔✔An increase in renal metabolism is always accompanied by an increase in renal
oxygenextraction across the kidney (ie. An increased arterial - venous (A-V) oxygen
difference) - ✔✔F . Renal metabolism is linked to renal sodium reabsorption. An
increase in renal sodium reabsorption will occur when more sodium is filtered, due most
often to an increased RPF (and renal blood flow, RBF). Because an increased RBF
delivers more oxygen to the kidney there is no need to increase oxygen extraction, so
usually renal A-Voxygen difference doesn't change although absolute oxygen utilization
increases
✔✔Acute kidney injury involves a rapid loss of function (fall in GFR) due to falls in both
RPFand PGC - ✔✔True
, ✔✔During the development of chronic kidney disease the plasmas creatinine falls. -
✔✔F.Creatinine is removed from the body by glomerular filtration and excretion in the
urine. As GFR falls, plasma creatinine increases
✔✔Everywhere in the renal tubule, the Na-K ATPase is located on the luminal
membrane. - ✔✔F. It is only on the peritubular (outside) membrane because Na has to
be able to enter the luminal membrane for reabsorption
✔✔Less than 5% of the filtered Na is reabsorbed in the proximal tubule. - ✔✔F. ~65%
of the Nais reabsorbed proximally; this is the site of "bulk" reabsorption
✔✔The Na K 2Cl co-transporter (NKCC2) is the major Na transporter in the thick
ascending limb of the loop of Henle (TALH) - ✔✔T. The NHE3 (Na-H exchanger) plays
a minor role inTALH
✔✔Aldosterone stimulates proximal Na reabsorption. - ✔✔F. Aldosterone regulates
NCC and ENaC in the distal tubule and collecting duct
✔✔The diuretic Amiloride causes potassium wasting. - ✔✔F. Amiloride inhibits the
ENaC in collecting duct, which prevents K wasting. The upstream diuretics (lasix/TALH
and thiazide (distal tubule) cause K wasting by stimulating ENaC activity which indirectly
promotes K excretion.
✔✔When excess Na is retained in the body it leads to large increases in plasma Na and
nochange in blood volume - ✔✔F. Plasma Na does not change much (except under
pathological conditions) but the retained Na also causes expansion of the water in the
ECF to ECFV and plasma volume increase
✔✔The only regulation of total body sodium content is by the kidney which regulates
Naoutput - ✔✔True
✔✔Most people eat just enough Na each day to remain in balance. - ✔✔F. We all eat
Na that isgreatly in excess of our needs
✔✔We filter and reabsorb large amounts of Na each day. - ✔✔True
✔✔Most of the filtered Na (>90%) is reabsorbed in the distal tubule and collecting duct.
- ✔✔F.Together the proximal tubule (65%) and the TALH (25%) reabsorb ~ 90% of the
filtered Na.~ 9-9.5% of the filtered Na is reabsorbed in the distal tubule and collecting
duct
✔✔An increase in GFR leads to increase filtration and excretion of Na. - ✔✔True
