GMS 6401 COMPREHENSIVE ANSWERS AND
QUESTIONS SET A+
✔✔An abrupt increase in arterial blood pressure (renal perfusion pressure) by 20 mmHg
above normal increases GFR which causes an increase in Na excretion - ✔✔F. Renal
autoregulation prevents an increased GFR when BP increases within the autoregulatory
range. Na excretion does increase but this is due to direct proximal tubular inhibition
ofNa reabsorption
✔✔In the normal person renal Na handling accurately maintains plasma volume within a
narrow range - ✔✔T. When environmental conditions are normal, the normal kidney has
such a range of mechanisms that control Na excretion, that the plasma volume remains
euvolemic
✔✔When blood loss during an acute hemorrhage reaches 10.5 %, death occurs due to
a massive fall in BP and loss of organ perfusion, leading to multi organ failure - ✔✔F.
With 10.5% hemorrhage BP is maintained close to normal and organ perfusion is
marinated, due to the combined actions of the activated RAAS, SNS and release of
vasoconstrictor levels of ADH (AVP). Hemorrhagic shock and organ failure usually
occurs with > 25%blood loss
✔✔As long as the total ECF volume is maintained, plasma volume is normal. - ✔✔F.
When fluid shifts from the vascular space into the interstitium (as occurs in septic shock;
nephrotic syndrome: liver cirrhosis), the circulation becomes "underfilled" despite an
absolute increase in ECFV
✔✔Everyone with salt sensitive hypertension also has severe edema. - ✔✔F. There is
an initial volume expansion but once BP increases sufficiently to active the blunted
pressure natriuresis, volume decreases. At the same time, to prevent large increases in
organ perfusion, the blood vessels constrict, raising total peripheral resistance, which
maintains the high BP, despite almost complete volume restoration.
, ✔✔In advanced chronic kidney disease, edema is often seen. - ✔✔T. the failing kidney
cannot maintain Na balance, and very strict dietary Na restriction is necessary to
prevent edema.
✔✔About 95% of the Ca in the body is present in the extracellular fluid. - ✔✔F. ~99%
isintracellular, a lot of it is in bone
✔✔Calcium excretion is controlled mainly by how much is reabsorbed in the TALH and
distal tubule - ✔✔T. These are the sites of regulation, mainly by Parathyroid hormone,
PTH
✔✔Thiazide diuretics are prescribed for people with Ca-forming kidney stones. - ✔✔T.
Thiazidespromote proximal and TALH Na reabsorption (secondary to Na loss by
inhibiting distal tubule NCC) which promotes secondary Ca reabsorption in these sites.
This lowers the delivery of Ca to the distal tubule and collecting duct, which inhibits
stone formation
✔✔Most of the filtered phosphate is reabsorbed in the collecting duct. - ✔✔F. ~80% of
thefiltered phosphate is reabsorbed in the proximal tubule. There is little or no
phosphatereabsorption in the collecting duct
✔✔Increased parathyroid hormone (PTH) leads to increased phosphate excretion. -
✔✔T. PTHinhibits proximal PO4 reabsorption
✔✔When extracellular (plasma) K increases, skeletal muscle becomes more excitable. -
✔✔T .The resting membrane potential becomes less negative (due to a decreased
diffusion gradient for K, out of the cell).
✔✔The renal excretion of K is dependent on how much K is filtered. - ✔✔F. Most of the
filtered K is reabsorbed. The normal determinant of K excretion is the amount secreted
in to the collecting duct
✔✔A fall in collecting duct Na reabsorption will increase K excretion. - ✔✔F. Increased
CD Na reabsorption (by ENaC) increases the lumen -ve transepithelial potential
difference (PD)which increases secretion of K+.
✔✔Aldosterone increases renal K excretion. - ✔✔T. Aldo promotes K+ entry into cells
bystimulation of Na+-K+ ATPase; opens luminal membrane K channel and increases
lumennegativity by stimulating ENaC
✔✔When plasma H+ conc increases (pH falls), the plasma conc of K+ falls. - ✔✔F.
Some H+enters the cell for buffering (see later) and K moves out in exchange, so
plasma K increases
QUESTIONS SET A+
✔✔An abrupt increase in arterial blood pressure (renal perfusion pressure) by 20 mmHg
above normal increases GFR which causes an increase in Na excretion - ✔✔F. Renal
autoregulation prevents an increased GFR when BP increases within the autoregulatory
range. Na excretion does increase but this is due to direct proximal tubular inhibition
ofNa reabsorption
✔✔In the normal person renal Na handling accurately maintains plasma volume within a
narrow range - ✔✔T. When environmental conditions are normal, the normal kidney has
such a range of mechanisms that control Na excretion, that the plasma volume remains
euvolemic
✔✔When blood loss during an acute hemorrhage reaches 10.5 %, death occurs due to
a massive fall in BP and loss of organ perfusion, leading to multi organ failure - ✔✔F.
With 10.5% hemorrhage BP is maintained close to normal and organ perfusion is
marinated, due to the combined actions of the activated RAAS, SNS and release of
vasoconstrictor levels of ADH (AVP). Hemorrhagic shock and organ failure usually
occurs with > 25%blood loss
✔✔As long as the total ECF volume is maintained, plasma volume is normal. - ✔✔F.
When fluid shifts from the vascular space into the interstitium (as occurs in septic shock;
nephrotic syndrome: liver cirrhosis), the circulation becomes "underfilled" despite an
absolute increase in ECFV
✔✔Everyone with salt sensitive hypertension also has severe edema. - ✔✔F. There is
an initial volume expansion but once BP increases sufficiently to active the blunted
pressure natriuresis, volume decreases. At the same time, to prevent large increases in
organ perfusion, the blood vessels constrict, raising total peripheral resistance, which
maintains the high BP, despite almost complete volume restoration.
, ✔✔In advanced chronic kidney disease, edema is often seen. - ✔✔T. the failing kidney
cannot maintain Na balance, and very strict dietary Na restriction is necessary to
prevent edema.
✔✔About 95% of the Ca in the body is present in the extracellular fluid. - ✔✔F. ~99%
isintracellular, a lot of it is in bone
✔✔Calcium excretion is controlled mainly by how much is reabsorbed in the TALH and
distal tubule - ✔✔T. These are the sites of regulation, mainly by Parathyroid hormone,
PTH
✔✔Thiazide diuretics are prescribed for people with Ca-forming kidney stones. - ✔✔T.
Thiazidespromote proximal and TALH Na reabsorption (secondary to Na loss by
inhibiting distal tubule NCC) which promotes secondary Ca reabsorption in these sites.
This lowers the delivery of Ca to the distal tubule and collecting duct, which inhibits
stone formation
✔✔Most of the filtered phosphate is reabsorbed in the collecting duct. - ✔✔F. ~80% of
thefiltered phosphate is reabsorbed in the proximal tubule. There is little or no
phosphatereabsorption in the collecting duct
✔✔Increased parathyroid hormone (PTH) leads to increased phosphate excretion. -
✔✔T. PTHinhibits proximal PO4 reabsorption
✔✔When extracellular (plasma) K increases, skeletal muscle becomes more excitable. -
✔✔T .The resting membrane potential becomes less negative (due to a decreased
diffusion gradient for K, out of the cell).
✔✔The renal excretion of K is dependent on how much K is filtered. - ✔✔F. Most of the
filtered K is reabsorbed. The normal determinant of K excretion is the amount secreted
in to the collecting duct
✔✔A fall in collecting duct Na reabsorption will increase K excretion. - ✔✔F. Increased
CD Na reabsorption (by ENaC) increases the lumen -ve transepithelial potential
difference (PD)which increases secretion of K+.
✔✔Aldosterone increases renal K excretion. - ✔✔T. Aldo promotes K+ entry into cells
bystimulation of Na+-K+ ATPase; opens luminal membrane K channel and increases
lumennegativity by stimulating ENaC
✔✔When plasma H+ conc increases (pH falls), the plasma conc of K+ falls. - ✔✔F.
Some H+enters the cell for buffering (see later) and K moves out in exchange, so
plasma K increases
