Q.1
Why are patients with eating disorders generally protected from nephrolithiasis?
A. Because the associated loss of muscle mass results in a low urinary urate excretion.
B. Because the associated ECF volume depletion results in a low urinary calcium excretion.
C. Because the associated metabolic alkalosis results in a low urinary oxalate excretion.
D. Because the associated hypokalemia results in a high urine pH.
Q.2
Patients with eating disorders frequently develop hypokalemia from vomiting or laxative abuse. Hypokalemia promotes stone formation mainly by:
A. Inducing metabolic alkalosis and increasing urinary trivalent citrate.
B. Promoting growth and agglomeration of calcium crystals.
C. Inducing intracellular acidosis and increasing citrate uptake by proximal tubular cells.
D. Decreasing activity of the NaDC-1 co-transporter and increasing urinary oxalate excretion.
Q.3
Which of the following pathogenic mechanisms has not been implicated in the increased ammoniagenesis associated with hypokalemia?
A. Increased expression of the basolateral glutamine transporter (SN1).
B. Increased expression of the Na+-K+-2Cl- cotransporter (NKCC2).
C. Increased expression of the enzymes glutaminase, glutamate dehydrogenase, and phosphoenolpyruvate carboxykinase.
D. Increased expression of the Rh glycoproteins.
Q.4
Which of the following is not a consequence of hypokalemia?
A. Decreased renin and angiotensin II levels.
B. Decreased aquaporin-2 expression.
C. Increased bicarbonate reabsorption in the proximal tubule.
D. Central polydipsia.
Q.5
Which of the following pathogenic mechanisms has not been implicated in the development of hypokalemic nephropathy?
A. Increased ammoniagenesis.
B. Abnormalities in the expression of multiple growth factors (ie, IGF-I).
C. Upregulation of osteopontin expression.
D. Decreased angiotensin II levels.