I posted this on the official NBME 15 thread but I guess it's not active anymore. So I'm posting it here. If anyone wants to have a discussion...
Q1. 6 year girl with known renal tubular acidosis with "a defect in renal ammoniagenesis suspected". The question is "the source of ammonia production in THIS patient".
Would someone like to discuss this? I know the answer for this is glutamine but I have my doubts. Glutamine is deaminated by glutaminase in the kidney to produce glutamate + NH3. The ammonia is then used to buffer protons for acid excretion. Now in context to this question there is a "defect in renal ammoniagenesis" so I'm thinking defective glutaminase. How can glutamine serve to be the source of ammonia then? "Glutamate" would have been a much better answer I reckon.
Q2. 50 year old man with fatigue. pO2=96 mm Hg, pCO2=30 mm Hg, arterial O2 'content' is significantly low and so is mixed venous O2 content. The answer is obviously anemia as the oxygen content is low inspite of fairly normal pO2. Can someone explain the low pCO2? Or are they just playfully messing with our already traumatized brains?
Over-thinking cost me these two. I hope the questions could be a bit more accurate and a bit less redundant in the real exam. I didn't like this NBME so much.
Q1. 6 year girl with known renal tubular acidosis with "a defect in renal ammoniagenesis suspected". The question is "the source of ammonia production in THIS patient".
Would someone like to discuss this? I know the answer for this is glutamine but I have my doubts. Glutamine is deaminated by glutaminase in the kidney to produce glutamate + NH3. The ammonia is then used to buffer protons for acid excretion. Now in context to this question there is a "defect in renal ammoniagenesis" so I'm thinking defective glutaminase. How can glutamine serve to be the source of ammonia then? "Glutamate" would have been a much better answer I reckon.
Q2. 50 year old man with fatigue. pO2=96 mm Hg, pCO2=30 mm Hg, arterial O2 'content' is significantly low and so is mixed venous O2 content. The answer is obviously anemia as the oxygen content is low inspite of fairly normal pO2. Can someone explain the low pCO2? Or are they just playfully messing with our already traumatized brains?
Over-thinking cost me these two. I hope the questions could be a bit more accurate and a bit less redundant in the real exam. I didn't like this NBME so much.