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Discussion Starter · #1 ·
A 45 year old smoker, non-alcoholic on phenytoin develops gradually increasing paleness and dyspnea with exertion. Neurological examination is normal. The patient appears to have an inflamed tongue. His blood workup shows an MCV of 110. What is the most likely mechanism contributing to this patient's clinical complains:

A-Inhibition of monoglutamate absorption
B-Increased gastric acidity
C-Inhibition of intestinal conjugase polyglutamate
D-Decreased vegetable intake
E-Decreased folate absorption in the large bowel
 

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C... inhibition of intestinal conjugase which converts polyglutamate into monoglutamate. folate in food is present in the form of polyglutamate.. decreased monoglutamate leads to folate deficiency.
 

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Discussion Starter · #3 ·
yup veeeeery goood :) correct answer is C

If the patient was an alcoholic or on OCP the answer would have been A
 

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Discussion Starter · #5 ·
Ok, in order to answer you have to know the physiology of folate absorption. Also you have to know that this patient has Macrocytic anemia (from the symptoms and MCV) due to folate (as there are no neurological symptoms)

Folate is found in plants as "Polyglutamate PG". PG can't be absorbed in the bowel in this form (Just like sugars have to be broken down to be absorbed in the bowel).
So, they have to be broken down in the BOWEL into "Monoglutamate MG". MG form CAN be absorbed in the jejunum to be turned into folate in the intestinal cells.

Phenytoin acts by inhibiting the breakdown of PG by inhibiting "Intestinal conjugase polyglutamate" (the enz. that breaks it down)

As I also mentioned earlier. The second step (which is absorption of MG after the breakdown process) is inhibited by Alcohol and OCPs.

Choice B- would be correct in the case of Zollinger Ellison Syndrome.
Choice E- Incorrect as folate is absorbed in the jejunum which is part of the small bowel NOT the large bowel.

Don't worry about this question as I made it up. The info is in Goljan and it's in the blue prints as high yield. Didn't see it in FA.
 

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