CLINICAL CASES
389
C O M P R E H E N SIO N Q U E ST IO N S
[42.1] A patient with a tentative diagnosis of cobalamin deficiency is await-
ing a comprehensive blood analysis. Which of the following perturba-
tions would NOT fit with the putative diagnosis?
A. Elevated levels of methylmalonic acid
B. Elevated levels of propionic acid
C. Elevated levels ofpara-hydroxyphenylpyruvate
D. Decreased levels of erythrocytes
E. Elevated levels of megaloblasts
[42.2] In evaluating the case presented above your resident asks questions of
the role of cobalamin in metabolism. Which of the following state-
ments is true?
A. Cyanocobalamin is
the principal form of cobalamin used
physiologically
B. Cobalamin is equally active with an iron cofactor
C. Enterocytes produce an intrinsic factor required for uptake of
cobalamin in the gut
D. Cobalamin is transported in the blood to tissues by proteins named
transcobalamins
E. Cobalamin is active in its 3+ oxidation state
[42.3] Megaloblastic anemia has two most likely causes, deficiency of folate
and deficiency of cobalamin. Often treatment of patients with cobal-
amin deficiency improves in terms of their hematologic features with
treatment with folate but not in their neurologic symptoms. What is the
most likely explanation for this explanation?
A. Cobalamin deficiencies are not serious
B. Excess folate blunts the trapping of folate as A5-methyltetrahydrofolate
C. Folate in high concentrations can serve as cofactor for the conver-
sion of homocysteine to methionine
D. Excess folate directly inhibits the destruction of red blood cells
E. Excess folate stimulates erythropoietic tissues to synthesize cobal-
amin in situ
previous page 403 Case Files   Biochemistry read online next page 405 Case Files   Biochemistry read online Home Toggle text on/off