Answer Key

Answer Key
Dr. Manning
1. C (They are epimers, since they differ in the non-hemiacetal carbon; also it is at the carbon 4
position, not 3)
2. E (There are 2 glucose residues so you eliminate A & D; You know it’s a reducing sugar since a
free anomeric carbon is present so you eliminate B & C; Lactose consists of Galactose & glucose
and F says it contains both Glucose Residues so that is incorrect. Cellobiose is correct since it is
verbatim definition).
3. A (Phosphofructokinase is the rate limiting step. AMP stimulates it)
4. B (The metabolism scheme goes from ethanol being oxidized to acetaldehyde to acetic acid)
5. C (ribulose 5-phosphate is already converted to xylulose 5-P & ribose 5-P before transketolase
comes into play).
6. B(Glucanolactase acts on 6-phosphoglucanolactone to produce 6-phosphogluconate)
7. D (Lack of fructokinase and buildup of fructose is characteristic of essential fructose uria)
8. B (From objectives, it says we lack L-gulonolacetone (oxidase) so we cannot synthesize vitamin
C. The other answers were all there to throw you off)
9. B (Biotin participates in carboxylation reactions. The reaction in answer B is not one of the 3
carboxylation reactions listed by Dr. Manning).
Dr. Maltese
A (Straight from page 33)
C (Straight from page 43)
C (Straight from page 122)
B (ATP Citrate Lyase converts Citrate to OAA & Acetyl CoA in cytoplasm; page 130)
D (Page 287)
A (7 alpha hydroxylase affects formation of bile salts. It is the rate limiting step in bile salt
formation. Taurocholate and Glycocholate would both be affected sincethey are bile salts)
B (page 197)
D (When you lack energy, you have lots of AMP. You don’t have any energy rich ATP. Thus
energy poor AMP activates the AMP activated protein kinase, which puts a phosphate group on
Acetyl CoA carboxylase preventing fatty acid synthesis)
D (This is a reasonable clinical vignette since I just make it look confusing until the end where it
says ‘a lack of glucoerebrosidase’ which is directly on page 224 for Gaucher’s Disease. The
disease in answer choice B was made up. Answer choice A would be a lack of a
sphingomyelinase enzyme. Answer choice C was a deficiency in an enzyme in the salvage
pathways of nucleobases
B (This is found on page 231 verbatim from the text. Answer choice A relates to Aspirin. Answer
C & D were made up).
B (This is found on page 300. Keep in mind the key word ‘immediate’ product, meaning the first
product after that enzyme would do its job, which is pregnenolone.
21. C (It is a deoxyribose. Also guanine is the only purine (not including hypoxanthine or xanthine)
with a carbonyl group. Adenine does not have this group. Answer choice D is not correct due to
it being a nucleotide. The structure is clearly a nucleoside. Answer choice B implies a ribose
22. B (IMP, AMP & GMP, on page 85, are the regulators of feedback inhibition in purine synthesis)
23. B (It is useful for gout treatment, page 89)
24. A (Glutamate is not a starting component of this synthesis. Glutamine is one of the 3 starting
components, along with CO2 & aspartate)
25. B (UTP as indicated on page 101)
26. C (I threw in Beta Glycine as a trick. Page 104 reflects how NH3, CO2, Beta-alanine & Baminoisobutyrate are the end products of pyrimidine catabolism)
27. D (dGTP as well as dTTP both inhibit reduction of pyrimidine nucleoside diphosphates, page 108)
28. B (Uracil has Uracil Phosphoribosyl transferase, Guanine & Hypoxanthine have hypoxanthineGuanine Phosphoribosyl Transferase, Adenine has Adenine Phosphoribosyl Transferase).
29. B (page 159)
30. D (I tried to cause confusion between answers C & D. Keep in mind that serine glycine
hydromethyl transferase uses 5,10-methlyene THF. We never discussed anything about serine
alanine hydromethyl transferase).
31. B (I know this is specific but this is a reasonable question. On page 267, he gives a list to the left
of different growth factors. It is a recognition question. I made up the growth factor in answer
choice B).
32. B (Answer A is the transactivation process, Answer C is the Transrepression process, Answer D is
the Transduction process. We did not discuss any way where the glucocorticoid prevents the
binding of the actual interleukin or any other inflammatory stimulating protein to the receptor
of the cell membrane; page 269).
33. G (verbatim from page 274)