2005 Edition of First Aid for the USMLE Step 1 - Official Errata Thread

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Pox in a box

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List the errors you find. Include the page number(s), section, and the correction that needs to be made. Also list the source if you know one to validate your correction.

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pg 148 under glycolysis regulation... Says that glucose6P inhibits glucokinase and hexokinase. Only hexokinase is inhibited, see the above box on HK/GK.

pg 149 states that pyruvate dehydrogenase is activated by increased NADH --> NAD. Not sure what this is trying to say, but PDH is activated by NAD. It is inhibited by NADH (by PDH Kinase).
 
betz said:
pg 148 under glycolysis regulation... Says that glucose6P inhibits glucokinase and hexokinase. Only hexokinase is inhibited, see the above box on HK/GK.

pg 149 states that pyruvate dehydrogenase is activated by increased NADH --> NAD. Not sure what this is trying to say, but PDH is activated by NAD. It is inhibited by NADH (by PDH Kinase).

along those same lines...i was confused by the statement on 149 that says that PDH is activated by exercise...i thought exercise increases NADH which would inhibit PDH??

Also, page 159, should that arrow pointing from lead poisoning to ALA synthetase be there?
 
P. 343: Smooth Muscle Contraction - When MLCK goes to work and phosphorylates the myosin, it would result in contraction; NOT relaxation. The phosphatase would then result in muscle relaxation.
 
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The brain diagram on the bottom of page 229 is mislabeled (I believe) for low-grade pilocytic astrocytoma (labeled F). They are most often found in the posterior fossa (cerebellum), can arise in the hypothalamus (3rd ventricle). Looks like it's labeled (F) in the frontal lobe of the anterior fossa in the diagram.



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Don't get fvcked by the institvte
 
Bounty said:
along those same lines...i was confused by the statement on 149 that says that PDH is activated by exercise...i thought exercise increases NADH which would inhibit PDH??

Also, page 159, should that arrow pointing from lead poisoning to ALA synthetase be there?

I think what they mean is, that exercise increases the need for energy. ADP will increase, thus the need for PDH for entry into the TCA cycle for energy. Yes, exercise will increase NADH in the muscle tissue, but pyruvate --> lactate will replenish the NAD needed for anaerobic glycolysis. Therefore, NADH will not accumulate.

And the arrow on ALA synthetase shouldnt be there. Good catch! :cool:
 
zeloc said:
page 71, doesn't the zona fasciculata just do the glucocorticoids and the zona reticularis does the glucocorticoids plus sex hormones?
I had always thought that the ZF and ZR both work in the synth. of GC and sex hormmones, because they both have 17 hydroxylase and 17,20 lyase responsible for producing androgens. While ZG does not have 17 hydroxylase, therefore limited only to MC production. But, correct me if I am wrong.
 
HiddenTruth said:
I had always thought that the ZF and ZR both work in the synth. of GC and sex hormmones, because they both have 17 hydroxylase and 17,20 lyase responsible for producing androgens. While ZG does not have 17 hydroxylase, therefore limited only to MC production. But, correct me if I am wrong.

This means that First Aid is wrong then. In First Aid it is listed that the ZR just does the sex hormones. I looked in my Histology syllabus and it confirmed that the ZF and ZR both do GC and sex hormones.
 
zeloc said:
This means that First Aid is wrong then. In First Aid it is listed that the ZR just does the sex hormones. I looked in my Histology syllabus and it confirmed that the ZF and ZR both do GC and sex hormones.
yea, i think PRIMARILY ZR makes sex, and ZF makes GC, but they both can synth. both
 
on Smooth muscle contraction p.343 , it says Myosin~P + actin work to relax muscle. I think it should say contract/cross-bridge formation.
funny thing is that the exact same page in the 2004 edition is switched but correct.
 
bumping this for those on the FA error thread.
 
Robbins and Cotran Pathologic Basis of Disease 7ed, Page 1166

Hyperthyroidism

Clinical Course

From Robbins - Some patients with thyrotoxicosis develop a reversible diastolic dysfunction and a 'low-output' failure, so-called thyrotoxic dilated cardiomyopathy.

I think thyrotoxicosis causes "high-output" cardiac failure with systolic dysfunction. Can anyone verify this?
 
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