Step I First Aid 2013 Errata

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BelieveTheHype

Mad Widgetry
10+ Year Member
I took the plunge and got the 2013 edition because I couldn't be hassled to go through a 28 page errata and making the 2012 edition look like it came out of an explosion from the printing press. Have any of you gotten a head start on this new edition and came across any errors? If so please post here for the benefit of others, thanks!
 
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crunchymedicine said:
on page 366-->polycythemia table
shouldn't RCC, Wilm's tumor, cyst, HCC, and hydronephrosis go under polcythemia vera and NOT inappropriate absolute?
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My understanding is that FA is correct. PCV (aka absolute polycythemia without hypoxic stimulus) is due to an acquired mutation on the JAK2 gene of chromosome 9 that affects myeloid stem cells.

Meanwhile, RCC (for instance), causes exogenous EPO production. Inappropriate polycythemia is an RBC count increase without hypoxic stimulus, yes, but it's distinguished from polycythemia VERA by the plasma volume:

Inappropriate absolute polycythemia from ectopic EPO production → normal PV.

Inappropriate absolute polycythemia from polycythemia vera → increased PV.

That's my understanding from GT, at least.

...In PCV, you have ↑ RBC mass, RBC count, and plasma volume but LOWER Epo because the mutation makes the receptor just act like it's constantly being stimulated (I think. That part is from memory, so I'm not 100%).
 
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crunchymedicine said:
also, this seems nit picky, but isn't hereditary spherocytosis associated with defects in enkyrin, spectrin and band 4.1 (NOT band 3)??

probably doesn't matter...
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According to this article: https://www.sciencedirect.com/science/article/pii/S0140673608615883

"...due to defects in the membrane proteins ankyrin, band 3, β spectrin, α spectrin, or protein 4.2."

So it seems like FA is correct here too.

I have my STEP 1 in about a week, so keep an eye out for any more errors! So far, I haven't found any, and I annotated most of UWORLD into my FA, double checking what FA said along the way. Like I said, so far, nothing, but if anyone sees anything, please post!

EDIT: I also agree with hrain that FA is correct about PV.
 
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incubusfanclm said:
Pg. 444 - Multiple Sclerosis

I've learned several times that there is relative axon preservation within MS demyelination plaques. Is FA correct in saying there is axon destruction?
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From Wikipedia
More specifically, MS destroys oligodendrocytes, the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals (action potentials).[4] MS results in a thinning or complete loss of myelin and, as the disease advances, the cutting (transection) of the neuron's axons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.[4] A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes cannot completely rebuild the cell's myelin sheath.[26] Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons.[26] Different lesion patterns have been described.[27]
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Perhaps it would be best to say early MS is mostly myelin destruction and late MS progresses to actual axon destruction?
 
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roberco0908 said:
Pg. 78...

Currently reads "Type I or Type V collagen most frequently affected"

Should read "Type I or Type III Collagen most frequently affected"

Agreed?
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From Robbins Basic Pathology, 9E:
The molecular bases for three of the more common variants are as follows:
- Deficiency of the enzyme lysyl hydroxylase. Decreased hydroxylation of lysyl residues in types I and III collagen interferes with the formation of cross-links among collagen molecules. As might be expected, this variant (kyphoscoliotic EDS), resulting from an enzyme deficiency, is inherited as an autosomal recessive disorder.
- Deficient synthesis of type III collagen resulting from mutations affecting the COL3A1 gene. This variant, the vascular type, is inherited as an autosomal dominant disorder and is characterized by weakness of tissues rich in type III collagen (e.g., blood vessels, bowel wall), predisposing them to rupture.
- Deficient synthesis of type V collagen due to mutations in COL5A1 and COL5A2 is inherited as an autosomal dominant disorder and results in classical EDS.
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In summary:
- Types I, III and V collagen are all commonly affected.
- Type I collagen deficiency is due to deficiency of lysyl hydroxylase (AR)
- Type III collagen deficiency is either due to deficiency of lysyl hydroxylase (AR) or mutation of the enzyme coding for type III collagen (AD) - this is the most common subtype associated with Berry aneurysms
- Type V collagen deficiency is due to mutation of the genes coding for type V collagen (AD).
 
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Is there an error on pg 83 in regards to imprinting a/w Prader-Willi syndrome and Angelman's syndrome? FA says Prader-Willi syndrome is where the paternal allele is NOT expressed. However, I've been searching on the internet the whole night and kept finding that in PW syndrome, maternal gene is turned off??? I'm confused...

Here is the website that I was browsing on...

http://ghr.nlm.nih.gov/condition/prader-willi-syndrome
 
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uncgirl501 said:
Is there an error on pg 83 in regards to imprinting a/w Prader-Willi syndrome and Angelman's syndrome? FA says Prader-Willi syndrome is where the paternal allele is NOT expressed. However, I've been searching on the internet the whole night and kept finding that in PW syndrome, maternal gene is turned off??? I'm confused...

Here is the website that I was browsing on...

http://ghr.nlm.nih.gov/condition/prader-willi-syndrome
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FA's right. It's when the paternal gene is either deleted or not inherited. I think you're getting mixed up because of the wording from that website.

"Some genes are turned on (active) only on the copy that is inherited from a person's father (the paternal copy)...". They should've followed with how a deletion or a non-inheritance in that gene would cause Prader-Willi syndrome.

Also, the next paragraph says, "Most cases of Prader-Willi syndrome (about 70 percent) occur when a segment of the paternal chromosome 15 is deleted in each cell. People with this chromosomal change are missing certain critical genes in this region because the genes on the paternal copy have been deleted, and the genes on the maternal copy are turned off (inactive). In another 25 percent of cases, a person with Prader-Willi syndrome has two copies of chromosome 15 inherited from his or her mother (maternal copies) instead of one copy from each parent."

When it says "genes on maternal copy are turned off (inactive)," it's referring to the earlier portion where only the paternal gene is active (caused by genomic imprinting).
 
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so first off, imprinting is inactivating a gene.

If the father's gene is inactivated, then only the mother's gene is expressed. When that mother's gene is deleted, then you have angelman's. When the mother's is inactivated (imprinted) and the father's is deleted, it's prader-willi.

It's sort of like the two hit hypothesis with cancer. One doesn't work form the beginning, and when the second is deleted, you have problems.

Page 83 is misleading. Neither paternal nor maternal is expressed. One is silenced and one is missing.

Reference: Robbins Path pg 172, Medical Genetics pg 89
 
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Under insulin regulation, shouldn't B2-AGONISTS, not ANTAgonists increase insulin release? ALso, the diagram is labeled wrong i think...i think it's GLUT-2 receptors in the pancreatic cell that bring glucose in, not GLUT-1. Feedback anyone?
 
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First Aid 2013 ... Has omitted some information....


So far the one that has managed to get under my skin is that...it has omitted Uncal Herniation clinical signs and causes (FA12 470) ...which it says in the index is page 448 but its NOT EVEN THERE.....nor is differential diagnosis of brain lesions....(FA12 page 471)

Man how much booze do they consume when they makes these books...geez....
 
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jenniferhan1987 said:
Under insulin regulation, shouldn't B2-AGONISTS, not ANTAgonists increase insulin release? ALso, the diagram is labeled wrong i think...i think it's GLUT-2 receptors in the pancreatic cell that bring glucose in, not GLUT-1. Feedback anyone?
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you're right about both.

I seriously wonder if anyone with any medical background even looks at this f*cking book. They should send it out to faculty/students from january-may, make adjustments and release it in july.
 
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