Error in First Aid and BRS Path?

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MCG

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Just started cramming for this test and i noticed on page 332 of BRS path it says the most common malignancy in women is Lung CA with Breast CA second (shouldnt this say deaths not incidence). Also, in First Aid on page 290 under ESR, it says it is increased in polycythemia vera (shouldnt this be decreased). Can someone please explain the concept of ESR if I am wrong. Thanks

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Good catch on the ESR. That should be decreased in polycythemia vera. And I dont have First Aid in front of me, but the order of incidence of CA always has lung second (behind prostate/breast), although it is first in mortality. So, if those mistakes are in there, your corrections are right.
 
What edition do you have because I just checked my 2004 First Aid about the ESR & Polycythemia and on page 281 under ESR it says, "Decreased with sickle cell anemia, CHF, and polycythemia." Maybe it's been corrected since past editions of the book.
 
Originally posted by MCG
Just started cramming for this test


Just STARTED cramming? Damn...you're leagues ahead of most people I know....
 
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actually my test is in 3 weeks - and i am losing it, someone please tell me anatomy and embryo will not be more than 10 q's
 
It has been asserted over and again that 90% of the possible gross/neuro material is in First Aid, which accounts for about 30 pages in that book. It seems to be pretty superficial.
 
continuing on the compilation of errors in board review books.

pg. 139 physiology in big costanzo. (surprised to find an error in one of her books)

"....inspiration delays closure of the pulmonic valve and causes splitting of the second heart sound; that is, during inspiration, the pulmonic valve closes distinctly before the aortic valve..."

this is wrong. it should be distinctly AFTER the aortic valve.
 
Originally posted by nuclearrabbit77
continuing on the compilation of errors in board review books.

pg. 139 physiology in big costanzo. (surprised to find an error in one of her books)

"....inspiration delays closure of the pulmonic valve and causes splitting of the second heart sound; that is, during inspiration, the pulmonic valve closes distinctly before the aortic valve..."

this is wrong. it should be distinctly AFTER the aortic valve.

She was just making sure you were paying attention :p
 
<saga continues...>

pg. 48. High-Yield Gross Anatomy. 2nd edition.

"pulmonary valve is the outflow valve of the right ventricle. it is composed of three cusps (right, left, and posterior)..."

The pulmonary valves cusps are named right, left and ANTERIOR---while the aortic valve has right, left and posterior.
 
Originally posted by nuclearrabbit77
<saga continues...>

pg. 48. High-Yield Gross Anatomy. 2nd edition.

"pulmonary valve is the outflow valve of the right ventricle. it is composed of three cusps (right, left, and posterior)..."

The pulmonary valves cusps are named right, left and ANTERIOR---while the aortic valve has right, left and posterior.

That will not be tested
 
agreed. regardless, if anyone else comes across errors in any commonly used step1 review books please post them here.
 
came across another disagreement between first aid (says mutation, NOT deletion) page 236, and BRS path 376 (says segmental deletions), i believe this question came up on a kaplan exam, so probably a little more important than the others.

sorry, the question was, what is the mutation in Beckers Dystrophy, a deletion, or a just a mutation with a truncated protein?
 
Originally posted by MCG
came across another disagreement between first aid (says mutation, NOT deletion) page 236, and BRS path 376 (says segmental deletions), i believe this question came up on the NBME practice exam, or a kaplan exam, so probably a little more important than the others.

sorry, the question was, what is the mutation in Beckers Dystrophy, a deletion, or a just a mutation with a truncated protein?

First of all, I belive that a deletion=mutation. Regarding Beckers Muscular dystrophy, from emedicine.com:
"Advancements in diagnosis of genetic conditions have revealed that BMD is a type of recessive X-linked dystrophinopathy. Exon deletions exist in the dystrophin gene Xp21 (ie, X-chromosome, short arm p, region 2, band 1). Patients in approximately 30% of known cases of BMD phenotype do not have demonstrable deletion. A reading frame or in-frame mutation hypothesis has been proposed to explain abnormal translation of the dystrophin gene. Abnormal but functional dystrophin may be produced, in contrast to the pathology in DMD where frame-shift mutation leads essentially to failure to produce dystrophin. Dystrophin levels in BMD generally are 30-80% of normal, rather than less than 5% as in Duchenne."
 
Thanks for the info, looks like First aid is wrong again. Also, i know its detailed, but deletion is not the same as mutation. A mutation can lead to an early stop codon, therefore a truncated protein, but a it jsut changes the base sequence without deleting anything, and usually doesnt affect the protein at all. on the other hand, a deletion almost always leads to an early stop codon, because the sequence downstream becomes out of Whack. at least thats my take on it.
 
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I also forgot, another disagreement between the 36 page Golgan review, sorry cant remember the page, and BRS path page 381. Golgan says Legg Calve Perthes and Osgood Schattler disease are NOT due to avascular necrosis, while BRS says it is.

also, the common association we all make with osteomyelitis and sickle cell is SALMONELLA! i think this is in every review book, but the goljan review says staph is more common (sorry forget the page #), while kaplan says salmonella is the cause of 80% of the cases if i can remember correctly. I think this is an important question, because you know theyll put both as answers.

some of you guys must think i'm a pyscho, but when youre down to your final 2.5 weeks before showtime, you eat, drink, and crap 1st aid and Brs path.
 
Originally posted by MCG
Thanks for the info, looks like First aid is wrong again. Also, i know its detailed, but deletion is not the same as mutation. A mutation can lead to an early stop codon, therefore a truncated protein, but a it jsut changes the base sequence without deleting anything, and usually doesnt affect the protein at all. on the other hand, a deletion almost always leads to an early stop codon, because the sequence downstream becomes out of Whack. at least thats my take on it.

The way that I was taught was that a deletion was a type of mutation. Oh well, it doesn't matter for your test. Minor avascular necrosis has been theorized to play some role in the pathogenisis of osgood schlatter's disease, but for test taking purpose, I would say that it's not because the term "avascular necrosis" is not associated with osgood schlatters out in clinical practice. Think of osgood schlatters as a common ped's pretibial pain problem associated with the bone growing. Avascular necrosis is part of the pathogenesis of Legg Calves Perthes though. Staph aureus osteomyelitis is the most common type of osteomyelitis in sickle cell patients, but salmonella is mainly known to only cause osteomyelitis in sickle cell patients (rare in non-sicklers).
 
This is actally a mistake. Salmonella paratyphi is the MCC of osteomyelitis in sickle cell patients. That is in the current literature and is in Goljans newest notes and lectures. He hasnt lectured about Osgood-Schlatter or Legg Calves Perthes yet, tho:(

MCG, Most Duchennes (96%) have a frameshift, resulting in an early stop, and no dystrophin production, while Beckers typically has an inframe deletion (i.e. 3,6,9 bases), that results in a semi-functional state.
 
Originally posted by Idiopathic
This is actally a mistake. Salmonella paratyphi is the MCC of osteomyelitis in sickle cell patients. That is in the current literature and is in Goljans newest notes and lectures.

Interesting. I was pimped on S. Aureus being the most common cause of osteomyelitis by an elderly ID doc, but after reviewing the most recent literature, it does appear that you are correct. I wonder why there was so much confusion about etiologies causing osteomyelitis in sicklers, I was only able to find a few articles which even suggested that S. Aureus was the most common cause. Anyways, here is a recent peds paper saying that salmonella is the most common cause:

http://www.ncbi.nlm.nih.gov/entrez/...ics.org/cgi/pmidlookup?view=full&pmid=9445507
 
Yeah, its true. I think the confusion comes from Staph aureus as being almost universal as the MCC in Px without sickle cell. But for some reason it flips in these patients. Also, many people make the mistake of thinking it is Salmonella typhi, when in reality it is Salmonella paratyphi...just remember Salmonella paratyphi = Sickle cell patients


Thats how it works for me....kinda dorky, I know.
 
i agree with the above post that Duchenne's in complete absence of dystrophin whereas Becker's is decreased functionality in dystrophin...both arre due to mutations but i think the mutation in Becker's causes premature stop in translation = truncated protein...this comes from what i recall during my genetics elective.

also, i thought lung ca was the most common ca in women...is it really BCC across the board?

-s.
 
skin cancers are more common than lung, prostate, breast CA. but since the numbers are so high and it is so hard to keep track of all the skin cancers they are not included in the typical stats of CA.
 
Another difference between BRS path(76, says I) and First Aid(217 says II) suggesting which HLA (I or II) is the most important determinant of graft rejection. can anyone answer this.

Also make an edit on page 82 of BRS path, it says DiGeorge is a defect in the 3rd and 4th arches not pouches. cant believe i never caught that before. schneider probably had too much to drink the night he typed that one.
 
Originally posted by MCG
skin cancers are more common than lung, prostate, breast CA. but since the numbers are so high and it is so hard to keep track of all the skin cancers they are not included in the typical stats of CA.

I did mean to mention this....it is true in both men and women.
 
Error on page 182 of BRS Path, 2nd edition, regarding abnormal hemolobin tetramers seen in a-thalassemias.

- claims that Hemoglobin H is a gamma-4 tetramer and that Hemoglobin Barts is a beta-4 tetramer

Should be exactly the opposite.
 
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