First Aid 2006 Errata

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missbonnie

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Hey, I dont think one has been started yet so..here it goes.
A bunch of emails have been going around my class with the First Aid 2006 errata..there are tons, and even missing pages!!!

I've copied & pasted what I can find so far, and obviously, use at your own risk but most are obvious... and 2 attachments of 2 PDF files of missing pages - one for micro (Rickettsia) & Cardio drugs.,

age#--correction

72--it should read "Kubler-Ross Dying Stages" (not grief stages)

161--Micro - Most common cause of bacterial meningitis in adults 18-60 is Strep pneumo. N meningitidis is still the most common for 6 - 18 yr olds (from uptodate)

187--the complement cascade show C4b2*b* as classic C3 convertase and C4b2*b as classic C5 convertase. It should be C4b2_*a*_ = classic C3 convertase and C4b2_*a*_3b = classic C5 convertase

208--St. John's Wort is an inducer of CYP (3A4), not an inhibitor. (checked JAMA)

221--EDV and ESV are swapped in the pressure-volume relationship in the cardiovascular section

221--the PV-curve shows what happens with an increase in afterload AND contractility. So put a little "[up-arrow] contractility" next to "[up-arrow] afterload"

259--In "Other hypothalamic/pituitary drugs" GH is somatoTROPIN. Octreotide is the analogue of somatostatin.

274--Barrett's esophagus is replacement of nonkeratinized squamous epithelium with INTESTINAL columnar epithelium in the distal esophagus (not gastric)

275--"Usually squamous cell carcinoma" Actually, squamous cell CA and adenocarcinoma of the esophagus currently have almost equal incidence due to a rapid rise in adenocarcinoma rates in recent decades (from UpToDate, Qbank)

283--Pirenzepine causes TACHYcardia, not bradycardia as a toxicity (from micromedex)

295--Wilm's tumor is a mutation on 11p (not 11q) (according to BRS and emedicine and Miglet) (for both WT1 and WT2)

310--Imatinib (Gleevec) is NOT an antibody or myclonal. But it is a tyrosine kinase inhibitor.

322--Pemphigus vulgaris = intraEPIDERMAL bullae

344--cavernous sinus syndrome should include opthalmoplegia, opthalmic and MAXILLARY sensory loss

345--swap SR with IO at the top, and IR with SO at the bottom

346--pupillary light reflex sends signal via CN2 not CN3

353--Syringomyelia is from damage to crossing SPINOTHALAMIC TRACT FIBERS in the anterior white commissure.

368--the mechanism of ethosuxamide blocks thalamic Ca+2 channels, NOT thalamic Ca+1

385--#5) SLE - in DIFFUSE PROLIFERATIVE form you get wire-loop abnormality with subendothelial immune complex deposits

Color img 48B--is actually a pilocytic astrocytoma, not a glioblastoma (those are Rosenthal fibers)

Color img 104--Sarcoidosis does NOT have caseation

they're the
area immediately posterior to the central sulcus.

pg 346: Pupillary light reflex -> light in either retina sends a signal
via
CN II (NOT III). the pupils contract bilaterally (consensual reflex)
via CN
III (= solid lines)

pg352- diagram on left: F, which is supposed to be pilocytic
astroctoma, is
usually in the posterior fossa but they drew it in the frontal lobe.

pg353- the spinal cord section diagram for syringomelia- corticospinal
should be spinothalamic

pg 357- herniation syndromes- the uncus is mislabelled.

Differences In the definition of cleft lip on page 117 and 124. What
it
says on page 124 is correct and page 117 should read "failure of fusion
of
the maxillary and medial nasal processes leading to cleft lip."

pg 149 it states that Loa Loa (nematode) is transmitted by the deerfly.
this is incorrect. it is transmitted by the bite of a mango fly,
Chrysops.

Pg 63 – Second chart should be disease vs. exposure, not disease vs. test [Annie Garment]

Pg 87 – Pyruvate Kinase is shown as reversible in the diagram. It’s
irreversible. [From Mike Su and Christian Song]

Pg 97 – Liver, Fasting State: Amino acids can indeed enter the TCA cycle directly (after deamination) but this is not true for glycerol or lactate. Glycerol enters the glycolytic pathway by being metabolized to Dihydroxyacetone Phosphate (DHAP) while lactate enters the pathway by being metabolized to pyruvate. Therefore, the arrows should be changed accordingly.

Pg 118 – Under the heading "Embryologic Derivatives", surface ectoderm is said
to give rise to the "epithelial linings". This is mostly incorrect. The ectodermal germ layer gives rise to the *sensory* epithelium of the ear, nose, and eye. Epithelial linings of the gut, UG tract, and respiratory tract are derived from the *endodermal* germ layer. [DT Jacobs]

Pg 140 – “Salmonella has an animal reservoir.” Not true of Salmonella Typhi, the strain the causes Typhoid fever! (i.e. it’s only in humans).

Pg 141 – E. Coli O157:H7 is a subtype of EHEC, not EIEC.

Pg 154 – The process explained is called “Phenotypic Masking” not “Phenotypic Mixing”, which is a different process. I verified this with a research paper which describes the process in the journal of Evolution. [from James Toussaint]

Pg 166 (Chart) – Amoxicillin/Ampicillin can be used for E. Coli, as it says on the very next page.

Pg 302 – Follicular Lymphoma: “bcl-2 is involved in apoptosis.” Okay, technically this isn’t an actual mistake, but at the very least it’s HIGHLY misleading. It should really say “bcl-2 is involved in INHIBITION of apoptosis.” It’s important to realize that this isn’t a matter of underexpression of a pro-apoptotic gene, but rather overexpression of an anti-apoptotic gene.

Pg 319 – Osteomalacia/rickets. Vitamin D deficiency causes a DECREASE in serum phosphate (due to increased renal excretion, which, in turn, is due to increased PTH).

Pg 324 – Temporal Arteritis affects medium and LARGE arteries

Pg 325 – Cox-2 inhibitors: the IMPORTANT toxicity is an increased risk of thrombosis (stroke or MI).

Pg 326 – Etanercept: Mechanism – inhibits BOTH TNF-ά AND TNF-β

Pg 404, Testicular non-germ cell tumors, Leydig cell: "androgen producing leads to gynecomastia in men, precocious puberty in boys." While it is true that Leydig cell tumors are androgen-secreting (at least initially) and it is also true that later in life
they can lead to gynecomastia, it is incorrect to say that these two facts are
related to each other. Not only does this not make any sense, but it turns out
that adults with leydig cell tumors actually have DECREASED levels of androgens.

Pg 485 – ALL is Acute LymphoBLASTIC Leukemia, not “lymphocytic” leukemia

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Whats the deal with the typos....is it wise to just stick to 2005 edition???I know that has its fair share of problems?
 
I was about to order a subscription to the umslerx q bank (by the First Aid people), but after seeing this, I have changed my mind!!
 
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Most of these are helpful (thanks!) but I disagree partially with some. I haven't read them all, but here are a few that stood out. (I also don't have 2006 edition so I can't say that what FA has is correct either)

Kubler-Ross stages are for grief -- they are not restricted to the person who is dying, but apply to anyone who is grieving.

The C4b2b nomenclature is seen quite often in the literature (Robbins for instance uses it) and shouldn't be regarded as incorrect (ie. you may see it in an answer choice and it won't make it incorrect).

The deer fly and horsefly (mango fly) are both vectors for Loa Loa.

According to Robbins, wire loop lesions can be seen in focal, diffuse, and membranous types of glomerulonephritis. However for testing purposes it may be sufficient to say they go with the diffuse proliferative type, because that is most common. It is correct that they are subendothelial deposits.

#275: note that this is true for the United States only.
 
TIMMY said:
Whats the deal with the typos....is it wise to just stick to 2005 edition???I know that has its fair share of problems?


Isn't the 2005 edition almost the exact same as the 2006 edition? The only difference being that the 2005 edition is organized by subject (ie, Anatomy, Biochem, Path, etc) and the 2006 edition is organized by organ system (ie Cardiovascular, Musculoskeletal, etc). Anybody have a preference to one organization over another?
 
TIMMY said:
Whats the deal with the typos....is it wise to just stick to 2005 edition???I know that has its fair share of problems?
I've got both 2005 and 2006. I thought the organ-system based organization might be more useful, but I don't really see the utility behind it. What's more annoying is that some subjects were split b/w Section 1 (which contains Beh Science, Micro/Immuno, Pharma, Embryo and Biochem as stand-alone content) and Section 2 which contains the organ systems. I prefer to study subject-wise and don't really like flipping back and forth b/w section 1 and section 2 to look up all the FA facts for a certain subject. Either they should have made the whole thing organ-based or stuck to keeping the subjects totally separate. As it is, the division in the subjects is difficult to follow because few popular review books approach the Step 1 material that way. I might just stick to the 2005 edition.
 
how do I access the pdfs for the missing pages? the link doesn't seem to work.
 
missbonnie said:
Hey, I dont think one has been started yet so..here it goes.
A bunch of emails have been going around my class with the First Aid 2006 errata..there are tons, and even missing pages!!!

I've copied & pasted what I can find so far, and obviously, use at your own risk but most are obvious... and 2 attachments of 2 PDF files of missing pages - one for micro (Rickettsia) & Cardio drugs.,

age#--correction

72--it should read "Kubler-Ross Dying Stages" (not grief stages)

161--Micro - Most common cause of bacterial meningitis in adults 18-60 is Strep pneumo. N meningitidis is still the most common for 6 - 18 yr olds (from uptodate)

187--the complement cascade show C4b2*b* as classic C3 convertase and C4b2*b as classic C5 convertase. It should be C4b2_*a*_ = classic C3 convertase and C4b2_*a*_3b = classic C5 convertase

208--St. John's Wort is an inducer of CYP (3A4), not an inhibitor. (checked JAMA)

221--EDV and ESV are swapped in the pressure-volume relationship in the cardiovascular section

221--the PV-curve shows what happens with an increase in afterload AND contractility. So put a little "[up-arrow] contractility" next to "[up-arrow] afterload"

259--In "Other hypothalamic/pituitary drugs" GH is somatoTROPIN. Octreotide is the analogue of somatostatin.

274--Barrett's esophagus is replacement of nonkeratinized squamous epithelium with INTESTINAL columnar epithelium in the distal esophagus (not gastric)

275--"Usually squamous cell carcinoma" Actually, squamous cell CA and adenocarcinoma of the esophagus currently have almost equal incidence due to a rapid rise in adenocarcinoma rates in recent decades (from UpToDate, Qbank)

283--Pirenzepine causes TACHYcardia, not bradycardia as a toxicity (from micromedex)

295--Wilm's tumor is a mutation on 11p (not 11q) (according to BRS and emedicine and Miglet) (for both WT1 and WT2)

310--Imatinib (Gleevec) is NOT an antibody or myclonal. But it is a tyrosine kinase inhibitor.

322--Pemphigus vulgaris = intraEPIDERMAL bullae

344--cavernous sinus syndrome should include opthalmoplegia, opthalmic and MAXILLARY sensory loss

345--swap SR with IO at the top, and IR with SO at the bottom

346--pupillary light reflex sends signal via CN2 not CN3

353--Syringomyelia is from damage to crossing SPINOTHALAMIC TRACT FIBERS in the anterior white commissure.

368--the mechanism of ethosuxamide blocks thalamic Ca+2 channels, NOT thalamic Ca+1

385--#5) SLE - in DIFFUSE PROLIFERATIVE form you get wire-loop abnormality with subendothelial immune complex deposits

Color img 48B--is actually a pilocytic astrocytoma, not a glioblastoma (those are Rosenthal fibers)

Color img 104--Sarcoidosis does NOT have caseation

they're the
area immediately posterior to the central sulcus.

pg 346: Pupillary light reflex -> light in either retina sends a signal
via
CN II (NOT III). the pupils contract bilaterally (consensual reflex)
via CN
III (= solid lines)

pg352- diagram on left: F, which is supposed to be pilocytic
astroctoma, is
usually in the posterior fossa but they drew it in the frontal lobe.

pg353- the spinal cord section diagram for syringomelia- corticospinal
should be spinothalamic

pg 357- herniation syndromes- the uncus is mislabelled.

Differences In the definition of cleft lip on page 117 and 124. What
it
says on page 124 is correct and page 117 should read "failure of fusion
of
the maxillary and medial nasal processes leading to cleft lip."

pg 149 it states that Loa Loa (nematode) is transmitted by the deerfly.
this is incorrect. it is transmitted by the bite of a mango fly,
Chrysops.

Pg 63 – Second chart should be disease vs. exposure, not disease vs. test [Annie Garment]

Pg 87 – Pyruvate Kinase is shown as reversible in the diagram. It’s
irreversible. [From Mike Su and Christian Song]

Pg 97 – Liver, Fasting State: Amino acids can indeed enter the TCA cycle directly (after deamination) but this is not true for glycerol or lactate. Glycerol enters the glycolytic pathway by being metabolized to Dihydroxyacetone Phosphate (DHAP) while lactate enters the pathway by being metabolized to pyruvate. Therefore, the arrows should be changed accordingly.

Pg 118 – Under the heading "Embryologic Derivatives", surface ectoderm is said
to give rise to the "epithelial linings". This is mostly incorrect. The ectodermal germ layer gives rise to the *sensory* epithelium of the ear, nose, and eye. Epithelial linings of the gut, UG tract, and respiratory tract are derived from the *endodermal* germ layer. [DT Jacobs]

Pg 140 – “Salmonella has an animal reservoir.” Not true of Salmonella Typhi, the strain the causes Typhoid fever! (i.e. it’s only in humans).

Pg 141 – E. Coli O157:H7 is a subtype of EHEC, not EIEC.

Pg 154 – The process explained is called “Phenotypic Masking” not “Phenotypic Mixing”, which is a different process. I verified this with a research paper which describes the process in the journal of Evolution. [from James Toussaint]

Pg 166 (Chart) – Amoxicillin/Ampicillin can be used for E. Coli, as it says on the very next page.

Pg 302 – Follicular Lymphoma: “bcl-2 is involved in apoptosis.” Okay, technically this isn’t an actual mistake, but at the very least it’s HIGHLY misleading. It should really say “bcl-2 is involved in INHIBITION of apoptosis.” It’s important to realize that this isn’t a matter of underexpression of a pro-apoptotic gene, but rather overexpression of an anti-apoptotic gene.

Pg 319 – Osteomalacia/rickets. Vitamin D deficiency causes a DECREASE in serum phosphate (due to increased renal excretion, which, in turn, is due to increased PTH).

Pg 324 – Temporal Arteritis affects medium and LARGE arteries

Pg 325 – Cox-2 inhibitors: the IMPORTANT toxicity is an increased risk of thrombosis (stroke or MI).

Pg 326 – Etanercept: Mechanism – inhibits BOTH TNF-ά AND TNF-β

Pg 404, Testicular non-germ cell tumors, Leydig cell: "androgen producing leads to gynecomastia in men, precocious puberty in boys." While it is true that Leydig cell tumors are androgen-secreting (at least initially) and it is also true that later in life
they can lead to gynecomastia, it is incorrect to say that these two facts are
related to each other. Not only does this not make any sense, but it turns out
that adults with leydig cell tumors actually have DECREASED levels of androgens.

Pg 485 – ALL is Acute LymphoBLASTIC Leukemia, not “lymphocytic” leukemia


you find all these yourself?

great job!
 
Is anyone still using the 2004 First Aid? I bought it at the time, & I don't really want to buy another one. Has anyone found any errors or disadvantages of using 2004?

Thank you!!
 
The First Aid Mafia needs to wise up. If you're going to have this review book racket then at least put out a product that isn't riddled with mistakes. I picked up my obligatory copy of FA 2006 a few months ago but didn't use it much until studying for final exams, but I did catch myself saying "Wait a minute. That isn't right???"

I still think FA is great to use as your review source after you have learned the material. FA is usually just a bunch of facts regurgitated onto the page, and I find that it helps me best as a superficial review after already memorizing and understanding the material. I guess this is why people say to make sure you understand the material in there and not just memorize the book.
 
Thanks for the post! I looked on the mcgraw website (link is above) and was able to find the missing rickettsia page (182_errata), but couldn't find the cardio drug page. Has anyone else been able to find it? and if so how? I notices there are no drugs on tx dyslipidemia (ie statins etc) in the 2006 book...thanks for the help! And good luck to all!
 
Here are some corrections to your corrections...

208--St. John's Wort is an inducer of CYP (3A4), not an inhibitor. (checked JAMA)

- also isn't quinidine is an inhibitor not an inducer

274--Barrett's esophagus is replacement of nonkeratinized squamous epithelium with INTESTINAL columnar epithelium in the distal esophagus (not gastric)

-Robbins says "gastric" and Wheater's says "gastric or intestinal"

pg 149 it states that Loa Loa (nematode) is transmitted by the deerfly. this is incorrect. it is transmitted by the bite of a mango fly, Chrysops.

-CDC says it's transmitted by both deer and mango fly which are both species of the genus chrysops

Pg 485 – ALL is Acute LymphoBLASTIC Leukemia, not “lymphocytic” leukemia[/QUOTE]

-sources seem to use both lymphoblastic and lymphocytic
 
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DrJessie said:
274--Barrett's esophagus is replacement of nonkeratinized squamous epithelium with INTESTINAL columnar epithelium in the distal esophagus (not gastric)

-Robbins says "gastric" and Wheater's says "gastric or intestinal"

Here's a correction to your corrections to her corrections

Big Robbins 7th Ed. says it must be intestinal metaplasia. (pg. 804)
 
lord_jeebus said:
Here's a correction to your corrections to her corrections

Big Robbins 7th Ed. says it must be intestinal metaplasia. (pg. 804)

this is kinda funny. i think the confusion is that it different types of metaplasia can happen, not just intestinal (and includes gastric) but it is generally agreed upon that it must be intestinal to be called Barrett's, and that only intestinal type has higher risk of adenocarcinoma... i'm thinking for boards, just know intestinal type. source - my gi class at P&S, uptodate.

bonnie
 
this is incorrect: "pg. 345--swap SR with IO at the top, and IR with SO at the bottom"

the diagram on pg. 345 in FA 2006 is correct
 
doctorTT said:
this is incorrect: "pg. 345--swap SR with IO at the top, and IR with SO at the bottom"

the diagram on pg. 345 in FA 2006 is correct


may i ask how it is correct??

the obliques of the eye Abduct. the diagram has them adducting towards the nose. the recti are the one that adduct.
 
woowoo said:
may i ask how it is correct??

the obliques of the eye Abduct. the diagram has them adducting towards the nose. the recti are the one that adduct.

I took the diagram to mean that the superior oblique depresses when adducted. Also that the superior oblique intorts the eye (and thus towards nose).
 
woowoo said:
may i ask how it is correct??

the obliques of the eye Abduct. the diagram has them adducting towards the nose. the recti are the one that adduct.

The confusion lies in that both are correct. I encountered this at an ophthalmology exam so this could be one for the ophtho residents. The diagram pictured on 345 is correct in that those are the primary movements of the eye, with each muscle working as an independent unit.

The confusing bit is that in actuality, all the muscles work together at all times and so in conjoined movement, the obliques appear to abduct and the recti muscles adduct, which is the way it appears in Moores and is the reason why when you get a 3rd nerve palsy, the eye appears "down and out" with both the LR and SO acting together. The obliques abducting and the recti adducting is what appears in all the textbooks, but the diagram on p. 345 is also correct.

As to what the USMLE wants, it's hard to know. I guess you'll have to read the question very carefully.
 
Two very minor corrections:
p. 390, the heading should say "Renal--Pharmacology" instead of Pathology.
Color Image 41, picture A is gross and B is microscopic, but the descriptions are reversed in the caption.

And, one question. On p. 394, the vignette says a woman with a C-section scar is at risk for developing placenta previa. While this may be true, both FA and BRS Path associate C-section scar with placenta accreta, so shouldn't that be the more 'likely' answer? Or is the important part the location of the scar (close to the opening of the os)?
 
I think you should realize that accreta is for all intents and purposes a subset of previa. Therefore, to have an accreta, you must also have a previa. And yes, C-section is a major risk factor for previa (which is itself a major risk factor for accreta)
 
leorl said:
The confusion lies in that both are correct. I encountered this at an ophthalmology exam so this could be one for the ophtho residents. The diagram pictured on 345 is correct in that those are the primary movements of the eye, with each muscle working as an independent unit.

The confusing bit is that in actuality, all the muscles work together at all times and so in conjoined movement, the obliques appear to abduct and the recti muscles adduct, which is the way it appears in Moores and is the reason why when you get a 3rd nerve palsy, the eye appears "down and out" with both the LR and SO acting together. The obliques abducting and the recti adducting is what appears in all the textbooks, but the diagram on p. 345 is also correct.

As to what the USMLE wants, it's hard to know. I guess you'll have to read the question very carefully.

thanks leorl! thats the way it appears in moore's essential clinical anatomy on pg 539 (2nd edition) so thats how i'm going to remember it. i just have more trust in moore than in first aid when it comes to anatomy so i'll learn it their way. if anyone has a different explanation as to what we should remember, please post!
 
pg 151


"Naked nucleic acids of most dsDNA (except poxvirus and HBV) and (+) strand ssRNA viruses are infectious. Naked nucleic acids of (-) strand ssRNA and dsDNA viruses are not infectious"

Can someone translate this for me...I'm on 10 hours of studying and this statement is confusing the hell out of me
 
Arsenic said:
thanks leorl! thats the way it appears in moore's essential clinical anatomy on pg 539 (2nd edition) so thats how i'm going to remember it. i just have more trust in moore than in first aid when it comes to anatomy so i'll learn it their way. if anyone has a different explanation as to what we should remember, please post!

yes leorl you are right.
to elaborate: the superior oblique is used to depress the aDducted eye, and the inferior oblique is used to elevate the aDducted eye. whereas the superior rectus elevates the aBducted eye and the inferior rectus depresses the aBducted eye.
thats what FA is getting at- the combined use of the EO muscles-which is what you should know for step-1

you should also know what happens with CN3, CN4, and CN6 palsys.--thats where the individual role of the muscles is important to know (as mentioned in moore)
 
woowoo said:
may i ask how it is correct??

the obliques of the eye Abduct. the diagram has them adducting towards the nose. the recti are the one that adduct.

The diagram is confusing but i think it's correct. The recti are oriented to be parallel with the eye's axis when it's looking temporally(so they work best temporally), and the obliques elevate/lower the eye best when it's looking nasally.

The confusing part is all the arrows. They start you thinking about muscle insertions or direction of pull on the eyeball itself. A better way to go would be to draw the vertical lines between SR-->IR and IO-->SO. Now you have the "H" that you would use in a clinical exam
 
Not sure if it has been mentioned but on 291 plasmin (not plasminogen) actives complement.
 
Hey all,

Sources seem to be mixed on this, but we learned that Lente is an intermediate-acting insulin. The sources are not, however, mixed on the fact that Lente is always mentioned with NPH (which, in FA, is deemed intermediate). After all, if Lente was long-acting, where would the fun be in having an "ultra-"lente. If only for Latin's sake, I'm deeming it intermediate.

The (potential) error, by the way, is on p. 258.
 
On PAGE 264 (GI section) it lists the Portal-Systemic anastomoses, under # 2 it lists the Superior to lnferior Rectal vein anastomoses leading to EXTERNAL hemorroids (if backed up due to portal HTN) -- I got a question wrong in USMLERx (ironically by the same company that makes First Aid) b/c the question required that you know that external hemorrhoids is generally NOT assoc. w/ portal htn while internal hemorroids is. If I am wrong in this reasoning someone please set me straight!! :eek:

Sallazar
 
Does anyone know if FIRST AID HAS put out an errata sheat in addition to providing their missing pages? Last time I checked the only things listed as an error was the page cross-reference table on the inside cover WAS NOT updated for the 2006 edition so the pages are wrong-- other than this there was nothing listed as errors.

Jeremy
 
bump.
This book is full of mistakes that people need to be aware of.

Another one:

p. 324 -- says Polyarteritis Nodosa is not associated with ANCA
it is associated with p-ANCA (and Wegener's is c-ANCA)
 
Dunce said:
bump.
This book is full of mistakes that people need to be aware of.

Another one:

p. 324 -- says Polyarteritis Nodosa is not associated with ANCA
it is associated with p-ANCA (and Wegener's is c-ANCA)

According to Robbins, majority of Polyarteritis Nodosa cases are not associated with p-ANCA (they got that Hep B thing going on). Microscpic polyangitis is the one associated with p-ANCA.
 
that's right, we debated it in class - PAN is not associated with anca, but microscopic polyangiitis is. :) brs and goljan have it wrong ...
 
dara678 said:
that's right, we debated it in class - PAN is not associated with anca, but microscopic polyangiitis is. :) brs and goljan have it wrong ...

I was counting on Goljan to be infallible. Isn't he a superhero or something?
 
Dunce said:
I was counting on Goljan to be infallible. Isn't he a superhero or something?

lol he is a superhero! actually i think it's just a matter of timing -- the goljan lectures are from 2002 and in those 4 years they probably found out that it wasn't p-anca after all ...
 
Idiopathic said:
I think you should realize that accreta is for all intents and purposes a subset of previa. Therefore, to have an accreta, you must also have a previa. And yes, C-section is a major risk factor for previa (which is itself a major risk factor for accreta)


I just wanted to clarify... Previous C/S is always a risk factor for placenta accreta (any time you mess with the myometrium there's a risk for abnormally deep implantation). Independently of the risk for accreta, prior C/S can also be a RF for placenta previa as long as the C/S was a low transverse incision in the lower uterine segment rather than the "classical" incision at the fundus which is rarely used anymore. So, h/o C/S can be a RF for both accreta and previa, but definitely neither of those is a "subset" for the other, and the manifestations clinically are quite different. The management of the term patient with history of C/S and current placenta previa is just, automatic repeat C/S; previa is typically diagnosed before the woman presents to L&D. Accreta, however, may not be diagnosed until the woman with prior C/S has already undergone a trial of labor and the implanted placenta won't deliver or causes a uterine inversion or massive hemorrhage or something...

Just finished my OB/Gyn rotation.
 
Amiodarone is listed on page 242 as a Class IA agent and class III agent on page 243.

It is actually only a Class III agent.

I dont understand why the authors of this books have not corrected the all the mistakes in this book.
 
Angel said:
Amiodarone is listed on page 242 as a Class IA agent and class III agent on page 243.

It is actually only a Class III agent.

I dont understand why the authors of this books have not corrected the all the mistakes in this book.

Amiodarone is actually all four classes rolled into one! But it is primarily Class III (K+ block). But it also has Na+ block and beta-blocking AND Ca2+ blocking activity. what a doozie
 
exmike said:
Amiodarone is actually all four classes rolled into one! But it is primarily Class III (K+ block). But it also has Na+ block and beta-blocking AND Ca2+ blocking activity. what a doozie

ditto on that, exmike is right. :)
 
True Amiodorone does do a little bit of everything, but it is considered to be a only a class III agent, according to Goodman and Gillman.
 
Angel said:
True Amiodorone does do a little bit of everything, but it is considered to be a only a class III agent, according to Goodman and Gillman.

Where does G&G say that? I see a lot in it on Amiodarone but not that it should be "considered to be only a class III agent." In a table of antiarrhythmics it lists it with the class III drugs but that's not saying that it should only be considered Class III.
 
SInce it is listed under the class III section in the book. It is considered a class III agent. My pharm professor verified this. He was the person who looked at the First Aid Book and said it was a mistake. I looked in Goodman and Gillman to see what class they listed the drug in.
 
They're not going to list a drug 4 times if it has 4 mechanisms of action.

What you said was that it should be considered only a Class III drug. You cannot conclude this from where the drug is found in Goodman and Gilman.

If you read the section on Amiodarone in G&G or look at their table on antiarrhythmics and their mechanisms it should be very clear that to call Amiodarone "only Class III" would be quite incorrect.
 
Pg 63 – Second chart should be disease vs. exposure, not disease vs. test [Annie Garment]

exposure to a risk factor

OR

Risk Factor +/-

OR

(generally) FACTOR +/-
could be a risk factor, could be a protective factor (healthy diet, drug trial)
 
Angel said:
SInce it is listed under the class III section in the book. It is considered a class III agent. My pharm professor verified this. He was the person who looked at the First Aid Book and said it was a mistake. I looked in Goodman and Gillman to see what class they listed the drug in.
tomato tomatoe. its really not a big deal where it is classified. its is FAR more important to know that amiodarone as class I, II, IV activity than to pidgeonhole it into Class III. If anything, Step I will say which class III is blah blah taking but exhibiting b-blocking activity or something. What makes amiodarone special is that it has OTHER class drug actions and it is thus VERY important to know those. If you just memorize it as STRICTLY class III, you'll get burned.
 
does anyone have the list of errors..the links on the first page doesnt work and their official site only has three errors on it ..

thanks.
 
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