Discrepancy between Goljan and FA

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Peutz Jehger causes increase in risk of colon cancer?

Goljan says no
FA says yes

There are a few others I've come across listening to his audio. Any input or any additions to this list?

i dont know where you are seeing this; RR 3rd edition pg 351: increased risk of colorectal cancers in PJ.

Now, in FA it says PJ is nonmalignant hamartomas, so maybe you mistyped? But the GI cancers arise independently of polyps due to tumor suppressor gene mux (Robbins 8th ed pg 817).

Hope that helps
 
on a side note, maybe we can make this a dedicated thread where we can bring up and discuss discrepancies or unclear items in 2010 FA since the errata will not be up for a while??
 
hmmm Goljan's Audio is where I got it from. I relistened to it and he said...."PJ is hamartomatous = non malignant = no increase in risk of CRC". I guess maybe he changed his mind in his new book? haha ok thanks for finding that.
 
You misheard him on the audio. He indicates that the polyps are hamartomas and themselves have no increased risk and that they most often are in the small intestine. He specifically mentions increased risk to malignancy including colorectal cancer (just not from THOSE polyps)
 
hmmm Goljan's Audio is where I got it from. I relistened to it and he said...."PJ is hamartomatous = non malignant = no increase in risk of CRC". I guess maybe he changed his mind in his new book? haha ok thanks for finding that.

I remember what you are talking about when I listened to it last semester. I think he might have just been hammering the point that hamartomas themselves are NOT malignant. "the PJ polyps are not malignant" meaning that the hemartoma polyps are not malignant.
 
I remember what you are talking about when I listened to it last semester. I think he might have just been hammering the point that hamartomas themselves are NOT malignant. "the PJ polyps are not malignant" meaning that the hemartoma polyps are not malignant.

Ah thanks so much guys for clearing things up! Makes sense.

Another thing...so FA says THYMOMA--> MG

Goljan says....B-Cell Hyperplasia in the Thymus (DONT PUT THYMOMA ON TEST) --> MG

What's the deal wit dat?
 
Ah thanks so much guys for clearing things up! Makes sense.

Another thing...so FA says THYMOMA--> MG

Goljan says....B-Cell Hyperplasia in the Thymus (DONT PUT THYMOMA ON TEST) --> MG

What's the deal wit dat?

If you have a question that asks, "What will a MG patient most likely have?" And the choices include both 1) thymoma and 2)germinal centers in thymus, the answer would be 2... Because it is more prevalent. But I don't think he meant, don't put thymoma on the test. If you had that same question and they didn't put "germinal centers in the thymus" as one of the choices, the answer would likely be thymoma.
 
hmmm Goljan's Audio is where I got it from. I relistened to it and he said...."PJ is hamartomatous = non malignant = no increase in risk of CRC". I guess maybe he changed his mind in his new book? haha ok thanks for finding that.

He's changed his mind on a few things. One key one is colon CA, he makes a big deal about it being the 2nd overall killer in men and women combined in the audio (despite being third for men or women independently), in most recent notes it's 3rd for men and women together.
 
Another discrepancy I found:

FA 2010 (pg. 348) -- below the diagram, it says the heme has a negative feedback relationship with ALA dehydratase.

RR (3rd edition, pg. 203) -- states this feedback relationship is with ALA synthase.

Discuss? I haven't found many sources apart from random googling, but think Goljan is correct...
 
Another discrepancy I found:

FA 2010 (pg. 348) -- below the diagram, it says the heme has a negative feedback relationship with ALA dehydratase.

RR (3rd edition, pg. 203) -- states this feedback relationship is with ALA synthase.
Discuss? I haven't found many sources apart from random googling, but think Goljan is correct...

I believe that Goljan is correct too. From the RPI website:

"Heme functions as a feedback inhibitor, repressing transcription of the gene for d-Aminolevulinate Synthase"
 
Another discrepancy

Membranoproliferative GN....

In FA 2010 p 467, it says that Type I MPGN is more associated with HBV than HCV

In Goljan 3rd p 403 AND his audio, he says that Type I MPGN is more associated with HCV while HBV is more associated with diffuse membranous glomerulopathy. My class notes also agree with Goljan. I guess this is a FA error?
 
Another discrepancy

Membranoproliferative GN....

In FA 2010 p 467, it says that Type I MPGN is more associated with HBV than HCV

In Goljan 3rd p 403 AND his audio, he says that Type I MPGN is more associated with HCV while HBV is more associated with diffuse membranous glomerulopathy. My class notes also agree with Goljan. I guess this is a FA error?

i learned it the same way - good eyes all
 
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