Goljan RR path Errors.

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Teejay

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I just wanted to start this thread for those of us who are using Goljan RR for step one study.
On page 443, it says that prolactin enhances testosterone synthesis and spermatogenesis.
I thought this was the opposit since Prolactin inhibits GnRH which inturn decreases LH and FSH. BRS phys 3rd edition 262 also says Prolactin inhibits spermatogenesis.
Anyone has an answer for this discrepancy?

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I got you, you mean it's a typo and he meant reduced NAD+.

I thought that whole exchange was hilarious.

Here is what it says:
C. IMPORTANT PRODUCTS of ALCOHOL METABOLISM:
1) Reduced nicotinamide adenine dinucleotide (NADH).


Then he goes on to list the functions it has. There is no typo. He was merely refreshing our memories that the reduced form of NAD has an extra electron (hydrogen).
 
Hey guys. Ive noticed you guys have spotted many errors here, which concerns me. I just started listening to Goljan recently, by recommendation of one of my M3 friends, and it has been simply AMAZING. He makes alot of sense out of concepts that I hadnt really understood, and just memorized.

However, if there are this many mistakes, I am unsure about whether or not I should continue with it. Its great that I am understanding, but I do not wish to understand for the wrong reasons. How helpful have you found his lectures and High Yield notes, overall?
 
Hey guys. Ive noticed you guys have spotted many errors here, which concerns me. I just started listening to Goljan recently, by recommendation of one of my M3 friends, and it has been simply AMAZING. He makes alot of sense out of concepts that I hadnt really understood, and just memorized.

However, if there are this many mistakes, I am unsure about whether or not I should continue with it. Its great that I am understanding, but I do not wish to understand for the wrong reasons. How helpful have you found his lectures and High Yield notes, overall?

Very helpful. I consider RR to be better than BRS path (plus it has pictures). Goljan's lectures have been recommended to me by more people than I can count, many of whom scored very well on the boards.

Every book has it's mistakes. I've found plenty in Robbins, too.
 
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Hey guys. Ive noticed you guys have spotted many errors here, which concerns me. I just started listening to Goljan recently, by recommendation of one of my M3 friends, and it has been simply AMAZING. He makes alot of sense out of concepts that I hadnt really understood, and just memorized.

However, if there are this many mistakes, I am unsure about whether or not I should continue with it. Its great that I am understanding, but I do not wish to understand for the wrong reasons. How helpful have you found his lectures and High Yield notes, overall?
he keeps an updated list of errors on his website (as posted earlier in this thread): http://www.healthsciences.okstate.edu/college/biomedical/pathology/goljan.cfm

problem solved
 
Hey guys. Ive noticed you guys have spotted many errors here, which concerns me. I just started listening to Goljan recently, by recommendation of one of my M3 friends, and it has been simply AMAZING. He makes alot of sense out of concepts that I hadnt really understood, and just memorized.

However, if there are this many mistakes, I am unsure about whether or not I should continue with it. Its great that I am understanding, but I do not wish to understand for the wrong reasons. How helpful have you found his lectures and High Yield notes, overall?

goljan is overrated

i would argue that studyin from his RR Path book is counterproductive since it contains more incorrect info than correct info

if you want my advice, you should round up all your goljan materials and store them in that circular file you have at the side of your desk

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:thumbdown:
 
I thought that whole exchange was hilarious.

Here is what it says:
C. IMPORTANT PRODUCTS of ALCOHOL METABOLISM:
1) Reduced nicotinamide adenine dinucleotide (NADH).


Then he goes on to list the functions it has. There is no typo. He was merely refreshing our memories that the reduced form of NAD has an extra electron (hydrogen).

Yeah, admittedly my reading comprehension is pretty terrible. This isn't the first time I've been really wrong.
 
Very helpful. I consider RR to be better than BRS path (plus it has pictures). Goljan's lectures have been recommended to me by more people than I can count, many of whom scored very well on the boards.

Every book has it's mistakes. I've found plenty in Robbins, too.

he keeps an updated list of errors on his website (as posted earlier in this thread): http://www.healthsciences.okstate.edu/college/biomedical/pathology/goljan.cfm

problem solved

Sweet, thanks for the help guys! Thats definitely a relief.
 
Yeah, admittedly my reading comprehension is pretty terrible. This isn't the first time I've been really wrong.

It's easy to do with the format of the book. The outline format makes it confusing (the book doesn't bold many of the sub-topics and has to use numbers more than once under one topic so you are sometimes unsure when he is starting a new topic).



I've heard that Goljan's lectures basically follow the format of RR (so you can follow along in the book with the lecture). Anyone know if this is true?
 
It's easy to do with the format of the book. The outline format makes it confusing (the book doesn't bold many of the sub-topics and has to use numbers more than once under one topic so you are sometimes unsure when he is starting a new topic).



I've heard that Goljan's lectures basically follow the format of RR (so you can follow along in the book with the lecture). Anyone know if this is true?
they follow it close enough.....and the index is really good....ie not difficult to follow


and about the format....its way better then the 1st edition...but this is the first time I've ever had to use a highlighter in my life....the whole RR series could take a lesson from the new editions of BRS books about bolding and highlighting to make it easier to follow
 
Another error - I checked Dr. Goljan's website and it isn't posted there. I skimmed through this thread and haven't seen it, so here goes.

Nutritional Disorders, Page 128:

D. Vitamin K
3.a.1. - Procoagulants include factors II (prothrombin), VII, IX, X, protein C, and protein S.


Protein C and Protein S are anti-coagulants, not pro-coagulants.



EDIT: My bad, this was covered in post #99 on this thread. Thanks to phassett for pointing this out.
 
they follow it close enough.....and the index is really good....ie not difficult to follow


and about the format....its way better then the 1st edition...but this is the first time I've ever had to use a highlighter in my life....the whole RR series could take a lesson from the new editions of BRS books about bolding and highlighting to make it easier to follow
seriously, I love the 'nuggets of info' on the side, but how hard is it to BOLD the key points here and there?
 
Another error - I checked Dr. Goljan's website and it isn't posted there. I skimmed through this thread and haven't seen it, so here goes.

Nutritional Disorders, Page 128:

D. Vitamin K
3.a.1. - Procoagulants include factors II (prothrombin), VII, IX, X, protein C, and protein S.


Protein C and Protein S are anti-coagulants, not pro-coagulants.

Check thread #99
 
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Sorry guys this is not a book mistake but a question/comment. Have any of you gone to the studentconsult.com website to do the RR of Path questions? Because it seems that they only have a couple chapters (about 8) up unless I am doing something wrong. Can anybody care to clarify please.

Thanks
 
When discussing intravascular hemolysis on page 215 in the blue box in the middle of the page he says that

"The amot Hb that complexes (to haptoglobin) is so small that unconjugated bilirubin is not significantly increased"

This does not make any sense since if the unconjugated bilirubin did not increase, (and there is no reason why conjugated bilirubin would increase) there would be no jaundice in patients with intravascular hemolysis. However there is jaundice in patients with intravascular hemolysis such as G6PD deficiency.

according to emedicine: In G6PD deficiency:

"Jaundice and splenomegaly may be present during a crisis."

http://www.emedicine.com/med/topic900.htm

Also my hemotology professor confrmed this and said that there is jaundice in intravascular hemolysis.

Any takes on this??
thanks
 
When discussing intravascular hemolysis on page 215 in the blue box in the middle of the page he says that

"The amot Hb that complexes (to haptoglobin) is so small that unconjugated bilirubin is not significantly increased"

Any takes on this??
thanks

I'm not too sure, but perhaps it's different for intravascular vs. extravascular hemolysis. If you check out page 367 he lists extravascular hemolysis as a cause for increased unconjugated bilirubin (producing jaundice), however with no mention of intravascular hemolysis (interesting?). However, Up-to-date conflicts with this and also has intravascular hemolysis listed under a cause of jaundice: http://patients.uptodate.com/image.asp?file=hepa_pix/classi21.htm. Can anyone help clarify what Goljan is trying to say?
 
hmmm...i encountered a question in qbank which assumed u knew that unconj bilirubin was associated with extrav. not intravas. hemolysis.
 
It's painful according to Stenchever: Comprehensive Gynecology.

I try to avoid using Robbins to cross-check clinical signs.

Fat necrosis is a rare condition of the breast but is of clinical importance because it produces a mass, often accompanied by skin or nipple retraction, that is clinically indistinguishable from carcinoma. Trauma is the presumed etiology, although only about half of patients recall a history of injury to the breast. Ecchymosis is occasionally observed in conjunction with the mass. Tenderness may or may not be present. If untreated, the mass associated with fat necrosis gradually disappears. Should the mass not resolve after several weeks, a biopsy should be considered. The entire mass should be excised, primarily to rule out malignant processes.

according to Matthew M. Poggi, MD, & Kathleen Harney, MD
Current OB/GYN > Chapter 63. The Breast > Diseases of the Breast
(cannt give page number I found it on e-book through my school library)

Also on Day 1 of Goljan's lecture series, under "Cell Injury 2" (34:33) he says that calcification due traumatic fat necrosis of breast is painful vs calcification in a cancer which is painless
 
Page 320
Second blue high yield fact: Should say increase in NaCl in sweat...
 
Page 307 under Silicosis d. (2):

Book says that it increases risk for TB AND lung cancer

My class notes and BRS path both have it as only increasing the risk for TB and NOT cancer.
 
Page 320
Second blue high yield fact: Should say increase in NaCl in sweat...
its the same thing - increased NaCl in sweat is how you lose NaCl from the body.......maybe he should have been clearer by saying loss of NaCl via sweat
 
If anyone's interested...

I don't think this has been mentioned yet. Sorry if it has. Pg 592 (top) it states there is "Increased CSF protein and lymphocytes" in Guillain-Barre Syndrome.

GBS is actually characterized by an albuminocytological dissociation, in which CSF protein is elevated without a corresponding pleocytosis. I was thinking the lymphocyte count should be normal, not increased as Goljan says.
 
Found another possible error:

Pg. 490 in the margin states "Water Deprivation Test: defines the type of diabetes insipidus"

I thought that whether you had Central or Nephrogenic, the end result is the same: no ADH effect, so you have decreased urine osmolarity and increased plasma osmolarity.

I think it should read "Injection of ADH: defines the type of diabetes insipidus"

Please correct me if I screwed this up.
 
Found another possible error:

Pg. 490 in the margin states "Water Deprivation Test: defines the type of diabetes insipidus"

I thought that whether you had Central or Nephrogenic, the end result is the same: no ADH effect, so you have decreased urine osmolarity and increased plasma osmolarity.

I think it should read "Injection of ADH: defines the type of diabetes insipidus"

Please correct me if I screwed this up.

the water deprivation test includes that part.
 
hoping ppl still check this posting

i wasnt able to find this in the posted erratas document

in the text on p 526, table 23-1 under osteochondroma it states "outgrowth of bone (exocytosis) capped by benign cartilage." Several times in the audio lectures he states it is an outgrowth of cartilage capped by bone. Can anyone clarify which it is? thanks
 
On page 123, the margin note for Anorexia Nervosa says the most common cause of death in due to ventricular arrhythmia. On the very next page, in the actual notes, ventricular arrhythmia is listed as the most common cause of death for Bulimia Nervosa.

I know that patients with either AN and BN have associated heart conditions, but this doesn't look right, and, I even remember associating Ventricular arrhythmia with Bulimia Nervosa. I've checked in the Goljan Errata and Classification doc, and I did not find anything, so I am posting this info.
 
There is a minor discrepancy between pages 209-210:

p 209
Blue margin note states "Folate deficiency: alcohol most common cause"

p 210
Table 11-4 states "Decreased intake [of folate] most common cause of folate deficiency"

Page 209 should state "Folate deficiency: decreased intake most common cause"
 
There is a minor discrepancy between pages 209-210:

p 209
Blue margin note states "Folate deficiency: alcohol most common cause"

p 210
Table 11-4 states "Decreased intake [of folate] most common cause of folate deficiency"

Page 209 should state "Folate deficiency: decreased intake most common cause"

Goljan can be a bit undisciplined with his explanations. I had the same question upon first read, here's my take:
I think the point he was trying to make is that chronic alcoholism is the most common cause of folate defeciency in the US.

Alcohol blocks the reabsorbtion of monoglutamate folate (pg. 209), thereby decreasing folate uptake. Also, chronic alcoholics are genrally malnourished, as alcohol drinking takes precedence over eating solid food (table 11-4 under causes of decreased intake).

Just my thoughts; Goljan is AMAZING, but I agree, sometimes his associations are loose.
 
Hi, when reviewing the cardiology chapter I noticed that on page 187 it says that chronic rheumatic fever causes aortic stenosis and on page 188 it says that chronic rheumatic fever causes aortic regurgitation. Is this an error? I find it surprising that chronic RF can cause both AS and AR when RF causes mitral regurgitation and chronic RF causes mitral stenosis. I tried emailing Dr Goljan this question but since he never responded, but any clarification would be a huge help.
 
Hi, when reviewing the cardiology chapter I noticed that on page 187 it says that chronic rheumatic fever causes aortic stenosis and on page 188 it says that chronic rheumatic fever causes aortic regurgitation. Is this an error? I find it surprising that chronic RF can cause both AS and AR when RF causes mitral regurgitation and chronic RF causes mitral stenosis. I tried emailing Dr Goljan this question but since he never responded, but any clarification would be a huge help.

I thought both can occur simultaneously? Stenosis can lead to resistance in systole due to a partially occluded valve (not able to fully open) and patency during diastole (inability of the valve to completely close) leading to regurg
 
wow, these errors are just as bad as those in FA.

I hope there aren't anymore errors. =-/
 
From what I remember in Hematology it goes something like this:
First of all G6PD deficient patients can have bouts of intravascular hemolysis WITH A MILD EXTRAVASCULAR COMPONENT as well - this would explain the slight jaundice and splenomegaly. For the most part Goljan's associations are spot on:
With intravascular you are supposed to think increased LDH, hemoglobinuria, and decreased haptoglobin
With extravascular you are supposed to think jaundice (due to unconj bilirubin), increased LDH, macrophage phagocytosis (explaining the splenomegaly) etc.
Moreover, there might be slight jaundice from pure intravascular hemolysis alone (as in Malaria) but I believe it is more profound with extravascular hemolysis.

I am not sure if that is a hundred percent correct but that is how I remember studying it. If anyone has a better explanation I would be glad to learn from it.


When discussing intravascular hemolysis on page 215 in the blue box in the middle of the page he says that

"The amot Hb that complexes (to haptoglobin) is so small that unconjugated bilirubin is not significantly increased"

This does not make any sense since if the unconjugated bilirubin did not increase, (and there is no reason why conjugated bilirubin would increase) there would be no jaundice in patients with intravascular hemolysis. However there is jaundice in patients with intravascular hemolysis such as G6PD deficiency.

according to emedicine: In G6PD deficiency:

"Jaundice and splenomegaly may be present during a crisis."

http://www.emedicine.com/med/topic900.htm

Also my hemotology professor confrmed this and said that there is jaundice in intravascular hemolysis.

Any takes on this??
thanks
 
Hi, when reviewing the cardiology chapter I noticed that on page 187 it says that chronic rheumatic fever causes aortic stenosis and on page 188 it says that chronic rheumatic fever causes aortic regurgitation. Is this an error? I find it surprising that chronic RF can cause both AS and AR when RF causes mitral regurgitation and chronic RF causes mitral stenosis. I tried emailing Dr Goljan this question but since he never responded, but any clarification would be a huge help.


RF causes both mitral stenosis and regurgitation.

Stenosis takes many years to develop.

RF causes a myocarditis that may bring about cardiac dilation. This dilation may evolve into functional mitral regurgitation.


Hope that helps.
 
Goljan can be a bit undisciplined with his explanations. I had the same question upon first read, here's my take:
I think the point he was trying to make is that chronic alcoholism is the most common cause of folate defeciency in the US.

Alcohol blocks the reabsorbtion of monoglutamate folate (pg. 209), thereby decreasing folate uptake. Also, chronic alcoholics are genrally malnourished, as alcohol drinking takes precedence over eating solid food (table 11-4 under causes of decreased intake).

Just my thoughts; Goljan is AMAZING, but I agree, sometimes his associations are loose.

This is, in fact, correct. According to Goljan's & Pelley's RR Biochemistry book pg. 60, "Folic acid defienciency is most commonly caused by alcoholism."
 
Page 403, table 19-5:
Adult polycystic kidney disease --> Other findings...risk for developing renal cell carcinoma

AND

Page 426:
Renal cell carcinoma --> Risk factors --> (3) Adult polycystic kidney disease.

I couldn't find this association in any of my other review books. Screwed me on a Q-bank question, too. Anyone else?
 
So are there anymore errors in this book? or are the ones listed on Goljan's website pretty much it?

Does he update that errata list?
 
^^ Thanks for the informative post, but I was asking if Goljan updates that errata list on his website, or is it the same errata list that's been posted before?
 
I'm also curious to know if any of the errata in that staggering list have been corrected in subsequent printings.

I didn't check all but randomly went through the errata and looks like all are fixed.

I got mine a couple of months ago from Amazon.
 
hmm, this thread looks to have been bumped, so.........


Were there any added errors to this errata list? I'm not going to go through the list again to check; just thought maybe someone already knew.

Thanks.
 
I'm also curious to know if any of the errata in that staggering list have been corrected in subsequent printings.

Looked at the errata and maybe corrected 1 thing in my RR path book. It looks like it everything has been corrected in my edition.
Got mine off ebay 2 weeks ago. :hardy:
 
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