Goljan RR path Errors.

[Teejay]

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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[guitarguy09]

Pg 54,
Total confusion in this one . In Wiskott-aldrich syndrome, he says there is normal IgG and Increased IgA and IgE. First aid says you have normal IgE and harrisons say you have normal IgA..
Who do we believe now?

According to eMedicine: "Always interpret quantitative immunoglobulin levels based on age-related reference range values. Classic WAS shows low IgM and IgG, with normal-to-high IgA and IgE. Young infants in particular, however, may not show classic immunoglobulin abnormalities because WAS shows attrition in immunologic functions."

http://www.emedicine.com/ped/topic2443.htm

Sounds like they all may be right in some respects, I don't know. It seems like you have to do an "age-related" reference, and that people often don't present with the "classic" values. Hope this helps some.

 

[albertoss]

Errata list can be found in MS Word form on his website:

http://www.healthsciences.okstate.edu/college/biomedical/pathology/goljan.cfm

 

[fakin' the funk]

According to eMedicine: "Always interpret quantitative immunoglobulin levels based on age-related reference range values. Classic WAS shows low IgM and IgG, with normal-to-high IgA and IgE. Young infants in particular, however, may not show classic immunoglobulin abnormalities because WAS shows attrition in immunologic functions."

http://www.emedicine.com/ped/topic2443.htm

Sounds like they all may be right in some respects, I don't know. It seems like you have to do an "age-related" reference, and that people often don't present with the "classic" values. Hope this helps some.

This is the kind of thing that the USMLE will not be testing. Values that are "sometimes" normal or "sometimes" elevated don't make for cut & dry enough questions on the exam...

 

[guitarguy09]

Errata list can be found in MS Word form on his website:

http://www.healthsciences.okstate.edu/college/biomedical/pathology/goljan.cfm

thanks

 

[Teejay]

Pg 52,
Dermatomyositis is commonly caused by Ovarian cancers. (The Lancet)

 

[Old_Mil]

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?

I haven't looked them all up - but at least some of these errors aren't in the Red & Black 2004 edition...

 

[EricVorheese]

I haven't looked them all up - but at least some of these errors aren't in the Red & Black 2004 edition...

yes but the red and black 2004 ed doesnt have some of the stuff that the blue 2007 ed has..........its better to have the newer ed and correct the mistakes......

 

[Inquisitive]

pg. 579. Argyll- Robertson pupil: pupils DO accomodate but do NOT react.

Pg. 586 Werdnig- Hoffman disease: ONLY LMN disease, DOES NOT involve UMN. It is a degeneration of the anterior horns seen in babies.

 

[UCLAstudent]

On page 300, there's a mistake in the division between bacteria and viruses. Chlamydia, Rickettsia, Coxiella, and Mycoplasma should be listed under bacteria.

 

[Medikit]

On page 300, there's a mistake in the division between bacteria and viruses. Chlamydia, Rickettsia, Coxiella, and Mycoplasma should be listed under bacteria.

Yeah, I think there was supposed to be a separate subheading called "Intracellular bacteria"

 

[lekky]

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

i think id made that mistake too before when i saw it written elsewhere in his book, i thought he had a typo but he doesn't, he just wrote reduced NAD, which means NADH. (but i'd taken it to mean decreased NAD, whereas he is simply referring to the reduced form of NAD) (unless that is not what you were referring to)

 

[EricVorheese]

http://www.healthsciences.okstate.edu/college/biomedical/pathology/goljan.cfm

look right in the center of the page when it loads for "Updated Errata"

 

[Inquisitive]

Pg. 195 says that there is an increase in EPO production when the Oxygen binding curve is shifted to the left. It also says that EPO increases at high altitudes. Shouldn't EPO go up if the oxygen binding curve is shifted to the right? I thought at high altitudes, there is more production of 2,3 BPG, which causes a right shift in the oxygen binding curve, hence increased EPO production. What do you guys think? I could be totally off.

 

[Teejay]

Pg. 195 says that there is an increase in EPO production when the Oxygen binding curve is shifted to the left. It also says that EPO increases at high altitudes. Shouldn't EPO go up if the oxygen binding curve is shifted to the right? I thought at high altitudes, there is more production of 2,3 BPG, which causes a right shift in the oxygen binding curve, hence increased EPO production. What do you guys think? I could be totally off.

From my understanding of this topic, i think you're probably correct in your argument. All those factors listed for EPO release causes a right shift, so the listed left-shift is in total contrast to all those listed variables. I think is should say a right-shifted O2-binding curve.

 

[dsm4]

I think the text is correct as written. I think that high altitude and hypoxemia stimulate epo production (to increase the carrying capacity of the blood) as well as shifting the curve to the right to increase unloading of 02 at the tissue. Additionally, a left shift of the curve caused by decreased O2 carrying capacity (inhaling CO - high affinity for hemoglobin) will stimulate epo production to increase carrying capacity of the blood.


From Pub med

Biomed Biochim Acta. 1987;46(2-3):S304-8.
Dependence of erythropoietin production on blood oxygen affinity and hemoglobin concentration in rats.
Jelkmann W, Seidl J.

Plasma erythropoietin titers (Ep) were compared in rats subjected to different kinds of systemic hypoxia. Ep increased exponentially, when hypoxia was induced by exposure to simulated altitude (from less than 0.025 IU Ep/ml plasma at sea-level up to 3.65 IU Ep/ml at 7000 m). An acute increase in the O2 affinity of blood augmented Ep production in normal rats but not in rats exposed to hypobaria. Ep also rose exponentially when isovolemic anemia was induced (e.g., 0.5 IU Ep/ml plasma were found at 7 g Hb/dl blood). When the same reduction in blood O2 carrying capacity was produced by CO-inhalation (0.1% CO in air), Ep increased to 5.57 IU/ml plasma. This very high value was considered to be partly due to the very high O2 affinity of carboxyhemoglobin. These results indicate that a left shift in the hemoglobin-O2 dissociation curve produces a stimulation of Ep production, particularly, when the O2-carrying capacity of blood is lowered.

 

[JayneCobb]

Pg. 195 says that there is an increase in EPO production when the Oxygen binding curve is shifted to the left. It also says that EPO increases at high altitudes. Shouldn't EPO go up if the oxygen binding curve is shifted to the right? I thought at high altitudes, there is more production of 2,3 BPG, which causes a right shift in the oxygen binding curve, hence increased EPO production. What do you guys think? I could be totally off.

If you exclude the Sherpa's in the Himalaya's, many people who live at very high altitudes have problems with polycythemia. Hypoxemia, despite the increase in 2,3 BPG, is going to be a stimulant for EPO production.

 

[Taus]

have you looked at page 3 in the middle?....he has a box explaining the high altitude shift in detail

 

[DrThom]

pg. 122.

3. Digestion of dietary triglycerides
(3) Packaged into chylomicrons which enter the lymph system (Not
the blood)

 

[dsm4]

page 41
1. Acute inflammation (see Fig. 2.13A
2. Chronic inflammation (see Fig. 2.13B

page 377
A. Alcohol realted disorders
1. should say (see Chapter 6)
2. should say (see Chapter 6)
4. should say (see Chapter 6)

 

[Pianoboe01]

Does any one also have the 1st edition? Is there much difference in the 2nd edition other than color pictures? I'm debating whether or not I should buy it (the 1st edition was given to me by an upperclassman).

 

[SwissB4]

Yes, it's subendothelial --- that's how the "tram tracks" form.

...Not really...Tram tracks are due to the mesangium proliferating into the GBM

 

[DrThom]

Does any one also have the 1st edition? Is there much difference in the 2nd edition other than color pictures? I'm debating whether or not I should buy it (the 1st edition was given to me by an upperclassman).

Apparently the 2nd edition is a somewhat of an overhaul w/ not only the pictures but some new info as well. It might be worth a buy but I have to tell you that I haven't seen the 1st edition.

 

[Teejay]

pg 142,
Retinoblastoma-is he talking about hereditary or sporadic cases when he mentioned the one-hit theory.

 

[pleaseletmepass]

p488 - "Prolactin release is inhibited by estrogen and progesterone during pregnancy"

i believe estrogen/progesterone blocks prolactin's stimulatory activity on the breast tissue (and hence inhibits lactogenesis), rather than block its release from the anterior pituitary, because prolactin levels rise during pregnancy. please correct me if i am wrong.

-plmp

 

[Teejay]

Pg 479,
Fat necrosis of the breast presents with painless mass not painful. I got a question wrong in q-bank b/c of this mistake. I also cross-checked with robbins- pg1126.

 

[guitarguy09]

pg 142,
Retinoblastoma-is he talking about hereditary or sporadic cases when he mentioned the one-hit theory.

I believe he is talking about hereditary and "one-hit" is a mistake. It should be "two-hit" theory.

 

[Medikit]

p488 - "Prolactin release is inhibited by estrogen and progesterone during pregnancy"

i believe estrogen/progesterone blocks prolactin's stimulatory activity on the breast tissue (and hence inhibits lactogenesis), rather than block its release from the anterior pituitary, because prolactin levels rise during pregnancy. please correct me if i am wrong.

-plmp

Estrogen increases dopamine inhibition I do believe.

 

[UCLAstudent]

Page 173: there's an INCREASE in endothelin with Prinzmetal's angina (confirmed on Up-to-Date).

 

[DrThom]

pg 85.

"In Beta-thalassemia major, a nonsense mutation produces a stop codon that causes premature termination of protein translation of Beta-globin chain. (Not premature termination of DNA transcription)

 

[Medikit]

P. 323, bottom of table 16-5:
Bronchial hamartoma should be listed as peripheral according to Robbins pg. 765.

Goljan listed it as central.

 

[mesoderm]

OK, you know what? I am just as endeared to Poppy as the next 2nd year med student who felt like getting hold to his audio lectures no matter the twinges of guilt in the back of the mind, then buying RR Path, 2nd ed. was like gaining possession to the Holy Grail. However, as this thread of errors gets longer and longer, I am picking up my RR Path book less and less. I have gone back to BRS Path. I still love Dr. G, but something's gotta give!

 

[BSR1]

C. Impetigo p. 544
Most often caused now by S. aureus NOT S. pyogenes!!! I missed this on a quiz. In Robbins it talks about how S. pyogenes used to be the number one cause, but now it is S. aureus

 

[Teejay]

234
My mistake. No errors on this page.

 

[domer621]

Pg 479,
Fat necrosis of the breast presents with painless mass not painful. I got a question wrong in q-bank b/c of this mistake. I also cross-checked with robbins- pg1126.

It's painful according to Stenchever: Comprehensive Gynecology.

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

 

[mesoderm]

Painless breast masses are the cancerous ones, right? Whereas painful masses are benign?

 

[domer621]

234
in the schematic for relative polycythemia, i believe the ARROW for RBC/PV should be going up not down.

Why would it go up? It's due to a decrease in PV with no change in RBC mass... that's why it's "relative". Having an increase in PV would have the exact opposite effect.

Painless breast masses are the cancerous ones, right? Whereas painful masses are benign?

Yes, sir.

 

[Teejay]

Why would it go up? It's due to a decrease in PV with no change in RBC mass... that's why it's "relative". Having an increase in PV would have the exact opposite effect.
I'm not a professional at this but looking at it mathematically, i felt it should go up. It doesn't make any sense to me why it should go down. If you have any concerete explantions apart from the fact that its relative, i''ll appreciate it if you''ll elucidate.

 

[Teejay]

Why would it go up? It's due to a decrease in PV with no change in RBC mass... that's why it's "relative". Having an increase in PV would have the exact opposite effect.

I'm not a professional at this but looking at it mathematically, i felt it should go up. It doesn't make any sense to me why it should go down. i can undersand why it should stay normal but not go down. If you have any concerete explanations apart from the fact that its relative, i''ll appreciate it if you''ll elucidate.

 

[domer621]

I'm not a professional at this but looking at it mathematically, i felt it should go up. It doesn't make any sense to me why it should go down. If you have any concerete explantions apart from the fact that its relative, i''ll appreciate it if you''ll elucidate.

If you're getting volume depleted (e.g. sweating), the only thing you are losing is plasma volume (that's why there is a down arrow for PV in the figure). The total number of RBCs in your body (i.e. RBC mass) has no reason to change - it is normal. If your plasma volume is lowering and your RBC mass is staying the same, that means you'll have more RBCs per microliter of blood - your RBC count increases. Increased RBC count means polycythemia.

 

[Teejay]

If you're getting volume depleted (e.g. sweating), the only thing you are losing is plasma volume (that's why there is a down arrow for PV in the figure). The total number of RBCs in your body (i.e. RBC mass) has no reason to change - it is normal. If your plasma volume is lowering and your RBC mass is staying the same, that means you'll have more RBCs per microliter of blood - your RBC count increases. Increased RBC count means polycythemia.[/QUOTE

Do you know what, i'm stupid. I thought that arrow represented the entire ratio(RBC count). Looking at the whole schematic closely, i now realize the arrow is just for the plasma volume. That was why i was thrown-off. Thanks for the input though.

 

[domer621]

haha no problem, dude.

 

[jav5652]

Hi guys, my second post here. I am also using the RR book, I am little disappointed with the quantity of errors also, but it is a good book, especially with all the corrections we are making now!! . Sometimes I wish he had the book on a regular paragraph format, like BRS but containing all the information BRS misses and that Dr. Goljan puts in the book. Nevertheless, here are 2 small errors I found on the Hepatobiliary chapter, just typos.

Page 371: bottom of the page. E (1) ....."converts to anti-BHc-IgG" should be anti-HBc-IgG

Page 375: top of the page in the Blue High Yield margin: The Arrow on PT and ammonia is going Down instead of UP. He has it right on the regular text on the left side....the blue HY is wrong about PT and ammonia decreasing in Fulminant Hepatitis.

 

[DrThom]

Yet another.

Pg. 579

Argyll Robertson pupil (Pupils accommodate but do NOT react)

He wrote that they react but do not accommodate

 

[domer621]

pg. 579. Argyll- Robertson pupil: pupils DO accomodate but do NOT react.

^^

 

[DrThom]

^^

HAHA, sorry, the thread was so long and and I'm lazy

 

[leverp2000]

Not sure if this has been mentioned already, but:

p.128 D3(1) "Procoagulants include facotrs II (prothrombin), VII, IX, X, protein C, and protein S"

Protein C and Protein S are anticoagulants.

 

[phassett74]

Keep them coming people. I have submitted the latest errata, and the following are his corrections:

See my website under Pathology Department for complete up-to-date listing

ADDITIONAL ERRATAS

Page 41
Under 1. Acute inflammation (see Fig. 2-13A)
Under 2. Chronic inflammation (see Figure 2-13B)

Page 162
Table 9-1
Under Sturge-Weber syndrome
Delete (AD)
Actually, it is now considered somatic mosacism

Page 173
Under Prinzmetal’s angina
increase in endothelin

Page 300
Put Chlamydia, Rickettsia, Mycoplasma under Bacteria not Viruses heading

Page 323
Under Bronchial hamartoma
Put Peripheral (90%), Central (10%)

Page 371
Under e. Chronic HBV, (1) …converts to anti-HBc-IgG

Page 375
Margin Note
Fulminant hepatic failure: arrow for decrease transaminases, arrow for increase PT and ammonia

Pages 377 and 378
Under A. Alcohol related disorders
1. should say (Chapter 6)
3. should say (Chapter 6)
4. should say (Chapter 6)

Page 479
Under 3. Traumatic fat necrosis
c. Painless, indurated mass
add: • Painful in acute stage

Page 544
Under C. Impetigo
1. Most often caused by Staphylococcus aureus
• Streptococcus pyogenes second most common cause
3. Presence of bullae commonly occurs with Staphylococcus aureus

Page 569
Under 4. Sturge-Weber syndrome
a. Somatic mosacism
It is not autosomal dominant

Page 579
Under Table 25-4: Treponema pallidum
Argyll-Robertson pupil (pupils accommodate but do not react)

 

[Teejay]

Keep them coming people. I have submitted the latest errata, and the following are his corrections:

See my website under Pathology Department for complete up-to-date listing

ADDITIONAL ERRATAS

Page 41
Under 1. Acute inflammation (see Fig. 2-13A)
Under 2. Chronic inflammation (see Figure 2-13B)

Page 162
Table 9-1
Under Sturge-Weber syndrome
Delete (AD)
Actually, it is now considered somatic mosacism

Page 173
Under Prinzmetal’s angina
increase in endothelin

Page 300
Put Chlamydia, Rickettsia, Mycoplasma under Bacteria not Viruses heading

Page 323
Under Bronchial hamartoma
Put Peripheral (90%), Central (10%)

Page 371
Under e. Chronic HBV, (1) …converts to anti-HBc-IgG

Page 375
Margin Note
Fulminant hepatic failure: arrow for decrease transaminases, arrow for increase PT and ammonia

Pages 377 and 378
Under A. Alcohol related disorders
1. should say (Chapter 6)
3. should say (Chapter 6)
4. should say (Chapter 6)

Page 479
Under 3. Traumatic fat necrosis
c. Painless, indurated mass
add: • Painful in acute stage

Page 544
Under C. Impetigo
1. Most often caused by Staphylococcus aureus
• Streptococcus pyogenes second most common cause
3. Presence of bullae commonly occurs with Staphylococcus aureus

Page 569
Under 4. Sturge-Weber syndrome
a. Somatic mosacism
It is not autosomal dominant

Page 579
Under Table 25-4: Treponema pallidum
Argyll-Robertson pupil (pupils accommodate but do not react)

 

[phassett74]

Morning Delivery:

Page 128
Under D. Vitamin K, 3. Function
a. Gamma-Carboxylates glutamate residues in vitamin K-dependent procoagulants and anticoagulants (protein C and S)
(1) Procoagulants include factors II (prothrombin), VII, IX, and X (delete protein C and S, which are anticoagulants)

 

[Ypo.]

I don't foresee this simplification being addressed. For all practical and clinical purposes it doesn't matter, especially to a 2nd year student when this detail is unlikely to be on boards. And when serum creatinine is actually overestimated by standard serum assays and negates much of the 10% (until you start getting into serum creatinine levels above ~2.0)

This is all clinically speaking of course. .

Yep. Creatinine is secreted a little which raises it's actual urinary concentration about 20%, but the colorimetric method used to measure plasma creatinine usually overeestimates it by 20%. When calculating the GFR, the numerator (urine creatinine conc.) and denominator (plasma creat. conc.) cancel out and you get a fairly accurate representation of the real number.

For intents and purposes of the boards, we're going to have to know that creatine is used clinically to approximate the GFR because it is filtered and not reasborbed and only secreted a little (for all practical purposes the secretion is not important) and that the clearance of Inulin is the gold standard for measuring GFR because is ONLY filtered and not reabsorbed or secreted (but inulin isn't used often to determine the GFR because you have to catheterize the patient and do an iv infusion).