errors in FA 2007

[viostorm]

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I suggest we post any errors we find in FA 2007 here.

I'll start:

P. 106 - Deficient enzyme on Von Gierke's disease is Glucose-6-phosphotase not glucose-6-phosphate.

 

[DrThom]

Isn't that more of a typo than an error?

 

[viostorm]

Isn't that more of a typo than an error?

Isn't a typo a type of error?

Ok, just kidding ....

Sure ... who knows, I was just reviewing my biochem and was like WTF?!?

 

[guitarguy09]

On page 145 it has E. coli O157:H7 listed as Enteroinvasive (EIEC) when it should be under Enterohemorrhagic E. coli (EHEC).

 

[epalantequevoy]

pg 194 Hashimoto's is a type II hypersensitivity

 

[automan]

PG 98 - Uncoupling agents increase (not decrease) the permeability of the membrane, causing a drop in the proton gradient and a increase (not decrease) in oxygen consumption. (That's why there is a risk of hyperthermia, everything keeps churning because no ATP is being made and the energy produces heat - it's like brown fat)

I don't know how they managed to screw this up, as the 2006 version is correct. Also, if I am wrong, please let me know.

 

[lord_jeebus]

I don't know how they managed to screw this up, as the 2006 version is correct.

***Conspiracy Theory***

If FA didn't have a steady supply of errors, who would buy a newer edition fresh with "corrections"?

 

[domer621]

***Conspiracy Theory***

If FA didn't have a steady supply of errors, who would buy a newer edition fresh with "corrections"?

Yep, it's all about the money. Every version will have errors.

 

[guitarguy09]

(p.223) Quinidine INHIBITS cytochrome P-450 (enzyme 2D6), it is not an inducer (as listed).

 

[Teejay]

I suggest we post any errors we find in FA 2007 here.

I'll start:

P. 106 - Deficient enzyme on Von Gierke's disease is Glucose-6-phosphotase not glucose-6-phosphate.

This is a great thread. Thanks viostorm for starting it. Hope to contribute my best to it. Good luck everyone.

 

[Marigold]

OK, I'm definitely not a biochem whiz, so correct me if I'm wrong, but it seems that there is an error on page 96:

In the "Regulation by F2,6BP" box, the arrows between Fructose-6-phosphate and Fructose-2,6-bisphosphate should be reversed. That, or you could switch FBP2 and PFK2 so that they're beside the correct arrows.

 

[TheEleventhReel]

On page 394, under E. Collecting Tubules, the pic shows a Na/H ATPase antiporter. The pic it's taken from in Katzung shows the ATPase as only secreting protons (no sodium involved).

 

[automan]

On page 394, under E. Collecting Tubules, the pic shows a Na/H ATPase antiporter. The pic it's taken from in Katzung shows the ATPase as only secreting protons (no sodium involved).

Another example where 2006 was correct, yet 2007 somehow got screwed up..........

 

[TheEleventhReel]

Jeebus is right. It is a conspiracy...

 

[Game Point]

Seeing as how there are a few errors in the 2007 version that aren't present in the 2006, and obviously vice versa, is it overall worth it to get the new First Aid 2007 if you already have the 2006? What are your opinions?

 

[domer621]

I think if you've already written in your 2006 FA, you shouldn't buy the 2007 edition. Don't forget that there's already a big errata thread for 2006, too, so at least you know most of what to correct.
If you haven't marked up your 2006 FA, you might as well buy the new one. They did add some more material, like a new general path section (which is pretty much worthless since every student uses BRS or RR for path, anyway) and some more diagrams.
Just my 2 cents.

 

[Quiscribit]

The upper right kidney anatomy diagram on page 391 is partially inaccurate. Where interlobular artery & vein is shown, is in fact the arcuate artery & vein. This mistake is in both 2006 and 2007 FA.

 

[studentdr9123]

Pulmonic area - murmur of pulmonic stenosis is a systolic murmur (not diastolic as listed)

Correct me if this in wrong.

 

[Teejay]

273? Please correct me if i am wrong, but Metformin is normally used in patients who have type 2 diabetes mellitus because it increases insulin sensitivity(Lippincott Pharm) and it sometimes requires insulin for its action. So why would they say it is used in patients without islet fuction which is basically type 1 diabetes mellitus.

 

[justin334]

273? Please correct me if i am wrong, but Metformin is normally used in patients who have type 2 diabetes mellitus because it increases insulin sensitivity(Lippincott Pharm) and it sometimes requires insulin for its action. So why would they say it is used in patients without islet fuction which is basically type 1 diabetes mellitus.

Eventually the islet cells of a Type II diabetic will crap out because they're cranking out so much insulin over a long period of time. Metformin is useful in this case because, unlike sulfonylureas and glitazones, it doesn't act by increasing insulin production.

 

[automan]

Eventually the islet cells of a Type II diabetic will crap out because they're cranking out so much insulin over a long period of time. Metformin is useful in this case because, unlike sulfonylureas and glitazones, it doesn't act by increasing insulin production.

I agree that metformin can be used in both.

Metformin acts via an unknown mechanism to decrease hepatic gluconeogenesis. This would be beneficial for both type 1 and type 2.

It is used mostly for type 2 instead of type 1 because type 1 is easily managed with insulin, however, it would also work in type 1 pts.

 

[lord_jeebus]

273? Please correct me if i am wrong, but Metformin is normally used in patients who have type 2 diabetes mellitus because it increases insulin sensitivity(Lippincott Pharm) and it sometimes requires insulin for its action. So why would they say it is used in patients without islet fuction which is basically type 1 diabetes mellitus.

I do not think the USMLE would offer a question in which the answer is to give metformin to a type 1 diabetic. There doesn't seem to be strong enough evidence for its use in the type 1 DM population on the whole -- in my opinion they like to stick to things with very strong evidence.

That's not to say there's no benefit to doing so. For instance, one small study:

Diabet Med. 2006 Oct;23(10):1079-84

The effect of metformin on blood glucose control in overweight patients with Type 1 diabetes.

In a randomized, double-blind, cross-over study, we investigated the effect of metformin on blood glucose control and daily insulin dose in overweight patients with Type 1 diabetes. METHODS: We studied 15 C-peptide-negative patients, aged 48 +/- 12 years, with a body mass index of 31.3 +/- 2.6 kg/m(2). Each patient had a 'screening visit', followed by a 4-week 'run-in' period. This was followed by two separate 16-week 'study' (treatment) periods, separated by a 4-week 'wash-out' period. Patients received either metformin or placebo during the 'study' periods, in random order. RESULTS: HbA(1c) was significantly lower following 16 weeks of treatment with metformin (7.8 +/- 1.1%) compared with baseline (8.5 +/- 1.4%; P < 0.005) and placebo (8.6 +/- 1.2%; P < 0.005). Fasting plasma glucose, following 16 weeks of metformin treatment, was significantly lower (8.3 +/- 2.8 mmol/l) compared with baseline (12.4 +/- 3.0 mmol/l; P < 0.01) and placebo (12.6 +/- 3.4 mmol/l; P < 0.01). Compared with baseline (60 +/- 14 units), total daily insulin dose was significantly lower following the addition of metformin (50 +/- 13 units; P < 0.05) and this final total daily insulin dose in the metformin group was lower compared with placebo (58 +/- 12 units, P < 0.05). Body weight did not change following metformin or placebo treatment. CONCLUSION: Metformin can effectively improve glycaemic control and reduce the total daily insulin dose in overweight people with Type 1 diabetes.

 

[pristine21]

Pulmonic area - murmur of pulmonic stenosis is a systolic murmur (not diastolic as listed)

Correct me if this in wrong.

You are correct, the diagram should say Systolic murmur here, however it does have it correct on the left hand side where it shows both pulmonic and aortic Regurg are diastolic...

I also don't know what a "flow murmur" is, and I also thought both VSD and ASD could be heard more during systole, but it only says that VSD is heard then and ASD is heard during diastole...???

This makes me nervous

 

[pristine21]

Another example where 2006 was correct, yet 2007 somehow got screwed up..........

I actually came across this prob during my renal theme- and my professor said that almost all the channels primarily use one ion but in disease states it will take others- this may be an example of this ( another one is Cl at the distal tubule instead of H+ in metabolic alkalosis with severe diarrhea...)

 

[pristine21]

PG 98 - Uncoupling agents increase (not decrease) the permeability of the membrane, causing a drop in the proton gradient and a increase (not decrease) in oxygen consumption. (That's why there is a risk of hyperthermia, everything keeps churning because no ATP is being made and the energy produces heat - it's like brown fat)

I don't know how they managed to screw this up, as the 2006 version is correct. Also, if I am wrong, please let me know.

Wouldn't O2 consumption decrease if it was no longer needed for respiration to make ATP?

 

[Pepsy]

PG 98 - Uncoupling agents increase (not decrease) the permeability of the membrane, causing a drop in the proton gradient and a increase (not decrease) in oxygen consumption. (That's why there is a risk of hyperthermia, everything keeps churning because no ATP is being made and the energy produces heat - it's like brown fat)


Wouldn't O2 consumption decrease if it was no longer needed for respiration to make ATP?

P/O ratio - ATP molecules produced per O atom reduced.
NADH - P/O ratio of 3
FADH - p/O ratio of 2
2,4-dinitrophenol, an uncoupler that dissipates the H+ gradient has a P/O ratio of 0. [info from kaplan, pg. 34]

Having said that, Uncoupling agents 2,4-DNP, aspirin, Thermogenin [protein in brown fat], UCP, CCCP, FCCP would cause:

Increase permeability of membrane
Decrease proton gradient
Decrease O2 consumption

CCCP --> carbonyl cyanide m-chloro phenyl hydrazone.This is a lipid-soluble weak acid which is a very powerful mitochondrial uncoupling agent.
FCCP --> p-trifluoromethoxy carbonyl cyanide phenyl hydrazone (similar to above)
UCP --> from FA, dont know this one. neone?

 

[Pepsy]

Pg. 97 -

PDH def - said to result in lactic acidosis --> (leads to metabolic acidosis)

Rx - increase intake of ketogenic nutrients.

----- doesnt ketosis lower plasma pH causing a metabolic acidosis (ketoacidosis) as well. Initially, i thought the arrow should face down but i could be wrong. can anyone clarify. thnx in advance.

 

[Teejay]

Pg. 97 -

PDH def - said to result in lactic acidosis --> (leads to metabolic acidosis)

Rx - increase intake of ketogenic nutrients.

----- doesnt ketosis lower plasma pH causing a metabolic acidosis (ketoacidosis) as well. Initially, i thought the arrow should face down but i could be wrong. can anyone clarify. thnx in advance.

Hmmmmm! Lippincott biochem says PHD is the most common cause of congenital lactic acidosis. Whats your source? You might wanna cross-Check it again. Maybe it causes both i don't know.

 

[automan]

I am sorry, but I can't make sense of your post.

I can tell you for sure that what you said in the middle is half correct, but you are missing the main idea of this entire concept.

Here's what I know for sure:

Mitochondrial uncouplers, such as UCP, 2-4DNP, asprin, thermogenin disrupt the proton gradient across the innner mitochondrial membrane. Without a proton gradient, there is nothing driving ATPsynthase and thus no ATP being produced.

What happens inside the cell when ATP gets low.............. the cell will try to make more ATP. How does a cell make more ATP...................it increases electron transport. This is where the cell runs into trouble.

It is shunting all of its energy down the electron transport chain, and using up all of its oxygen (because oxygen is the terminal electron acceptor). Thus, increasing oxygen consumption But the poor cell is fighting an uphill battle. All of the protons that are being pumped to the mitochondrial intermembrane space are sneaking back into the matrix because of the uncoupling agent. Thus, no ATP is being produced.

Bottom line: The uncoupler decreases the proton gradient, decreases ATP synthesis, but INCREASES oxygen consumption becuase it is still trying to make ATP, it just can't. So ATP synthesis stops, but oxygen utilization continues as the cell tries to make up for it's decreased ATP.

Now think about the hyperthermia effect, the whole reason you get hyperthermia is the cell is constantly producing excess heat from the excess electron flow. The only way electrons can flow is if oxygen is waiting at the end ready to take them away. So you can't get hyperthermia if oxygen consumption stops.

I hope that helps, and sorry in advance for typos.

[/I]


P/O ratio - ATP molecules produced per O atom reduced.
NADH - P/O ratio of 3
FADH - p/O ratio of 2
2,4-dinitrophenol, an uncoupler that dissipates the H+ gradient has a P/O ratio of 0. [info from kaplan, pg. 34]

Having said that, Uncoupling agents 2,4-DNP, aspirin, Thermogenin [protein in brown fat], UCP, CCCP, FCCP would cause:

Increase permeability of membrane
Decrease proton gradient
Decrease O2 consumption

CCCP --> carbonyl cyanide m-chloro phenyl hydrazone.This is a lipid-soluble weak acid which is a very powerful mitochondrial uncoupling agent.
FCCP --> p-trifluoromethoxy carbonyl cyanide phenyl hydrazone (similar to above)
UCP --> from FA, dont know this one. neone?

 

[automan]

Hmmmmm! Lippincott biochem says PHD is the most common cause of congenital lactic acidosis. Check your source again. May be it causes both.

I agree, PDH deficiency = lactic acidosis, decreased acetly CoA, and it is usually fatal at an early age.

 

[Pepsy]

The only way electrons can flow is if oxygen is waiting at the end ready to take them away. So you can't get hyperthermia if oxygen consumption stops.

well said, automan.

PDH deficiency = lactic acidosis, decreased acetly CoA, and it is usually fatal at an early age

i agree that PDH def does cause lactic acidosis. But my question is why treat it with "increase ketogenic nutrients" (as said in FA, pg. 97), if ketosis (overproduction of ketones) causes metabolic acidosis as well. thnx.

 

[JDWflash44]

well said, automan.


i agree that PDH def does cause lactic acidosis. But my question is why treat it with "increase ketogenic nutrients" (as said in FA, pg. 97), if ketosis (overproduction of ketones) causes metabolic acidosis as well. thnx.

You treat it that way because if you are using ketones(fats basically) as your energy source, then you bypass the PDH reaction and can convert the ketones to acetyl co-a and use this in aerobic respiration. This alleviates the need for PDH, right?? I think its one of these "better of two evils" situations.

 

[Marigold]

well said, automan.


i agree that PDH def does cause lactic acidosis. But my question is why treat it with "increase ketogenic nutrients" (as said in FA, pg. 97), if ketosis (overproduction of ketones) causes metabolic acidosis as well. thnx.

Ketones, for a PDH deficiency baby, serve as an ALTERNATE source of energy (since they are unable to get energy the normal way, i.e. from making Acetyl CoA out of Pyruvate).

 

[Marigold]

You treat it that way because if you are using ketones(fats basically) as your energy source, then you bypass the PDH reaction and can convert the ketones to acetyl co-a and use this in aerobic respiration. This alleviates the need for PDH, right?? I think its one of these "better of two evils" situations.

Better of two evils, exactly.

 

[Teejay]

263 It is supposed to be 3-B-hydroxysteroid dehydrogenase (Lippincott biochem) not 33 hydroxysteroid dehydrogenase FOR pregnenolone--to--progesterone

 

[etlee]

Pg. 105 Glycogen

Glycogen synthase catalyzes the rxn with UDP-glucose as the substrate not the product. Also, the arrow is incorrectly shown as irreversible on the main diagram pg 94 between G-6-P and G-1-P.

 

[Pepsy]

Pg. 105 Glycogen

Glycogen synthase catalyzes the rxn with UDP-glucose as the substrate not the product. Also, the arrow is incorrectly shown as irreversible on the main diagram pg 94 between G-6-P and G-1-P

you're right on pg. 105. thnx. i changed the enzyme (1) to UDP-glucose pyrophosphyrlase and for the bottom reaction, added an enzyme (1.5) which would be glycogen synthase. product being glycogen, with white circle and 4 black dots.

as for pg. 94, i dont think they meant to show many rxns as reversible/irreversible other than glycolysis and the ones with stars. Look at HMP shunt and TCA cycle, for example. I also added few more key enzymes to that diagram that might be worth mentioning to some.

19) "isocitrate dehydrogenase" - RLS of TCA
20) "carboamoyl phosphate synthase" - RLS of Urea cycle
21) "Acetyl-CoA carboxylase" - RLS of FA synthesis
21) "CAT-I" - RLS of FA oxidation (I drew an arrow from Fatty acids to "acetly-coA" that i wrote myself on the side)
22) MCAD (clinically relevant)

 

[Hosklal]

Hey everyone, this forum is great, so i thought i would add one.

On page 287, under liver anatomy, Zone III is actually the most sensitive part of the liver to toxic injury(not Zone I). Zone III contains most of the P450 enzymes that make it the reason it is so sensitive.

 

[automan]

Hey everyone, this forum is great, so i thought i would add one.

On page 287, under liver anatomy, Zone III is actually the most sensitive part of the liver to toxic injury(not Zone I). Zone III contains most of the P450 enzymes that make it the reason it is so sensitive.

Thanks for the post, I have a quick question as I used to think the same way as first aid. (Now I am not sure what to think)

Since zone 1 gets the biggest dose of toxin, wouldn't that be the area most likely to be damaged?

Open to discussion and I don't really know. I can see the p450s converting benign things into damaging things and thus, if most of the p450s are in zone 3, then it could be damaged more.

We'll see what the super sluths come up with..........

 

[Taus]

zone 3 is the furthest away from the source of oxygen

 

[guitarguy09]

I can definitely see that Zone III is most affected in bouts of ischemia. However, the toxin issue is a little different. I'm thinking that Zone I would show the most effects if the toxin was already activated and causing damage, because most would then be delivered to Zone I. However, if the drug/toxin needs to be metabolized to its toxic form first, then maybe more effects would be seen in Zone III (do to the P-450 system, where the drug is metabolized).

This is of course not supported with a source, I attempted a brief search, but couldn't find much so I'm just going off of my own reasoning. Therefore, don't hold me to anything. Anyone else know for sure?

 

[justin334]

Hey everyone, this forum is great, so i thought i would add one.

On page 287, under liver anatomy, Zone III is actually the most sensitive part of the liver to toxic injury(not Zone I). Zone III contains most of the P450 enzymes that make it the reason it is so sensitive.

Zone 1 = most sensitive to toxins
Zone 3 = most sensitive to ischemic injury

and I seem to remember Zone 2 being succeptible to infection but I would have to look that up and I don't want to.

 

[Hosklal]

I apologize for the earlier post. It does appear that Zone I is most sensitive to toxic injury b/c it does not have the P450 enzymes to detox the toxins. Zone III is most sensitive to ischemia. In order to make it up to you guys, I posted an example of ISCHEMIC injury!

This is the question:
A donor liver arrives in NYC from Chicago 7 hrs after harvest. A biopsy is performed on arrival to check for ischemic injury. The sensitive oxidase P450 system is very susceptible to ischemia. In which of the following regions of the liver is this system located?
ANSWER: Pericentral Vein Zone(Zone III)

 

[Taus]

I apologize for the earlier post. It does appear that Zone I is most sensitive to toxic injury b/c it does not have the P450 enzymes to detox the toxins. Zone III is most sensitive to ischemia. In order to make it up to you guys, I posted an example of ISCHEMIC injury!

This is the question:
A donor liver arrives in NYC from Chicago 7 hrs after harvest. A biopsy is performed on arrival to check for ischemic injury. The sensitive oxidase P450 system is very susceptible to ischemia. In which of the following regions of the liver is this system located?
ANSWER: Pericentral Vein Zone(Zone III)

phew...now I can finally sleep at night..

jk..thank you for clearing that up

 

[TN Aaron]

Lupus deposits should be subendothelial, not subepithelial accoring to both the grid book and the Goljan audio lecture Renal 1

(EDIT) The sentence above on page 400 is referring to the membranous form (Type V) of lupus. In membranous form, the immune complex deposits are subepithelial (but this accounts for only 10% of Lupus patients).

BRS Pathology page 260 says that Type iV SLE (diffuse proliferative form) is the prototype of lupus nephropathy and is the most severe form of the disease. This is the type that has subendothelial deposits.

 

[guitarguy09]

p.295 where it talks about Jaundice:

Goljan's RR Path (2nd ed.) p.367 & 369 say that hepatocellular (mixed unconj./conj.) bilirubinemia has an increased urine urobilinogen because it is redirected from the liver to the kidneys (and thus more appears in urine). However, FA on p.295 says urobilinogen is normal/decreased in hepatocellular (mixed) jaundice. I know this is being "nit-picky" or whatever, but I'm just trying to understand the processes. So which is correct??

(Please don't quote BRS because I think FA's chart is essentially copied from there. Thanks.)

 

[automan]

I'll give it a shot......

I agree with Goljan, here's why:

As you said, in a mixed hyperbilirubinemia (EX: viral/alcoholic hepatitis) the liver is damaged and lab results show increased CB and UCB. The liver cells are damaged, therefore they have decreased ability to produce CB which leads to increased in UCB. However, they are still able to produce CB, (if they couldn't, it wouldn't be a mixed hyperbilirubinemia and only UCB would be elevated) and that accounts for the increased CB in the urine. Now, let's talk about UBG.

If the cells are able to produce CB, and there isn't an obstruction (which there isn't because your stool isn't white and your AlkP/GGT enzymes are not sky high when you have hepatitis), then a substantial amount of CB will still be excreted in the bile allowing the bacterial to produce UBG. Most of this UBG is pooped out, but some is reabsorbed into the portal circulation. However, instead of being taken up be the liver cells, much of it shunts past due to the extensive liver damage. Because UBG is soluable, it ends up in your urine at higher concentrations than normal.

Therfore, I would change First Aid and BRS - this is a double whammy and another point for the great Goljan!

As always, this is just me thinking out loud. If I am way off base and/or crazy, let me know.

p.295 where it talks about Jaundice:

Goljan's RR Path (2nd ed.) p.367 & 369 say that hepatocellular (mixed unconj./conj.) bilirubinemia has an increased urine urobilinogen because it is redirected from the liver to the kidneys (and thus more appears in urine). However, FA on p.295 says urobilinogen is normal/decreased in hepatocellular (mixed) jaundice. I know this is being "nit-picky" or whatever, but I'm just trying to understand the processes. So which is correct??

(Please don't quote BRS because I think FA's chart is essentially copied from there. Thanks.)

 

[guitarguy09]

thanks... i came to a similar conclusion, but i wanted reinforcement since that would mean that both BRS and FA were wrong. Goljan's the man!

 

[etlee]

Pg. 125 Fetal circulation

This has to be one of the most blatant "mistakes" yet. There was obviously some crafty editing of this image from the correct 2006 version. At least they got the "Adapted, with permission" part correct. The shading does not match up properly as the umbilical vein has the highest O2 content in the fetal circulation. I wish someone would open up an investigation into these authors, because this one is pretty obvious as to what is going on with their yearly "revisions". And yet, it continues to sell thousands...

 

[NEATOMD]

pg 194 Hashimoto's is a type II hypersensitivity

I think you might be wrong about this. Hashimoto's IS a type IV hypersensitivity. It is a type 2 autoimmune thyroiditis(specifically type 2A). I found it listed as a type II in wiki-pedia, but I'm almost certain that it is wrong.