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.

 

[lord_jeebus]

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). The only place I found it listed as a type II was wiki-pedia, and considering that it is wiki-pedia, it is probably wrong.

Both Type II and Type IV mechanisms underlie Hashimoto.

If you had to pick one, and I don't think you will, I'd go with IV.

 

[guitarguy09]

It's listed as Type II by Merck (as well as wiki-pedia).

http://www.merck.com/mmpe/sec13/ch165/ch165a.html

 

[Skills of House]

Hashimoto's does have Type II and Type IV mechanisms. According to Parham, it's mainly a CD4 Th1 response. However, there are antibodies and T cells directed against the thyroid antigen. Kaplan also agrees with FA in listing it overall as a type IV...as opposed to Graves which is of course type II

 

[Davelee]

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

I have checked several references, I think you're right! Good job! Interesting enough,two QUEENs (Quinidine and Quinupristin) are P450 inhibitors.

 

[mohaven]

pg 194 Hashimoto's is a type II hypersensitivity

Actually according to Robbins Pathologic Basis of Disease there seems to be three immunologic mechanisms that may contribute to the death of thyrocytes... The initial event is CD8+ sensitization... Release of IFN-gamma by CD4+ T cells causes recruitment and damage by macrophages, and finally antibody dependent cell mediated cytotoxicity (ADCC)... SO it seems that both Type II and IV hypersensitivity may be involved... First Aid was not wrong in this case but was not completely correct... I guess that can be expected since it is a high yield book with the skeleton of what is required to be known for the Step 1...

 

[sfgboy]

Apple core lesions representing colon ca can somtemes be on barium enema radiographs, NOT barium swallow x-rays

 

[Taus]

Page 385

It says typical anti-pyschotics have extrapyramidal sx and anti-chol sx....and that atypicals have less EPS and less anti-chol

I'm pretty sure typicals do have more EPS sx....but the Atypicals have the stronger anti-cholinergic effects.

 

[Taus]

FA states:
1. most common bacterial meningitis in newborns is E. Coli....should be Group B Strep according to Goljan and several other sources

2. Most common in children is H. Flu...not unless they meant to say un-vaccinated kids...

 

[lord_jeebus]

Page 385

It says typical anti-pyschotics have extrapyramidal sx and anti-chol sx....and that atypicals have less EPS and less anti-chol

I'm pretty sure typicals do have more EPS sx....but the Atypicals have the stronger anti-cholinergic effects.

Low potency typicals (eg. thioridazine) have more anticholinergic effects
High potency typicals (eg. haloperidol) have more EPS
Atypicals have little of either.

 

[Megalofyia]

page 163

Under HIV immunity it should have CXCR4 as the chemokine receptor that when mutated leads to a more rapid progression to AIDS.

 

[guitarguy09]

page 163

Under HIV immunity it should have CXCR4 as the chemokine receptor that when mutated leads to a more rapid progression to AIDS.

Is this correct? I for some reason am thinking that mutations in CXCR4 and CCR5 both SLOW the progression of AIDS, or am I way off? Also, I really don't know much, if anything, about CXCR1 and its mutation effects, that's why I was just trusting FA to be correct. I haven't found any support of this online either. Anyone know what is correct?

 

[KNightInBlue]

Is this correct? I for some reason am thinking that mutations in CXCR4 and CCR5 both SLOW the progression of AIDS, or am I way off? Also, I really don't know much, if anything, about CXCR1 and its mutation effects, that's why I was just trusting FA to be correct. I haven't found any support of this online either. Anyone know what is correct?

this might help -

http://en.wikipedia.org/wiki/HIV_tropism

 

[mountainman123]

According to RR Path- it is a type IV reaction. The thyroid is destroyed by CD8 T-cells and the antimicrosomal Ab come as a result of the injury.

 

[Pepsy]

this is a great thread.. thnx everyone.

 

[guitarguy09]

I noticed FA 2007 p.255-256 lists "amiodarone" as being both a Class Ia and Class III antiarrhythmic, while Lippinocott's and Wikipedia list is being solely Class III. Does it act in some other way aside from blocking K+ channel outflow during phase 3 (prolonging the AP and effective refractory period)? Lippincott's says that it has Class I, II, III, and IV actions, but that it is unlike Class I because it does not prolong the QT interval (although it's listed with the other Class III antiarrhythmics as increasing QT in FA). What's up with this??

 

[medinah]

http://wordpress.com/tag/errors-in-first-aid-for-the-usmle/

 

[surprisedgirl]

im sure this has been asked, but is it maybe a better idea to stick w/ FA 2006 b/c i heard there are possibly more erros in 2007?

 

[Teejay]

im sure this has been asked, but is it maybe a better idea to stick w/ FA 2006 b/c i heard there are possibly more erros in 2007?

NO! NO! NO!. 2006 is full of errors. Some old errors from 2006 have been corrected already in the 07 version. Besides, the 07 version has a new pathology and psychiatry chapter.

 

[Darth Asclepius]

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

I just looked this up. ASD has both. Look under the "physical" heading http://www.emedicine.com/ped/topic1686.htm

 

[Teejay]

Page 111,
In the heme synthesis, it says that porphobilinogen is converted to Pre-uroporphyrinogen whereas in lippincotts, it says hydroxymethylbilane. On that same note, in acute intermittent porphyria, it says that the affected enzyme is Uroporphyrinogen l synthase but lippincotts says its hydroxymethylbilane synthase. Goljan Rapid Review agrees with first aid but i don't know who to believe now because all of them have a history of frivolous mistakes.
Somebody should cross-check this just to make sure. There could be double names for these enzymes but i would'nt know that.

 

[Teejay]

PG 117
In Duchenne's Muscular dystrophy, it says that elevated CPK is used for diagnosis. I have no idea what CPK stands for in this context because in both BRS and RR, its says elevated CK which i know stands for creatine Kinase.

 

[lord_jeebus]

PG 117
In Duchenne's Muscular dystrophy, it says that elevated CPK is used for diagnosis. I have no idea what CPK stands for in this context because in both BRS and RR, its says elevated CK which i know stands for creatine Kinase.

CK = CPK

 

[Teejay]

Pg 165😕
I'm now confused because i'm getting different answers from different sources. What is the most common cause of nosocomial pneumonia? Is it Staph Aureus or Psuedomas Aureginosa?

 

[rumorsweretrue]

Thanks for starting this thread; finding errors when you're studying is a pain in the ass. I'm taking Step 1 on March 14th, and in the meantime I started organizing all of the errors to the FA by section and adding things to them like graphs, drawings, mnemonics and the like. I've gotten pretty far through the book, and other than Micro, HemeOnc, Psych and Repro, I've put everything I've found online.

Other than catching a few errors that haven't been mentioned here and changing some of the sillier mnemonics around, that's all I really have to offer. Hope it helps, topher.

Here are two examples from Neuro:

Instead of the current mnemonic “ALexander Bell with STD: AIDS, Lyme, Sarcoid, Tumors, Diabetes” I suggest the shorter “BLASTeD: Bell’s palsy from Lyme, AIDS, Sarcoid, Tumors, Diabetes”. A small change, but somewhat easier to remember. Or, if you like, “Bell-LASTeD“.

Instead of the current mnemonic “B.B. King on OPIATES PROPOses FOOLishly” for memorizing Barbiturates, Benzodiazepines, Ketamine, Opiates and Propofol, I think this is better:

KOPs keep them BEhind BARs: Ketamine, Opiates, Propofol, BEnzodiazepines, BARbiturates.

Bonus: …where they are put to sleep by IV anesthetics.
​

 

[rumorsweretrue]

I noticed FA 2007 p.255-256 lists "amiodarone" as being both a Class Ia and Class III antiarrhythmic, while Lippinocott's and Wikipedia list is being solely Class III. Does it act in some other way aside from blocking K+ channel outflow during phase 3 (prolonging the AP and effective refractory period)? Lippincott's says that it has Class I, II, III, and IV actions, but that it is unlike Class I because it does not prolong the QT interval (although it's listed with the other Class III antiarrhythmics as increasing QT in FA). What's up with this??

Awesome question with a cool answer. Unfortunately, it requires some detail to explain. Here's a table I made when I was sorting it out for myself.

​

The Na+ channels of the SA and AV nodes are always firing (more or less) and are termed "active". This is in contrast to the Na+ channels of the ventricles that are usually off or "inactive". This all makes sense when you remember that the slow depolarization of the SA/AV is via Na+ channel, whereas the Na+ channels of the ventricles are off except for a very brief phase 0 upstroke (not a lot of time for a drug to take effect).

So, what makes a Class I a Class I is its action on these active Na+ channels. From this, you expect their action to be in the nodes and not in the ventricles. What makes Quinidine a Ia is its additional K+ action. In the SA/AV, this would prolong repolarization. In the ventricles, this would also prolong repolarization. Now, the prolonged QT, the slowing HR, etc begin to make sense.

If you can keep the differences between the SA/AV and the Ventricles straight AND commit the table I included to memory, then the effects of these drugs start to come together. Shockingly, more detail up front requires less memorization later on and leads to a real understanding of antiarrhythmials.

So when people say that Amiodarone is also a Class I, they're missing it! Amiodarone doesn't have the basic action that makes a Class I a Class I, and instead includes the actions that make a Ia and a Ib different from a standard Class I.

Lot of details, but interesting nonetheless. The only thing I'll add is that the Na+ channel in the SA/AV is a "funny" channel and that the Ca2+ channel in the SA/AV is an L-type channel. Why do you care? Well, the actions of Beta-Blockers don't make sense otherwise. Beta-blockers like Propranolol can act at the Funny channel and the L-type channels in the SA/AV, and can also act at the Ca2+ in the ventricle, but you don't see them affect the Na+ channel in the ventricles.

You should be able to piece together the rest. In the meantime, here are the bullet points.

Block: Effect

K+: Delays repolarization ↑AP duration, ↑ ERP, ↑ QT interval (risk for Torsade de pointes)
Na+ (SA/AV): ↓ automaticity, ↓ slope of phase 4, ↓ cell excitability
Na+ (Vent) : ↓ conduction, ↓ slope of phase 0 depolarization
Ca2+: ↓ conduction (SA/AV), ↓ slope of phase 4, ↓ phase 2 plateau (Vent), ↓ contractility, ↓ QT interval
Beta-receptor: Na+ (SA/AV)-block and Ca2+-block; negative chronotropic, dromotropic, and inotropic

Mg2+: Functional Ca2+ blocker; first line in Torsades de Pointes, Digitoxin toxicity
Adenosine: Receptors on SA and AV node; ↑ K+ and ↓ Ca2+ conductance, hyperpolarizes; may cause AV block; DOC in diagnosing/abolishing AV nodal arrhythmias. Toxicity: flushing, chest burning. t1/2 = 10s.

Hope it helps, topher.
http://rumorsweretrue.wordpress.com

 

[Teejay]

👍

 

[goodies]

Awesome question with a cool answer. Unfortunately, it requires some detail to explain. Here's a table I made when I was sorting it out for myself.

​

The Na+ channels of the SA and AV nodes are always firing (more or less) and are termed "active". This is in contrast to the Na+ channels of the ventricles that are usually off or "inactive". This all makes sense when you remember that the slow depolarization of the SA/AV is via Na+ channel, whereas the Na+ channels of the ventricles are off except for a very brief phase 0 upstroke (not a lot of time for a drug to take effect).

So, what makes a Class I a Class I is its action on these active Na+ channels. From this, you expect their action to be in the nodes and not in the ventricles. What makes Quinidine a Ia is its additional K+ action. In the SA/AV, this would prolong repolarization. In the ventricles, this would also prolong repolarization. Now, the prolonged QT, the slowing HR, etc begin to make sense.

If you can keep the differences between the SA/AV and the Ventricles straight AND commit the table I included to memory, then the effects of these drugs start to come together. Shockingly, more detail up front requires less memorization later on and leads to a real understanding of antiarrhythmials.

So when people say that Amiodarone is also a Class I, they're missing it! Amiodarone doesn't have the basic action that makes a Class I a Class I, and instead includes the actions that make a Ia and a Ib different from a standard Class I.

Lot of details, but interesting nonetheless. The only thing I'll add is that the Na+ channel in the SA/AV is a "funny" channel and that the Ca2+ channel in the SA/AV is an L-type channel. Why do you care? Well, the actions of Beta-Blockers don't make sense otherwise. Beta-blockers like Propranolol can act at the Funny channel and the L-type channels in the SA/AV, and can also act at the Ca2+ in the ventricle, but you don't see them affect the Na+ channel in the ventricles.

You should be able to piece together the rest. In the meantime, here are the bullet points.

Block: Effect

K+: Delays repolarization ↑AP duration, ↑ ERP, ↑ QT interval (risk for Torsade de pointes)
Na+ (SA/AV): ↓ automaticity, ↓ slope of phase 4, ↓ cell excitability
Na+ (Vent) : ↓ conduction, ↓ slope of phase 0 depolarization
Ca2+: ↓ conduction (SA/AV), ↓ slope of phase 4, ↓ phase 2 plateau (Vent), ↓ contractility, ↓ QT interval
Beta-receptor: Na+ (SA/AV)-block and Ca2+-block; negative chronotropic, dromotropic, and inotropic

Mg2+: Functional Ca2+ blocker; first line in Torsades de Pointes, Digitoxin toxicity
Adenosine: Receptors on SA and AV node; ↑ K+ and ↓ Ca2+ conductance, hyperpolarizes; may cause AV block; DOC in diagnosing/abolishing AV nodal arrhythmias. Toxicity: flushing, chest burning. t1/2 = 10s.

Hope it helps, topher.
http://rumorsweretrue.wordpress.com

what about Ic? and what does "down" in bold mean? the predominant effect? i thought 1b just affected fast Na+ channels and ischemic tissue rather than nodal tissue "SA/AV"??

 

[fakin' the funk]

In the Cardiovascular chapter, under Cardiomyopathies...

Hemochromatosis is a cause of restrictive cardiomyopathy, NOT dilated. A rare one, but this is an error nonetheless. Verified in Cecil's.

 

[fakin' the funk]

http://wordpress.com/tag/errors-in-first-aid-for-the-usmle/

I would recommend using any of these corrections very cautiously.

E.g.: author states that Marfans predisposes to ruptured aortic aneurysm. Marfans predisposes to aortic dissection.

Additionally, most of these "corrections" are nitpicky differences of preference as to how diagrams are laid out.

 

[rumorsweretrue]

I would recommend using any of these corrections very cautiously.

E.g.: author states that Marfans predisposes to ruptured aortic aneurysm. Marfans predisposes to aortic dissection.

Additionally, most of these "corrections" are nitpicky differences of preference as to how diagrams are laid out.

I agree that the corrections should be used very cautiously; the Marfan's example you quoted is downright dangerous in the wrong hands.

Too nit-picky or appropriate, it's up to you. If you're the guy that reads something in FA, thinks it's wrong, and then just moves past it without caring, then I can't imagine you care enough to look online for the correction. If you are instead the type that (when they see something that conflicts) spends several minutes cross-referencing sources to settle the issue, then those things can waste a good portion of your time. I don't think it makes sense for us all to repeat that step, so that's why I took the time to post the things I found. If you disagree with any of them, I INVITE you to offer a correction.

Or you could complain.

 

[Sureshot83]

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

Cardiology was a long time (4 months) ago, but here is what I remember. Someone please correct if wrong.

Flow murmur = murmur resulting from excess blood flow. NOT from turbulence, as occurs in aortic stenosis.

ASD has a diastolic murmur because the right atrium is collecting blood from BOTH the systemic circulation and the left atrium (through the ASD). When this excessive volume of blood flows through the tricuspid valve, it causes a flow murmur. Since this occurs during ventricular filling, it is a diastolic murmur. This excess amount of blood is also pushed out across the pulmonic valve, causing another flow murmur heard loudest in the pulmonic area.


PS - I just happened to browse across this thread, and it certainly is making me realize just how many concepts seem vaguely familiar, even though I don't really know any of the details. Yikes. Ahhhhhh.......fun times until June 11th.

 

[viostorm]

Pg 165😕
I'm now confused because i'm getting different answers from different sources. What is the most common cause of nosocomial pneumonia? Is it Staph Aureus or Psuedomas Aureginosa?

According to both Harrison's Internal Medicine AND UptoDate the most common cause of nosocomial pneumonia is staph aureus.

From UptoDate:

Pathogen Prevalence Mortality
MRSA 59 (14.8) 19 (32.2)*
P aeruginosa 57 (14.3) 16 (28.6)
Other Staphylococcus spp 35 (8.8) 8 (22.9)
Klebsiella pneumoniae 13 (3.3) 3 (23.1)
Enterobacter 13 (3.3) 1 (7.7)
Escherichia coli 12 (3.0) 3 (25.0)
Acinetobacter 8 (2.0) 4 (50.0)
No major organism identified 146 (36.7) 29 (19.9)
Neither BAL nor TRACH culture performed 25 (6.3) 9 (36.0)
BAL or TRACH culture identified as "none" 30 (7.5) 8 (26.7)

 

[Teejay]

Pg 195
In Wiskott-aldrich syndrome, it says there is Increased IgA and normal IgE. Goljan says you have increasedIgE and harrisons say you have normal IgA..
Who should we believe?

 

[guitarguy09]

Pg 195
In Wiskott-aldrich syndrome, it says there is Increased IgA and normal IgE. Goljan says you have increasedIgE and harrisons say you have normal IgA..
Who should we believe?

Check out my post for you in the Goljan's RR Path thread...

 

[fakin' the funk]

Pg 195
In Wiskott-aldrich syndrome, it says there is Increased IgA and normal IgE. Goljan says you have increasedIgE and harrisons say you have normal IgA..
Who should we believe?

Harrison's. ALWAYS Harrison's.

 

[goodies]

page 255 under class I antiarrhythmics, it says that they decrease slope of phase 4 depolarization, but in Kaplan Pharm and Lange Pharm cards it says that they decrease phase 0 depolarization. Which is it?

page 249 under Libman-Sacks endocarditis, it says "vegetations develop on both sides of valve --> mitral valve stenosis," but in Goljan's book it says mitral regurgitation. Which is correct?

 

[TheEleventhReel]

page 255 under class I antiarrhythmics, it says that they decrease slope of phase 4 depolarization, but in Kaplan Pharm and Lange Pharm cards it says that they decrease phase 0 depolarization. Which is it?

page 249 under Libman-Sacks endocarditis, it says "vegetations develop on both sides of valve --> mitral valve stenosis," but in Goljan's book it says mitral regurgitation. Which is correct?

For Class 1, they slow phase 0 depolarization in purkinje cells. I think they also act to decrease the slope of phase 4 depolarization in AV/SA nodal tissues. So, it depends on which type of cardiac tissue you're referring to. At least that's my understanding of it. Anyone else care to comment?

 

[IzzyMD09]

This uncal herniation business

ok L side mass, brain squeezed out ipsilaterally

stretching ipsilateral CNIII (so far fine)

contralteral homonymous hemianopia because PCA compression ipsilaterally (also fine)

but this ipsilateral paresis ....wtf, im thinking L side mass compressed corticospinal/bulbar nerves on R wouldnt it be contralateral paresis, i thought it was ipsilateral if the damage was in the spinal cord (HY Neuroanatomy pg 68 3rd edition)

help me

izzy

 

[IzzyMD09]

its ipsilater paresis, ipsilateral to the lesion
any lesion above the decussation is contralateral paresis
contralateral to the lesion

but FA 2007 means ipsilateral paresis with regards to the mass not the lesion

aaaaaaaaahhhhhh


izzy

 

[drbetty]

FA states:
1. most common bacterial meningitis in newborns is E. Coli....should be Group B Strep according to Goljan and several other sources

2. Most common in children is H. Flu...not unless they meant to say un-vaccinated kids...

*I agree that H. influenza type B is definitely no longer the 'most frequent cause' of meningitis in kids! This is b/c of the conjugated vaccine, and FA even mentions that on pg 165. S. penumoniae or N. meningitidis are actually most common bacterial causes in children.

**Another mistake in FA rapid review chart: page 439
C-ANCA -->Wegener's granulomatosis (correct)
P-ANCA -->polyarteritis nodosa (incorrect!) - BRS path 3rd edition pg 138, Goljan audio, and older FA editions also are mistaken here. FA page 333 & Robbins page 539 states that PAN is "typically not associated with ANCA". also verified on emedicine & uptodate

 

[Teejay]

249
TB causes caseous pericarditis not hemorrhagic.

 

[lord_jeebus]

249
TB causes caseous pericarditis not hemorrhagic.

I would recommend looking up the most common causes of hemorrhagic pericarditis, and coming back to tell us what you learn.

 

[blz]

In the Cardiovascular chapter, under Cardiomyopathies...

Hemochromatosis is a cause of restrictive cardiomyopathy, NOT dilated. A rare one, but this is an error nonetheless. Verified in Cecil's.

This isn't verified from any source but I remember back in the day when we learned about hemochromatosis in class the professor said it is a cause of dilated cardiomyopathy. I only remember this fact because it showed up on our exam. I wouldn't be surprised if it did both.

 

[acl3623]

P 242
Teratology of fallot- it says patient learns to squat to improve sx: compression of femoral arteries increases pressure, thereby R to L shunt. should say DECREASES R to L shunt, so cyanosis can be diminished.

 

[Merlin3]

From the cleveland clinic: "Hemochromatosis may result in a restrictive or dilated cardiomyopathy with characteristic histologic features."
From emedicine (and similar sources) "dilated left ventricle with restrictive physiology"
There is a great proportion of sources stating dilated more than restrictive; however, both are indeed taking place!
--My work is done! Time for a nap. 😴

 

[dr.weiner]

NO! NO! NO!. 2006 is full of errors. Some old errors from 2006 have been corrected already in the 07 version. Besides, the 07 version has a new pathology and psychiatry chapter.

I took a quick look at the 2007 edition and its pretty much the same stuff as 2006 just reorganized. For example the new stand-alone pathology section just contains pages that were in other sections (mostly oncology) from the 2006 just put under a new heading. From what I saw the only new stuff was one new page containing general cell injury and inflammation facts. I would guess the new psychiatry section is just taken out of the neurology/psychiatry section of 2006's.

If you (anyone in general i mean) have a 2006 and have gotten familiar with the layout and have been annotating it already, I see no need to change to 2007. If you haven't been using the 2006 much and have an extra 40 bucks to spare, then go ahead and get 2007.

 

[drbetty]

pg 84 - subtitle reads "mutations in DNA" --->should be "mutations in mRNA"

pg 107 (very bottom) - end product of sphnigolipid metabolism should be ceramide, not cerebroside

pg 426 (picture of bronchial tree) - right bronchus is shorter, wider, and straighter, unlike pictorial representation

http://www.bartleby.com/107/237.html

 

[Taus]

kinda random and insignificant...but the diagram at the bottom of p. 177 of antivirals lists "rifampin (vaccinia)" as the blocker of packaging and assembly....

Shouldn't HIV protease inhibitors should be in that box?

thats gotta just be a typo...vaccinia is cowpox and I can't see how rifampin would fit there but I could be mistaken...

 

[drbetty]

page 184 - T cells in PALS, which is part of white pulp, not red pulp

RED pulp = sinusoids (filtration and degration of senecent/abnormal RBC)

WHITE pulp = PALS (T-cells) + germinal centers (B-cells)
(fight infxn)

http://www.lab.anhb.uwa.edu.au/mb140/CorePages/Lymphoid2/lymph2.htm#Spleen

 

[drbetty]

pg 101- subtitle "transport of ammonium by alanine and glutamine"

• Contrary to the title, the 2 pathways seem to depict the "removal of ammonium by alanine and aspartate", although it is true that the transport of toxic NH3 to liver is via glutamine (from most tissues) and alanine (from muscle).
• Problem with the 2nd pathway:
  • amino acid + ketoacid -->ketoacid + amino acid (swap NH3 to the corresponding carbon skeleton)
  • thus: glutamate + OAA -->alpha-ketoglutarate + aspartate
    • catalyzed by AST (SGOT)
  • not: glutamate + OAA -->glutamine + aspartate
    • obviously wrong! product is not 2 AAs!