Step I First Aid Mistake

[Jalby]

Advertisement - Members don't see this ad

Not that this one matters in the slightest, but I'm proud of myself for finding one. One page 159, homocystinuria, they have a reaction catalyzed by cystathionine synthase that magically spits out cysteine. Alright, back to biochemistry. I don't think a single person is going to get a question right or wrong because of that mistake.

 

[Idiopathic]

brilliant...somebody was paid for that

 

[Jalby]

Go to bed..

 

[Jalby]

There are two genetic defects that turn urine dark. What are they and whats the difference on how they turn the urine dark??

 

[OneStrongBro]

Let me ask Archibald Garrod. He should know.

There are two genetic defects that turn urine dark. What are they and whats the difference on how they turn the urine dark??

 

[Idiopathic]

edit: after giving the answer, I realized that I am way too much of a nerd....still not off to bed yet though.

 

[Jalby]

tick tock, tick tock

 

[mpp]

That's not quite a a mistake...they just skipped a reaction. Cystathionine sythase catalyzes homocysteine to cystathionine (with Vit B6 as a cofactor) and then cystahionase catalyzes the last reaction to cysteine.

 

[Jalby]

...they just skipped a reaction.

Hence, a mistake....otherwise known as an innacuracy.

 

[StringBean]

I agree w/ it not being a mistake. First Aid does that in a few places (skips a reaction in a pathway). I think sometimes they just want to highlight the most important steps. Sometimes it helps, sometimes it confuzes the heck out of me for a few 😕

 

[AlexRusso]

There are two genetic defects that turn urine dark. What are they and whats the difference on how they turn the urine dark??

Alkptonuria which is due to amino acids accumulating in the urine

PNH which is due to complement mediated hemolysis with subsequent hemoglobin in the urine.

 

[Jalby]

I agree w/ it not being a mistake. First Aid does that in a few places (skips a reaction in a pathway). I think sometimes they just want to highlight the most important steps. Sometimes it helps, sometimes it confuzes the heck out of me for a few 😕

Fine. I'll just say that first AID has something that is wrong.

 

[Idiopathic]

Alkptonuria which is due to amino acids accumulating in the urine

PNH which is due to complement mediated hemolysis with subsequent hemoglobin in the urine.

I actually had acute intermittent porphyria over PNH. Any intravascular hemolysis will turn the urine darker than normal, but few think make it look like something else entirely.

 

[Jalby]

And what is the difference between the darkness of the urine??? (i.e. a patient comes in with dark urine. How do you tell which is which??)

 

[Jalby]

The other one I was sure is a mess up. This one, I'm 90% confident. On page 160, fatty acid metabolism sites it states:

"Fatty acid entry into cytosol is via citrate shuttle"

This is inaccurate. The citrate shuttle shuttles Acetyl-CoA. Now, you might be able to stretch it to say that acetyl is a fatty acid, but I think that's hard to do. They should have said:
"Acetyl CoA for FA synthesis is transported into the cytosol via the citrate shuttle"

idiopathic, go to bed.

 

[Idiopathic]

And what is the difference between the darkness of the urine??? (i.e. a patient comes in with dark urine. How do you tell which is which??)

The urine in AIP looks normal upon voiding, but after sitting out ("windowsill test") it turns black. Also, the AIP Px are often nuts...

 

[drdrtoledo]

Is this a mistake too?
Pg. 141, top right under "Principal Cell". It has a "+" then Aldosterone reabsorbs K+.
I thought aldosterone caused a secretion of K+, Hence when spironalactone (an aldosterone blocker) binds it led to K+ sparing. I am burned out...10 hours straight... let me know if I'm just not thinking clearly. 😴
ATnS

 

[Idiopathic]

two pumps mediated by aldosterone: one, a Na+ in/K+ out pump is in the distal tubule and two, a K+ in/H+ out pump, in the collecting duct (principal cell). The reason why spironolactone spares K+ is it blocks the first pump, which keeps K+ from ever being secreted (and also keeps H+ from leaving in the second pump, leading to the met. acidosis)

Case: Conn's syndrome (primary aldosteronism) causes a metabolic alkalosis because the second pump spits out H+ in an effort to reclaim K+...

 

[drdrtoledo]

Thanks.... Oh, and if you wanna laugh... I was looking at Step up NOT FA... I need sleep. I have no clue what I'm looking at
ATnS

 

[BlackPuma]

Not that this one matters in the slightest, but I'm proud of myself for finding one. One page 159, homocystinuria, they have a reaction catalyzed by cystathionine synthase that magically spits out cysteine. Alright, back to biochemistry. I don't think a single person is going to get a question right or wrong because of that mistake.

news flash BRS path and first aid are full of mistakes... 🙄 if u have found only one...u have a lot of studying to do buddy

 

[AlexRusso]

FA 2004 pg 69

Pt. cannot protrude tongue to LEFT side and has a right-sided spastic paralysis. Where's the lesion? answer: left medulla, CN XII

Wouldn't the tounge protrude to the left side if the left CNXII was damaged? Shouldn't that questions read "pt cannot protrude tongue to Right..." Unless his lession clipped the descending corticobulbar fibers before they crossed. As far as I remember the tongue points ipsilateral to the CN XII lession. Am I goin crazy?

 

[Claymore]

2004 FA p 82: Rotator Cuff mm.
Says the Teres Minor adducts and medially rotates. According to my Anatomy text it adducts and laterally rotates.

p 258 Bullous Pemphigoid
Says IgG is against the epidural membrane, think it should be epidermal membrane.

Please correct me if I'm wrong.

 

[Resident Alien]

Edit: thanks mpp for the correction.

 

[mpp]

But a lesion to the left nucleus of XII would lead to deviation of the toungue to the left when protruding (as the left genioglossus muscle would be paralyzed). I agree with Alex that it should read:

'can't protrude tongue to the right' or 'tongue deviates to the left on protrusion'

 

[grunermann]

I'll give an easy one:
I think that on pg 369 the determination of physiologic dead space should read:
Vd = Vt x (PaCO2-PeCO2)/PaCO2

I was wondering why a weird line was drawn in for the longest. I need a break.

 

[nuclearrabbit77]

pg. 119 high yield gross anatomy. that's not a penis, that's cartman's face.

 

[mycin1600]

what about on page 169 of 2004 under vitamin D where it's listing causes of hypercalcemia. it lists paget's disease. in paget's disease labs typically show normal calcium and normal phosphorus, with the primary defect being increased APh.

 

[drdrtoledo]

pg. 119 high yield gross anatomy. that's not a penis, that's cartman's face.

Now that's funny! Damn, we're nerds... 🙂

 

[nuclearrabbit77]

what about on page 169 of 2004 under vitamin D where it's listing causes of hypercalcemia. it lists paget's disease. in paget's disease labs typically show normal calcium and normal phosphorus, with the primary defect being increased APh.

during the lytic phase of paget's, overactivity of osteoclasts can increase levels of calcium.

 

[nuclearrabbit77]

i take that back. calcium and phosphate levels should be in reference range for paget's, but there over a 10-15% coincidence of hyperparathyroidism in paget's.

"Secondary hyperparathyroidism may occur in 10-15% of patients with Paget disease. This development may be due to inadequate calcium intake in the face of increased demand from extensive bone remodeling." -emedicine. http://www.emedicine.com/pmr/topic98.htm

 

[mycin1600]

yeah, but in first aid under that same subheading of causes of hypercalcemia, it lists hyperparathyroidism and paget's disease as two separate entities, effectively making paget's disease incorrect. paget's disease with coexistent hyperparathyroidism would cause increased calcium, sure. bleh, anyways...

 

[Idiopathic]

But a lesion to the left nucleus of XII would lead to deviation of the toungue to the left when protruding (as the left genioglossus muscle would be paralyzed). I agree with Alex that it should read:

'can't protrude tongue to the right' or 'tongue deviates to the left on protrusion'

No...the tongue cannot protrude the side of the lesion. A left-sided lesion paralyzes the genioglossus on that side, causing the tongue to 'point toward the lesion'. So, the tongue does point to the left, because the right side pushes it that way

 

[Idiopathic]

yeah, but in first aid under that same subheading of causes of hypercalcemia, it lists hyperparathyroidism and paget's disease as two separate entities, effectively making paget's disease incorrect. paget's disease with coexistent hyperparathyroidism would cause increased calcium, sure. bleh, anyways...

obviously you can get hypercalcemia with Pagets early on...

"Paget's disease occurs in three phases.1,4 The initial phase consists of intense osteoclastic activity and bone resorption, with bone turnover as high as 20 times the normal rate.5 This phase is followed by an osteolytic-osteoblastic phase during which osteoblasts begin to produce an abundance of woven bone, but mineralization is ineffective. In the final phase, dense cortical and trabecular bone deposition dominates, but it is sclerotic, disorganized, and weaker than normal bone.4 "

 

[AlexRusso]

No...the tongue cannot protrude the side of the lesion. A left-sided lesion paralyzes the genioglossus on that side, causing the tongue to 'point toward the lesion'. So, the tongue does point to the left, because the right side pushes it that way

Yes...thats what mpp and I were saying, that the tongue points to the left. However the question says that the pt. CANNOT point his tongue to the left.

 

[jakstat33]

two pumps mediated by aldosterone: one, a Na+ in/K+ out pump is in the distal tubule and two, a K+ in/H+ out pump, in the collecting duct (principal cell). The reason why spironolactone spares K+ is it blocks the first pump, which keeps K+ from ever being secreted (and also keeps H+ from leaving in the second pump, leading to the met. acidosis)

Case: Conn's syndrome (primary aldosteronism) causes a metabolic alkalosis because the second pump spits out H+ in an effort to reclaim K+...

idiopathic, i thought that aldosterone mediated H secretion in intercalated cells by stimulating the H-ATPase, not the K-H Exchange...

 

[Jalby]

Not a good day for idiopathic yesterday.

 

[OneStrongBro]

That's right...It is a H ATPase in the intercalated cells.

ThERE IS NO H-K+ EXCHANGE at the intercalated cells of the collecting duct affected by aldosterone.

idiopathic, i thought that aldosterone mediated H secretion in intercalated cells by stimulating the H-ATPase, not the K-H Exchange...

 

[mpp]

There is an H+/K+ ATPase in the luminal membrane of the alpha-intercalated cells which serves to resorb K+ when in a hypokalemic state.

 

[Idiopathic]

Yes...thats what mpp and I were saying, that the tongue points to the left. However the question says that the pt. CANNOT point his tongue to the left.

I thought you were saying that it cannot protrude the tongue on the left (which is correct), obviously the tongue points to the left, but because the genioglossus on that side cant protrude.

 

[Idiopathic]

Not a good day for idiopathic yesterday.

suck it, i'm on all the time

 

[EctopicFetus]

Under twinning it states that "monozygotes develop 2 placentas, chorions and amniotic sacs" obviously this is true for Dizygotes. As monozygotes have 2 amnions, but 1 placenta and 1 chorion.

BOOO YAH!!! Boards be coming sooon!!! June 5th im gunna get all up in that tests ASS!!

 

[phllystyl]

Under twinning it states that "monozygotes develop 2 placentas, chorions and amniotic sacs" obviously this is true for Dizygotes. As monozygotes have 2 amnions, but 1 placenta and 1 chorion.

BOOO YAH!!! Boards be coming sooon!!! June 5th im gunna get all up in that tests ASS!!

not completely. Monozygotes which split late are as such, but early monozygotes can be diamniotic and dichorionic.