Step I First Aid Mistake

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Jalby

Jalby

I fight crime at day when Batman are sleeping.
20+ Year Member
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.
 
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There are two genetic defects that turn urine dark. What are they and whats the difference on how they turn the urine dark??
 
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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.
 
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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 😕
 
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Jalby said:
There are two genetic defects that turn urine dark. What are they and whats the difference on how they turn the urine dark??
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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.
 
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StringBean said:
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 😕
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Fine. I'll just say that first AID has something that is wrong.
 
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AlexRusso said:
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.
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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.
 
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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??)
 
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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.
 
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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
 
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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+...
 
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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
 
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Jalby said:
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.
Click to expand...

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 :laugh:
 
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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?
 
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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.
 
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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'
 
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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.
 
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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.
 
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mycin1600 said:
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.
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during the lytic phase of paget's, overactivity of osteoclasts can increase levels of calcium.
 
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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
 
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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...
 
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mpp said:
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'
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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
 
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mycin1600 said:
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...
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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 "
 
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Idiopathic said:
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
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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.
 
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Idiopathic said:
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+...
Click to expand...

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

jakstat33 said:
idiopathic, i thought that aldosterone mediated H secretion in intercalated cells by stimulating the H-ATPase, not the K-H Exchange...
Click to expand...
 
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AlexRusso said:
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.
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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.
 
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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!!
 
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EctopicFetus said:
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!!
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not completely. Monozygotes which split late are as such, but early monozygotes can be diamniotic and dichorionic.
 
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