HelpPleaseMD

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pg 210 Clindamycin it binds 50s and inhibits translocation like the macrolides? instead of the mechanism they have listed.

I emailed FA and got no response. Am I wrong?
 

Phloston

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pg 210 Clindamycin it binds 50s and inhibits translocation like the macrolides? instead of the mechanism they have listed.

I emailed FA and got no response. Am I wrong?
As far as I'm aware, clindamycin binds to 50S and inhibits peptide bond formation. Translocation is macrolides.
 

Dr McSexy

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As far as I'm aware, clindamycin binds to 50S and inhibits peptide bond formation. Translocation is macrolides.
I had thought so as well (due to FA)....

but all sources I've seen (Wiki and otherwise) say it has the same mechanism as macrolides. I had a UWorld question on this that I missed on this as well.
 

VisionaryTics

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As far as I'm aware, clindamycin binds to 50S and inhibits peptide bond formation. Translocation is macrolides.
According to Katzung, clindamycin has the same binding site as the macrolides, and inhibits translocation.

I'll take Katzung.
 

ijn

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Clindamycin is definitely acting by inhibition of translocation. Chloramphenicol is the only board relevant antibiotic that acts on peptidyl transferase.
 

Phloston

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First Aid is very specific by saying that macrolides "inhibit protein synthesis by blocking translocation" (209) and that clindamycin "blocks peptide bond formation" (210).

First Aid wins. No debate.

Macrolides and clindamycin both bind to the peptidyl transferase loop of the 23S rRNA, as does lincomycin, but the way the mechanisms for how these drugs work are phrased are where the points are going to come in on the USMLE. It's not good enough in their eyes to say that many of them do the same thing.

Macrolides --> inhibit translocation
Clindamycin --> inhibit peptide bond formation
Chloramphenicol --> inhibit peptide bond formation AND peptidyl transferase
Tetracyclines --> prevent attachment of aminoacyl-tRNA to the A site
Aminoglycosides --> inhibit initiation complex and cause misreading of the mRNA

These exact descriptions have also shown up in Rx.
 

VisionaryTics

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K, Phloston. You should write Katzung, Lippincott, and Goodman & Gilman while you're on it. They were all pretty specific, too.

I have to say, your obstinacy when corrected borders on ridiculous. That's a ****ty quality to have, both as a student and physician. I generally appreciate your contributions to this forum, but sometimes you need to take a moment to realize that other people have something to offer.
 
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ijn

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Macrolides and clindamycin both inhibit transpeptidation. That isn't a useful differential between the two.

You don't know how the USMLE phrases things unless you are writing the questions or have access to STEP 1 recall banks.
 

ijn

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K, Phloston. You should write Katzung, Lippincott, and Goodman & Gilman while you're on it. They were all pretty specific, too.

I have to say, your obstinacy when corrected borders on ridiculous. That's a ****ty quality to have, both as a student and physician. I generally appreciate your contributions to this forum, but sometimes you need to take a moment to realize that other people have something to offer.
Yeah, I wanted to say something too. It almost seems pathological.

Anyway, here's the UpToDate articles on the drugs:

" Clindamycin works primarily by binding to the 50s ribosomal subunit of bacteria. This agent disrupts protein synthesis by interfering with the transpeptidation reaction, which thereby inhibits early chain elongation."

" [Macrolides] bind to the 50S subunit of bacterial ribosomes, leading to inhibition of transpeptidation, translocation, chain elongation and, ultimately, bacterial protein synthesis "

That sounds pretty damn similar. They also have identical modes of resistance (methylation of the 50S).

Regardless this kind of hair splitting is extremely low yield. They are more likely going to test clindamycin on how it's distinctly different than macrolides - i.e. it's good for S. aureus osteomyelitis, it's good for anaerobic abscess infections, it's associated with pseudomembranous colitis.
 

Phloston

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This isn't about me. This is about First Aid. It is our job to comment on FA's errata regarding its misplaced down arrow's, images, etc., but regarding the super-high-yield descriptions of antibiotic mechanisms, those are based on numerous people having taken the test and reporting back. There are quite a few resources that will say different things. First Aid wins.
 

Dr McSexy

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It's a shame that this board will have to suffer another 6 months of this. Good thing I'll be finished in 2.5 weeks.
 

ijn

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This isn't about me. This is about First Aid. It is our job to comment on FA's errata regarding its misplaced down arrow's, images, etc., but regarding the super-high-yield descriptions of antibiotic mechanisms, those are based on numerous people having taken the test and reporting back. There are quite a few resources that will say different things. First Aid wins.
It's soooooooo set in stone that it's been the same in First Aid 2010, 2011, and 2012, right? It's not possible at all this is another case of extreme schizophrenia that First Aid has shown throughout the years like with constant revisions on the unhappy triad.

(Hint: look at 2010. In there they say translocation three times for clindamycin. 2011 has internal contradictions on its mechanism of action; in the cell biology section they say clindamycin inhibits translocation, and in the antibiotic section they say it inhibits peptide bond formation but the overall antibiotic section graphic on the page before it says it inhibits translocation)
 

lrkoehle

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This isn't about me. This is about First Aid. It is our job to comment on FA's errata regarding its misplaced down arrow's, images, etc., but regarding the super-high-yield descriptions of antibiotic mechanisms, those are based on numerous people having taken the test and reporting back. There are quite a few resources that will say different things. First Aid wins.
Those people taking the test know they got it correct how? I don't remember there being an "expanded feedback" option on the real exam like the practice NBME's. FA doesn't win just because it is FA. Honestly, there is nothing special about FA, it's just another book. Despite its many shortcomings, it still happens to be the best collection of high yield step I info in one book, but that by no means makes it perfect or infallible, as is clearly demonstrated by the pages and pages of errata every year.

I usually like your posts and you seem to be very intelligent, but this attitude of "it's in FA, so that's that; First Aid wins," really needs to stop. It makes you look bad. It comes across like you don't want to think, but instead you just want to memorize word for word what's in FA and not go any further. I know you're able to dig deeper, reason things for yourself, and know when FA is wrong.
 
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tjquinn

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Words cannot describe my awe... Phloston you truly trust FA over any other pharmacology source, even with the errata for FA 2012 that is almost as long as FA 2012 itself? What an amazing mind you have, the way it rationalizes and justifies what to accept and what to reject.
 
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This thread has gone nuclear. :laugh:

I will say though that Katzung is a more reliable source in pharm than FA. In fact, FA regularly borrows images/diagrams from Katzung. FA is like the Jackie Chan of pharm while Katzung is Bruce Lee.
 
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lrkoehle

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I wasn't meaning to attack Phloston. Based on what I've seen here, I respect the guy's work ethic and knowledge base.
 

missmedschool

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This isn't about me. This is about First Aid. It is our job to comment on FA's errata regarding its misplaced down arrow's, images, etc., but regarding the super-high-yield descriptions of antibiotic mechanisms, those are based on numerous people having taken the test and reporting back. There are quite a few resources that will say different things. First Aid wins.
Welp FA 2011 errata replaced "peptide bond formation" with "translocation" for clindamycin ... So yeah ... what does that mean Phloston?