Lactulose vs Neomycin

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You’re probably wondering why I wrote a post about two seemingly weird drugs. Yeah I know, weird. By all means, I could have not mentioned the following HY points at all, but I figured it’s better to at least get them out there.

If you’re ever asked about the treatment of hyperammonemia on the USMLE, it will be one of two drugs: lactulose or neomycin.

Lactulose increases gut excretion of ammonia by enabling its conversion to ammonium. Since we are not able to break it down, gut bacteria are able to ferment it. This fermentation leads to acid production, so more intraluminal NH3 is converted to NH4+.  Since charged entities are not absorbed as readily, excretion is increased. Pretty straightforward.

The USMLE also wants you to know that neomycin, an aminoglycoside, kills urease (+) organisms, therefore decreasing NH3 production. If they ever ask you about an antibiotic that can treat hyperammonemia, look for neomycin as an answer. This drug is floating around on the newer NBMEs as well.

That’s literally it. Two weird HY drugs out of the way.

Some texts might mention benzoate or phenylbutyrate as drugs that bind amino acids in the bloodstream and increase their excretion before their amine groups can be liberated via catabolism, but I’d be wildly surprised if either of these ever shows up on a real exam. The only reason I’m mentioning them here is because someone who’s pedantic might otherwise say, “Yeah but Michael, you didn’t mention benzoate or phenylbutyrate.” So there you go. I did. But once again, they’re not HY. Just know lactulose and neomycin.

1. How does lactulose work in terms of decreasing ammonia in the blood?

2. How does neomycin decrease blood ammonia levels?

3. What is the mechanism of action of neomycin? (select one answer; two points)