Med students help! Question about aspirin vs. other NSAIDs

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

golgiapparatus88

Full Member
15+ Year Member
Joined
Jun 20, 2008
Messages
614
Reaction score
5
Hi med students. Like the title says, I have a question about aspirin compared to NSAIDs such as ibuprofen and acetaminophen, specifically pertaining to influenza.

My question is why is Aspirin so much more harmful than taking ibuprofen or acetaminophen? I know Aspirin can cause Reye's syndrome but are their other reasons besides that? Aren't they all NSAIDS? <-- (that's what confusing me the most).

Thanks!
- A confused pre-med 😀

Members don't see this ad.
 
Hi med students. Like the title says, I have a question about aspirin compared to NSAIDs such as ibuprofen and acetaminophen, specifically pertaining to influenza.

My question is why is Aspirin so much more harmful than taking ibuprofen or acetaminophen? I know Aspirin can cause Reye's syndrome but are their other reasons besides that? Aren't they all NSAIDS? <-- (that's what confusing me the most).

Thanks!
- A confused pre-med 😀

It's a loaded question, since there are several concepts that need to be addressed. First of all, ASA (Aspirin) and Ibuprofen (IBU) are both considered non-steroidal anti-inflammatory drugs (NSAIDs), while APAP (acetaminophen or Tylenol) is not. They both work by non-selectively blocking the cyclooxygenase (COX) pathway, thus inhibiting the production of prostaglandins, an class of factors that are inflammatory and pain mediators. This is how they reduce inflammation, pain, and fever. Both also block the formation of TXA2 (thromboxane A2) in your platelets, which prevents platelet aggregation and the formation of clots, and can increase the risk of upper GI symptoms (such as bleeds), since they also block the COX-1 pathway (you get the anti-inflammatory effects from the blocking of COX-2), which produces a prostaglandin involved in protecting the stomach. ASA happens to be a non-competitive inhibitor of the COX pathway (a property that is taken advantage of for the effective blocking of platelet aggregation), so it carries a much higher risk of upper GI symptoms and bleeding than IBU. Also, ASA is a salicylate, while IBU is not, which is a class of meds that some people can be sensitive or allergic to and have adverse reactions when taken (Steven's-Johnson syndrome, Reye's syndrome, ototoxicity, etc.). ASA toxicity is also notorious and well-documented. Aspirin can also cause or exacerbate respiratory symptoms in those who have triad asthma.

APAP has analgesic and anti-pyretic effects, but it is not a COX inhibitor and is not an NSAID. It has no significant anti-inflammatory effects. Consequently, it also does not carry the same risks or adverse effects. It can, however, be toxic to the liver when taken in excess. APAP is metabolized into a damaging free-radical by your body, when present in excess can cause harm to your liver and kidneys. Your body has an ability to handle free-radicals through the glutathione system. When you OD on APAP, you are exhausting that system, which you can replenish by giving N-acetyl-cysteine, the antidote for APAP overdose. Another point of trivia, which is may not be so trivial to your body, is that if you continually combine APAP with NSAIDS, it will lead to drug-induced damage to your kidneys and may lead to failure because of free-radical damage (from APAP) that is facilitated by diminished blood supply (NSAIDS).

Hope that begins to answer your question.
 
Last edited:
Tylenol is not an NSAID it is an analgesic. Aspirin and ibuprofen are NSAIDs, but aspirin is an irreversible inhibitor of both COX1 and 2, whereas ibuprofen is reversible. Tylenol acts in a similar mechanism but only in the CNS (no peripheral anti inflammatory.) They will all lower a fever through hypothalamic mechanisms.

In general the reason that NSAIDS are toxic is that they can exacerbate ulcers and bleeding disorders (due to their COX 1 inhibition) but there is another whole mess that comes from selective COX 2s (like Celebrex), as they inhibit both thromboxane A2 (this is a good thing as it stops blood clots from forming) and prostacyclin (this is a bad thing as it causes blood clots.) Each different NSAID does this to a different degree so each has a different degree of safety vs effectivness. I think Naproxin is technically the best for pain relief compared to side effects (don’t quote me on that.)

All that said, Tylenol is unsafe at high doses because it is broken down into a toxic metabolite.

Don’t take either for pain, just pure morphine, or codeine, if you can get it without all the Tylenol. 👍
 
Members don't see this ad :)
Dang Spice, you beat me to the punch!
 
Dang Spice, you beat me to the punch!

I was feeling nostalgic for my Step 1 review days...and had flashbacks of listening to Goljan on this topic. 😀

I like your explanation and noticed you mentioned some things that I had forgotten. If you combine our posts, it is quite comprehensive. 🙂
 
I was feeling nostalgic for my Step 1 review days...and had flashbacks of listening to Goljan on this topic. 😀

I like your explanation and noticed you mentioned some things that I had forgotten. If you combine our posts, it is quite comprehensive. 🙂

Lol. I'll have to print this thread off and stuff it in the back of my First Aid book for later...🙂
 
I was feeling nostalgic for my Step 1 review days...and had flashbacks of listening to Goljan on this topic. 😀

I like your explanation and noticed you mentioned some things that I had forgotten. If you combine our posts, it is quite comprehensive. 🙂

get a room.
 
I think Naproxin is technically the best for pain relief compared to side effects (don't quote me on that.)

I actually use a lot of meloxicam with my patients. Once daily dosing. Extremely effective. 4 dollar drug. Lowest incidence of GI side effects of any of the NSAIDs, with the possible exception of celecoxib. (no different from placebo in fact)

Another thing is that in our rush to demonize Rofecoxib we may have painted with too broad of brush strokes, which isn't unsurprising given the natural human urge for sensationalism. There actually isn't any evidence that Celecoxib is any worse from a cardiovascular standpoint than Ibuprofen. And naproxen probably isn't 'protective' as once thought.

One thing about meloxicam is that there is little to no data available on cardiovascular risk. Given that Rofecoxib is the most selective (at like 1000:1 or more cox2:cox1) and has the worst incidence of vasoocclusive events, celecoxib (at 200:1--off the top of my head) is no different from nonselectives, and Meloxicam (at 10:1--again from memory) is the least cox2 selective of the cox2s, I'm guessing that there isn't a particularly bad risk profile with it from that aspect.

As far as I'm concerned, meloxicam combines being cheap, easy to take, and having a ridiculously low side effect in one very sexy package.

Edit: found this with a quick google search. http://jama.ama-assn.org/cgi/content/full/296.13.jrv60011v1
 
Top