Out of curiosity - and not because I feel any burning need to stock up on either OTC or prescription pain killers - how do different pain killers compare? Seems like whenever an acquaintance or FOF ends up in the ER for a broken limb, kidney stone, bad back, one of the first questions is “what’d you get” and then there’s congratulations for Demerol or sympathy for ibuprofen.
I figure the scale looks something like this:
tylenol/aspiren w/ caffeine
tylenol w/ codeine
(a lot of other pain killers like Demerol, Vicodin, percocet, etcetera)
You’re comparing apples and oranges there. Some people get wondrous relief from headaches with tylenol, while demerol just makes them throw up. Others can’t seem to handle the pain of a hangnail with anything less than heroin.
Best to compare by classes.
Tylenol (APAP or acetaminophen) is pretty much in a class by itself. Even so, on the whole most tests show its pain relief properties are about equal to aspirin or ibuprofen.
NSAIDS (aspirin, ibuprofen, indocin, naproxen, aleve, advil, toradol, etc etc about 50 different types). Effectiveness depends a lot on absorption, which in turn relates a lot to what else is in the pill, what is taken with the medicine, and the patient’s individual physiology. What works great for one patient may not help another one. Intially there was great excitement that the new COX II NSAIDS (vioxx, celebrex, etc) would be better pain relievers with less GI upset. Sadly, that early promise is not being realized. They may be no better than aspirin. In summary, most NSAIDS are pretty equivalent. Finding the right one for you may be mostly trial and error.
Opiates. Here, the effectiveness can be measured by the binding strength of the opiate molecule to the opiate receptor. Specifically the opiate receptor subtype, of which there are 4: Kappa, Lambda, Mu[sub]1[/sub] and Mu[sub]2[/sub]. For pain relief, strong binding to the Kappa receptors in the spinal cord and the Mu[sub]1[/sub] receptors in the brain is necessary. Some opiates active certain receptor types while blocking others, so that muddies the waters. But in general, here is a hierarchy of opiate potency.
Some pain relievers have multiple modes of action, and sometimes drugs not normally used for analgesia are the only source of relief.
Ultram (tramadol) is both an opiod, as well as a serotonin and norepinephrine reuptake inhibitor, and it’s thought these effects act synergistically.
A closely-related molecule, venlafaxine (otherwise known as Effexor), has very weak mu receptor agonist properties, and but is a stronger SNRI. It appears to be quite effective for pain disorders like fibromyalgia.
Anticonvulsants have been shown to be effective for some neuralgias. Carbamazepine for trigeminal neuralgia is one example.
Pain is a very complicated phenomenon, and even within classes there’s often no clear way to say what will work, and how well.
Loopydude makes good points, but most of the drugs he mentions are for use in people with chronic pain, which is quite a different kettle of fish than acute pain or malignant pain.
I do not care for tramadol. Its opiate receptor activity makes it a liability for anyone with a history of addiction, even tho the drug company tries to market it as “safe” vis a vis dependency. That has not been my and my colleagues experience with patients with a history of addiction.
Likewise its activity in another area, that of serotonin and norepi, makes it seem to me sort of a shotgun approach and not appropriate for acute pain.
I’ve had better luck with the tricyclics and anticonvulsants (particularly gabapentin, if the chronic pain is not too longstanding) than I have with the SSRI’s for chronic pain.
Qadgop or another pharmacologically competent member, could you discuss, objectively, the values of the four main OTC NSAIDs (using that term a bit more generically than is technically appropriate): Aspirin, Acetomenaphin, Ibuprofen, and Naproxen? This would be in terms of which is least likely to cause stomach problems, which functions best for muscle/joint pain, which reduces fever best, which can most safely be used in high doses to alleviate pain-severe-enough-to-call-for-massive-doses-but-not-sufficient-to-call-for-an-ER-visit., etc.
Obviously, each makes claims that emphasize its good points but do not address any negatives. And a good reference to what’s appropriate when would be of inestimable value.
Acetaminophen isn’t an NSAID (which Qadgop actually mentioned). As such, it’s less useful for pain involving inflammation, such as typical joint and muscle aches, as it doesn’t act as an anti-inflammatory along with its analgesic properties.
The thing to remember with NSAIDS is that they really do not reduce inflammation significantly unless taken regularly for a few weeks. In fact, some evidence shows they may make inflammation from acute trauma actually worse when used early in the course of the injury, by inhibiting some of the prostaglandins which help mediate bleeding and acute inflammatory response. I know a few orthopedists that recommend acetaminophen for mild to moderate acute injury pain because it will not inhibit prostaglandins.
Frankly, it’s six of one, half a dozen of another as far as I’m concerned. Use acetaminophen (tylenol) if you have a history of ulcers, severe heartburn history, or a history of GI intolerance to NSAIDS. Heck, acetaminophen is safer all around if you don’t plan on taking more than 2 grams a day for only a few days, and don’t have significant liver disease. And odds are it’ll be about as effective as most NSAIDS in fighting pain and fever.
As for the NSAIDS, whatever works for you best is best. Just take 'em with food, and follow package or prescription directions. I won’t get into stuff like safe maximum dosing, as that is an individual judgement call.
I think that is a very difficult question to answer. People (and animals, as I have found in dealing with this very question) simply react differently to different drugs, and it’s impossible to predict beforehand. FWIW, as an example, a paper I read in the British Journal of Medicine (Henry, et al.1996 Jun 22;312(7046):1563-6.) gave a meta-analysis from a number of studies of ranking risk of negative GI side-effects. The study seemed to indicate that ibuprofren might be superior to other NSAIDS, but the discussion was so filled with caveats, what I came away with was little more than “lower the dose of the drug as much as possible”, meaning whatever drug the doctor happens to be using and seems to be effective. In the end, I just gave up and used aspirin (sodium acetylsalicylate, in this case), because it’s cheap.
Wow, this is some good info. Do you mind expanding a little? What exactly is hydrocodone? Vicodin? Percocet versus percodan? When I injured a muscle in my back that then pinched a nerve running through my arm, the ER doc gave me hydrocodone and muscle relaxants. When I had my tonsils out last summer, I got 4 mgs of morphine in recovery (and learned that morphine is a wonderful thing), and then took percocet in crushed tablet form (it worked, but man, did it taste bad) and Tylenol 3 in liquid form (yummy 50 proof orange flavor). How do doctors make choices about which pain killers are appropriate for which kinds of pain and injury?
Every one of those drugs you mentioned is an opioid, an opiate, or contains an opiate. I imagine the reasons for choosing one or another may range anywhere from highly rational mechanistic concerns to “this kills pain fast”.
Pretty much based what’s on the formulary for that patient’s drug plan combined with that patient’s medical diagnoses and whatever mood the prescriber is in at the moment (Hey, the oxycontin guy just gave me a nice new pen! Next 10 patients get oxycontin!)
Vicodin has hydrocodone and acetaminophen. Vicoprofen has hydrocodone and ibuprofen. Percocet is oxycodone and acetaminophen. Percodan is oxycodone and aspirin. Lumping a narcotic pain killer with a non-narcotic pain killer is often done mainly because it seems like a good idea. If the patient is not aided by one ingredient, maybe they will get pain relief from the other. And maybe in that person, the two of them working together will do even more good. Or maybe not.
One reason for prescribing Tylenol #3 (codiene and acetaminophen) instead if plain old codiene is that T3’s are Schedule III and easier to prescribe, while codiene by itself is Schedule II and that has more restrictions on it.
One problem with mixing opiates and acetaminophen or NSAIDS in 1 pill is that a heroin addict who wants to get the same buzz off of percocet may take up to 100 pills at a time for the equivalent opiate effect of his usual heroin dose, but the acetaminophen dose ends up killing him.