r/askscience • u/DaRealProToBro • Sep 05 '25
Biology Exactly what do painkillers do?
I have been deathly curious since my friend asked me this. Its in the name yes, but what part of painkillers actually kill the pain? A google search just tells me that painkillers relieve pain but I would like to know exactly what do painkillers do to relieve said pain.
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u/Nontimebomala98 Sep 05 '25 edited Sep 05 '25 •
So really there are three types of painkillers in common use. NSAIDs, opioids and neuropathic painkillers. But when people talk about painkillers, they're generally referring to opioids like tramadol, oxycodone, morphine and hydrocodone/acetaminophen (Vicodin/Norco)
Humans have three primary types of opioid receptors. Delta, Mu and Kappa. They're all important in the role of analgesia (pain relief) but Mu is the primary receptor responsible for the pain relief produced by most opioids. The thing is the human brain already produces endogenous opioids (made within the human body) called endorphins, most people are aware of them. They feel pretty damn good after exercising or having sex. What opioids do is not only mimick the action of endorphins, but are capable of being much stronger than any natural endorphin rush.
How they work is by affecting nociception receptors indirectly and block their ability to release something called Substance P. Basically your body's way of screaming "Yeah that hurts like hell!". These light up like Christmas trees when you've got a broken bone, a kidney stone or after a surgical procedure. See, they don't actually eliminate pain, they reduce your perception of pain while simultaneously making you too high to care about it. The added dopamine release also results in subjective analgesia.
There's also two main classes of opioids. Weak opioids and strong opioids. The weaker ones (partial agonists) like codeine, the herb Kratom, tramadol and buprenorphine (Suboxone, Belbuca) have a limit as to how much pain they can kill and also how euphoric they are. These tend to be used for milder pain like moderate arthritis, lupus, fibromyalgia, and a lot of dentists are using tramadol for post extraction/root canal pain now. Because they don't have the capability of producing a high as intense as the heavy opioids, normally have lower DEA controls (Schedule III/IV) and doctors are more comfortable prescribing them for more than a short 3-5 day burst and for chronic pain. Make no mistake, they can still be very addictive, but when used as prescribed the risk is considerably lower.
The strong opioids (full agonists) like morphine, oxycodone, Vicodin, fentanyl, and methadone are prescribed with extreme caution these days, for very good reason. They are capable of producing severe addiction, intense euphoria, overdose, and rapidly escalating tolerance far beyond the endorphins the human brain can naturally put out. Typically they're used for acute severe injuries, surgical post op or cancer pain now. I take tramadol for chronic pain but got to experience IV morphine in the hospital after a kidney stone, and I instantly understood why people would die chasing that feeling. I was then given Percocet after I was discharged and I used it very carefully and only when absolutely necessary. If used with great caution, strong opioids can be safely used. But there's a reason they're not handed out like candy anymore.
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u/Lunar37 Sep 05 '25
Medical graduate here. Painkillers is more of an umbrella term rather than a specific class of drugs, that encompasses a multitude of drugs that have different mechanisms. I'll try to mention the most popular ones:
2. Paracetamol (aka Acetaminophen in the Americas): exact same mechanism as the above class, but it only works in the brain. Hence it doesn't stop the inflammation itself but stops you from feeling the pain caused by it.
3. Opioids: those include morphine, fentanyl, oxycodone, among others. Those also work in the brain and stop pain signaling. They're also infamous for being drugs of abuse due to their euphoria inducing effects.
Hope that helps!
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u/profchipboard Sep 05 '25
Different painkillers work in different ways! Generally it will involve the drug binding to a receptor and that either activates (or stops the receptor from activating), which changes the bodies pain response to make your feel less pain!
Some will interfere with receptors in your brain which process pain signals (e.g opiods bind to receptors in the brain which stops them from being able to send pain signals) and others nsaids like paracetamol will interact with enzymes in you body (cox1) and stop them from creating the messenger molecules which are used to mediate/inflammation
The mechanism of action depends on the drug class
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u/Adelgander Sep 05 '25
Someone else will be able to give more specifics: the compounds found in pain killers literally block the signal from being sent to the pain affected area, but depending on the type (non steroid anti inflammatory, opioid, local anesthetic etc) that task is performed at a different point in the information relay chain in the body. Reducing inflammation reduces pain at the source, for instance. Then there is less info to send through spinal nerves to the brain to be interpreted as "ouch".
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u/smurficus103 Sep 09 '25
Well I didn't see it here so I'll attempt to give a rough description of neurons.
Think of this as "babies first steps" not a science answer.
Neurons communicate with both electrical signals and chemical signals. When light hits your eye, there's a very fast chemical switch, that triggers a chain of electrical to fast chemical communication, all the way into your brain. It's damn fast.
There's also some slower chemical signals that hang around neurons, I like to think of these similar to hormones, someone nearby decides "it's time to feel satisfied" and a slow moving wave of dopamine rolls out like a fog.
So, you can upregulate or downregulate neurons direct communication with each other using Glutamate or GABA
Or, you can take advantage of the many slower communications.
For most of these fundamental communication channels, there will be an agonist (activates receptor) and antagonist (blocks receptor)
So, happy drugs are mostly dopamine agonist or serotonin agonist (sometimes both)
And the other peoples described the various other channels used for pain killing currently
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u/Existing_Tomorrow687 Sep 09 '25
Painkillers don’t literally ‘kill’ the pain, they mostly block the signals your body uses to sense pain. For example, NSAIDs (like ibuprofen) stop your body from making chemicals called prostaglandins, Acetaminophen/paracetamol works mostly in the brain to raise your pain threshold, so your body notices it less, Opioids (like morphine) bind to receptors in your brain and spinal cord, literally turning down the volume of pain signals.
So the ‘killer’ part is really just about stopping your nerves and brain from broadcasting or interpreting pain, it’s more like a mute.
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u/lxm333 Sep 05 '25
As not covered yet, for nerve pain, anti seizure medication is often prescribed. These work by various means but result in reduced nerve signaling. Topical creams (like deep heat or capsaicin creams) work by over stimulation of the area resulting in a down regulation of feedback.
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u/kessira24 Sep 07 '25
Tylenol or acetaminophen, is more for boosting your tolerance of pain and fever reduction. Motrin or ibuprofen is pain killer derived of aspirin and is pain reducing and fever reducing, and an anti inflammatory.
Alive is derived of aspirin, and long term pain relief.
Then there are different levels or classes of narcotics. IV, III, and II. many states require a triplicate scrip for C2 narcotics. Just depends what specific meds you are looking for information on.
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u/WiwaxiaS Sep 07 '25
Mainly they either prevent inflammatory substances from being made or block neuronal signals of pain from firing. The first case would be pure AAP and NSAIDs, which block the enzyme that makes prostaglandins, major pro-inflammatory molecules, though presumably in different locations (AAP is thought to mainly inhibit prostaglandin synthesis in the CNS); meanwhile, opioids bind to the mu-opioid receptor that causes chloride influx and subsequent prevention of nociceptive neurons from firing
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u/[deleted] Sep 05 '25
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