Asking this as I have a horrible throat infection making it incredibly painful to swallow, and therefore difficult to eat and drink. I have to stay on top of my painkillers every four hours or the pain starts to come back, I’d just love to know how this actually works.
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Depends. I mean, its really all relative. If the pain is gone temporarily, then one could argue that it killed the pain, completely, temporarily.
If the problem is inflammation, then there may be an allergy related post nasal drip happening that is drying your throat up, making it hurt. Drinking water is the key.
You can also have an infection without a fever. If the throat ache goes on for a week, it helps to get a throat culture done to see if there is any infection.
As far as how painkillers work, they might indeed kill or dull the pain temporarily, but they dont kill any infection, or treat the root cause of the pain.
Theres a product out, AZO, which claims.to help with bladder infections. The problem with this OTC product is that some people use it when they start feeling a bladder infection, to FEEL better, and can end up with a kidney infection, because they used an analgesic or anti-inflammatory, and didnt get their doctor to prescribe an antibiotic. Its okay to FEEL better, but if the problem is lasting for a week, its time to get an antibiotic to kill the infection.
Once the infection is gone, along with the antibiotics, this will end the pain.
Pain is a personal experience of each person experiencing pain.
You have “sensors” in your body called nociceptors. They tend to react to certain inputs, in a way as smoke detectors work. If there is smoke, they signal alarm. They respond to various inputs (compression, as in an actual hit, if I hit you), heat, cold, traction (touch) etc.
Your nervous system is a wiring system that passes through your spine, like cars on a high way. Destination? Your Operator.
So, smoke detector (nociceptors) > nerve (wire) > spine (high way) > brain (Operator).
Now, pain is a sensation you experience if Operator deems signal too loud for what’s normal, and what its used to feel/hear. It then uses previous experiences, the signal strength (how loud your smoke detector yells) and interprets what’s going on: that something dangerous happened. Operator is also responsible for an action as a response: like jerking your hand away from fire, because skin got burned.
Now, each pain drug have their own method of working.
1) Blocking nociceptors from triggering (like a plastic bag over a smoke detector) by attaching to them like Lego. No other piece can then be attached to them any more. See point 3.
2) Blocking wires from transmitting. Like epidural that blocks your spine (high way) from passing the signal on.
3) Removing source of pain. Inflammation creates chemical things that attach to nociceptors like Lego. Your Operator doesn’t really know if something is inflamed without those chemicals. Some drugs remove Inflammation, and with that the chemicals that trigger nociceptors (smoke alarm).
4) Some block your Operator from knowing anything is up. No signal gets through to it, so as far as Operator is concerned, everything is peachy.
I’m sure there is at least one pain scientist and a chemist that can correct me here 😀
This is not really a ELI5 topic. This sorta thing is a doctorate study. But to if you want understand pain and pain receptors at a very rudimentary form imagine it like you are on you bicycle and witnessing a fight and a kid getting knocked out.
You want to ride home on your bicycle and tell your mom what happened.
Only on your ride home, you notice the street you’re riding on has construction signs and a buncha back goes and you can’t ride through (narcotics, mu receptors).
So you decide your going to ride around all that on your way home on the sidewalk but it is also barricaded off and it abruptly ends ending up in a grass patch (NSAIDs/Acetaminophen)
So you say “fuck it” and ditch your bike where it stands and your going to run across the grass to your house to go tell mom what happens, only to find there’s some stupid big ass fence in the way (etc. Pathways, alpha 2 blockers, misc pain pathways ) and you can’t actually get home so you just stand there and yell from where you’re at and your mom can’t really figure out wtf is going on.
Yeah. It’s kinda like that. Mom is the brain which interprets and reacts to all the information. The incident/fight is the painful incident and the messenger, little kid on the bike, is the communicator.
If the communicator can’t relay the message of pain the brain can’t process what to make of it or how to respond to the incident so nothing happens.
This is not really a ELI5 topic. This sorta thing is a doctorate study. But to if you want understand pain and pain receptors at a very rudimentary form imagine it like you are on you bicycle and witnessing a fight and a kid getting knocked out.
You want to ride home on your bicycle and tell your mom what happened.
Only on your ride home, you notice the street you’re riding on has construction signs and a buncha back goes and you can’t ride through (narcotics, mu receptors).
So you decide your going to ride around all that on your way home on the sidewalk but it is also barricaded off and it abruptly ends ending up in a grass patch (NSAIDs/Acetaminophen)
So you say “fuck it” and ditch your bike where it stands and your going to run across the grass to your house to go tell mom what happens, only to find there’s some stupid big ass fence in the way (etc. Pathways, alpha 2 blockers, misc pain pathways ) and you can’t actually get home so you just stand there and yell from where you’re at and your mom can’t really figure out wtf is going on.
Yeah. It’s kinda like that. Mom is the brain which interprets and reacts to all the information. The incident/fight is the painful incident and the messenger, little kid on the bike, is the communicator.
If the communicator can’t relay the message of pain the brain can’t process what to make of it or how to respond to the incident so nothing happens.
This is not really a ELI5 topic. This sorta thing is a doctorate study. But to if you want understand pain and pain receptors at a very rudimentary form imagine it like you are on you bicycle and witnessing a fight and a kid getting knocked out.
You want to ride home on your bicycle and tell your mom what happened.
Only on your ride home, you notice the street you’re riding on has construction signs and a buncha back goes and you can’t ride through (narcotics, mu receptors).
So you decide your going to ride around all that on your way home on the sidewalk but it is also barricaded off and it abruptly ends ending up in a grass patch (NSAIDs/Acetaminophen)
So you say “fuck it” and ditch your bike where it stands and your going to run across the grass to your house to go tell mom what happens, only to find there’s some stupid big ass fence in the way (etc. Pathways, alpha 2 blockers, misc pain pathways ) and you can’t actually get home so you just stand there and yell from where you’re at and your mom can’t really figure out wtf is going on.
Yeah. It’s kinda like that. Mom is the brain which interprets and reacts to all the information. The incident/fight is the painful incident and the messenger, little kid on the bike, is the communicator.
If the communicator can’t relay the message of pain the brain can’t process what to make of it or how to respond to the incident so nothing happens.
It depends on the painkiller.
Some of them stop the processes that send pain-inducing chemicals, like aspirin. In this case, yes, the pain is actually “gone” because those pain signals stop sending.
In stronger things like opioids, the pain receptors are blocked. The pain is still “there” but you can’t even receive those pain signals.
So for example, you can’t take something like aspirin and feel no pain if you suddenly cut your hand, because aspirin doesn’t stop that type of of pain process. While someone high on opioids may not even notice they cut their hand.
It depends on the painkiller.
Some of them stop the processes that send pain-inducing chemicals, like aspirin. In this case, yes, the pain is actually “gone” because those pain signals stop sending.
In stronger things like opioids, the pain receptors are blocked. The pain is still “there” but you can’t even receive those pain signals.
So for example, you can’t take something like aspirin and feel no pain if you suddenly cut your hand, because aspirin doesn’t stop that type of of pain process. While someone high on opioids may not even notice they cut their hand.
It depends on the painkiller.
Some of them stop the processes that send pain-inducing chemicals, like aspirin. In this case, yes, the pain is actually “gone” because those pain signals stop sending.
In stronger things like opioids, the pain receptors are blocked. The pain is still “there” but you can’t even receive those pain signals.
So for example, you can’t take something like aspirin and feel no pain if you suddenly cut your hand, because aspirin doesn’t stop that type of of pain process. While someone high on opioids may not even notice they cut their hand.
This is the same as saying “if a tree falls in the woods and no one is there to hear it, does it make a sound?”
Pain is your body telling you something is wrong. Painkillers block that message.
The tree fell… the painkillers made sure you didn’t hear it.
This is the same as saying “if a tree falls in the woods and no one is there to hear it, does it make a sound?”
Pain is your body telling you something is wrong. Painkillers block that message.
The tree fell… the painkillers made sure you didn’t hear it.
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