How Do Pain Relievers Work? - George Zaidan

3,981,414 views ・ 2012-06-26

TED-Ed


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Translator: Ido Dekkers Reviewer: Ariana Bleau Lugo
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Say you're at the beach, and you get sand in your eyes.
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How do you know the sand is there?
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You obviously can't see it, but if you are a normal, healthy human,
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you can feel it,
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that sensation of extreme discomfort, also known as pain.
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Now, pain makes you do something,
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in this case, rinse your eyes until the sand is gone.
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And how do you know the sand is gone?
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Exactly. Because there's no more pain.
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There are people who don't feel pain.
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Now, that might sound cool, but it's not.
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If you can't feel pain, you could get hurt, or even hurt yourself
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and never know it.
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Pain is your body's early warning system.
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It protects you from the world around you, and from yourself.
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As we grow, we install pain detectors in most areas of our body.
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These detectors are specialized nerve cells
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called nociceptors
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that stretch from your spinal cord to your skin, your muscles, your joints,
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your teeth and some of your internal organs.
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Just like all nerve cells, they conduct electrical signals,
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sending information from wherever they're located back to your brain.
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But, unlike other nerve cells,
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nociceptors only fire if something happens that could cause
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or is causing damage.
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So, gently touch the tip of a needle.
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You'll feel the metal, and those are your regular nerve cells.
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But you won't feel any pain.
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Now, the harder you push against the needle,
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the closer you get to the nociceptor threshold.
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Push hard enough, and you'll cross that threshold
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and the nociceptors fire,
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telling your body to stop doing whatever you're doing.
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But the pain threshold isn't set in stone.
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Certain chemicals can tune nociceptors, lowering their threshold for pain.
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When cells are damaged, they and other nearby cells
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start producing these tuning chemicals like crazy,
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lowering the nociceptors' threshold to the point
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where just touch can cause pain.
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And this is where over-the-counter painkillers come in.
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Aspirin and ibuprofen
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block production of one class of these tuning chemicals,
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called prostaglandins.
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Let's take a look at how they do that.
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When cells are damaged, they release a chemical called arachidonic acid.
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And two enzymes called COX-1 and COX-2
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convert this arachidonic acid into prostaglandin H2,
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which is then converted into a bunch of other chemicals
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that do a bunch of things,
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including raise your body temperature, cause inflammation
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and lower the pain threshold.
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Now, all enzymes have an active site.
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That's the place in the enzyme where the reaction happens.
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The active sites of COX-1 and COX-2
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fit arachidonic acid very cozily.
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As you can see, there is no room to spare.
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Now, it's in this active site that aspirin and ibuprofen do their work.
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So, they work differently.
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Aspirin acts like a spine from a porcupine.
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It enters the active site and then breaks off,
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leaving half of itself in there,
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totally blocking that channel and making it impossible
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for the arachidonic acid to fit.
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This permanently deactivates COX-1 and COX-2.
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Ibuprofen, on the other hand,
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enters the active site,
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but doesn't break apart or change the enzyme.
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COX-1 and COX-2 are free to spit it out again,
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but for the time that that ibuprofen is in there,
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the enzyme can't bind arachidonic acid, and can't do its normal chemistry.
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But how do aspirin and ibuprofen know where the pain is?
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Well, they don't.
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Once the drugs are in your bloodstream,
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they are carried throughout your body,
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and they go to painful areas just the same as normal ones.
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So that's how aspirin and ibuprofen work.
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But there are other dimensions to pain.
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Neuropathic pain, for example,
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is pain caused by damage to our nervous system itself;
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there doesn't need to be any sort of outside stimulus.
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And scientists are discovering that the brain controls
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how we respond to pain signals.
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For example, how much pain you feel can depend on
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whether you're paying attention to the pain, or even your mood.
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Pain is an area of active research.
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If we can understand it better, maybe we can help people manage it better.
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