A pharmacy of natural chemicals dampens the initial pain of a broken finger but when the shock wears off and the hurt kicks in medical science, thankfully, comes to the rescue.

My column has been missing the past two weeks after I slipped and managed to embed my hand into a volcanic rock in Hawaii.

Staring at the broken bones protruding from my hand immediately after my accident, I remember thinking "this should hurt more than it does". I was surprised at how little I actually felt. My scientific brain kicked in - I wanted to know more.

The International Association for the study of Pain describes pain as an unpleasant sensory and emotional experience associated with tissue damage. This makes pain a subjective experience - it cannot be measured, and there is huge variability in how different people experience it.

Pain is usually divided into two groups: acute, which usually occurs after trauma or surgery and is typically confined to a period of time and severity; and chronic, often defined as pain lasting for more than 12 weeks, and which sometimes has no identifiable cause.

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The first documented relationship between stress and pain came from the World War II battlegrounds. Medics noticed that seriously wounded soldiers would fail to report pain immediately after being wounded, but would then report significant increases of pain one to two days later once the effects of shock had worn off.

When the brain senses a serious injury it releases a whole pharmacy of natural chemicals to dampen the pain - a process called "stress-induced analgesia". Some of these include opioids from the adrenal and pituitary glands.

In Hawaii, staring at a broken finger and degloved hand, my heart rate increased and my sense of time seemed to make things move very slowly - I knew my "fight or flight" sympathetic nervous system had already kicked in.

Once in the safety of the hospital, I lay listening to the medical professionals discussing the bone and tendon damage in my hand. They talked titanium screws and plates, and mentioned surgery and long-term recovery plans.

My sense of pain increased dramatically - my body's initial response had passed. Thankfully, the question of pain relief came up - again my scientific brain kicked in - I wondered how the medicine would know where my pain was and how to stop it.

I was given an injection of science (labelled "morphine") to help with my pain. Morphine and codeine are sourced from the opium seedpod found in the poppy plant. They are thought to relieve pain sensation by binding to opiate receptors in the central nervous system, interfering with the transmission of pain signals to the brain while also working inside the brain to alter the sensation of pain.

Rather than "finding" the pain, they reduce the patient's perception of the pain. My hand was still broken, but my brain wasn't receiving the pain signals to let me know.

Later, after my surgery, I was given an NSAID (non-steroidal anti-inflammatory drug), which works by inhibiting an enzyme called cyclooxygenase or COX. After a part of the body is injured, protective mechanisms go into action causing swelling, heat, redness and pain - the inflammatory response.

Inflammation-causing chemicals called prostaglandins are produced by the COX enzyme, and NSAIDs (eg aspirin, ibuprofen and naproxen) inhibit this production, reducing the inflammation and pain.

I've learned that pain is a very personal experience for each of us.

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My final synthetic pain relief was paracetamol, which also binds to enzymes at the site of cell damage, preventing them from sending pain signals to the brain.

Although paracetamol doesn't treat inflammation, it is effective in reducing pain with far fewer side effects than other painkiller drugs, making it more suitable for long-term use.

Through this journey I've learned that pain is a personal experience for each of us. The body has some amazing natural painkillers of its own and when those aren't enough, thankfully medical science has created some amazing solutions to help manage and control pain, each with their own mechanism of action.