Pharmacology in Pain Management

Welcome to PPA Pain Project. This page is being developed by participants of a project to populate the Pain section of Physiopedia.  The project is supervised and co-ordinated by the The Physiotherapy Pain Association.

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Tips for writing this page:

• Describe the principles of the pharmacology of medications used to treat pain: non-opioid medications, opioids, adjuvants and topical analgesics and local anaesthetics.
• Include limitations of the pharmacological management of chronic pain and barriers such as social and professional stigma/stereoypes associated with medication use and prescription
  
• The role of AHP and Physiotherapy prescribing

Introduction: A wide range of drugs are used to help manage pain which may result from inflammation in response to tissue damage, chemical agents or pathogens (nociceptive pain) or nerve damage ( neuropathic pain ). Most drugs act by binding to protein targets on the cell membrane and affect the biochemical processes of the body. Protein targets are specific to specific tissues allowing drugs to be precisely targeted at organs or cells (specificity). Drugs exhibiting high specificity require lower doses and have fewer side effects than those with lower specificity.
Originally developed by the World Health Organisation (WHO) as an attempt to improve the management of cancer pain; the 3 step WHO analgesic ladder is also widely used as the framework for providing stepwise pain relief for pain due to other causes.

== Non opioid medications: (step 1 WHO Analgesic ladder – mild to moderate pain) Non steroidal anti inflammatory drugs (NSAIDs) such as asprin, ibuprofen, naproxen, diclofenac weaken and reduce the levels of chemical mediators (prostaglandins) produced during inflammation, relieving symptoms of pain, swelling and redness. They inhibit the enzyme cyclo-oxygenase (COX 2) which is integral in the synthesis of prostaglandins. During infection the effect of prostaglandins on the hypothalamus results in a higher body temperature (pyrexia). NSAIDs weaken the production of prostaglandins enabling the temperature to reduce towards normal. NSAIDS do not just inhibit prostaglandin production at the site if pain but throughout the body producing side effects including in the gastrointestinal tract(GIT). GIT side effects are explained by NSAIDs interference with the normal homeostasis role of prostaglandins (mediated by COX 1 enzyme) in maintaining gastric mucosa and regulating stomach acids. Side effects affecting GIT may include indigestion, nausea and vomiting, and diarrhoea and can result in ulceration and bleeding.. Other side effects include rashes, photosensitivity, bronchospasm, dizziness and haematuria.
NSAIDs must be used with caution in the elderly, and people with diabetes, asthma and impaired renal or cardiac function.
NSAIDs are contraindicated for people with a previous history of adverse reaction, a history of peptic ulcer or clotting disorders and those taking anticoagulants or another NSAID medication.
Paracetamol. Although it is the most widely used pain relieving medication the exact mechanism of action of paracetamol is relatively poorly understood. It is thought to act on the COX 3, a recently discovered type of COX present in the brain and spinal cord. Paracetamol has mainly anti-pyretic (reducing the levels of prostaglandins in the hypothalamus) and analgesic properties; it does not interfere with COX 2 and does not affect the other components of inflammation ( swelling and redness). As paracetamol has no action on COX 1 at a therapeutic dose it has few side effects. The maximum recommended daily therapeutic dose of paracetamol for adults is 4g ( 8 x500mg tablets). It is hepatotoxic at only 2-3 times the therapeutic dose causing necrosis of the liver and resulting in 226 deaths in 2013 in England and Wales ( ref)
Asprin. Thromboxanes are inflammatory mediators derived from platelets that cause vasoconstriction and aggregation of platelets leading to clotting. Asprin inhibits the production of COX 2 enzymes, which are also essential to the production of thromboxanes, inhibiting platelet aggregation and clots leading to its use in the treatment and prophylaxis of cardiovascular disease or myocardial infarction.  ==

Limitations of the pharmacological management

It is important to understand the limitations of the pharmacological management of chronic pain, the importance of combining pharmacological approaches with non-pharmacological management of chronic pain and the use of such strategies alongside appropriate evidence-based active self management strategies.