Analgesic (patient information)

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An analgesic (colloquially known as a painkiller) is any member of the diverse group of drugs used to relieve pain (achieve analgesia). This derives from Greek an-, "without", and -algia, "pain". Analgesic drugs act in various ways on the peripheral and central nervous systems; they include paracetamol (acetaminophen), the nonsteroidal anti-inflammatory drugs (NSAIDs) such as the salicylates, narcotic drugs such as morphine, synthetic drugs with narcotic properties such as tramadol, and various others. Some other classes of drugs not normally considered analgesics are used to treat neuropathic pain syndromes; these include tricyclic antidepressants and anticonvulsants.

Contents

The major classes

Paracetamol and NSAIDs

The exact mechanism of action of paracetamol/acetaminophen is uncertain, but it appears to be acting centrally. Aspirin and the other NSAIDs inhibit cyclooxygenase, leading to a decrease in prostaglandin production; this reduces pain and also inflammation (in contrast to paracetamol and the opioids).[citation needed]

Paracetamol has few side effects, but dosing is limited by possible hepatotoxicity (potential for liver damage). NSAIDs may predispose to peptic ulcers, renal failure, allergic reactions, and hearing loss.[citation needed] They may also increase the risk of hemorrhage by affecting platelet function. The use of certain NSAIDs in children under 16 suffering from viral illness may contribute to Reye's syndrome.

COX-2 inhibitors

These drugs have been derived from NSAIDs. The cyclooxygenase enzyme inhibited by NSAIDs was discovered to have at least 2 different versions: COX1 and COX2. Research suggested that most of the adverse effects of NSAIDs were mediated by blocking the COX1 (constitutive) enzyme, with the analgesic effects being mediated by the COX2 (inducible) enzyme. The COX2 inhibitors were thus developed to inhibit only the COX2 enzyme (traditional NSAIDs block both versions in general). These drugs (such as rofecoxib and celecoxib) are equally effective analgesics when compared with NSAIDs, but cause less gastrointestinal hemorrhage in particular. However post-launch data indicated increased risk of cardiac and cerebrovascular events with these drugs, and rofecoxib was subsequently withdrawn from the market. The role for this class of drug is currently hotly debated.

Opiates and morphinomimetics

Morphine, the archetypal opioid, and various other substances (e.g. codeine, oxycodone, hydrocodone, diamorphine, pethidine) all exert a similar influence on the cerebral opioid receptor system. Tramadol and buprenorphine are thought to be partial agonists of the opioid receptors. Dosing of all opioids may be limited by opioid toxicity (confusion, respiratory depression, myoclonic jerks and pinpoint pupils), but there is no dose ceiling in patients who tolerate this.

Opioids, while very effective analgesics, may have some unpleasant side-effects. Up to 1 in 3 patients starting morphine may experience nausea and vomiting (generally relieved by a short course of antiemetics). Pruritus (itching) may require switching to a different opioid. Constipation occurs in almost all patients on opioids, and laxatives (lactulose, macrogol-containing or co-danthramer) are typically co-prescribed.

When used appropriately, opioids and similar narcotic analgesics are safe and effective, carrying relatively little risk of addiction. Occasionally, gradual tapering of the dose is required to avoid withdrawal symptoms.

Specific agents

In patients with chronic or neuropathic pain, various other substances may have analgesic properties. Tricyclic antidepressants, especially amitriptyline, have been shown to improve pain in what appears to be a central manner. The exact mechanism of carbamazepine, gabapentin and pregabalin is similarly unclear, but these anticonvulsants are used to treat neuropathic pain with modest success.

Specific forms and uses

Combinations

Analgesics are frequently used in combination, such as the paracetamol and codeine preparations found in many non-prescription pain relievers. They can also be found in combination with vasoconstrictor drugs such as pseudoephedrine for sinus-related preparations, or with antihistamine drugs for allergy sufferers.

The use of paracetamol, as well as aspirin, ibuprofen, naproxen, and other NSAIDS concurrently with weak to mid-range opiates (up to about the hydrocodone level) has been shown to have beneficial synergistic effects by combating pain at multiple sites of action—NSAIDs reduce inflammation which, in some cases, is the cause of the pain itself while opiates dull the perception of pain—thus, in cases of mild to moderate pain caused in part by inflammation, it is generally recommended that the two are prescribed together.[1]

Topical or systemic

Topical analgesia is generally recommended to avoid systemic side-effects. Painful joints, for example, may be treated with an ibuprofen- or diclofenac-containing gel; capsaicin also is used topically. Lidocaine and steroids may be injected into painful joints for longer-term pain relief. Lidocaine is also used for painful mouth sores and to numb areas for dental work and minor medical procedures.

Psychotropic agents

Tetrahydrocannabinol (THC) and some other cannabinoids, either from the Cannabis sativa plant or synthetic, have analgesic properties, although the use of cannabis derivatives is illegal in many countries. Other psychotropic analgesic agents include ketamine (an NMDA receptor antagonist), clonidine and other α2-adrenoreceptor agonists, and mexiletine and other local anaesthetic analogues.

Atypical and/or adjuvant analgesics

Orphenadrine, cyclobenzaprine, scopolamine, atropine, gabapentin, first-generation antidepressants and other drugs possessing anticholinergic and/or antispasmodic properties are used in many cases along with analgesics to potentiate centrally acting analgesics such as opioids when used against pain especially of neuropathic origin and to modulate the effects of many other types of analgesics by action in the parasympathetic nervous system. Dextromethorphan has been noted to slow the development of tolerance to opioids and exert additional analgesia by acting upon the NMDA receptors; some analgesics such as methadone and ketobemidone and perhaps piritramide have intrinsic NMDA action.

The use of adjuvant analgesics is an important and growing part of the pain-control field and new discoveries are made practically every year. Many of these drugs combat the side effects of opioid analgesics, an added bonus. For example, antihistamines including orphenadrine combat the release of histamine caused by many opioids, methylphenidate, caffeine, ephedrine, dextroamphetamine, and cocaine work against heavy sedation and may elevate mood in distressed patients as do the antidepressants. The one indisputably true benefit of THC to chronic pain patients on opioids may be its superior anti-nauseant action. However, it would make more sense to use the Marinol capsule, or oral, rectal, or vapour administration of hash oil, rather than smoking cannabis, for the same reasons most doctors advise against smoking tobacco.

Addiction

In the United States in recent years, there has been a wave of new addictions to prescription narcotics such as oxycodone (Percocet) and hydrocodone (Vicodin, Lortab etc.) when available in pure formulations as opposed to combined with other medications (as in Percocet which contains both oxycodone and acetaminophen/paracetamol). Hydrocodone is only available in pure form in some European countries as the original hydrocodone pharmaceutical, Dicodid tablets. Far from reducing addiction liability, the paracetamol content of many codeine, dihydrocodeine, hydrocodone, and oxycodone pharmaceuticals in the United States only saddles users with the high risk of severe liver damage, and extraction of the opioids with cold water or solvents reduces this problem for the sophisticated abuser, self-medicator, and legitimate prescription holder alike [2].

See also

References

  • Cancer pain relief and palliative care. Report of a WHO expert committee [World Health Organization Technical Report Series, 804] . Geneva, Switzerland: World Health Organization; 1990. pp. 1–75. ISBN 92-4-120804-X.
  • Bandolier pain site (Oxford pain group)

External links

Overview

Related Key Words and Synonyms:

Epidemiology and Demographics

Risk Factors

Screening

Pathophysiology & Etiology

Molecular Biology

Genetics

Natural History

Diagnosis

Differential Diagnosis

History and Symptoms

Physical Examination

Appearance of the Patient

Vital Signs

Skin

Eyes

Ear Nose and Throat

Heart

Lungs

Abdomen

Extremities

Neurologic

Other

Laboratory Findings

Electrolyte and Biomarker Studies

Electrocardiogram

Chest X Ray

MRI and CT

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Risk Stratification and Prognosis

Treatment

Pharmacotherapy

Acute Pharmacotherapies

Chronic Pharmacotherapies

Surgery and Device Based Therapy

Indications for Surgery

Pre-Operative Assessment

Post-Operative Management

Transplantation

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

"The Way I Like To Do It ..." Tips and Tricks From Clinicians Around The World

Suggested Revisions to the Current Guidelines

References

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Acknowledgements

The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.

Initial content for this page in some instances came from Wikipedia

List of contributors:

Suggested Reading and Key General References

Suggested Links and Web Resources

For Patients


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