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Pharmacologic treatment is the mainstay of pain therapy. Almost half of individuals who suffer from pain choose a nonprescription analgesic as their initial choice for pain relief.1 Up to one in five Americans take an over-the-counter or prescription analgesic on a daily basis.2 As with types of pain, multiple systems for classifying analgesics exist. In the below system, analgesics are broadly categorized as: ■ Nonopioid analgesics (nonopioids): acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and other salicylic acid derivatives ■ Opioid analgesics (opioids): mu opioid agonists (i.e., morphine-like agonists) and agonist-antagonist opioids ■ Adjuvant analgesics or co-analgesics: a diverse group of drugs, with primary indications for conditions other than pain, with analgesic properties relevant to some conditions. Commonly used adjuvant analgesics include antiepileptic drugs (AEDs), tricyclic antidepressants (TCAs), and local anesthetics (LAs). Variations of this classification system exist,a and terminology in the field is also evolving. The term “opioids” has replaced “narcotics,” and “co-analgesics” is an alternate term for “adjuvant analgesics.” 2. Common Analgesic Agents a. Nonopioids i. Mechanism of action and effects The primary mechanism of action of NSAIDs is inhibition of the enzyme cyclooxygenase (COX) which blocks prostaglandin synthesis.4,5 Acetaminophen, another nonopioid, appears to act mostly via a central mechanism.3,6-7 All nonopioids have anti-inflammatory, antipyretic, and analgesic effects, but the anti-inflammatory effect of acetaminophen is essentially negligible.8 The analgesic effect of NSAIDs is prompt (minutes to hours), whereas the antiinflammatory effect may take longer (1-2 weeks or longer).9 This latter effect can indirectly relieve some pain by reducing tissue swelling. The relatively recent discovery that COX has two isoforms, COX-1 and COX-2, has advanced NSAID pharmacology. COX-1 is constitutively expressed in most normal tissues,10 but plays an especially important role in the gastrointestinal (GI) tract, kidneys, and platelets; COX-1 primarily produces prostaglandins with beneficial effects (e.g., regulation of blood flow to the gastric mucosa and kidneys).8,11 In contrast, COX-2 is normally not present but may be induced in response to inflammatory stimuli; COX-2 primarily produces prostaglandins that activate and sensitize nociceptors (see I.B).b Nonselective NSAIDs inhibit COX-1 and COX-2, which contributes to both their therapeutic actions and side effects. The recently introduced COX-2 selective inhibitors (or “coxibs”) selectively inhibit COX-2 without affecting COX-1 at therapeutic doses.15,16 Thus, coxibs offer the advantage of efficacy comparable to that of nonselective NSAIDs, with a reduced risk of certain side effects.17-18 The coxibs affect COX-2 both centrally and peripherally. ii. Indications and uses Nonopioids relieve a variety of types of acute and chronic pain (e.g., trauma, postoperative, cancer, arthritis pain) and are especially effective for certain types of somatic pain (e.g., muscle and joint pain, bone/dental pain, inflammatory pain, postoperative pain) (Table 19).19-21 Acetaminophen and NSAIDs, alone, often relieve mild pain, and some NSAIDs relieve certain types of moderate pain (Table 19).51 Even National Pharmaceutical Council 33 Section III: Types of Treatments a Because acetaminophen has some, albeit extremely limited, anti-inflammatory properties,3 some experts consider acetaminophen an NSAID and use the term “NSAIDs” rather than “nonopioids.” Other experts disagree with this classification due to the different mechanisms of action and side effects of these drugs. b The division of function between COX-1 and COX-2 is not perfect. COX-1 produces some prostaglandins that contribute to inflammation.12 COX-2 is constitutively expressed in some organs (e.g., the kidney) where it produces prostaglandins with protective effects.13-14 34 Pain: Current Understanding of Assessment, Management, and Treatments Section III: Types of Treatments Table 19. Examples of Nonopioid Analgesics Usual Oral Dosage Dosing Forms and Chemical Generic Interval or Routes of Major Side Class Name Indications Frequency Administration Effects Comments Paraaminophenols Acetamin- Mild to moderate q 4-6 ha Multiple oral Acute overdose: Lacks anti-inflammatory ophen pain due to (e.g., tablets, hepatic necrosis effects of NSAIDs, but multiple causes caplets, (liver damage)b no adverse effects on including head- powder, elixir, gastric mucosa or ache, toothache, suspensions, Chronic platelets muscular aches, liquid); rectal overdose: liver Analgesic and backache, suppositories toxicity, antipyretic effects menstrual cramps, nephrotoxicity, comparable to aspirin arthritis, common thrombocytopenia Useful in patients cold, and flu; intolerant of NSAIDs fever reduction and for fever control in children with flu Salicylates Aspirin Mild to moderate ASA: Multiple oral NSAID class effectsc Combination pain due to q 4-6 ha (caplet, tablet, formulations available Diflunisal multiple causes gelcap, Diflunisal (aspirin and including headache, Diflunisal: effervescent hypersensitivity: acetaminophen, and/or CMT toothache, sinus q 8-12 h tablet, gum, life-threatening caffeine) pain, muscular liquid); rectal reaction that Diflunisal
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