Pharmacology and Medical Management of Pain
Core concepts
Know mechanisms and receptor targets: NSAIDs (COX inhibition, GI/renal/cardiovascular risk), acetaminophen (central, hepatic ceiling), gabapentinoids (alpha-2-delta subunit), SNRIs and TCAs (descending modulation), topical agents (lidocaine, capsaicin), and opioids (mu agonism). Match drug class to mechanism: neuropathic pain responds to gabapentinoids, SNRIs, and TCAs, not to NSAIDs.
Safety and interactions
High-yield safety: NSAID avoidance in renal disease, heart failure, and anticoagulation; serotonin syndrome risk with combined serotonergic agents; anticholinergic burden of TCAs; gabapentinoid sedation and renal dosing. Opioid questions emphasize equianalgesic conversion, tolerance versus hyperalgesia, bowel prophylaxis, and misuse risk assessment.
Traps
- Assuming one neuropathic agent fits all; titration and combination are often needed.
- Ignoring renal function for gabapentinoids and NSAIDs.
- Confusing physical dependence with addiction.
- Missing steroid side effects (hyperglycemia, insomnia, adrenal suppression with chronic use).
Worked rule of thumb
Start low, titrate to effect or intolerance, reassess function not just pain score. For neuropathic pain, a reasonable sequence is gabapentinoid or SNRI first-line, then add a mechanistically different agent before switching classes.
Regulatory context
Opioid prescribing carries documentation and monitoring expectations; know that urine drug testing and prescription monitoring queries are risk-management tools, not proof of misuse.