Pain Management
Chronic pain syndromes, CRPS, neuraxial opioids, multimodal analgesia, neuropathic pain, interventional pain. ← Back to Q-Bank
Q1. CRPS classification
The defining difference between CRPS type I and type II is:
A. Severity of pain
B. Type I occurs without identifiable nerve injury; Type II occurs after major nerve trunk injury
C. Type I is acute, Type II is chronic
D. Type I affects upper extremity only
E. Type II is psychogenic
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Answer: B. CRPS I (formerly RSD) — trivial injury, no specific nerve identified. CRPS II (formerly causalgia) — known nerve trunk injury (gunshot, surgical). Both: burning pain, allodynia, autonomic dysfunction (temperature, sweating, skin color changes), trophic changes. Treatment: PT, sympathetic blocks (stellate for UE, lumbar for LE), gabapentinoids, TCAs, ketamine infusion, spinal cord stimulator for refractory.
Q2. Neuraxial morphine respiratory depression
Respiratory depression risk after intrathecal morphine peaks at:
A. 30 min
B. 6–12 hours (delayed because of slow cephalad spread in CSF)
C. 24 hours
D. 48 hours
E. Immediately after injection
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Answer: B. Intrathecal morphine (hydrophilic) → slow cephalad spread to brainstem → delayed respiratory depression peak 6–12 hr. Monitor for 24 hr postop. Fentanyl (lipophilic) → rapid local uptake, peak respiratory depression at injection. ASRA guidelines: monitor for ≥20 min continuously then hourly for 2 hr after lipophilic, hourly for 12 hr then q2h × 12 hr for hydrophilic opioid.
Q3. Multimodal analgesia rationale
The advantage of multimodal analgesia is:
A. Higher total opioid dose
B. Synergistic effect at multiple pathways reduces total opioid requirement, side effects, and chronic pain transition
C. Single high-dose opioid is equivalent
D. Multimodal increases PONV
E. Cheaper only
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Answer: B. Acetaminophen + NSAID + gabapentinoid + regional + ketamine (low-dose) + dexmedetomidine — multimodal reduces opioid use 30–50%, less PONV, less constipation, less sedation, better outcomes. Cornerstone of ERAS protocols.
Q4. Methadone for chronic pain
Methadone is useful for chronic neuropathic pain because of:
A. Strong α-blocker effect
B. NMDA antagonism + μ-opioid agonism + SNRI properties
C. Anti-inflammatory effects
D. Direct nerve regeneration
E. GABA agonism
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Answer: B. Methadone unique combination — NMDA antagonism (neuropathic pain), μ-agonist (analgesia), serotonin/NE reuptake inhibition. Useful in opioid tolerance and neuropathic pain. Side effects: QT prolongation, long and unpredictable half-life (13–58 hr) → titrate carefully.
Q5. Buprenorphine in chronic pain
A patient on buprenorphine for opioid use disorder presents for major surgery. The most current recommendation is:
A. Stop buprenorphine 1 week preop
B. Continue buprenorphine perioperatively, use multimodal analgesia, add high-dose full-agonist opioid (will need higher doses than usual)
C. Switch to methadone preop
D. Use naloxone postop
E. Avoid all opioids
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Answer: B. Current ASAM/ASRA recommendations (2021) favor continuing buprenorphine perioperatively. Multimodal + regional. Use higher-than-usual doses of full agonists if needed (high mu affinity of buprenorphine displaces other opioids). Avoid stopping (risk of relapse, worse pain control). Hydromorphone or fentanyl tend to work better than morphine.
Q6. Opioid-induced hyperalgesia
Opioid-induced hyperalgesia is characterized by:
A. Tolerance to opioid analgesia
B. Increased sensitivity to pain after opioid administration, often diffuse and worse with escalating doses
C. Acute opioid withdrawal
D. Allergic reaction
E. Respiratory depression
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Answer: B. OIH: paradoxical increased pain with increased opioid dose, often diffuse beyond original pain area. Mechanism: NMDA upregulation, dynorphin, descending facilitation. Treatment: rotate opioid (especially to methadone — NMDA antagonist), reduce dose, add ketamine, multimodal regional.
Q7. Ketamine for chronic pain
Low-dose ketamine for chronic neuropathic pain works via:
A. μ-opioid agonism
B. NMDA receptor antagonism → modulates central sensitization and reduces wind-up
C. α₂-adrenergic agonism
D. GABA potentiation
E. COX inhibition
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Answer: B. NMDA antagonism reverses central sensitization. Low-dose ketamine infusion (0.1–0.5 mg/kg/hr) reduces opioid consumption in opioid-tolerant patients, CRPS, chronic neuropathic pain. Side effects: dissociation, hypertension, hallucinations (less at sub-dissociative doses).
Q8. Tricyclic antidepressants for neuropathic pain
TCAs (amitriptyline, nortriptyline) treat neuropathic pain via:
A. Direct sodium channel blockade in peripheral nerves
B. Inhibition of serotonin and norepinephrine reuptake → enhances descending inhibition of pain
C. NMDA antagonism
D. μ-opioid agonism
E. GABA agonism
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Answer: B. TCAs enhance descending noradrenergic and serotonergic inhibition. First-line for many neuropathic pain conditions (diabetic neuropathy, post-herpetic neuralgia, fibromyalgia). Side effects: anticholinergic, sedation, QT prolongation, orthostasis. Nortriptyline better tolerated than amitriptyline.
Q9. Fibromyalgia treatment
First-line pharmacologic treatment for fibromyalgia includes:
A. Opioids
B. Duloxetine, milnacipran (SNRIs), pregabalin (FDA-approved), amitriptyline
C. NSAIDs alone
D. Steroids
E. Benzodiazepines
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Answer: B. Three FDA-approved drugs: duloxetine, milnacipran, pregabalin. TCAs (amitriptyline) also effective. Combine with non-pharmacologic: aerobic exercise, CBT, sleep hygiene. Opioids generally avoided (limited efficacy, abuse potential).
Q10. Lumbar sympathectomy CRPS
Lumbar sympathectomy is appropriate for CRPS of the:
A. Upper extremity
B. Lower extremity
C. Face
D. Trunk
E. Both upper and lower extremities
Show answer
Answer: B. Lumbar sympathetic chain (L2–L4) for lower extremity CRPS, peripheral vascular disease, ischemic ulcers, phantom limb. Approach: prone or lateral, needle to lateral aspect of L3 vertebral body, walk off, advance ~0.5 inch, inject 12–15 mL local. Complications: genitofemoral neuralgia, intravascular injection, epidural/intrathecal spread.
Q11. Intrathecal drug delivery
The most common intrathecal medications delivered via implanted pump include:
A. Morphine, hydromorphone, fentanyl, bupivacaine, clonidine, ziconotide
B. Aspirin
C. Acetaminophen
D. Lidocaine alone
E. Methotrexate
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Answer: A. ITDD for refractory chronic pain or severe spasticity (baclofen). Polyanalgesic Consensus Conference guidelines: morphine and ziconotide as first-line for nociceptive and neuropathic pain respectively. Ziconotide = N-type calcium channel blocker (from cone snail toxin) — no respiratory depression but psychiatric and CNS side effects.
Q12. Phantom limb pain treatment
Phantom limb pain prevention may be reduced by:
A. Perioperative regional anesthesia (epidural or peripheral nerve block continued postoperatively), gabapentinoid, mirror therapy
B. Opioids alone
C. Avoidance of regional anesthesia
D. NSAID monotherapy
E. SSRIs
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Answer: A. Perioperative regional analgesia may reduce chronic phantom limb pain (evidence mixed). Gabapentin/pregabalin, TCAs, mirror visual feedback therapy, transcutaneous electrical nerve stimulation. Memantine and ketamine targeted at NMDA mechanism. Spinal cord stimulator for refractory.
Q13. Cancer pain — WHO ladder
Step 3 of the WHO cancer pain ladder includes:
A. Acetaminophen only
B. Strong opioid ± non-opioid ± adjuvant for severe pain (morphine, oxycodone, hydromorphone, methadone, fentanyl)
C. Tramadol only
D. Codeine
E. Steroids alone
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Answer: B. WHO ladder: Step 1 (mild) = non-opioid (acetaminophen, NSAIDs) ± adjuvant. Step 2 (moderate) = weak opioid (tramadol, codeine, hydrocodone) ± non-opioid ± adjuvant. Step 3 (severe) = strong opioid ± non-opioid ± adjuvant. Adjuvants: TCAs, gabapentinoids, bisphosphonates (bone mets), steroids (edema, pressure).
Q14. Lidocaine infusion for chronic pain
IV lidocaine infusion for chronic neuropathic pain works via:
A. Selective sodium channel blockade of ectopic neuronal discharge from injured nerves
B. NMDA antagonism
C. GABA agonism
D. μ-opioid agonism
E. Histamine blockade
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Answer: A. IV lidocaine 1–3 mg/min targets ectopic sodium channels in injured nerves → modulates wind-up. Used in CRPS, neuropathic pain, refractory cancer pain. Toxicity monitor: levels ideally <5 mcg/mL.
Q15. Postherpetic neuralgia
First-line therapy for postherpetic neuralgia includes:
A. Topical lidocaine patches, gabapentinoids, TCAs
B. Acyclovir only
C. Opioid monotherapy
D. Steroids alone
E. NSAIDs as first-line
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Answer: A. PHN first-line: 5% lidocaine patches, gabapentinoids, TCAs (nortriptyline preferred over amitriptyline for tolerability). Second-line: opioids, capsaicin. Prevention: zoster vaccine in older adults. Antiviral therapy for acute zoster reduces but doesn't eliminate PHN risk.
Q16. Migraine headache treatment
Status migrainosus first-line treatment includes:
A. Opioids
B. IV ketorolac, prochlorperazine or metoclopramide, IV fluids, magnesium, dexamethasone; triptans if not contraindicated
C. Benzodiazepines
D. Steroids only
E. β-blockers (acute)
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Answer: B. Status migrainosus: IV fluids, NSAID, antiemetic (D2 antagonist — also has direct anti-migraine effect), magnesium, dexamethasone (prevents recurrence). Avoid opioids (rebound). Triptans contraindicated in CAD, basilar/hemiplegic migraine. Sphenopalatine ganglion block for refractory.
Q17. Epidural steroid injection for radiculopathy
The best evidence for epidural steroid injection is for:
A. Mechanical low back pain alone
B. Lumbar radiculopathy from disc herniation (short-term improvement)
C. Spinal stenosis (limited benefit)
D. Facet joint pain
E. Sacroiliac dysfunction
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Answer: B. ESI evidence: lumbar radiculopathy → short-term (1–3 months) pain reduction; minimal long-term benefit. Spinal stenosis: more controversial. Approaches: interlaminar, transforaminal (better target but higher risk of vascular complication), caudal. Triamcinolone or dexamethasone. Risks: epidural hematoma (especially on anticoagulants), infection, intravascular injection (transforaminal — paraplegia risk if particulate steroid into radicular artery).
Q18. Trigeminal neuralgia
First-line pharmacotherapy for trigeminal neuralgia is:
A. Opioids
B. Carbamazepine (or oxcarbazepine)
C. Acetaminophen
D. NSAIDs
E. Antidepressants
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Answer: B. Carbamazepine is first-line for trigeminal neuralgia (number needed to treat ~2). Side effects: hyponatremia, neutropenia, drug interactions. Oxcarbazepine alternative with fewer interactions. Refractory: microvascular decompression (Janetta procedure), gamma knife, radiofrequency rhizotomy.
Q19. Acetaminophen mechanism
Acetaminophen is now thought to provide analgesia primarily via:
A. Peripheral COX inhibition
B. Central COX-2 inhibition, possible activation of descending serotonergic pathways, indirect cannabinoid effect
C. NMDA antagonism
D. μ-opioid agonism
E. GABA potentiation
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Answer: B. Acetaminophen acts centrally — limited peripheral COX inhibition (hence no anti-inflammatory effect). Less GI/renal/platelet side effects than NSAIDs. Hepatic toxicity via CYP2E1 → NAPQI → glutathione depletion. Max 4 g/day adults (3 g/day chronic ETOH or hepatic disease).
Q20. Liposomal bupivacaine
Liposomal bupivacaine (Exparel) is intended to provide:
A. 24-hour pain relief
B. 72-hour analgesia through slow release from liposomal vesicles
C. No clinical benefit
D. Permanent nerve block
E. Faster onset than standard bupivacaine
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Answer: B. Liposomal bupivacaine claims 72-hour analgesia. Evidence mixed; recent meta-analyses suggest modest benefit over standard local. Cost-effectiveness questionable. Don't combine with other locals (lipid disruption). FDA-approved for surgical site infiltration and interscalene block.
Q21. Myofascial pain syndrome
Diagnostic criteria for myofascial pain syndrome include:
A. Palpable taut band, exquisite tender nodule (trigger point), reproduction of patient's pain with pressure, painful limitation of passive ROM
B. Lab abnormalities
C. Imaging findings
D. EMG abnormalities required
E. Genetic test
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Answer: A. Myofascial pain = trigger points in taut bands. Treatment: trigger point injection (local anesthetic, dry needling, botox for refractory), stretching, PT, postural correction. Differentiate from fibromyalgia (widespread tender points without taut bands, more centralized).