NURS 533 Exam 2 Study Guide
WEEK 5: Pain: Management
Types (how they differ):
• Acute pain: sudden, short duration; protective; sympathetic signs (↑HR, ↑BP). Treat cause + short-term analgesia.
• Chronic pain (>3 mo): persists beyond healing; biopsychosocial; goals = function/QOL; avoid long-term high-dose opioids.
• Nociceptive pain: tissue injury/inflammation. o Somatic: well-localized, aching (skin, bone, joints).
o Visceral: diffuse, cramping/pressure (organs), may refer.
• Neuropathic pain: nerve injury/dysfunction; burning, shooting, tingling, allodynia; responds best to adjuvants (SNRIs, TCAs,
gabapentinoids).
• Malignant (cancer) pain: often mixed (nociceptive + neuropathic); prioritize comfort, use WHO ladder more liberally. Non-
pharmacologic approaches (use with meds in all patients):
• Education, goal-setting, CBT, mindfulness
• Physical therapy, graded exercise, heat/ice
• TENS, acupuncture, spinal manipulation
• Sleep hygiene; weight loss; ergonomics; pacing; splints/braces
WHO 3-step ladder (with examples)
Step 1 – Mild pain: non-opioids ± adjuvants
• APAP, NSAIDs (e.g., ibuprofen, naproxen); topicals (diclofenac gel, lidocaine patch); adjuvants if neuropathic.
Step 2 – Moderate pain: weak/short-acting opioids + Step 1 ± adjuvants
• Tramadol or low-dose short-acting opioid (hydrocodone/APAP, oxycodone IR) + NSAID/APAP.
Step 3 – Severe pain: strong opioids + Step 1 ± adjuvants
• Morphine, hydromorphone, oxycodone, fentanyl, methadone; consider nerve blocks, spinal analgesia in cancer pain. Use
validated pain scales (NRS 0–10; Figure 35-1) and follow a stepwise algorithm (Figure 35-2; Table 35-1 aligns analgesic
selection with pain intensity).
NSAIDs
MOA: inhibit COX-1/COX-2 → ↓ prostaglandins → ↓ peripheral/central sensitization (analgesic, anti-inflammatory, antipyretic).
Indications: inflammatory nociceptive pain (musculoskeletal, osteoarthritis, sprains, dysmenorrhea).
Precautions/adverse effects:
• GI irritation/ulcer/bleed (↑ risk with age, steroids, anticoagulants)
• Renal vasoconstriction → AKI, Na /H₂O retention; avoid in advanced CKD⁺
• CV risk (MI/stroke), ↑ BP; naproxen may have the most favorable CV profile
• Platelets: nonselective NSAIDs inhibit TXA₂ (reversible); ibuprofen can blunt aspirin’s antiplatelet effect (separate dosing)
COX-2 (celecoxib): ↓ GI risk, but caution in CV disease Is one NSAID safer/better?
• Analgesic efficacy is similar at equipotent doses; choose by patient risk: GI (consider PPI or COX-2), CV (avoid COX-2/high-
dose diclofenac), renal (avoid class).
Ceiling effect: yes—once analgesic ceiling reached, higher doses ↑ toxicity without more pain relief (e.g., ibuprofen >400 mg/dose
gives little extra analgesia).
Special: ketorolac max 5 days (GI/renal risk).
Acetaminophen (APAP)
MOA: central prostaglandin (COX) inhibition → analgesic + antipyretic (minimal anti-inflammatory).
Indications: mild pain/fever; OA when NSAIDs risky; combine with other classes for multimodal analgesia. Dosing/limits:
1
, • Typical adult: 325–1,000 mg q4–6h PRN
• Absolute max: 4 g/day (all sources)
• Many practices cap at 3 g/day (safer)
• Older adults, liver disease, chronic alcohol use: keep ≤2 g/day, avoid if active severe hepatic disease.
Precautions: hepatotoxicity (esp. with alcohol/fasting/overdose); check combination products.
Spectrum vs NSAIDs: APAP lacks anti-inflammatory effect; safer GI/renal profile when inflammation isn’t prominent.
Adjuvant analgesics (what & when)
Use when neuropathic features (e.g., DPN, PHN), fibromyalgia, central sensitization, or as opioid-sparing agents.
• Antidepressants: SNRIs (duloxetine, venlafaxine), TCAs (nortriptyline, amitriptyline)
• Anticonvulsants: gabapentin, pregabalin, carbamazepine (trigeminal neuralgia)
• Topicals: lidocaine 5% patch (PHN), capsaicin
• Muscle relaxants: tizanidine, baclofen (spasticity)
• Others (specialist): ketamine (NMDA antagonist) in refractory pain; clonidine/dexmedetomidine (α2 agonists);
corticosteroids for cancer/bone pain or nerve compression
Opioids
MOA: μ-opioid receptor agonism (± κ/δ) → ↓ neurotransmitter release & postsynaptic excitability in pain pathways (spinal &
supraspinal).
Common adverse effects & management:
• Constipation (no tolerance): prophylax with stimulant laxative (senna ± docusate) and fluids/fiber; refractory OIC →
peripherally acting μ-antagonists (PAMORAs: methylnaltrexone, naloxegol, naldemedine)
• Nausea/vomiting: usually transient; ondansetron or prochlorperazine
• Sedation: dose-reduce, space doses, consider stimulant in palliative settings
• Respiratory depression: avoid rapid titration, caution with sedatives; naloxone for overdose
• Pruritus: antihistamine or rotate opioid (often histamine-release with morphine)
• Endocrine (↓ HPG axis), urinary retention, QT prolongation (methadone), opioid-induced hyperalgesia (consider dose
reduction/rotation)
Tolerance develops to most effects except constipation & miosis.
True opioid allergy (anaphylaxis) – reasonable alternatives:
Opioids fall into 3 main chemical classes—cross-reactivity is more likely within a class:
• Phenanthrenes: morphine, codeine, hydromorphone, oxycodone, hydrocodone
• Phenylpiperidines: fentanyl, meperidine
• Diphenylheptanes: methadone
→ If true IgE to a phenanthrene (e.g., morphine), switch to a phenylpiperidine (fentanyl) or diphenylheptane (methadone)
and monitor.
Equianalgesic dosing, incomplete cross-tolerance, rotation
Equianalgesic dose: a dose of opioid B that provides ~the same analgesia as opioid A.
Incomplete cross-tolerance: when switching opioids, the patient is less tolerant to the new opioid → reduce the calculated
equianalgesic dose by ~25–50% (more reduction for high doses, frail/older adults), then titrate.
Example manual conversion (illustrative):
• Patient takes morphine 60 mg PO/day (15 mg q6h).
• Oral morphine : oxycodone ≈ 1.5 : 1 (approximate). o 60 mg morphine/day ≈ 40 mg oxycodone/day.
• Apply 30–50% reduction for incomplete cross-tolerance → new target 20–28 mg/day. o Practical regimen: oxycodone IR 5
mg q6h (20 mg/day) with PRN rescue, reassess in 24–48 h.
2
, (You’d choose different products/intervals to match patient factors and pain pattern.)
Always reassess pain, function, adverse effects, and total daily MME, and document goals/risks.
Quick reference: picking & protecting
• Start with non-pharm + APAP/NSAID (if safe).
• Add adjuvant if neuropathic features.
• Escalate to short-acting opioid for breakthrough severe pain; convert to long-acting only when stable.
• Bowel regimen from day 1 with any opioid.
• Revisit goals frequently; deprescribe/rotate as needed.
_________________________________________________________________________________________________Headaches
Migraine & Cluster Headaches — What to Know
1) IHS Classification (diagnostic criteria)
Migraine without aura
• ≥5 attacks lasting 4–72 h (untreated/unsuccessfully treated)
• ≥2 of: unilateral, pulsating, moderate–severe intensity, aggravated by routine activity
• During HA ≥1 of: nausea/vomiting OR photophobia + phonophobia
• Not better explained by another diagnosis Migraine with aura
• ≥2 attacks with fully reversible aura (visual, sensory, speech/language; ± brainstem, retinal; motor aura may last longer)
• ≥3 of: gradual spread (≥5 min), ≥2 aura symptoms in succession, each aura 5–60 min (motor up to 72 h), ≥1 unilateral, ≥1
positive (scintillations/tingling), headache during aura or within 60 min after
Cluster headache
• Severe/very severe unilateral orbital/supraorbital/temporal pain 15–180 min
• Frequency: 1 every other day → 8/day during a cluster period
• With ipsilateral autonomic signs (≥1): conjunctival injection/tearing, nasal congestion/rhinorrhea, eyelid edema,
forehead/facial sweating, miosis/ptosis and/or marked restlessness/agitation
2) Headache diary, triggers & red flags
Headache diary
• Track date/time, duration, severity, associated symptoms, meds used/response, sleep, stress, menses, foods,
caffeine/alcohol, weather. Helps identify triggers & medication-overuse headache (MOH).
Common migraine triggers (Table 36-2 style)
• Lifestyle: stress, let-down after stress, sleep loss or excess, skipped meals/fasting, dehydration
• Hormonal: menses, ovulation
• Dietary: alcohol (esp. red wine), aged cheeses (tyramine), processed meats (nitrates), MSG, artificial sweeteners, caffeine
withdrawal or excess
• Environmental: bright/flickering lights, strong odors, weather/barometric changes
• Medication-related: vasodilators (nitroglycerin), OCPs/hormone shifts
Headache red flags — “SNOOP10” (Table 36-1 style)
• Systemic symptoms/illness (fever, weight loss, cancer, HIV)
• Neurologic deficits (confusion, focal signs, seizures)
• Onset abrupt (“thunderclap”), Older age at onset (>50), Occipital w/ exertion
• Pattern change/progressive, Papilledema, Pregnancy/postpartum, Post-trauma
• Also: positional HA, precipitated by Valsalva/exertion, immunosuppression, anticoagulation → Urgent evaluation
(neuroimaging ± LP) if present.
3) Stepwise management
A) Migraine (acute → preventive)
3
WEEK 5: Pain: Management
Types (how they differ):
• Acute pain: sudden, short duration; protective; sympathetic signs (↑HR, ↑BP). Treat cause + short-term analgesia.
• Chronic pain (>3 mo): persists beyond healing; biopsychosocial; goals = function/QOL; avoid long-term high-dose opioids.
• Nociceptive pain: tissue injury/inflammation. o Somatic: well-localized, aching (skin, bone, joints).
o Visceral: diffuse, cramping/pressure (organs), may refer.
• Neuropathic pain: nerve injury/dysfunction; burning, shooting, tingling, allodynia; responds best to adjuvants (SNRIs, TCAs,
gabapentinoids).
• Malignant (cancer) pain: often mixed (nociceptive + neuropathic); prioritize comfort, use WHO ladder more liberally. Non-
pharmacologic approaches (use with meds in all patients):
• Education, goal-setting, CBT, mindfulness
• Physical therapy, graded exercise, heat/ice
• TENS, acupuncture, spinal manipulation
• Sleep hygiene; weight loss; ergonomics; pacing; splints/braces
WHO 3-step ladder (with examples)
Step 1 – Mild pain: non-opioids ± adjuvants
• APAP, NSAIDs (e.g., ibuprofen, naproxen); topicals (diclofenac gel, lidocaine patch); adjuvants if neuropathic.
Step 2 – Moderate pain: weak/short-acting opioids + Step 1 ± adjuvants
• Tramadol or low-dose short-acting opioid (hydrocodone/APAP, oxycodone IR) + NSAID/APAP.
Step 3 – Severe pain: strong opioids + Step 1 ± adjuvants
• Morphine, hydromorphone, oxycodone, fentanyl, methadone; consider nerve blocks, spinal analgesia in cancer pain. Use
validated pain scales (NRS 0–10; Figure 35-1) and follow a stepwise algorithm (Figure 35-2; Table 35-1 aligns analgesic
selection with pain intensity).
NSAIDs
MOA: inhibit COX-1/COX-2 → ↓ prostaglandins → ↓ peripheral/central sensitization (analgesic, anti-inflammatory, antipyretic).
Indications: inflammatory nociceptive pain (musculoskeletal, osteoarthritis, sprains, dysmenorrhea).
Precautions/adverse effects:
• GI irritation/ulcer/bleed (↑ risk with age, steroids, anticoagulants)
• Renal vasoconstriction → AKI, Na /H₂O retention; avoid in advanced CKD⁺
• CV risk (MI/stroke), ↑ BP; naproxen may have the most favorable CV profile
• Platelets: nonselective NSAIDs inhibit TXA₂ (reversible); ibuprofen can blunt aspirin’s antiplatelet effect (separate dosing)
COX-2 (celecoxib): ↓ GI risk, but caution in CV disease Is one NSAID safer/better?
• Analgesic efficacy is similar at equipotent doses; choose by patient risk: GI (consider PPI or COX-2), CV (avoid COX-2/high-
dose diclofenac), renal (avoid class).
Ceiling effect: yes—once analgesic ceiling reached, higher doses ↑ toxicity without more pain relief (e.g., ibuprofen >400 mg/dose
gives little extra analgesia).
Special: ketorolac max 5 days (GI/renal risk).
Acetaminophen (APAP)
MOA: central prostaglandin (COX) inhibition → analgesic + antipyretic (minimal anti-inflammatory).
Indications: mild pain/fever; OA when NSAIDs risky; combine with other classes for multimodal analgesia. Dosing/limits:
1
, • Typical adult: 325–1,000 mg q4–6h PRN
• Absolute max: 4 g/day (all sources)
• Many practices cap at 3 g/day (safer)
• Older adults, liver disease, chronic alcohol use: keep ≤2 g/day, avoid if active severe hepatic disease.
Precautions: hepatotoxicity (esp. with alcohol/fasting/overdose); check combination products.
Spectrum vs NSAIDs: APAP lacks anti-inflammatory effect; safer GI/renal profile when inflammation isn’t prominent.
Adjuvant analgesics (what & when)
Use when neuropathic features (e.g., DPN, PHN), fibromyalgia, central sensitization, or as opioid-sparing agents.
• Antidepressants: SNRIs (duloxetine, venlafaxine), TCAs (nortriptyline, amitriptyline)
• Anticonvulsants: gabapentin, pregabalin, carbamazepine (trigeminal neuralgia)
• Topicals: lidocaine 5% patch (PHN), capsaicin
• Muscle relaxants: tizanidine, baclofen (spasticity)
• Others (specialist): ketamine (NMDA antagonist) in refractory pain; clonidine/dexmedetomidine (α2 agonists);
corticosteroids for cancer/bone pain or nerve compression
Opioids
MOA: μ-opioid receptor agonism (± κ/δ) → ↓ neurotransmitter release & postsynaptic excitability in pain pathways (spinal &
supraspinal).
Common adverse effects & management:
• Constipation (no tolerance): prophylax with stimulant laxative (senna ± docusate) and fluids/fiber; refractory OIC →
peripherally acting μ-antagonists (PAMORAs: methylnaltrexone, naloxegol, naldemedine)
• Nausea/vomiting: usually transient; ondansetron or prochlorperazine
• Sedation: dose-reduce, space doses, consider stimulant in palliative settings
• Respiratory depression: avoid rapid titration, caution with sedatives; naloxone for overdose
• Pruritus: antihistamine or rotate opioid (often histamine-release with morphine)
• Endocrine (↓ HPG axis), urinary retention, QT prolongation (methadone), opioid-induced hyperalgesia (consider dose
reduction/rotation)
Tolerance develops to most effects except constipation & miosis.
True opioid allergy (anaphylaxis) – reasonable alternatives:
Opioids fall into 3 main chemical classes—cross-reactivity is more likely within a class:
• Phenanthrenes: morphine, codeine, hydromorphone, oxycodone, hydrocodone
• Phenylpiperidines: fentanyl, meperidine
• Diphenylheptanes: methadone
→ If true IgE to a phenanthrene (e.g., morphine), switch to a phenylpiperidine (fentanyl) or diphenylheptane (methadone)
and monitor.
Equianalgesic dosing, incomplete cross-tolerance, rotation
Equianalgesic dose: a dose of opioid B that provides ~the same analgesia as opioid A.
Incomplete cross-tolerance: when switching opioids, the patient is less tolerant to the new opioid → reduce the calculated
equianalgesic dose by ~25–50% (more reduction for high doses, frail/older adults), then titrate.
Example manual conversion (illustrative):
• Patient takes morphine 60 mg PO/day (15 mg q6h).
• Oral morphine : oxycodone ≈ 1.5 : 1 (approximate). o 60 mg morphine/day ≈ 40 mg oxycodone/day.
• Apply 30–50% reduction for incomplete cross-tolerance → new target 20–28 mg/day. o Practical regimen: oxycodone IR 5
mg q6h (20 mg/day) with PRN rescue, reassess in 24–48 h.
2
, (You’d choose different products/intervals to match patient factors and pain pattern.)
Always reassess pain, function, adverse effects, and total daily MME, and document goals/risks.
Quick reference: picking & protecting
• Start with non-pharm + APAP/NSAID (if safe).
• Add adjuvant if neuropathic features.
• Escalate to short-acting opioid for breakthrough severe pain; convert to long-acting only when stable.
• Bowel regimen from day 1 with any opioid.
• Revisit goals frequently; deprescribe/rotate as needed.
_________________________________________________________________________________________________Headaches
Migraine & Cluster Headaches — What to Know
1) IHS Classification (diagnostic criteria)
Migraine without aura
• ≥5 attacks lasting 4–72 h (untreated/unsuccessfully treated)
• ≥2 of: unilateral, pulsating, moderate–severe intensity, aggravated by routine activity
• During HA ≥1 of: nausea/vomiting OR photophobia + phonophobia
• Not better explained by another diagnosis Migraine with aura
• ≥2 attacks with fully reversible aura (visual, sensory, speech/language; ± brainstem, retinal; motor aura may last longer)
• ≥3 of: gradual spread (≥5 min), ≥2 aura symptoms in succession, each aura 5–60 min (motor up to 72 h), ≥1 unilateral, ≥1
positive (scintillations/tingling), headache during aura or within 60 min after
Cluster headache
• Severe/very severe unilateral orbital/supraorbital/temporal pain 15–180 min
• Frequency: 1 every other day → 8/day during a cluster period
• With ipsilateral autonomic signs (≥1): conjunctival injection/tearing, nasal congestion/rhinorrhea, eyelid edema,
forehead/facial sweating, miosis/ptosis and/or marked restlessness/agitation
2) Headache diary, triggers & red flags
Headache diary
• Track date/time, duration, severity, associated symptoms, meds used/response, sleep, stress, menses, foods,
caffeine/alcohol, weather. Helps identify triggers & medication-overuse headache (MOH).
Common migraine triggers (Table 36-2 style)
• Lifestyle: stress, let-down after stress, sleep loss or excess, skipped meals/fasting, dehydration
• Hormonal: menses, ovulation
• Dietary: alcohol (esp. red wine), aged cheeses (tyramine), processed meats (nitrates), MSG, artificial sweeteners, caffeine
withdrawal or excess
• Environmental: bright/flickering lights, strong odors, weather/barometric changes
• Medication-related: vasodilators (nitroglycerin), OCPs/hormone shifts
Headache red flags — “SNOOP10” (Table 36-1 style)
• Systemic symptoms/illness (fever, weight loss, cancer, HIV)
• Neurologic deficits (confusion, focal signs, seizures)
• Onset abrupt (“thunderclap”), Older age at onset (>50), Occipital w/ exertion
• Pattern change/progressive, Papilledema, Pregnancy/postpartum, Post-trauma
• Also: positional HA, precipitated by Valsalva/exertion, immunosuppression, anticoagulation → Urgent evaluation
(neuroimaging ± LP) if present.
3) Stepwise management
A) Migraine (acute → preventive)
3
