Pain Flashcards
(234 cards)
1
Q
A
2
Q
What is nociception?
A
The process of detecting and transmitting noxious stimuli to the brain.
3
Q
What is the difference between pain and nociception?
A
Pain is the conscious experience; nociception is the neural process.
4
Q
Where are nociceptors located and what do they detect?
A
In skin and viscera; detect mechanical, thermal, and chemical damage.
5
Q
What are A-delta fibres?
A
Small, myelinated fibres for sharp, well-localised pain.
6
Q
What are C fibres?
A
Unmyelinated fibres for dull, burning, poorly localised pain.
7
Q
Describe the ascending pain pathway.
A
Signal travels from nociceptors → spinal cord (dorsal horn) → thalamus → cortex.
8
Q
What is peripheral sensitisation?
A
Increased sensitivity of nociceptors due to inflammation mediators like bradykinin and prostaglandins.
9
Q
What is central sensitisation (‘wind-up’)?
A
Repeated stimulation causes increased synaptic transmission via NMDA and NK receptors.
10
Q
What is allodynia?
A
Pain from a normally non-painful stimulus.
11
Q
What is hyperalgesia?
A
Increased response to a mildly painful stimulus.
12
Q
What is the gate control theory of pain?
A
Non-painful input (A-beta fibres) can inhibit pain transmission via spinal interneurons.
13
Q
What role does the periaqueductal grey (PAG) play in pain?
A
It is part of the descending inhibitory pain pathway.
14
Q
Which brainstem areas modulate pain?
A
PAG (descending pain inhibition )RVM (rostral ventromedial medulla), locus coeruleus. (Release noradrenaline to regulate pain)
15
Q
How do NSAIDs reduce pain?
A
They inhibit COX enzymes, reducing prostaglandin synthesis and inflammation.
16
Q
Which enzyme do NSAIDs target?
A
Cyclooxygenase (COX-1 and COX-2).
17
Q
How does paracetamol differ from NSAIDs?
A
Not anti-inflammatory; acts centrally with unclear COX inhibition.
18
Q
What are the main opioid receptors?
A
Mu (μ), kappa (κ), delta (δ) – all GPCRs.
19
Q
Which opioid receptor mediates most analgesia?
A
Mu receptor.
20
Q
How do opioids work at synapses?
A
They inhibit Ca²⁺ channels and open K⁺ channels → hyperpolarisation and reduced neurotransmitter release.
21
Q
What central effects are caused by mu opioid receptor activation?
A
Analgesia, euphoria, respiratory depression, sedation.
22
Q
What is a key side effect of opioids in the gut?
A
Constipation due to reduced motility.
23
Q
What is opioid tolerance?
A
Reduced effect with repeated use, requiring higher doses.
24
Q
Why is co-use of opioids and benzodiazepines risky?
A
Can cause fatal respiratory depression.
25
Why are fentanyl patches long-acting?
They form a subcutaneous reservoir and continue release after removal.
26
What is tramadol's dual mechanism?
Weak mu-opioid agonist and inhibits reuptake of noradrenaline and serotonin.
27
How do TCAs like amitriptyline help in pain?
Inhibit NA and 5HT reuptake, enhancing descending inhibition.
28
What class of drugs are pregabalin and gabapentin?
Calcium channel blockers used in neuropathic pain.
29
What are cannabinoid receptors involved in pain?
CB1 and CB2 – act in CNS and periphery for neuropathic pain.
30
How might NMDA antagonists (e.g. ketamine) help in pain?
Block central wind-up, but may cause psychosis.
31
What is nociplastic pain?
Persistent pain from altered nociception without obvious tissue damage (e.g. fibromyalgia).
32
What are the most common paediatric analgesic suspensions?
Paracetamol (Calpol®) and ibuprofen (Nurofen®).
33
Why should 'shake well' instructions be reinforced for suspensions?
To ensure even distribution of the drug throughout the liquid.
34
Why is paediatric paracetamol elixir BP not recommended?
Contains 8.4% ethanol – not suitable for children.
35
When are suppositories preferred in paediatric analgesia?
When oral dosing is difficult due to vomiting or nausea.
36
Name two analgesic drugs available as suppositories for children.
Paracetamol and diclofenac.
37
What are orodispersible dosage forms?
Forms that dissolve quickly in the mouth and are swallowed.
38
List the four types of orodispersible dosage forms.
Orodispersible tablets, oral lyophilisates, films, and granules.
39
What excipients aid orodispersible tablet disintegration?
Croscarmellose sodium, crospovidone (superdisintegrants).
40
How are sublimation-based orodispersible tablets made?
Using volatile solids like camphor that leave pores after sublimation.
41
What is the main manufacturing method for oral lyophilisates?
Freeze-drying (lyophilisation).
42
What are the four stages of freeze-drying?
Freezing, vacuum application, sublimation, secondary drying.
43
Why can’t Zydis® tablets be pushed through foil?
They are soft and fragile due to lyophilisation.
44
Give one drug example using Zydis® technology.
Rizatriptan (Maxalt Melt®).
45
What are orodispersible films?
Sheets that dissolve in the mouth; limited use in analgesia.
46
What method is used to make orodispersible films?
Solvent casting (mixing drug + polymer + solvent).
47
What is the buccal route and give one example drug.
Delivery via the inner cheek; e.g., fentanyl lozenges (Actiq®).
48
How is fentanyl administered transdermally?
Via adhesive patches for chronic pain management.
49
What is the use of the MAD® device?
To atomise drugs for intranasal, oral, or laryngeal mucosal absorption.
50
What is Entonox®?
A 50:50 mixture of oxygen and nitrous oxide used for short-term analgesia.
51
Why are oral lyophilisates not common in paediatric-only analgesia?
They are used more widely for other conditions but not yet standard for analgesia in children.
52
What is PEGylation?
The process of attaching polyethylene glycol (PEG) to protein or peptide drugs to improve their pharmacokinetics.
53
What are two main problems with protein drugs?
Poor absorption (especially orally) and rapid clearance from the body.
54
Name four routes by which protein drugs are cleared from the body.
Renal excretion, proteolysis, opsonisation (liver/macrophages), and immune response (neutralising antibodies).
55
What is the effect of PEGylation on drug half-life?
It increases the drug's physiological half-life by reducing clearance.
56
List three physiological benefits of PEGylation.
Reduces renal excretion, shields from proteases, and reduces opsonisation.
57
What properties make PEG ideal for PEGylation?
Biocompatible, non-immunogenic, water-soluble, easy to attach, and cleared after metabolism.
58
What is the 'halo effect' in PEGylation?
Hydrated PEG molecules form a protective barrier around the protein, shielding it from enzymes and immune cells.
59
Why should PEG be attached away from the active site?
To avoid reducing the drug's activity or efficacy.
60
What is certolizumab pegol?
A PEGylated Fab fragment that binds TNF-α for treating rheumatoid arthritis.
61
What is the half-life of certolizumab pegol and how often is it dosed?
13 days; dosed fortnightly.
62
What is a biosimilar medicine?
A biologic highly similar to an existing approved biologic, but not identical like a generic.
63
Name another PEGylated drug used in gout.
Pegloticase – a PEGylated uricase enzyme.
64
How many lysine residues in each subunit of pegloticase are PEGylated?
9 of 30 residues per unit.
65
What other drugs have been PEGylated to extend half-life?
Filgrastim, asparaginase, interferons, BDNF, IL-6.
66
What is the PEGylation strategy for nanoparticles?
PEG moieties are added to nanoparticle surfaces to reduce opsonisation and immune clearance.
67
How were COVID-19 mRNA vaccines stabilised using PEGylation?
PEGylated lipids were used in the lipid nanoparticle (LNP) shells to protect mRNA and aid delivery.
68
What concern arose with PEG in COVID-19 vaccines?
Rare serious reactions possibly linked to anti-PEG antibodies in some individuals.
69
What are alternatives being explored to PEG?
Zwitterionic polymers, XTEN polypeptides, poly(thioglycidyl glycerol), and polysaccharides.
70
What is efanesoctocog alfa?
A fully recombinant fusion protein using XTEN chains, approved for haemophilia A.
71
Why is PEGylation especially useful for protein drugs?
It overcomes fast clearance and immunogenicity, allowing less frequent dosing and better efficacy.
72
Who first isolated codeine and in what year?
Pierre-Jean Robiquet in 1832.
73
What plant is the natural source of codeine and morphine?
Papaver somniferum (opium poppy).
74
What is the main difference between morphine and codeine?
Morphine is an active analgesic; codeine is a pro-drug.
75
Which receptor do morphine and codeine bind to?
Mu-opioid receptor (µ).
76
Why is codeine less potent than morphine?
It binds moderately to µ receptors and requires metabolism to morphine.
77
What is the key structural difference between morphine and codeine?
Morphine has a hydroxyl group; codeine has a methoxy group.
78
What is the Log P of morphine vs codeine?
Morphine: -0.21; Codeine: 1.19 (more lipophilic).
79
What is heroin chemically?
Diacetylated morphine (more lipophilic and potent).
80
What is the opioid pharmacophore?
A key structural feature required for activity at opioid receptors.
81
What type of drug is fentanyl?
A synthetic, lipophilic opioid agonist that binds to µ receptors.
82
How much more potent is fentanyl compared to morphine?
Approximately 100 times more potent.
83
Why is fentanyl effective in patches and mucosal routes?
Its high lipophilicity allows rapid and easy absorption through membranes.
84
What is the main danger associated with fentanyl?
High overdose risk due to potency; contributes to most opioid overdose deaths in the US.
85
What are the main properties of paracetamol?
Analgesic and antipyretic, but not anti-inflammatory.
86
What is a major toxicity risk with paracetamol?
Hepatotoxicity in overdose.
87
What is the synthesis route of paracetamol?
Acetylation of p-aminophenol.
88
What type of drug is ibuprofen?
A non-steroidal anti-inflammatory drug (NSAID) with analgesic, antipyretic, and anti-inflammatory effects.
89
What is the key structural feature of ibuprofen?
(±)-2-(p-isobutylphenyl)propionic acid – a racemic mixture.
90
What is the industrial synthesis route of ibuprofen?
Boots synthesis process from isobutylbenzene.
91
What is the clinical caution with ibuprofen?
Risk in patients with GI disorders, hypertension, or cardiovascular disease.
92
What is the primary goal of palliative pain therapy?
Ensure no patient lives or dies in pain.
93
What is palliative care?
Care that relieves pain, affirms life, integrates psychological and spiritual support, and helps both patients and families.
94
What are the types of factors contributing to pain in palliative care?
Psychological, psychosocial, physical/biological, and other contextual factors.
95
What should be assessed when evaluating a patient's pain?
History, type, intensity, cause, treatment response, and medication side effects.
96
List three common causes of cancer-related pain.
Bone destruction, post-radiation pain, diabetic neuropathy.
97
What is Step 1 of the WHO analgesic ladder?
Non-opioid analgesics (e.g., paracetamol, NSAIDs).
98
What is Step 2 of the WHO analgesic ladder?
Weak opioids (e.g., codeine, dihydrocodeine, tramadol).
99
What is Step 3 of the WHO analgesic ladder?
Strong opioids (e.g., morphine, oxycodone).
100
How should morphine be initiated in an opioid-naive patient?
20–30 mg/day in divided doses, titrated to effect.
101
How are rescue doses of morphine calculated?
1/10th to 1/6th of the 24-hour total dose.
102
What is the equivalent 24-hour s/c morphine dose for 400 mg oral morphine?
200 mg s/c morphine.
103
What is the equivalent 24-hour s/c diamorphine dose for 400 mg oral morphine?
Approx. 133 mg (one-third of oral dose).
104
What is a syringe driver used for?
Continuous subcutaneous infusion for patients unable to swallow or with persistent vomiting.
105
When are fentanyl or buprenorphine patches used?
If morphine causes persistent adverse effects and pain is stable.
106
Why are patches not used for breakthrough pain?
They have a slow onset of action.
107
What are common opioid side effects?
Nausea, vomiting, constipation, respiratory depression, urinary retention, drowsiness.
108
How is opioid-induced nausea managed?
Use anti-emetics based on cause: cyclizine, haloperidol, or metoclopramide.
109
How is opioid-induced constipation managed?
Routine laxatives: stimulant (senna), osmotic (macrogols), softeners (docusate).
110
What is opioid-induced neurotoxicity?
Syndrome with agitation, hallucinations, confusion, especially in renal impairment.
111
List 3 adjuvants for poorly responsive pain.
Radiotherapy, NSAIDs, TCAs, anticonvulsants, corticosteroids.
112
Which adjuvants are useful in bone pain?
NSAIDs, radiotherapy, corticosteroids.
113
Which adjuvants are useful in nerve pain?
Anticonvulsants, TCAs, corticosteroids, nerve blocks.
114
What is the principle for oral morphine to s/c morphine conversion?
Reduce the total oral dose by 50% for the s/c dose.
115
Why should weak opioids not delay step-up to strong opioids?
They may be insufficient for severe pain and cause unnecessary delay in effective treatment.
116
What distinguishes strong opioids like fentanyl and buprenorphine?
Different onset, duration, lipophilicity, and route-specific absorption.
117
When is methadone used in palliative care?
As an alternative strong opioid, especially in neuropathic pain.
118
Why is regular review of rescue doses important?
To adjust maintenance dosing appropriately and ensure adequate pain control.
119
What route is preferred for stable pain in palliative care?
Oral if possible; otherwise s/c via syringe driver.
120
What is the role of diamorphine in end-of-life care?
Preferred for s/c use due to higher solubility and potency vs morphine.
121
What principle guides palliative pain treatment?
Treat based on pain severity and previous analgesia, not disease stage.
122
What Schedules of CDs require recording in a CD register?
Schedule 1 and Schedule 2 CDs.
123
How should a CD register be structured?
Bound book; separate parts for each class; separate pages for each strength/form.
124
How long must CD registers be kept?
Two years from the date of the last entry.
125
What must be recorded for CDs received?
Date received, name/address from whom received, quantity received.
126
What must be recorded for CDs supplied?
Date supplied, name/address of recipient, prescriber details, quantity, collector info, ID requested/provided.
127
What are the requirements for making entries in the CD register?
Chronological, prompt, ink/indelible, unaltered with signed/dated corrections.
128
What are requirements for electronic CD registers?
Attributable, auditable, compliant, accessible, and secure against later alterations.
129
How often should running balances and stock checks be done?
At least weekly; visually checked with each CD supply.
130
What is an instalment direction on a CD Rx?
Specifies dose per instalment and interval between supplies.
131
When must the first instalment be dispensed?
Within 28 days of the appropriate date.
132
What must be done if 3+ doses are missed in instalment dispensing?
Consult the prescriber due to overdose risk from lost tolerance.
133
Who may lawfully possess Schedule 2-5 CDs?
Pharmacists, prescribers, patients, and others with authority or licence.
134
Who can administer Schedule 2-4 CDs?
Doctors, dentists, independent prescribers, or by direction of such prescribers.
135
When is a special Home Office licence required?
To prescribe diamorphine, cocaine or dipipanone for addiction.
136
How much CD supply may a patient travel with?
Up to three months' supply with a prescriber-signed letter.
137
What form is required to requisition Schedule 2/3 CDs?
WP10CDF or equivalent; exempt for hospices, prisons, ambulance orgs.
138
What must a midwife supply order contain?
Midwife's name/occupation, recipient details, drug purpose, quantity, medical officer signature.
139
How must requisitions be handled on receipt?
Marked indelibly with supplier info and sent to NHS agency; retain copy.
140
Who may witness destruction of Schedule 2 CDs?
Police constables, authorised persons; not the accountable officer themselves.
141
What must be done before disposing of CDs?
Denature (render irretrievable) and place in pharmaceutical waste for incineration.
142
Do patient-returned CDs require witnessed destruction?
No, witnessing not required for returned meds from patients.
143
Why are CDs denatured before disposal?
To prevent misuse, environmental harm, or theft.
144
What PPE is advised during CD destruction?
Gloves, mask, goggles in a well-ventilated area.
145
How should CD tablets be destroyed?
Crush and mix with CD denaturing kit; add water to minimise dust.
146
What is the definition of public health?
The science and art of preventing disease, prolonging life, and promoting health through organised societal efforts.
147
Name three current public health challenges in England.
Smoking, obesity, alcohol consumption.
148
What percentage of men and women in England are overweight or obese?
70% of men and 60% of women.
149
What is the aim of population health?
To improve the health of an entire population, particularly the poorest, fastest.
150
What are social determinants of health?
Conditions like housing, education, green space, and income that impact health.
151
What does the Marmot Review highlight?
Health inequalities are linked to socioeconomic factors and are largely preventable.
152
How do death rates from CVD differ by socioeconomic status?
Death rates are six times higher in lower socioeconomic groups.
153
Why are pharmacies key to delivering public health?
They serve deprived communities and have daily health-related contact with the public.
154
Give four examples of public health services provided by pharmacies.
BP checks, smoking cessation, emergency contraception, chlamydia screening.
155
What is 'Make Every Contact Count'?
A strategy encouraging brief health interventions during routine interactions.
156
What is social prescribing?
Referring patients with non-medical needs to local non-clinical community services.
157
List three potential referral sources for social prescribing.
Self-referral, healthcare professionals, third sector organisations.
158
Name five examples of social prescribing activities.
Dance groups, choirs, healthy lifestyle groups, community food projects, befriending groups.
159
What are three health outcomes improved by social prescribing?
Mental wellbeing, self-confidence, reduced medication use.
160
What is the role of a social prescribing link worker?
To connect individuals to community support and build a trusting relationship.
161
What are the cost-related benefits of social prescribing?
Fewer GP visits, reduced prescribing, savings across the NHS care pathway.
162
What barriers must inclusive services overcome?
Disability, language barriers, sensory impairments, marginalisation.
163
What is a key reason why patients consult GPs unnecessarily?
About 20% of patients present with social rather than medical issues.
164
How can pharmacists contribute to mental health through public health?
By holding supportive conversations that improve self-efficacy and emotional wellbeing.
165
What are voluntary and community sector (VCS) organisations?
Groups providing non-clinical community-based support services.
166
Give two ways social prescribing strengthens communities.
Builds community resilience and increases awareness of local resources.
167
How can social prescribing improve employability?
By reducing isolation, building confidence, and improving mental health.
168
What key principle underpins both public health and social prescribing?
Prevention and early intervention improve quality of life and reduce health inequalities.
169
What NHS initiative helps identify risky drinking levels?
Alcohol brief interventions provided through community pharmacy.
170
What does 'Make Every Contact Count' involve for pharmacists?
Using routine consultations to promote healthy behaviours.
171
What are three types of health promotion offered in pharmacies?
Smoking cessation, sexual health, weight management.
172
What key outcome does social prescribing aim to reduce?
Frequent primary care visits and medicine prescribing.
173
What does 'activation' mean in social prescribing?
Enabling people to take control of their health and make sustained lifestyle changes.
174
What is the purpose of connecting people to local choirs in social prescribing?
To improve lung function and mental wellbeing, especially in COPD.
175
How can pharmacists support people with substance misuse?
By identifying misuse, offering support, and signposting to services.
176
How does the IASP define pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
177
What are the three main types of pain by mechanism?
Nociceptive, neuropathic, and nociplastic pain.
178
What is the purpose of pain?
It acts as a protective warning signal to prevent harm.
179
What is nociceptive pain?
Pain from actual or threatened non-neural tissue damage due to activation of nociceptors.
180
Give examples of nociceptive pain causes.
Fractures, burns, muscle spasm, osteoarthritis, peptic ulcers, angina.
181
What drugs are used for nociceptive pain?
Paracetamol, NSAIDs, opioids, antispasmodics, and treating the cause.
182
What is neuropathic pain?
Pain caused by a lesion or disease affecting the somatosensory system.
183
Give examples of neuropathic pain conditions.
MS, spinal cord injury, shingles, carpal tunnel, diabetic neuropathy, CRPS.
184
What drugs are used for neuropathic pain?
TCAs, pregabalin, gabapentin, duloxetine, carbamazepine.
185
What is nociplastic pain?
Pain from altered nociception without clear tissue damage or nervous system lesion.
186
Give examples of nociplastic pain conditions.
Fibromyalgia, IBS, TMJ disorder, CRPS Type 1.
187
What are features of central sensitisation?
Increased NMDA activity, cortical reorganisation, diminished GABA/NA inhibition, immune activation.
188
How is nociplastic pain managed?
Non-drug first: exercise, sleep, diet, stress reduction; pharmacological: pregabalin, duloxetine (multi-modal).
189
What is opioid-induced hyperalgesia (OIH)?
A state of nociceptive sensitisation caused by opioid exposure leading to worsened pain.
190
How is OIH treated?
Reduce or stop opioids; symptoms may improve after 1–3 months.
191
What are risk factors for developing chronic pain?
Surgery, chronic opioid use, genetics, anxiety/depression, female sex, obesity, youth.
192
What changes occur in acute to chronic pain transition?
Peripheral & central sensitisation; reduced inhibitory neurotransmission (GABA); neuroplasticity.
193
What is central sensitisation?
Persistent increased responsiveness of CNS neurons to pain stimuli.
194
What is the recommended approach to chronic pain management?
Multimodal: combine pharmacological and non-pharmacological therapies.
195
Why is chronic pain often difficult to treat?
Pain may be severe with no clear pathology, unpredictable, and unresponsive to analgesics.
196
What is the WHO analgesic ladder?
A stepwise approach to pain management starting from non-opioids to strong opioids as needed.
197
What is the role of exercise in chronic pain?
Improves function, reduces sensitisation, and enhances quality of life.
198
How does mood affect chronic pain?
Anxiety and depression can worsen pain perception and response to treatment.
199
What educational resources are recommended for chronic pain patients?
Live Well with Pain, NICE NG193, British Pain Society.
200
What role does the immune system play in chronic pain?
Glial cell activation and release of cytokines contribute to pain sensitisation.
201
How do TCAs and SNRIs help in chronic pain?
Enhance descending inhibition via increased NA and serotonin levels.
202
Why might opioids fail in chronic pain?
Tolerance, opioid-induced hyperalgesia, lack of efficacy in nociplastic pain.
203
Why are non-drug treatments first-line in nociplastic pain?
Drugs often have small effects; lifestyle changes better improve function and QoL.
204
What is diffuse allodynia?
Pain from non-painful stimuli across widespread areas – common in OIH and central sensitisation.
205
Why should opioids be reviewed carefully in chronic pain?
They may worsen pain (OIH), impair function, and pose long-term harm.
206
What is the wider impact of chronic pain on a person?
It can affect mood, sleep, mobility, work, relationships, hobbies, and family role.
207
Do tablets cure chronic pain?
No – 70% of people taking painkillers still report significant pain.
208
What is a key issue with long-term painkiller use?
Unpleasant side effects often outweigh the benefits.
209
How does chronic pain change brain activity?
fMRI shows a shift from nociceptive to emotional brain circuits.
210
What three brain domains modulate pain experience?
Somatosensory, cognitive, and affective components.
211
List three cognitive factors that increase pain.
Anxiety, depression, anger.
212
What are examples of positive psychological factors in pain management?
Acceptance, goal setting, pacing, mood, having fun, routine.
213
What is a vicious cycle in chronic pain?
Pain → inactivity → low mood → more pain.
214
What helps break the chronic pain vicious cycle?
Exercise, pacing, goal setting, sleep hygiene, mindfulness.
215
What does the Biopsychosocial (BPS) model of pain address?
Biological, psychological, and social factors influencing pain.
216
What does the NICE guidance say about paracetamol in chronic primary pain?
Do not initiate.
217
Name four drug classes NOT recommended in chronic primary pain by NICE.
Opioids, anti-epileptics, antipsychotics, benzodiazepines.
218
What antidepressants are recommended for chronic primary pain?
Duloxetine, sertraline, citalopram, fluoxetine, paroxetine (off-label).
219
How should off-label use of antidepressants be approached?
Discuss benefits and risks with the patient.
220
What neurotransmitters do TCAs affect?
Noradrenaline and serotonin.
221
What are side effects of TCAs like amitriptyline?
Drowsiness, dry mouth, urinary issues, constipation, cardiac issues.
222
What is a safer TCA alternative to amitriptyline?
Nortriptyline – less sedating.
223
What is the MOA of duloxetine?
Combined serotonin and noradrenaline reuptake inhibition.
224
What are common side effects of duloxetine?
Nausea, dry mouth, drowsiness, raised BP.
225
How is pregabalin dosed for pain?
Start at 150mg/day; titrate to 300mg bd; reduce slowly if stopping.
226
What are side effects of pregabalin?
Dizziness, drowsiness, ataxia, nausea, respiratory depression.
227
What is the half-life of pregabalin?
6.3 hours; longer in renal impairment or elderly.
228
What is the Number Needed to Treat (NNT)?
No. of patients needed to treat for one to benefit with ≥50% pain relief.
229
Is a low or high NNT better?
Lower NNT = more effective treatment.
230
What is Number Needed to Harm (NNH)?
No. of patients needed to treat for one to experience harm – higher is better.
231
What type of pain is fibromyalgia?
Nociplastic pain.
232
What is the role of education in chronic pain management?
Helps patients understand pain and engage in self-management.
233
Why is opioid use discouraged in chronic primary pain?
Lack of evidence for benefit and risk of harm.
234
What model should be used to assess pain holistically?
Biopsychosocial (BPS) model.
