Clinical CNS Pain Flashcards

(131 cards)

1
Q

What are the questions to ask patients how to measure pain?

A

How long have they felt the pain?
What could have caused it?
Where is the pain?
What makes it better/worse time of day?
Does it come or go?
Does it vary with position?
What does the pain feel like?
What have they tried to help?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are there ways of measuring a patient’s pain?

A

VAS (visual analogue scale) 0-10
NRS (numerical rating scale):
0-10 123= mild, 456=moderate, 789=severe
For younger patients can use facial expressions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are aspects to examine on a patient in terms of pain?

A

Colour changes
Swelling
Tenderness
Asymmetry
Any weakness
Range of movement
Sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do we classify pain?

A

Duration- acute/chronic
Underlying mechanisms
Physical origin
Cause e.g cancer/ post op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the underlying mechanisms of pain?

A

Nociceptive
Neuropathic
Nociplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the physical origin of pain?

A

Visceral (internal organs)
Somatic (external- bone, muscle)
Referred pain (e.g MI pain in arm/jaw)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe acute pain:

A

Comes on suddenly
Treated by resolving the cause of the pain
Usually due to trauma, injury or surgery
Lasts less than 6 months
OTC treatments/ analgesic ladder
Best to rest area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe chronic pain?

A

Comes on gradually
Usually, the result of a condition that is difficult to treat/diagnose
Lasts more than 6 months
Difficult to find lasting relief
Better to mobilise the area
Musculoskeletal pain 50-80% of UK pop at a time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the factors contributing to pain?

A

Social
Psychological
Biological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is nociceptive pain?

A

E.g reflex arc, hand near flame
Nociception- the ability to detect painful stimuli via nociceptors that respond to painful stimuli
Preventing or in repsonse to tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is neuropathic pain?

A

Malfunction in the NS or damage to the nerves e.g diabetic neuropathy
Central pain, peripheral neuropathy, complex regional pain syndrome
Burning, electric shocks, shooting pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is nociplastic pain?

A

Altered nociception in the absence of tissue or nerve damage
Widespread intense pain e.g fibromyalgia
Exercise/psychological/accupuncture
Antidepressants off label

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the first step in the WHO analgesic ladder:

A

Non-opioid:
Paracetamol
NSAIDs
Topical treatments (NSAIDs, lidocaine, capsaicin)
± adjuvant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the second step in the WHO analgesic ladder:

A

Mild opioid as an alternative or an addition:
Mild to moderate pain
Codeine/ dihydrocodeine/ tramadol
Limited potency at the MU receptor
± adjuvant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the third step in the WHO analgesic ladder:

A

Strong opioid to replace the mild opioid:
Moderate to severe pain
Morphine/ diamorphine/ oxycodone
Fentanyl/buprenorophine/ alfentanil
Strong potency at the MU receptor
± adjuvant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name and give examples of adjuvant therapies in the WHO ladder:

A

Anti-epileptics (neuropathic)- pregabalin, gabapentin, carbamazepine (TN)
Anti-depressants- TCA, SSRIs
Other- dexamethasone, bone pain in palliative
Non pharmaceutical- physio, exercise, psychological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the evidence for the use of opioids?

A

Acute pain in palliative care
Limited evidence of efficacy in long term pain:
-if don’t achieve useful pain relief in 2-4 weeks unlikely to gain long term benefit
No efficacy with high dose (>120mg/ day morphine/ equivalent) due to lack of trial data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the risk of treatment with weak opioids?

A

Metabolism of weak opioids
Cyp2D6 enzyme- converts codeine into morphine
Interpatient variability dependent on gene expression (if a supermetaboliser and breastfeeding can pass more morphine to baby)
Unpredictable variation in efficacy and toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the SEs of opioids?

A

N&V- likely to reduce with time
Constipation, drowsiness, sedation, resp depression
-use stim and osmotic
Renal function- increase morphine in body
Dependence/ addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the signs of overdose of an opioid?

A

Pinpoint pupils
Pale skin
Blue lips (cyanosis)
Unconscious
Shallow/slow breathing
Snoring/gasping for breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe how pinpoint pupils are a sign of opioid overdose:

A

Stimulation of parasympathetic NS causes contraction pinpoint pupils
Less/no response to light or abnormal movements
Use eye examination and light test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe how pale skin and blue lips are a sign of opioid overdose:

A

Hypoxia- low blood oxygen, low blood circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe how unconsciousness and the breathing abnormalities are a sign of opioid overdose:

A

Resp depression
Activation of the µ-opioid receptors in the brain stem that co-ordinate respiratory rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the aspects of the NEWS2 score that indicates an opioid overdose?

A

Resp rate <8bmp (normal= 12-20)
O2 sats can be <85% (96-99%)
HR= tachycardia
BP= high or low
Sedation score= VPU higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does VPU stand for in the NEWS2 score?
V= verbally P= pain U= unconscious/unresponsive
26
What is the non-pharmacological treatment for lower back pain (musculoskeletal)?
Exercise (aerobic) programmes and manual therapies- spinal manipulation, massage (as part) Psychological therapies- CBT (as part) Return to work programmes
27
What is the pharmacological treatment for lower back pain (musculoskeletal)?
NSAIDs- look at CI Weak opioids for acute lower back pain if NSAIDs CI or ineffective Do not offer paracetamol alone
28
What is sciatica?
Musculoskeletal pain Leg pain 2º to lumbosacral nerve root pathology due to compression or irritation to the sciatic nerve- shooting pain
29
What is the pharmacological treatment for sciatica?
Do not offer gabapentinoids/antiepileptics/ benzodiazepines If already prescribed, discuss problmes and withdrawal Limited evidence of NSAID benefit Do not offer opioids Epidural injections (acute and severe sciatica)
30
What are the surgical treatments for sciatica?
Spinal decompression surgery Other surgical intervention depending on cause
31
What are the symptoms of osteoarthritis?
Pain Stiffness Tenderness Grating sensation Swelling Bone spurs
32
What is the non-pharmacological treatment for osteoarthritis?
Exercise/ physiotherapy Weight loss if indicated to decrease pressure on joints Manual therpaies
33
What are the pharmacological treatments for osteoarthritis?
Topical NSAID, if ineffective/ CI oral can be considered Paracetamol and weak opioid may be considered Intra-articular corticosteroid if others ineffective/unsuitable Joint replacement
34
What are the main medications indicated for neuropathic pain?
Amitriptyline Duloxetine Gabapentin Pregabalin
35
What should be the process of using medications for neuropathic pain?
Each indicated for things slightly different If initial treatment ineffective/ not tolerated then try another
36
What are other medications that can be used for neuropathic pain?
Tramadol only if acute rescue therapy needed Capsaicin cream for localised pain who with to avoid oral- normal for burning/stinging Carbamazepine for trigeminal neuralgia
37
What is the initial pain relief in palliative care?
24 hour pain relief- simple analgesia or strong opioid, no max dose of opioid Begin with anticipatory (PRN) injection
38
Name and state the doses of the anticipatory injection in palliative care:
Morphine SC 2.5-5mg 2-4 hrly (eGFR >60) Oxycodone SC 1.25-2.5mg 2-4 hrly (eGFR 30-60) Alfentanil SC 125-250mcg 2-4 hrly (eGFR <30)
39
When would a patient need a syringe driver in palliative care?
If needing 3 or more injections in a 24 hour period, may be less than 3 in certain situations
40
What is the treatment for breathlessness in palliative care?
Opioid/ midazolam- slows down breathing
41
What should be co-prescribed with opioids in palliative care?
Naloxone- toxicity
42
What are syringe drivers?
Battery powered pump delivering a 24hr continuous SC infusion of medication Usually matches PRN injections Need a diluent to provide volume- WFI/NaCl Compatibility- can put other drugs in there as well
43
Which surgeries would NSAIDs not be used for pain and why?
Not in fracture of hip or pelvis as affects bone recovery IV paracetamol is used
44
When would you use oral opioids for post-operative pain?
Moderate/severe pain expected- larger/complex procedure Not with PCA or opiate epidural Aids in recovery- get coughing relax back and mobilise pt quicker
45
When would gabapentin be used for post-operative pain?
If neuropathic post op pain- orthopaedic/ thoracic chest drain insertion (temporary treatment)
46
What is PCA?
Patient controlled analgesia Pts determine when and how much analgesia they receive (presses button) IV admin Opiates most common Loading dose in recovery then PCA
47
What are the monitoring requirements for patients on PCA?
BP/pulse/RR/sedation/pain score/nausea (opioid effects) First 8 hours= hourly 8-24 hours= 2 hourly 48 hours- end= 4 hourly
48
What is the typical PCA admin?
100mg morphine in 100ml NaCl 0.9% (1mg/1ml) -administers 1mg at a time -lockout 5 mins
49
What are the benefits of PCA?
Patient ownership and independence Faster alleviation of pain Decrease distress in waiting for nursing staff Less time consuming for nurse Easy to titrate accoring to response Fewer peaks/ troughs than bolus
50
What are the disadvantages of PCA?
Patient may to be responsive or dextrous enough Patient may lack understanding or be scared to use Decrease mobility Liable to abuse (comes with lockout) SEs- normal opioids
51
What should be administered for N&V in PCA?
Cyclizine (oral/IM prn) Ondansetron (oral/IV/IM) Can have protocols so nurse can give without prescribing
52
What should be administered for pruritis in PCA?
Chlorphenamine 4mg TDS
53
What should be administered for respiratory depression in PCA?
Oxygen and monitor sats Stop PCA Consider naloxone 200-400mcg- may need repeated admin as short t1/2
54
What should be administered for excessive sedation in PCA?
Remove PCA Oxygen sats, pain, sedation Ensure adequate non-opioid analgesia presented
55
What is an epidural?
Numb nerves that carry pain impulses from birth canal to brain Injection into spinal column into epidural space Can be used post-op
56
What is the subarachnoid space?
Consists of the CSF for lumbar puncture
57
Describe an epidural infusion:
Does not induce paralysis- just uncoordinated when walking There will still be sensation and movement both above and below Bathing the nerve fibres- block transmission of sensory impulses from afferent nerves to the spinal nerve, and ongoing transmission to the efferent Target a particular nerve root and to dampen the nociceptive transmission Block groups of 3 to block out one dermatome
58
Describe the different dermatomes:
Cervical region- C1-C8 Thoracic region- T1-T11 Lumbar region- L1-L5 Sacral region S1-S5 Common injection sites are low thoracic/ high lumbar T10-L3
59
Describe the order of central nerve blockade and where an epidural works:
Small unmyelinated fibres Autonomic pre ganglionic fibre (response to temp) Pain (Touch)- target of block Deep pressure Vibration and proprioception During birth mother can't feel pain but can feel pressure of baby
60
Name the two classes of drugs in an epidural bag:
Opioid analgesic Anaesthetic
61
Describe opioid analgesics in an epidural bag:
E.g morphine Diffuses into CSF Inhibits pain transmission in spinal cord Spinal opioid receptors-main site of action No effect on motor or sensory functions Reversible (naloxone) Doesn't migrate
62
Describe the anaesthetic in an epidural bag:
E.g bupivacaine Diffuses across myelin sheath into nerve cell Inhibits Na+ channels, preventing depolarisation of the membrane, nerve impulse conduction and conduction Reversible Doesn't migrate
63
What doesn't an epidural migrate and why is this good?
Don't want migration as don't want it to travel to other areas of the spine and cause loss of pain sensation in other areas Also if they do migrate there will be a decreased conc at the site they need to be, so lower efficacy Balance between density: -more dense than medium injection= sink down to spinal column -less dense float to brain
64
What are the properties of fentanyl in an epidural?
Stable in CSF Penetrates neurones Doesn't migrate Onset 4-10 mins Duration 2.5-4 hours
65
What are the properties of bupivacaine in an epidural?
Block sensory fibres, maintain motor function Migration limited by slow infusion rate Onset 15-20 mins Duration 2-3 hours
66
What are epidurals co-administered with and why?
Both emergency only Naloxone Ephedrine- combat any hypotension due to epidural
67
What are the advantages of epidurals?
High quality pain relief and smaller opioid doses than systemic Reduced incidence of DVT Less sedation Post-op lower over 24 hours if infusion Improved pulmonary function Decreases cardiac morbidity and sepsis Faster re-establishment of oral intake
68
What are the disadvantages of epidurals?
Accidental injection into the spinal cord (total spinal block) Risk of permanent spinal damage Accidental IV admin Dural puncture headache (within 72 hours) Epidural bleed/haematoma Migration of drug can lead to resp paralysis Infection risk
69
What are the SEs of epidurals?
Resp arrest (opioid)- migration to C3-C5 blocking phrenic nerves Resp depression Hypotension/ hypothermia due to vasodilation Decreased CO if T1-T4 affected Reflex tachycardia Overdose or IV given- depression of myocardial excitability Reduced hepatic/ renal perusion More common: Tinnitus/ headache/ N&V/ pruritis/ sedation
70
What is the rescue therapy for administering IV bupivacain?
Intralipid 20% to reverse cardiac arrest risk of life threatening toxicity
71
What is the rescue therapy for a dural puncture headache?
Blood patch Injected with own blood in hope of creating a seal around hole
72
What is a dural puncture headache?
The hole has been made by the spinal needle, sometimes can cause leakage of CSF and can cause pressure in rest of fluid e.g in CNS to be decreased so can lead to severe headache- late onset
73
What are the CI of epidurals?
Pt refusal Infection at the site Clotting abnormalities Severe resp impairment Uncorrected hypovolemia Raised intracranial pressure Neurological disease Difficult anatomy Tattoos
74
Why are tattoos CI in epidurals?
Some say yes, some say no Due to risk of ink bleeding into epidural space- ink toxicity If tattoo is old/ healed some anaesthetists would say no risk
75
Name the different classifications of primary headaches:
Tension-type Cluster headache Migraine Miscellaneous
76
What is a tension headache?
Most common cause Thought to be due to muscle spasm in neck/scalp Can be caused by emotional stress (tension, anxiety, fatigue, dehydration)
77
What is the pain like in a tension headache?
Mild to moderate Non-throbbing, vice like, a feeling of 'tightness or squeezing', weight pressing down on head Usually affects both sides of the head- mainly front of head May worsen throughout the day
78
What is a cluster headache?
Rare but is 6-9x more common in men
79
What is the pain like in cluster headaches?
Excruciating unilateral headache Accompanied by red eye, lacrimation, nasal congestion, rhiborrhoea (runny nose), facial sweating, miosis (pupil constriction), droopy eye lid and eye lid oedema May be mistaken for an eye injury
80
What is the duration of a cluster headache like?
Sudden onset- may wake them up from sleep Intermittent onset- can occur up to 8x a day Lasts between 10mins- 3 hrs
81
What is the differential diagnosis in cluster headaches?
Meningitis Head bleed (arachnoid haemorrhage)- back of head Cranial arteritis- inflammation, joint sitffness, go up side of head near jaw Temporal arteries- scalp painful to touch, older patients
82
What is the first line treatment for headaches if they don't impact the patients life?
Paracetamol
83
What is the second line treatment for a headache if it does impact a patients life?
Paracetamol Codeine (30-60mg 4-6 hourly)- OTC doesn't reach evidence based dosages ±ibuprofen
84
What is the third line treatment for a headache if it means a patient can't carry on with every day activities?
Paracetamol Opioid e.g morphine, fentanyl, oxycodone ±Ibuprofen
85
What should be used for breakthrough pain with a headache?
If ongoing daily pain relief not helping- give 1/6 amount of main opioid getting in a day
86
What are the symptoms of a migraine?
Episodic- patients are well between attack Prodrome Aura Headache Postdrome- washout feeling
87
Describe the symptoms of the headache in a migraine?
Lateralised (one side of head) and pulsating Associated with N&V, phono/photophobia
88
What is the epidemiology of migraines?
Common (15% population) 3x women greater, possible hormonal link 190,000 each day in UK Underdiagnosed and under treated
89
What is the onset of age of migraines?
Peaks at young children- 5 years Peaks at early 20s then drop off Very rare to get around 50-55 and above so red flag
90
Name the divisions of migraines:
Classical migraine Common migraine Abdominal migraine Migraine associated with childhood travel sickness
91
Describe a classical migraine:
Migraine with aura (15%) Focal neurological disturbance
92
Describe a common migraine:
Migraine without aura (85%)
93
Describe an abdominal migraine:
Migraine in children (3-10%) 50% remission after puberty Often GI symptoms- stomach cramps, withdrawing from play, not like loud noises, nausea
94
Describe the pathophysiology of migraines:
Genetic link, from familiar hemiplegic migraine (FHM) Chromosome 19 and 1 10 potential polymorphism of Ca2+ channels which involve 5HT release Brain hypothesis Sensory nerve hypothesis 5HT implicated
95
Describe the brain hypothesis in the pathophysiology of migraines:
Increased extracellular [K+] so decreased blood flow Wave of neuronal inhibition
96
Describe the sensory nerve hypothesis in the pathophysiology of migraines:
AKA inflammatory hypothesis Activation of trigeminal nerve- feeds up side of head- meninges Inflammatory mediators released- cytokines, PG, CGRP
97
How is 5HT implicated in migraines?
Sharp increase in serotonin main metabolites during attack If inject serotonin, can relieve migraine Blood serotonin decrease Can stimulate migraines which cause 5HT depletion
98
Name and describe the trigger factors for a migraine:
Foods- alcohol, caffeine, choc, dairy Hormonal changes- HRT, pill, pregnancy (stops during) Environmental- emotion, weather Points system- every trigger is a point until reach trigger threshold, keep a diary
99
Describe the prodrome phase in a migraine:
Heightened sensations e.g craving Foreboding- know its not gonna be a good day
100
Describe the aura phase in a migraine:
Fortification spectra (visual field affected) Flashing lights Scotoma (black/blind spot on visual field) Paraethesiae- pins and needles, can be prodrome
101
Describe the symptoms of meningitis syndrome:
Headache, N&V, dislike of bright light, noises Different symptoms for meningitis: -rash (late onset), neck movement- can't put chin on chest
102
Describe the diagnosis points to be classed as a migraineur:
At least 5 repeated attacks of headaches lasting 4-72 hours which have these features: At least 2 of: -unilateral pain -throbbing pain -aggravated by movement -moderate/severe intensity At least 1 of: -N&V -phono/photophobia
103
When should a patient be referred to the GP with a migraine/ headache?
Lasting more than 24 hours Worse in morning (eases as day progresses)- effortless vomiting in morning (indicate growth) Headache with unsteadiness/ clumsiness- esp in children Children under 12 Suspected ADRs e.g nitrates/ CCBs
104
What is the acute simple analgesic for migraines?
Dispersible/ effervescent preps preferred -aspirin 900mg -ibuprofen 400mg -paracetamol 1000mg
105
Describe the use of OTC caffeine and codeine for migraines:
Caffeine can increase absorption but can be a trigger factor Codeine not evidence based dosage Chronic daily headache- analgesic induced Dependence
106
Name the OTC treatments for migraines:
Migraleve Buccastem M Triptans
107
Describe Migraleve as an acute treatment for migraines:
Do not suggest Pink tabs (onset of attack): -buclizine- doesn't work at right part of brain, antihistamine to cause drowsiness, paracetamol, codeine Yellow tabs (during) -paracetamol, codeine BNF says less suitable for prescribing
108
Describe Buccastem M as an acute treatment for migraines:
3mg Buccal prochlorperazine- works on the CTZ
109
Describe how the triptans work for treating acute migraines:
5HT1 agonists Specifically working on 5HT1B and 5HT1D Constrict blood vessels back to normal
110
What are the CI of the triptans?
IHD- 5HT subtypes in coronary area Uncontrolled hypertension Over 65
111
What are the SEs of the triptans?
Tiredness and dizziness (common) Heaviness on chest and throat
112
Name some triptans:
Sumatriptan Zolmitriptan Naratriptan
113
Describe the +/-ve of sumatriptan:
+ve: SC: very fast acting Nasal: fast acting+ can use on under 18 -ve: Poorly absorbed by mouth
114
Describe the +ve of zolmitriptan:
Melt: orange flavour so decreased taste disturbances
115
Describe the +/-ve of naratriptan:
+ve: long t1/2 for prolonged and recurrent migraines -ve: Less effective at 2 hours
116
What should be the counselling points with the triptans?
If the migraine disappears but then reappears can take a second dose after 2 hours have passed If doesn't disappear originally then not effective to take a second dose
117
What are medication overuse headaches?
Taking meds too often for headaches 1 in 50 people affected at some point (more common in women) Pain oppressive, worse in morning as body used to chemical
118
What is the treatment for medication overuse headaches?
Stop current therapy Pain gets worse before it gets better
119
Which are the patients at risk of getting a medication overuse headache?
Using analgesics/ triptans >15 days per month Refer requests for ≥4 sumatriptan/ month
120
How would you prevent medication overuse headache?
<15 days/month 3-4 doses over 1-2 days is okay Don't take consecutively for more than 2 days Avoid codeine containing products
121
When would it be ideal to use migraine prophylaxis?
Functional impairment- how much every day life affected Headache more than 2x per week Amount of acute med used Will patient comply Success or failure of previous therpay
122
Describe counselling points for patients for migraine prophylaxis:
50% of patients have 50% relief Will not provide migraine free living Still need acute break through treatment
123
What are the SEs of migraine prophylaxis?
Diminish with time (e.g valproate + nausea) Weight gain/contraceptionn
124
What should be the treatment time for migraine prophylaxis?
6-12 months effective therapy, if not withdraw Need without time period to see if can not have anymore
125
Name drugs that can be used for migraine prophylaxis:
B blockers- propranolol Pizotifen (rare) Methysergide TCA- amitriptyline Anticonvulsants (valproate/topiramate) OTC feverfew- limited evidence
126
Describe the SEs of BBs:
Fatigue, bronchoconstriction Cold extremities
127
Describe how pizotifen works and its SEs:
5HT2 antagonist- antihistamine Weight gain, sedation
128
Describe how methysergide works and its SEs:
5HT2 antagonist N&V Rare- fibrotic conditions
129
Why are anticonvulsants used for migraine prophylaxis?
Prolonged or atypical migraine aura (no headache)
130
Name and describe an injection for the prophylaxis of migraines:
Botulinum toxin type A (botox)- liscensed Non systemic medication- mechanism is unknown Relaxes muscles- blocks pain feedback Repeated injections to head and neck
131
Name potential future migraine prophylaxis:
CGRP antagonist- no vasoconstriction effects but liver toxicity Serotonin receptor agonists (5HT1D/1F only) Nitric oxide antagonists- vasodilator, no evidence