pain clinical Flashcards

1
Q

what is pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

how is pain classified

A

duration - acute or chronic
mechanism- nociceptive, neuropathic or neoplastic

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3
Q

what is acute pain

A

sudden onset
resolved by treating cause
<6m
OTC/WHO ladder for treatment

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4
Q

what is chronic pain

A

gradual onset
usually the result of a condition that is heard to diagnose/treat
>6m duration
musculoskeletal pain

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5
Q

what is nociceptive pain

A

pain preventing or in response to tissue damage

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6
Q

what is neuropathic pain

A

malfunction of the nervous system or nerve damage

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7
Q

what is oncoplastic pain

A

altered nociception in the absence of tissue or nerve damage

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8
Q

what are the 3 rules of the WHO pain ladder

A

by the clock - as often as possible
by the mouth - unless not possible
by the ladder

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9
Q

what are the steps on the WHO pain ladder

A
  1. non-opioid (paracetamol, NSAIDs, COX)
  2. mild opioid (codeine, dihydrocodeine, tramadol)
  3. strong opioid (morphine, oxycodone, fentanyl)
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10
Q

what adjuvant therapies can be used for pain

A

neuropathy - AEDs (gaba, pregab and carba)
- TCAs/SSRIs
palliative bone pain - dexamethasone
non-pharmacolog - physio, exercise, physological treatment, acupuncture

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11
Q

what are opioids used for

A

acute pain and palliative care

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12
Q

opioid metabolism

A

CYP2D6 - varies between patients

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13
Q

opioid side s/e

A

N&V - may settle
constipation - co prescribed w/ laxatives
drowsiness/sedation
resp depression
renal function
addiction

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14
Q

what are the signs of opioid overdose

A

pinpoint pupils
hypoxia
resp depression
NEWS2
- RR <8
- O2 <85% on air
- tachycardia
- sedation

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15
Q

what are the non-pharmacological interventions for lower back pain and sciatica

A
  • exercise and manual therapies
  • psychological activities
  • return to work programs
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16
Q

pharmacological treatment for lower back pain

A
  • NSAIDS (GI/renal/age - PPI and stop date)
  • weak opioids if NSAID C/I or not tolerated
  • paracetmol alone not recommended
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17
Q

pharmacological treatment of sciatica

A
  • no gabapentinoids, AEDs, benzos - stop if on
  • limited evidence for NSAIDs
  • no opioids
  • epidural injections or surgery
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18
Q

how is osteoarthritis treated

A
  • exercise/weight loss
  • manual therapies
  • oral/topical NSAID
  • paracetamol/weak opioids considered
  • intraarticular steroids
  • joint replacement
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19
Q

how is neuropathic pain treated

A
  • if initial C/I or not tolerated
    amitriptyline/duloxetine/gaba/pregab
  • tramadol only for acute rescue therapy
  • capsaicin can be used for local if oral not tolerated
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20
Q

what is palliative care

A

aim is to improve QoL at end of life

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21
Q

what pain relief is used in palliative care

A

24 hr simple analgesia or weak opioid
- PRN injection but if >3 then syringe driver
naloxone for toxicity

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22
Q

what is used to treat breathlessness in palliative care

A

opioid or midazolam

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23
Q

what is PCA

A

patient controlled analgesia - usually 1mg/ml morphine but if renal function reduced give fentanyl

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24
Q

monitoring for PCA

A

BP
pulse
RR
sedation
pain score
- hourly for 8
- every 2 for 8-24
- every 48 hours after

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25
Q

PCA s/e

A

N&V - cyclizine
pruritis - chlorphenamine
RR <8 - O2, monitor and stop - consider naloxone
excess sedation - stop, monitor, non-opioid analgesia

26
Q

what is an epidural

A

delivery of analgesics with or without adjuvants o epidural space

27
Q

where are epidurals given

A

epidural space

28
Q

epidural space physiology

A

dorsal route ganglion - cell bodies from afferent and efferent nerves, communication between peripheral and central nervous systems
- Spinal meninges - dura mater is outer layer (arachnoid mater and then pia mater) - tough and strong to protect the spine
○ Subarachnoid space - space between the subarachnoid mater and the pia mater - filled with CSF, accessed for lumbar punctures
○ Epidural space between dura mater and bone - fatty matter and space for epidural to be injected

29
Q

what are the components of epidural

A

opioid analgesic
- inhibits pain transmission at spinal cord
- reversible, no migration
anaesthetic
- diffuses across myelin sheath into nerve
- inhibits sodium channel preventing depolarisation
ephedrine for hypotension
naloxone
cyclizine for sickness

30
Q

what are the advantages of epidural

A
  • better relief for smaller doses
  • reduced DVT incidence
  • less sedation
  • covers post-op
  • improved pulmonary function
  • reduced cardiac and sepsis issues
31
Q

what are the disadvantages of epidural

A
  • Accidental injection into spinal cord - total spine block
  • Risk of permanent damage
  • Accidental IV administration
  • Dural puncture headache
  • Epidural bleed
  • Drug migration can lead to respiratory paralysis
  • Infection risk
  • Requires informed consent
32
Q

s/e of epidural

A
  • resp arrest (C3-C5)
  • resp depression
  • hypotension/hypothermia
  • reduced cardiac output
  • reflex tachycardia
  • overdose/IV - myocardial depression
  • reduced hepatic/real perfusion
  • dural headache
  • tinnitus
  • pruritis
  • N&V
  • sedation
33
Q

what rescue therapies are used for epidurals

A
  • IV bupivacaine - reverse cardiac arrest or toxicity
  • opioid toxicity - naloxone
  • hypotension - ephedrine
  • dural puncture headache - CSF leakage causes drop in pressure
34
Q

C/I for epidurals

A
  • Refusal
  • Infection at site
  • Clotting abnormalities
  • Severe respiratory impairment
  • Uncorrected hypovolaemia
  • Raised intracranial pressure
  • Neurological disease
  • Injury or deformity changing anatomy
  • Tattoos - site of injection would be up to clinician (could cause ink leakage/bleeding)
35
Q

what is a tension headache

A

most common form, thought to be due to neck/scalp muscle spasm - can be due to stress

36
Q

symptoms of a tension headache

A

mild to moderate pain
non-throbbing and vice like
unilateral
may worsen throughout the day

37
Q

what is a cluster headache

A

sudden onset lasting 10m to 3hr

38
Q

what are the symptoms of a cluster headache

A
  • Excruciating- severe pain on one side of the head
    • Nasal or eye symptoms
    • Accompanied by red eye, lacrimation, nasal congestion, rhinorrhoea, facial sweating, miosis, droopy eye lids and eye lid oedema
39
Q

what are the differential diagnosis for cluster headaches

A

meningitis - non blanching rash, light sensitivity
bleeding - trauma, confusion
cranial arteritis - pre-existing joint issues

40
Q

what are medication overuse headaches

A

Pain is oppressive - worse in morning caused by painkiller overuse

41
Q

how are medication use headaches treated

A

stop therapy
pain gets worse before it gets better
gp for prophylaxis

42
Q

what medications put patients at risk of medication overuse headaches

A

using analgesics or triptans for more than 15 days/month

43
Q

how should painkillers be used for headaches

A

<15 days a month
3-4 doses / 2 days
no consecutive use
avoid codeine

44
Q

what are the symptoms of migraines

A

prodrome - pre-headache
- aura
headache
- lateralised and pulsing
- N&V
- dislike for bright light and loud noises

45
Q

what are the theories for pathophysiology of migraines

A
  • vascular theory - disproven
  • brain hypothesis - increased extracellular potassium causing decreased flow and neuronal inhibition
  • inflammation - activation of trigeminal nerve
    5HT implicated in pathogenesis - metabolites present in urine
46
Q

what are the three types of migraine

A

classical
common
abdominal

47
Q

what are the symptoms of a classical migraine

A

aura
slurred speech
visual phenomena

48
Q

what are the symptoms of common migraines

A

no aura

49
Q

what are the symptoms of abdominal auras

A

usually in children
headaches
GI symptoms
withdrawing from play
not liking loud noises
cyclic

50
Q

what are some trigger factors of migraines

A

certain foods
hormonal changes
environmental issues
change in standard routine

51
Q

how are migraines diagnosed

A

repeated attacks lasting 4-74 hours with at least TWO
- unilateral pain
- throbbing pain
- aggravated by movement
- moderate or severe intensity
and ONE
- nausea and vomiting
- phono/photophobia

52
Q

which migraine patients need to be referred to GP

A

> 24 hrs
no nausea but vomiting in the morning
unsteadiness
under 12s
suspected ADRs

53
Q

how are migraines managed

A

elimination of triggers
acute intervention for breakthrough
if >4/month offer prophylaxis

54
Q

what is the acute treatment of migraines

A
  1. dispersible or effervescent ibuprofen 400, aspirin 900 or paracetamol 1g
  2. OTC prochlorperazine or triptans
55
Q

what are the triptans

A

5HT1B and 1D agonists
C/I in IHD, HT, 65 +
s/e dizziness, tiredness, tight chest and throat
1 tab - 2nd dose if goes away ad comes back

56
Q

which medications can be used for migraine prophylaxis

A

beta blockers
pizotifen
methysergide
TCAs
topiramate
valproate

57
Q

beat blockers s/e

A

fatigue
bronchoconstriction
cold extremities

58
Q

what is methysergide and its s/e

A

5HT antagonist
N&V
rare fibrotic conditions

59
Q

what is pizotifen and its s/e

A

5HT agonist
weight gain
sedation

60
Q

what issue needs to be accounted for when using valproate and topiramate for migraines

A

teratogenic

61
Q

what are the trigger factors for migraines and how to reduce them

A

anxiety - coping strategies
change of habits - reversal to normal
foods - exclude
bright lights and noise - avoid
strenuous exercise - avoid

62
Q

when is migraine prophylaxis indicated

A
  • functional impairment
  • > 2 headaches a week
  • patient compliance