Post-op pain relief Flashcards

1
Q

What is the definition of pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or expressed in terms of such damage

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2
Q

Can you be in pain if unconscious?

A

no, but can still respond to noxious stimuli

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3
Q

What is the definition of chronic pain?

A

Duration of pain exceeds 6 months, or persists beyond the time for tissue healing

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4
Q

What are 3 aspects to pain?

A
  1. Physical
  2. Emotional
  3. Rational - e.g. avoiding things that are painful; pain itself might not do much harm but damage assoc. w pain may
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5
Q

What element of pain was Descartes involved in?

A

Described idea of pain involving peripheral sensation and ascending centrally; i.e. 2 aspects, peripheral and central components of pain

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6
Q

What general pathway do the majority of pain pathways follow?

A
  • First order neuron from periphery to spinal cord; decussates at spinal level
  • Second order neuron via lateral spinothalamic tract to thalamus
  • Third order neuron from thalamus to cortex
  • The many sensory pathways e.g. pain, movement, light touch etc. interact
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7
Q

Which spinal tract do pain signal ascend via in the spinal cord?

A

Lateral spinothalamic tract

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8
Q

What is the relationship between pain receptors and the first order neuron that carries pain signals?

A

Peripheral receptors of several types are connected to the primary sensory neurons

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9
Q

What is the anatomy of first order neurons which transmit pain signals?

A

Have their cell bodies in the dorsal root ganglion (DRG), and a central connection terminating on the second order neuron in the dorsal horn substantia gelatinosa (SG)

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10
Q

What are 4 types of neurons which transmit somatosensory pain?

A
  1. A delta (12-30m/sec)
  2. C fibres (0.5-2m/sec)
  3. B fibres - sympathetic pregnanglionic fibres
  4. A beta (30-70m/sec) - under abnormal conditions
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11
Q

What type of receptors are A delta neurons associated with? 2 types

A

Mechanoreceptors and nociceptors

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12
Q

What type of receptors are C fibres associated with? 2 types

A

Mechanoreceptors, nociceptors

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13
Q

What type of receptors are A beta neurons associated with? 2 types

A

Cutaneous touch and pressure

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14
Q

What is important to remember about A beta fibres and pain?

A

normally they’re not involved in signally noxious stimuli but can do so under abnormal conditions

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15
Q

Why is it pertinent to anaesthetics that A beta fibres don’t normally signal noxious stimuli?

A

they are more resistant to local anaesthetic blockage than A delta and C fibres

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16
Q

Why might a patient under spinal or epidural analgesia stilll sense touch and movement but not pain and temperature?

A

because these are transmitted by A beta fibres which are more resisntat to local anaesthetic blockage

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17
Q

Which type of nerve fibres are primarily being targeted by local anaesthetic?

A

C fibres (pain and temperature)

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18
Q

Why might a patient be able to move when under local anaesthetic but not be aware of doing so? For example, moving toes on command but can’t feel it

A

all but A alpha (i.e. motor neurons) are blocked

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19
Q

Give 2 ways that A delta fibres differ from C fibres/others in their properties?

A

A delta fibres transmit faster, are more readily injured by pressure and ischaemia e.g. sciatica, residual nerve dysfunction

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20
Q

Which type of noxious signalling fibre is more easily blocked by local anaesthetics and what effect does this have?

A

C fibres are more easily blocked; possible to remove sensation of pain and temperature elaving light touch and movement intact

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21
Q

What are 3 types of physical pain?

A
  1. Somatosensory pain
  2. Visceral pain
  3. Sympathetically maintained pain
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22
Q

How do somatosensory and visceral pain differ?

A
  • Somatosensory is cutaneous, well-localised, sharp pain; pain from deeper structures may be diffuse and less localised
  • Visceral is poorly localised, often referred to surface areas innervated by the same spinal segments e.g. myocardial ischaemic pain refers to arms or neck
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23
Q

What are 13 tissue injury factors released when acute tissue trauma occurs?

A
  1. K+
  2. H+
  3. Bradykinins
  4. ATP
  5. Prostaglandins
  6. 5-HT
  7. Histamine
  8. Cytokines
  9. IL-1
  10. IL-6
  11. IL-8
  12. TNF-alpha
  13. NGF (nerve growth factor)
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24
Q

What are 4 neuropeptides involved in the neurochemistry of sensory neurons?

A
  1. substance P
  2. excitatory amino acids (EAAs)
  3. glutamate
  4. aspartate
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25
Q

What are 3 types of channels invovled in the neurochemistry of pain?

A

sodium, potassium, calcium

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26
Q

What are 2 types of inflammation pathways involved with pain and 3 chemicals involved in each?

A
  1. Arachidonic acid pathways: prostaglandins, thromboxanes, leukotrienes
  2. Lysosomes: histamine, bradykinin, other kinins
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27
Q

What are 5 things caused by inflammation?

A
  • Pain (dolor)
  • Erythema (rubor)
  • Heat (calor)
  • Swelling (tumor)
  • Loss of function
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28
Q

What is the neuro-transmitter involved in acute pain and what are the 2 relevant receptors?

A

Glutamate is the transmitter; NMDA and AMPA receptors

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29
Q

What neurotransmitters are involved in chronic pain?

A

substance P and othe rless recognised neurotransmitters

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30
Q

What is the gate theory of pain?

A
  • Idea of rubbing skin to inhibit pain signal, described by Ron Melzack and Patrick Wall in 1965
  • Nociceptive signal arrives on projection neurone in the spinal cord
  • If a non-painful stimulus e.g. rubbing skin occurs, this is transmitted down a different fibres which may act on an interneuron that blocks transmission through the original synaptic neurone
  • Reduces transmission of original nociceptive signal
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31
Q

Why can rubbing a bumped knee reduce pain?

A

Inhibits projection neuron which carried pain signal by acting on inhibitory interneuron: gate theory

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32
Q

How has the gate theory of pain been made use of in medicine?

A

TENS: transcutaneous electrical nerve stimulation; stimulates non-nociceptive neurons that inhibit traffic of nociceptive neurons

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33
Q

What is the theory behind pre-emptive analgesia?

A

by preventing noxious stimuli from reaching the spinal cord and CNS, central sensitisation will not occur, minimising neuron changes and reducing post-operative pain

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34
Q

In practice, what does pre-emptive analgesia involve?

A

Local anaesthetic infiltration into tissues prior to incision, block of peripheral nerves or nerve plexuses, epidural or spinal injection

Using local anaesthetic with/without opioids, plus systemic opioids, NSAIDs and NMDA receptor blockers

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35
Q

What is the outcome of properly administered pre-emptive analgesia?

A

Major reduction in post-operative pain, with earlier discharge from hospital (e.g. following thoracotomy, radical prostatectomy)

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36
Q

What are 6 common drugs used to treat pain?

A
  1. Opioids
  2. Paracetamol (IV)
  3. NSAIDs
  4. Tricyclic antidepressants (more for chronic pain)
  5. Anticonvulsants (chronic)
  6. Sodium channel blockers (LA)
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37
Q

What are 6 examples of opioids?

A
  1. Codeine
  2. Morphine
  3. Diamorphine
  4. Fentanyl
  5. Alfentanil
  6. Remifentanil
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38
Q

How can paracetamol be administered?

A

often used orally but in recent years more commonly given IV

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39
Q

What is the mechanism of action of NSAIDs?

A

COX2 (cyclooxygenase 2) selective inhibitors

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40
Q

What are 4 examples of NSAIDs?

A
  1. ASA amino-salyclic acid aka aspirin
  2. naproxen
  3. ibuprofen
  4. Diclofenac
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41
Q

What are 2 examples of TCAs used for pain?

A
  1. Amitriptyline
  2. Nortriptyline
42
Q

What are 3 examples of anti-convulsants used for pain?

A
  1. Gabapentin
  2. Carbamazepine
  3. Valproate
43
Q

What are 2 examples of sodium channel blockers used for pain (i.e. LA)?

A

lidocaine, flecainide

44
Q

What are 2 things that NSAIDs are good analgesics for?

A
  1. Body wall
  2. orthopaedics
45
Q

What is a highly beneficial effect of NSAIDs as analgesics?

A

Excellent opioid sparing effect

46
Q

What are 5 key side effects of NSAIDs?

A
  1. peptic ulceration
  2. bronchospasm (especially aspirin)
  3. renal failure (prostaglandins used to preserve renal blood flow in hypotension, blocked by NSAIDs)
  4. blood thinning - increased bleeding and bruising
  5. hypersensitivity reactions
47
Q

Why shouldn’t NSAIDs be given in major surgery e.g. cardiac surgery?

A

they cause renal failure due to blocking the action of prostaglandins, which are naturally occuring and preserve renal blood flow in hypotension

48
Q

What type of analgesia are opioids good at?

A

Good as visceral analgesics, poor somatic analgesics

49
Q

Via which receptor do opioids act to produce analgesia?

A

mu receptor

50
Q

What is the only opioid drug that is strange and whose effects differ from the others?

A

buprenorphine - rarely used

51
Q

What are the 2 key features of opioid toxicity?

A
  1. low respiratory rate
  2. large tidal volume
52
Q

What effect does an opioid overdose have on the CO2 response curve?

A

Pushes the curve upwards - smaller response to CO2 at the same concentration

53
Q

What can occur due to the effects of opioid toxicity?

A

some people then arrest; muscles of airway patency likely to be affected; appear sleepy and drowsy then leads to obstructive respiratory arrest

54
Q

What are 4 desirable effects of opioids?

A
  1. Effective analgesia
  2. Relief of anxiety
  3. Sedation
  4. Euphoria
55
Q

What are 9 undesirable effets of opioids?

A
  1. Tolerance
  2. Dependence
  3. Dysphoria (state of unease)
  4. Nausea and vomiting
  5. Smooth muscle spasm
  6. Constipation
  7. Respiratory depression
  8. Depression of cough reflex
  9. Muscle rigidity
56
Q

What are 6 routes for administering opioid analgesia?

A
  1. Conventional IM opioid
  2. Bolus IV opioid
  3. Continuous infusion
  4. PCA: patient controlled analgesia
  5. Local nerve blocks
  6. Regional nerve blocks
57
Q

What are 2 places that bolus IV opioids are commonly used?

A

ITU, emergency units

58
Q

What are 3 disadvantages of IM opioids?

A
  1. Delay leads to discomfort - i.e. takes a while to work
  2. Heavy manpower requirements
  3. Underdose is probable
59
Q

What are 2 advantages of IV opioids?

A
  1. Simple
  2. Overdose unlikely (but underdose probable)
60
Q

What are 3 disadvantages of bolus IV opioids?

A
  1. Danger of short-term complications
  2. Large swings in plasma levels and give repeated doses: need to be careful in hypovolaemic, shocked patients
  3. Not suitable for long-term post-operative pain
61
Q

What are 3 advantages of bolus IV opioid analgesia?

A
  1. No discomfort on administration
  2. Rapid onset - useful in trauma
  3. Large swings in plasma levels means it works quickly
62
Q

What are 2 advantages of a continuous infusion of opioid for analgesia?

A
  1. Better analgesia
  2. Reduces nursing workload
63
Q

What are 3 disadvantages of continuous infusion opioid analgesia?

A
  1. Safety margin reduced
  2. unpredictable response due to large variability of patient pharmacodynamics
  3. risk of accumulation is big here
64
Q

How does patient-controlled analgesia (PCA) to deliver opioid work?

A
  • when patient presses a button they get a bolus. Then there is a pre-set lockout time.
  • can get a background infusion from some devices, so don’t fall asleep and wake up in agony
65
Q

What are 3 advantages of PCA for opioid analgesia?

A
  1. Addresses both physical and emotional components of analgesia
  2. Overdose almost impossible lif used appropriately due to lockout time
  3. Reduced nursing work
66
Q

What are 3 disadvantages of PCA to deliver opioid analgesia?

A
  1. Expensive
  2. Safety considerations imperative
  3. Need education to know how to use - not good for very young, confused, semi-conscious
67
Q

When should the decision to used PCA be decided and implemented?

A

pain team introduce it pre-operatively

68
Q

What are the 3 key steps of the WHO analgesic ladder?

A
  1. Non-opioid with/without adjuvant e.g. NSAID or paracetamol (virtually everyone gets venous paracetamol)
  2. Opioid for mild to moderate pain e.g. codeine, dyhidrocodein, co-codamol with or without a non-opioid and adjuvant
  3. Opioid for moderate to severe pain e.g. morphine, diamorphine, fentanyl, with or without a non-opioid and adjuvant
69
Q

What are 3 ways to determine the level of a patient’s pain (and thus determine which step of the WHO pain ladder to go for)?

A
  1. Scale 1-10 (Step 1: pain severity 2-5, 2: 5-8, 3: 8-10)
  2. Asking what pain prevents them from doing, e.g. sleeping
  3. Examining for altered physical signs e.g. increased respiratory and heart rates
70
Q

What is the best regimen to use when prescribing medicines and why?

A

Best to prescribe them every few hours rather than PRN, particularly in hospital, as otherwise patient is likely to be in pain between the doses

71
Q

In which 3 groups of people is there a risk of reduced renal perfusion when using NSAIDs?

A

Those who have cardiac, renal and liver problems

72
Q

What is the mechanism of action of paracetamol?

A

Not clearly understood, but known to act weakly on COX enzymes (but doesn’t explain its full effects)

73
Q

What are some example prescribing schedules for paracetamol/diclogenac/ibuprofen?

A
  • Paracetamol: 1g QDS PO
  • Diclofenac: 50mg TDS PO
  • Ibuprofen: 400mg QDS PO
74
Q

What is the maximum dose of paracetamol?

A

1g per dose (up to 2 500mg tablets) and 4g per day. Must be at least 4 hours between doses

75
Q

What are the 3 types of receptors that opioids act on in the CNS (not just pain)?

A
  • Mew µ 1 and 2
  • Kappa
  • Delta
76
Q

What are the actions of type 1 and type 2 mew opioid receptors?

A

Type 1 reduces the sensation of pain by inhibiting transmission of pain signals ascending the nerves of the spinal cord

Type 2 produces side effects e.g. constipation, drowsiness, nausea and vomiting, respiratory depression

77
Q

What are 2 drugs that can be used to treat an excess of opioid?

A

Naloxone or naltrexone

78
Q

What are example prescribing schedules for co-codamol, codeine and morphine?

A
  1. Co-codamol: 8/500, 2 tables QDS PO
  2. Codeine: 60mg QDS PO
  3. Morphine: 10mg QDS SC/IM
79
Q

What are 2 reasons why alternative analgesics may be tried?

A
  1. Pain is too chronic for patient to continue taking strong opioids
  2. No other analgesics have worked
80
Q

What are 4 alternative analgesic approaches?

A
  1. Benzodiazepines e.g. diazepam
  2. Tricyclic antidepressants e.g. amitriptyline
  3. Anticonvulsants e.g. carbamazepine
  4. Pain management programme/ physical methods e.g. nerve blocks, joint injections, acupuncture
81
Q

What type of pain are benzodiazepines good for an what is an example dosing regimen?

A

Muscle spasm

3mg TDS PO

82
Q

What are tricyclic antidepressants good analgesics for? What is an example dosing regimen?

A

Neuropathic pain

Amitryptyline 75mg NOCTE PO

83
Q

What type of pain are anticonvulsants used for?

A

Neuropathic pain

84
Q

What is the best type of analgesic for musculoskeletal pain?

A

NSAIDs

85
Q

What are 3 contraindications to prescribing NSAIDs?

A
  1. Renal impairment
  2. History of GI ulcers
  3. Caution in elderly
86
Q

What should be done when giving NSAIDs regularly?

A

Give PPI e.g. lansoprazole

87
Q

What 2 additional drugs should be considered to be given in conjunction with any opioid (including weak opioids)?

A
  1. Laxative e.g. sodium docusate
  2. Antiemetic e.g. metoclopramide
88
Q

When should nursing staff be told to contact a doctor, regarding patient’s pain relief?

A

Tell them to contact a docotr if patient needs more than 2x PRN in a 24 hour period –> may need to increase regular dose, or the regular drug isn’t working (e.g. due to vomiting, bowel obstruction, faecal loading)

89
Q

What is a key non-pharmacological pain treatment to remember?

A

TENS (massage, art therapy, acupuncture)

90
Q

If paracetamol overdose is untreated, what proportion have liver damage and what proportion die?

A
  • Liver damage: <10%
  • Mortality: <2%
91
Q

What is the mortality rate following a treated paracetamol overdose?

A

<0.4%

92
Q

What can paracetamol overdose lead to and what is this dependent on?

A

Hepatotoxicity, dose and age dependent

93
Q

What is the management of paracetamol overdose?

A
  • Minority who present <1 hour may benefit from activated charcoal to reduce absoprtion
  • N-Acetylcysteine should be given if:
    • there staggered overdose or there is doubt over time of ingestion OR
    • plasma paracetamol conc. is on or above single treatment line joining points of 100mg/L at 4 hours an 15mg/L at 15 hours
  • NAC infused over 1 hour
    • ​stop at begin again at lower rate if anaphylactoid reaction
94
Q

What are 2 instances when NAC should be given to treat paracetamol overdose?

A
  • staggered overdose or doubt over time of ingestion
  • plasma paracetamol concentration on or above a single treatment line joining points of 100mg/L at 4 hours and 15mg/L at 15 hours
95
Q

What are the King’s College Hospital criteria for liver transplantation for paracetamol liver failure?

A
  1. Arterial pH <7.3 24 hours after ingestion
  2. Or ALL of the following met:
    1. prothrombin time >100s
    2. creatinine >300umol/L
    3. grade III or IV encephalopathy
96
Q

When are opioids often given IV/IM/orally?

A

IV: emergency medicine

IM: on the ward, especially in palliative care

orally: chronic pain

97
Q

What should be monitored when giving a patient IV morphine?

A

Oxygen and pulse oximetry

98
Q

What kind of IV doses of morphine are typically given in ED to children/ adults/ the elderly?

A

children: 0.1mg/kg as initial dose

Adults: 5mg boluses IV

Elderly: 1-2.5mg boluses IV

99
Q

What form of morphine is often taken by chronic pain patients and what are typical daily doses?

A

MST - morphine sulfate. 40-200mg

100
Q
A