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ANAESTHETICS & PERI-OPERATIVE MEDICINE > 1: Pain Management > Flashcards

1: Pain Management Flashcards

1
Q

define pain and distinguish between acute and chronic pain

A

pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage
- acute: painful with rapid onset/short course
- chronic: painful persisting beyond the normal time of healing

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2
Q

how is pain transmitted

A

nociceptors

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3
Q

what are nociceptors

A

free nerve endings of afferent neurones that transmit pain perception via spinothalamic tract

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4
Q

what do nociceptors respond to

A
  • mechanical deformation (e.g. severe pressure)
  • excessive heat
  • certain chemicals
  • neuropeptide transmitters e.g. bradykinin, histamine, cytokines, prostaglandins)
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5
Q

all sensory information transmitted to the CNS can be modulated - how can afferent neurone transmission be inhibited

A
  • collateral branches of other ascending neurones
  • cerebral cortices via descending neurones
  • specific synapses (indirect inhibition)
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6
Q

how is pain modulated (3)

A
  • afferent input from nociceptors is continually inhibited
  • allows ‘disinhibition’ during severe tissue damage which increases pain signal
  • allows complete inhibition to completely block pain signal
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7
Q

how can pain be augmented

A
  • emotion e.g. anxiety
  • suggestion
  • activation of other sensory modalities
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8
Q

what are risk factors for developing chronic pain

A

patient factors
- pyschological
- female
- younger age
- genetics
- depression

medical factors
- repeat surgery
- nerve damage
- RT to area
- duration of postop pain treatment

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9
Q

what is hyperalgesia

A

increased pain sensation to the same stimulus (pain perception disproportionate to the stimulus)

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10
Q

what is allodynia

A

sensation of pain in absence of painful stimulus

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11
Q

what are the benenfits of post-op analgesia

A
  • ↓ sympathetic effects of pain
  • earlier mobilisation
  • ↓ risk of post op resp complications
  • ↓ chronic pain syndromes
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12
Q

what key aspects of assessment of pain

A
  1. history
    - SQITARS
    - effects on function
    - response to treatment
    - medical/surgical hx
  2. examination
    - obs e.g. HR, BP, RR
    - spO2 - pain may lead to desaturation in adults
    - exam of painful site
    - mobilising without pain?
    - deep breathing
    - able to eat/drink where appropriate
  3. qualitative
    - pt describes pain
    - appearance e.g. sweating, distress
  4. pain measurement tools
    - categorical scales
    - VAS
    - NRS
    - paediatric faces
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13
Q

WHO pain ladder

A

minimal side effects but most analgesic benefit

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14
Q

what is the MOA of paracetamol

A

? inhibits PG synthesis in CNS
? modulates endogenous cannabinoid system

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15
Q

what are the side effects of paracetamol

A
  • CVS: hypotension and bradycardia if given rapid IV
  • CNS: analgesia and antipyretic
  • rare: rash, idiopathic thrombocytopenia
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16
Q

what is the absorption/distribution of paracetamol

A
  • absorbed in small bowel
  • 80% oral bioavailability
  • 10% protein bound
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17
Q

what is the dosing of paracetamol

A
  • adults >50kg: 1g, 6 hourly
  • children & adults <50kg: 15mg/kg 6 hourly
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18
Q

what is the metabolism/excretion of paracetamol

A
  • hepatic metabolism to glucoronide, excreted in urine
  • 10% metabolised by P450 system to toxic NAPQI (genetic enzyme polymorphism determines amount of NAPQI produced)
  • normal dose: NAPQI conjugated by glutathione and harmless product excreted in urine
  • overdose: glutathione exhausted and NAPQI accumulation –> liver failure
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19
Q

what is the MOA of NSAIDs

A

inhibits cyclo-oxygenase which reduces the production of inflammatory prostanoids e.g. PG, thromboxane, prostacyclin

20
Q

what is the function of prostacyclin

A
  • vasodilator
  • prevents platelet plug formation
21
Q

what is the function of thromboxane

A
  • vasoconstrictor
  • potent platelet aggregator
22
Q

what are the functions of various PGs

A
  • PGE2: ↓ gastric acid secretion, ↑ gastric mucous secretions
  • PGI2: vasodilation, platelet aggregation
  • PGF2: uterine contraction, bronchoconstriction
23
Q

what is the mechanism of NSAID-induced asthma

A

leukotriene production ↑ due to COX inhibition

24
Q

give examples of non-selective COX inhibitors

A

aspirin
ibuprofen
diclofenac

25
Q

give an example of a selective COX-2 inhibitor

A

parecoxib

26
Q

how are NSAIDs absorbed/distributed

A
  • significant first pass metabolism, well absorbed by all routes
  • highly protein bound
27
Q

how are NSAIDs metabolised/excretion

A

hepatic metabolsim, excreted in bile

28
Q

what are the side effets of NSAIDs

A
  • bronchospasm sensitivity in 20% asthmatics
  • ↓ PG required to maintain gastric mucosal intregity
  • PG & prostacyclin inhibition –> local hypoxia and ↓ renal perfusion for potential for AKI
  • reversible inhibition of platelet function
29
Q

what are opioids

A

synthetic substances that stimulate opioids receptors e.g. fentayl, alfentanil

30
Q

give 4 types of opioid receptors

A
  • MOP µ
  • KOP k
  • DOP δ
  • NOP (nociceptin)
31
Q

what is tolerance

A

decreasing response to repeated dosing of drug - over time a larger dose is required to produce the same effect

32
Q

what is dependence

A

requirement for repeated administration of a drug to avoid withdrawal symptoms

33
Q

what is addiction

A

patient’s behaviour as a result of their drug dependence e.g. lack of control, cravings, drug-seeking, compulsiveness

34
Q

state some opioid withdrawal symptoms

A
  • anxiety and fear
  • adrenergic hyperactivity
  • malaise
  • abdo cramps
  • sweating
  • yawning
35
Q

what is the MOA of morphine

A

MOP & KOP agonist - stimulates pre-synaptic GPCRµ
- closure of VGCC
- ↓cAMP production
- K+ efflux
- hyperpolarisation of cell membrane
- ↓ excitability of the cell - ↓NT release - reduced pain transmission

36
Q

what is the absorption/distribution of morphine

A
  • good oral absorption from SB - extensive first pass metabolism
  • 15-20% oral F, 20-40% protein bound
  • peak effect 10-30 mins, duration 3-4 hours
37
Q

what is the metabolism/excretion of morphine

A
  • hepatic metabolism to morphine-3-glucuronide (inactive) and morphine-6-glucoronide (x13 potency)
  • ‼️ liver impairment
  • excreted in urine - active metabolites accumulates in renal failure
38
Q

what are CVS side effects of morphine

A
  • no direct effects
  • hypotension if histamine release occurs
  • mild bradycardia due to ↓ sympathetic tone
39
Q

what are respiratory side effects of morphine

A
  • dose dependent resp depression
  • ↓sensitivity to rising pCO2
  • antitussive
  • bronchospasm if histamine release
40
Q

what are CNS side effects of morphine

A
  • analgesia
  • sedation
  • euphoria
  • hallucinations
  • meiosis via EDW nucleus
  • seizures/muscle rigidity at high doses
41
Q

what are GI side effects of morphine

A
  • ↓ motility
  • ↓ gastric acid, pancreatic, bile secretions
  • N&V - CTZ stimulation via 5HT3 & dopamine receptors
42
Q

GO

what are GU side effects of morphine

A

↑ tone in bladder detrusor and sphincter muscles - urinary retention

43
Q

what are skin side effects of morphine

A

rash
pruritus

44
Q

what are endocrine side effects of morphine

A
  • ↓ACTH
  • ↓ gonadotrophic hormones
  • ↑ ADH causing hypernatremia & water retention
45
Q

what is regional analgesia

A

targeted analgesia depending on specific surgery e.g. complexity, site, etc
- optimises peri-op analgesia to enhance recovery & reduce requirement for systemic meds esp opiates

46
Q

give 3 subtypes of regional analgesia

A
  • neuraxial blocks e.g. spinal (intrathecal morphine single shot), epidural (thoracic/lumbar)
  • truncal regional nerve blocks e.g. TAP, rectus sheath block +/- continuous infusion via nerve catheter, ilioinguinal
  • peripheral nerve blocks e.g. fem/pop, brachial plexus

ANAESTHETICS & PERI-OPERATIVE MEDICINE (5 decks)

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