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Pain Management Flashcards

1
Q

classification of pain

A

acute
chronic
neuropathic
nociceptive
nociplastic

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2
Q

acute pain

A

recent onset
short duration of less than 6 weeks
associated with acute trauma
limited to the area of damage
resolves without healing

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3
Q

chronic pain

A

not associated with normal tissue healing process
persists beyond normal course of acute illness or beyond normal times

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4
Q

pain that arises from non-neural tissue damage

A

nociceptive pain

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5
Q

pain that is somatosensory and arises from neural tissue damage

A

neuropathic pain

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6
Q

pain that arises from altered nocireceptors with no clear evidence of actual or threatened tissue damage

A

nociplastic pain

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7
Q

Nociception

A

neural process of encoding noxious stimuli

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8
Q

quality of somatic pain

A

sharp, dull aching localised

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9
Q

quality of visceral pain

A

cramping squeezing that is diffuse or referred

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10
Q

quality of neuropathic pain

A

sharp, shooting electric shocks that is diffuse or dermatomal
- tingling
- numbness
- allodynia

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11
Q

hyperalgesia

A

increased pain from stimulus that normally causes pain

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12
Q

allodynia

A

pain from stimulus that doesn’t normally provoke pain

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13
Q

chronic pain mx

A
  • multi team
    a. gabapentanoids = gabapentin and pregabalin
    b. low dose TCA = amitriptyline
    c. SNRIs = venlafaxine and duloxetine
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14
Q

acute pain mx

A

Ladder
1. simple = panado, NSAIDS
2. weak = tramadol, codeine
3. strong = morphine, fentanyl

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15
Q

pain pathophysiology

A

injury –> nocireceptors stimulated and inflammatory soup sensitisation —> primary order neurons –> dorsal horn –> secondary order neurons in spin thalamic tract –> thalamus –> 3rd order –> somatosensory cortex

  • PAG inhibits facilitation
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16
Q

what makes up the inflammatory soup?

A
  • histamines
  • prostaglandins
  • bradykinin
  • serotonin
  • K
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17
Q

NSAIDS MOA

A

inhibits COX1 = physiological and COX 2 = inflammation and pain, that normally allow for prostaglandins and thromboxane, hence anti-inflammatory but also have complications

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18
Q

examples of NSAIDS

A

ibuprofen
diclofenac
indomethacin
ketorolac

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19
Q

major risk of NSAIDS in anaesthesia

A

breakdown of arachidonic acid - LOX - leurkotriene release = bronchospasm

20
Q

NSAID side effects

A
  • gastric irritation
  • renal dysfunction
  • platelet dysfunction
  • bronchospasm
  • hepatotoxicity
  • MI
21
Q

long vs short acting opioids

A

Weak opioids: codeine, tramadol

Strong opioids
Long acting: morphine
Short acting: fentanyl, remifentanil, sufentanyl & alfentanyl

22
Q

side effects of opioids

A

Nausea and vomiting
Constipation
Urinary retention
Itchiness/ pruritis
Respiratory depression
Sedation
Histamine release (morphine)
Bradycardia (fentanyl and Remi)
Muscle rigidity

23
Q

opioid antagonist

A

1-4mcg/kg/IV naloxone

24
Q

side effects of naloxone

A
  • arrhythmias
  • hypertension
  • pulmonary oedema
  • anti-analgesic
25
MOA of ketamine
NMDA receptor antagonist
26
side effects of ketamine
- bronchodilator - salivation - emergence agitation
27
where do opioids act?
at MOP / mu receptors located in the CNS and hence is centrally acting
28
useful effects in opioids
1. centrally mediated analgesia that is intense and decreased neural discharge 2. less sympathetic response 3. sedation and sometimes LOC in high doses 4. cough suppression ( methadone and codeine )
29
side effects of opioids
> resp depression > foetal distress as it crosses the placenta > chest wall rigidity > dysphoria > prolonged recovery > nausea, vomiting and constipation > addiction > severe pruritis
30
use of opioids in anaesthesia
Mainstay of intraoperative analgesia Mainly fentanyl and morphine Establishing pre-emptive analgesia Maintaining intraoperative analgesia (IV boluses or infusion) Dampening of intubation response (alfentanil) Additive to LA in neuraxial blockade Target controlled infusion of remifentanil for intraoperative analgesia Opioid-based anaesthesia Cardiovascular instability (trauma, emergencies, cardiac surgery)
31
Morphine routes and when
IV - in theatre and ICU IM - in ward every 4-6 hrs and in labour Oral = PCA, palliative care
32
morphine pro-drug that is naturally occurring with varied metabolism and is combined with there drugs
codeine
33
semi-synthetic opioids
Heroin Oxycodone
34
Synthetic opioids
pethidine fentanyl derivatives
35
Sublimaze
fentanyl
36
fentanyl onset of action
10 minutes and is intense for 30-45 mins hence best as pre-emptive analgesia
37
is fentanyl potent and why?
yes, 100 more than morphine accumulative risk for resp depression
38
can fentanyl be used in CVS instability
yes can be used in high doses where induction agents not safe
39
when else can fentanyl be used
PCA bolus and added to spinal
40
fentanyl derivative with a rapid onset of 5 minutes
afentanil = rapifen - does not cross placenta - blunting of intubation response - emergency rescue - diagnostic use for insufficient analgesia
41
pros of sufentanil
- few CVS effects - potent - good post-operative anaesthesia
42
why is remifentanil unique?
Ultra-short acting, spontaneous recovery regardless of dose - metabolised out after 10 minutes
43
how is Remi given?
IV infusion pump
44
indications for Remi
sleep apnea obesity avoiding resp depression deep intra-op required ** NEED ADDED ANALGESIA AFTER
45
weak synthetic opioid and MOA
tramadol - act on NA and serotonin receptors - usually combined
46
naloxone use
Rapidly displaces opioids from receptors Useful for emergency management of respiratory depression Neonates: opioid reversal in mothers who have received opioids in labour or as part of GA pre-delivery Diagnostic value NOT A CURE—patient must be carefully monitored as opioids can bind again Sudden opioid withdrawal can be extremely distressing for the patient

Anaesthesia (10 decks)

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