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BB2 > Pharmacology of Pain > Flashcards

Pharmacology of Pain Flashcards

1
Q

How can pain occur within seconds to minutes?

A

Activation of nociceptive/specific wide dynamic range neurons proportional to intensity of stimulus

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2
Q

How can pain occur within minutes to days?

A

Sensitisation of nerve terminals at the injury site and delayed central sensitisation

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3
Q

How can pain occur within days to months?

A

Changes in supply of trophic growth factors, sprouting of fibres, abnormal innervation and trans-synaptic degeneration

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4
Q

What are the 3 types of pain?

A
  • nociceptive (acute noxious mechanical/thermal/electrical stimuli)
  • inflammatory (semi-acute or chronic ischaemia/infection/local degeneration)
  • neuropathy (chronic maladaptive plasticity/disease affecting somatosensory nervous system)
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5
Q

What is the formation of the local circuits in the dorsal horn?

A
  • first synapse between C fibre and dorsal neuron releases multiple transmitters which bind to various receptors
  • NO, PG, glutamate
  • interneuron modulates neuron so multitude of possible targets even just at first synpase
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6
Q

What is the role of opoids?

A

In the efferent pathway:

  • activate PAG
  • inhibits transmission directly at first synapse
  • activates NRPG
  • inhibits transmission at secondary neuron in periphery
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7
Q

Which parts of the brain do nociceptive stimuli activate?

A
  • spinal cord
  • thalamus
  • somatosensory cortex
  • anterior cingulate cortex
  • insula
  • amygdala
  • prefrontal cortex
  • hippocampus
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8
Q

What factors influence pain perception?

A
  • cognition (attention/distraction/control/hypervigilance)
  • mood (depression/anxiety)
  • context (beliefs/expectations/placebo)
  • chemical and structures (atrophy/dopaminergic dysfunction)
  • injury (peripheral and central sensitisation)
  • genetics
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9
Q

Which factors modulate the risk of developing chronic pain?

A
  • hardware at birth (gender, genotype, epigenetic profile)
  • environmental influences (acute injury/disease at critical developmental periods, stressful life events)
  • gene + environment interactions (personality and psychology - pessimism/anxiety)
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10
Q

What are the 3 main families of opoids?

A

Proopiomelanocortin
Proenkephalin
Prodynorphin

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11
Q

What are the main receptors which opoids act on?

A
  • Mu (1 and 2, widespread)
  • Delta (1 and 2)
  • Kappa (1,2,3)
  • also pro-nociceptive endogenous systems such as CCK
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12
Q

What explains the broad spectrum of effects of opoids?

A
  • Mu receptors being widely distributed
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13
Q

What are the problems of direct administration of opoids?

A

Very short half-lives so rapidly inactivated in circulation

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14
Q

Why can Mu receptors be negative?

A
  • when opoids bind react most intensely which can cause adverse effects:
  • increased dependence, respiratory depression, pupillary constriction
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15
Q

How can receptors to opoids be targeted in different patients?

A
  • cause difference is responses
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16
Q

What are the 3 types of analgesia?

A

Supraspinal
Spinal
Peripheral

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17
Q

Which opoid receptors cause supraspinal analgesia?

A

Mu receptors

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18
Q

Which opoid receptors cause spinal analgesia?

A

Mu receptors
Delta receptors
Kappa receptors may

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19
Q

Which opoid receptors cause peripheral analgesia?

A

Mu receptors

Kappa receptors

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20
Q

Which opoid receptors cause pupillary depression?

A

Mu receptors highly
Delta receptors
Kappa receptors may

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21
Q

Which opoid receptors cause pupillary constriction?

A

Mu

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22
Q

Which opoid receptors cause reduced GI motility?

A

Mu
Delta
kappa may

23
Q

Which opoid receptors cause sedation?

A

Mu

Kappa

24
Q

Which opoid receptors cause euphoria?

A

Mu

25
Q

Which opoid receptors cause dysphoria?

A

KAPPA!!!

26
Q

Which opoid receptors cause dependence?

A

Mu!!!

27
Q

What effects may opoids have on the CNS?

A 
Analgesia,
nausea & vomiting
Respiratory depression
Drowsiness/lethargy
Miosis
28
Q

What effects may opoids have on the CV system?

A

Hypotension

29
Q

What effects may opoids have on the GI system?

A

Delayed gastric emptying

30
Q

What are some examples of opoids?

A
  • morphine
  • heroin
  • dextromoramide
  • methadone
  • meptazinol
  • pethidine
31
Q

What is the mechanism of morphine?

A

Forms active metabolite M6G

  • decreased excitability and release of neurotransmitters
  • activation of K+ conductance and decreased Ca2+ conductance
32
Q

What is the mechanism of heroin?

A

High solubility compared to morphine

- cachexia is drug of choice

33
Q

What is the mechanism of dextromoramide?

A

Active sublingually

34
Q

What is the mechanism of methadone?

A

Half life increases on repeated dosing

35
Q

What is the mechanism of meptazinol?

A

U1 receptor agonist

36
Q

What is the mechanism of pethidine?

A

Forms metabolite

37
Q

What is the significance of tolerance?

A
  • not equivalent to development of addiction
  • not important in terms of chronic pain
  • natural neurobiological adaptation
38
Q

What is the significance of personalised analgesia?

A

Patient variability
Affects different backgrounds
Possible to switch opoid when patient is becoming tolerant

39
Q

What are the main non-opoids?

A
  • paracetamol
  • NSAIDs
  • anticonvulsants
  • tricyclic antidepressants
40
Q

How does paracetamol work?

A

Reduces active oxidised form of COX2

Analgesic, antipyretic, little anti-inflammatory effect

41
Q

How do NSAIDs work?

A

Inhibit COX2

42
Q

What are examples of NSAIDs? What do they do?

A
  • aspirin (COX1 and 2 inhibitor and anti-inflammatory
  • ibuprofen/diclofenac/ketoprofen (COX1 and 2 inhibitiors)
  • rofecoxib (selective COX2 inhibitors)
43
Q

What are some indications for non-opoids?

A 
Rheumatoid arthiritis
Osetoarthiritis
Dysmenorrhea
Gout
Muscle Spasms
44
Q

What are the side effects of non-opoids?

A

Nausea

GI bleeding

45
Q

What are anticonvulsant used for?

A
  • neuropathic pain and trigeminal neuralgia
46
Q

What are some examples of anticonvulsants and what do they act on?

A
  • carbamazepine (Na+ channels)
  • sodium valproate (Na+ channels)
  • pregabalin (Alpha2delta subunit)
47
Q

What is an example of a tricyclic anti-depressant and how does it work?

A
  • amitriptyline

- inhibit reuptake of amine, block Na+ and Ca2+ channels

48
Q

What is the WHO analgesics ladder for pain management?

A

1) Non-opoids and adjuvant
2) Moderate efficacy opoids - codeine (+1)
3) High efficacy opoids - morphine (+1)

49
Q

Which drugs should be used for complex pain types?

A
  • antidepressants
  • anticonvulsants
  • calcium channel ligands (gabapentin)
  • vanilloid receptor agonists (capsaicin)
  • NMDA glutamate receptor antagonists
  • GABA receptor agonists
  • opoid agonists (tramadol)
  • local anaesthetics
50
Q

How should you manage neuropathic pain?

A

1) offer convulsant or TCA + calcium channel ligands
2) try switching if initial drug is not tolerant
3) consider tramadol if acute rescue therapy needed
4) capsaicin cream if oral treatment not tolerated

51
Q

How do local anaesthetics work?

A
  • block sodium channels (risk of systemic toxicity = hypotension/respiratory depression)
  • administered through surface/infiltration/epidural
52
Q

What are examples of local anaesthetics?

A

Lignocaine

Prilocaine

53
Q

How do general anaesthetics work?

A

Activation of inhibitory receptors/inhibition of excitatory receptors
- induce CV depression so monitored in surgery

BB2 (31 decks)

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