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Neuropharmacology > Lecture 12 > Flashcards

Lecture 12 Flashcards

1
Q

Definition of pain

A

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

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2
Q

What affects pain experience?

A
  • context - previous experience - expectation - culture - attention - anxiety
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3
Q

What are the effects of pain behaviour which decrease quality of life?

A
  • withdrawal from social network - physical deconditioning - helplessness, depression
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4
Q

What are the two pain pathways?

A
  • peripheral nociceptive afferent neurons - central mechanisms
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5
Q

What is the peripheral pain pathway?

A

Afferent neurons are activated by noxious stimuli

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6
Q

What is the central mechanisms pathway?

A

Afferent input generates a pain sensation

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7
Q

What can go wrong with the central mechanisms?

A

Conditions like stroke and infection can lead to chronic pain without tissue damage- pain circuit becomes hypersensitive

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8
Q

Which type of fibre is responsible for fast pain e.g. sharp, short, localised pain?

A

A𝛿 fibres

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9
Q

Which type of fibre is responsible for slower pain e.g. dull, diffuse, poorly localised pain?

A

C fibres

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10
Q

What are the features of A𝛿 fibres?

A
  • myelinated - 1-5µm diameter - fast conductance - mechanosenstive - temperature sensitive
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11
Q

What are the features of C fibres?

A
  • unmyelinated - 0.1-1.5µm diameter - slow conductance - mechanosensitive - temperature sensitive - chemical (capaiscin) etc
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12
Q

How do you knock out A𝛿 fibres and what would you expect to happen?

A
  • anoxia - loss of fast pain sensation
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13
Q

How do you knock out C fibres and what would you expect to happen?

A
  • local anaesthetics - loss of slow pain sensation
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14
Q

What would you expect if both A𝛿 and C fibres were knocked out?

A

No pain sensation

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15
Q

What is released by both A𝛿 and C fibres?

A
  • glutamate - neuropeptides e.g. substance P
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16
Q

Can you block A𝛿 and C fibres using neuromuscular blocking agents?

A

No because acetylcholine is not involved in pain transmission- glutamate is

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17
Q

What is one theory of why both fast and slow pain exist?

A
  • rapid withdrawal (prevent further damage) - immobilisation (healing)
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18
Q

How does head and neck pain enter the CNS?

A

Via trigeminal nerve

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19
Q

What are the areas associated with the spinothalamic tract?

A

Spinal cord > medulla > pons > midbrain > thalamus > somatosensory cortex

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20
Q

What root does pain enter?

A

Dorsal root

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21
Q

What is the substantia gelatinosa?

A

the dorsal region of the spinal cord where both fast and slow pain fibers synapse with sensory neurones at the spinal cord

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22
Q

According to the gate theory, what pathways modulate pain sensation?

A

Descending pathways (either analgesic or hypersensitive)

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23
Q

What is the gate theory of pain?

A

Pain sensation is reduced when a distractive somatosensory signal activates larger peripheral nerve fibres, activating inhibitory interneurons which inhibits pain sensation from reaching the brain

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24
Q

What are the emotional effects of pain?

A
  • loss of motivation - depression, loss of appetite - loss of self-esteem and confidence
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25
What are the three origins of the three descending pathways?
- cortex - reticular formation - raphe nuclei
26
What is a key component of the descending system?
The periaqueductal gray (PAG)
27
Why is the PAG a key part of the descending pathway?
Acts through various nuclei and can produce inhibition of pain
28
What is an opiate?
Describes drugs derived from the opium poppy Papaver somniferum
29
What is an opioid?
Refers to both opiates and synthetic substances
30
What are the CNS effects of opioids?
- profound analgesia (acute and chronic pain)- respiratory depression (PCO2 sensitivity of respiratory centre in medulla) - nausea and vomiting (activates medulla chemotrigger zone)
31
How do we stimulate breathing in patients who have taken opioid drugs?
For a given CO2, it does not become effective at driving breathing, therefore we need larger increases in CO2
32
What are the further CNS effects of opioids?
- euphoria, contentment and well-being - dry mouth - drowsiness - depression of cough reflex (Pholcodeine) - pupillary constriction (stimulation of occulomotor nucleus)
33
What are the effects of opioids on the GI tract?
- increases tone and reduces gut motility - constipation - delays gastric emptying (slows drug absorption)
34
What are the effects of opioid on histamine?
- urticaria (hives) - bronchoconstriction (bronchospasm), hypotension
35
What are the effects of opioid antagonists?
Reverse the effects of opioid analgesics
36
What evidence suggested that there are opioid receptors?
- opioid antagonists - strict structure-activity relationship
37
How were the opioid receptors first identified?
- binding study - labelled radioisotopes of morphine - looked at the binding curve to identify whether there was specific binding - identified as the μ opioid receptor
38
How were endogenous opioids discovered?
- fractionated assays morphine derivatives - compound must induce contractions in ileum - must be blocked by an antagonist e.g. naloxone
39
What are the two types of endogenous opioid peptides?
- enkephalins - endorphins
40
Where are opioid peptides distributed?
- areas associated with nociception (PAG, rostral ventral medulla, substantia gelatinosa) - periphery in adrenal medulla, heart, kidney etc (role is unclear)
41
Where are enkephalins distributed?
Diffuse distribution so may play a role in many processes
42
Where are β endorphins distributed?
- less diffuse distributions - hypothalamus which send projections to PAG and noradrenergic nuclei in brain stem
43
What is the role of endogenous opioid peptides?
- modulate pain perception - reward - stress response - autonomic control
44
How do opioid analgesics affect endogenous opioid ligands?
Either replace or supplement the endogenous ligands
45
What is the evidence for multiple opiate receptors?
- many different opioid analogs - different effects in different parts of the body - studies using cross-tolerance and withdrawal suggested at least 3 different receptor subtypes
46
What is a physiological example for how we know there are different opioid receptor subtypes?
- guinea pig ileum= morphine > enkephalins for inhibiting induced contractions (potently blocked by naloxone) - vas deferens= enkephalins > morphine for inhibiting induced contractions (weakly blocked by naloxone)
47
What are the opiate receptor subtypes?
- mu (MOP) - delta (DOP) - kappa (KOP)
48
Where are MOP receptors distributed?
- CNS and periphery - cortex - thalamus - PAG - rostral ventral medulla - substantia gelatinosa
49
Where are KOP receptors distributed?
- hypothalamus - PAG - substantia gelatinosa
50
Where are DOP receptors distributed?
- pontine nuclei - amygdala - olfactory bulb - cortex
51
What are the side effects of MOP receptor activation?
- respiratory depression - reduce gastrointestinal motility - euphoria in the VTA - high physical dependence
52
Which receptor subtypes do clinical agonists and antagonists target?
MOP
53
What type of receptors are opioid receptors?
GPCRs
54
What are the mechanisms of opioid GPCR activation?
- inhibit Ca2+ channels - activate K+ channels - inhibit cAMP
55
How are the opioid peptides stored and how do they become involved in transmission?
- stored as large protein molecules - active components get cleaved off
56
What are the main effects of opioid on pain transmission?
- directly inhibit pain perception by acting at the spinal cord (lamina II) - increase descending inhibition (euphoria)
57
What is tolerance?
Increase in doses required to produce a pharmacological effect
58
Describe opioid tolerance
- occurs rapidly, and affects most opioid effects, including analgesia, euphoria and respiratory depression - less so to constipation and pupil-constriction
59
What are the mechanisms of opioid tolerance?
- receptor desensitisation - phosphorylation - receptor internalisation
60
Describe the pharmacokinetics of opioids
- short half life, erratic oral absorption - hepatic metabolism and some undergo entero-hepatic cycling - used on demand (infusion pump, patient-controlled anaesthesia (PCA))
61
What are some examples of opioid analgesics?
- morphine - fentanyl - codeine - pethidine - methadone
62
Morphine as an opioid analgesic
- acute and chronic pain - premedication, postoperative pain, myocardial infarction - injected and oral formulation
63
What is diamorphine (heroin)?
- powerful analgesic - less nausea than morphine - greater water solubility so can be used in palliative care when patient is emaciated
64
Fentanyl as an opioid analgesic
- acute pain and anaesthesia - 100X more potent than morphine - rapid onset and short duration - failed attempt to cut heroin and cocaine use
65
Codeine as an opioid analgesic
- naturally occurring in opium - weaker analgesic than morphine - less respiratory depression than morphine - less liable to produce constipation - co-codamol= combined with paracetamol
66
Pethidine as an opioid analgesic
- short-lasting analgesia, less potent than morphine - antimuscarinic (dry mouth, blurred vision) - less constipating than morphine - analgesia in labour without forced contractions - eliminated in neonates with naloxone
67
What are examples of opioid antagonists?
- nalorphine, naloxone, naltrexone
68
Which opioid antagonist is non-competitive?
Nalorphine
69
Why would you use an opioid antagonist?
- overdose - respiratory depression in babies - precipitates withdrawal in addicts
70
What is an example of a partial opioid agonist?
Buprenorphine
71
Why would you use buprenorphine?
- less respiratory depression than morphine but has similar effects - chronic pain and dependence - precipitates withdrawal in patients dependent on morphine

Neuropharmacology (15 decks)

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