Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What affects pain experience?

A
  • context - previous experience - expectation - culture - attention - anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
  • withdrawal from social network - physical deconditioning - helplessness, depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the two pain pathways?

A
  • peripheral nociceptive afferent neurons - central mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the peripheral pain pathway?

A

Afferent neurons are activated by noxious stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the central mechanisms pathway?

A

Afferent input generates a pain sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

A𝛿 fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

C fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of A𝛿 fibres?

A
  • myelinated - 1-5µm diameter - fast conductance - mechanosenstive - temperature sensitive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the features of C fibres?

A
  • unmyelinated - 0.1-1.5µm diameter - slow conductance - mechanosensitive - temperature sensitive - chemical (capaiscin) etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A
  • anoxia - loss of fast pain sensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A
  • local anaesthetics - loss of slow pain sensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

No pain sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is released by both A𝛿 and C fibres?

A
  • glutamate - neuropeptides e.g. substance P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A
  • rapid withdrawal (prevent further damage) - immobilisation (healing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does head and neck pain enter the CNS?

A

Via trigeminal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the areas associated with the spinothalamic tract?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What root does pain enter?

A

Dorsal root

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Descending pathways (either analgesic or hypersensitive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the emotional effects of pain?

A
  • loss of motivation - depression, loss of appetite - loss of self-esteem and confidence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the three origins of the three descending pathways?

A
  • cortex - reticular formation - raphe nuclei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is a key component of the descending system?

A

The periaqueductal gray (PAG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why is the PAG a key part of the descending pathway?

A

Acts through various nuclei and can produce inhibition of pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is an opiate?

A

Describes drugs derived from the opium poppy Papaver somniferum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is an opioid?

A

Refers to both opiates and synthetic substances

30
Q

What are the CNS effects of opioids?

A
  • profound analgesia (acute and chronic pain)- respiratory depression (PCO2 sensitivity of respiratory centre in medulla) - nausea and vomiting (activates medulla chemotrigger zone)
31
Q

How do we stimulate breathing in patients who have taken opioid drugs?

A

For a given CO2, it does not become effective at driving breathing, therefore we need larger increases in CO2

32
Q

What are the further CNS effects of opioids?

A
  • euphoria, contentment and well-being - dry mouth - drowsiness - depression of cough reflex (Pholcodeine) - pupillary constriction (stimulation of occulomotor nucleus)
33
Q

What are the effects of opioids on the GI tract?

A
  • increases tone and reduces gut motility - constipation - delays gastric emptying (slows drug absorption)
34
Q

What are the effects of opioid on histamine?

A
  • urticaria (hives) - bronchoconstriction (bronchospasm), hypotension
35
Q

What are the effects of opioid antagonists?

A

Reverse the effects of opioid analgesics

36
Q

What evidence suggested that there are opioid receptors?

A
  • opioid antagonists - strict structure-activity relationship
37
Q

How were the opioid receptors first identified?

A
  • 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
Q

How were endogenous opioids discovered?

A
  • fractionated assays morphine derivatives - compound must induce contractions in ileum - must be blocked by an antagonist e.g. naloxone
39
Q

What are the two types of endogenous opioid peptides?

A
  • enkephalins - endorphins
40
Q

Where are opioid peptides distributed?

A
  • areas associated with nociception (PAG, rostral ventral medulla, substantia gelatinosa) - periphery in adrenal medulla, heart, kidney etc (role is unclear)
41
Q

Where are enkephalins distributed?

A

Diffuse distribution so may play a role in many processes

42
Q

Where are β endorphins distributed?

A
  • less diffuse distributions - hypothalamus which send projections to PAG and noradrenergic nuclei in brain stem
43
Q

What is the role of endogenous opioid peptides?

A
  • modulate pain perception - reward - stress response - autonomic control
44
Q

How do opioid analgesics affect endogenous opioid ligands?

A

Either replace or supplement the endogenous ligands

45
Q

What is the evidence for multiple opiate receptors?

A
  • 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
Q

What is a physiological example for how we know there are different opioid receptor subtypes?

A
  • 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
Q

What are the opiate receptor subtypes?

A
  • mu (MOP) - delta (DOP) - kappa (KOP)
48
Q

Where are MOP receptors distributed?

A
  • CNS and periphery - cortex - thalamus - PAG - rostral ventral medulla - substantia gelatinosa
49
Q

Where are KOP receptors distributed?

A
  • hypothalamus - PAG - substantia gelatinosa
50
Q

Where are DOP receptors distributed?

A
  • pontine nuclei - amygdala - olfactory bulb - cortex
51
Q

What are the side effects of MOP receptor activation?

A
  • respiratory depression - reduce gastrointestinal motility - euphoria in the VTA - high physical dependence
52
Q

Which receptor subtypes do clinical agonists and antagonists target?

A

MOP

53
Q

What type of receptors are opioid receptors?

A

GPCRs

54
Q

What are the mechanisms of opioid GPCR activation?

A
  • inhibit Ca2+ channels - activate K+ channels - inhibit cAMP
55
Q

How are the opioid peptides stored and how do they become involved in transmission?

A
  • stored as large protein molecules - active components get cleaved off
56
Q

What are the main effects of opioid on pain transmission?

A
  • directly inhibit pain perception by acting at the spinal cord (lamina II) - increase descending inhibition (euphoria)
57
Q

What is tolerance?

A

Increase in doses required to produce a pharmacological effect

58
Q

Describe opioid tolerance

A
  • occurs rapidly, and affects most opioid effects, including analgesia, euphoria and respiratory depression - less so to constipation and pupil-constriction
59
Q

What are the mechanisms of opioid tolerance?

A
  • receptor desensitisation - phosphorylation - receptor internalisation
60
Q

Describe the pharmacokinetics of opioids

A
  • short half life, erratic oral absorption - hepatic metabolism and some undergo entero-hepatic cycling - used on demand (infusion pump, patient-controlled anaesthesia (PCA))
61
Q

What are some examples of opioid analgesics?

A
  • morphine - fentanyl - codeine - pethidine - methadone
62
Q

Morphine as an opioid analgesic

A
  • acute and chronic pain - premedication, postoperative pain, myocardial infarction - injected and oral formulation
63
Q

What is diamorphine (heroin)?

A
  • powerful analgesic - less nausea than morphine - greater water solubility so can be used in palliative care when patient is emaciated
64
Q

Fentanyl as an opioid analgesic

A
  • acute pain and anaesthesia - 100X more potent than morphine - rapid onset and short duration - failed attempt to cut heroin and cocaine use
65
Q

Codeine as an opioid analgesic

A
  • naturally occurring in opium - weaker analgesic than morphine - less respiratory depression than morphine - less liable to produce constipation - co-codamol= combined with paracetamol
66
Q

Pethidine as an opioid analgesic

A
  • 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
Q

What are examples of opioid antagonists?

A
  • nalorphine, naloxone, naltrexone
68
Q

Which opioid antagonist is non-competitive?

A

Nalorphine

69
Q

Why would you use an opioid antagonist?

A
  • overdose - respiratory depression in babies - precipitates withdrawal in addicts
70
Q

What is an example of a partial opioid agonist?

A

Buprenorphine

71
Q

Why would you use buprenorphine?

A
  • less respiratory depression than morphine but has similar effects - chronic pain and dependence - precipitates withdrawal in patients dependent on morphine

Neuropharmacology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions