opioids Flashcards
(106 cards)
1
Q
what are narcotic analgesics
A
drugs that produce analgesia - reduction of pain without anaesthesia but promote a sense of relaxation and sleep and at overdoses lead to coma and death
2
Q
what are the acute effects of opioids
A
- analgesia
- cough suppression
- respiratory depression
- relaxation and sleep
- decreased blood pressure
- constipation
3
Q
what are withdrawal signs of opioids
A
- pain and irritability
- panting and yawning
- dysphoria and depression
4
Q
what are the physiological effects of heroin
A
- crosses blood brain barrier more quickly
- strong high
- heroin is converted to morphine in the brain
5
Q
what are the physiological effects of codeine
A
- less analgesic
- less side effects and less addictive
- potent cough suppression
6
Q
what is naloxone
A
- opioid receptor antagonist
- blocks effect of opioid
7
Q
what is the history of opioid use and misuse
A
- medical use
- recreational use
- today - medical use is strictly regulated and recreational use is illegal
8
Q
what is the main cause of overdose deaths
A
opioids
9
Q
where is the highest opioid use
A
united states
10
Q
what are signs of opioid overdose
A
- respiratory depression
- miosis - pupil constriction
- stupor - unresponsiveness
- hepatic injury
- hypothermia
11
Q
how can opioid overdose be treated
A
opioid overdose can be treated by an injection with the opioid antagonist naloxone
12
Q
what are the four types of opioid receptors
A
- mu
- kappa
- delta
- nociceptin
13
Q
what hormone is produced from the mu receptor
A
- endomorphins and endorphins (POMC)
14
Q
what hormone is produced from the delta receptor
A
enkephalin an endorphins
15
Q
what hormone is produced from the kappa receptor
A
- dynorphins
16
Q
what hormone is produced from the nociceptin receptor
A
nociceptin
orphanin FQ
17
Q
where is the mu receptor and what is it’s function
A
- thalamus, periaqueductal gray, raphe nuclei, spinal cord, striatum, brain stem, nucleus accumbens, amygdala, hippocampus
- analgesia, reinforcement feeding, cardiovascular and respiratory depression, antitussive, vomiting, sensorimotor integration
18
Q
location and function of delta receptor
A
- neocortex, striatum, olfactory areas, substantia nigra, nucleus accumbens, spinal cord
- analgesia, reinforcement, cognitive function, olfaction, motor integration
19
Q
function and location of the kappa receptor
A
pituitary, hypothalamus, amygdala, striatum, nucleus accumbens
- neuroendocrine function, water balance, feeding, temperature control, dysphoria, analgesia
20
Q
location and function of the nociceptin receptor
A
- cortex, amygdala, hypothalamus, hippocampus, periaqueductal gray, thalamus, substantia nigra, brain stem, spinal cord
- spinal analgesia, supraspinal pronociception, feeding, learning, motor function, neuroendocrine function
21
Q
where are peripheral opioid receptors
A
- peripheral nerve endings
- gastrointestinal tract
22
Q
what type of receptors are opioid receptors
A
g-protein coupled receptors
23
Q
what is a g protein
A
- after activation from opioid - knock on effects mediate other responses e.g. interactions with ion channels, depolarisation or another enzyme
24
Q
what does activation of opioid receptors tend to do
A
- inhibit neural activity or neurotransmitter release of the neurons carrying the opioid receptor.
25
what happens in postsynaptic inhibition
- opioid receptors sit on the postsynaptic neuron
- opening of potassium channels
- inhibition of neuron
26
what happens in axoaxonic inhibition
- closing of calcium channels from opioids
- reducing neurotransmitter release
27
what happens in presynaptic autoreceptors
- inhibition of neurotransmitter release from presynaptic terminal
28
what is the definition of pain
- an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
29
what is the definition of nociception
- the neural process of encoding noxious stimuli i.e. stimuli causing tissue damage
30
what is the definition of chronic pain
- pain that lasts or recurs for longer than 3 months, can be symptoms of disease in itself i.e. with no clear relation to tissue damage - affects about 20% people world wide
31
what is the leading cause of disability in the UK
pain
32
what happens is the function of the ascending pathway
- transmits pain signals from the body to the brain
33
what is the function of the descending pain pathway
- modulates pain signals, often inhibiting them
34
where do primary sensory neurons originate
- in the dorsal root ganglion
35
what type of fibers are associated with 'second/slow/late' pain
c fibers
36
what type of fibers are associated with first/fast pain
a-delta fibers
37
where does the brain signal travel after leaving the dorsal horn of the spinal cord
to the thalamus
38
where does the pain signal travel after the thalamus
- to the somatosensory cortex
39
what is the role of the somatosensory cortex in pain perception
- it processes and localises pain
40
where does the descending pain pathway originate
in the midbrain, specifically the periaqueductal gray
41
what is the function of the periaqueductal gray in the descending pathway
- plays a key role in modulating pain signals
42
what other brain structures are involved in the descending pathway
- locus coeruleus and raphe nuclei
43
what is the overall effect of the descending pathway on pain processing
- inhibits pain processing
44
where does the descending pathway send signals to modulate pain
to the spinal cord
45
what is the overall effect of opioids on pain processing
- opioids inhibit pain processing
46
how do opioids affect the descending pain pathway
opioids disinhibit the descending pathway that normally inhibits pain
47
what happens when opioids inhibit inhibitory neurons in the descending pathway
- removes the inhibition on neurons that communicate with the nucleus raphe magnus
48
what is the role of the nucleus raphe magnus in pain modulation
- part of the descending pathway that helps reduce pain signals
49
where in the brain does this disinhibition process start
- in the periaqueductal gray matter in the midbrain
50
how do opioids affect the ascending pathway
- opioids inhibit the ascending pain pathway
51
where do opioids act on the neurons of the ascending pathway
on receptors located on the axons of these neurons
52
what is the effect of opioids binding to these receptors
it inhibits the transmission of pain signals to the brain
53
do opioids inhibit chronic pain
- limited evidence to show they work
54
what is the primary neurotransmitter involved in the mesocorticolimbic system
dopamine
55
what happens when reward is experienced
the mesocorticolimbic dopamine system is activated, leading to dopamine release
56
where do dopamine neurons originate in the mesocorticolimbic system
the ventral tegmental area
57
what brain structure is a primary target of dopamine release and crucial for reward processing
the nucleus accumbens
58
what is the role of the frontal cortex in the mesocorticolimbic system
- involved in higher-level cognitive functions related to reward
59
what is the role of the amygdala and hippocampus in the mesocorticolimbic system
contribute to emotional and memory aspects of reward
60
what type of receptors are important in the nucleus accumbens for mediating dopamine's effects
d1 and d2 receptors
61
what is the effect of dopamine binding to d1 and d2 receptors
contributes to the feeling of reward
62
what type of neurons regulate dopamine release in the mesocorticolimbic system
- GABA
63
how do GABAergic interneurons regulate dopamine release
- through disinhibition - inhibiting inhibitory neurons, leading to dopamine release
64
how may opioids increase dopamine release in the nucleus accumbens
Disinhibition of dopaminergic neurons in the VTA: opioids stimulate opioid receptors of GABA neurons, inhibiting GABA release by these neurons, thereby allowing an increase of dopaminergic VTA neurons
65
how do opioids acting on mu-opioid receptors in the VTA affect dopamine release in the nucleus accumbens
- increase dopamine release
66
what is the behavioural effect of increased dopamine release in the nucleus accumbens due to mu receptor activation
reinforcement - reward
67
what endogenous opioid is associated with activating mu receptors in the mesocorticolimbic system
- beta-endorphin
68
how do opioids acting on kappa receptors affect dopamine release in nucleus accumbens
- decrease dopamine release
69
what is the potential behavioural effect of decreased dopamine in the nucleus accumbens due to kappa receptors
aversion
70
what endogenous opioid is associated with activating kappa receptors in the mesocorticolimbic system
dynorphin
71
what is the main distinction between reward and pleasure
distinction between wanting and liking
72
how can 'liking' be measured
using facial expressions to sweet or bitter tastes
73
what brain region is specifically related to liking
the nucleus accumbens
74
what is the affect of stimulating opioid receptors in the nucleus accumbens shell
- it increases liking
75
what is the effect of stimulating dopamine receptors in the nucleus accumbens shell
it reduces liking
76
how does morphine affect 'liking' responses
increases liking
77
how does amphetamine affect liking responses
decreases liking
78
what type of reactions does morphine increase in context of liking
- hedonic reactions
79
what type of reactions does amphetamine increase in the context of liking
aversive
80
what are the key components of substance dependence
- tolerance, withdrawal, preoccupation with drug use, and persistent desire to reduce use
81
how does repeated opioid use lead to tolerance
it reduces the acute effects of the drug
82
what is a potential consequence of developing tolerance to opioids
- the user may increase the dose or take a stronger opioid
83
what causes withdrawal symptoms in opioid dependence
long term compensatory changes in neural mechanisms due to repeated opioid use
84
how are withdrawal symptoms related to acute effects of opioids
they are generally the opposite
85
what withdrawal symptom corresponds with analgesia
pain and irritability
86
what withdrawal symptom corresponds with respiratory depression
panting and yawning
87
what withdrawal symptom corresponds with euphoria
dysphoria and depression
88
what withdrawal symptom corresponds with relaxation and sleep
restlessness and insomnia
89
what withdrawal symptom corresponds with decreased blood pressure
increased blood pressure
90
what withdrawal symptom corresponds with constipation
diarrhoea
91
what withdrawal symptom corresponds with pupil constriction
pupil dilation
92
what withdrawal symptom corresponds with hypothermia
hyperthermia
93
what withdrawal symptom matches with drying of secretions
tearing, runny nose
94
what withdrawal symptom matches with reduced sex drive
spontaneous ejaculation
95
what withdrawal symptom matches with flushed and warm skin
chilliness and gooseflesh
96
what are the main types of treatments used for opioid dependence
detoxification, maintenance therapy, abstinence with opioid antagonist
97
what is often use during opioid detoxification to manage withdrawal symptoms
substitution with long acting opioids like methadone or buprenorphine
98
how do methadone and buprenorphine compare to heroin in terms of highs and withdrawal symptoms
they have lower highs and less pronounced withdrawal symptoms
99
what drugs are used in maintenance therapy for opioid dependence
buprenorphine or methadone
100
what is a benefit of maintenance therapy with methadone or buprenorphine
it reduces mortality from overdose and other causes
101
what is a drawback of using substitution drugs like methadone or buprenorphine
they have adverse effects and can interfere with normal life
102
how does buprenorphine compare to methadone in terms of adverse effects
buprenorphine may have reduced adverse effects but this isn't proven
103
what type of drug is used for treatment aimed at full abstinence from opioids
opioid antagonists
104
what is an example of an opioid antagonist
naloxone
105
what does an opioid antagonist do
it makes opioid administration ineffective
106
what is a challenge with using opioid antagonists for abstinence
typically very low adherence and requires highly motivated patients
