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PSYT 301 > Opioids > Flashcards

Opioids Flashcards

1
Q

difference bw opiates and opioids

A

opiates -> everything derived from poppy (natural opium products)
opioids -> including semi-synthetic and synthetic substances (actions similar to morphine; reacting with opioid receptors as agonist or antagonist)

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2
Q

what can influence the potency of opioids

A

their structure

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3
Q

characteristics of codeine (3)

A
  1. weaker analgesic
  2. fewer side effects
  3. cough suppressant
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4
Q

characteristics of heroin compared to morphine (3)

A
  1. 2-4x stronger IV
  2. quicker action
  3. more liposoluble
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5
Q

what is naloxone

A

opioid antagonist (binds to receptor and blocks effect); also partial inverse agonist (blocks receptor + makes opioids leave the receptor); induces withdrawal when in overdose

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6
Q

natural narcotics (4)

A
  1. opium
  2. morphine
  3. codeine
  4. thebaine
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7
Q

semisynthetic narcotics (4)

A
  1. heroin
  2. hydromorphone (dilaudid)
  3. oxycodone (percodan)
  4. etorphine
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8
Q

synthetic narcotics (6)

A
  1. pantazocine (talwin)
  2. meperidine (demerol)
  3. fentanyl (sublimaze)
  4. methadone (dolophine)
  5. LAAM
  6. propoxyphene (darvon)
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9
Q

endogenous opioids (4)

A
  1. enkephalins
  2. endorphins
  3. dynorphins
  4. endomorphins
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10
Q

(a) absorption (b) medical administration ways (c) recreational administration ways (d) metabolism of opioids

A

(a) only small fraction crosses BBB, but can easily cross placenta barrier
(b) IM, PO
(c) inhalated, intranasal, subcutaneous, IV
(d) metabolized by liver, metabolites excreted in urine in 24h

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11
Q

why do inhalated or IV opioids act faster that in pill (oral) or subcutaneous form

A

go into oxygenated blood, which goes straight to the brain; pill is slower because takes a while to be absorbed and is metabolized (loses potency) ad subcutaneous slows absorption

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12
Q

what is the main active ingredient of narcotic analgesics

A

morphine

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13
Q

what allowed doctors to prescribe specific doses of painkillers

A

identification of main active ingredient of narcotic analgesics

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14
Q

what influences psychological and behavioral effects of opioids (2)

A

dose and speed of absorption

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15
Q

main subjective effects of weak doses of opioids (5-10 mg) (3 elements)

A
  1. sleepiness
  2. reduced sensitivity to the environment
  3. decreased focus
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16
Q

elements of psychological pain that weak doses of opioids (5-10 mg) target (3)

A
  1. reduced anxiety
  2. reduced feeling of inadequacy
  3. reduced hostility
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17
Q

main effects of weak doses of opioids (5-10 mg) (3 elements)

A
  1. pain relief
  2. respiratory depression
  3. miosis (pupil constriction)
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18
Q

what is morphine used for (not pain)

A

cough suppressant

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19
Q

brain area (1) that morphine acts on and effects (4)

A

hypothalamus; decreased appetite, drop in body temperature, reduced sex drive, variety of hormonal changes

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20
Q

positive effects of high doses of opioids (> 10 mg)

A

euphoria, elation, ‘whole-body orgasm’

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21
Q

negative effects of high doses of opioids (> 10 mg) (4 elements)

A
  1. dysphoria
  2. agitation
  3. anxiety
  4. nausea and vomiting
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22
Q

effects of highest doses (close to overdose) of opioids (5 elements)

A
  1. sedative (loss of consciousness)
  2. drastic decrease in temperature
  3. drastic decrease in BP
  4. severe respiratory depression
  5. miosis
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23
Q

main peripheral effect of opioids and why

A

constipation -> because the receptor it binds to also plays a role in the digestive tract

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24
Q

which medication plays on the constipation side effect of opioids and what does it treat

A

loperamide -> treating diarrhea (no effect on CNS, but effect on GIT)

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25
Q

tolerance of peripheral side effects of opioids

A

there is no tolerance to constipation

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26
Q

what is the usual cause of death of people who consume opioids

A

respiratory depression -> cardiac arrest

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27
Q

subtypes of opioid metabotropic receptors (4)

A
  1. mu
  2. delta
  3. kappa
  4. nociceptin/orphanin FQ (NOP-R)
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28
Q

characteristics of mu receptors (2)

A
  1. high affinity for morphine and derivatives
  2. widespread in the brain and spinal cord
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29
Q

roles of mu receptors (4)

A
  1. morphine-induced analgesia
  2. feeding and positive reinforcement
  3. CV and respiratory depression, cough control and nausea/vomiting
  4. sensorimotor integration
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30
Q

brain regions regulating (a) morphine-induced analgesia (4) (b) feeding and positive reinforcement (c) CV and respiratory depression/cough control/nausea & vomiting (d) sensorimotor integration (2)

A

(a) medial thalamus + periaqueductal gray + median raphe (raphe nuclei) + spinal cord
(b) NAcc
(c) brainstem
(d) thalamus + striatum
(also located in amygdala and hippocampus)

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31
Q

in which brain region are delta receptors predominant (5)

A

forebrain:
1. neocortex
2. striatum
3. olfactory areas
4. substantia nigra
5. NAcc
(also spinal cord)

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32
Q

roles of delta receptors (4)

A
  1. olfaction
  2. motor integration
  3. reinforcement
  4. cognitive functions
    (also analgesia)
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33
Q

do delta receptors have a role in analgesia

A

they overlap with mu receptors suggesting modulation of spinal analgesic response (so yes)

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34
Q

location of kappa receptors (5)

A
  1. striatum
  2. amygdala
  3. hypothalamus
  4. pituitary
  5. NAcc
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35
Q

roles of kappa receptors (8)

A
  1. regulation of pain perception
  2. gut motility
  3. dysphoria
  4. water balance
  5. feeding
  6. temperature control
  7. neuroendocrine/hormonal function
  8. analgesia
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36
Q

location of NOP-R receptors (9)

A
  1. cerebral cortex
  2. amygdala
  3. hypothalamus
  4. hippocampus
  5. periaqueductal gray
  6. thalamus
  7. substantia nigra
  8. brainstem nuclei (including raphe nuclei)
  9. spinal cord
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37
Q

roles of NOP-R receptors (7)

A
  1. spinal analgesia
  2. feeding
  3. learning
  4. motor function
  5. neuroendocrine regulation
  6. mood -> limbic effect (5-HT, NE)
  7. perception of pain
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38
Q

which receptors are important for withdrawal symptoms

A

kappa receptors -> neuroendocrine/hormonal problems when stop use

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39
Q

endogenous ligands of 4 receptors

A

mu -> endomorphins, endorphins
delta -> enkephalins, endorphins
kappa -> dynorphins
NOP-R -> nociceptin, orphanin, FQ

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40
Q

what can increase the risk of respiratory depression

A

mixing alcohol with opioids

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41
Q

where do endogenous peptides imitating morphine come from

A

precursor peptides (propeptides; inactive) -> broken into smaller active opioids by proteases in golgi apparatus + axonal transport in vesicles

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42
Q

effect of electrostimulation of specific regions in CNS

A

produces analgesia -> effect partially reduced with opiate antagonist

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43
Q

inhibitory mechanisms of endogenous opioids (3)

A
  1. postsynaptic inhibition
  2. axoaxonic inhibition
  3. presynaptic autoreceptors
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44
Q

which protein are the 4 receptor subtypes linked to

A

Gi protein (inhibitory GPCR)

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45
Q

explain postsynaptic inhibition (4 elements)

A
  1. opioid neuron releases endo-opioids
  2. when opioid binds, opioid receptor produces G protein modulation of K+ channels (opens them) -> hyperpolarization of neuron
  3. decrease firing rate & inhibits release of NT
  4. decreases excitability of membranes/neurons
46
Q

explain axoaxonic inhibition (4 elements)

A
  1. opioid neuron releases endo-opioids on presynaptic neuron (non-opioid neuron)
  2. when opioid binds, opioid receptor on presynaptic neuron terminal produce G protein modulation of Ca2+ channels (closes them)
  3. inhibits vesicle fusion to membrane and NT release into cleft
  4. decreases excitability of membrane/neurons
47
Q

explain presynaptic autoreceptor inhibition (4 elements)

A
  1. endorphins released by neuron (colocalized NT and opioid) in cleft bind to autoreceptors on presynaptic neuron
  2. decreases signal to send NTs to cleft
  3. inhibits release of NT
  4. reduced postsynaptic effect
48
Q

main role of 3 inhibitory actions of endogenous opioids

A
  1. postsynaptic inhibition -> opening K+ channels
  2. axoaxonic inhibition -> closing Ca2+ channels (neuromodulator)
  3. presynaptic autoreceptors -> reducing NT release (only neurons that have colocalized NT and opioids)
49
Q

how do opioids reduce pain (3)

A
  1. in spinal cord by small inhibitory interneurons (ascending?)
  2. by 2 descending pathways from periaqueductal gray (goes to raphe nuclei and locus coeruleus -> release of 5-HT and NE that have inhibitory effect)
  3. at higher level sites in brain (emotional and hormonal aspects)
50
Q

explain descending inhibitory pathway (2)

A
  1. sensory afferent excites projection neuron
  2. descending inhibitory neuron inhibits effect of sensory afferent (synapses on body of projection neuron)
51
Q

explain descending modulatory pathway (3)

A
  1. sensory afferent synapses on excitatory interneuron
  2. excitatory interneuron synapses on projection neuron
  3. descending modulatory neuron inhibits excitatory interneuron (body)
52
Q

explain descending excitatory pathway (3)

A
  1. sensory afferent synapses on projection neuron
  2. opioid neuron inhibits projection neuron (body)
  3. descending excitatory neuron stimulates opioid neuron
53
Q

mechanism of reinforcement (2 steps)

A
  1. (in VTA) b-endorphin neuron inhibits GABA neuron projecting on mesolimbic cell (disinhibition)
  2. mesolimbic cell stimulates DA neuron in NAcc (DA release)
    (3. DA release onto neuron in ventral pallidum)
54
Q

mechanism of kappa agonists/dynorphin on DA pathway in reinforcement

A

inhibit mesolimbic cell (at level of terminal) -> inhibition of DA cell -> inhibition of DA release

55
Q

link between treating pain and potential for opioid abuse

A

opioid action intertwined with DA pathway

56
Q

how do kappa receptors cause dysphoria

A

kappa receptors on terminal of DA neurons -> causes decrease of DA release in NAcc

57
Q

effect of lesions in DA/opioid network

A

partial decrease in self-administration (other regions must be implicated)

58
Q

opioid tolerance (4)

A
  1. for all opioids, even endorphins
  2. metabolic -> increased metabolism when use more opiates (need to take more to have same effect)
  3. pharmacodynamic -> neurons compensate for chronic use of opiates (happens quickly after use)
  4. not at same level for all pharmacological effects (analgesia = quick tolerance; miosis = no tolerance)
59
Q

opioid cross-tolerance

A

reduced effect on other opioid receptors

60
Q

opioid sensitization (2)

A
  1. substance abuse -> motivation to approach (craving) undergoes sensitization (every time use = craving increase)
  2. neural mechanism responsible for high (liking of drug) is unchanged or decreases (become less sensitive) when develop tolerance
61
Q

physical dependance (2)

A
  1. neuroadaptations in response to long-term occupation of opioid receptors
  2. when drug no longer present (abstinence) -> cell function returns to normal (loss of inhibitory action) + overshoots basal levels (creates opposite symptoms/rebound)
62
Q

withdrawal (3)

A
  1. non-lethal
  2. extremely unpleasant (pain, dysphoria, restlessness, fearfulness, flu-like symptoms)
  3. length depends on factors
63
Q

what does length of withdrawal depend on (5)

A
  1. dose
  2. frequency
  3. duration of drug use
  4. general health
  5. personality
64
Q

withdrawal of long-acting opioids like methadone (4)

A
  1. takes more time
  2. show less severe withdrawal symptoms
  3. can decrease dosage slowly without causing intense withdrawal symptoms
  4. have to be careful because could induce relapse (methadone is an opioid)
65
Q

location of withdrawal (3)

A
  1. periaqueductal gray
  2. locus coeruleus
  3. NAcc implicated in aversive response + reinforcing values of opiates
66
Q

treatment options for opioid addiction (5)

A
  1. support groups
  2. rehabilitation facilities
  3. medicated-assisted treatment (methadone)
  4. cognitive therapies (mindfulness, cognitive reappraisal)
  5. neurostimulation
67
Q

effects of tDCS of dlPFC (3)

A
  1. decreased self-reported cravings
  2. decreased risk-taking behaviors
  3. decreased drug-related cue reactivity
68
Q

elements of mindfulness-oriented recovery enhancement (4)

A
  1. mindfulness
  2. reappraisal
  3. savoring
  4. transcendence
69
Q

mechanism and target of (a) mindfulness (b) reappraisal (c) savoring (d) transcendence

A

(a) attentional control over automaticity -> cognitive & behavioral habits (cognitive impairments preceding addiction; thoughts)
(b) shift from affective to sensory processing -> physical & emotional pain (reframe thoughts)
(c) restructuring reward valuation -> positive affect, pleasure & meaning (rebalance brain to respond to natural pleasures; change salience)
(d) craving regulation -> addiction (acknowledgement; know have control over thoughts)

70
Q

ways to detox (2)

A
  1. medication-assisted (methodone; usually with clonidine)
  2. non-assisted (cold turkey)
71
Q

biggest risk of medication-assisted detox

A

overdose -> methodone/buprenorphine are opioids

72
Q

why use methadone (5)

A
  1. cross-dependence - withdrawal
  2. cross-tolerance - chronic usage (tolerance to euphoric effect of opioids)
  3. oral administration
  4. long acting
  5. medically safe even long-term and doesn’t interfere with daily activities
73
Q

WM in ctl vs abstainers vs CUD vs OUD

A
  1. little difference between ctl and abstainers -> brain recovered
  2. CUD -> a lot of WM impairments
  3. OUD -> even more impairments
74
Q

what do WM abnormalities (in WM diffusivity) in SUD brains suggest

A

less integrity of WM tracts in individuals with SUD -> axonal packing attenuation & demyelination

75
Q

WM impairments reflect (2)

A
  1. neurotoxic effect of cocaine and heroin
  2. association with neuroinflammatory brain responses
76
Q

effect of methadone on WM

A

still see impairments because methadone is an opioid

77
Q

what is WM recovery associated with

A

reduced cravings (not cue-induced cravings)

78
Q

WM changes in the brain with abstinence (3)

A
  1. normalization/regeneration of axonal processes
  2. remyelination
  3. reduced neuroinflammatory brain responses
79
Q

cytokines involved in (3)

A
  1. neuroimmune effects
  2. neuroinflammatory effects
  3. BBB disruption
80
Q

relationship bw neuroinflammation, opioids and WM (2)

A
  1. chronic opioid exposure -> direct impact on neuroimmune microglia cells
  2. opioids known to afect gene expression in oligodendrocytes (cells responsible for myelinating axons in CNS)
81
Q

how can cytokines be useful for looking at WM

A

can be used as a proxy measure for WM integrity

82
Q

what is (a) prevention (b) treatment (c) harm reduction (d) enforcement

A

(a) preventing problematic drug and substance use
(b) supporting innovative approaches to treatment and rehabilitation
(c) supporting measures that reduce the negative consequences of drug and substance use
(d) addressing illicit drug production, supply and distribution

83
Q

why did opioid antagonists appear

A

because respiratory depression became of clinical importance

84
Q

what is an opioid use disorder (2)

A
  1. combines 2 disorders: opioid dependence and opioid abuse
  2. includes broader range of illegal and prescribed drugs
85
Q

abstinence (1) vs harm reduction (4)

A
  1. abstinence: state of (in)voluntary non-engagement in behavior (ie. cold turkey)
  2. harm reduction: prevent overdose and infectious disease transmission + improve wellbeing + offer low-threshold options for treatment + prevention, treatment and recovery
86
Q

non-pharmacological therapies for OUD (6)

A
  1. 12-step program
  2. CBT
  3. contingency management
  4. family therapy
  5. group counselling and support groups
  6. motivational interviewing
87
Q

con of therapy for OUDs

A

in some cases, cannot be sole form of treatment because doesn’t help with physical withdrawal symptoms

88
Q

what do opioid agonist treatments (OATs) do (5)

A
  1. replace short-acting opioids with longer-acting opioid medication
  2. don’t result in a high
  3. affect body more slowly and for longer than opioids
  4. prevent opioid withdrawal symptoms for 24-36 hours
  5. helps eliminate cravings
89
Q

most commonly used OATs (2)

A
  1. methadone
  2. buprenorphine/naloxone
90
Q

benefits of methadone (3)

A
  1. high bioavailability
  2. long elimination/half-life ~24h
  3. prevents withdrawal symptoms
91
Q

benefits of buprenorphine (3)

A
  1. long elimination half-life -> helps relieve withdrawal symptoms
  2. lower risk of overdose than methadone
  3. comes in many forms, less restrictive treatment modalities
92
Q

benefits of diacetylmorphine (heroin) as treatment for OAT (2)

A
  1. responds to specific needs of patients who don’t respond to available medication-assisted treatments
  2. non-contaminated
93
Q

limitations of methadone (4)

A
  1. potential risk of overdose
  2. modalities (dose obtained daily at pharmacy)
  3. has to be taken under supervision
  4. training and license required for physicians
94
Q

limitations of buprenorphine (2)

A
  1. needs to be combined with naloxone (to avoid misuse)
  2. presence of naloxone is sometimes perceived as negative by people who use opioids
95
Q

limitations of diacetylmorphine (heroin) as treatment for OUDs (2)

A
  1. access to treatment restricted
  2. modalities low acceptability from patients (each injection obtained in medical space, following planned schedule)
96
Q

difference between methadone and buprenorphine

A

methadone = full agonist
buprenorphine = partial agonist

97
Q

subutex vs suboxone

A

subutex: contains buprenorphine (proved to be addictive to many and has been abused)
suboxone: contains buprenorphone and naloxone

98
Q

what do antagonist interventions do (3)

A
  1. opioid antagonist drugs one of most powerful tools in treatment of opioid addiction
  2. block one or more of the opioid receptors in CNS
  3. help people who are addicted to opioids manage withdrawal symptoms or recover from opioid overdose
99
Q

most popular opioid antagonists (2)

A
  1. naloxone (suboxone)
  2. naltrexone
100
Q

benefits of naltrexone (3)

A
  1. antagonizes heroin
  2. long duration of action (~4h) compared to naloxone
  3. works well for long-term treatment
101
Q

benefits of naloxone (3)

A
  1. for overdose intervention -> can temporarily stop the effects of opioid use
  2. available in nasal spray
  3. easy to administer
102
Q

limitations of naltrexone (2)

A
  1. decreases, but doesn’t eliminate cravings
  2. chronic exposure may result in upregulation of opioid receptors (increase their sensitivity)
103
Q

limitations of naloxone (3)

A
  1. cost of nasal spray
  2. requires legal and medical authorization
  3. induces withdrawal symptoms, so don’t necessarily want to take it
104
Q

what is safer supply (4)

A
  1. provide prescribed medications to people who use drugs
  2. goal of preventing overdoses and saving lives
  3. provided in less clinical and more flexible way compared to OATs
  4. include opioid medications, stimulant medications and BZDs
105
Q

chronic pain leading to iatrogenic OUD (4)

A
  1. chronic pain (3+ months)
  2. no pain relief + increasing doses (opioid tolerance)
  3. loss of prescriber + opioid-related problems + withdrawal + find opioids elsewhere
  4. finding competent healthcare team + long-term process
106
Q

what is PROFAN (3)

A
  1. community-based peer-led training program initiative
  2. uses harm reduction approach
  3. to empower peers in responding to opioid overdoses they are likely to witness
107
Q

objectives of PROFAN 1.0 (2)

A
  1. demonstrate that the administration of naloxone by peers is effective in saving lives
  2. demonstrate the feasibility and credibility of this initiative in order to sustain it
108
Q

what is the PROFAN effect

A

experiential knowledge transfer via a peer combined to clinical knowledge transfer via intervention worker

109
Q

PROFAN: transversal challenges faced (6)

A
  1. pandemic context
  2. state disengagement
  3. exacerbated overdoses
  4. instabilities in the media
  5. multiplicity of actions and initiatives
  6. lack of concernation
110
Q

what could be done to improve situation of PWOUD (5)

A
  1. safe supply
  2. access to treatments
  3. safe environment
  4. stigmatization/infantilization
  5. decriminalization

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