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PSYT 301 > Cannabis > Flashcards

Cannabis Flashcards

1
Q

7 priorities of cannabis act (7)

A
  1. protect health of young persons by restricting their access to cannabis
  2. minimize inducements to use cannabis
  3. allow legal production of cannabis to replace illicit market
  4. deter illicit cannabis production and sale
  5. reduce burden of dealing with cannabis offences imposed on criminal justice system
  6. enable cannabis users to have quality-controlled supply of cannabis
  7. increase public awareness of health risks of using cannabis
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2
Q

tight regulations of quebec on cannabis (6)

A
  1. minimum legal purchase age of 21 years
  2. only SQDC can sell cannabis
  3. reduced amount of cannabis that adult can legally possess
  4. banned growing of cannabis for personal use
  5. limits THC content of cannabis edibles and extracts (max of 5 mg/edible and 30% weight in extracts)
  6. banned additives to any cannabis product that would increase attractiveness or flavor or enhance psychoactive effects
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3
Q

what happened since legalization of cannabis (2)

A
  1. cannabis use increase in > 25 year olds
  2. slight decline in adolescents 15-17 years (goal of protecting youth has not been met)
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4
Q

fastest growing population of cannabis users

A

aging adults over 55

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5
Q

consequences of cannabis legalization (7)

A
  1. increased patterns of cannabis use (decreased perceived harmfulness -> perceive cannabis to be more beneficial than harmful + increased cannabis availability and accessibility)
  2. hasn’t created any health benefits -> linked to serious concerns instead
  3. outcomes related to health have increased (or remained steady)
  4. increase in cannabis intoxications in young children
  5. lack of education campaigns of public health messages on cannabis
  6. lack of health warning messages on cannabis products
  7. reduction in criminal arrests and charges related to cannabis use
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6
Q

what is cannabis (3)

A
  1. mixture of cut, dried and ground flowers, leaves, stems of hemp plant
  2. stimulant and depressant
  3. has hallucinogenic properties
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7
Q

what is responsible for the aroma of cannabis

A

terpenes

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8
Q

what is responsible for the pigment and flavor of cannabis

A

flavanoids

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9
Q

THC vs CBD

A

THC: psychoactive + addictive (acts on DA system)
CBD: non-psychoactive, but biologically active (doesn’t cause a high, not addictive)

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10
Q

3 strains + properties

A
  1. sativa -> higher ratio of THC to CBD, more stimulating, psychotropic effects
  2. indica -> higher ration of CBD to THC, typically more sedating
  3. ruderalis -> low THC strain
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11
Q

effect of mode of administration on pharmacokinetics (3)

A

different onset of effects, duration of action and distinct health effects

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12
Q

vaporized cannabis vs smoked cannabis

A

vaporized cannabis produces greater subjective drug effects (and higher THC blood concentrations) than am doses of smoked cannabis

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13
Q

endocannabinoid system (6)

A
  1. widespread neuromodulatory system
  2. role in CNS development
  3. regulates many physiological and cognitive processes
  4. works to maintain homeostasis: controls levels of other NTs, influences and is influenced by other signalling pathways
  5. active even without cannabis
  6. implicated in pathological conditions (scz)
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14
Q

role of endocannabinoid system (14)

A
  1. memory
  2. new neuron formation
  3. inflammatory responses
  4. fetal cell differentiation
  5. pain perception
  6. emotions
  7. appetite
  8. thermogenesis
  9. metabolism
  10. sleep
  11. motility
  12. response to stress
  13. addiction processes
  14. immunomodulation
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15
Q

endogenous cannabinoid system (3)

A
  1. endocannabinoids
  2. cannabinoid receptors
  3. endocannabinoid enzymes
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16
Q

forms of cannabinoids (3)

A
  1. phytocannabinoids: derived naturally from flora
  2. endocannabinoids: produced endogenously
  3. synthetic cannabinoids: created artificially
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17
Q

what are endocannabinoids and how do they work (3)

A
  1. lipid molecules synthesized on demand (not really NTs) -> anandamide and 2-AG
  2. retrograde messengers: released from postsynaptic cells and travel backwards across synapse
  3. bind to cannabinoid receptor on presynaptic cell
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18
Q

enzymes that metabolize endocannabinoids (2)

A
  1. fatty acid amino hydrolase (FAAH) -> degrades AEA
  2. monoacylglycerol lipase (MAGL) -> degrades 2-AG
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19
Q

cannabinoid receptors (4)

A
  1. CB1R mostly found in CNS
  2. CB2R mostly found in periphery and immune cells
  3. AEA is partial agonist of both
  4. 2-AG is full agonist of both
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20
Q

brain areas where CB1R are found (8)

A
  1. cerebellum* -> movement coordination
  2. brainstem
  3. hippocampus* -> learning and memory
  4. amygdala
  5. hypothalamus
  6. NAcc* -> reward and motivation
  7. basal ganglia* -> movement control
  8. neocortex
    * = highly concentrated
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21
Q

tetrahydrocannabinol (THC) (8)

A
  1. main psychoactive component
  2. responsible for addictive properties -> dose-dependently increases DA in shell of NAcc
  3. partial agonist
  4. metabolized into THC-COOH (inactive) by cytochrome P450s
  5. deposits in adipose tissue (peak = 4-5 days later) and later re-released in blood
  6. long half-life (20-30h)
  7. metabolites remain detectable for ~28 days after last use
  8. rapidly absorbed through lungs -> peak blood concentration in 6-10 minutes, peak brain concentration in 15-30 minutes
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22
Q

why is cannabis addictive and how (3)

A
  1. THC dose-dependently increases DA in shell of NAcc and striatum
  2. increase in cannabis potency (%THC)
  3. THC increases DA neural firing by decreasing GABAergic inhibition of DA neural activity (disinhibition)
  4. THC allosterically modulates opioid receptors (additional indirect routes for altering DA transmission?)
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23
Q

system that underlies THC adversive effects

A

inhibition of VTA glutamatergic transmission -> decreases DA release

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24
Q

short-term/acute effects of THC (12)

A
  1. red eyes
  2. dry mouth
  3. skin sensation
  4. memory loss
  5. paranoia
  6. impaired motor coordination
  7. increased appetite
  8. pleasure/bliss
  9. delayed response
  10. altered perception
  11. muscle relaxation
  12. increased heart rate
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25
Q

short-term/acute effects of THC at very high doses (5)

A
  1. chest pain
  2. rapid heartbeat
  3. nausea/vomiting
  4. psychotic episode - hallucinations/delusions
  5. respiratory depression
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26
Q

long-term/chronic effects of THC (4)

A
  1. physical health risk (respiratory and cardiovascular problems)
  2. psychiatric symptoms and disorders (addiction)
  3. psychosocial problems (academics)
  4. cognitive dysfunction
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27
Q

long-term/chronic effect of THC at very high doses

A

cannabinoid hyperemesis syndrome: recurrent episodes of nausea, vomiting and dehydrations + frequent visits to emergency department -> may involved chronic overstimulation of cannabinoid receptors

28
Q

cannabinoid hyperemesis syndrome (a) demography (b) treatment (c) when is it resolved

A

(a) typically young adults with long history of cannabis use
(b) hot showers
(c) when cannabinoids are discontinued

29
Q

neurobiological changes with chronic cannabis use (3)

A
  1. CB1Rs are downregulated
  2. amygdala volume negatively correlated with severity of CUD
  3. hippocampus volume negatively correlated with weekly cannabis use
30
Q

therapeutic properties of cannabidiol (CBD) (6)

A
  1. anxiolytic
  2. antidepressant
  3. antipsychotic
  4. analgesic
  5. anti-inflammatory
  6. add-on therapy for social anxiety disorders, scz, non-motor symptoms in PD, SUD
    *7. lack of evidence
31
Q

MOA of CBD (3)

A
  1. little binding affinity for CB1 and CB2 receptors
  2. non-competitive NAM of CB1R
  3. inhibits FAAH
32
Q

effects of non-competitive NAM of CB1R mechanism of CBD (2)

A
  1. reduces affinity/efficacy of THC and AEA
  2. improves tolerability and safety of THC by antagonizing effects of THC (psychosis, anxiety, sedation, tachycardia)
33
Q

effect of inhibition of FAAH by CBD

A

FAAH metabolizes AEA, so inhibiting it increases AEA, increasing bliss/mood

34
Q

non-cannabinoid targets of CBD (3)

A
  1. agonist of 5HT1A receptor (mood enhancer)
  2. allosteric modulator of opioid receptors
  3. agonist at transient potential vanilloid-1 receptor (TRPV1) - multisensory receptor (temperature, etc.)
35
Q

CBD pharmacokinetics (6)

A
  1. metabolized by CYPs: 2C9, 2C19 and 3A4
  2. active metabolite = 7-OH-CBD
  3. inactive metabolite = CBD-COOH
  4. lipid soluble
  5. prolonged elimination
  6. half-life = 1-30h
36
Q

risks and harms associated with CBD (6)

A
  1. decreased alertness (drowsiness and sedation)
  2. changes in mood (irritability and agitation)
  3. decreased appetite
  4. gastrointestinal symptoms/distress (diarrhea)
  5. drug interaction effects with over-the-counter and prescription medications (acts as inhibitor/inducer of CYPs)
  6. inaccurate labels (unreliable info about product purity and safety)
37
Q

CBD as approved therapy

A

approved only to treat seizures associated with Lennox Gastaut syndrome, Dravet syndrome or tuberous sclerosis complex

38
Q

cannabis withdrawal (7)

A
  1. severity is similar to that of tobacco/nicotine withdrawal
  2. correlates with functional impairment
  3. reduces odds of initiating a quit attempt
  4. increases risk of relapse
  5. severity of symptoms proportional to severity of cannabis use
  6. tobacco co-use increases severity and duration of cannabis withdrawal symptoms (increases risk for cannabis relapse)
  7. > 50% of people with regular cannabis use experience withdrawal
39
Q

clinically significant CUD symptoms (13)

A
  1. cravings
  2. irritability
  3. anxiety
  4. depression
  5. decreased appetite
  6. sleep disturbances
  7. weird dreams
  8. restlessness
  9. somatic symptoms (headaches, sweating, nausea, vomiting, abdominal pain)
40
Q

cannabis withdrawal timeline (3)

A
  1. symptoms begins 24h after cessation
  2. peak within 7 days
  3. dissipate following 28 days of abstinence
41
Q

cannabis treatments (3)

A
  1. behavioral treatments yield moderate abstinence rates that decline once treatment is discontinued
  2. no approved pharmacological treatments
  3. harm reduction approach
42
Q

harm reduction for cannabis use (3)

A
  1. avoid adding tobacco
  2. use safer routes (edible/tincture > vaporize > smoking)
  3. use a regulated supply when able (medical or recreational)
43
Q

behavioral therapies for cannabis (3)

A
  1. CBT
  2. motivational enhancement therapy
  3. contingency management
    *combining all 3 has greatest efficacy
44
Q

pharmacotherapies for cannabis use disorder (5)

A
  1. sedatives (zolpidem)
  2. antidepressants (bupropion)
  3. synthetic cannabinoid (oral THC, nabilone)
  4. CB1R antagonist (rimonabant) -> severe side effects, removed from market
  5. FAAH inhibitor -> most promising
    *all target withdrawal
45
Q

FAAH inhibitor treatment (4)

A
  1. lower self-reported cannabis use after 4 weeks
  2. reduced symptoms of cannabis withdrawal
  3. lower urinary [THC-COOH]
  4. well tolerated (no SE yet)
46
Q

novel avenues for cannabis treatment (2)

A
  1. repetitive transcranial magnetic stimulation (rTMS): changing magnetic field to caused electric current at specific area via electromagnetic induction (dlPFC and PCC/precuneus)
  2. transcranial direct current stimulation (tDCS): direct electrical current to stimulate specific parts of brain (dlPFC)
47
Q

what is self-medication

A

using a substance to alleviate, cope with, or reduce psychological or physical symptoms

48
Q

medicating with cannabis (3)

A
  1. in low doses can produce anxiolytic effects for some people (but doesn’t last)
  2. shouldn’t be recommended as treatment for affective symptoms
  3. chronic cannabis use and CUD are associated with negative mental health outcomes
49
Q

cannabis use disorder

A

problematic pattern of cannabis consumption that leads to clinically significant levels of impairment or distress to the user (can become dependent; impairment in day-to-day life)

50
Q

vulnerability to CUD (4)

A
  1. daily or almost daily users
  2. adolescents and young adults, especially under the age of 25
  3. family history of addiction or problematic use
  4. those with psychiatric history
51
Q

cognitive impairments due to acute cannabis intoxication (6)

A
  1. memory
  2. learning
  3. attention
  4. perceptual motor skill
  5. executive functions
  6. processing speed
52
Q

cognitive impairments that remain after acute intoxication (residual effects) (4)

A
  1. memory (small-high)
  2. verbal learning (small-moderate)
  3. executive functioning (small)
  4. attention, processing speed, language (none)
53
Q

vulnerabilities to residual cognitive deficits (2)

A
  1. adolescent vs adult brain
  2. level of use (chronic, frequent, heavy use)
54
Q

cannabis and education (3)

A
  1. less likely to complete homework, attend class, achieve high marks
  2. CUD severity better predictor of educational impairment than MDD and PTSD (undergrads)
  3. craving predicted cannabis use and reduced academic motivation
55
Q

psychosis (3)

A
  1. mental state/behaviors characterized by a loss of contact with reality (hallucinations + delusions)
  2. hallucinations: disorder in experience of sensory events
  3. delusions: disorder in the representation of reality (persecution, grandiosity, paranoia)
56
Q

scz symptoms (3)

A
  1. positive symptoms: hallucinations and/or delusions
  2. negative symptoms: flat affect, avolition, anhedonia, alogia
  3. disorganized symptoms: disorganized speech, inappropriate affect
57
Q

dose-dependent relationship of THC (effects)

A

low [THC]: anxiolytic ~ feeling calm, less anxious, relaxed, slowed down
high [THC]: can produce feelings of anxiety, hallucinations, delusions (paranoia), derealization

58
Q

intravenous administration of THC to healthy controls findings (5)

A

transient increase in:
1. positive symptoms
2. negative symptoms
3. perceptual alterations (spaced out, detached)
4. anxious
5. tired

59
Q

scz and cannabis (5)

A
  1. cannabis is a risk factor to the development of scz
  2. dose-response relationship: more frequent cannabis use associated to higher risk of developing scz
  3. sex effects: link more prevalent in males
  4. timing of use: using in adolescence increases strength of link
  5. genetics: polymorphisms (COMT, AKT1, DAT1, BDNF)
60
Q

COMT polymorphism linked with scz and cannabis (4)

A
  1. COMT = enzyme responsible for breakdown of DA in brain
  2. polymorphism = substitution at codon 158 of COMT gene (Val -> Met)
  3. changes speed of DA breakdown (slower?)
  4. cannabis use in adolescence increased risk of scz at 26, but only in carriers of 1 or 2 Val alleles
61
Q

cognition: scz and cannabis (2)

A
  1. impairment in verbal memory with higher doses of THC (and in people with scz+thc)
  2. improvements in verbal memory in people with scz after 28 days of cannabis abstinence
62
Q

cannabis use and mental health (6)

A
  1. cannabis use during adolescence increases risk of developing depression and suicidal ideation
  2. cannabis use can be harmful to mental health (causality cannot be established)
  3. adolescent cannabis use associated with adult MDD and suicidality, but not with GAD
  4. young age of use and increased frequency: increased risk
  5. greater cannabis use at baseline predicted slower improvements in anxiety (maintenance of symptoms over time) *anxiety at baseline did not predict change in cannabis use -> causality link
  6. flourishing (positive mental health/wellbeing) associated with lower cannabis use
63
Q

endocannabinoid system and mental health (2)

A
  1. involved in anxiety regulation and emotion processing
  2. high [CB1R] in hypothalamus, amygdala, cerebral cortex, hippocampus (emotion, memory, neuroendocrine function)
64
Q

evidence of dysregulation of endocannabinoid system after chronic use of cannabis (2)

A
  1. downregulation of CB1R (reversed in abstinence)
  2. dysregulation in plasma and CSF endocannabinoid levels
65
Q

why wait 28 days to measure changes in outcome (3)

A
  1. 28 days for complete urinary elimination of cannabis
  2. most withdrawal symptoms dissipate after 28 days of abstinence
  3. evidence that downregulation of CB1R reverses after 28 days of abstinence
66
Q

limitations to measuring changes in outcome in abstinence study (5)

A
  1. MDD comorbidity
  2. psychosis comorbidity
  3. medical conditions (MS)
  4. veterans
  5. adolescents (only group that didn’t have comorbidities)
67
Q

overall summary (6)

A
  1. frequent cannabis self-medication for affective symptoms
  2. cannabis use can progress to CUD
  3. cannabis use can lead to cognitive impairments that impact functioning
  4. cannabis has dose-dependent effects: high doses produce anxiety and psychotic symptoms
  5. cannabis is a risk factor for scz in vulnerable people
  6. evidence that cannabis can increase risk of depression and suicidality, and maybe GAD

PSYT 301 (9 decks)

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