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PMCOL 305 > cannabis 2 > Flashcards

cannabis 2 Flashcards

1
Q

what temperature does THC vaporize at

A

180-200 degrees C

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2
Q

why are vaporizers safer than smoking

A

because cannabis is heated but not burned

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3
Q

can vaporizers deliver equal amounts of THC as smoking

A

yes

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4
Q

do vaporizers produce as many combustion products as smoking

A

no

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5
Q

what happens to receptors (which ones) with chronic THC exposure

A

CB1 receptors are internalized

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6
Q

what are 7 withdrawal symptoms of THC

A

hot flashes, sweating, runny nose, loose stools, irritability, anxiety, insomnia (opposite of what THC does_

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7
Q

what causes THC tolerance

A

internalization of CB1 receptors

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8
Q

why is withdrawal usually not severe

A

because of long-half life of drug and metabolites, so there is a very gradual decrease (no immediate symptoms)

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9
Q

what does pyrolysis of cannabis generate (3)

A

mutagenic polycyclic hydrocarbons, phenols, cresols

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10
Q

what does smoking cannabis do to airways

A

increases precancerous lesions and airway inflammation

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11
Q

can smoking cannabis cause lung cancer

A

there is no correlation

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12
Q

can smoking cannabis cause larynx cancer

A

there is no correlation

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13
Q

can smoking cannabis cause pharynx cancer

A

there is no correlation

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14
Q

can smoking cannabis cause mouth cancer

A

there is no correlation

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15
Q

can smoking cannabis cause testicular cancer

A

there is a link

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16
Q

what % of all schizophrenia cases are linked to weed use

A

8%

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17
Q

what is the increased risk of schizophrenia in average users over long term (like 10-15 times in life)

A

2 times the average risk

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18
Q

what is the increased risk of schizophrenia in heavy users over long term

A

6 times the average risk

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19
Q

what increases the risk of schizophrenia with cannabis users

A

high THC to low CBD varieties

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20
Q

what does age and cannabis use link to schizophrenia + why

A

increased risk with earlier first exposure (neuroplasticity)

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21
Q

what 2 gene mutations may cause a link with schizophrenia and how

A

COMT gene mutation, it metabolizes DA

AKT controls gene transcription and cell death in neurons

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22
Q

what is the timeline of cannabis use and schizophrenia

A

cannabis use precedes schizophrenia by 1-5 years

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23
Q

why is the argument that “cannabis is used for schizophrenia self-medication” likely wrong

A

because cannabis use typically worsens symptoms

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24
Q

what is a positive symptom of schizophrenia

A

hallucinations

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25
Q

what is a negative symptom of schizophrenia

A

apathy

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26
Q

can THC mimic schizophrenia symptoms and how

A

yes by THC intoxication

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27
Q

what are 3 mental illnesses that cannabis has been linked to

A

depression, amotivational syndrome, schizophrenia

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28
Q

what can cannabis use do to IQ (from age 18-30)

A

drop by 8

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29
Q

what are 3 ways that cannabinoids stimulate food intake

A

increased: olfaction, pleasure when eating food and activity of hunger signalling pathways

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30
Q

what do cannabinoids do to olfaction

A

increase

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31
Q

what do cannabinoids do to pleasure when eating food

A

increase

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32
Q

what do cannabinoids do to activity of hunger signalling pathways

A

increase

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33
Q

what kind of cells are in the main olfactory bulb that sense neuronal information

A

mitral cells

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34
Q

what are mitralcells

A

cells in main olfactory bulb that sense neuronal information

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35
Q

where do mitral cells transmit their sensory information

A

to the prefrontal cortex and amygdala

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36
Q

what kind of neurons project onto mitral cells

A

GABA releasing neurons

37
Q

what stimulates GABA releasing neurons onto the mitral cells (what is step 1)

A

glutamate releasing neurons

38
Q

what is the 3 neuron pathway that controls hunger

A

glutamate projection onto GABA releasing neurons onto mitral cells

39
Q

what do glutamate releasing neurons do when you are not hungry

A

they release glutamate onto GABA relasing neurons

40
Q

what do GABA releasing neurons do when you are not hungry and why

A

release GABA onto mitral cells (because glutamate excites the GABA releasing neurons)

41
Q

what happens to mitral cells when you arent hungry

A

they dont transmit olfactory information to other brain regions

42
Q

what do glutamate releasing neurons do when you are hungry

A

glutamate release is prevented due to CB1 activation on glutamate-releasing nerve endings

43
Q

what do glutamate releasing neurons do when you have cannabinoids in you

A

glutamate release is prevented due to CB1 activation on glutamate-releasing nerve endings

44
Q

what do GABA releasing neurons do when you are hungry and why

A

they do not release GABA because they arent activated by glutamate

45
Q

what happens to mitral cells when you are hungry

A

they will transmit olfactory info to other brain regions (no GABA inhibition)

46
Q

what do GABA releasing neurons do when you are high and why

A

they do not release GABA because they arent activated by glutamate

47
Q

what happens to mitral cells when you are high

A

they will transmit olfactory info to other brain regions (no GABA inhibition)

48
Q

in the hunger pathway, where are the CB1 receptors localized

A

on the nerve endings on glutamate releasing neurons

49
Q

what does THC do to pleasure and reward from food

A

increase

50
Q

does THC make water even more rewarding

A

no

51
Q

does THC make a small dose of sucrose (one that wouldn’t cause pleasure before) even more rewarding

A

yes

52
Q

what NT is the primary signal for nausea and vomiting

A

serotonin

53
Q

what does THC do to 5HT release

A

prevents its release

54
Q

how does THC prevent serotonin release (2)

A

via CB1 activation (Gi) and binds to 5HT3 receptors to decrease their activity

55
Q

what does THC do to 5HT3 receptors

A

binds and decreases their activity

56
Q

what is CBD to 5HT1A autoreceptors

A

agonist (prevents 5HT release)

57
Q

what is CBD to 5HT3 + what does this cause

A

antagonist (its post synaptic)

causes a reduced nausea

58
Q

what does CBD do to 5HT release

A

prevents

59
Q

what is cannabinoid hyperemesis syndrome

A

constant vomiting and stomach pains

60
Q

what causes cannabinoid hyperemesis syndrome

A

long term frequent cannabis users

61
Q

what can relieve symptoms of cannabinoid hyperemesis syndrome

A

compulsive hot showers

62
Q

what part of the body controls body temperature

A

hypothalamus

63
Q

what may cause the link of cannabinoid hyperemesis syndrome and hot showers

A

lots of CB1 receptors in hypothalamus (controls body temp)

64
Q

what kind of driving task is most effected by cannabis use

A

automated tasks (staying in lane)

65
Q

what kind of driving task is least effected by cannabis use

A

concentration-intensive tasks (reversing, distance keeping)

66
Q

are automated or concentration-intensive tasks more severely affected by cannabis use

A

automated

67
Q

how does acute cannabis risk change with motor vehicle accident risk

A

doubles risk

68
Q

what are the effects of alcohol and cannabis to driving

A

additive

69
Q

where do the chemicals found in synthetic/herbal marijuana come from

A

cast-offs of various research programs that were trying to find new drugs to characterize CB1 and CB2 receptors

70
Q

what is JWH-018

A

synthetic marijuana

71
Q

what is UR-144

A

synthetic marijuana

72
Q

what is XLR-11

A

synthetic marijuana

73
Q

what is the potency of JWH-018

A

middle, 102nm required to get same effect as 250nm THC

74
Q

what is the potency of UR-144

A

not very potent, 421nm required to get same effect as 250nm THC

75
Q

what is the potency of XLR-11

A

fairly potent, 98nm required to get same effect as 250nm THC

76
Q

what is the structural difference of XLR-11 and UR-144

A

XLR-11 has an F group as its R substituent

77
Q

what does the F group as a substituent do to potency

A

makes it more potent

78
Q

what causes the potency difference of XLR-11 and UR-144

A

XLR-11 (more potent) has an F as the R group and UR-144 has an H group as the R group

79
Q

what is “spiceophrenia”

A

psychosis that is induced from synthetic cannabinoids

80
Q

what do synthetic cannabinoids do to BP

A

increase

81
Q

what do synthetic cannabinoids do to HR

A

increase

82
Q

what do synthetic cannabinoids do to respiration rate

A

increase

83
Q

what kind of agonist is THC

A

partial agonist

84
Q

what kind of agonist is synthetic cannabinoids

A

full agonists

85
Q

why do the synthetic cannabinoids have a larger effect on the cardiovascular system and psychologically

A

because they are more potent agonists at CB2 receptors than THC

86
Q

what are 2 main differences in the effects of synthetic cannabinoids than THC (like 2 new things that happen)

A
  • stimulate intracellular signalling pathways (not simulated by THC or endocannabinoids)
  • more rapid desensitization and internalization of receptors
87
Q

which receptor is responsible for synthetic cannabinoids effects on the cardiovascular system

A

CB2

88
Q

for the nausea stuff, where are 5HT1A receptors

A

presynaptic

89
Q

for the nausea stuff, where are 5HT3 receptors

A

post synaptic

PMCOL 305 (26 decks)

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