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345A > Marijuana: Nov 20-22 > Flashcards

Marijuana: Nov 20-22 Flashcards

1
Q

what parts of the Cannabis plant do you use

A

resin and leaf

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2
Q

what is the drug that comes from the leaf vs the resin

A 
resin= hash 
leaf= mj
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3
Q

did they start using the resin or the leaf first

A

resin 2737 BCE China, 1000 CE North Africa

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4
Q

when was THC first isolated and synthesized

A

for horses in 1964

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5
Q

street names often differ. what do they refer to

A

method of intake and preparation e.g. inhalation=Blunt, doobie, joint, refeer

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6
Q

is hemp a drug

A

no it is the plant fibres used for material items

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7
Q

does the resin and leaf have the same potency

A

no

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8
Q

can someone like mj but not hashish

A

yes they have different chemicals = 2 separate things

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9
Q

what does phytocanabinoid get its name from

A 
phyto= plant 
cannabinoid= class of chemical
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10
Q

Δ9-Tetrahydrocannabinoid :T

A

THC

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11
Q

generic name for THC

A

dronabinol= medical mj

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12
Q

is the potency of medical mj always the same

A

not to original plant substance

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13
Q

are Δ9-THC metabolites active or inactive

A

active

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14
Q

what are the 2 metabolites of Δ9-THC

A

cannabinol and cannabidiol

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15
Q

does Δ9-THC cannabinol and cannabidiol have the same effects

A

no all different

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16
Q

Cannabinol, cannabidiol are only produced by THC metabolites

A

f can be indepedently found in the leaf

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17
Q

when ingested …. is formed in the liver from THC

A

11-hydroxy-Δ9-THC

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18
Q

if you smoked or ate THC changes the active chemical compounds in your body

A

t

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19
Q

Δ9-THC: what are the effects

A

depends on route of admin

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20
Q

what’s wrong with all the hype around THC

A

there are unique effects of metabolites which can potentiate or interact with THC compounds

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21
Q

what is it you actually want

A

the canabidiol THC will give you a panic attack

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22
Q

why are buttery cocoay pot brownies the best way to make an edible

A

Highly lipid-soluble (butter), however molecule is protein- bound (coca) = problem for fat people drug testing

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23
Q

Highly lipid-soluble, however molecule is protein- bound why is this a complication

A

potency and distribution differ widely

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24
Q

2 things synthetics try and do

A
  1. interact with receptor without molecule looking like original molecule
  2. try to derive the molecule from everything else= get it on its own
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25
Q

what is a partial vs a full synthetic

A 
partial= dereiviate 
full= generate in lab
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26
Q

street names for synthetic cannabinoid alternatives

A

K2 or spice

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27
Q

what 2 systems do synthetic cannabinoids target

A

seretonin and cannabinoid

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28
Q

synthetics Emerged from scientific research meant to study the
effects on …

A

receptors

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29
Q

3 types of synthetics

A

classic, non classical and hybrid

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30
Q

what is an example of a classic synthetic

A

dronabinol =derived from chemical choosing pieces you need

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31
Q

T: synthesized analgesics

A

nonclassical

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32
Q

Aminoalkylindoles what can we tell from this name

A

indole= seretonin

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33
Q

synthetic anti-inflamatory, antihyperalgesia :T

A

Aminoalkylindoles

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34
Q

synthetic: synthesized endo; immune response, pain

perception :T

A

eicosanoid (look at molecule in body not leaf)

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35
Q

3 quadrants of syntheitcs?

A

classical, aminoalkylindoles, eicosanoid

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36
Q

which of the 3 quadrants of synthetics is focused on for medical use

A

aminoalkylindoles

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37
Q

synthetic can are Marketed under different street names what are 2

A

“potpourri” and “incense”

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38
Q

why called incense

A

you don’t smoke it you burn and inhale it

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39
Q

synthetic cannabinoids show properties of what 2 drug classes

A

stimulant and hallucinogen

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40
Q

are synthetic cannabinoids partial or full agoinsts

A

full

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41
Q

what is the problem with synthetic can

A

contamination with other chemicals

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42
Q

4 things synthetic can are cut with

A

Oleamide, harmine/harmaline, cathinone, MAO-I

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43
Q

are synthetic can strictly street drugs

A

they have them in pharm research but not being distributed

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44
Q

is hashish more potent than Mj

A

hard to say

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45
Q

3 problems in deciphering if hash or mj is more potent

A
  1. dose depedant
  2. variable concentrations in modern strains
  3. stews comparing these 2 in research
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46
Q

why can’t you just give same dose of hash and mj

A

how much inhaled smoking mj vs inhaling resin and doses vary due to strain

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47
Q

THC: …% in 1980s to …% in 2000’s depending on strain

A

2, 8-20

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48
Q

high potency makes it easier to have a good time

A

f a bad time

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49
Q

T: marijuana of a variety that has a particularly high concentration of psychoactive agents.

A

sinsemilla (skunk)

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50
Q

“buzz” -> “high” -> “stoned” what does each of these feel like

A

Light-headed, tingling → euphoric, exhilarated → calm, relaxed

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51
Q

2 most popular methods of intake

A

inhalation and ingestion

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52
Q

how long does ti take for it to hit you when you’re inhaling it and how long does it last

A

1 min – 2/4 hr (how long it lasts depends on strain, and what in joint)

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53
Q

… of the Δ9-THC is released into smoke

A

Only 50%

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54
Q

how much of that 50 % is then absorbed into lungs

A

20%

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55
Q

what effects absorption in lungs

A

time held in lungs

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56
Q

T: second-hand inhalation can result in

psychoactive levels

A

contact high

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57
Q

is contact high really a thing

A

Little evidence that this is a possibility in casual social situations

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58
Q

how long to kick in and how long did it last with ingestion

A

1hr- 4/6hr (slowly released into blood stream)

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59
Q

first-pass metabolism deactivates …% of THC

A

50

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60
Q

ingestion: Requires… more to achieve comparable high to inhalation

A

x3 (because of slow onset)

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61
Q

Requires x3 more to achieve comparable high to inhalation why does this make it dangerous

A

slow onset: people don’t realize they are high

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62
Q

is a pot brownie or smoking more detectable on a drug test

A

pot brownie bcs highly lipid soluble

63
Q

4-5 days of use leads to ~ … day long-term pharmacological action

A

7 (still in urine- lingers)

64
Q

problem with the long lasting action of ingested canniboids

A
  1. potency- if you eat again 4 days after your adding to what’s already in system
  2. LT effects? cannabinoid hypermesis syndrome
65
Q

Debate with ingestion: Evolutionary “gatekeeper” mechanism?

A

??

66
Q

at what dose do you get euphoria

A

high

67
Q

problem with ingestion?

A

lack of immediate effects makes users eat more

68
Q

4-5 days of use leads to ~ … day long-term pharmacological action

A

7

69
Q

when endogenous system cannaboids work on

A

endocannabinoid

70
Q

“Gateway” or “Stepping-stone” Theory was supported by the process of illicit drug use: what were the 3 stages in the process

A

Alcohol → Marijuana → stim/opioid/halluc.

71
Q

does this route support gateway theory

A

no has nothing to do with the way the drug makes you feel but about availability in societies

72
Q

any evidence for gateway

A

no support for process not for outcome

73
Q

2 problems with process supporting gateway

A

Not all users progress to the next step (~ only 10-20%) – Users still make use of earlier process drugs

74
Q

T: Drug use is accounted for by the user’s

characteristics (i.e. propensity for drug use)

A

correlated vulnerabilities

75
Q

what does correlated vulnerability theory say the relationship between cannabis and elicit drug use is

A

Users will use anything, not a function of kind of drug (psychological state of user not drug itself)

76
Q

what LT effects found in users vs non users cognitively 2

A

users= lower Verbal fluency & Divided attention (correlation not causation)

77
Q

LT mj users showed … focus on one task = no divided attention

A

perseverating (struggle with attention)

78
Q

differences found b/wn heavy users, former heavy

users, light users, and nonusers?

A

Intellectual impairment reversed with abstinence (heavy users spew intellectual impairments)

79
Q

how were heavy users impaired

A

severe verbal IQ deficits(maybe these people had less schooling)

80
Q

heavy users had 40% higher chance for …. 3

A

schizophrenia, GAD, and depression

81
Q

how did heavy users brains differ

A

Changes in dopaminergic pathway (developmental trend in those who started use before 17= LT changes in endocan system)

82
Q

re adverse consequences caused by changes to endocannabinoid system

A

no brain changes maybe interacts with dopamine pathway which could cause adverse effects

83
Q

3 confounds that could also account for adverse effects from correlational study

A

reflect effect of cannabis on development, traits of user, or social ramification of use?

84
Q

is there tolerance with cannabinoids

A

yes but rapidly dissipate

85
Q

in the 8 week, in-lab study; 1-4 weeks free access to joints how did how many joints they took a day change

A

Day 1: 1 per day, Day 21: 19 per day

86
Q

what were the reports from participants during tolerance study

A

Participants complained joints were becoming weak

87
Q

what were the negative outcomes by the end of tolerance study with heavy use

A

suspiciousness, paranoid, agitated, apathetic,

withdrawn and depressed

88
Q

what did the in lab joint study tell us about tolerance

A

Implies downregulation of receptors

89
Q

what happened when they cut people off from the joints? week 5

A

irritability, uncooperativeness, resistance, and hostility, appetite suppression, insomnia (tolerance mechanisms)

90
Q

does mj have an effect on seretonin

A

yes

91
Q

what happened at week 6

A

symptoms dissipate

92
Q

2 cannabis related syndromes?

A

cannabis dependance and cannabis withdrawl syndrome

93
Q

does light use do to tolerance

A

none= no dependance

94
Q

T: general criteria of substance dependence

A

cannabis dependance

95
Q

T: 3 of the following
• Irritability, anger/aggression, anxiety, depressed mood, difficulty sleeping, decreased appetite, and physical symptoms

A

cannabis withdrawl syndrome

96
Q

why separate dependance from withdrawl syndrome

A

might have life disruptions without having withdrawl

97
Q

unique withdrawl symptom to mj?

A 
Nausea, vomiting and colicky abdominal pain1 as a
result of (weekly) cannabis use2 following a history of cannabis use for years3  (why we used it for horses)
98
Q 
T: Nausea, vomiting and colicky abdominal pain1 as a
result of (weekly) cannabis use2 following a history of cannabis use for years3
A

cannabinoid hypermesis syndrome

99
Q

what’s interesting about can hyp syndrome

A

time frame

100
Q

what is cannabinoid hyperemesis syndrome caused by 2

A

toxicity or changes to hypothalamus

101
Q

support for hypothalamus disregulation explanation for Cannabinoid Hyperemesis Syndrome

A

Compulsive hot baths (for symptom relief)= temp influ by hypothalamus

102
Q

what is support for toxicity explanation of can hyp syndrome

A

buildup in tissue in intestine= toxicity

103
Q

which explanation for can hyp syndrome explains temporal onset and defunct elimination

A

toxicity

104
Q

Δ9-THC how many overdoses from this

A

none= low toxicity

105
Q

T: is used to treat loss of appetite that causes weight loss in people with AIDS.

A

dronabinol (only Δ9-THC no other chemicals)

106
Q

how many mg per kg is dronabinol prescribed at

A

30mg / kg = we do see toxicity because this is so much in pill

107
Q

side effects of dronabinol

A

lethargy, decreased motor coordination, slurred speech, and postural hypotension

108
Q

T: walking very thud thud torso swaying with heavy gait

A

postural hypotension

109
Q

how accurate are people at telling if they are on THC or placebo

A

100% accuracy

110
Q

could they discriminate between against benzodiazepine, opioid, or stimulant or THC

A

Accuracy of 100% on small doses, and 85% on larger doses

111
Q

which drugs were THC confused with at high doses

A

Confound with analgesics and methylphenidate: sensitive to pain relief and attentional component of mj

112
Q

what can we tell from discriminatory studies

A

Δ9-THC results in unique stimulus effects

113
Q

could people discriminate between different doses

A

90% accuracy of “high” vs. “stoned” reports correlating with dosage= medium from high

114
Q

people usually have a good first experience with mj

A

f have to be coached to engage in experience

115
Q

T: First-time users require “instruction” to experience effects

A

learned response = guided = not only physiological?

116
Q

… affect positive or negative outcome

A

Attitudes

117
Q

what parts of mj have pain relieving and relaxing effects

A

cannabidiol and cannabinol

118
Q

2 natural endocannaboids

A

anaamide, 2-AG

119
Q

what kind of receptor is CB1

A

Metabotoropic (G-protein coupled) Receptors

120
Q

3 areas of brain CB1 causes motor inhibiton

A

basal ganglia, substantia nigra, cerebellum

121
Q

3 areas where CB1 causes mood elevation and psychosis

A

nucleus accumbens, ventral tegmental area, hippocampus

122
Q

where does CB1 effect memory

A

hippocampus

123
Q

where does CB1 cause cognition and pain relief

A

cerebral cortex

124
Q

where does CB1 cause pain relief

A

spinal cord and thalamus

125
Q

where does CB1 effect appetite

A

hypothalamus

126
Q

what kind of agonism in cannabis

A

partial

127
Q

what NT and where is stimulating effect of cannabinoids

A

increased dopamine in the NA

128
Q

T: modulates release of neurotransmitter, reducing firing rate

A

retrograde NT molecule

129
Q

what effect does the retrograde NT molecule

A

calming

130
Q

what does CB2 do and where is it made

A

in hippocampus, immunofacilitative function

131
Q

where are CB2 receptors

A

on glial cells, [white blood cells, leukocytes, and mast cells]

132
Q

Lack of 2-AG correlated with ….

A

bowel cancer

133
Q

Cancer has CB2 receptors that when triggered causes …

A

apoptosis (cell death)

134
Q

Behavioural Effects of Δ9-THC

A

dose dependent

135
Q

how are ❖Motor coordination and reaction time influenced

A

Low dosage: increase in motor activity decrease coordination • High dosage: decrease motor activity increase in reaction time

136
Q

…. to disruptions in vigilance

A

Compensatory reactions

137
Q

T: Persistent lack of motivation to engage in productive activities

A

amotivational syndrome

138
Q

is there evidence for motivational syndrome

A

No evidence for the effects of cannabinoids in research focusing on reward-based strategies
but maybe for self motivated or unrewarded tasks
Not found in cross-cultural studies

139
Q

how did cannabis make effortful tasks seem

A

less effortful but were worse at it

140
Q

are both the behavioural and cognitive effects dose dep

A

yes

141
Q

what happens to ST memory

A 
low= memory deficit with no attentional impairment 
high= memory reasoning and attentional impairment
142
Q

how were cognitive deficits shown in the brain

A

less LTP in hippocampus

143
Q

what did developmental persistence studies find

A

permenant decline for every 5 mj years of exposure (strategies, proactive/retroactive interference)

144
Q

T: perception of time is slowed down= cognitive effect

A

decelerated time

145
Q

what phase of high does decelerated time occur

A

stoned

146
Q

what’s happening in brain that accounts for decelerated time

A

reduced blood flow to cerebellum

147
Q

T: alteration in perceptions associated with time

A

temporal disintegration

148
Q

e.g. of temporal disintegration

A

tempo and sequence errors

149
Q

T: Spontaneous, seemingly random ideas

A

flight of ideas

150
Q

what causes flight of ideas

A

orienting and time perception deficits (?)

• Cognitive threshold impairment (?)

151
Q

Debate: low should cause confusion, high should cause “numbing”

A

??

152
Q

how are executive functions altered

A

Shift/Inhibit activities= impaired while abstinent for chronic users

153
Q

Debate: associated with developmental milestones

A

??

345A (20 decks)

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