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PMCOL 200 > Cannabis > Flashcards

Cannabis Flashcards

1
Q

what is cannabis?

A

genus of a flowering plant

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2
Q

what 2 bioactive compounds does cannabis contain that are most studied? (has more)

A

tetrahydrocannabinol (THC) and cannabidiol (CBD)

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3
Q

what is the primary psychoactive compound in cannabis?

A

THC

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4
Q

what are cannabinoids?

A

class of chemical compounds that act at cannabinoid receptors

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5
Q

t/f: cannabis contains few phytocannabinoids

A

false, contains hundreds of phytocannabinoids (∆9 THC and CBD most popular)

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6
Q

t/f: cannabis contains hundreds of non-cannabinoid substituents

A

true

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7
Q

what are terpenoids?

A

substances that give cannabis its characteristic smell

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8
Q

what have in vivo and in vitro studies of terpenoids found?

A

terpenoids have anti-inflammatory, anti-bacterial and anti-anxiety effects (no clinical trials)

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9
Q

what may explain difference btwn experiences of cannabis based on strains?

A

possible synergy btwn cannabis ingred. in diff strains (difficult for clinical use-hard to isolate effective compounds)

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10
Q

what is absorption/bioavailability?

A

fraction of an administered drug that reach effectors (plasma to CNS)

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11
Q

what ingred. does most pharmacokinetic info. on cannabis pertain to?

A

THC

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12
Q

what is the difference btwn bioavailability and peak plasma conc. for smoking vs ingesting THC?

A

smoking: 25% bioavail., peak conc in 6-10 min
ingesting: 6% bioavail., peak conc in 2-6 hours

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13
Q

t/f: it is easier to overdose on THC when it is smoked

A

false, easier to overdose when ingested as it has decr bioavail. and reaches peak plasma conc slower (may cause incr dose)

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14
Q

t/f: THC is highly lipophilic and is taken up in tissues w/ high blood flow

A

true (in heart, lungs, brain, and liver)

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15
Q

t/f: tissues w/ less blood flow don’t accumulate THC such as adipose tissue

A

false, adipose tissue can accumulate THC slowly and release it for days (chronic cannabis smokers)

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16
Q

which enzyme in the liver metabolizes THC?

A

cytochrome P450 2C9 (CYP2C9)

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17
Q

what is the active vs inactive metabolites for CYP2C9 degradation of THC?

A

active: 11-OH-THC
inactive: THC-COOH (excreted)

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18
Q

in 5 days, __-__% of THC is excreted, __% in feces and __% in urine

A

80-90% THC excreted, 65% in feces, 25% in urine

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19
Q

how long can THC be detected in urine after low vs chronic/daily dose?

A

low: 2-5 days

chronic/daily: weeks (accumulates in adipose tissue)

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20
Q

what kind of receptors are cannabinoid receptors?

A

Gi protein-coupled receptors (decr cAMP)

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21
Q

what are the 2 cannabinoid receptors?

A

CB1 and CB2

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22
Q

what does a decr in cAMP from cannabinoid binding to its receptor cause?

A

decr influx of Ca into firing neuron and decr NT release (decr synaptic transmission)

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23
Q

what is THC?

A

partial CB1 agonist

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24
Q

what is a theorized mechanism of action for cannabidiol (CBD)?

A

negative allosteric modulator at CB1 (blunt THC effects)

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25
Q

t/f: CB1 receptors are rarely found in the body

A

false, CB1 receptors are that most abundant GPCRs in the body

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26
Q

where are CB1 receptors found in the body? (3)

A

brian (sparse), peripheral organs (heart, liver, fat, stomach, testes), and peripheral nerves

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27
Q

where are CB2 receptors mostly?

A

immune cells (non-neuronal cells-can explain anti-inflammatory effects)

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28
Q

what does preclinical research suggest are CBD’s potential therapeutic effects? (6)

A

manage inflammation, anxiety, emesis, nausea, inflammatory pain, and epilepsy (lacks clinical data)

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29
Q

what are 6 general effects of THC?

A

euphoria, relaxation, disinhibition, changed perception, vasodilation, incr HR

30
Q

what are 4 therapeutic effects of THC?

A

decr nausea, incr appetite, decr intraocular P, chronic pain relief

31
Q

what are 5 unwanted effects of THC?

A

memory impairment, dysphoric state, hallucination, depersonalization, psychotic episodes

32
Q

what are 6 acute effects of high doses of THC?

A

panic attacks, severe anxiety, psychosis, paranoia, convulsions, and hyperemesis

33
Q

what are prenatal effects of cannabis?

A

can cause neuroanatomical and behavioural changes of fetus

34
Q

t/f: smoking cannabis can cause lung cancer

A

true

35
Q

what are the effects of driving w/ cannabis?

A

incr risk for motor accident (decr perception, psychomotor performance, cognitive functions, and rxn times)

36
Q

t/f: there is documented evidence cannabis overdose can cause death

A

false (due to sparsity of CB1 receptors in brain)

37
Q

what does data suggest about cannabis use (in adolescence) and developing psychotic disorders/schizophrenia?

A

lots of correlative data but don’t indicate causation (reverse causality, bias or confounding variables), can elicit acute psychosis, worsen existing schiz., or trigger development of schiz. in at-risk populations

38
Q

what is psychological dependence?

A

compulsive drug-seeking behaviour for personal satisfaction, despite risks to health

39
Q

what is physiological dependence?

A

symptoms produced by drug withdrawal, are usually opposite to desired effects

40
Q

what is cannabis withdrawal like?

A

mild and short-lived (restless, irritable, agitated, insomnia, nausea, cramping) but worse in chronic users

41
Q

what is addiction/substance use disorder defined as?

A

inability to control use of legal or illegal substances despite negative consequences

42
Q

how many criterion do individuals have to meet to be diagnosed w/ addiction/substance use disorder?

A

11 (tolerance and withdrawal are not mandatory)

43
Q

what is the severity of substance use disorder determined by?

A

of criterion person meets (2-mild, 4-moderate, 6-severe)

44
Q

approx. what % of ppl who use cannabis develop a substance use disorder?

A

~9% (regardless, chronic use can incr risk for dependence/addiction)

45
Q

what are synthetic cannabinoids?

A

manufactured compounds that imitate properties of active constituents of cannabis (THC)

46
Q

what are 4 pros of synthetic cannabinoids?

A

incr specificity, decr off-target effects, easier dosing, more controlled studies

47
Q

what 3 diseases have multiple randomized clinical trials confirmed effectiveness of cannabinoids?

A

nausea/vomiting, anorexia (to incr appetite), weight loss from HIV/AIDS/cancer

48
Q

what is nabilone? what is it used for?

A

synthetic THC analog for chronic pain, multiple sclerosis, etc.

49
Q

what is dronabinol? what is it used for?

A

trans isomer of ∆9-THC for nausea/vomiting after chemotherapy or anorexia in AIDS wasting syndrome

50
Q

what are 3 similarities btwn nabilone and dronabinol?

A

both are partial CB1 agonists, taken orally, and less psychotropic effects than cannabis

51
Q

what are nabiximols (sativex)?

A

sublingual botanical drugs (cannabis extract-1:1 ratio of THC and cannabinol)

52
Q

why were nabiximols (sativex) created?

A

to relieve pain in ppl w/ multiple sclerosis and cancer (less psychotropic effects than smoked cannabinoids)

53
Q

what is rimonabant?

A

inverse CB1 agonist (opposite effects)

54
Q

why was rimonabant created but later withdrawn?

A

to treat obesity (inverse agonist-decr appetite) but caused depression and suicidal ideation

55
Q

what are endocannabinoids?

A

endogenous cannabinoids (made by body) that regulate mood, feeding, and motor function

56
Q

t/f: cannabinoid receptors evolved in response to cannabis

A

false, we have endogenous cannabinoids

57
Q

what are 2 endocannabinoids?

A

anandamide (AEA) and 2-arachinoyl glycerol (2-AG)

58
Q

how are AEA and 2-AG made in the body?

A

from the phospholipid bilayer of cell memb (~arachidonic acid)

59
Q

what is the biochemical synthesis pathway for AEA?

A

N-acetyltransferase converts phosphatidylethanolamine (PE) to N-arachydonoil-PE (NAPE), phospholipase D converts NAPE to AEA

60
Q

what is the biochemical synthesis pathway for 2-AG?

A

phospholipase C converts phospholipid to DAG, DAG lipase converts DAG to 2-AG

61
Q

what does “AEA and 2-AG are retrograde NTs” mean?

A

act on cannabinoid receptors on presynaptic memb.

62
Q

how do AEA and 2-AG sort of act in a negative feedback loop?

A

are synthesized on demand in postsyn. cell w/ AP, are released back into synapse where they bind to Gi CB1 receptors which inhibits future NT release

63
Q

how do endocannabinoids act like THC?

A

decr neuronal release of other NTs (Glu)

64
Q

when and where are AEA and 2-AG synthesized?

A

w/ incr intracellular [Ca] in depolarized postsynaptic neuron; only active regions of brain

65
Q

what enzymes metabolize AEA va 2-AG in presynaptic cell?

A

AEA: fatty-acid amide hydrolase (FAAH)

2-AG: monoacylglycerol (MAGL)

66
Q

what does suppression of FAAH and MAGL cause?

A

incr activity of AEA and 2-AG

67
Q

why were FAAH/MAGL inhibitors created?

A

to incr activity of AEA and 2-AG in active areas of brain (not entire brain) to decr pain (analgesic effects) wo/ psychoactive effects, sedation, catalepsy, or hypothermia

68
Q

why was a clinical trial of a FAAH inhibitor (BIA-2474) halted?

A

had several, severe off-target effects (death/hospitalization)

69
Q

Genetic variation in which gene had been associated with incr risk of developing psychotic disorders with cannabis use?

A

Catechol-O-methyltransferase (COMT)

70
Q

t/f: AEA and 2 -AG are stored in vesicles in postsynaptic memb

A

false, they’re generated on-demand after enzymatic transformation

PMCOL 200 (27 decks)

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