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PCL200 > Cannabis > Flashcards

Cannabis Flashcards

1
Q

cb1 receptors are the most abundant ________ in the brain

A

g-protein coupled receptor

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2
Q

what are cb1 receptors activated by

A

endocannabinoids and thc

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3
Q

thc is the _____ of cb1 receptor

A

agonist

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4
Q

what receptor did cannabis help us discover

A

cb1 receptor

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5
Q

where are cb1 receptors expressed in the body

A

brain (in diff levels), lungs, liver, kidney, pancreas, bone

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6
Q

what are cb2 receptors thought as

A

“nonbrain receptor” - bc present in much less abundance than the cb1 receptor
“peripheral cannabinoid receptors” - more expressed in the body than the brain

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7
Q

where are cb2 receptors found

A

in the brain (lower levels), in immune cells

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8
Q

what nt activates cb2 receptors

A

thc and endocannabinoids

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9
Q

describe the endocannabinoid system

A

makes second by second adjustment in which neurons are firing and which isn’t = when you manipulate this system, a lot of brain function is impacted

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10
Q

name 2 examples of endocannabinoids

A

anandamide, 2ag

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11
Q

explain the process of 2 AG in the brain (specifically on the CB1 receptor)

A

Intense activation of the neuron causes the production of 2AG. 2-AG leads to activation of an enzyme which cuts/clips the 2-AG and then the 2-AG floats everywhere (diffuses locally) and lands/binds on CB1 receptors (pre-synaptic) –> 2AG activates the CB1 receptor which causes less glutamate to be released by decreasing the the likelihood of synaptic vesicles fusing ==> less glumate release means more normal activation

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12
Q

are endocannabinoids made by the pre or post synaptic neuron

A

post synaptic neuron

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13
Q

what are endocannabinoids made by

A

made on demand by enzymes that convert membrane lipids into eCBs

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14
Q

explain the process of endocannabinoids in the brain (specifically on the CB1 receptor)

A

eCBs diffuse out (postsynaptic neuron) and bind to the nearby cb1 receptors on the presynaptic neurons (at axon terminal) - these are quickly degraded by other enzymes so they act for short time - they are agonists(?) and activate the cb1 receptor = presynaptic neuron to release less NT

the presynaptic neuron could be glutamate or gaba

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15
Q

difference in the action timing of thc and eCBs

A

eCB short and thc long

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16
Q

compare and contrast thc to endocannabinoids:
- the degradation time
- effects on appetite
- effects on pain and how
- effects on learning and memory
- anything else:

A

endocannabinoids
- quickly degraded - fast acting modulators to correct level of neurotransmission
- appetite stimulant
- reduces pain (part of descending pathway - same pathway that morphine works)
- promotes learning and memory (difficult without eCB)
- promotes bone formatoin

thc
- long lasting - acute effects last for hours, accumulation in fat tissue, lasts in body for weeks
- appetite stimulant and anti-emitic (reduce vomiting) –> may cause hyper-emesis
- reduces pain (analgesic) and muscle spasticity
- impairs learning and memory
- hallucinations (sensory & time distortion)
- psychosis at high doses

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17
Q

plants make different cannabinoids that are ______ in structure

A

similar

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18
Q

where does the name cannabinoid come from

A

they go to the cb receptors

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19
Q

what comprises phytocannabinoids

A
  • Δ^9THC (tetrahydrocannabinol)
  • cbd (cannabidiol)
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20
Q

effects of Δ^9THC

A
  • euphoric
  • munchies
  • analgesic
  • anti-emitic
  • psychosis
  • memory loss
  • hallucinations
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21
Q

cbd

A
  • does not cause a “high”
  • anti-epilepsy
  • anti-psychotic
  • anti-cancer
22
Q

endocannabinoids

A
  • appetite stimulation
  • pain processing
  • learning and memory
  • bone formation
23
Q

overall effects of cannabis

A
  • pain relief in multiple sclerosis (myelination of motor neurons)
  • anti nausea
  • appetite stimulation - important for people with AIDS
  • epilepsy treatment
  • impairs short-term memory
  • impairs attention, judgment, and other cognitive functions
  • impairs learning skills
  • risk of psychosis and schizophrenia in vulnerable individuals
  • can lead to cannabis use disorder (dependence, addiction)
24
Q

effects of eCBs and cannabis on diff parts of the brain:
striatum, amygdala, brain stem & spinal cord, cortex, hypothalamus, hippocampus

A

striatum
eCBs: reward, pleasure
Cannabis: high

amygdala
eCBs: emotion, fear
Cannabis: effects on mood

brain stem and spinal cord
eCBs: vomit reflex, pain control
Cannabis: anti-nausea, pain relief

cortex
eCBs: cognitive function
Cannabis: cognitive impairment (chronic, high dose)

hypothalamus
eCBs: appetite
Cannabis: muchies (acute)

hippocampus
eCBs: learning, memory
Cannabis: memory impairment

25
Q

relationship between cannabis and psychosis (new zealand study)

A

cannabis use is associated w an increased risk of experiencing schiz symptoms, even after psychotic symptoms. early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). did not predict later depression.

26
Q

what does daily cannabis use lead to

A

tolerance (down regulation of CB1 receptors), dependence & withdrawal

27
Q

what is the dsm-v

A

the instruction manual that pharmacologists use. cannabis use disorder (cannabis addiction) and cannabis withdrawal are apart of it

28
Q

what are withdrawal symptoms of cannabis (may take weeks to subside)

A

depression and anxiety, insomnia, gi distubrances, reduced appetite

29
Q

__% of those who use cannabis may have some degree of cannabis use disorder

A

30

30
Q

what are the withdrawal that peaks within the first week after quitting (and can last up to 2 weeks)

A

irritability, mood and sleep difficulties, decreased appetite, cravings, restlessness, and/or various forms of physical discomfort

31
Q

when does the cannabis use disorder become an addiction

A

when the person cannot stop using the drug even though it interferes with many aspects of his or her life

32
Q

what are the names of the drugs used for medicinal cannibis

A

(know the first names)
- nabiximol - sativex (mouth spray) made up on 1:1 thc and cbd
- cannabidiol - epidiolex
- dronabinol - marinol from
(pure) thc
- nabilone from thc

33
Q

what are the uses for nabiximol

A
  • mouth spray
  • reduces muscle spasticity and pain that accompanies multiple sclerosis
  • reduces pain in cancer patients
34
Q

what are the uses for cannabidiol

A
  • approved to treat childhood epilepsy
  • cbd is tested for treatment of chronic pain and inflammatory disorders
35
Q

what are the uses for dronabinol

A
  • treat anorexia in hiv/aids
  • treat nausea and vomiting induced by chemotherapy
36
Q

how is dronabinol prescribed (injested)

A

as a capsule containing thc

37
Q

what is the relationship between dronabinol and nabilone

A

nabilone is a synthetic analog of dronabinol

38
Q

what are the (directed) uses for nabinol

A
  • treats anorexia associated w hiv/aids
  • treat nausea and vomiting with chemo
39
Q

what are the off-label uses of nabilone

A

treatment of chronic pain/neuropathic pain and fibromyalgia

40
Q

what does off-label uses mean

A

practice of prescribing a drug for a different purpose than what the FDA approved

41
Q

what was the intended purpose of rimonabant

A

reduced food intake and promoted weight lost

42
Q

rimonabant is a CB1______

A

antagonist

43
Q

why was rimonabant taken off the market (in 2008)

A

caused suicidal ideation

44
Q

why were pharmaceutical companies interested in drugs that blocked the cb1 receptor

A

cb1 receptors in the liver and adipose tissue also promote fat storage, so blocking the receptor could reduce fat deposition

45
Q

why is it important to prevent obesity

A

Obesity sets them up for diabetes, CVD, heart attack so the CB1 antagonists might be able to help them with this

46
Q

since cb1 agonists (eg thc) can cause psychosis, would a cb1 antagonist bc effective as an antipsychotic

A

possibly

47
Q

current treatments for schizophrenia and bpd cause weight ____, so a treatment that reduces __________ and weight ____ could be a substantial improvement for therapy

A

gain, psychosis, gain

48
Q

why might cb1 antagonists cause suicidal ideation

A

it impacts the ability to feel pleasure. the loss of appetite may be caused by a loss of dopamine
^ depends on part of the brain causing the appetite suppression

49
Q

why is it difficult to find appropriate obesity medication

A

it mostly impacts the ability to feel pleasure - matter of concern

50
Q

activating cb1 receptor = ______ dopamine
blocking cb1 receptor = _____ dopamine

A

more, less

PCL200 (5 decks)

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