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Cannabis Flashcards

1
Q

Cannabinoid actions are receptor-dependent because: (3)

A
  1. Modulate intracellular signal cascades
  2. Temperature dependent
  3. Saturable
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2
Q

If CB1 is activated on an inhibitory neuron, what happens?

A

It blocks the release of inhibitory neurotransmitter (double-negative), meaning something is going to be activated

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3
Q

What is the type 1 cannabinoid receptor (CB1R)? (2)

A
  1. G𝜶i/o-coupled G protein-coupled receptor (clasically)
  2. Most-abundant GPCR in the CNS
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4
Q

What is CB1R activated by? (3)

A
  1. 2-AG (2-arachidonyl glycerol) and AEA (anandamide)
  2. THC (the high)
  3. Spice/K-2 compounds (e.g. CP55,490 and JWH-120)
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5
Q

What is CB1R inhibited by? (2)

A
  1. Rimonabant (SR141716A)
  2. CBD (indirectly)
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6
Q

What is the type 2 cannabinoid receptor (CB2R)? (2)

A
  1. Also G𝜶i/o-coupled G protein-coupled receptor (classically)
  2. Expressed and induced at immunomodulatory cells
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7
Q

What is an orphan receptor?

A

A receptor for which we do not know the endogenous ligand

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8
Q

What are 3 orphan GPCRs that have been identified that respond to exogenous cannabinoids?

A
  1. GPR55 – expressed predominantly in immune cells and osteoclasts/osteoblasts. Activated by THC. Endogenous ligand may be lysophosphatidyl inositol
  2. GPR18 – expressed in microglia. Activated by THC and CBD. Endogenous ligand may be N-arachidonoyl glycine (related to 2-AG)
  3. GPR119 – expressed in pancreas and gut. Activated by derivates of 2-AG and AEA. Endogenous ligand may be N-palmitoylethanolamine
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9
Q

Where is the transient receptor potential vanilloid 1 (TRPV1) receptor found?
What activates it?

A
  1. Ligand-gated Ca2+ channel expressed on central and peripheral nociceptive neurons
  2. Activated by AEA and also capsaicin
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10
Q

What are some important endocannabinoid recpeptors to be aware of? (3)

A
  1. CB1
  2. CB2
  3. TRPV1
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11
Q

What was found in humans with FAAH (C/A or A/A) genotypes?

A

Humans with a C/A or A/A genotype show less anxiety, greater propensity to substance use disorder and obesity, and heightened pain perception

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12
Q

Where is CB1R mostly distributed in the brain? (6)

A
  1. Caudate nucleus
  2. Amygdala
  3. Hypothalamus
  4. Substansia nigra
  5. Cerebellum
  6. Dorsal vagal complex
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13
Q

Explain ‘greening out’

A

When you green out, there is so much THC present that it overwhelms the inhibitory process in the dorsal vagal complex and you have an overwhelming urge to vomit

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14
Q

At what age do we (currently) think the human brain reaches mature neuronal development?

A

25

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15
Q

How does activation of CB1 affect memory?

A

Activation of CB1 impairs long-term potentiation in the hippocampus and reduces short-term memory

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16
Q

CB1 activates neurogenesis in the _______ _____ and ___________ ____

A

dentate gyrus; subgranular zone

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17
Q

Cannabinoids can facilitate short-term depression via ___ vs. long-term depression via _____

A

CB1; TRPV1

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18
Q

Explain what happens with CB1R and the HPA axis

A

Activation of CB1R habituates the HPA axis
- AEA decreases corticosterone secretion
- 2-AG inhibits excessive glucocorticoid release

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19
Q

Activation of CB1R in the amygdala is __________. Examples? (3)

A

anxiolytic
1. In GABAergic neurons this improves socialization, NORT, and exploration (mice)
2. In glutamatergic neurons this reduces aggression and excessive arousal
3. 2-AG and AEA levels are also circadian, peaking during slow-wave sleep

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20
Q

Explain the role of cannabinoids in pain perception (3)

A
  1. CB1R activation inhibits GABAergic interneuron transmission, which disinhibits descending, pain-attenuating pathways from the brainstem
  2. TRPV1, GPR55, and PPAR are also involved
  3. One possible mechanism for acet is the inhibition of AEA catabolism (i.e., endocannabinoid augmentation)
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21
Q

What role do cannabinoids play in thermoregulation? (2)

A
  1. In humans and non-human primates, TRPV1 regulates temperature through hypothalamic and vasodilatory mechanisms (AEA and N-arachidonoyl dopamine)
  2. In other mammals, CB1R also contributes to thermoregulation, with CB1R activation –> hypothermia
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22
Q

Explain how cannabinoids play a role in appetite (4)

A
  1. Acute activation of CB1R stimulates appetite
  2. Chronic stimulation of CB1R reduces appetite
  3. Inhibition of CB1R reduces food intake and weight (central and peripheral mechanisms)
  4. The effect of CB1R inhibition on food intake has implications for addiction as well (e.g., rimonabant was used for smoking cessation, too)
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23
Q

What role do cannabinoids play in adipocytes? (metabolism)

A

Activation of CB1R increases lipogensis

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24
Q

What role do cannabinoids play in hepatocytes? (metabolism)

A

Activation of CB1R increases fatty acid oxidation, VLDL-TG clearance, de novo lipogenesis; chronic activation of CB2R stimulates fibrosis

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25
Q

What role do cannabinoids play in the GIT? (metabolism)

A

Activation of CB1R decreases GI motility and permeability

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26
Q

What role do cannabinoids play in skeletal muscle? (metabolism)

A

TRPV1, PPAR, and CB1R activation increases insulin sensitivity

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27
Q

What role do cannabinoids play in the pancreas? (metabolism)

A

CB1R activation stimulates insulin release (can lead to insulin resistance)

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28
Q

What role do cannabinoids play in the hypothalamus? (metabolism)

A

CB1R activation stimulates leptin release (eventual leptin resistance), decreases adiponectin release

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29
Q

What role do cannabinoids play in immune function?

A

CB1R < CB2R limits TNFa and pro-inflammatory chemokines
- CB2R upregulated in response to inflammation
- Esp. in macrophages & mast cells

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30
Q

What utility do cannabinoids have in MS? (3)

A

CB2R activation increases:
1. Oligodendrocyte survival and growth
2. Microglial proliferation
3. Schwaan cell survival and growth

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31
Q

What role do cannabinoids have in reproduction - females specifically? (2)

A
  1. CB1R levels rise and fall alongside progesterone, which may help to initiate menses
  2. CB1R expressed on sensory and sympathetic fibres throughout the uterus
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32
Q

What role do cannabinoids have in reproduction - males specifically? (2)

A
  1. CB1R expressed at high levels on spermatocytes and sperm
  2. Cannabinoids inhibit sperm maturation, motility, acrosome reaction, and mitochondrial function
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33
Q

What role do cannabinoids have in reproduction (for both sexes)

A

Exogenous cannabinoids are sex hormone mimetics that inhibit the activity of testosterone and augment the activity of estrogen

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34
Q

Name the endocannabinoids (6)

A
  1. 2-Arachidonoylglycerol (2-AG)
  2. 1-Arachidonoylglycerol
  3. Noladin ether
  4. 2-Oleoylglycerol
  5. Anandamide (AEA)
  6. Palmitoylethanolamide
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35
Q

What are the phytocannabinoids? (2)

A
  1. Δ9-tetrahydrocannabinol (THC) - gets you high - CB1R and CB2R partial agonist
  2. Cannabidiol (CBD) - multiple MOAs
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36
Q

What are the 4 types of synthetic cannabinoids?

A
  1. “Classic” Cannabinoids
  2. 1st Gen Aminoalkylindoles
  3. Antagonists (Rimonabant)
  4. “Spice” Compounds
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37
Q

What is ligand bias?

A

The ability of ligands to differentially activate certain receptor signaling responses compared with others

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38
Q

How might ligand bias potentially be used in cannabinoids? (2)

A
  1. In theory, receptor signaling can be directed toward a preferred pathway and away from an unwanted pathway
  2. For cannabinoids this link is less clear but may be useful for avoiding drowsiness, metabolic effects, Beta-arrestin-mediated downregulation at CB1R
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39
Q

What is positive allosteric modulation (PAM)?
How about negative allosteric modulation (NAM)?

A
  1. Binds somewhere on the receptor, and promotes signaling by orthosteric ligand. Makes the environment better for the receptor to work. Net outcome is increased signaling. PAM should do nothing by itself though if no orthosteric agonist present
  2. NAM does the opposite of PAM basically (decreased signalling)
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40
Q

How might PAM and NAM potentially be used in cannabinoids (formulation?)?

A

In theory: reduced likelihood for dependence, tolerance, adverse effects because the drug is only effective in the presence of an orthosteric ligand

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41
Q

An example of a novel CB1R PAM is?

A

GAT211 - can turn up the volume of cannabinoid receptor signaling but cannot activate the receptor itself

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42
Q

True or False? PAMs produce tetrad effects

A
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43
Q

Which of the following is not considered a cannabinoid receptor?
a. CB1R
b. CB2R
c. 5HT1A
d. TRPV1

A

c.

44
Q

Which of the following is an endogenous cannabinoid?
a. Δ9-tetrahydrocannabinol
b. Anandamide
c. Arachidonic acid
d. Cannabidiol

A

b.

45
Q

How do the synthetic cannabinoids (aka ‘spice’ compounds) differ from Δ9-tetrahydrocannabinol (THC)?
a. Synthetic cannabinoids are receptor full agonists
b. Synthetic cannabinoids are receptor antagonists
c. Synthetic cannabinoids cannot be smoked
d. Synthetic cannabinoids have fewer adverse effects

A

a.

46
Q

Which of the following is the enzyme that catabolizes (i.e., breaks down) anandamide?
a. Monoacylglycerol lipase (MAGL)
b. Cytochrome P450 2C9 (CYP2C9)
c. Serine hydrolase 6 (ABHD6)
d. Fatty acid amide hydrolase (FAAH)

A

d.

47
Q

In theory an allosteric modulator should have fewer adverse effects than a ‘typical’ orthosteric compound because:
a. Allosteric modulators directly activate their target receptor
b. Allosteric modulators only effect their target receptor when an endogenous ligand is present
c. Allosteric modulators are metabolized by different enzymes
d. Allosteric modulators tend to be more water soluble and therefore are better absorbed into the blood stream

A

b.

48
Q

What enzyme catabolizes 2-Arachidonoylglycerol (2-AG)?

A

MAGL (Monoacylglycerol lipase)

49
Q

Touch on smoked and vapourized cannabis.
That is, how quickly to get into the blood?
Bioavailability?
Where it is metabolized?
Threshold?

A
  1. Rapidly partitions into the blood from the lungs (< 30 min)
  2. Bioavailability of ~35 (2-56)%
  3. Transformed in the liver to 11-OH-THC (primary) and THC-COOH (secondary) – both are psychoactive (11-OH-THC > THC-COOH)
  4. Thresholds for intoxication vary based on genetics, past use, etc.
50
Q

Touch on sublingual and nasopharyngeal cannabis.
That is, how does it get into circulation
Bioavailability?
Duration of action?

A
  1. Sublingual and oromucosal (e.g. Sativex) administration bypasses the liver to enter the systemic circulation
  2. Bioavailability ~13%
  3. Duration of action is much longer – in the example graph THC still readily detectable > 50 ng/mL at 8 h
51
Q

How does oral cannabis differ from sublingual/nasopharyngeal? (2)

A
  1. Similar to oromucosal but F is lower (~6%) due to 1st pass metabolism
  2. Delayed onset of action and lower Cmax but longer duration of action
52
Q

Very few clinical studies have been performed on topical/transcutaneous cannabis, but in general, what do they show? (2)

A
  1. Good local bioavailability (~5 ng/mL within 1 h and maintained for 48 h)
  2. Being explored for nausea, hyperemesis, addiction, glaucoma (topical) and pain control
53
Q

What is the concern with topical/transcutaneous cannabis?

A

Concern that individuals may extract drug from patches (similar to fentanyl)

54
Q

Discuss oral absorption of cannabis.
That is, what is the F?
Onset, tmax, cmax?
T1/2?

A
  1. Oral absorption across the gut epithelium is ~100% but 1st pass makes bioavailability ~6%
  2. Onset is 0.5-1h, tmax 2-4h, Cmax 1.32 ng/mL (for a 5mg dose)
  3. T1/2 varies widely based on genetics, body fat content, and frequency of use
    - THC: 18h-4.1d (4h and 25h)
    - 11-OH-THC & THC-COOH 3d-12.6d
55
Q

Discuss cannabis distribution in the body
That is, where does it accumulate? (2)
Plasma protein binding?
Placenta and breast milk?

A
  1. As a lipophilic drug, THC concentrates in fatty tissue (and in lungs if smoked)
  2. Ratio of ~ 21:1 adipose:brain in multiple species, including humans
    – Vd ~ 3.4 – 10 L/kg (very high)
    3.~95% plasma protein bound; otherwise rapidly cleared from plasma and liver
  3. THC partitions into the placenta and breast milk (8.4:1 breast milk to plasma)
56
Q

Discuss cannabinoid metabolism (4)

A
  1. THC (and other cannabinoids) are metabolized in liver by CYP2C9 > CYP3A4 + CYP2D6 to become 11-OH-THC and/or THC-COOH
  2. Extra-hepatic beta-glucoronidases in the gut, cerebellum, and brain stem also transform THC
  3. Cannabinoids may interfere with each other’s metabolism
  4. Metabolite levels peak 0.5-4 h after administration and are detectable for several days
57
Q

Discuss cannabinoid elimination (3)

A
  1. 80-90% of THC is eliminated in 5 d and detectable by current techniques (~ 5 ng/mL) for up to 5 weeks
  2. 65% feces vs. 20% urine
  3. Clearance average from human studies is 0.2 L/kg/h with a range of (0.001 – 2), which is hugely variable
58
Q

What are 2 cannabis DIs to be aware of?

A
  1. Opioids
  2. NSAIDs
59
Q

What is a poor metabolizer (PM)?

A

At least 2 loss of function alleles

60
Q

What is a normal metabolizer (NM) also known as?

A

Also known as extensive metabolizer; EM

61
Q

What is an ultra metabolizer (UM)?

A

At least 3 copies of functional alleles

62
Q

What are the 3 major themes when it comes to gene polymorphisms and cannabis?

A
  1. If drugs are pro-drugs or metabolism produces an active compound, then polymorphisms that increase metabolism will increase drug efficacy & ADRs = reduced safety
  2. Polymorphisms that reduce metabolism may lead to high [drug] and = reduced safety
  3. Polymorphisms that enhance drug metabolism will reduce drug efficacy and may be misconstrued as drug-seeking behaviour
63
Q

Cannabinoids and opioids have PD effects that __________

A

synergize

64
Q

Cannabis and cannabinoids were prohibited and controlled substances (and still are in many jurisdictions), which made clinical research challenging. The studies that do exist typically suffer from? (7)

A
  1. Low power
  2. Lack of binding
  3. Heterogeneity of disease
  4. Heterogeneity of drug (what’s in this cannabis)
  5. Heterogeneity of exposure route
  6. Poor dosing criteria
  7. No PK assessment
65
Q

What is cachexia? Who typically gets it?

A
  1. Wasting syndrome characterized by loss of weight, muscle weakness, fatigue, atrophy, and loss of appetite
  2. Late-stage cancers, patients receiving chemotherapy, AIDS, COPD, late-stage MS, congestive heart failure, etc.
66
Q

How might cannabis be used in cachexia?

A
  1. Medical cannabis widely prescribed to help improve diet and appetite
    - Acts to inhibit orexin and enhance ghrelin signaling
  2. Also prescribed as a palliative care measure
67
Q

As of right now, is there cannabis actually approved for cachexia?

A

No rigorous Phase I or II clinical trials or validated PK demonstration of reliable benefit (2016)
- Dronabinol is approved

68
Q

How might cannabis be used to treat glaucoma? (4)

A

Topical applications of CB1R agonists reduces IOP:
- Reduced production of aqueous humor
- Increased outflow through the trabecular meshwork
- Localized decrease in blood pressure

69
Q

What has been found with the following in MS spasticity treatment:
1. Nabiximols
2. THC
3. Smoked cannabis

A
  1. No improvement
  2. Inconsistent results
  3. Worsened balance
70
Q

What has been found with the following in MS central pain and spasm treatment:
1. Nabiximols
2. THC or THC/CBD
3. Smoked cannabis

A
  1. No improvement or reduced pain intensity
  2. 28-31% of pts reduction in pain and spasm
  3. Reduced pain and spasm
71
Q

What was found with cannabinoids and MS bladder dysfunction and tremor? (2)

A
  1. Nabiximols are effective for reducing bladder dysfunction, whereas THC is not.
  2. 6 published clinical trials to investigate tremor
    - THC and oral cannabis extracts are ineffective for tremor
72
Q

Of the 6 placebo-controlled trials of CBD conducted to date about cannabis and epilepsy, what was found? (3)

A
  1. 39-50% reduction in seizure frequency
    - Incl. Dravet and Lennox-Gastaut Syndromes
  2. Side effects are mild & infrequent:
    - Tiredness, diarrhea, reduced appetite
  3. Dose between 200 – 750 mg or 25 – 50 mg/kg
73
Q

How do CB receptors play a role in pain? (3)

A
  1. CB receptors inhibit nociceptive transmission centrally
  2. Inflammation and nociceptive peripherally
  3. CB1R, CB2R, TRPV1, GPR18, GPR55
74
Q

What has been found in cannabis studies regarding chronic pain?

A

Moderate-quality evidence to support the use of cannabis-based medicines for the treatment of chronic pain but not as a 1st line therapy

75
Q

What has been found in cannabis studies regarding rheumatic disease and fibromyalgia (pain)?

A

Insufficient evidence to recommend any cannabis-based medicine for symptom management

76
Q

What have been the benefits of cannabis in IBD? (6)

A
  1. Decreased nausea and vomiting
  2. Improve appetite
  3. Decreased intestinal motility
  4. Decreased lower esophageal sphincter relaxation
  5. Improved epithelial wound healing
  6. Inhibition of cell proliferation
77
Q

What is the obesity cannabinoid drug?

A

Rimonabant

78
Q

What was found when using rimonabant to treat obesity?

A

Weight loss complimentary to diet and exercise in BMI > 30, type 2 diabetes, or CVD

79
Q

What were the side effects of rimonabant? (2)

A
  • 16x more like to experience depression
  • 8x more likely to express suicidal ideation
80
Q

What does acute cannabis intoxication look like?

A

Clinically significant psychological changes: impaired motor coordination, euphoria, anxiety, a sensation of slowed time, impaired judgement, social withdrawal

81
Q

What are the perceptual disturbances associated with acute cannabis intoxication?

A

Auditory, visual, or tactile illusions occur in the absence of delirium

82
Q

What is cannabis withdrawal defined as?

A

Cessation of cannabis use that has been heavy and prolonged (i.e., daily or almost daily >= 3 months). >= 3 symptoms develop ~ 1 week after cessation

83
Q

What are some symptoms of cannabis withdrawal? (7)

A
  1. Irritability, anger, or aggression (may lead to cannabis-induced delirium or psychoses)
  2. Nervousness or anxiety (may lead to cannabis-induced anxiety)
  3. Sleep difficulty (i.e., insomnia, disturbing dreams) (may lead to cannabis-induced insomnia)
  4. Decreased appetite or weight loss
  5. Restlessness
  6. Depressed mood
  7. > = 1 physical symptoms: abdominal pain, shakiness/tremors, sweating, fever, chills, or a headache
84
Q

When do symptoms of cannabis withdrawal begin? When do they peak? How long can it last?

A

Usually within 24 hours, peak by day 3, and can last for up to 2 weeks. Increased use and more recent use can predict the severity of withdrawal

85
Q

According to the DSM-5, CUD is a problematic pattern of cannabis use leading to clinically significant impairment or distress, as manifested by >= 2 of the following occurring within a 12-month period: (11)

A
  1. Cannabis is often taken in larger amounts or over a longer period than was intended.
  2. There is a persistent desire or unsuccessful efforts to cut down or control Cannabis use.
  3. A great deal of time is spent in activities necessary to obtain cannabis, use Cannabis, or recover from its effects.
  4. Craving, or a strong desire or urge to use Cannabis.
  5. Recurrent Cannabis use results in failure to fulfill role obligations at work, school, or home
  6. Continued Cannabis use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of Cannabis.
  7. Important social, occupational, or recreational activities are given up or reduced because of Cannabis use.
  8. Recurrent Cannabis use in situations in which it is physically hazardous.
  9. Cannabis use continues despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by cannabis.
  10. Tolerance, as defined by either: (1) a need for markedly increased cannabis to achieve intoxication or desired effect or (2) a markedly diminished effect with continued use of the same amount of the substance.
    11.Withdrawal, as manifested by either (1) the characteristic withdrawal syndrome for Cannabis or (2) Cannabis is taken to relieve or avoid withdrawal symptoms.
86
Q

What is early remission of CUD?

A

After full criteria for CUD were previously met, none of the criteria for CUD has been met for 3-12 months (with an exception provided for craving)

87
Q

What is sustained remission of CUD?

A

After full criteria for CUD were previously met, none of the criteria for CUD has been met at any time during >12 months (with an exception provided for craving)

88
Q

What are the adverse effects and toxicities associated with synthetic cannabinoids (spice or K-2)? (6)

A
  1. HTN
  2. Tachycardia
  3. Myocardial infarction
  4. Psychoses
  5. Seizures
  6. Intoxication and death due to CNS depression and hypothermia
89
Q

The National Academies of Science created a report commissioned to determine the state of Cannabis knowledge, producing 4 wide-sweeping recommendations. What are they?

A
  1. Address Research Gaps in (i) clinical and observational research, health policy and economics, public health and safety.
  2. Improve Research Quality through the creation of workshops and mechanisms for research quality standards.
  3. Improve Surveillance Capacity to better understand the short- and long-term consequences of Cannabis use.
  4. Address Research Barriers and change regulatory systems to enhance research.
90
Q

The Lower Risk Cannabis Use Guidelines are aimed at ________ ____, not _________ __________

A

reducing risk; enforcing abstinence

91
Q

What are the 10 recommendations that the Lower Risk of Cannabis Use Guidelines make?

A
  1. The only way to completely avoid these risks is by choosing not the use cannabis
  2. You’ll lower your risk of cannabis-related health problems if you choose to start using cannabis later in life
  3. If you use, choose low-strength products, such as those with a lower THC content or a higher ratio of CBD to THC
  4. Don’t use synthetic cannabis products
  5. Smoking cannabis is the most harmful way of using cannabis b/c it directly affects your lungs
  6. If you choose to smoke cannabis, avoid inhaling deeply or holding your breath
  7. Try to limit your use as much as possible
  8. Cannabis use impairs your ability to drive a car or operate other machinery. Don’t engage in these activities after using cannabis, or while you still feel affected by cannabis in any way.
  9. Specifically, people with a personal or family history of psychosis or substance use problems, and pregnant women should not use cannabis at all
  10. Avoid combining any of the risky behaviours described above
92
Q

Cannabis use and pregnancy, what is no good here? (2)

A
  1. Cannabis exposure during pregnancy is correlated with reduced body weight and foot length
  2. Cannabis exposure during pregnancy is associated with reduced sociability and cognitive performance (pre-clinical)
93
Q

In the states, __._% of the population now lives in a state where marijuana has been legalized

A

59.3

94
Q

What has been the history of cannabis legality in Canada? (4) (up to 2001)

A
  1. 1st banned in Canada in 1923
  2. Regulated by Health Canada under the Controlled Drugs and Substances Act
  3. 1972: Le Dain Commission Cannabis should be decriminalized
  4. 2001: Medical cannabis made available in “Marijuana Medical Access Regulations” MMAR
95
Q

What has been the history of cannabis legality in Canada? (3) (from 2012)

A
  1. 2012 “Medical Marijuana Access Program” revised the MMAR to create the “Marijuana for Medical Purposes Regulations” MMPR
    - Allowed licensed applications for personal and commercial growth
    - Amended in 2013 to allow sale of oils and non-dried products
  2. 2016 Transition to the “Access to Cannabis for Medical Purposes Regulations” ACMPR
    - Greater freedom for personal cultivation to transition into full legalization July 2017, Schedule II drug
  3. 2017: The Liberal government announced that by summer 2018 Canada will move to legalize cannabis completely*
96
Q

What are the laws for recreational cannabis in Saskatchewan? (5)

A
  1. 19+
  2. No use in public or vehicles
  3. May be gifted but not sold
  4. May be transported ONLY if sealed in original packaging, in the trunk if possible
  5. 4 plants/house
97
Q

Considering the pharmacokinetics of THC, complete the following sentence: inhaling THC leads to ______ Cmax, and a _______ duration of action
a. Lower, longer
b. Higher, longer
c. Lower, shorter
d. Higher shorter

A

d.

98
Q

Which of the following cytochrome P450 enzymes does NOT break down cannabinoids and NSAIDs?
a. CYP2D6
b. CYP2C9
c. CYP3A5
d. CYP3A4

A

c.

99
Q

What is the MOA by which Epidolex (cannabidiol) reduces seizure occurrence?
a. Inhibition of the metabolism of other anti-convulsants
b. Activation of inwardly-rectifying potassium channels
c. Inhibition of voltage-gated calcium channels
d. The mechanism of action is unknown

A

d.

100
Q

Generally the evidence for using cannabinoids to relieve pain is weak. However, among the different forms of pain, what pain modality seems to receive the most benefit from THC use?
a. Neuropathic pain
b. Fibromyalgia pain
c. Arthritis pain
d. Emotional pain

A

a.

101
Q

Rimonabant was a drug that targeted the type 1 cannabinoid receptor (CB1R) and was briefly approved in the EU for the treatment of obesity and CVD. What was Rimonabant’s MOA?
a. Fatty acid amide hydrolase (FAAH) inhibitor
b. Type 1 cannabinoid receptor (CB1R) agonist
c. Monoacylglycerol lipase (MAGL) agonist
d. Type 1 cannabinoid receptor (CB1R) antagonist

A

d.

102
Q

Which of the following is a symptom of cannabis withdrawal?
a. Auditory hallucinations
b. Severe itchiness
c. Insomnia
d. Physical pain

A

c.

103
Q

Which of the following is an adverse effect of synthetic cannabinoids, but not THC?
a. Euphoria
b. Myocardial infarction
c. Delayed reaction time
d. Impaired short term memory

A

b.

104
Q

Cannabis use during pregnancy is discouraged because:
a. Cannabis use in pregnancy may be associated with lower birthweight
b. Cannabis use in pregnancy may be associated with learning impairments in offspring
c. Cannabis use in pregnancy may alter blood flow through the placenta
d. All of the above

A

d.

105
Q

In Saskatchewan what is the legal age of cannabis use?
a. 18
b. 19
c. 21
d. 25

A

b.

106
Q

What is the sales model used by cannabis stores in Saskatchewan?
a. Public Government-owned
b. Private Pharmacy-owned
c. Private Retailer-owned
d. Public Health Authority-owned

A

c.

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