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PMCOL 200 > 17 Cannabis > Flashcards

17 Cannabis Flashcards

1
Q

What is cannabis?

A

Genus of flowering plant;

  • contains many bioactive compounds but most studied are tetrahydrocannabinol (THC) and cannabidiol (CBD)
  • THC is primary psychoactive compound
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2
Q

What are cannabinoids?

A

Class of chemical compounds that act at the cannabinoid receptors

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3
Q

What constituent of cannabis gives it its characteristic smell?

A

Terpenoids

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4
Q

In vitro and in vivo studies have found that some terpenoids have _________, _________ and _________ effects, but no clinical trials have been conducted to support this

A

In vitro and in vivo studies have found that some terpenoids have anti-inflammatory, antibacterial and anti-anxiety effects, but no clinical trials have been conducted to support this

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5
Q

Why is it difficult to create a clinically appropriate form of cannabis?

A

Cannabis contains hundreds of phytocannabinoids at varying concentrations between different plants and the effect of cannabis is possibly due to surround effect, or synergy between the compounds

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6
Q

Pharmacokinetics of THC:

ADME

  • Bioavailability of smoked THC vs ingested
  • Time to peak plasma concentration?
A

Absorption (bioavailability):

  • smoking provides rapid and efficient delivery from lungs to the brain
    • bioavailability of smoked THC is 25%, reaching peak plasma concentration in 6-10 minutes
  • Ingested:
    • bioavailability ~6% (because of 1st pass metabolism)
    • Time to peak plasma concentration is 2-6 hours
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7
Q

Pharmacokinetics of THC:

ADME

How is THC distributed?

A
  • THC is highly lipophilic so rapidly taken up by tissues with high blood flow (heart, lungs, brain, liver)
  • Tissues with less blood flow accumulate THC more slowly and release it over a longer period of time (eg adipose tissue)
  • THC stored in fat in chronic, frequent smokers can be released into the blood for days
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8
Q

THC metabolism occurs mostly in the ______ by the enzyme __________

A

THC metabolism occurs mostly in the liver by the enzyme cytochrome P450 2C9 producing the metabolites:

  • 11-OH-THC
  • THC-COOH
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9
Q

THC metabolism occurs mostly in the liver by the enzyme cytochrome P450 2C9 producing what 2 metabolites?

A

THC metabolism occurs mostly in the liver by the enzyme cytochrome P450 2C9 producing the metabolites:

  1. 11-OH-THC
  2. THC-COOH
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10
Q

How long does it take for THC to be excreted and in what form?

A

Within 5 days 80-90% of a THC dose is excreted, primarily as metabolites

  • 65% in feces
  • 25% in urine

Can detect THC in urine 2-5days for low dose, and longer (weeks) for chronic users (because it accumulates in fat tissue)

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11
Q

What kind of receptors are cannabinoid receptors?

What are the 2 “flavours”?

A

Inhibitory G-protein coupled receptors (Gi coupled)

  1. CB1
  2. CB2
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12
Q

What effect does an agonist binding to a CB receptor have?

A

CB receptors leads to decrease in cAMP (cyclic adenosine monophosphate) accumulation which inhibits the influx of Ca2+ in the firing neuron and inhibits NT release

(↓cAMP → ↓Ca2+ → ↓NT release

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13
Q

What effect do CB receptors have on synaptic transmission and NT release?

A

decrease synaptic transmission

inhibit NT release

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14
Q

THC is a _________ at CB1

(partial agonist, full agonist, antagonist)

A

THC is a partial agonist at CB1

(partial agonist, full agonist, antagonist)

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15
Q

Cannabidiol (CBD) is poorly understood but some evidence suggests that it acts as a ______ at CB1

A

Cannabidiol (CBD) is poorly understood but some evidence suggests that it acts as a Negative Allosteric Modulator at CB1 (binds outside the binding pocket to block receptor activation)

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16
Q

How do CBD and THC compete at the CB1 receptor?

A

CBD can blunt psychotropic effects of THC

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17
Q

Which of the two CB receptors are more abundant in the brain?

A
  • CB1 receptors are among the most abundant GPCRs
    • Found in brain, peripheral organs (heart, liver, fat, stomach testes) and peripheral nerves (ie found almost everywhere)
  • CB2 mostly on immune cells
    • glial cells in the brain
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18
Q

What does preclinical research suggest about CBD therapeutic potential?

A

CBD has potential for management of inflammation, anxiety, emesis, nausea, inflammatory pain, and epilepsy

  • may influence effects of THC
  • No clinical data for these claims
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19
Q

What are 6 general effects of THC?

A
  1. euphoria
  2. relaxation
  3. disinhibition
  4. changes in perception
  5. vasodilation
  6. increase pulse
20
Q

What are four potential therapeutic effects of THC?

A
  1. attenuation of nausea
  2. increased appetite
  3. decreased intraocular pressure
  4. chronic pain relief
21
Q

What are five unwanted effects of THC?

A
  1. memory impairment
  2. dysphoric state
  3. visual hallucinations
  4. depersonalization
  5. psychotic episodes
22
Q

What are four adverse effects of cannabis use?

A
  1. Acute effects (rare and usually associated with high doses of THC)
    • Panic attacks
    • severe anxiety
    • psychosis
    • paranoia
    • convulsions
    • hyperemesis
  2. Prenatal effects
    • may lead to neuroanatomical and behavioural changes in offspring
    • fetal growth, particularly neurodevelopment, but dose-response relationship not identified
  3. Lung cancer : particularly through smoked cannabis
  4. Driving:
    • increase risk of MVA
    • Impairs perception, psychomotor performance, cognitive functions and affective functions
    • Decreased rxn time
23
Q

What is the probable reason why there have been no documented evidence of death exclusively linked to cannabis overdose?

A

Because of sparsity of CB1 receptors in the brain stem region that controls respiratory and cardiovascular systems

24
Q

How is cannabis linked to schizophrenia?

A

Strictly through correlation

  • correlative data suggests schizophrenics are more likely to use cannabis and early cannabis use dose-dependently predicts the development of schizophrenia later on
  • these studies do not indicate causation
  • Majority of cannabis users do not develop schizophrenia
    • however, cannabis can elicit acute psychosis and can worsen course of pre-existing schizophrenia
      • may be trigger in the development of schizophrenia in at-risk populations (ie those with genetic predisposition)
25
Q

How is tolerance achieved from cannabis use?

A

Chronic activation of CB1 receptor uncouples from intracellular downstream signal transduction events or receptor downregulation (internalization or degradation of receptor)

26
Q

Define psychological dependence?

A

compulsive drug-seeking behaviour in which the individual uses the drug receptively for personal satisfaction, often in the face of known risks to health

27
Q

What is physiological dependence?

A

revealed when withdrawal of the drug produces symptoms and signs that are frequently opposite of those sought by the user

28
Q

What are the symptoms associated with cannabis withdrawal?

A

Cannabis withdrawal is relatively mild and short-lived

Symptoms:

  • restlessness
  • irritability
  • mild agitation
  • insomnia
  • nausea
  • cramping

May be worse in chronic, long-term users and may contribute to continued drug use

29
Q

How is substance use disorder (addiction) defined and how is it diagnosed? How many cannabis users develop a substance use disorder?

A

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

  • diagnosed by 11 diagnostic criteria
    • severity is determined by the number of criteria the person meets (mild 2/11; 4/11 moderate; 6+/11 severe)
  • Approximately 9% of those who use cannabis develop a substance use disorder (taken prior to legalization)
30
Q

What are synthetic cannabinoids and why bother developing them?

A

Synthetic cannabinoids: a manufactured compound whose properties imitate those of the active constituents of cannabis

Why?

  • increased specificity
  • decreased off-target effects
  • easier dosing
  • better controlled studies
31
Q

What are three well-confirmed clinical uses of cannabinoids?

A
  1. Refractory nausea/vomiting
  2. anorexia appetite loss
  3. HIV/AIDS/cancer cachexia
32
Q

What is nabilone?

A
  • Synthetic analog of THC
  • partial agonist at CB1 receptor
  • taken orally (less psychotropic effects than cannabis)
33
Q

What is dronabinol?

A
  • (-) trans isomer of delta9-THC
  • Approved for nausea and vomiting in patients who undergo chemotherapy and anorexia in AIDS wasting syndrome
  • Partial agonist at the CB1 receptor
  • Taken orally = less psychotropic effects
34
Q

What is nabiximols (sativex)?

When was it first licensed in Canada and for what use?

A

Botanical drug (cannabis extract)

  • 1:1 mixture of THC and cannabinol, sublingual spray
  • First licenced in Canada for relief of pain in those with multiple sclerosis or cancer
  • Less psychotropic effects than smoked cannabinoids
35
Q

What is Rimonabant?

What was it approved to treat and what are its adverse effects?

A

Rimonabant is an inverse agonist at the BC1 receptor

  • originally approved for the treatment of obesity but withdrawn due to serious adverse effects (depression and suicide)
36
Q

What are endocannabinoids?

Two types?

A

Endogenous cannabinoids that mediate mood, feeding and motor function

  • Two types
    • Anandamide (AEA)
    • 2-arachidonoyl glycerol (2-AG)
37
Q

Where are AEA and 2-AG made?

A

AEA and 2-AG (the endocannabinoids) are made from the phospholipid bilayer of the cell membrane

38
Q

AEA and 2-AG are ___________ (act on receptors on pre-synaptic membrane)

A

AEA and 2-AG are retrograde NT’s (act on receptors on pre-synaptic membrane)

39
Q

In contrast to most NT’s, AEA and 2AG are not stored in vesicles, but rather _________ when and where they are needed

A

In contrast to most NT’s, AEA and 2AG are not stored in vesicles, but rather synthesized on demand when and where they are needed

40
Q

Like THC, endocannabinoids ______ neuronal release of other transmitters

A

Like THC, endocannabinoids decrease neuronal release of other transmitters

  • via hyperpolarizing membrane
41
Q

What stimulates the synthesis of 2AG or AEA?

A

Synthesis of 2AG or AEA (endocannabinoids) is stimulated by increase in intracellular [Ca2+] when the postsynaptic neuron becomes depolarized by the action of a NT

  • therefore, produced only in regions of brane that are activated
42
Q

AEA and 2AG are rapidly cleared from the synapse and inactived by ____________ or ___________.

A

AEA and 2AG are rapidly cleared from the synapse and inactivated by fatty-acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL).

43
Q

Suppression of fatty-acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL) would have what effect?

A

These enzymes (FAAH and MAGL) inactivate and clear AEA and 2AG so suppression of these enzymes prolongs the activity of endocannabinoids

44
Q

Inhibition of AEA or 2AG metabolism would have what effect on CB1?

A

Because AEA and 2AG are synthesized and released on demand at the site of action, inhibition of their metabolism would enhance CB1 activation where AEA and 2AG levels are highest

  • FAAH/MAGL inhibitors
45
Q

What are the effects of FAAH/MAGL inhibitors in comparison to effects of THC? What halted clinical trials?

A

FAAH/MAGL inhibitors do not produce typical psychoactive effects of thc, sedation, catalepsy or hypothermia BUT do have analgesic effects

  • several compounds under development for the treatment of chronic pain
  • Clinical trials halted because of several severe adverse events from a FAAH inhibitor
    • brain damage, one death

PMCOL 200 (30 decks)

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