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PMCOL II > Cannabis > Flashcards

Cannabis Flashcards

1
Q

What is Cannabis

A

A genus of flowering plant

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2
Q

What are the primary bioactive compounds studied in Cannabis

A

Tetrahydrocannabinol (THC)
Cannabidiol (CBD)

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3
Q

Define Cannabinoids

A

Class of chemical compounds that act act the cannabinoid receptor (Includes THC and CBD)

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4
Q

Define phytocannabinoids

A

Cannabinoids originating from the natural cannabis plant

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5
Q

What gives cannabis its plant smell

A

terpenoids

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6
Q

What non-cannabinoid compound is in cannabis, what do they do

A

Terpenoid and hundreds more, they do not bind to the cannabinoid receptor

Terpenoids have anti-inflammatory, anti-bacterial, and anti-anxiety effects
No clinical trial to support this

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7
Q

Why is Cannabis hard to understand

A

Cannabis contains hundreds of different chemicals, hard to know all of the chemical interactions

Different strains vary in the compounds they contain and thus, it becomes hard to standerdize

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8
Q

Define absorption, how does it relate to Cannabis

A

Bioavailability of a drug
Fraction of the administered drug that reaches effectors

Mostly involved in pharmacokinetic info of THC

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9
Q

What is the bioavailability of THC when smoked
How quick to reach peak plasma concentration

A

25%
6-10 minutes

Pretty good absorption and quick
Liver is not involved

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10
Q

What is the bioavailability of THC when ingested
How quick to reach peak plasma concentration

A

6%
2-6 hours

Has to pass through digestive tract
Metabolized into metabolites

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11
Q

What is the distribution of THC

A

Highly lipophilic (Hangs out in fat)
Tissues with high blood flow rapidly take up THC

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12
Q

THC effect in tissues with low blood flow

A

Accumulate THC slowly and release it over a longer period of time (Adipose tissue (fat))

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13
Q

THC and fat relationship

A

THC is stored in fat in chronic/frequent cannabis smokers, can be released into the blood for days

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14
Q

Can THC cross the BBB

A

Yes

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15
Q

What enzyme helps with THC metabolism, where does this occur

A

Occurs in liver by cytochrome p450 2C9

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16
Q

What are the metabolites created from THC metabolism

A

Active: 11-OH-THC
Inactive: THC-COOH

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17
Q

THC Dose Elimination
Length: ____
Amount: ____
Composition: ____

A

Length: 5 days
Amount 80%-90% of THC dose
Composition: Primary in metabolites, 65% feces, 25% urine

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18
Q

How long can low dose THC be detected in urine

A

2-5 days

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19
Q

How long can chronic daily cannabis smokers THC dose be detected for. Why?

A

Can detect THC for weeks

THC is lipophilic and can accumulate in adipose tissue
Released slowly
Excretion takes place over a month

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20
Q

What kind of receptors are Cannabinoid Receptors. What kinds of Cannabinoid Receptors are there

A

Inhibitory G-protein coupled receptors (Gi coupled)
CB1 and CB2

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21
Q

What is the overall effect of Cannabinoid Receptors

A

Decrease synaptic transmission
Inhibit neurotransmitter release

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22
Q

What is the mechanism of Cannabinoid Receptors

A

decrease cAMP
Inhibits influx of Ca2+ in the firing neuron
Inhibits neurotransmitter release

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23
Q

What kind of agonist is THC. What receptor?

A

Partial agonist at CB1

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24
Q

What kind of agonist is CBD. How does it work? What receptor?

A

Negative allosteric modulator at CB1

Binds outside of the binding pocket to block receptor activation by reducing effects of THC
Not very understood

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25
Q

Potential Use and Issues of CBD

A

Could blunt psychotropic effects of THC
Hard to study because of placebo

Low bioavailability
Poorly absorbed

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26
Q

Where are CB1 receptors found? How abundant are they?

A

Among the most abundant of GPCRs

Found in the brain, peripheral organs (Heart, liver, fat, stomach, testes), and peripheral nerves

27
Q

Where are CB2 receptors found? How abundant are they?

A

Limited distribution. Distributed mostly on immune cells
Only found in the brain on glial cells

28
Q

What are the general effects of Cannabis (THC) (6)
Issues?

A

Euphoria
Relaxation
Disinhibition
Changes in perception
Vasodilation
Increase pulse rate

Doses to achieve therapeutic effects is many folds higher than what is biologically possible in vivo. Such high doses could lead to off target effects

29
Q

Potential therapeutic effects of Cannabis (THC)

A

Reduction of nausea
Increased appetite
Decreased intraocular pressure (Eye pressure)
Chronic pain relief

30
Q

Unwanted effects of Cannabis (THC)

A

Memory impairment
Dysphoric state (Unhappiness, Anger)
Visual hallucinations
Depersonalization
Psychotic episodes

31
Q

Adverse Acute effects of high doses of THC

A

Panic attacks, severe anxiety, psychosis, paranoia, convulsions, hyperemesis (severe nausea)

32
Q

Adverse Prenatal effects of cannabis use

A

May cause neuroanatomical and behavioural changes in offspring

Fetal growth affected (specifically neurodevelopment)
No dose-response relationship identified

33
Q

What kind of cancer can cannabis use cause

A

Smoked cannabis can cause lung cancer

34
Q

How has the legalization of Cannabis impacted motor vehicle accident

A

Probably only a mild effect
Despite impairing perception, cognitive functions, and reaction time there has been no drastic increase in accidents

35
Q

Cases of overdosing with Cannabis? Why?

A

No documented evidence of death from purely cannabis

Probably because lack of CB1 receptors in the brain stem region that control respiratory and cardiovascular systems

36
Q

What is the relationship between schizophrenics and cannabis use (Correlative)

A

Mostly correlative data that cannabis use predicts development of schizophrenia.

Lots of bias, confounding variables (unknown factor that increases risk of cannabis use and psychosis), and reverse causality (people already with psychosis are more likely to use cannabis)

37
Q

What is the relationship between psychosis and cannabis use (Conclusion)

A

In most people cannabis does not lead to the development of schizophrenia
- Cannabis can be a trigger in the development of schizophrenia in at-risk populations (those with the genetic predisposition)
- Cannabis can worsen pre-existing schizophrenia
- Cannabis can elicit acute psychosis

38
Q

Psychological dependence

A

Behavioural

Continued compulsive use of a drug for personal satisfaction despite knowing its risks

39
Q

Physiological dependence

A

Physical

Withdrawal of drug causes symptoms and signs that are opposite of what the user wants
Weight changes
Flu like symptoms
Depression

40
Q

Effects of Cannabis withdrawal

A

Relatively mild and effects are short-lived
Restlessness, Irritability, Mild agitation, Insomnia, Nausea, and Cramping

May be worse in chronic, long term users

41
Q

What is the definition of Addiction (Substance use disorder)

A

Inability to control the use of legal/illegal substances despite their negative consequences

42
Q

How id Addiction diagonesed

A

11 Diagnostic criteria

2/11 mild
4/11 moderate
6+/11 severe

43
Q

What percentage of cannabis users develop a substance use disorder

A

9%

44
Q

What are synthetic cannabinoids

A

Manufactured compounds whos properties are meant to imitate the active constitutions of cannabis

45
Q

Why do we use synthetic cannabinoids

A

Increased specificity
Decreased off target effects
Easier dosing
Better controlled studies (Clinical studies fail less often)

46
Q

What is Nabiline, how is it administered

A

Synthetic analog of THC (Oral)

Partial agonist

47
Q

What is Dronabinol, how is it administered

A

Trans-isomer of THC (Oral)

Partial agonist

48
Q

What does Dronabinol treat

A

Nausea and vomiting during chemotherapy

Anorexia in AIDS wasting syndrome

49
Q

What is Nabiximol

A

Cannabis extract, a botanical drug

50
Q

What does Nabiximol contain and what does it treat

A

1:1 mixture of THC and CBD

Multiple sclerosis or Cancer

51
Q

What has more psychotropic effects
Smoked Cannabis or Sublingual Spray

A

Smoked Cannabis

52
Q

What has less psychotropic effects
Smoked Cannabis or Oral THC Analogs

A

Oral THC Analogs

53
Q

What is Rimonabant

A

Inverse agonist at CB1 receptor

54
Q

What was Rimonabant used for

A

Used to treat obesity
Had serious side effects (depression and suicide ideation)

55
Q

Why do Humans evolve to have Cannabinoid receptors

A

Not because of Cannabis

Endocannabinoids
Endogenous cannabinoids that mediate mood, feeding, and
motor function

56
Q

What are the two types of endocannabinoids

A

Anandamide (AEA)

2-arachinoyl glycerol (2-AG)

57
Q

How are endocannabinoids made

A

Formed from the phospholipid bilayer of the cell membrane

58
Q

What are AEA and 2-AG and what are there functions

A

Retrograde neurotransmitters used in endocannabinoid signaling

Synthesized on demand, and works as a break to shut off neuron

59
Q

What are the overall effects of endocannabinoid

A

Similar to THC

Decreases neuronal release of other transmitters. Acts as a break in active neurons

60
Q

Where are endocannabinoids produced? Why?

A

Produced in active regions of the brain

Synthesis of 2AG and AEA is initiated by an increase of intracellular Ca2+ which occurs when postsynaptic neuron is depolarized by a neurotransmitter

61
Q

How are endocannabinoids deactivated? What happens if these enzymes are not around?

A

Fatty-acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL) clear endocannabinoids from the synapse and inactivate them

Suppressing these enzymes will prolong the activity of endocannabinoids

62
Q

What are the effects

and side effects of FAAH and MAGL inhibitors

A

Analgesic effects, treatment of chronic pain

Sudden death

63
Q

What conditions will enhance CB1 activity the most when using FAAH and MAGL inhibitors

A

A2G and AEA are released on demand at the site of action

Thus, the greater the A2G and AEA levels the greater the CB1 activation when these endocannabinoids are inhabited

64
Q

What effects do FAAH and MAGL inhibitors not have

A

Do not have the typical THC effects: sedation, catalepsy, hypothermia, and psychoactive effects in general

PMCOL II (10 decks)

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