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PSYT 301 > L6 - NICOTINE > Flashcards

L6 - NICOTINE Flashcards

1
Q

List short-term effects of tobacco.

A
  • Increased heart-rate, blood pressure and breathing rate
  • CO blocks O2 from getting into bloodstream
  • Stimulates nausea
  • Bad breath
  • Stimulates neurochemical systems
    • Dopamine
    • Norepinephrine (appetite suppression)
    • Acetylcholine
    • GABA
    • B-Endorphin
    • Glutamate
    • Serotonin
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2
Q

Associate the follow neurotransmitters with a state/function:
- Dopamine
- Norepinephrine
- Acetylcholine
- GABA
- B-Endorphin
- Glutamate
- Serotonin

A
  • Dopamine -> reward
  • Norepinephrine -> arousal
  • Acetylcholine -> arousal
  • Glutamate -> learning
  • GABA -> reduction of anxiety
  • B-Endorphin -> reduction of anxiety
  • Serotonin -> mood
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3
Q

List long-term effects of tobacco.

A
  • Tobacco addiction
  • Emphysema and bronchitis
  • COPD
  • Heart and artery disease
  • Cancer of lung, bladder, pancreas
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4
Q

Name three major coindicent long-term effects of adolescent tobacco use. List their implications.

A

Altered trajectory of normal brain development:
- Dendritic remodeling
- Lower gray matter volume in thalamus and amygdala
- Aberrant functional connectivity between dlPFC and amygdala and striatum
- Modified reward system
- Changes in 5HT synaptic function
Diminished cognitive function, persisting into adulthood:
- Reduced attention span
- Poorer memory
- Lower inhibitory control
Greater mental health problems
-Increased anxiety and depressive-like behaviour
-More severe tobacco dependence

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5
Q

True or false: there is consensus about the relationship between adolescent tobacco use and its consequences in adulthood.

A

False.

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6
Q

True or false: nicotine has behavioural implications.

A

True.

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7
Q

In what organ is nicotine from smoked tobacco entering the bloodstream?

A

Lungs.

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8
Q

True or false: nicotine is toxic at high concentrations.

A

True.

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9
Q

Provide a hormonal basis for the tranquilizing effects of nicotine.

A

Decreases CORT.

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10
Q

To what receptors bind nicotine?

A

Nicotinic acetylcholine receptors (nAChR).

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11
Q

How many subunits does a nAChR have? What are the two types of subunits?

A
  1. Alpha and beta.
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12
Q

How many isoforms of nAChR subunits are there?

A

9 for alpha and 3 for beta.

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13
Q

What are the most abundant nAChR subtypes in brain?

A

α4β2 and α7.

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14
Q

True or false: nicotine has equal affinity for α4β2 and α7.

A

False: highest affinity for α4β2.

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15
Q

How do you call nAChRs made up only of one type of subunit? Made of different types?

A

Homomeric vs heteromeric.

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16
Q

Where are nAChRs mostly located?

A

Thalamus, but also basal ganglia, frontal and insular cortices.

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17
Q

What NTs are binding nAChRs?

A

Acetylcholine and nicotine (presynaptically).

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18
Q

What are the three states of nAChRs?

A

Closed.
Open.
Desensitized.

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19
Q

Which state of nAChR is the most prevalent between open and desensitized?

A

Desensitized.

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20
Q

Describe implications of nAChR desensitization.

A

Acute effects are limited.
Reduced satisfaction.
Facilitates the emergence of withdrawal symptoms.
Chronic nicotine use leads to neuroadaptive changes: upregulation of nAChRs.

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21
Q

What specific nAChR has been found in higher densities in living human smokers? In what parts of the CNS?

A

Beta2 nAChR. In the striatum, cerebellum, and cerebral cortex compared to nonsmokers.

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22
Q

With what aspects of tobacco consumption are the adaptations in β2 nAChRs thought to be involved?

A

In tobacco addiction, tolerance and dependence.

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23
Q

What behavioural tests support the evidence that nicotine is addictive?

A

Self-administration and CPP (conditioned place preference).

24
Q

What is the effect of nicotine on DA release in the NAcc?

A

Very intense peak (very addictive).

25
Q

On what cell types are nAChRs found in the VTA?

A

Dopaminergic.
GABAergic.
Glutamatergic.

26
Q

Which nAChR regulates many of addiction-relevant behavioural responses to nicotine? How is it experimentally supported?

A

Alpha4beta2 nAChRs:
-Alpha4 subunit KO decreases self-administration.
-Genetically-modified alpha4 subunit for increased sensitivity to nicotine increases self-administration.

27
Q

Where is nicotine mostly metabolized?

A

Liver.

28
Q

By which enzyme is nicotine mostly metabolized?

A

Cytochrome P450 enzymes (CYP2A6).

29
Q

What is the implication of the half life of nicotine being only 2 hours?

A

Explains recurrent smoking in a single day.

30
Q

What is nicotine’s principle metabolite?

A

Cotinine.

31
Q

Why are smokers carefully balancing their nicotine consumption?

A

Narrow window between withdrawal and OD.

32
Q

Why are smokers almost certainly smoking in the first minutes of waking?

A

Nicotine is most likely out of their blood (4h>). They therefore have to smoke to avoid withdrawals.

33
Q

List primary (4) and secondary (4) risk factors for TUD.

A

Primary:
- Acute withdrawal syndrome
- Negative affect (mood)
- Positive effects (satisfaction)
- Conditioned cues
Secondary:
- Stress
- Antinociception (pain relief)
- Weight control
- Cognitive enhancement

34
Q

List 5 neurotransmitters regulated by nicotine.

A

DA
NE
5-HT
ACh
Glu

35
Q

What is one simple behavioural treatment for TUD that tends to be underrated?

A

Brief advice from physician or other health professional

36
Q

Provide four behavioural treatments for TUD.

A

Motivational interviewing
Coping skills
Community support groups
Rapid smoking

37
Q

What are the four broad classes of TUD pharmacotherapies? Give an example for each.

A

Slow-acting NRT: patch
Fast-acting NRT: gum
Antidepressant: SR bupropion
Nicotinic partial agonist: varenicline

38
Q

What is the most efficient pharmacotherapy for TUD?

A

Varenicline (nicotinic partial agonist)

39
Q

Each of the four broad classes of TUD pharmacotherapies is associated with which respective predominant side effect?

A

Slow-acting NRT: local irritation
Fast-acting NRT: oropharyngeal irritation
Antidepressant: insomnia (activation)
Nicotinic partial agonist: insomnia

40
Q

Varenicline acts on which receptor?

A

alpha4beta2-selective nAChR partial agonist

41
Q

Up to how many weeks is varenicline preventing smoking relapse?

A

24 weeks

42
Q

Why does it make sense that the side effects of nicotine are nicotine-like?

A

Varenilcine binds to alpha4beta2 (but partial effects).

43
Q

True or false: varenicline has no behavioural side effects.

A

False: no scientific consensus. Reports of neuropsychiatric treatment-emergent adverse effects.

44
Q

What treatment between varenilcine and bupropion has the highest rate of continuous abstinence in clinical studies?

A

Varenicline, significantly.

45
Q

From studies on the pharmacogenetics of smoking cessation, what treatments can we expect to be particularly efficacious for slow metabolizers and normal metabolizers?

A
  • For slow metabolizers (low CYP2A6 activity), nicotine patch and varenicline are expected to be equally efficacious.
  • For normal metabolizers, varenicline is expected to be more efficacious than nicotine patch.
46
Q

True or false: quitting smoking in MI populations leads to better psychiatric and substance use disorder outcomes.

A

True.

47
Q

True or false: rates of tobacco smoking in MI populations are higher AND rates of quitting smoking are significantly lower.

A

True.

48
Q

Name four broad risk factors that make Sz vulnerable to TUD?

A

Biochemical
Genetic
Behavioural
Neurocognitive

49
Q

What is the most significant biochemical difference between Sz and neurotypical smokers?

A

Lower density of beta2*nAChRs in Sz smokers.

50
Q

Different densities of beta2*nAChRs in Sz smokers were observed in which brain areas?

A

-Parietal cortex
-Frontal cortex
-Thalamus
-Striatum
-Hippocampus

51
Q

Based on previous case reports, why would it be counter-intuitive to prescribe varenicline to a neuroatypical individuals? Is this reluctancy founded?

A

There are reports implicating varenicline in treatment-emergent adverse events such as suicidality, homicidality, psychosis and mania. However, recent studies have shown that varenicline seemed safe and efficacious in both Sz and bipolar populations.

52
Q

Name three research findings that attest varenicline’s efficacy for smoking cessation in Sz populations.

A
  • Increased abstinence
  • Varenicline effects do not seem to generate different positive or negative effects from control
  • Works for replase-prevention
53
Q

Provide 4 reasons that might explain why co-use of tobacco and cannabis is so high.

A
  • Both are smoked products, cross cuing
  • Substitution effects (one can temporarily replace the other)
  • Interaction between endocannabinoid and nicotinic receptor systems
  • Common social determinants
54
Q

Why an association between tobacco use and transition to psychosis is presumed?

A

-Majority of early psychosis patients smoke tobacco
-In average, psychotic patients have been using tobacco 5.3 years before before the onset of their illness.

55
Q

Why is the relationship between Sz populations and cannabis unexpected?

A

Tobacco co-morbidity is generally associated with other substance use disorders (SUDs). However, it does not seem like it is the case for cannabis: Sz with current cannabis dependence history smoke less tobacco than Sz with no history of cannabis dependence.

56
Q

Provide two possible mechanisms that could explain why Sz individuals tend to be cannabis-abstinent.

A

-Increase in tobacco use with cannabis abstinence in SZ versus CTL subjects could represent compensation
-Sz patients might be more neurobiologically sensitive to cannabis, supported by selective improvements in neurocognition in SZ versus CTL subjects with cannabis abstinence

57
Q

For what purpose has rTMS been advised for Sz tobacco-smokers?

A

rTMS reduces tobacco cravings in patients with schizophrenia.

PSYT 301 (8 decks)

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