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PSYT 301 > lecture 5: nicotine > Flashcards

lecture 5: nicotine Flashcards

1
Q

what happened why smoke-free laws were introduced?

A

slight decrease in tobacco smoke and dramatic decrease in second-hand smoke

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2
Q

what is the number 1 cause of preventable death?

A

smoking

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3
Q

what are some chemicals found in tobacco?

A

any of the following:
- acetone
- acetic acid
- ammonia
- arsenic
- Benzene
- Butane
- cadmium
- CO
- formaldehyde
- hexamine
- lead
- methanol
- nicotine
- tar
- toluene

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4
Q

what are the short-term effects of tobacco use?

A
  • euphoria
  • enhanced cognition
  • decreased appetite
  • stimulate nausea/vomiting reflex
  • increased HR and BP
  • CO blocks O2 from getting into bloodstream
  • bad breath
  • stimulate reward system/other neurochemical systems
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5
Q

what neurotransmission systems does tobacco use affect?

A
  • dopamine (reward)
  • NE (arousal/decreased appetite)
  • acetylcholine (enhance cognition/arousal)
  • glutamine (learning)
  • endorphin (decreased anxiety)
  • GABA (decreased anxiety)
  • serotonin (mood modulation)
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6
Q

what are long-term effects of tobacco use?

A
  • bronchitis
  • COPD
  • heart disease
  • cancer (lung, bladder, pancreas)
  • diabetes
  • osteoporosis
  • addiction
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7
Q

what are risk factors of tobacco use disorder?

A
  • genetics (family history)
  • parent exposure
  • lower socioeconomic status
  • peer pressure/low self-esteem
  • poor academic performance
  • impulsivity
  • mental disorder/illness
  • other substance use
  • early use (childhood/teenager)
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8
Q

what are some long-term effects of adolescent tobacco use?

A
  • Alters trajectory of normal brain development
  • Diminished cognitive function that persists into adulthood
  • Greater mental health problems (anxiety, depression)
  • Tobacco exposure in adolescence has effects that last into adulthood;
    adults do not show comparable effects
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9
Q

what brain developmental changes are seen in long-term use of tobacco in adolescents?

A
  • dendritic remodeling
  • lower gray matter volume in thalamus and amygdala
  • aberrant functional connectivity
  • changes in reward system
  • change in 5-HT synaptic function
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10
Q

what are some cognitive functions that persist into adulthood which long-term tobacco use in adolescents?

A
  • reduced attention span
  • poor memory
  • enhanced impulsivity and lower inhibitory control
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11
Q

how much nicotine does a cigarette contain and how much is actually absorbed?

A

9 mg but about 1 mg is absorbed

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12
Q

what is nicotine?

A

the main psychoactive constituents in tobacco – stimulant

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13
Q

what is the most common mode of delivery for nicotine?

A

cigarette

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14
Q

what are the basic pharmacokinetics when nicotine is smoked?

A
  • nicotine is distilled from the tobacco and is carried in smoke particles into the lungs
  • Moves quickly to the brain (10-15s); faster than by intravenous injection
  • Binds to nicotinic acetylcholine receptors (nAChR) in the brain
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15
Q

what type of receptor is the nicotinic acetylcholine receptor? what does it do?

A

ligand-gated ion channel that modulates neuronal excitability (regulate flow of cations (Na, K, Ca)

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16
Q

what are the different subunits of the nAChR and how many are there?

A

5 membrane-spanning subunits (a mix of a and b):
- 9 types of a and 3 types of b

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17
Q

what are the most abundant nAChR subtypes?

A

a4b2 and a7

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18
Q

Nicotine has _______ affinity for α4β2; ________ affinity for α7

A

highest ; low

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19
Q

which nAChR subunit mediate the rewarding and aversive effects
of nicotine in brain?

A

B2

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20
Q

where in the brain can nAChRs be found?

A
  • Cortex
  • Hippocampus
  • Amygdala
  • Striatum: nucleus accumbens,
    caudate, putamen
  • VTA
  • Cerebellum
  • Thalamus
  • Insula
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21
Q

In brain, nAChRs are mostly expressed ___-synaptically

A

pre

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22
Q

what activates nAChRs and what happens when it opens?

A

(1) Activation of nAChRs occurs when acetylcholine or nicotine binds to receptor
(2) Conformational change that opens the channel pore to allow influx of sodium and calcium cauing depolarization of neuron
(3) then, goes into a desensitized state. Desensitized nAChRs still have a high affinity for ACh and other ligands, but the receptor is inactive

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23
Q

what is the advantage of receptor desensitization, normally?

A

Limits duration of acute effects which is enhanced by fact that the desensitized phase is longer than the activation phase

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24
Q

what is the effect of nAChR desensitization in the context of cigarette smoking?

A

Results in decreased receptor responsiveness for a subsequent stimulus following repetitive stimulation – Acute tolerance of nicotine and reduced satisfaction
This also means that with chronic use, the receptors spend more time in the desensitized state, leading to upregulation, which is a compensation mechanism to augment nAChR response

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25
Q

looking in the context if neurobiology, when do the craving/withdrawal symptoms appear in a person with tobacco use disorder?

A

once previously desensitized α4β2 nAChRs become unoccupied and recover to a responsive state during a period of abstinence, and because this is a change that lasts a while, it may contribute to why its hard to quit

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26
Q

which nAChR subtypes desensitize fast/slow?

A

a7 very fast (milliseconds) and non-a7 (e.g. a4b2) slower (seconds)

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27
Q

Receptor upregulation appears to primarily involve which nAChR subtypes?

A

those involving b2 subunits

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28
Q

how does the capture rate of tobacco compare to other subsances?

A

very high (~32%)

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29
Q

what are the rewarding effects of nicotine? i.e. what makes nicotine so rewarding?

A
  1. Nicotine directly
    activates VTA dopamine neurons, which releases dopamine in the NAcc
  2. Simultaneously, nicotine activates α7 nAChRs glutamatergic neurons, which indirectly increases NAcc dopamine release
    * α7 are less prone to desensitization due to their low affinity for nicotine, so this effect is sustained
  3. Nicotine activates GABA neurons which express β2-containing nAChRs which inhibits dopamine release. This occurs at the same time that dopamine neurons themselves are directly activated and Glu is indirectly activated
    * Because the α4β2 nAChRs rapidly desensitize, GABAergic drive to the dopamine neurons is reduced over a longer time frame when low levels of nicotine are continually present, helping to sustain dopamine levels for a longer duration
30
Q

α4β2 nAChRs are highly expressed in __________ pathways

A

midbrain dopamine

31
Q

α4β2 regulate what type of behaviours?

A

addiction-relevant behavioral responses to nicotine

32
Q

β2 nAChR subunit control _________

A

dopamine release

33
Q

α4 nAChR subunits control ______

A

nicotine sensitivity

34
Q

what behaviour do β2 nAChR subunit knockout mice show?

A

do not self-administer nicotine

35
Q

what behaviour do Mice with genetic mutations that increase nicotine sensitivity of α4 nAChR subunit show?

A

enhanced addiction-relevant behavior to nicotine

36
Q

nAChRs containing α3 and β4 subunits are ___-affinity and enriched in brain sites involved in __________

A

low; aversion

37
Q

other than nicotine, what are other rewarding chemicals?

A

MAOIs, which decrease the breakdown of DA, which increases DA in rewarding regions of the brain (enhances nicotine self-administration in animals)

38
Q

do we see the effect of cigarette MAOIs immediately, like nicotine?

A

no, it requires long-term exposure, but that also means that it is not rapidly reversible

39
Q

what are nicotine pharmacokinetics (metabolism, T1/2, major metabolite)

A
  • Majority of nicotine is metabolized in the liver by cytochrome P450 enzymes (CYP2A6)
  • Half life of nicotine in the blood is 2 hours (so people that smoke titrate the dose within quite narrow limits)
  • Major metabolite is cotinine, which is inactive
40
Q

what do nicotine withdrawal symptoms begin, when do they peak, and when do they stop?

A
  • begin: 4-24 hrs
  • peak: 2-5 days
  • dissipate: 4 weeks
41
Q

what are some nicotine withdrawal symptoms?

A
  • Irritability
  • Anxiety
  • Difficulty concentrating
  • Restlessness/impatience
  • Depressed mood/depression
  • Insomnia
  • Impaired performance
  • Increased appetite/weight gain
  • Cravings
42
Q

tobacco use disorder diagnosed by ______

A

DSM-5 criteria and the Fagerstrom Test for Nicotine Dependence

43
Q

what is the nicotine addition cycle?

A
  1. cigarette smoking
  2. nicotine absorption
  3. arousal, mood modulation, pleasure
  4. tolerance and physical dependence
  5. abstinence produces withdrawal symptoms
  6. craving for nicotine to self-medicate withdrawal symptoms
44
Q

what are some tobacco use disorder comorbidities and why is this thought to be seen?

A

psychiatric disorders are more vulnerable to addictive properties of cigs
thought to tie into the self-medication hypothesis where nicotine counteracts specific impairments associated with their disorder

45
Q

e-cigs deliver nicotine via ____…

A

aerosol to users by heating a solution typically made up of propylene glycol or glycerol (base) and nicotine

46
Q

what factors affect nicotine exposure with e-cigs?

A
  • e-liquid nicotine concentration
  • Power of the e-cigarette
  • User consumption patterns
47
Q

why were e-cigs perceived as healthier than tobacco?

A

Nicotine is delivered to the upper and lower respiratory tract without any combustion and was advertised as a way to stop smoking

48
Q

what are the main parts of an e-cig and their main function?

A

device/battery: Provides power to heat the coil
coil: This is the heating element inside the pod/tank that heats up the vape juice to create vapor
cartridge/pod/tank: Attached to the battery and holds the vape juice

49
Q

1 JUUL pod = __ cigs

A

20

50
Q

why would you want to use nicotine salts in e-cigs?

A

allow for markedly higher levels of available nicotine to be readily inhaled by masking the harshness of nicotine with less irritation than the free-base nicotine used in traditional tobacco product

51
Q

what are some toxic chemical found in vapes?

A
  • propylene glycol
  • carcinogens (acetaldehyde, formaldehyde)
  • acrolein
  • diacetyl
  • diethylene glycol
  • heavy metals (nickel, tin, lead)
  • cadmium
  • benzene
52
Q

what makes vapes appealing to youth?

A
  • flavour
  • discreetness
  • accessible
  • perception that they are safer
  • advertising and marketing that targets them
  • unaware that they contain nicotine
53
Q

health concerns for vaping?

A
  • nicotine addiction
  • later neurodevelopment trajectory in youth
  • increase risk of psychopathology (mood disorder, anxiety, suicide, depression)
  • destruction of lung tissue (popcorn lung) and EVALI
  • cancer
  • cardiovascular effect
  • explosion
54
Q

what are some future concerns with vape use?

A
  • e-cigarette use is a risk factor for subsequent cigarette smoking
  • “Renormalizing” smoking
  • Long-term effects are unknown
55
Q

what positive effects are seen when someone stops smoking?

A
  • Reducing smoking leads to some health improvements (e.g., better breathing and exercise tolerance)
  • Reductions in cardiac, pulmonary, and oncological disease are only seen when quitting smoking
56
Q

what are some behavioural treatments for nicotine cessation?

A
  • Brief advice from physician or other health professional
  • Motivational Interviewing (MI)
  • Coping Skills
  • Relapse-Prevention
  • Community Support Groups (HSFO, CCS)
  • Hypnosis
  • Acupuncture
  • Rapid Smoking (Aversive Therapy
57
Q

what are some pharmacotherapies for smoking cessation?

A
  • slow-acting NRT: patch
  • fast-acting NRT: gum, inhaler, lozenge
  • antidepressant: bupropion
  • nicotinic partial agonist: varenicline (champix)
58
Q

what are some side effects of the nicotine patch?

A

local irritation

59
Q

what are some side effects of the fast-acting NRTs?

A

oropharyngeal irritation

60
Q

what are some side effects of buproprion for nicotine cessation?

A

insomnia, dry mouth

61
Q

what are some side effects of champix (varenicline)

A

GI effects, insomnia

62
Q

what is Varenicline?

A

a α4β2 nAChR partial agonist and Prevents smoking-relapse with treatment up to 24 weeks

63
Q

what was there a black-box warning against Varenicline?

A

anecdotal reports of treatment-emergent suicidality, homocidality, aggression, psychosis and mania

64
Q

which smoking cessation method was the best?

A

varenicline

65
Q

what are the different patterns of co-use?

A

sequential (on separate occasions)
simultaneous (at the same time)

66
Q

why are rates of nicotine and cannabis co-use so high?

A
  1. qualitative reports (“burns better”, cost-effective, “better high”)
  2. common route of administration, so easy to add on
  3. nicotine may counteract selective cognitive and clinical effects associated with cannabis (e.g. memory performance, sedation, appetite)
67
Q

how are cannabis and nicotine associated?

A

their distribution highly overlap, suggesting cross-talk between the two

68
Q

consequence of nicotine/cannabis co-use?

A
  • higher risk of developing cannabis/nicotine use disorder
  • additive adverse effects (e.g. depression)
  • greater physical health problems
  • increased toxicant exposure
  • reduced likelihood of stopping cannabis
69
Q

what is the cannabis withdrawal trajectory?

A

begin: 24 hrs
peak: within 7 days
dissipate: after 28 days

70
Q

What is Driving Elevated Cannabis Withdrawal Severity in people who co-use tobacco?

A
  • chronic cannabis use alters endocannabinoid system (downregulate CR1, decreased anandamide)
  • withdrawal is linked to dysregulation of the system, which may be exacerbated with tobacco use
71
Q

how did FAAH levels differ in people who just use cannabis or that co-use? what does this mean?

A

higher in co-use, which means that more endocannabinoids broken down, which dysregulates the system further

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