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PSYT 301 > Nicotine and tobacco > Flashcards

Nicotine and tobacco Flashcards

1
Q

impacts of smoke-free laws and policies (2)

A
  1. ~7% decrease in tobacco use
  2. dramatic reduction of second-hand smoke exposure
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2
Q

prevalence of smoking in canada

A

daily -> 8%
daily + non-daily -> 12%

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3
Q

short-term effects of tobacco use (8)

A
  1. euphoria (the high)
  2. enhances cognition (ex. attention)
  3. decreases appetite
  4. stimulates nausea and vomit reflex
  5. increases HR, breathing rate and BP
  6. CO blocks O2 from getting into bloodstream
  7. bad breath
  8. stimulates reward system and other neurochemical systems
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4
Q

systems that tobacco stimulates and what they’re involved in (7)

A
  1. DA -> pleasure, reward
  2. NE -> arousal, appetite suppression
  3. ACh -> arousal, cognitive enhancement
  4. Glu -> learning, memory enhancement
  5. b-endorphin -> reduction of anxiety and tension
  6. GABA -> reduction of anxiety and tension
  7. 5-HT -> mood modulation, appetite suppression
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5
Q

long-term effects of tobacco use (7)

A
  1. bronchitis and emphysema
  2. chronic obstructive pulmonary disease (COPD)
  3. heart and artery disease
  4. cancer (lung, bladder, pancreas)
  5. diabetes
  6. osteoporosis
  7. tobacco addiction
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6
Q

people who smoke die how many years earlier than non-smokers

A

13-14 years earlier

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7
Q

risk factors for tobacco use disorder (11)

A
  1. genetic predisposition
  2. parental exposure
  3. lower socioeconomic status
  4. peer pressure
  5. poor academic performance
  6. impulsivity
  7. low self-esteem
  8. mood disorders
  9. mental illness
  10. substance abuse
  11. onset of tobacco smoking during childhood or adolescence
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8
Q

long-term effects of /adolescent/ tobacco use (4)

A
  1. alters trajectory of normal brain development
  2. diminished cognitive function that persists into adulthood
  3. greater mental health problems
  4. effects that last into adulthood
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9
Q

how does adolescent tobacco use alter trajectory of normal brain development (5)

A
  1. dendritic remodelling
  2. lower GMV in thalamus and amygdala
  3. aberrant functional connectivity
  4. changes in reward system
  5. changes in 5-HT synaptic function
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10
Q

how does adolescent tobacco use diminish cognitive function (3)

A
  1. reduced attention span
  2. poorer memory
  3. enhanced impulsivity and lower inhibitory control
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11
Q

how does adolescent tobacco use cause greater mental health problems (2)

A
  1. increased anxiety, psychosis and depressive-like behaviors in adults
  2. more severe tobacco addiction later in life
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12
Q

what is nicotine (3)

A
  1. stimulant
  2. primary psychoactive constituent of tobacco
  3. underlies addictive properties
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13
Q

mode of delivery of nicotine: cigarette (4)

A
  1. nicotine is distilled from tobacco and carried in smoke particles into lungs
  2. moves quickly to brain (10-15s) -> faster than via IV
  3. binds to nAChR
  4. onset of CNS action within seconds
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14
Q

properties of nAChR (7)

A
  1. ligand-gated ion channel
  2. key role in modulating neuronal excitability
  3. regulates flow of cations across cell membrane
  4. 5 distinct membrane-spanning subunits (a and b) combine to form functional receptor
  5. each composed of various combinations of a/b subunits
  6. expressed pre-synaptically
  7. activated by nicotine and ACh
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15
Q

most abundant nAChR in brain (2)

A

a4b2 and a7

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16
Q

affinity of nicotine for a4b2 and a7

A

highest affinity for a4b2; low affinity for a7

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17
Q

brain areas with highest density of nAChRs (9)

A
  1. cortex
  2. hippocampus
  3. amygdala
  4. NAcc
  5. caudate, putamen
  6. VTA
  7. cerebellum
  8. thalamus
  9. insula
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18
Q

mechanism of nicotine/ACh binding to nAChR (4)

A
  1. binding induces conformational change
  2. cations flow through intrinsic channel -> depolarization of neuron
  3. after activation, nAChR become desensitized: channels close and receptor cannot be reactivated
  4. eventually regain sensitivity and become reactivated
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19
Q

how does nAChR desensitization influence effects of nicotine

A

limits duration of acute effects

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20
Q

desensitized nAChRs (3)

A
  1. still have high affinity for ACh and nicotine
  2. receptor is inactive -> binding has no effect
  3. decreased receptor responsiveness for subsequent stimulus
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21
Q

effect of chronic nicotine use on nAChR desensitized state

A

nAChR spend more time in desensitized state, causing an upregulation of nAChRs

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22
Q

effect of decreased nAChR responsiveness (2)

A
  1. acute tolerance of nicotine
  2. reduced satisfaction
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23
Q

upregulation of nAChRs due to chronic nicotine use (3)

A
  1. results from frequent desensitization of receptors
  2. compensation mechanism to augment nAChR response
  3. may contribute to difficulties with tobacco cessation
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24
Q

upregulation of nAChRs documented in (3)

A
  1. animal studies after chronic nicotine exposure
  2. postmortem tobacco smokers compared to non-smokers
  3. increased densities in striatum, cerebellum and cortex of living human smokers compared to non-smokers
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25
Q

level of upregulation of nAChR in abstinence (2)

A
  1. persists for up to 1 month abstinence
  2. normalizes to control levels after 6-12 weeks of abstinence
26
Q

nicotine and its rewarding properties (5)

A
  1. one of most addictive drugs
  2. repeated administration sensitizes response to nicotine (implicated in transition from experimentation to habitual smoking)
  3. repeated administration facilitates conditioned learning (smoking cues are very salient)
  4. most smokers find it difficult to quit despite knowing the harms
  5. brain nAChRs expressed in high densities in VTA
27
Q

what makes nicotine so addictive

A

DA surge happens very quickly and at high levels

28
Q

nAChRs found on which neurons in VTA (3)

A
  1. DA
  2. GABA
  3. glu
29
Q

what causes enhanced DA release in NAcc (vague)

A

stimulatory (DA, glu) and inhibitory (GABA) effects and differential desensitization of nAChRs

30
Q

nicotine mechanisms involved in DA release (3)

A
  1. direct activation of VTA DA neurons: DA release in NAcc
  2. activation of a7 nAChR on glu neurons (indirect mechanism)
  3. activation of GABA neurons (contain b2 nAChRs) (indirect mechanism)
31
Q

activation of a7 nAChR on glu neurons mechanism (3)

A
  1. release glutamate on DA neurons
  2. DA release in NAcc
    * a7 less prone to desensitization because have low affinity for nicotine -> effect is sustained
32
Q

activation of GABA b2-containing neurons mechanism (4)

A
  1. release GABA on DA neurons
  2. inhibition of DA release in NAcc
  3. a4b2 receptor desensitization -> decreased GABA release
  4. a4b2 receptor upregulation -> increased DA neuron excitability
    (a4b2 nAChRs rapidly desensitize -> GABAergic drive is reduced over longer time frame when constant presence of nicotine -> sustained DA levels)
33
Q

general activity of nicotine on DA, glu and GABA neurons in VTA (4)

A
  1. nicotine directly stimulate DA neurons in VTA
  2. nicotine stimulates release of glu -> more release of DA in NAcc
  3. VTA cells stimulate GABA release to counter DA increase
  4. minutes later, glu cells continue to release DA, but GABA release becomes inhibited (desensitization) -> results in sustained levels of DA in NAcc
34
Q

roles of different subunits in nAChRs (4)

A
  1. a4b2 -> regulate many of the addiction-relevant behavioral responses to nicotine (highly expressed in midbrain DA pathways)
  2. b2 -> DA release, self-administration
  3. a4 -> nicotine sensitivity (mutation that increases sensitivity of a4 = enhanced addiction-relevant behavior)
  4. a3 and b4 -> low-affinity nicotine binding sites (enriched in brain sites involved in aversion)
35
Q

non-nicotinic compound that promotes reinforcing action of nicotine

A

monoamine oxidase inhibitors (MAO enzymatic activity reduced in smokers)

36
Q

actions of MAOI (2)

A
  1. decrease breakdown of DA -> increases DA in rewarding regions of brain
  2. enhances nicotine self-administration
37
Q

when do MAOIs by smoke have an effect

A

after long-term exposure (not rapidly reversible) -> no change in MAO enzymatic activity after single cigarette

38
Q

nicotine pharmacokinetics (3)

A
  1. majority metabolized in liver by P450s (CYP2A6)
  2. half-life in blood = 2h
  3. major metabolite is cotinine
39
Q

how is nicotine titrated by smokers (3)

A
  1. smoke 1st cigarette within 5 minutes of waking (to counter withdrawal induced by sleeping)
  2. smoke more frequently in 1st hours after waking (try to get blood [nicotine] to specific level
  3. levels are maintained throughout the day by smoking cigarettes (to avoid withdrawal)
40
Q

nicotine withdrawal symptoms (10)

A
  1. irritability
  2. anxiety
  3. difficulty concentrating
  4. restlessness/impatience
  5. depressed mood/depression
  6. insomnia
  7. impaired performance
  8. increased appetite/weight gain
  9. cravings
  10. impaired cognition
41
Q

timeline of nicotine withdrawal (4)

A
  1. onset within 4 hours
  2. most symptoms manifest within first 1-2 days
  3. peak within 1st week
  4. subside within 2-4 weeks
42
Q

nicotine addiction cycle (6)

A
  1. cigarette smoking
  2. nicotine absorption
  3. arousal/mood modulation/pleasure
  4. tolerance and physical dependence
  5. drug abstinence produces withdrawal symptoms
  6. cravings for nicotine to self-medicate withdrawal symptoms
43
Q

people with TUD comorbidity (2)

A
  1. people with psychiatric disorders have heightened vulnerability to addictive properties of cigarettes
  2. more likely to progress to habitual smoking because nicotine counteracts impairments of disorders
44
Q

e-cigarettes (3)

A
  1. tool for smoking cessation
  2. heating solution of propylene glycol or glycerol and nicotine
  3. perceived as healthier alternative to tobacco smoking
45
Q

factors affecting nicotine exposure of e-cigarettes (3)

A
  1. e-liquid [nicotine]
  2. power of e-cigarette
  3. user consumption patterns
46
Q

how are e-cigarettes healthier than tobacco smoking

A

nicotine delivered to upper and lower respiratory tract without any combustion (less carcinogens delivered)

47
Q

harmful effects of e-cigarettes (14)

A
  1. respiratory irritation
  2. abnormalities in respiratory function
  3. lung oedema
  4. airway epithelial injury
  5. sustained tissue hypoxia
  6. EVALI
  7. cytotoxicity
  8. oxidative stress
  9. increased inflammatory markers
  10. impaired endothelial function
  11. increased platelet and leukocyte activation
  12. increased platelet aggregation
  13. increased arterial stiffness
  14. potential human carcinogen
48
Q

new way JUUL developed to deliver nicotine

A

nicotine salts: easier to inhale and more readily absorbed into bloodstream (rate similar to conventional cigarettes)

49
Q

toxic chemicals and metals in e-cigarettes (8)

A
  1. propylene glycol
  2. carcinogens (acetaldehyde, formaldehyde)
  3. acrolein
  4. diacetyl
  5. diethylene glycol
  6. nickel, tin, lead
  7. cadmium
  8. benzene
    *high [ultrafine particle and toxicants]
50
Q

people who use e-cigarettes (2)

A
  1. people who already smoke cigarettes (dual use)
  2. adolescents
51
Q

how are e-cigarettes appealing to youth (6)

A
  1. flavoring
  2. discreteness
  3. accessible
  4. perception that they are safer than cigarettes
  5. advertising and marketing towards young people
  6. unaware that e-cigarettes contain nicotine
52
Q

concerns about e-cigarettes (4)

A
  1. use on the rise, especially among adolescents
  2. risk factor for subsequent cigarette smoking
  3. renormalizing smoking
  4. long-term effects unknown
53
Q

quitting nicotine/tobacco (5)

A
  1. health improvements
  2. reductions in cardiac, pulmonary and oncological disease
  3. ~70% want to quit
  4. > 30 attempts before success
  5. current treatments show limited efficacy
54
Q

current treatments (4)

A
  1. behavioral treatment
  2. NRTs (nicotine patch, gum)
  3. antidepressants (bupropion)
  4. nicotinic partial agonist (varenicline)
  5. brain stimulation (rTMS)
55
Q

behavioral treatments (8)

A
  1. brief advice from physician or health professional
  2. motivational interviewing
  3. coping skills
  4. relapse-prevention
  5. community support groups
  6. hypnosis
  7. acupuncture
  8. rapid smoking (aversive therapy)
56
Q

slow (1) and fast (3) NRTs

A

slow -> nicotine patch
fast -> gum, lozenge, inhaler

57
Q

side effects of slow (1) and fast (1) NRTs, bupropion (3) and varenicline (5)

A

slow NRT -> local irritation
fast NRT -> oropharyngeal irritation
bupropion -> insomnia, activation, dry mouth
varenicline -> GI, insomnia, nausea, headache, abnormal dreams

58
Q

mechanisms of NRTs (3)

A
  1. rates of delivery which are less than that of cigarettes smoking
  2. acts as agonist alone, mimics MOA of nicotine
  3. peak levels are ~30-50% of those achieved by smoking
59
Q

varenicline (champix) (5)

A
  1. a4b2 nAChR partial agonist
  2. superior to bupropion and placebo
  3. prevents smoking-relapse with 24 week treatment
  4. main SE = nausea, insomnia, headache, abnormal dreams
  5. anecdotal reports of suicidality, homocidality, aggression, psychosis and mania
60
Q

treatment of TUD and types of metabolizers to optimize quitting (2)

A
  1. treat normal metabolizers with varenicline
  2. treat slow metabolizers with nicotine patch

PSYT 301 (9 decks)

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