nicotine 1 Flashcards

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1
Q

how much money is spent per year on treating tobacco-related illness

A

£1.7 billion

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2
Q

identify organs effected by tobacco

A
  • brain
  • heart
  • liver
  • kidneys
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3
Q

what does the enzyme MAO-B do?

A
  • enzyme that breaks down dopamine
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4
Q

what is the effect of tobacco on the MAO-B enzyme?

A
  • tobacco greatly reduces MAO-B enzyme activity
  • when activity of this enzyme is reduced activity of dopamine and noradrenaline increases
  • thought to increase addictive nature of nicotine
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5
Q

what is nicotine?

A
  • active ingredient in tobacco (tobacco = plant, nicotine = chemical found in plant)
  • responsible for addictive potential
  • functions as anti-herbivore chemical (to deter insects)
  • herbal drug
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6
Q

identify another use of nicotine

A

insecticide

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7
Q

identify different ways of nicotine entering the body

A
  • chewing tobacco leaves
  • making tobacco tea
  • dry smoking the leaves
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8
Q

what is required for nicotine to be absorbed across lung alveoli?

A
  • the acidity of environment needs to be suitable for absorption
  • this is achieved with tar molecules that is in tobacco
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9
Q

identify a difficulty that the nicotine replacement industry has faced

A
  • difficulty = replicating the fast, spiked absorption of cigarettes
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10
Q

identify 3 models of addiction for nicotine

A

1/ susceptibility and exposure model

2/ withdrawal model

3/ DA-mediated incentive effects

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11
Q

define tolerance

A
  • when taking the same dose of a drug doesn’t have the same effect it once did when initially started with that drug
  • an increase in dose of drug is needed to have effect it once did
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12
Q

define withdrawal

A

a syndrome that occurs after having stopped prolonged, heavy consumption of drug

symptoms include:
- nausea, insomnia, mood alterations, anxiety

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13
Q

define escalation of dose

A
  • where individual experiences period of using drug more than they intended to
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14
Q

define difficulty cutting down

A

where individual experiences wanting to stop or cut down drug use more than once

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15
Q

define reduce other activities

A

where individual cuts down or gives up on activities that they were once interested in due to drug not being permitted at that activity

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16
Q

define use despite problems

A

where individual continues to use drug despite causing health problems or making health problems worse

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17
Q

do all smokers become dependent?

A

no

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18
Q

what percentage of those who smoke become dependent, based on research by Anthony et al. (1994)?

A

32% exposed to tobacco become dependent

19
Q

what does data from Anthony et al. (1994) show about nicotine dependence?

A
  • of 75.6% exposed to nicotine, 31.9% become dependent
  • nicotine in tobacco is more addictive than heroin
    (32% became dependent vs 23% becoming dependent on heroin)
20
Q

what % of smokers meet the DSM criteria for nicotine dependence?
(Donny & Dierker, 2007)

A

60%

21
Q

what % of smokers are chippers? (only uses drug recreationally)
(Hyland, 2005)

A

10%

22
Q

what does the findings from Donny & Dierker (2007) and Hyland (2005) suggest about nicotine and dependence?

A
  • suggests tobacco dependence is not inevitable consequence of exposure to tobacco
  • tobacco dependence = interaction between exposure and individual vulnerability (susceptibility and exposure model)
23
Q

identify a vulnerability factor of tobacco dependence

A

age of first exposure

24
Q

what age is tobacco usage higher in?

A
  • higher in smokers aged 18 - 25 years
25
Q

is there a gender difference in tobacco usage?

A

yes

males use more tobacco than females

26
Q

Outline Levin et al. (2003) study into adolescent rats and smoking

A
  • conducted controlled animal study
  • rats were given opportunity to self-administer nicotine using lever press

results showed:
- adolescent rats worked harder for nicotine

  • adolescent rats took larger amounts of nicotine

results suggest that adolescents are vulnerable to nicotine addiction

27
Q

how is nicotine delivered to the brain?

A
  • nicotine is delivered to brain through blood in arteries
  • concentration of nicotine in arteries (carries blood away from heart and lungs) rose more rapidly and reached higher peak than nicotine in veins (carries blood back to heart and lungs)
28
Q

what is nicotine’s primary mechanism of action when it reaches the brain?

A
  • primary action is at ACh receptors
  • nicotine has correct molecular shape to take over ACh function
  • this means nicotine can function on same receptor
29
Q

what is the name of the receptors that nicotine act on?

A

nicotinic cholinergic receptors

30
Q

what is ACh?

A
  • it is a neuromodulator (a messenger released from a neuron that affects the transmission of the signals between neurons)
  • ACh can influence activity in target cells over long periods
  • plays important role in learning and intellectual function
  • degeneration of ACh seen in Alzheimer’s disease
31
Q

what primary effects does nicotine addiction have on ACh?

A
  • ACh receptors become desensitised through chronic coupling (meaning more ACh or nicotine is needed to produce same response)
  • leads to withdrawal response when nicotine = stopped
  • because ACh activation within normal range is insufficient to keep neuronal activation within normal range
32
Q

what secondary effects does nicotine have on ACh?

A
  • increased activity in target cell, particularly dopamine
  • this thought to drive rewarding/reinforcing effects on nicotine
33
Q

what does NRT stand for?

A

nicotine replacement therapy

  • used to help reduce the urge to smoke
34
Q

explain NRT

A
  • thought to stop withdrawal
  • done by maintaining ACh receptor occupancy
  • however, this can result in transfer of dependence (using e-cigarette or nicotine lozenge)
35
Q

what is the issue with transference of dependence?

A

despite smoking habit being broken, addiction never truly broken if dependence transfers to other source of nicotine

36
Q

how do antidepressants help with

A
  • urge to smoke is reduced by treatment with anti-depressants
  • anti-depressants thought to block negative emotional state associated with withdrawal (protecting against relapse)
37
Q

what is the success rate of using antidepressants as a way to treat nicotine addiction? (Wang, 2008) , (Wu, 2006)

A

in 12 month sustained abstinence success rate:
- 2% with placebo
- 5% with nicotine patch (NRT) or antidepressant

38
Q

how does antidepressant work?

A
  • inhibits reuptake of dopamine (and noradrenaline)
  • increasing availability of postsynaptic dopamine
39
Q

what effect does nicotine have on dopamine?

A

nicotine increases dopamine release indirectly

40
Q

outline Fa et al. (2000) study into dopamine and nicotine addiction in rats

A
  • administered tobacco smoke to rats
  • measured rats dopamine level with micro-electrodes
  • micro-electrodes were placed on ventral tegmentum (VTA) or substantia nigra
  • VTA = important in regulating reward through mediating dopamine release
  • SN = critical brain area for production of dopamine
  • administered mecamylamine (nicotinic receptor antagonist)
  • antagonist = blocks activity of receptor
  • administering mecamylamine found to block surge in firing of dopamine that is seen after exposure to tobacco smoke
  • this pattern was found in VTA but not SN
  • shows that the mesolimbic (reward) dopamine pathway is critical for addiction
41
Q

what is the effect of nicotine induced excitation of ACh neurons?

A
  • excite mesolimbic dopamine (reward) cells
  • via branching cholinergic pathways from pedunculopontine nucleus (ppt)
  • this is a source of cholinergic projections
42
Q

explain an animal (rat) study that confirms the role of dopamine in nicotine dependence

A
  • found that rats readily learn to press a lever
  • lever to obtain electrical brain stimulation reward (BSR) of mesolimbic dopamine pathway
  • unlike natural reward, this behaviour does not require deprivation
  • BSR can displace important rewards
  • found that rats choose BSR over food to point of starvation
  • emphasises the role dopamine has in reward
43
Q

outline David (2006) study into dopamine and self-administration

A
  • rats self-administered nicotine directly to VTA (ventral tegmentum)
  • the self-administering of nicotine can be stopped by antagonising activity at dopamine or ACh receptors
  • concluded that nicotine (via ACh receptors) increases activity of dopamine cells in VTA
  • increased activity moderates the addictive properties of nicotine