Nicotine Flashcards

1
Q

Levels of nicotine present in cigarettes?

How does nicotine enter the lungs?

Difference in nicotinic levels in venous vs arterial?

A
  • 6-11mg per cigarette;
    • only 1-3mg absorbed in bloodstream.

Nicotine entry to lungs:

  • via small particles known as TAR:
    • readily passes through the absorbent lungs.
      • Higher levels in arterial blood, having a more rapid increase at higher levels in comparison to venous.
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2
Q

Characteristics of Nicotine?

  • Half life?
  • tolerance for the following days?
    *
A
  • Half-life:
    • around 2 hours.
  • Tolerance dissipates the following day:
    • therefore strong craving the following day,
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3
Q

Receptors responsible for mechanism of action?

A
  • Activation of nicotinic cholinergic receptors( nAChRs).
    • Acting upon acetylcholine.

Nicotine; leading to persistent activation of nicotinic receptors and continuous depolarization of the post-synaptic cells.

  • Cell cannot fire until nicotinic is removed.
    • Biphasic effect:
      • Stimulation of nicotinic cholinergic function that turns to nicotinic receptor block.
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4
Q

Continuous nicotine administration to non-smokers enhances performance?

  • Results on smokers vs non-smokers?
A

Overall:

  • Nicotine shows an increased level of cognitive function.
    • This is as ACh is heavily involved in cognitive function.
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5
Q

Key pathway involved in reinforcement, and how nicotine attributes to this.

A

Mesolimbic dopamine pathway:

  • VTA——> NAcc.
    • high-affinity nicotinic receptors stimulate the firing of DA neurons, to increase DA release in the NAcc.
    • Other studies involve lesioning dopaminergic innervations in the NAcc, with 6-hydroxydopamine(6-OHDA), which reduces self-administration.
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6
Q

Other compounds in tobacco and its effects on MAO-B?

  • PET scans?
  • Function of MAO?
  • Other consequences of nicotine on the ANS?
    • and positive clinical symptoms?
A

PET scans:

  • inhibition of MAO as a result of smoking.
    • As MAO is important in the breakdown of DA.

Consequences:

  • As nicotine acts upon the ANS; PNS and SNS:
    • causes tachycardia and elevated blood pressure:
      • ++ Cardiovascular disease.
  • However: reduce appetite and increase metabolic weight.
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7
Q

Briefly describe the physiology of withdrawal syndrome.

A
  • Reduced DA release in the NAc,
    • increase in Corticotrophin releasing factor(CRF) within the amygdala.
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8
Q

What is the nicotine resource model?

A
  • That smoking relieves stress and enhances the ability to concentrate.
    • primarily based on environmental stress.
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9
Q

Deprivation reversal model?

A
  • Positive effects of smoking alleviation irritability, stress and poor concentration;
    • Bringing smokers into the same state as a non-smoker.
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10
Q

Side effects of smoking?

A
  • Can lead to respiratory diseases: such as Chronic Obstructive pulmonary disease(COPD):
    • increased risk of:
      • Heart attacks.
      • Stroke.
      • Atherosclerosis.
  • The decline in cognitive function.
  • During pregnancy:
    • decrease birth weight, delaying the infant’s development, and increases the risk of complications.
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11
Q

Treatments for nicotine dependence?

  • State examples of the medications(pharmacological) use.
A
  • Behavioural interventions, high taxes on products and health warning on packaging.
  • Counselling, social support or/and training in coping in skills.
  • Pharmacological interventions: nicotine replacement:
    • nicotine gum, nasal sprays and inhalers.
    • Buproprion:
      • smoking cessation(ending smoking), initially used as an antidepressant.
    • Varenicline:
      • partial agonist, high affinity for a4B2 nicotinic receptors, expressed in VTA.
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12
Q
A
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