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PSYC 207 > (8) nicotine & caffeine > Flashcards

(8) nicotine & caffeine Flashcards

1
Q

Why do plants produce nicotine?

A
  • produced in plants of nightshade family (tomato, potato, eggplant, bell pepper)
  • acts as anti-herbivore: dissuade animals from eating, feel unpleasant from nicotine
  • acts as insecticide: neonicotinoid (synthetic nicotine)
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2
Q

What are various routes of nicotine administration? How do these routes relate to peak absorption?

A
  • cigarettes
  • cigars
  • pipes
  • smokeless tobacco
  • vaporisers: free based form of nicotine
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3
Q

What is Juul? Why is it different from other e-cigarettes?

A
  • nicotine salts
  • reduced harshness
  • faster peak effects: 5 mins
  • tremendously potent: each pod = nicotine in 1 pack of cigarettes
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4
Q

How does our previous learning on dose and route of administration relate to the addictive potential of Juul? What features make it potentially a problem?

A
  • v. potent & fast effects: recreational users want fast & intense high
  • predictors of addiction: v. large amounts & regular frequent use - both gained in Juul
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5
Q

In what ways is tobacco unhealthy? (II Ie I)

A

in cigarettes, associated w/ adverse health consequences:

  • increased rates of cancer: nitrosamines is carcinogen (cancer-causing substance)
  • increased rates of cardiovascular disease
  • increased rates of pulmonary disease:
    • emphysema: progressive disease of lungs leads to shortness of breath
  • increased pregnancy complications: teratogen - chemical/substance that negatively alters process of dvpm in fetus
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6
Q

What is first-, second-, and third-hand smoke?

A
  • first-hand: person smoking
  • second-hand: around ppl who exhale smoke & breath in cigarette smoke
  • third-hand: substance in smoke sticks to physical objects
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7
Q

What is the pharmacokinetics of nicotine? (administration & absorption) (AI P O)

A
  • absorbed thru mouth, nose, throat, lungs
  • inhalation most effective for nicotine delivery - exception: e-cigs
  • peak absorption:
    • 5-7mins for cigarettes
    • 20-30mins for other products
  • other variables affecting absorption: tricky to measure amount of drug used
    1. # of inhalations
    2. quality of inhalation
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8
Q

What is the pharmacokinetics of nicotine? (biotransformation & elimination) (N Mbmps Hlc E)

A
  • nicotine readily crosses bbb
  • metabolised in liver:
    • broken down into active metabolite: cotinine
    • mentholation slows metabolism: longer lasting & more intense effects → smoke less
    • polymorphisms affect rate of metabolism
    • slower metabolisers likely light smokers
  • half-life of nicotine: 2 hours
    • less for chronic smokers
    • cotinine: 17 hours
  • eliminated via urine
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9
Q

What is the pharmacodynamic mechanism of nicotine?

A

nicotine is cholinergic agonist at nicotinic receptors (nAChRs)

- i.e. for acetylcholine
- ionotropic receptors: when nicotine binds, cause them to open & ions to flow thru
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10
Q

What are the rewarding properties of nicotine? (I Ni Ra O)

A
  • increases DA in NAcc: mimics actions of acetylcholine & activates DA cells
  • nicotine receptors activated in VTA/NAcc increase DA:
    • ionotropic: allows calcium & sodium, causes depolarisation & APs
  • release in NAcc:
    • AP in VTA causes more DA to be released
  • other constituents of tobacco smoke may enhance these effects
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11
Q

What is nAChR desensitization? What effect does it have on the experience of subsequent nicotine use and the amount of subsequent nicotine use? (NN Dfa)

A
  • nicotine = acetylcholine receptor agonist
  • nicotine binds for extra long time & receptor closes even w/ nicotine binded
  • desensitized state:
    • functional antagonism?
    • acetylcholine cannot bind to receptor
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12
Q

What is nAChR desensitization? What effect does it have on the experience of subsequent nicotine use and the amount of subsequent nicotine use? (Ucn Rsl)

A
  • upregulation:
    • more acetycholine receptors come up to membrane
    • more receptors for nicotine to bind to
  • related to acute tolerance: after taken drug once, next time will have weaker effect
    • strongest is first cigarette
    • leads to more smoking
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13
Q

Where are nAChRs located? How do differing locations lead to differing effects? (Fng Fhpv)

A
  • found in PNS:
    • neuromuscular junction
    • ganglia of ANS
  • found in CNS:
    • hippocampus & cerebral cortex
    • basal ganglia
    • VTA & NAcc
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14
Q

What are the pharmacological effects of nicotine? (Psiba Cic B)

A
  • physiological effects:
    • sympathomimetic
    • increase BP & HR
    • blood vessels constrict
    • appetite suppressant
  • cognition & movement:
    • involved in movement stability
    • cognitive enhancer (e.g. Stroop test, memory test)
  • but consider acute tolerance
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15
Q

How do effects differ between habitual and naïve users? (H:rble)

A
  • naïve: report negative subjective effects
  • habitual:
    • report positive subjective effects
    • build tolerance to negative subjective effects
    • likely to become addicted
    • exception: chippers
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16
Q

What are chippers? (SRC Glbb)

A
  • “social smokers”
  • resistant to addictive effects of nicotine
  • common
  • genetic & environmental mechanisms:
    • less stressed
    • better support & social structure
    • better coping skills
17
Q

What are the results of studying nicotine’s subjective effects in animal models?

A

animal models confirm negative subjective effects:

  • drink from bottle of water or water w/ nicotine
  • over trials, drink less from bottle of water w/ nicotine
18
Q

What best predicts long-term abstinence?

A

the magic timeframe: 2 weeks

- biggest predictor of long-term abstinence

19
Q

What are the various strategies for quitting and their success rates?

A
  1. nicotine replacement therapy
  2. nAChR agonists
  3. antidepressants
20
Q

What is nicotine replacement therapy for quitting smoking?

A
  • e.g. gum, patches, nasal spray, vapes
  • more similar to smoking cigarette, more effective
  • Juul?
21
Q

What are nAChR agonists for quitting smoking?

A
  • e.g. Varenicline (Chantix, Champix): bind to acetylcholine receptor & activate it
  • success rate: less than half
  • should we consider this replacement therapy?
22
Q

What are antidepressants for quitting smoking?

A
  • e.g. Buproprion (Zyban, Wellbutrin), NDRI & nAChR antagonist:
    • NDRI: norepinephrine dopamine reuptake inhibitors
  • helps 20% of individuals in decreasing amount of smoking
23
Q

What are the effects of caffeine?

A
  • Physiological:
    • increased HR
    • blood vessel constriction
    • BR
    • reduced appetite
  • Behavioural:
    • attention
    • alertness
  • Subjective effects: positive mood
  • Adverse effects: caffeinism
24
Q

What is caffeine dependence?

A
  • caffeine tolerance: mood, alertness, anxiousness
  • no/reduced tolerance: cardiovascular activity, blood vessel constriction
  • but caffeine intoxication (caffeinism) & withdrawal are in the DSM-5
25
Q

Why do people consume caffeinated products?

A
  • increased sense of energy & improved mood but diminishes w/ tolerance
  • physical dependence
  • incentive sensitization
    • products containing caffeine taste good (especially recently)
26
Q

What family of molecules does caffeine belong to?

A
  • mild psychostimulant of xanthine family
  • found in number of plants
  • most widely used drug

xanthine found in:

  • kola nuts
  • cocoa tree nuts
  • tea leaves
  • coffee beans:
    • longer roast, more caffeine
    • dark roast: less caffeine, light roast: more caffeine
27
Q

What is the relative caffeine content of various foods and beverages (in coarse terms)?

A

energy drinks:

  • contain around 75mg of caffeine + other xanthines
  • fastest growing beverage market
  • caffeinated alcoholic beverages are mixing energy drinks
  • high sugar content
28
Q

What is caffeine’s pharmacokinetics?

A
  • oral administration: food, beverage, pills
  • absorption across intestinal walls
  • peak concentrations: 40mins after ingestion
  • crosses BBB
  • metabolised in liver
  • active metabolites: theobromine, theophylline, paraxanthine
  • half-life varies: b/w 3-10hrs
  • elimination via urine
29
Q

What is the pharmacodynamic mechanism of caffeine?

A
  • A1 & A2 adenosine receptor antagonist:
    • adenosine receptors omnipresent thruout body
    • i.e. CNS, PNS & non-nervous-system effects
  • some sympathomimetic effects
  • high doses can lead to caffeinism
  • acute subjective effects tend to tolerate
  • physiological effects may not tolerate
30
Q

What is caffeinism?

A

v. high dose of caffeine leading to:
- anxiety
- agitated
- negative mood
- v. fast HR
- higher BP
- discomfort in guts
- unable to sleep

31
Q

What are the effects of caffeine withdrawal?

A
  • headache
  • difficulty concentrating
  • fatigue
  • irritability
  • functional impairment
  • anxious mood
  • depressed mood
32
Q

Should caffeine be considered addictive?

A
  • caffeine not considered substance of concern by DSM-5

- caffeine not addictive, doesn’t lead to persistent/adverse effect on life

33
Q

Is nicotine neuroprotective? (alzheimer’s disease)

A

affects cholinergic neurons early

  • cholinergic neurons: produce acetylcholine
  • potential therapeutic: nAChR agonists
  • evidence: no clear benefits
34
Q

Is nicotine neuroprotective? (schizophrenia)

A

smoking disproportionately high

  • the “self-medication hypothesis”: nicotine administration may be instrumental
  • evidence (human studies & animal models):
    • smoking lessen negative symptoms, improves sensory processing, speeds up antipsychotic medication metabolism, act as mild cognitive enhancer
35
Q

Is nicotine neuroprotective? (neurodegeneration)

A
  • smoking cigarettes associated w/ some increased neurodegenerative risk (Alzheimer’s, dementia)
    BUT
  • smoking cigarettes inversely correlated w/ risk of Parkinson’s disease
  • nicotine w/o smoking may be neuroprotective
36
Q

Is caffeine neuroprotective? (neurodegeneration)

A
  • coffee & caffeine: good neuroprotective effect on brain
  • co-administering caffeine w/ PD-causing chemical (MPTP) protects rodent brain from PD
    • PD: Parkinson’s disease
  • similar effects for amyotrophic lateral sclerosis (ALS)
  • decent potential benefit for Alzheimer’s
  • may speed up arrival of symptoms in Huntington’s disease
  • coffee & caffeine delays/reduces age-related cognitive decline, especially in women
    • heavy coffee drinkers

PSYC 207 (12 decks)

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