Nicotine; Caffeine Flashcards

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1
Q

Plant of nicotine

A

Produced in plants of the nightshade family: insecticide properties
Nicotiana tabacum is most commonly cultivated

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2
Q

Juul and modern vaporizers

A
Nicotine salts (protonated nicotine)
Earlier nicotine peak
Tremendously potent
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3
Q

Tobacco use/exposure: Increased rates of cancer due to

A

nitrosamines in tobacco smoke

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4
Q

Tobacco use/exposure: Increased rates of

A

cancer, cardiovascular disease (CVD), pulmonary disease (Emphysema), pregnancy complications

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5
Q

Tobacco use/exposure: Teratogen

A

Increased pregnancy complications: malformation of embryo

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6
Q

First, second, third hand smoke

A

First - smoking
Second - through air
Third hand (smoke adhered to objects)
All convey risks

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7
Q

History of tobacco use

A

Mayans, incas, Toltecs, aztecs - religious purposes
First introduced to europe in 15th century. Mid 16th century = widespread
An important trade crop
Questions about safety date to early 17th century
The early 20th century saw researchers focus on adverse effects

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8
Q

Absorption of nicotine

A

Absorbed via mouth, nose, throat, lungs
Inhalation = most effective for nicotine delivery - exception: e-cigs
Peak absorption: 5-7 min for cigarettes (lungs)
20-30 Min for most other products

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9
Q

Biotransformation and elimination of nicotine

Blood brain barrier

A

Nicotine readily crosses blood-brain barrier

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10
Q

Biotransformation and elimination of nicotine

Metabolization

A

In liver
Active metabolite: cotinine
Mentholation slows metabolism (menthols)
Polymorphisms can affect rate of metabolism
Slower metabolizers are more likely to be light smokers

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11
Q

Half life nicotine

A

Half-life of nicotine: 2 hours (Less for chronic smokers)
Cotinine: 17 hours
Eliminated via urine

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12
Q

Nicotine agonist or antagonist?

A

Nicotine is a cholinergic agonist (increases the function of receptor)

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13
Q

What receptor does nicotine bind to?

A

nicotinic receptors = nAChRs acetylcholine receptors

Ionotropic receptors

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14
Q

When nicotine binds to acetylcholine receptors it creates an excitatory or inhibitory post synaptic potential?

A

EPSP

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15
Q

Nicotinic receptor desensitization

A

Desensitized state - Functional antagonism: high binding affinity - stays for a long time. Channel closes, molecule stays = blocks it in the long term. Becomes an antagonist.
Upregulation (acute tolerance) - first cigarette of the day feels better than second

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16
Q

Distribution of nicotinic receptors (AChRs)

Peripheral nervous system

A

Neuromuscular junction

Ganglia of autonomic nervous system

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17
Q

Distribution of nicotinic (AChRs) receptors

Central nervous system

A

Hippocampus and cerebral cortex
Basal ganglia
Ventral tegmental area (projecting to) nucleus accumbens (and other areas)

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18
Q

Rewarding (addictive) properties of nicotine

A

Indirect dopamine release
Nicotine receptors activated in the VTA or NA increase dopamine release in NA
Other constituents of tobacco enhance effects

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19
Q

Pharmacological effects

A
Wide ranging Sympathomimetic effects
\+
Movement stability
Cognitive enhancer (stroop test, memory test)
Acute tolerance
Hunger decreases
20
Q

Habitual versus naive users

A

Naive users report negative subjective effects
Habitual users report positive subjective effects
+ build tolerance to negative subjective effects

21
Q

Chippers

A

“social smokers” - common
Habitual users but unlikely to be addicted due to resistance to addictive effects of nicotine
Resistance bc of: genetic and environmental/social mechanisms

22
Q

Why do people smoke?

A

Social pressures
Most chronic users will become addicted
Hard to quit

23
Q

How do people quit?

A

Magic timeframe: 2 weeks - more about withdrawal
“Cold turkey” or with
- Nicotine replacement therapy
- nAChR agonists (Varenicline)
- Antidepressants (Bupropion, NDRI and nAChR antagonist)

24
Q

Gender, ethnicity, and SES in quitting

A

Better rates of abstinence in men, european americans, higher socioeconomic status

25
Q

Nicotine quitting studies

A

Groups usually don’t achieve higher than 50% quitting

26
Q

Caffeine - type of drug, plant

A

Mild psychostimulant of the xanthine family
Found in many plants
The most used drug on earth
Found in kola nuts, cocoa tree nuts, tea leaves, coffee beans

27
Q

Dark vs. light roast

A

The longer you roast, the less caffeine.

Light roast = more caffeine

28
Q

Energy drinks

A

75mg of caffeine plus other xanthines
Fastest growing beverage market
alcohol mixed with energy drinks - dangerous because of different half lives

29
Q

Caffeine pharmacokinetics

A
Administration: Oral
Absorption: intestines
Crosses BBB -> adenosine receptors
Metabolized in liver
Eliminated via urine (the metabolites)
30
Q

Active metabolites

A

theobromine, theophylline, paraxanthine

31
Q

Peak concentration and half life

A

40min after ingestion

Half-life varies tremendously

32
Q

Cigarettes and coffee

A

Polydrug use
Smoking increases CYP-1A2 activity (which breaks down caffeine)
Smoking increases elimination of the caffeine

33
Q

Caffeine Pharmacodynamics

A

A1 and A2 adenosine receptor antagonists

Adenosine receptors are omnipresent throughout entire body

34
Q

Caffeinism

A

High doses of caffeine = can lead to caffeinism
Adverse effects of caffeine >500mg - start to emerge
Sweating, high HR anxiety, agitation and insomnia.
No tolerance towards physiological effects, just acute subjective

35
Q

Physiological effects of caffeine

A

Increased heart rate
Blood vessel constriction
Increased breathing rate
Reduced appetite

36
Q

Behavioral and subjective effects

A
Attention
Alertness
\+
Positive mood
Elevated sense of wellbeing
37
Q

Dependence - tolerance

A

We build tolerance with: mood alertness, anxiousness, acute subjective effects (feeling awake)
No tolerance: cardiovascular activity, blood vessel constriction, physiological effects

38
Q

Dependence - withdrawal

A

Just mornings
Not considered a substance of concern by the DSM5 not “addictive”
But caffeinism and withdrawal are in the DSM-5

39
Q

Why do people consume caffeinated products?

A

Increased sense of energy/mood (go away with chronic use)
Physical dependence
Incentive sensitization - dopamine
Products with caffeine taste good

40
Q

Neuroprotection

A

Alzheimer’s: affects cholinergic neurons early - Potential therapeutic: nAChR agonists

41
Q

Nicotine and schizophrenia

A

smoking is disproportionately high

42
Q

Why is nicotine smoking disproportionately high in people with schizophrenia?

A

The self-medication hypothesis: nicotine administration may be instrumental
Smoking may lessen negative symptoms, improves sensory processing, speeds antipsychotic medication metabolism (take away side effects), act as cognitive enhancer

43
Q

Smoking cigarettes and neurodegeneration

A

Smoking cigarettes associated with increased neurodegeneration (alzheimer’s, dementia)

44
Q

Nicotine and neurodegeneration

A

Inversely correlated with risk of Parkinson’s disease. Nicotine without smoking may be neuroprotective.

45
Q

Caffeine and neuroprotection

A
  • Caffeine + parkinson’s causing chemical protects rodent from parkinson (Similar effects for amyotrophic lateral sclerosis and alzheimer’s)
  • Delays age-related cognitive decline, especially in women
  • 2-3 coffee cups a day = 25% lower risk of dementia/ stroke
46
Q

Caffeine and neurodegeneration

A

May speed up the arrival of symptoms in huntington’s disease (genetic disease)