Nicotine; Caffeine Flashcards by olive oil

Plant of nicotine

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

How well did you know this?

Not at all

Perfectly

Juul and modern vaporizers

Nicotine salts (protonated nicotine)
Earlier nicotine peak
Tremendously potent

How well did you know this?

Not at all

Perfectly

Tobacco use/exposure: Increased rates of cancer due to

nitrosamines in tobacco smoke

How well did you know this?

Not at all

Perfectly

Tobacco use/exposure: Increased rates of

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

How well did you know this?

Not at all

Perfectly

Tobacco use/exposure: Teratogen

Increased pregnancy complications: malformation of embryo

How well did you know this?

Not at all

Perfectly

First, second, third hand smoke

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

How well did you know this?

Not at all

Perfectly

History of tobacco use

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

How well did you know this?

Not at all

Perfectly

Absorption of nicotine

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

How well did you know this?

Not at all

Perfectly

Biotransformation and elimination of nicotine

Blood brain barrier

Nicotine readily crosses blood-brain barrier

How well did you know this?

Not at all

Perfectly

Biotransformation and elimination of nicotine

Metabolization

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

How well did you know this?

Not at all

Perfectly

Half life nicotine

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

How well did you know this?

Not at all

Perfectly

Nicotine agonist or antagonist?

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

How well did you know this?

Not at all

Perfectly

What receptor does nicotine bind to?

nicotinic receptors = nAChRs acetylcholine receptors

Ionotropic receptors

How well did you know this?

Not at all

Perfectly

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

EPSP

How well did you know this?

Not at all

Perfectly

Nicotinic receptor desensitization

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

How well did you know this?

Not at all

Perfectly

Distribution of nicotinic receptors (AChRs)

Peripheral nervous system

Neuromuscular junction

Ganglia of autonomic nervous system

How well did you know this?

Not at all

Perfectly

Distribution of nicotinic (AChRs) receptors

Central nervous system

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

How well did you know this?

Not at all

Perfectly

Rewarding (addictive) properties of nicotine

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

How well did you know this?

Not at all

Perfectly

Pharmacological effects

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

Habitual versus naive users

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

Chippers

“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

Why do people smoke?

Social pressures
Most chronic users will become addicted
Hard to quit

How do people quit?

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

Gender, ethnicity, and SES in quitting

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

Nicotine quitting studies

Groups usually don’t achieve higher than 50% quitting

Caffeine - type of drug, plant

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

Dark vs. light roast

The longer you roast, the less caffeine. | Light roast = more caffeine

Energy drinks

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

Caffeine pharmacokinetics

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

Active metabolites

theobromine, theophylline, paraxanthine

Peak concentration and half life

40min after ingestion | Half-life varies tremendously

Cigarettes and coffee

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

Caffeine Pharmacodynamics

A1 and A2 adenosine receptor antagonists | Adenosine receptors are omnipresent throughout entire body

Caffeinism

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

Physiological effects of caffeine

Increased heart rate Blood vessel constriction Increased breathing rate Reduced appetite

Behavioral and subjective effects

``` Attention Alertness + Positive mood Elevated sense of wellbeing ```

Dependence - tolerance

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

Dependence - withdrawal

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

Why do people consume caffeinated products?

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

Neuroprotection

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

Nicotine and schizophrenia

smoking is disproportionately high

Why is nicotine smoking disproportionately high in people with schizophrenia?

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

Smoking cigarettes and neurodegeneration

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

Nicotine and neurodegeneration

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

Caffeine and neuroprotection

- 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

Caffeine and neurodegeneration

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