(9) alcohol Flashcards
What are alcohol’s costs to society and to the individual? Is alcohol use safe? (M2E Eeiim)
- most commonly used depressant
- 2nd most used drug
- ethanol use: widespread
- ethanol vs. isopropanol & methanol:
- ethanol: low doses, relatively safe
- isopropanol & methanol: unsafe at any dose
- isopropanol: v. potent
- methanol: toxic
How does it fare compared to other drugs? What does this mean for alcohol regulation? What does this mean for regulation of other drugs? (Smml L)
- socially accepted, but
- most harm caused to user & others
- most dangerous drug
- largest societal cumulative toll
- law: most illicit drug, most harmful but not true
How is alcohol measured in a drink?
- percentage alcohol: alcohol by volume (ABV)
- # of grams of alcohol per 100ml of solution
- proof of alcohol:
- 100 proof = double of ABV
What is the difference between fermentation and distillation?
- fermentation: yeast eats sugar in solution, alcohol as byproduct
- beers & nonfortified wines
- max 15% ABV
- distillation: cook alcohol out of fermented solution & leave stronger alcohol beverage
- liquors & fortified wines
- at least 20% ABV
What is the pharmacokinetics of alcohol? What implications arise from these pharmacokinetics (e.g. eating on an empty stomach)? (EOA Ha I BP)
- ethanol both water & lipid-soluble: many tissues absorb alcohol
- oral administration
- absorbed by gastrointestinal tract
- high ABV irritates, slows absorption:
- absorption better w/ mix, esp. carbonated: reduce irritation
- interferes w/ thiamine (vita. B1) transporter
- blood-alcohol concentration (BAC)
- peak absorption: ~45mins after
What is blood-alcohol concentration (BAC)?
grams of alcohol per 100ml blood
What is the biotransformation of alcohol (identify one notable metabolite)?
- metabolism occurs in stomach & liver: more alcohol metabolised in stomach, less drunk
- acetaldehyde: stuff of hangovers
- biotransformation process:
- alcohol uses alcohol dehydrogenase to turn into acetaldehyde
- acetaldehyde broken down into acetic acid & acetate by alcohol dehydrogenase
- acetate broken down into water & CO2
What is alcohol dehydrogenase polymorphism?
- make enzyme more efficient: make acetaldehyde from alcohol more quickly
- v. unpleasant effects: nauseated, v. sick, headache
- drink less, less risk of addiction
What are zero-order kinetics?
- elimination follows zero-order kinetics:
- removal of alcohol follows slow & steady pace independent of concentration in body (10-14mL/hour)
What are first-order kinetics?
- drank a lot, elimination rate switches to first-order kinetics:
- higher the concentration of alcohol in system, faster it will be eliminated
What are the pharmacodynamic actions of alcohol on GABAa receptors?
- positive allosteric modulator:
- binds to GABA receptor & enhances effects of GABA on receptor
- GABAa: chloride channels
- chronic administration: # of GABAa receptors decreases
- location of receptors dictate effects
What are alcohol’s effects on the cerebral cortex, hippocampus and thalamus? (Dais)
depressant effects on cognition:
- binds to GABA receptor on GABA neurons - indirectly activates beta-endorphins - silences thing that inhibits DA neurons, cause more DA release
What are alcohol’s effects on the NAcc and VTA?
changes motivation, effects related to addiction & greater DA release:
- binds to cells w/ GABA receptors, increase inhibition of cells, driving addiction process
What are the pharmacodynamic actions of alcohol on glutamate receptors?
- inhibits NMDA glutamate receptors:
- likely an antagonist
- blocks long-term memory processes
- NMDARs are special:
- long-term potentiation
- i.e. memory
- chronic administration: upregulate NMDARs
- effect of downregulated GABAa & upregulated NMDARs
What is long-term potentiation?
when there’s strong connection b/w pre & post-synaptic sides, NMDARs activated & calcium signals many changes
