W 8 - Alcohol Flashcards
What are the three forms of alcohol?
- Isopropyl
- Methanol
- Ethanol (drinking alcohol)
What is the fermentation process?
- Sugar dissolved in water
- Yeasts multiply and convert sugar into ethanol and CO2
- Alcohol content about 10 - 15 %
- Fermented wines = extra alcohol
What is the distillation process?
- Fermentation –> Heated –> alcohol given off in vapor –> vapor cooled
- Alcohol content - 40 - 50%
Brandy = distilled wine
What is the main mode of administration?
- Oral
What is the absorption of alcohol like?
- Molecules cannot be ionized - pH levels have no effects upon absorption
- Readily dissolved in water & passes into blood from stomach lining, intenstines & colon
- 1st pass metabolism - alcohol dehydrogenase in stomach
What is the absorption rate and BAL affected by?
- Stomach contents
- Body fat (higher body fat means less water to dilute alcohol so greater concentrations)
- Medication
- Female sex (decrease in alcohol dehydrogenase, more body fat)
- alcohol concentration
- age
- usage (abstainers vs regular)
When the the BAL generally at a plateau
approx 1 hr after consumption
When is peak BAL?
approx 15 min after consumption (but depends when readings are take - after a few drinks levels reached sooner)
What drink types effect absorption
o Beer stays in stomach longer
o Absorption sparkling wines facilitated by carbination
o Higher concentration absorbed more quickly, up to a point ([~ 40 % alc.])
What is the expectance effect
Those who expect alcohol may have greater concentrations
What is the theoretical time course for BAL after single drink?
- A = Absorption Phase
- B & C = Plateau Phase
- D = Excretion Phase
What is the distribution of alcohol in body?
- Alcohol dissolves in water – distributed entirely in body water
- Crosses blood-brain barrier and placental barrier
- Circulates through lungs and vaporises in air (Breathalizer)
Where is alcohol excreted?
Some alcohol is excreted through breath,
sweat & urine
Most alcohol is metabolized in the liver (~90-98%)
– at rate ~ 1 SD/hr
How is alcohol metabolised by the liver?
- Alcohol is converted to acetaldehyde by alcohol dehydrogenase
- Acetaldehyde is converted into acetyl-coenzyme A
Acetyl-coenzyme A is then converted to water & CO2, via the Krebs cycle (or “citric acid cycle”)
What does having a genetic polymorphism in the kreb’s cycle mean?
Genetic polymorphism means they can’t break down acetaldehyde – can’t break down so often a protective factor
How does excretion vary between individuals?
- Excretion varies greatly between individuals
o Typical range ~ 10-20 mg/100ml/hr
What may affect the metabolism of alcohol?
- Rate of metabolism may depend on drinking experience
o Non-drinkers metabolize alcohol slightly slower - Eating speeds metabolism of alcohol – increases blood supply to the liver to speed up
What is the excretion of methanol and what are the effects of ingesting it?
- Excretion of methanol:
o Formaldehyde and formic acid
o Blindness and death if ingest methanol because of metabolites that lead to effects
o Ethanol treats methanol poisoning
What is the Microsomal ethanol-oxidizing system (MEOS)?
- Also responsible for metabolism of alcohol
- Increased activity with continuous drinking – thus heavy drinkers metabolize alcohol more quickly → metabolic tolerance
o Up regulation of MEOS system causes tolerance - Also responsible for metabolizing barbiturates → cross tolerance
o Used to be used similar the benzodiazepam
What are the interesting neuropharmacological traits of alcohol and what does this mean about alcohols site of action?
- Alcohol affects a variety of tissues
- Need a large dose to have an effect
- No drugs act as complete antagonists to all of the effects of alcohol
Therefore – conclude that alcohol does not work directly on specific receptor sites, but affects many sites of action
What is GABAA?
Inhibitory NT - GABBA-receptor-ionophor complex
Where are the sites of action of GABBA-receptor-ionophor complex?
Orthosteric & allosteric sites *– alcohol ¬ GABA effects (¯ neural activity) \ alcohol acts as a positive allosteric modulator
e.g. effects on cerebellum → inhibits pikinge neurons – causes stumbling and coordination
Where are the GABAB (metabotropic) receptors and what do they do?
May induce release of DA
- e.g., in VTA → less inhibition of DA release into NAcc
Inhibition of inhibition