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Psych 478 > Alcohol > Flashcards

Alcohol Flashcards

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1
Q

What is the economic burden in the US of alcohol per drink?

A

$1.90 per drink

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2
Q

What is the earliest historical evidence?

A

Archaeological evidence of fermentation
from Neolithic period (10,000 BCE)

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3
Q

What is alcohol?

A

Colloquially alcohol refers to ethyl
alcohol or ethanol (EtOH).

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4
Q

Describe pharmacology

A

EtOH administered by oral dose has high bioavailability

Alcohol has high caloric content but little nutritive value

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5
Q

Describe alcohol. absorption

A

Higher concentration of alcohol is absorbed faster

Food in stomach slows passage to intestine –
slower uptake
* Carbonation (e.g. champagne) accelerates passage
– faster uptake

Alcohol dehydrogenase (ADH) is secreted in
gastric fluids

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6
Q

Describe alcohol distribution

A
  • EtOH readily diffuses into all aqueous
    fluids/tissues via passive diffusion
  • Easy access through BBB and placental
    barrier
  • Excluded from fat tissues
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7
Q

Describe alcohol metabolism

A

Liver metabolism of alcohol depends
on the key enzymes alcohol
dehydrogenase and aldehyde
dehydrogenase.

  • Drug interactions caused by competition for P450 → elevated drug concentration
  • Induction of P450 with chronic use → decreased drug concentration
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8
Q

Describe specific effects of alcohol

A
  • Specific effects – result of interactions with receptors
  • Cause most of the acute and chronic effects of intoxication
  • Responsible for most subjective effects of intoxication
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9
Q

describe nonspecific effects of alcohol

A
  • Non-specific effects – result of interaction with
    phospholipid membranes or bodily fluids
  • EtOH interacts with cell membranes causing changes in membrane protein function and cellular dysfunction
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10
Q

Describe GABAA

A
  • EtOH acts as a positive allosteric
    modulator of GABAA
  • CNS depressant and sedative effects of
    EtOH moderated through GABA
  • EtOH can be cross-tolerant and cross-
    dependent with benzodiazepines and
    barbiturates
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11
Q

Describe NMDA and glutamate

A
  • At low doses EtOH antagonizes NMDA
    receptors
  • Decreases LTP
  • Impairs learning and memory
  • NMDAR responsible for amnesiac
    effects of ethanol
  • Blackouts
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12
Q

Describe one chronic effect on NMDA

A
  • Glutamate release increases as a result
    of EtOH withdrawal
  • Rebound hyperactivity
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13
Q

Describe dopamine

A
  • EtOH increases the firing rate of VTA
    dopamine projections into the nucleus
    accumbens
  • Dramatic decrease in VTA firing on
    withdrawal– may cause dysphoria of
    withdrawal
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14
Q

Describe opioid receptors and alcohol

A
  • Acute administration of ethanol increases
    endogenous opioid activity

NAc
* Opioid antagonists reduce EtOH self-
consumption in animal models

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15
Q

Describe physiological effects

A

At low doses:
* Diuretic (increased kidney output – dehydration)
* Inhibits antidiuretic hormone (vasopressin) release
* Sedative and hypnotic (sleep-inducing)

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16
Q

Describe alcohol, balance and coordination

A
  • Non-specific effects on vestibular system
  • Ethanol thins the fluid in the inner ear
  • Fluid moves more rapidly leading to
    overcompensation
17
Q

Describe alcohol tolerance

A
  • Cross-tolerance also develops with other sedative-hypnotic drugs, particularly benzodiazepines and barbiturates
18
Q

Describe acute alcohol tolerance

A

Effects associated with intoxication –
euphoria, anxiolysis, and mild
stimulation occur when blood alcohol
levels are rising.

19
Q

Describe alcohol metabolic tolerance

A
  • Drug disposition tolerance occurs
    relatively quickly – induction of liver
    enzymes (ADH and P450) increases the
    rate of alcohol metabolism
20
Q

Describe pharmacodynamic tolerance

A
  • Increased NMDA receptor function, increased glutamate release
  • Decreased GABA receptor function
  • Decreased synthesis and release of opioids
  • Decreased firing of mesolimbic dopamine neurons
21
Q

describe classical conditioning

A
  • Classical conditioning:
  • Similar to opiates
  • Environmental cues induce compensatory
    physiological changes
  • In rodent models alcohol administration
    decreases body temperature
  • Conditioning leads to a compensatory increase in
    body temperature based on expectancy
  • Tolerance diminished in novel environment
  • May play a strong role in craving
22
Q

Describe behavioural changes

A
  • Behavioural changes:
  • Practising behaviours under the influence of
    alcohol leads to improved performance
  • Rats trained run on a treadmill while
    intoxicated performed better with time
  • Rats trained on treadmill sober performed
    poorly when tested after alcohol
    administration
23
Q

Describe physical alcohol dependence

A
  • Prolonged intoxication can result in adaptive changes
  • Mechanisms of tolerance esp. pharmacodynamics
  • Restoration of homeostasis in presence of drug
  • Can be readily demonstrated by the development of
    symptoms of abstinence syndrome (withdrawal)
24
Q

Describe acute alcohol withdrawal

A

Hangover is often described as an early
component of withdrawal

  • May result from acute tolerance rather than
    dependence
25
Q

Describe contributors to hangovers

A
  • Toxicity:
  • Can be demonstrated by use of ALDH inhibitor -
    disulfuram
  • Dehydration:
  • Alcohol-induced gastric irritation:
  • Rebound effects on blood sugar:
  • Hypoglycemia, faintness, fatigue and malaise
  • Congeners:
  • Ingredients or fermentation byproducts that
    exacerbate condition
  • Red wine – tannins, sulfates
  • Distilled spirits – methanol
26
Q

Describe early component of early withdrawal

A
  • Early component (8-12 hours after last drink)
  • Agitation, tremors, muscle cramps, vomiting, nausea, sweating, vivid dreams (rebound effects on REM), irregular heartbeat
  • Typically lasts ~48 hours
  • Less severe component of alcohol withdrawal
  • Fewer than 5% of patients hospitalized for alcohol withdrawal go on to
    develop the late stage of withdrawal
27
Q

describe rebound effect at GABAA receptor

A
  • Rebound effects lead to development of
    hyperexcitability
28
Q

Describe rebound effect at NMDA receptor

A
  • Rebound effects lead to hyperexcitability
29
Q

Describe late withdrawal

A
  • Delirium tremens (DT)
30
Q

Describe risk with DT

A
  • Altered GABA homeostasis leads to
    unopposed sympathetic activation
  • Management of DT involves
    administration of benzodiazepines–
    effective due to cross tolerance at
    GABAA
31
Q

Describe cognitive deficits

A
  • Cognitive deficits occur with prolonged heavy drinking:
  • Abstract problem solving
  • Visuospatial abilities
  • Verbal learning
  • Perceptual motor skills
  • Motor skills
  • Memory
32
Q

Describe brain damage mechanisms

A
  • NMDA-mediated excitotoxicity
  • Homocysteine accumulation
  • Homocysteine is an agonist at glutamate and glycine sites of NMDAR (exacerbates excitotoxicity)
  • Neurotrophic factors
33
Q

Describe accumulation of toxic byproducts

A
  • Acetaldehyde:
  • Aldehydes are highly reactive with protein and DNA
  • General damage to protein function and DNA
  • Formation of aldehyde adducts correlates with liver damage
  • Acetaldehyde also shown to cause increased reinforcing effects in the mesolimbic dopamine pathway
  • Acetaldehyde microinjection to VTA can demonstrate self-administration in rats
34
Q

Describe Korsakoff syndrome

A
  • Alcoholism causes B1-vitamin deficiency
35
Q

Describe effects on the liver

A
  • At lower levels alcohol leads to fatty liver
  • Metabolism of alcohol decreases fat metabolism
    leading to reversible accumulation of fats
  • Prolonged use leads to alcoholic hepatitis
  • Inflammation, fever, jaundice
  • Potentially fatal

Psych 478 (28 decks)

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