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C81ADD > Alcohol > Flashcards

Alcohol Flashcards

1
Q

What are the three types of alcohol, and which do we consume?

A

Methyl, ethyl and isopropyl - consume ethyl alcohol, has 2 carbon atoms, 3H and O-H hydroxyl group.

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2
Q

What is BAC?

A

Blood alcohol concentration.

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3
Q

What BAC level does it take to produce measurable behavioural effects?

A

0.04%.

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4
Q

What measures are included in the drug harm scale?

A

Physical harm (acute, chronic, intravenous), dependence (pleasure, psych, physical), and social harms (intoxication, other and healthcare).

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5
Q

Who developed the drug harm scale, and what was it like?

A

Nutt et al (2007).

Each of the 9 criteria given a score between 0-3, totalled.

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6
Q

What did Nutt et al (2007) compare?

A

The drug harm scale mean score and classes of different drugs.

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7
Q

In what way did Nutt et al (2010) improve the drug harm scale?

A

Increased the number of criteria (from 9 to 16) and made scores from 0-100 rather than 0-3, as well as introducing differential weighting of criteria.

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8
Q

What did Nutt et al (2010) show?

A

That in terms of overall harm score, alcohol was worse than any other drug. Especially high in terms of harm to others. Therefore the drug classification system isn’t based on harm and alcohol harms should be targeted.

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9
Q

What happened to Nutt in 2009?

A

He was sacked as the government’s top drugs adviser.

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10
Q

What did White (2003) use as a simile for the psychological effects of alcohol?

A

If drugs were tools, alcohol would be a sledgehammer - few cognitive functions or behaviours escape.

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11
Q

What are the acute psychological effects of alcohol?

A
  • Decreased tension/anxiety (anxiolysis)
  • Impaired memory (amnesia)
  • Direct ‘reward’ (?)
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12
Q

What are the chronic psychological effects of alcohol?

A
  • Dependence, withdrawal symptoms

- Severe and chronic cognitive deficits due to brain shrinkage (Wernicke-Korsakoff Syndrome)

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13
Q

What are the brain systems that are first hit by alcohol?

A
  • Nt receptors (NMDA, GABA-A, Glycine, 5-HT3, nACh)

- Voltage-gated ion channels (L-type Ca2+ channels, GIRKs)

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14
Q

What nonspecific complex neuropharmacological effects does alcohol have?

A

Interactions with lipid bilayer, mainly at high concentrations.

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15
Q

What specific complex neuropharmacological effects does alcohol have?

A

Interaction with ligand-gated ion channels (i.e. nt receptors) and voltage-gated ion channels; at common consumption concentration levels.

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16
Q

What are some of the variables that affect the effects of alcohol in humans?

A
  • Environmental variables (social cues)
  • Cognitive set (expectancy)
  • Mood, arousal and personality factors
  • Age, sex and weight
  • Exposure to other drugs and nutritional state
  • Alcohol ingestion (dose, rate, time, type of beverage).
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17
Q

At 0.02-0.03 BAC, what effect can be observed on behaviour?

A

Slight relaxation and mild mood elevation.

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18
Q

At 0.05-0.06 BAC, what effect can be observed on behaviour?

A

Decreased alertness, relaxed inhibitions and mildly impaired judgement.

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19
Q

At 0.08-0.10 BAC, what effect can be observed on behaviour?

A

Loss of motor coordination, slower reaction times and less caution.

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20
Q

What is the legal driving limit in the UK?

A

0.08 BAC.

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21
Q

At 0.14-0.16 BAC, what effect can be observed on behaviour?

A

Major impairment of mental and physical control, slurred speech, exaggerated emotions, blurred vision, serious loss of judgement, large increases in reaction time.

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22
Q

At 0.20-0.25 BAC, what effect can be observed on behaviour?

A

Staggering, inability to walk/dress, tears/rage, mental confusion and double vision.

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23
Q

At 0.30 BAC, what effect can be observed on behaviour?

A

Conscious but in a stupor, unaware of surroundings.

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24
Q

At 0.50 BAC, what effect can be observed on behaviour?

A

Coma = lethal for 50% of population.

25
Q

What have studies on the relationship between alcohol and anxiety measures shown?

A

Variable effects, despite the widely held view that alcohol reduces tension and anxiety.

26
Q

What effect does alcohol have on GABA?

A

It enhances the response - it’s an indirect agonist at GABA-A receptors, similar to annxiolytics.

27
Q

What did Kushner et al (2000) find comorbidity between?

A

Anxiety disorders and alcohol abuse.

28
Q

What did Blanchard et al (1993) find about the effect of alcohol in rats?

A

It consistently reduces measures of anxiety.

29
Q

What did Gallate et al (2003) do?

A

Tested rats with the cat odour avoidance test and elevated plus maze test.

30
Q

What did Gallate et al (2003) find?

A

That the more alcohol rats consumed, the less time they spent hiding and the more time they spent approaching a cat odour; and they spent more time on the open arms and less on the closed arms of the elevated maze.

31
Q

What can be concluded from Gallate et al (2003)’s findings?

A

Alcohol decreases anxiety (and perhaps caution!)

32
Q

What did Spanagel et al (1995) find using the elevated plus maze?

A

Once anxious and non-anxious rats had been identified, the anxious rats had higher self-administration.

33
Q

With what particular memory process does alcohol interfere most with?

A

The encoding of new information into long-term declarative memory.

34
Q

What forms can alcohol-induced anterograde amnnesia take?

A
  • Little memory lapses (‘cocktail party memory deficits’)
  • Fragmentary (‘en block black outs’) i.e. partial or complete absence of memory for experiences under alcohol influence.
35
Q

What did White et al (2002) find about undergraduates and alcohol-induced amnesia?

A

That 51% of those who had ever consumed alcohol had awoken unable to remember things they had done the previous night.

36
Q

What are the possible mechanisms of alcohol-induced amnesia?

A
  • State dependence

- Selective interference with hippocampal memory mechanisms.

37
Q

What is the premise behind the state dependence mechanism of alcohol-induced amnesia?

A

Information encoded in a drugged state may be better remembered when in a comparable state (Overton, 1964).

38
Q

What experimental design has been used to test the state-dependence mechanism?

A

2x2 for encoding/retrieval state - alcohol (A) or sober (S).

39
Q

What does Duka et al (2001)’s finding of asymmetric state dependence mean?

A

That information encoded whilst drunk and retrieved whilst sober is worse recalled than information encoded sober and retrieved drunk.

40
Q

What did Goodwin et al (1969) find?

A

Alcohol has been shown to render some aspects of declarative memory (i.e. word-association memory) state dependent.

41
Q

According to Goodwin et al (1969), what type of amnesia does state-dependence account for?

A

Little memory lapses or fragmentary blackouts, rather than en block blackouts, which seem to be due to some other mechanism.

42
Q

Why is it theorised (White, 2003) that interference with hippocampal synaptic mechanisms of memory may conntribute to alcohol-induced amnesia?

A

Because problems encoding new declarative memories are also seen in hippocampal damage cases, e.g. HM.

43
Q

According to Bliss and Collingridge (1993), what does alcohol disrupt the induction of?

A

Hippocampal long-term potentiation (LTP), an activity-dependent long-lasting increase in synaptic strength and a candidate physiological mechanism of memory.

44
Q

What does long term potentiation involve?

A
  • Transmission of current (Na+): glutamate -> AMPA receptors.
  • Induction of LTP = intense stimulation, leads to expulsion of Mg2+ ions from NMDA receptors and influx of Na+ and Ca2+ ions.
  • This increases both no. of AMPA receptors and their efficiency.
  • Therefore a larger current is allowed through, leading to a larger epsp (excitatory postsynaptic potential).
45
Q

What did Givens and McMahon (1995) find?

A

That when LTP was induced in rats given saline or two levels of ethanol, ethanol-receiving rats’ LTP was lower and declined. Therefore ethanol selectively blocks the induction of LTP.

46
Q

Why is it suggested that people still drink alcohol, despite its negative consequences?

A

Because of the meso-corticolimbic dopamine system and reward (nucleus accumbens and VTA) - according to Spanagel and Weiss (1999), we learn reward associations from alcohol.

47
Q

What is microdialysis?

A

A sampling method that is used to determine the extracellular concentration of neurotransmitters in the brain through a probe, pumps and valves etc.

48
Q

What can intracerebral microdialysis be used to measure?

A

Neurotransmitters.

49
Q

What did Dichiara and Imperato (1988) find?

A 
That drugs (inc. alcohol) increase accumbal dopamine levels.
Implicates role of meso-corticolimbic dopamine system.
50
Q

What is the diagnostic criteria for substance abuse?

A
  • Impairs ability to function
  • Causes legal problems
  • Is used in a dangerous manner
  • Is used despite legal, social or medical problems.
51
Q

What is the diagnostic criteria for substance dependence?

A

Fulfills criteria for abuse and:

  • Development of tolerance
  • Withdrawal at abstinence
  • Frequent desire and effort to reduce use
  • Preoccupation directing most daily activity.
52
Q

According to Little (1999) and Vengeliene et al (2008), how can neuropharmacological adaptations to chronic alcohol use contribute to dependence?

A
  • Tolerance leads to reduced acute effects
  • Long-term compensatory changes in neural mechanisms lead to chronic psychological changes when sober
  • Compensatory changes are opposed to acute effects of alcohol.
53
Q

What is involved in the altered balance between excitatory and inhibitory neurotransmission in response to chronic alcohol, according to Little (1999) and Vengeliene et al (2008)?

A
  • Decreased GABA-A receptor function
  • Increased glutamate receptor stimulation and function
    (Both opposite of effects of acute alcohol).
54
Q

What is involved in withdrawal hyperexcitability?

A
  • Many withdrawal symptoms (seizures, tremors, withdrawal anxiety and craving)
  • Excitotoxic brain damage, resulting in long term cognitive deficits.
55
Q

What did Diana et al (1993) find?

A

That there is reduced nucleus accumbens dopamine during withdrawal and reduced spontaneous activity of dopaminergic neurons in the VTA.
This could reduce sensitivity to natural rewards and decrease motivation.

56
Q

What is the cause of Wernicke-Korsakoff syndrome?

A

Thiamine deficiency, most commonly in association with alcoholism.

57
Q

What is Wernicke syndrome?

A

The acute stage, characterised by ophtalmoplegia (paralysis of eye muscles), confusion and ataxia.

58
Q

What is Korsakoff amnesia?

A
  • Can remain after treatment of Wernicke syndrome.

- Global impairment of forming new declarative memories, severe brain shrinkage, degeneration of the mammilary bodies.

59
Q

What problems can be found in ‘uncomplicated’ alcoholics?

A
  • Deficits in sensori-motor and executive functions, learning and memory.
  • Marked fronto-cerebellar brain damage (Sullivan and Pfefferbaum, 2009).

C81ADD (13 decks)

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