Chapter 10: Alcohol Flashcards

1
Q

Describe the process of alcohol metabolism.

A

About 95% is metabolized by the liver at a rate of 1 to 1.5 ounces per hour and about 5% is excreted by the lungs.

The enzyme alcohol dehydrogenase metabolizes alcohol into acetaldehyde. Acetaldehyde (which is toxic) is degraded by the enzyme aldehyde dehydrogenase into acetic acid. Acetic acid is then oxidized into carbon dioxide, water, and energy.

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2
Q

What is acute alcohol tolerance?

A

Acute tolerance occurs within a single drinking episode and may lead to dangerous driving when binge drinkers perceive that they are less inoxicted on the descending limb of the blood alcohol curve.

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3
Q

How does the body adapt to chronic alcohol use?

A
  1. Causes metabolic tolerance by increasing cytochrome P450 enzymes
  2. Pharmacodynamic tolerance by producing compensatory changes in neuron function
  3. Behavioural tolerance of the operant type where performance improves when tasks are practiced while under the influence
  4. Behavioural conditioning of the classical conditioning type where repeated alcohol use in the same environment produces a compensatory response only in that environment
  5. Physical dependence
  6. Cross-tolerance with other sedative-hypnotic drugs
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4
Q

Describe alcohol withdrawal.

A

After chronic alcohol use withdrawal lasts for several days and includes tremor, anxiety, high BP and HR, sweating, rapid breathing, and nausea and vomiting. Severe effects are called delirium tremens. they are characterized by hallucinations, convulsions, disorientation, and intense anxiety.

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5
Q

Explain the behaviour effects of alcohol.

A

They are directly related to BAC but at low doses, the environment and expectations of effects also have significant effects.

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6
Q

What body organ systems does alcohol affect?

A
  1. Central nervous system
  2. Cardiovascular system
  3. Renal-urinary system
  4. Reproductive system
  5. GI system
  6. Liver
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7
Q

What effects does alcohol have on the central nervous system?

A

The effects are dose-dependent and include:

  1. relaxation
  2. reduced anxiety
  3. intoxication
  4. impaired judgment
  5. impaired memory
  6. sleep
  7. coma (high doses)
  8. death (high doses)
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8
Q

What vitamin deficiency does alcohol cause.

A

Vitamin B1 which leads to neurotoxic effects and brain damage caused by cell death in the periaqueductal gray, medial thalamus, and mammillary bodies. This B1 deficiency can cause Wernicke’s encephalopathy and Korsakoff syndrome.

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9
Q

What neurotransmitters does alcohol affect?

A
  1. glutamate
  2. GABA
  3. dopamine
  4. opioids
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10
Q

How does acute alcohol use affect glutamate?

A

inhibits transmission by reducing glutamate release and reducing its effects at the NMDA receptor

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11
Q

How does chronic alcohol use affect glutamate?

A
  1. up-regulates NMDA receptors

2. increases glutamate release

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12
Q

How does acute alcohol use affect GABA?

A

Works on GABA-A receptors to stimulate GABA release which increases chloride entry and hyperpolarization of the cell. This requires high levels of intoxication.

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13
Q

How does chronic alcohol use affect GABA?

A

Down-regulates GABA-A receptors

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14
Q

How does acute alcohol use affect dopamine?

A

Activates dopaminergic cells in the VTA causing the release of dopamine in the nucleus accumbens. This provides the positive reinforcement that leads to repeated drug taking.

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15
Q

What role does dopamine play in alcohol withdrawal?

A
  1. reduces firing rate of mesolimbic neurons
  2. decreases dopamine release in the nucleus accumbens
  3. causes rebound depression of reinforcement mechanisms
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16
Q

How does acute alcohol use affect opioid systems?

A

increases opioid release and increases gene expression of opioid peptides

17
Q

How does chronic alcohol use affect opioid systems?

A

reduces gene expression and lower levels of opioid peptides

18
Q

Explain alcohol use disorder.

A

It is a form of substance use that involves compulsive alcohol seeking and use despite damaging health and social consequences. Frequency and pattern of drinking are as important as the quantity consumed.

19
Q

What are the risk factors for alcoholism?

A
  1. personality
  2. stress
  3. vulnerability (i.e. family history, genetics, ACEs)
  4. novelty seeking (e.g. drinking before age 13, aversion to delayed gratification)
20
Q

What is the genetic contribution toward risk for alcoholism?

A

Genetics explains 50-60% of the variance of risk for alcohol dependence. Some people have genes for an inactive form of the enzyme aldehyde dehydrogenase which gives them low risk for AUD because they experience unpleasant effects from alcohol consumption.

21
Q

What are the two major pharmacotherapeutic approaches for treating alcoholism?

A
  1. disulfiram

2. naltrexone

22
Q

How does disulfiram work to treat alcoholism?

A

Disulfiram inhibits the enzyme aldehyde dehydrogenase which converts acetaldehyde into acetic acid. The result of this is that consuming alcohol causes very unpleasant effects such as nausea and vomiting, which discourages drinking.

23
Q

How does naltrexone work to treat alcoholism?

A

Naltrexone is an opioid receptor antagonist. It reduces the positive feelings caused by alcohol and has the effect of reducing alcohol consumption and craving.

24
Q

What is the most effective treatment for alcohol dependence?

A

Medical management along with either naltrexone or combined behavioural intervention.