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PSYC3030 > Alcohol > Flashcards

Alcohol Flashcards

1
Q

How commonly abused is alcohol?

A

After caffeine, is the most commonly abused psychoactive drug and most abused drug in general

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2
Q

What is mead and when was it created?

A

Fermented honey.

8000-10000 BC

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3
Q

When and where was the first official brewery formed?

A

3700 BC in Egypt

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4
Q

When did distillation first occur, and when was the process perfected?

A

Middle ages.

Perfected by the Dutch in 17th century

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5
Q

How is alcohol made?

A

Ethyl alcohol created by fermentation (yeast metabolizes sugar)

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6
Q

What is brewing beer?

A

Fermentation of starchy grains

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7
Q

What does fermentation do?

A

Gives maximum of about 15% alcohol

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8
Q

How soluble is alcohol?

A

It is a small molecule, so moderately soluble in fat and highly soluble in water

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9
Q

Where is alcohol absorbed?

A

It is easily absorbed in the GI tract. 10% is absorbed into blood directly from stomach, and remainder absorbed in upper small intestine

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10
Q

How much alcohol reaches brain immediately? Why?

A

90%.

Alcohol easily passes blood-brain barrier and placental barriers

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11
Q

What is blood alcohol concentration? How can it be estimated?

A

Grams of OH/100mL of blood expressed as %.

Can be estimated from body weight, number of standard drinks consumed, and hours elapsed since starting to drink

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12
Q

What is the LD50 of alcohol?

A

About 0.45

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13
Q

How is alcohol eliminated?

A

5% is eliminated by lungs, and remainder is eliminated in urine after biotransformation to CO2 and H2O

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14
Q

What is the body’s primary reaction to alcohol? How does this occur?

A

To metabolize it through oxidation. It is constant over time.

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15
Q

What is the enzyme that metabolizes alcohol? What is alcohol metabolized to? Where does this occur?

A

Alcohol dehydrogenase forms acetaldehyde from alcohol.

It is found in the stomach, where 20% is broken down before absorption. The remainder is metabolized by the liver

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16
Q

What happens to acetaldehyde?

A

Acetaldehyde dehydrogenase transforms acetaldehyde to acetic acid, which is oxidized to O2, CO2, and calories of energy.

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17
Q

What happens when acetaldehyde dehydrogenase is less active? How is this related to genetics?

A

Flushing, headaches, nausea, increased HR.

10% of Asians are homozygous for inactive form of acetaldehyde dehydrogenase, and 40% are heterozygous.

18
Q

What type of drug is alcohol?

A

A CNS depressant of the sedative hypnotic class

19
Q

Why is alcohol misperceived as a stimulant?

A

Release of cerebral cortex inhibitory control over subcortical systems and impaired judgement/thinking from loosening of social inhibitions

20
Q

What are the specific actions of alcohol?

A

Acts at neurotransmitter binding site, modifies gating mechanism inside channel, interacts directly with channel protein, and stimulates Gs (linked to adenylyl cyclase)

21
Q

What are the nonspecific actions of alcohol?

A

Alters lipid composition, interacts with polar heads of phospholipids, and disturbs relationship of protein in the membrane

22
Q

What are some behavioural effects of alcohol?

A

Anti-anxiety, reduced social inhibition, reduced attention, impaired judgement/self-perception (increased risk-taking behaviours), memory deficits that are dose- and task-dependent, reduced motor coordination

23
Q

Does alcohol have a reinforcing effect?

A

Yes. Mesolimbic system is important in reinforcement and motivational mechanisms. Alcohol increases VTA firing, and rats will work to have alcohol administered to VTA

24
Q

What is the role of endogenous opioids (endorphins) in alcohol?

A 
Endogenous opioids (endorphins) contribute to reinforcing properties of OH.
OH increases endorphin and enkephalin release in animals and humans.
25
Q

What are protective behaviours in alcohol consumption?

A

Vomiting and loss of consciousness

26
Q

What is Wernicke-Korsakoff syndrome?

A

AKA alcoholic dementia.
Encephalopathy and psychosis, cognitive deficits, confusion, disorientation abnormal eye movements, motor difficulties, chronic amnesia, general apathy, and confabulation.

27
Q

What neurologic changes may result from chronic alcohol consumption?

A

Loss of neurons, enlargement of vesicles due to vitamin B1 (thiamine) deficiency which is necessary for neurons to use glucose (also B2, B6, C, niacin, folacin, Zn, Mg)

28
Q

What other systems are affected by alcoholism?

A

Liver disease (hepatitis, cirrhosis), cardiovascular problems, cancer (esophagus, pharynx, larynx, as smoking is a comorbidity), renal-urinary (reduced ADH), reproductive, GI

29
Q

What is fetal alcohol syndrome?

A

Extreme susceptibility of fetus to what is in the mother’s bloodstream, as alcohol is teratogenic.
Fetus has low acetaldehyde dehydrogenase, so not metabolism.
Greatest risk occurs between 4-9 weeks.
Deficits in short-term memory, problem solving, hyperactivity, growth retardation, CNS abnormalities, skull and facial appearance

30
Q

What is metabolic tolerance with alcohol?

A

Cytochrome P450 family metabolizes many substrates, including alcohol. When alcohol is consumed regularly, these enzymes increase, which increases the rate of metabolism.

31
Q

Describe acute alcohol tolerance.

A

Behavioural and neural adaptation

32
Q

Describe chronic alcohol tolerance.

A

Increased alcohol dehydrogenase, decreased neural responsiveness, and behavioural tolerance.

33
Q

How long does withdrawal syndrome last for alcohol, and what are the symptoms?

A

Withdrawal syndrome lasts from hours to days.

Tremor, anxiety, increased BP/HR, sweating, respiration, nausea, and vomiting

34
Q

Why is competition a factor in alcohol’s interaction with other drugs?

A

Due to cytochrome P450 enzyme binding, when alcohol is taken with other drugs, it may lead to potentially dangerous levels of those drugs

35
Q

How does alcohol impact the glutamate system?

A

Alcohol reduces the effect of glutamate at NMDA receptors, reducing glutamate release.
NMDARs are important for learning and memory, synaptic plasticity, and spatial memory.
Chronic use leads up-regulation of NMDARs.

36
Q

How does post-alcohol withdrawal affect glutamate?

A

Post-alcohol withdrawal leads to increased glutamate release, which may result in excitotoxicity and neuronal cell death

37
Q

How does alcohol affect the GABA system?

A

Alcohol is a GABA agonist, so increases Cl influx.

Chronic use leads to decreased Cl flux, increased sensitivity to convulsants, and down-regulation of GABA-A receptors

38
Q

How do dopamine antagonists affect alcohol consumption?

A

Dopamine antagonists infused into NAcc shell reduce self-administration of alcohol

39
Q

How do opioid antagonists affect alcohol consumption?

A

Opioid receptor antagonists, such as naloxone, reduce alcohol use

40
Q

What is alcohol use disorder?

A

Caused by neurobiological, psychological, and sociocultural factors. Involves compulsive alcohol seeking and use despite damaging consequences

41
Q

How can alcohol use disorder be treated?

A

Individual needs to want to stop. Denial is prevalent. Detoxification occurs. Psychosocial rehabilitation prevents relapse.

42
Q

Which drugs can be used to treat alcohol use disorder?

A

Antabuse (inhibits acetaldehyde dehydrogenase), Naltrexone (inhibits opioid receptors), Acamprosate (NMDAR partial antagonist)

PSYC3030 (12 decks)

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