Alcohol Flashcards

(42 cards)

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
What are protective behaviours in alcohol consumption?
Vomiting and loss of consciousness
26
What is Wernicke-Korsakoff syndrome?
AKA alcoholic dementia. Encephalopathy and psychosis, cognitive deficits, confusion, disorientation abnormal eye movements, motor difficulties, chronic amnesia, general apathy, and confabulation.
27
What neurologic changes may result from chronic alcohol consumption?
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
What other systems are affected by alcoholism?
Liver disease (hepatitis, cirrhosis), cardiovascular problems, cancer (esophagus, pharynx, larynx, as smoking is a comorbidity), renal-urinary (reduced ADH), reproductive, GI
29
What is fetal alcohol syndrome?
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
What is metabolic tolerance with alcohol?
Cytochrome P450 family metabolizes many substrates, including alcohol. When alcohol is consumed regularly, these enzymes increase, which increases the rate of metabolism.
31
Describe acute alcohol tolerance.
Behavioural and neural adaptation
32
Describe chronic alcohol tolerance.
Increased alcohol dehydrogenase, decreased neural responsiveness, and behavioural tolerance.
33
How long does withdrawal syndrome last for alcohol, and what are the symptoms?
Withdrawal syndrome lasts from hours to days. | Tremor, anxiety, increased BP/HR, sweating, respiration, nausea, and vomiting
34
Why is competition a factor in alcohol's interaction with other drugs?
Due to cytochrome P450 enzyme binding, when alcohol is taken with other drugs, it may lead to potentially dangerous levels of those drugs
35
How does alcohol impact the glutamate system?
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
How does post-alcohol withdrawal affect glutamate?
Post-alcohol withdrawal leads to increased glutamate release, which may result in excitotoxicity and neuronal cell death
37
How does alcohol affect the GABA system?
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
How do dopamine antagonists affect alcohol consumption?
Dopamine antagonists infused into NAcc shell reduce self-administration of alcohol
39
How do opioid antagonists affect alcohol consumption?
Opioid receptor antagonists, such as naloxone, reduce alcohol use
40
What is alcohol use disorder?
Caused by neurobiological, psychological, and sociocultural factors. Involves compulsive alcohol seeking and use despite damaging consequences
41
How can alcohol use disorder be treated?
Individual needs to want to stop. Denial is prevalent. Detoxification occurs. Psychosocial rehabilitation prevents relapse.
42
Which drugs can be used to treat alcohol use disorder?
Antabuse (inhibits acetaldehyde dehydrogenase), Naltrexone (inhibits opioid receptors), Acamprosate (NMDAR partial antagonist)