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PSYC-2920 > Chapter 6: Alcohol > Flashcards

Chapter 6: Alcohol Flashcards

1
Q

According to Dr. D. Musto, Alcohol consumption in america tends to:

A

tends to peak every 60-70 years, followed by a decline in use. The decline was often accompanied by preoccupation with health and morality and by public concern over the harm of alcohol. (ex/ start of MADD)

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2
Q

What is BAC? what’re its units? how do you convert to percent alcohol?

A

BAC= Blood-alcohol concentration. Units in mg/100 ml of blood, but SI mmol/L. You can convert mg/ml by moving the decimal 3 places to the left to find alcohol percentage.

ex/ BAC of 80mg/100ml

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3
Q

T/F alcohol absorption is effected by PH of the stomach

A

false. Alcohol cannot ionize

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4
Q

What organ is the site of first pass metabolism for alcohol?

A

the stomach. NOT THE LIVER. There are high levels of alcohol dehydrogenase in the stomach, which breaks down alcohol before it gets absorbed into the blood and taken to the liver.

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5
Q

Why does eating before drinking prevent you from getting drunk?

A

because alcohol will spend more time in the stomach,making it exposed to first pass metabolism even further.

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6
Q

How does carbonation aid in alcohol absorption?

A

carbonation and carbonated drinks help pass alcohol through the stomach and into the blood stream faster.

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7
Q

How does Histidine H2 receptor antagonists effect alcohol absorption?

A

H2 antagonists reduce stomach levels of alcohol dehydrogenase and significantly reduces the amount of first pass metabolism, meaning the alcohol will arrive in larger concentrations into the blood stream

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8
Q

How to antacids such as Zantac affect alcohol absorption?

A

reduces stomach acidity and levels of first pass metabolism by reducing the amount of alcohol dehydrogenase present in the stomach, results in increased BAC levels

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9
Q

Why do women show higher levels of BAC even if they consumed the same amount as a male?

A

because they have less amounts of alcohol dehydrogenase, the alcohol is not metabolized as fast before entering the blood stream.

Additionally, because alcohol is distributed and excreted through body water, which women have less of (they have more fat), alcohol reaches higher concentrations in the blood since their is less body water to dilute the alcohol.

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10
Q

Why does alcohol inhalation cause higher BACs that oral ingestion of alcohol?

A

AWOL (alcohol without liquid) causes higher BACs because first pass metabolism is passed- the alcohol goes directly to the blood stream without going through the stomach.

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11
Q

Why would individuals that have a lesser % of muscle have higher levels of BAC compared to an individual who is ripped?

A

because alcohol is distributed, excreted and carried entirely in body water. A person with more fat will have higher BACs because the body with more fat has less water (in the muscles) to dilute the EtOH in the blood.

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12
Q

How does alcohol distribution get affected with age?

A

BAC’s increase as individuals get older because their fat: muscle ratio goes up, even if their body weight does not change. Fat= less body water= alcohol does not get diluted as much= higher concentrations.

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13
Q

What major organ is responsible for alcohol to be completely metabolized?

A

the liver; although the stomach is where first pass metabolism takes place, the liver is where most of it is metabolized.

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14
Q

What is the rate limiting step/ slowest step of alcohol metabolism?

A

the conversion of alcohol to acetaldehyde via alcohol dehydrogenase.

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15
Q

In addition to alcohol dehydrogenase, what other system helps the body metabolize alcohol?

A

the Microsomal Ethanol Oxidizing System (MEOS). A much smaller component of alcohol metabolism than alcohol dehydrogenase. MEOS is stimulated in heavy drinkers.

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16
Q

T/F Eating speeds up the rate of metabolism

A

TRUE. Eating speeds up the rate of metabolism but not absorption. This is a result of increased blood flow to the liver caused by food in the stomach

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17
Q

Two main neurotransmitters affected by alcohol

A

GABA and glutamate

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18
Q

Two ways that alcohol interacts with GABA or glutamate receptors

A

1) interacting with a pocket: an alcohol sensitive area on the receptor site
2) blocking the entire ion channel itself

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19
Q

Alcohol is a GABA ____

A

Alcohol is a GABA agonist. EtOH stimulates GABA activity and then decreases brain activity

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20
Q

2 types of GABA receptors

A

GABAa receptors- ionotropic

GABAb receptors- metabotropic

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21
Q

How is the function of the GABAa regulated in terms of structure?

A

the receptors are made of different types of subunits, alpha beta delta etc. Different varieties of subunits result in different GABAa receptor configurations. The variety of receptors determines its functions and how the receptor is affected by alcohol and other GABAergic drugs

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22
Q

Difference between orthosteric site and allosteric site

A

orthosteric site: binding site on the GABAa receptor where the natural ligand (aka GABA) binds to. When activated, the receptor opens its ion channel and permits an influx of Cl- ions, creating hyperpolarization of the cell. (More neg charge= more inhibition)

allosteric site: GABAa has alternative binding sites for alcohol and benzodiazepines, which creates conformational change, affecting the orthosteric site. Modification at the allosteric site by alcohol can change GABA binding affinity to GABAa.

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23
Q

Alcohol is a _____ modulator of GABAa receptors.

A

Alcohol is a positive allosteric modulator that enhances the ability of GABAa to open its ion channels via interaction of allosteric sites.

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24
Q

What kind of subunit must be present in order for alcohol to be able to allosterically modulate GABAa? Where are most of these subunit-containing GABAa receptors found?

A

EtOH only acts on GABAa receptors that have DELTA subunits.

DELTA-containing GABAa subunits are predominantly found in the cerebellum (PURKINJE NEURONS), which is involved in fine motor control, balance and coordination– issues that are compromised when a person has been drinking.

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25
Q

What type of neuron is found in the cerebellum and are found to interact with alcohol?

A

Purkinje Neurons are cerebellum neurons that are stimulated at low doses of alcohol, when alcohol acts on GABAa receptors. This causes the impairments in motor control.

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26
Q

What are the three varieties of GABAb receptors? Which one of these types of GABAb receptors can be modulated by alcohol?

A

1) autoreceptor GABAb= located on PREsynaptic cell and stimulates/modulates GABA release
2) located on the POST synaptic cell= blocks release of other neurotransmitters by altering the calcium channels
3) dopamine-stimulating GABAb receptors

EtOH alters GABAb receptors located on dopamine synapses that stimulate the release of dopamine.

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27
Q

Alcohol is a glutamate _____

A

alcohol is a glutamate antagonist

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28
Q

Which type of glutamate receptor is affected by the presence of alcohol? How is it affected?

A

NMDA receptors. Alcohol blocks the NMDA ion channels, which is responsible for excitatory responses. This results in the depression of the function of the glutamate ion channel. Magnesium release from ion channel of NMDA receptor is also disrupted.

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29
Q

What does chronic use of alcohol do to a person’s NMDA receptors? How might this contribute to withdrawal symptoms?

A

Chronic exposure UPREGULATES NMDA receptor-ion channel functioning. the brain thus becomes more sensitive to glutamate as a means for compensating for the prolonged depression caused by alcohol. When a person stops drinking, they are still very sensitive to glutamate (excitatory), which may responsible for the increased anxiety and agitation.

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30
Q

How does alcohol interfere with long term potentiation and prevention of new neuronal formation?

A

alcohol can affect hippocampus and memory formation because of its interactions with NMDA receptors.

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31
Q

How does alcohol affect upper level thinking and problem solving?

A

alcohol affects the PREFRONTAL CORTEX because the PFC contains GLUtaminergic pyramedal projection neurons, which get inhibited, as well as inhibitory GABAminergic interneurons, which get stimulated, which suppress activity of PYRAMEDAL neurons.

32
Q

Describe the mechanism as to how alcohol increases the activity of the mesolimbic dopamine system and increases dopamine via the nucleus accumbens.

A

Under normal conditions, the mesolimbic dopamine system is INHIBITED by GABAERGIC interneurons (operating on the DA neurons in the VTA), that are innervated by more GABAergic neurons projecting into the nucleus accumbens and VENTRAL PALLADIUM.

When alcohol is consumed, the nucleus accumbens and ventral palladium release increased amounts of GABA into the inhibitory interneurons of the VTA, decreasing the interneurons’ activity.

The interneurons are thus inhibited. They release less GABA into the mesolimbic dopamine system and VTA, resulting in increased activity of VTA dopaminergic neurons and increased dopamine output.

33
Q

Alcohol is a serotonin _____

A

a serotonin agonist, which facilitates dopamine release in the nucleus accumbens

34
Q

Alcohol is a mu opioid receptor _____. Is this receptor inhibitory or excitatory?

A

Alcohol is a mu opioid receptor agonist. The mu receptor is an inhibitory receptor linked to K+ ion movement.

35
Q

How does alcohol make the skin feel warm?

A

by acting as a dilator

36
Q

How does alcohol make you dehydrated?

A

it acts as a dieuretic by inhibiting the anti-diuretic hormone.

37
Q

When does increased urination occur? (when someone has been drinking)

A

When BAC levels begin to FALL, increased urination occurs.

38
Q

What does alcohol do to your sleep schedule?

A

it makes you fall asleep fast, but you do not get a good sleep because it decreases REM sleep

39
Q

Define Biphasic and how it relates to alcohol

A

when different doses (of alcohol in this case) give different effects.
low doses= stimulation and euphoria
high doses= sedation, depression adn anger.

40
Q

How might alcohol trigger aggression and violence?

A

high doses of alcohol may increase GABA levels, causing inhibition of the dorsal raphe nuclei, which plays a role in arousal and wakefulness.

41
Q

What is lateral inhibition and how might this affect perception when someone is under the influence of alcohol?

A

lateral inhibition: where excited neurons reduce the activity of neighboring neurons. This results in lowers scores in the critical flicker fusion threshold, increases and absolute and difference thresholds, decreases in peripheral vision, etc.

alcohol also decreases sensitivity to taste, small and pain.

42
Q

Generally, the more complex the task, the ____ the impairment seen at lower doses of alcohol.

A

Generally, the more complex the task, the greater the impairment seen at lower doses of alcohol.

43
Q

Why might performance in hand-eye coordination-requiring tasks be compromised under the influence of alcohol?

A

alcohol consumption DECREASES blood flow to the cerebellum and activates GABAa receptors that contain delta subunits, further inhibiting the cerebellum.

44
Q

What is nystagmus and how does Alcohol effect balance? How is balance tested?

A

balance is tested using the romberg sway test. the person stands on one food with eyes closed. EtOH disrupts inner-ear fluids, which causes nystagmus: eye movements responsible for dizziness, which causes swaying.

45
Q

T/F Alcohol does not increase errors in short-term verbal memory, but it does impair long term memory

A

true

46
Q

What two parts of the brain are affected when alcohol causes decreased verbal and visual memory and attention?

A

Decrease in verbal and visual memory and attention correspond with decreased functioning in the dorsolateral PREFRONTAL CORTEX and the ANTERIOR CINGULATE GYRUS

47
Q

What is a greyout

A

when an individual only remembers bits and pieces of events, but missing memories return if the drinker is reminded of these events or if he/she returns to the place where the events occurred.

this indicates that memories are formed and stored, but alcohol causes problems with RETRIEVAL

48
Q

What is an en bloc blackout? how is it different than a grey out?

A

an en-bloc black out is caused by a SUDDEN increase in BA levels. it has a DEFINITE beginning and end where there is NO EVIDENCE of memories being put into LONG TERM STORAGE. A person who is in “black out” may appear normal because their short-term memory is not compromised, but they will not remember what had happened when they wake up, even if they are “cued” and reminded, unlike grey outs.

49
Q

What is the mechanism of a blackout?

A

NMDA/glutaminergic receptors and the ion channels that are responsible for long term potentiation are blocked by alcohol. Because the excitatory receptors that aid in memory formation is blocked, memories cannot be stored long term.

50
Q

Which brain regions are responsible for reduced driving performance under the influence of alcohol?

A

1) the Anterioir cingulate gyrus and inferior frontal gyrus activity is decreased, which impairs cognitive control and ability to problem solve
2) orbitofrontal cortex and motor regions have decreased activity, resulting is poor performance

Intoxicated drivers are less able to orient themselves or detect novel stimuli because hippocampus, anterior cingulate gyrus and PFC are decreased in activity, resulting in poor decision making and poor detection of spatial location?

51
Q

What do the results of the Go-Stop Task show about how alcohol may impair motor performance?

A

Alcohol does not interfere with the GO signal, but decreases STOP signal latency. Shows disruption of inhibitory control. This is because EtOH WEAKENS THE CONNECTION BETWEEN THE PFC and the STRIATUM (motor area)

52
Q

alcohol ___ 5-HT3 receptors, causing the release of dopamine in nucleus accumbens, which is responsible for alcohol’s reinforcing effect

A

alcohol stimulates 5-HT3 receptors, causing the release of dopamine in nucleus accumbens, which is responsible for alcohol’s reinforcing effect.

53
Q

How does serotonin play a role in the biphasic affect of alcohol?

A

low doses of alcohol stimulates 5;HT3 receptors, increasing the excitatory effect of serotonin because serotonin stimulates glutamate release from the PFC.

chronic uses of alcohol however, decreases serotonin’s excitatory effect.

54
Q

A 5-HT3 antagonist blocks/inhibits alcohol or opiate effects?

A

A 5-HT3 antagonist blocks alcohol or opiate effects, because alcohol is a 5-HT3 agonist and enhances serotonin effects.

55
Q

What happens to the rate of response in punishment-suppressed behavior when an animal is under the influence of alcohol?

A

alcohol INCREASES the rate of response of behaviors that were originally suppressed by punishment. This indicates that alcohol loosens inhibitions and REDUCES the control of consequences on behavior.

56
Q

T/F Alcohol is highly generalizable

A

False. Alcohol is highly discriminable. It is easily discriminated against compared to benzodiazepines, and will only partly generalize to barbituates and opiates.

57
Q

Which neurotransmitter is responsible for mediating the subjective effects of alcohol?

A

Serotonin. this is proved because if one was to block 5-HT3 receptors, the effects of alcohol are removed.

58
Q

How does Naltrexone block the effects of alcohol?

A

By blocking the Mu Opioid receptors. Alcohol is usually an agonist of mu receptors, and by blocking the mu opioid receptors, alcohol cannot activate them.

59
Q

Does alcohol show acute tolerance?

A

yes, the effects of alcohol are better seen when the BAC is rising rather than falling. However, different effects are affected differently (lol); cognitive performance recovers from impairment to drug-free levels during declining BACs, whereas alcohol-increased errors do not diminish.

60
Q

How does chronic alcohol use results in metabolic tolerance?

A

due to increased levels of stimulation of alcohol dehydrogenase and MEOS.

61
Q

What 2 factors contribute to behavioral tolerance of alcohol?

A

1) behavioral effects of alcohol are mitigated by PRACTICE
2) behavioural effects of alcohol are mitigated by EXPECTANCY
- individuals who expected they were given alcohol were felt “less intoxicated” than individuals who did not know they received alcohol.
- shows that people who received beer may have better control of their behaviours

62
Q

Two stages of alcohol withdrawal

A

1) minor symptoms (partial hangovers, vomiting)

2) late symptoms

63
Q

Delirium Tremens, agitation, high anxiety and hallucinations are aspects of withdrawal due to the _____ mechanism of alcohol

A

Delirium Tremens, agitation, high anxiety and hallucinations are aspects of withdrawal due to the COMPENSATORY mechanism of alcohol. EtOH is a depressent that resulted in upregulation of NMDA excitatory receptors: the body is now super hyper/ glutamate sensitive now that there is no alcohol in the system to depress the excitatory system.

64
Q

What drugs can you use to reduce the withdrawal effects of alcohol?

A

benzodiazepam for anxiety reduction, haloperidol for hallucination reduction.

65
Q

2 phases of alcoholism

A

1) prodromal phase: characterization by frequent blackouts. Considered “problem drinking,” not actual alcoholism
2) Gamma alcoholics: TRUE alcoholics whose addictions are characterized by a) the INABILITY to CONTROL their drinking, and b) the onset of WITHDRAWAL symptoms if they do not drink.

66
Q

Difference between FHP and FHN individuals and their susceptibility to alcoholism

A

FHP (Familiy History Positive) individuals have heightened risk for alcoholism because one of their family members are an alcoholic. FHP subjects show greater sensitivity to the subjective and motor impairing effects of alcohol. This may be related to the fact that they have POLYMORPHISMS in genes related to EtOH metabolism and addictive personality characteristics.

FHN (family history negative) individuals have less risk of alcoholism because no family members are alcoholics.

67
Q

How is death by alcohol poisoning usually caused?

A

due to respiratory failure. Alcohol is a GABA agonist (inhibitor) and it depressed the respiratory system to stop working all together.

68
Q

How does the body prevent overdose? how does acute administration prevent the body from preventing overdose?

A

as you drink, the body can induce vomiting and unconciousness to prevent you from drinking more and poisoning yourself. If you acutely administer a large amount of alcohol, your body does not have time to react/make you go unconscious before alcohol depresses your respiratory system.

69
Q

Why do rats exhibit more anxiety on days 1 and weeks 6 in the elevated plus maze experiment than in the middle?

A

alcoholic rats open arm exploration DECREASES at one day of withdrawal, goes back to normal levels of exploration after 3 weeks, but decreasese again during prolonged abstinence.

This is due to corticotropin-releasing factor (stress factors) being dysregulated at day 1 and week 6, but being normal in the middle.

70
Q

Describe the mechanism of Antabuse

A

blocks aldehyde dehydrogenase and allows a buildup of acetaldehyde, which makes people sick. If you drink alcohol while on antabuse, you will get sick

71
Q

Describe how Buspirone works to treat alcohol addiction

A

it is a 5HT1A receptor agonist

72
Q

How does odansetrone work to treat alcohol addiction?

A

is blocks the 5HT3 receptor: recall, alcohol is a 5HT3 agonist.

73
Q

How does bromocriptine work to treat alcohol addictioN?

A

it is a dopamine D2 blocker, blocks the reinforcing and rewarding effects of alcohol

74
Q

How does Naltereoxine work to treat alcohol addiction?

A

it is a mu opioid receptor blocker: recall; alcohol is a mu receptor agonist.

75
Q

What ion is involved with glutamate? with GABA? with mu opioid receptors?

A

glutamate: Na+ and Ca2+, excitatory
GABA: Cl-, inhibitory
Mu opioid: K+ ion, inhibitory

PSYC-2920 (15 decks)

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