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PSYT 301 > L7 - ALCOHOL > Flashcards

L7 - ALCOHOL Flashcards

1
Q

What is wrong with “alcoholism”?

A

Term used to describe AUD, a medical disorder with a recognized diagnosis.

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2
Q

What does AUDIT stand for?

A

Alcohol Use Disorder Identification Test

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3
Q

Describe the trajectory of alcohol effects in terms of sedation and stimulation according to dosage.

A

At low dose:
1. Relaxation
2. Disinhibition

At moderate dose:
Loosing the stimulant properties.

At high dose:
1. Impaired motor function
2. Stupor (“pass out”)
3. Coma
4. Death

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4
Q

What is the reward phase of alcohol consumption neurobiologically characterized by?

A

DA, 5-HT and NE release

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5
Q

How does alcohol modulate the release of DA?

A

Likely via an opioid peptide, alcohol disinhibits GABA control over VTA DAergic neurons.

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6
Q

Neurobiologically, what is alcohol tolerance likely to signify for the mesolimbic pathway?

A

Regulation of GABA receptors is significant in the acquiring of tolerance.

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7
Q

What are collateral neurobiological implications of binge-drinking apart from GABAr regulation?

A

Also adaptations in DA + glutamate neurons + endocannabinoid systems.

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8
Q

How does alcohol tolerance put the health at risk?

A

Increased drug intake is necessary to produce reward, adverse health effects are coincidentally more likely.

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9
Q

On which subregions of the extended amygdala is ethanol acting on?

A

-NAcc
-Bed Nucleus of the Stria Terminalis (BNST)
-Central nucleus of Amygdala

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10
Q

List three neurobiological consequences of being in a withdrawal phase from alcohol.

A

-Activation of central amygdala stress circuit
-Decreased levels of DA, 5HT, enkephalin (opioid peptide involved in stress response) an endocannabinoids
-Increased levels of CRF (involved in stress response), dynorphin (opioid peptide), orexin (arousal), substance P (stress response)

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11
Q

True or false: VTA GABA neurons are significant in the withdrawal phase of AUD.

A

True.

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12
Q

Name 2 major psychological consequences of being in a withdrawal phase from alcohol.

A

-Negative affect (anxiety, depression and anhedonia)
-Increased salience for drug and decreased sensitivity to natural reinforcers

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13
Q

What are the two metabolizers charged of degrading ethanol under normal conditions?

A

ADH (alcohol dehydrogenase)
ALDH (acetaldehyde dehydrogenase)

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14
Q

In how many steps is ethanol metabolized?

A

2

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15
Q

On what molecular structures is the metabolizing of ethanol dependent under normal circumstances?

A

NAD and mitochondrial electron transport chain

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16
Q

When metabolizing reactions depending on NAD and the mitochondrial electron transport chain fail under excessive demand, what is metabolizing ethanol? What is the consequence?

A

Peroxisomes. Toxic oxygen radicals are produced and there is an accumulation of aldehyde = “hang over” state.

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17
Q

Where are ADH and ALDH mostly expressed?

A

Liver, digestive tract.

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18
Q

Why can it be counter-intuitive to characterize ethanol as a sedative?

A

Stimulatory effects at low dose.

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19
Q

In the alcohol addiction phase of regulated relapse, what neurobiological component is driving excessive drug taking?

A

Significant changes in NMDA and AMPA receptors.

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20
Q

True or false: during the regulated relapse phase of alcohol addiction, the midbrain stress system is becoming increasingly active.

A

True.

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21
Q

What are the CRF and NPY systems standing for? How are they respectively regulating stress-induced relapse? During the withdrawal phase, how are the two systems comparing in terms of activity?

A

The corticotropin-releasing factor system is promoting the stress-induced relapse and the neuropeptide Y system is blocking the stress-induced relapse. During the withdrawal phase of AUD, the CRF system overweights the NPY system.

22
Q

Neurobiological structures from which brain area are particularly involved in compulsive drug seeking?

A

PFC

23
Q

What neurobiological structure is underlying PFC control over DA release in the NAcc?

A

GLUergic neurons

24
Q

What system is hypersensitive during withdrawal periods of AUD, GABAergic or GLUergic?

A

GLU system is hypersensitive and that has repercussions on GABA levels.

25
Q

True or false: CB1 is a molecular target of ethanol.

A

True.

26
Q

List the 6 neuronal types that are characterized as molecular targets of ethanol.

A

-GABAergic
-GLUergic
-DAergic
-CRF neuron
-Opioid neuron
-Cholinergic neuron

27
Q

True or false: D1 but not D2 is a molecular target of ethanol.

A

False: D2 as well.

28
Q

Provide one clinical issue concerning the diagnosis of AUD.

A

Two recognized classifications of AUD:
-ICD-10 (WHO): recognizing harmful use of alcohol + hazardous use of alcohol
-DSM V (APA): integrates all cases under the spectrum of “AUD” (mild, moderate, severe)

29
Q

What are the cardinal features of AUD found in the DSM V and ICD-10 diagnoses of AUD.

A

-Pathological use of alcohol (behavioural criteria)
-Preoccupying social or legal consequences
-Tolerance and withdrawal

30
Q

List 5 medical complications objectively recognized to be associated with AUD.

A

-Cirrhosis (liver disease)
-Cardiomyopathy (heart struggling to pump blood to the rest of the body)
-Peripheral neuropathy (damage to PNS nerves)
-Cerebellar degeneration
-Dementia

31
Q

List 6 behavioural criteria for AUD.

A

-Daytime and morning intoxication
-Unsuccessful efforts to reduce SU
-Increased salience for drug
-Beneficial activities abandoned to SU
-Increased use despite physical impairments
-Complication of intoxication

32
Q

True or false: fetal alcohol spectrum disorders are usually only discovered at puberty.

A

True (expect for FASD cases with malformations).

33
Q

Name two behavioural or psychological impairments resulting from fetal alcohol spectrum disorders.

A

Learning impairment (cognitive) and impulsivity, depression (affective disturbances).

34
Q

What is the most common comorbid psychiatric condition to AUD?

A

Nicotine addiction.

35
Q

List 2 psychiatric conditions that are susceptible to be secondary outcomes to AUD.

A

-Anxiety
-Depression

36
Q

List 3 behavioural treatments for AUD.

A

-CBT (only woks if you WANT to stop drinking)
- AA (12-step)
-Motivational interviewing

37
Q

List 3 approved pharmacological interventions for AUD.

A

-Disulfuram: blocks ALDH (aversive)
-Naltrexone: prevents GABA disinhibition on NAcc DA (mu-receptor antagonist) release by blocking opioid release = decrease DA release
-Acamprosate (not always reliable):GABA-A receptor antagonist

38
Q

What is the single most determinant predictor of developing AUD?

A

Having a first-degree alcoholic relative.

39
Q

Is AUD a complex or simple Mendelian trait?

A

Complex, of course!

40
Q

What makes us think that there is genetic predisposition to AUD?

A

MZ twins tend to be more concordant that DZ. And 1° relatives tend be more concordant than 2° relative as well.

41
Q

Is AUD all about genetics?

A

No, environmental and personality components too.

42
Q

What are the two most known families of aldehyde hydrogenase (ALDH) genes?

A

AlDH-1 (cytoplasmic)
AlDH-2 (mitochondrial)

43
Q

Polymorphic variation in which gene of aldehyde hydrogenase is associated with low alcohol consumption and a substantially reduced risk of alcoholism?

A

ALDH-2

44
Q

How are Caucasians and East Asians differentiating in terms of ALDH cytosolic isozyme (-1) and mitochondrial isozyme (-2) expression?

A

Most Caucasians have two major isozymes, while approximately 50% of East Asians have the cytosolic isozyme but not the mitochondrial isozyme (polymorphic variation at ALDH-2).

45
Q

Linkage studies of familial alcoholism implicate the ADH region of which chromosome?

A

Chromosome 4

46
Q

What are the three main structures of the midbrain stress system that are activated by ethanol?

A

-Central Nucleus of the Amygdala (CeAmyg)
-Bed Nucleus of the Stria Terminalis (BNST)
-Nucleus Accumbens Shell (NaccS)

47
Q

Provide a function to the following peptides:

-Enkephalin
-CRF
-Dynorphin
-Orexin
-Substances P

A

-Enkephalin: mediating nociception by binding to opioid receptors
-CRF (corticotropin-releasing factor): neuropeptides activating the HPA axis
-Dynorphin: opioid peptide
-Orexin: arousal, wakefulness
-Substances P: involved in stress response

48
Q

What are the neuropeptides involved in the central amygdala microcircuitry?

A

GABA
CRF
NPY

49
Q

What are the effects of CRF and NPY systems on GABA levels in the microcircuitry of the central amygdala? What are the resulting effects on stress and anxiety?

A

CRF system increases intra-CeA GABA = pro-stress and anxiogenic
NPY system decreases intra-CeA GABA = anti-stress and anxiolytic

50
Q

What are the two systems hypersensitive in withdrawn individuals?

A

CRF and Glut.

51
Q

Signal from which neurotransmitter is mediating cravings?

A

Glutamate

PSYT 301 (8 decks)

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