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PSYT 301 > Alcohol > Flashcards

Alcohol Flashcards

1
Q

safe drinking levels

A

women -> 10 drinks/week; no more than 2/day
men -> 15 drinks/week; no more than 3/day

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2
Q

alcohol addiction vs alcoholism

A

alcohol addiction = medical disorder
alcoholism = not recognized as diagnosis

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3
Q

terms used to describe unhealthy levels of alcohol use

4 elements

A
  1. problematic alcohol use
  2. alcohol use disorder
  3. alcohol abuse
  4. as well as scores on structured interviews such as AUDIT
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4
Q

trajectory of alcohol effects

6 elements

A

stage #1 -> stimulation
1. relaxation (after 1-2 drinks)
2. disinhibition (after 3-4 drinks)
stage #2 -> sedation
3. impaired motor function
4. stupor
5. coma
6. death (in a single bout)

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5
Q

ethanol metabolism

4 elements

A
  1. ethanol -> acetaldehyde (via alcohol dehydrogenase/ADH)
  2. acetaldehyde -> acetate (via aldehyde dehydrogenase/ALDH)
  3. acetate enters tricyclic acid cycle -> converted to CO2
  4. reactions dependent on NAD and mt electron transport
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6
Q

when is ROS produced during ethanol metabolism

A

when ethanol is metabolized in peroxisomes

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7
Q

where are ADH and ALDH expressed

A

mostly in liver, some in parts of digestive tract

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8
Q

effect of regular alcohol consumption on ADH and ALDH

A

upregulation of enzymes

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9
Q

what causes symptoms of hangover

2 elements

A
  1. excess of aldehyde
  2. ROS
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10
Q

what happens when deficiency of ALDH

A

build up of aldehyde -> protection against addiction

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11
Q

effects of initial use of alcohol (2) + neurobiology involved (2)

A
  1. positive reinforcement + reward phase
  2. increased DA + opioid reward systems involved
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12
Q

effects of heavy or binge drinking (2) + neurobiology involved (4)

A
  1. tolerance (can drink large quantities/DAr become intolerant) + regulated drug-seeking
  2. neuroadaptations in DA, glutamate, GABA and endocannabinoid systems
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13
Q

effects of withdrawal (4) + neurobiology involved (2)

A
  1. negative affect + associated with anxiety + depression + anhedonia
  2. neuroadaptations in reward and stress systems drive compulsive consumption + increased value of drug stimuli and reduced sensitivity to natural reinforcers
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14
Q

effect of craving

A

compulsive drug seeking

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15
Q

mechanism of DA release in alcohol reward phase

A

disinhibiting GABA control of VTA DA release, via opioid peptide

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16
Q

acute effects in brain during reward phase

3 elements

A
  1. 5HT and NE released
  2. release pharmacological levels of DA activating D1 receptors
  3. initiate a ‘liking’ for the drug
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17
Q

primary site of reward phase activity

A

mesolimbic -> VTA and dorsal striatum

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18
Q

changes in brain during tolerance, regulated relapse phase

4 elements

A
  1. alcohol-dependent epigenetic changes become stabilized
  2. changes in NMDAr and AMPAr -> reinforces excessive drug taking
  3. glutamate projections to PFC still effective, but aversive signals competing with positive reinforcement
  4. midbrain stress system (CeAmyg, BNST, NAcc) increasingly active
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19
Q

brain effects in withdrawal phase

3 elements

A
  1. activation of CeAmyg stress circuit
  2. decreased levels/efficacy of DA, 5HT, enkephalin, endocannabinoids
  3. increased levels of CRH, CRH receptors, dynorphin, orexin, substance P
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20
Q

brain changes in compulsive drug seeking phase

4 elements

A
  1. morphological changes in striatal neurons
  2. changes in signalling
  3. CRH and glutamatergic systems hypersensitive in withdrawn individuals
  4. GABA dysregulated
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21
Q

relation bw D1 and GABAr

A

activation of D1 facilitates GABA-Ar sensitivity

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22
Q

neurons important in withdrawal phase

A

VTA GABA neurons

23
Q

activation of CeAmyg stress circuit in withdrawal phase leads to

A

increasingly negative affective states

24
Q

anatomy involved in compulsive drug seeking phase

3 elements

A

PFC, HC, corticostriatal glutamate system

25
Q

projections important in DA release in compulsive drug-seeking phase

A

glutamatergic projections to PFC

26
Q

what mediates craving

A

strong glutamate signals

27
Q

what circuits does stress-induced relapse involve

A

CRH and NE elements in CeAmyg

28
Q

neurotransmitter targets of ethanol

6 elements

A
  1. GABA
  2. glutamate
  3. DA
  4. CRH
  5. opioid
  6. Ach
29
Q

cardinal features of alcohol use disorders

3 elements

A
  1. pathological use of alcohol
  2. social, occupational or legal impairment; medical consequences
  3. tolerance and withdrawal
30
Q

objective criteria for alcohol use disorders

4 elements

A
  1. medical complications (cirrhosis, cardiomyopathy, peripheral neuropathy, cerebellar degeneration, dementia)
  2. impaired social relationships (disintegration of family, loss of friends)
  3. inability to fulfill role obligations (work, school)
  4. substance related legal problems
31
Q

behavioral criteria for alcohol use disorders

6 elements

A
  1. daytime intoxication, morning drinking
  2. persistent desire or unsuccessful efforts to reduce substance use
  3. increased time spent in obtaining drug or in thinking about obtaining drug
  4. other social and recreational activities abandoned or reduced in favor of substance abuse
  5. increased use of drug despite physical impairments
  6. complications of intoxication (blackouts)
32
Q

diseases secondary to alcoholism

3 elements

A
  1. liver: hepatitis, fatty liver, cirrhosis
  2. cancers: upper GI, liver, breast, lower GI (involves toxic byproduct of metabolism)
  3. brain disease: dementia, hallucinosis, FAS (vulnerability to psychosis)
33
Q

neurobehavioral problems in FAS

7 elements

A
  1. attention
  2. memory
  3. motor control
  4. language
  5. impulse control
  6. cognitive function
  7. coping skills
34
Q

dangers of adolescent drinking

3 elements

A
  1. death and major injuries (overdose, falls, burns, drowning, suicide, etc.)
  2. impaired jugdement and risky behavior (aggressiveness, violence, promiscuity, polydrug abuse)
  3. legal involvement
35
Q

myths of adolescent drinking

2 elements

A
  1. the earlier one starts drinking, the more likely they will become addicted
  2. will lead to irreparable brain damage
36
Q

anatomical problems in FAS

3 elements

A
  1. facial dysmorphology + holoprosencephaly
  2. microencephaly
  3. growth retardation + mental retardation
37
Q

comorbidities of drinking

4 elements

A
  1. smoking
  2. anxiety disorders
  3. depression
  4. personality traits (impulsivity)
38
Q

treatments for AUD

4 elements

A
  1. AA & 12-step programs
  2. CBT (not effective if no motivation to stop/reduce)
  3. brief interventions (motivational interviewing)
  4. supportive medication
39
Q

pharmacological interventions to drink less

3 elements

A
  1. disulfuram: blocks ALDH, very aversive
  2. naltrexone: blocks opioid release -> blocks GABA disinhibition on NAcc DA release (useful in early stages)
  3. acamprosate: GABA-Ar antagonist (useful in later stages)
40
Q

pharmacological interventions to drink less that aren’t approved

3 elements

A
  1. anxiolytics
  2. compounds that target CRH cascade
  3. GLP1 antagonists; FGF1 antagonists; ozempic (effective to decrease drinking, not for addiction)
41
Q

environmental aspects involved in AUD

9 elements

A
  1. ethanol itself
  2. education
  3. socioeconomic status
  4. religious prohibitions
  5. occupation
  6. childhood or sexual abuse
  7. cognitive function
  8. stress and coping mechanisms
  9. temperament and personality
42
Q

alcoholism in asians

3 elements

A
  1. chinese -> moderate, infrequent drinking (just important social occasions)
  2. japanese -> increase in consumption
  3. koreans -> extremes (abstinence or excess)
43
Q

genes responsible for alcoholism

2 elements

A
  1. ADH -> ADH-2 & ADH-3 associated with alcoholism; ADH-3 predisposition to FAS
  2. ALDH -> ALDH-2 mutation confers reduced rate of acetaldehyde clearance (reduced risk of alcoholism)
44
Q

strongest linkage signals for an addiction risk factor

3 elements

A
  1. FTO (diabetes, fat distribution)
  2. DRD2 (regulation of DAr)
  3. PDE4B (NT pathways)
45
Q

predispositions to becoming addicted to alcohol

3 elements

A
  1. epigenetics
  2. reduced resting EEG amplitude
  3. blunted subjective response to ethanol challenge (FH+)
46
Q

relation between acute ethanol administration and csf metabolites

A

acute ethanol administration increases csf metabolites of DA and 5HT

47
Q

levels of release of DA and drinking

A

animals that have lower release of DA drink more (reduced response (low LR) predicts high preference)

48
Q

results of study of adolescent monkeys with social exposure to alcohol

4 elements

A
  1. alc preference increased after 6 or 12 months of social alc exposure
  2. after 12 months of social ethanol exposure -> modest effect of social role models with high alc preference
  3. 12 or 24 months after cessation of social ethanol access -> main predictor of consumption level was baseline ethanol preference
  4. adolescent exposure to ethanol -> transient effect in individuals with low/moderate genetic vulnerability for preference drinking, but persistent effect in individuals with high genetic vulnerability
49
Q

implications of study of adolescent monkeys with social exposure to alcohol

2 elements

A
  1. early heavy use of beverage ethanol = marker of vulnerability (not environmental gateway to AUDs)
  2. gene-environment interactions in high-risk individuals mandate individualization of early screening and treatment programs
50
Q

services to families

3 elements

A
  1. counselling for susceptibility to alcoholism
  2. empiric risks and education
  3. counselling regarding prenatal drug use
51
Q

low and high LR responsiveness (amygdala-PFC connectivity) to angry and happy faces when drinking alcohol (compared to placebo)

A

low LR: decreased response to angry faces compared to placebo; increased response to happy faces compared to placebo
high LR: no difference in response to angry faces compared to placebo; increased response to happy faces compared to placebo

52
Q

raclopride function

A

estimate DA release and binding

53
Q

raclopride binding and ethanol

A

decreased raclopride binding in subjects with high LR (low DA release if high LR, higher DA release if low LR)

PSYT 301 (9 decks)

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