Addiction Flashcards

1
Q

voluntary motor behavior

A

BG

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2
Q

input stage of BG

A

caudate/putamen

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3
Q

caudate + putamen =?

A

corpus striatum

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4
Q

striatum –> pallidus –> thalamus

A

loop

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5
Q

planning, controlling impulsivity

A

PFC

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6
Q

early assessment of keys in env and linking to cues in emotional responses

A

amygdala

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7
Q

processing memory, general emotion regulation

A

hippocampus

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8
Q

circuit for translating emotion into action

A

CSPT:

PFC/Amygdala/Hippo –> nuc acc –> V pallidum –> MD thalamus –> cortical motor planning regions

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9
Q

nuclei that supply DA in the mesencephalon

A

SN, VTA

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10
Q

cells in striatum:accumbens that receive this input? what are they able to do w multiple inputs?

A

medium spiny neuron
receives GABA
INTEGRATORS!!! of glutamate from cortical regions with DA from VTA

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11
Q

lots of these are found in the striatum

A

opioids

DA+opioids involved in addiction

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12
Q

convey info

modulate info

A

DA

muOpioids

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13
Q

key site in brain to stimulate DA reward

A

VTA
can block D1 receptors to blunt this
destroying VTA blunts reward fxn

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14
Q
wanting chemical
liking chemical (hedonic response: liking chocolate cake after eating)
A

DA

opioids

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15
Q

which pathway will amphetamines effect?

A

wanting/goal-pursuit

NOT “liking”

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16
Q

neurochemical most predictive in reward stimulai

A

DA

most active when cues to predict reward, or when we have to learn something new (when env changes)

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17
Q

opponent process theory

A

A process: euphoria (e.g.)
B process: counteradaptation initiated to oppose the A process; over time this gets stronger and stronger

When A is removed then strong B leads to dysphoria

w/d theory: constantly taking drug to stave off B process

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18
Q

cue-elicited cocaine craving elicits?

A

DA release in the striatum

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19
Q

low striatal D2 receptor binding correlates with diminished activity where?

A

PFC

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20
Q

impulsivity results from impaired fxn of what?

A

PFC inhibitory control

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21
Q

compulsivity results from shift in what?

A

PFC-accumbens motor circuits to emphasis on dorsal striatal control (habit-mediator)

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22
Q

incentive-sensitization hypothesis

A

drug use leads to sensitization of DA ability to produce drug wanting

23
Q

reward-error prediction hypothesis

A

enhanced DA release during drug taking produces condition in which all stimuli encountered during this period are experienced as being better than expected

24
Q

big addiction characteristics

A

loss of control of limiting intake
taking persists despite negative consequences
alternatives no longer pursues
potential for relapse throughout lifespan

25
Q

def: a) tendency to choose immediate reinforcement over delayed gratification, even when smaller or less beneficial, and b) impairment of inhibiting a course of action once initiated

A

impulsive behavior

26
Q

def: perseveration in a certain behavior even in the face of unsuccessful/adverse outcomes

A

compulsive behavior

27
Q

a gradual decrease in the use of alcohol past 20 years of age or so

A

desistence: usually due to other reinforcers e.g. career/family etc

28
Q

epi of substance use d/o’s

A

70% of drug abusers are unemployed
300% higher med costs
50% of domestic violence, major crimes assoc
17% of pregnant women smoke, 13% use alcohol
24% of suicides have BAC >0.1

29
Q

genetic fx of alcohol abuse

low levels of what in CSF?

A

sons of fathers have 50% chance
inheritance of impulsivity as well as general addictive tendency
serotonin

30
Q

other factors assoc in development of addiction

A

parental discouragement and monitoring
focus on academics
defense mechanisms (denial/rationalization)
early psychoactive substance use

31
Q

almost all drugs of abuse elevate what neurochemical in the where?

A

DA in the nuc accumbens

32
Q

locations of DA-producing neurons

A

SN –>

VTA –> Acb/amyg/hippo/PFC (MCL pathway)

33
Q

how would you take away the “good” of food/drugs/other goal objects?
what projection plays role in wanting/seeking and reward-learning

A

block DA receptors

mesocorticolimbic projection

34
Q

system involved in “wanting”

peptides involved in liking

A

DA (VTA-Acb)

opioids (endorph/enkeph)

35
Q

3 components of the striatum
dorsal striatum?
ventral striatum?

A

caudate + putamen + nucleus accumbens
caudate + putamen
nuc accumbens

36
Q

loops that direct conscious control of voluntary motor action; hijacked in substance use d/o

A

cortico-striato-pallidal-thalamic

37
Q

inputs to Acb: motivation and emotion

A

amygdala and hippocampus

also PFC

38
Q

drugs augment the transmission of what where?

A

DA in the nuc accumbens

39
Q

hypothesis that states that DA codes for affective experience of reward

A

anhedonia

40
Q

neither reward-based nor w/d-based theories describe what?

A

lifelong propensity to relapse

41
Q

which theory does not require drug to cause subjective state of euphoria?
which theory describes increased wanting while decreased liking?

A

reward-learning

incentive-sensitiztion

42
Q

this theory posits that individuals w/addiction acts compulsively due to diminishment in these 2 brain regions

A

PFC and anterior cingulate cortex

43
Q

BAC levels: 50, 80, 200-300, 400-600

A

50 –> loss of cognition, judgment, coord
80 –> driving impaired
200 –> all faculties
400 –> coma/death

44
Q

tx for alcohol w/d (w/in 72h)

A

tx: supportive
w/d: BZD taper + thiamine, Mg (incr glutamate to offset opponent-process of dec GABA and incr glutamate) and anticonvulsants (gabapentin) modulate Glu, diazepam, lorazepam

45
Q

tx for opioid w/d

A

tx: naloxone

w/d: buprenorphine or methadone, clonidine/BZD regimen, suboxone, psychosocial support

46
Q

tx for stimulant w/d

A

tx: BZD’s

w/d: support + antidepressants

47
Q

wernicke’s encephalopathy

A

due to thiamine deficiency (give thiamine)

confusion, ataxia, ophthalmoplegia

48
Q

meds and psychosocial tx (3) for alcohol

A

naltrexone, acamposate, disulfuram, buprenorphine + methadone for cocaine

CBT: relapse prevention, motivational enhancement (learn to avoid stimuli and chose positive habits), 12 step

49
Q
timeline of w/d sx:
alcohol
BZD's
opioids
stimulants
A

sx subside in 72-96h; DT’s for 10+ days
depends on half-life (d-wks)
days (heroin/morphine) to wks (methadone)
cocaine shorter than methamphetamine

50
Q
dangerous sx of:
alcohol
BZD's
opioids
stimulants
A

psychosis, delirium, seizures
seizures
dehydration (NVD), leave to get more
leave to get more

51
Q
common sx of:
alcohol
BZD's
opioids
stimulants
A

anx, nausea, tremors, sleep, restlessness, sweating, headaches, pulse, HTN
same as above
NVD, craving, rhinorrhea, tearing, muscle aches/cramps, gooseflesh, dilated pupils

tired, prolonged sleeping, amotivational, depressed, overeating, craving

52
Q

tx of BZD w/d

A

switch to long-acting BZD and taper

some now use anticonvulsants

53
Q

goal of substance use tx

A

prevent relapse!

most common time is 1st month-1 yr

54
Q

MOA naltrexone
acamprosate effects which two systems?
MOA disulfiram (induction of fear)

A

interferes with + reinforcement (blocks effects of opioids released during use/cravings)
GABA/Glutamate; may decrease DA in nuc accumbens
antagonizes aldehyde dehydrogenase