Reward and Addictive Behaviours Flashcards

1
Q

Limbic System:

A

insert diagram

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2
Q

Reward Flowchart:

A

insert flowchart

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3
Q

Drug Use vs Drug Misuse:

A

any psychoactive recreational substance use/experimental use

any unsanctioned recreational substance use

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4
Q

Problematic/Hazardous Drug Use:

A

use of a psychoactive substance at amounts or rates likely to lead to problems

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5
Q

Harmful use of substances must be dependent.

True or False?

A

False

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6
Q

Dependent Use:

A

persistent uncontrolled drug use repeatedly leading to multiple harmful consequences

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7
Q

Addicition

A

a state in which a person engages in a compulsive behaviour, even when aware of potentially negative consequences - behaviour is reinforcing (rewarding or pleasurable)

loss of control in limiting intake

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8
Q

Tolerance:

A

a state in which a person no longer responds to a drug or substance

a higher dose is required to achieve the same effect

also referred to as the hyposensitisation syndrome

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9
Q

Dependence:

A

a state in which a person functions normally only in the presence of a drug

manifested as a physical homeostatic disturbance when the drug is removed

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10
Q

Categories of Harm Associated with Substance Abuse Disorders:

A

insert table

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11
Q

Life Cycle of Addiction:

A

insert diagram

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12
Q

What are the series of structures contributing to incentive salience?

A

The mesocorticolimbic circuit

also implicated in associative learning eg; taking cocaine in a nightclub, nightclubs are associated with craving for cocaine

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13
Q

What structures are used in the mesocorticolimbic circuit?

A
  • mesolimbic system
  • mesocortical system

addiction also involves:
- PFC
- amygdala
- hippocampus

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14
Q

When will the mesocorticolimbic system be activated?

A

in response to many stimuli

dopaminergic response

central to motivation

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15
Q

Pathway for Reward and Reinforcement:

A

addictive drugs activate this system

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16
Q

Addictive drugs cause more powerful and reliable activation of ——– than natural rewards/

A
  • behaviour activating system
17
Q

Mesocorticolimbic Circuitry:

A
  • initiates in the ventral tegmental
    area
  • travels along the mesolimbic
    pathway to the nucleus
    accumbens (linked to emotional
    processing)
  • mesocortical pathway originates
    from the ventral tegmental area
    and loops up into the prefrontal
    cortex and cingulate gyrus
  • cingulate gyrus is also linked to
    emotional processing
  • nucleus accumbens is the key
    structure in secreting the extra-
    cellular dopamine
18
Q

Nucleus Accumbens

A
  • inner core = linked to basal ganglia
    and implicated in movement
  • shell = part of amygdoloid
    complex and links into the limbic
    system and hence the reward-
    addiction pathway and responsible
    for the secretion of dopamine
19
Q

Dopaminergic processing in a normal reaction resulting in a

A

motivational state

20
Q

Reward-addiction: More than just Dopamine:

A

Opiates, cannabinoids and alcohol can act directly act on the nucleus accumbens via non-dopaminergic mechanisms

21
Q

Functions of the Reinforcement System:

A
  • detect reinforcing stimulus to
    recognise something positive has
    occurred and learning from
    experiences
  • strengthens neural connections
    via synaptic plasticity leading to
    long-term potentiation
22
Q

Dependence:

A

insert flowcharts

23
Q

Why do craving persist for years?

A

due to the previous homeostatic changes

the synaptic remodelling

24
Q

Cocaine and Amphetamines Effects:

A
  • psychosis; evidence of
    dopaminergic involvement in the
    positive symptoms of psychosis
  • cellular and molecular changes
    that promote dysregulation

can result in hypofrontality, in which there is decreased cerebral blood flow to the pre-frontal cortex

25
Q

Dopamine enhances Long0Term Potentiation:

A
  • dopamine binds to D1 receptor
  • modifies glutamatergic
    transmission allowing long term
    potentiation
  • synaptic remodelling: increased
    dendritic spine and branches
  • long term molecular and cellular
    changes remain months after
    abstinence
  • memories in these pathways may
    trigger relapse years later via
    associative learning
26
Q

Which dopamine receptors is found less in patients suffering with addiction?

A

D2 receptors

less found due to synaptic remodelling

impacts adversely upon classical conditioning (learning/memory) and motivational status

likely responsible for reduced sensitivity to natural rewards that often develops with addiction

27
Q

Why do patients who obtain abstinence often have mood disorders/ feel a lack of satisfaction in life?

A

Decrease in D2 receptors due to synaptic remodelling, which are highly implicated in motivation

the artificial reward triggers more dopamine than the natural reward

28
Q

What occurs on a molecular level to cause acute withdrawal symptoms in the context of opiate use?

A
  • opiate receptors present in
    mesocorticolimbic circuit
  • locus coeruleus is a noradrenergic
    nuclei, which is responsible for
    activating the fight or flight
    response
  • acute opiate use = acutely inhibits
    the firing of LC neurons
  • chronic opiate use = LC neurons
    return to normal firing rates due
    to compensatory mechanisms
  • in acute withdrawal:
    • substantial increase in LC firing
      • correlates with the physical
        withdrawal symptoms
      • triggers overactivation of the
        ANS
29
Q

Opiate Dependence: Treatment:

A
  • biopsychosocial interventions
  • stepwise process
  • needs to motivate patient
  • minimise harms related to taking
    substance
  • reduce criminal activity
30
Q

Alcohol:
- agonist?
- antagonist?

A
  • gaba agonist
  • NMDA antagonist

leads to inhibition of functioning of most voltage gated ion channels

alcohol leads to increased dopamine release in nucleus accumbulus and anticipation of alcohol in +ve valence

NMDA antagonism of cortical inputs to ventral tegmental area and inhibits dopaminergic neurons in this area resulting in increased dopamine release in nucleus accumbuls

31
Q

Alcohol Dependence Syndrome: Criteria:

A
  • strong desire/compulsion to take
    substance
  • difficulty in refraining from
    substance
  • physiological withdrawal state
    when substances have either been
    stopped or if dosage has been
    decreased. Physiological
    symptoms can be avoided by
    reintroducing the substance
  • evidence of tolerance
  • evidence of a progressive neglect
    of alternative pleasures or
    interests
  • persistent use of substance
    despite clear evidence of harm
32
Q

What are the acute effects of alcohol?

A
  • agonist at GABA
  • antagonist at NMDa
  • prevents influx of NA+, allows
    efflux of Cl-
  • less action potentials fired
33
Q

What are the molecular effects of chronic alcohol consumption?

A
  • downregulation of GABA receptors
  • upregulation of NMDA receptors
  • in the presence of alcohol firing
    rates return to normal as
    compensatory mechanisms allow
    the influx and efflux of ions as
    normal
34
Q

Alcohol Withdrawal:

A
  • absence of alcohol
  • firing rates increase as more influx
    and efflux due to compensation
  • alcohol not dampening the firing
    rates
  • agitation, tremors, confusion,
    seizures
35
Q

Alcohol Dependence Assessment:

A
  • extent of drinking
  • evidence of dependence
  • disabilities and co-morbidities
  • arrange psychiatric treatment for
    any co-morbid mental health
    problems
  • psychoeducation
  • motivation for change interview,
    self-help materials
36
Q

Treatment for Alcohol Dependence: Safe Withdrawal:

A

community based: benzodiazepines and oral thiamine

inpatient: same but management of complications

inpatient is better

37
Q

Treatment of Alcohol Dependence: Relapse:

A
  • outpatient follow-up
  • CBT
  • family therapy
  • vitamin supplementation
  • antidepressants for depression
  • assistance with employment,
    alcohol and legal issues