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
Dopamine enhances Long0Term Potentiation:
- 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
Which dopamine receptors is found less in patients suffering with addiction?
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
Why do patients who obtain abstinence often have mood disorders/ feel a lack of satisfaction in life?
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
What occurs on a molecular level to cause acute withdrawal symptoms in the context of opiate use?
- 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
Opiate Dependence: Treatment:
- biopsychosocial interventions - stepwise process - needs to motivate patient - minimise harms related to taking substance - reduce criminal activity
30
Alcohol: - agonist? - antagonist?
- 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
Alcohol Dependence Syndrome: Criteria:
- 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
What are the acute effects of alcohol?
- agonist at GABA - antagonist at NMDa - prevents influx of NA+, allows efflux of Cl- - less action potentials fired
33
What are the molecular effects of chronic alcohol consumption?
- 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
Alcohol Withdrawal:
- 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
Alcohol Dependence Assessment:
- 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
Treatment for Alcohol Dependence: Safe Withdrawal:
community based: benzodiazepines and oral thiamine inpatient: same but management of complications inpatient is better
37
Treatment of Alcohol Dependence: Relapse:
- outpatient follow-up - CBT - family therapy - vitamin supplementation - antidepressants for depression - assistance with employment, alcohol and legal issues