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psychology stage 3 > psychobiology of drug addiction > Flashcards

psychobiology of drug addiction Flashcards

1
Q

in 2021 how many drug related deaths were registered in England and Wales?

A

almost 5,000 deaths (according to office for national statistics)

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2
Q

how is a drug addiction characterised?

A
  • compulsion to seek out drug
  • loss of control in limiting intake of drug
  • negative emotions when access to drug is limited
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3
Q

is addiction a chronically relapsing disorder?

A

yes, most people who suffer with addiction will relapse

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4
Q

how does the DSM-V diagnose a substance use disorder?

A
  • 11 criteria
  • severity is determined based on the number of criteria the person meets
  • mild = 2-3
  • moderate = 4-5
  • severe = >6
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5
Q

when is someone most likely to get a diagnosis/ intervention?

A

when there starts to be impairment in day to day life

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6
Q

how many people stay abstinent without treatment?

A

around 12%

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7
Q

how many people stay abstinent with treatment?

A

around 30%

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8
Q

what is the average relapse rate for substance abuse disorders?

A

40-60%

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9
Q

do drugs impact neural circuits in the brain?

A

yes

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10
Q

are certain drugs more addictive than others?

A

yes

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11
Q

what is the learning process of addiction?

A

people become conditioned to a certain feeling and environment that is created from substance use (classical and operant conditioning)

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12
Q

how is an impulse control disorder characterised?

A
  • increased arousal before taking drug, regret after
  • positive reinforcement
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13
Q

how is a compulsive disorder characterised?

A
  • relief from stress or anxiety due to compulsion
  • negative reinforcement (negative feeling is take away from taking the drug)
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14
Q

when might people with an addiction realise it has became a problem

A

when they no longer use the substance for pleasure but instead use it to feel like they can function normally again

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15
Q

stages of addiction

A
  • binge/ intoxication
  • withdrawal/ negative affect
  • preoccupation/ anticipation
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16
Q

what is a possible explanation for why there is still such a high relapse rate with treatment?

A

treatments often do not target the mechanisms which lead to maladaptive behaviour
- usually try to modify behavioural symptoms when it may be the alterations in the brain that need treating

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17
Q

do different drugs impact the brain differently?

A

yes, through different mechanisms

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18
Q

what is the most common neurotransmitter that is influenced by drugs of abuse?

A

dopamine

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19
Q

what is comorbidity?

A

when individuals meet criteria for 2 or more disorders

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20
Q

what % of people receiving treatment for addiction also have another mental health disorder?

A

around 50-75%

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21
Q

how many individuals with a mental health disorder currently has (or has previously had) a substance abuse disorder?

A

25-50%

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22
Q

why can comorbidity be a problem?

A

it is difficult to determine which is causing the other, treatment should focus on the one that is causing the other

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23
Q

what did Friedman et al, 2013 find?

A

that there is not a great level of agreement (kappa) between different clinicians when diagnosing a patient

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24
Q

classical conditioning

A

associate an involuntary response with a stimulus
e.g. Pavlov’s dogs

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25
Q

operant conditioning

A

associate a voluntary behaviour with a consequence
e.g. Skinner box

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26
Q

positive reinforcement

A

behaviour followed by a reward

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27
Q

negative reinforcement

A

behaviour reinforced by taking away a negative stimulus as a result

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28
Q

positive reinforcement of drug use

A

the positive effects caused by the drug

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29
Q

negative reinforcement of drug use

A

more for addicted use - using the drug to take away the negative feelings of withdrawal
to take away a negative feeling

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30
Q

extinction in drug use

A

abstinence

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31
Q

definition of extinction in operant conditioning

A

disappearance of a conditioned response to a stimulus

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32
Q

meaning of spontaneous recovery in operant conditioning

A

the sudden reinstatement of a conditioned response to a stimulus

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33
Q

meaning of spontaneous recovery in relation to drug use

A

reinstatement of the conditioned response
relapse

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34
Q

spreading activation meaning in relation to drug use

A

associative process
may see a pub which may then remind the individual of drinking alcohol and the fun, reward, etc.

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35
Q

incentive salience

A

cognitive process that motivates an individual’s behaviour to or away from a certain stimulus

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36
Q

high incentive salience

A

high incentive salience will elicit motivation to pursue that stimuli for the reward it provides
- drugs typically have higher incentive salience than other rewarding behaviours which motivates drug users to engage in drug seeking

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37
Q

incentive-sensitisation theory

A

theory that drug addiction is the amplification of psychological ‘wanting’ without necessarily increasing ‘liking’

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38
Q

brain regions implicated in the incentive-sensitisation theory

A

neural changes after repeated drug use
- dopamine pathways in cortical regions linked to ‘wanting’
- dopamine pathways in dorsal striatum/ midbrain linked to ‘liking’

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39
Q

where is the ventral tegmental area (VTA) located?

A

midbrain

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40
Q

where is the nucleus accumbens (NAcc) located?

A

dorsal striatum

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41
Q

what neurotransmitter is released due to natural rewards?

A

dopamine

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42
Q

is cocaine a dopamine agonist?

A

yes

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43
Q

how does repeated drug use effect dopamine?

A
  • decreases in dopamine release (may be less in the vesicles)
  • decrease in DA2 receptors (downregulation)
  • then become reliant on external sources (drugs) for enhanced DA release
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44
Q

what did Volkow et al. (2001) find when comparing PET scans of meth users and control participants?

A
  • meth users had 24% less DA transporters in their striatum
  • after 14 months abstinence, DA transporters increased back to normal levels
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45
Q

what is the striatum involved in?

A

decision making, habit formation and reward

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46
Q

how is allostasis related to drug addiction?

A
  • previous reward point may have been changed by allostatic process
    addicts may no longer gain satisfaction from natural rewards
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47
Q

what is allostasis?

A

allostasis is the maintenance if physiological state around a setpoint that has deviated from the body’s normal setpoint
- process which changes the homeostatic setpoint

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48
Q

example of allostatic process in drug use

A

the dopamine level needed to feel reward may be raised in someone with an addiction
- repeated drug use does this
- eventually everyday things are no longer rewarding (anhedonia)

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49
Q

how do allostatic changes lead to craving and drug seeking behaviour?

A
  • brain adapts to new dopamine levels due to repeated drug use
  • when drugs are removed the reward circuits are ‘underwhelmed’
  • so this leads to negative reinforcement
  • drugs to reduce unpleasant withdrawal symptoms
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50
Q

opponent-process theory of drug addiction (theoretical model)

A
  • repeated drug use activates anti-reward processes
  • A process = occurs first, fast acting effects of drug, euphoric effect
  • B process = follows after, lasts longer, leads to withdrawal effects
  • the countereffects by the body (B process) become stronger and quicker which leads to shorter/ weaker experience of the drug
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51
Q

what does the B process do in the opponent-process theory of drug addiction?

A

opposes the drugs immediate effects (A process)

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52
Q

what is the B process for alcohol?

A

glutamate
- excitatory neurotransmitter as alcohol is inhibitory

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53
Q

what is the B process for opioid?

A

glutamate/ substance P

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54
Q

what is the B process for cocaine?

A

GABA
- inhibitory neurotransmitter as cocaine is excitatory

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55
Q

what is glutamate?

A

the most abundant excitatory neurotransmitter

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56
Q

does context/ environment play a role in B process (opponent-process theory)?

A

yes, in a certain environment due to associative learning the body may start releasing enzymes/ start its countereffects before you even take the drug
- how often overdose occurs in unfamiliar environment

57
Q

what enzyme is released to break down alcohol?

A

alcohol dehydrogenase
- this is a B process in the body for alcohol

58
Q

how does context environment effect the impact of drugs?

A
  • if you always consume drugs in a certain environment associative learning allows the body to start the B process before you even take the drug
  • so you would have a stronger tolerance for the drug in that environment
    -if you take the same amount of drug in an unfamiliar environment then it will have stronger effects
59
Q

study on rats that shows how environment can impact B processes/ cause overdose?

A
  • rats were injected with heroin in a certain cage
  • build up a tolerance in this environment
  • then the cages were swapped and the death rate of the rats doubled from 32.4% to 64.3%
    (old study, 1982)
60
Q

self-control model of addiction

A

behavioural control and inhibition is limited
- exerting control is an effort which causes fatigue and stress
- this then leads to stress-induced craving/ reinstatement

61
Q

what did Ferrari et al. (2009) find?

A

higher trait self-control was a predictor of abstinence from alcohol abuse, greater impulse control
- showing self-control is important component to prevent relapse

62
Q

areas of the brain involved in self-control

A
  • orbitofrontal cortex (OFC)
  • dorsolateral PFC (dlPFC)
  • anterior cingulate cortec (ACC)
63
Q

what was found by Wagner et al. (2013) in relation to self-control and the brain?

A

study looking at lack of self-control, used fMRI to look at a control vs. depleted group
- increased sensitivity to rewarding stimuli (OFC)
- decreased connectivity between OFC and dlPFC
- reduced inhibition
- poorer risk assessment and decision making

64
Q

what did Inzlicht et al. (2007) find in relation to self-control and the brain?

A
  • looked at control vs. depleted groups
  • EEG
  • diminished ACC activity (diminished impulse control)
  • less likely to detect errors in their behaviour
65
Q

where do most neurotransmitters start and project out from?

A

the midbrain

66
Q

areas of the midbrain involved in addiction

A
  • dorsal raphe nucleus (DRN)
  • ventral tegmental area (VTA)
  • substantia nigra (SN)
67
Q

ventral tegmental area (VTA) in addiction

A
  • ‘origin’ of reward pathways
  • dopamine projections
68
Q

substantia nigra (SN) in addiction

A
  • reward seeking
  • dopamine
69
Q

areas of the forebrain involved in addiction (subcortical structures)

A
  • thalamus
  • hypothalamus
  • hippocampus
  • amygdala
  • basal ganglia (several structures: NAcc particularly)
  • anterior cingulate cortex
70
Q

what is the role of the hypothalamus?

A

homeostasis

71
Q

what is the role of the hippocampus?

A

memory

72
Q

what is the role of the thalamus?

A

relay, signals go through the thalamus

73
Q

what is the role of the amygdala?

A

consolidates emotional memories (rewarding behaviours)

74
Q

what is the role of the nucleus accumbens (NAcc)?

A
  • works to make sure we don’t forget rewarding stimuli
  • reinforcement
  • stimulated by the VTA
  • key role in addiction
75
Q

what is the role of the anterior cingulate cortex?

A
  • impulse control
  • modulates emotional response
  • reward anticipation
76
Q

areas of the forebrain involved in addiction

A
  • dorsolateral PFC (dlPFC)
  • medial PFC (mPFC)
  • ventrolateral PFC (vlPFC)
  • obitofrontal cortex (OFC): ventromedial PFC
77
Q

what is the role of the dorsolateral PFC in addiction?

A
  • response selection
  • decision making and planning
  • risk assessment
78
Q

what is the role of the medial PFC in addiction?

A
  • retrieval of prior memories
  • reinstatement of drug seeking behaviour
79
Q

what is the role of the ventrolateral PFC in addiction?

A

inhibition

80
Q

what is the role of the ventromedial PFC in addiction?

A
  • assigns value to behaviour
  • estimates risk/ benefit
  • decision making
81
Q

which brain areas are involved in the self-control network?

A
  • dorsal anterior cingulate cortex (dACC) (conflict processing)
  • mPFC (memory retrieval)
  • rostral anterior cingulate cortex (rACC) (monitoring external cues)
  • dlPFC (response selection)
82
Q

which dopamine pathway is considered the start of addiction?

A

mesolimbic

83
Q

which dopamine pathway is considered to lead to the pursuit of drugs?

A

mesocortical

84
Q

mesolimbic dopamine pathway

A
  • cell bodies in VTA, axons terminate in limbic system
  • nucleus accumbens (NAcc), amygdala and hippocampus
85
Q

mesocortical dopamine pathway

A
  • cell bodies in VTA, axons terminate in PFC
  • motivation, behaviour planning and emotion regulation
86
Q

corticolimbic dopamine pathway

A
  • connections between PFC and limbic system
  • guides motivation and drug seeking
87
Q

pharmacokinetics

A

refers to how drugs pass through the body

87
Q

pharmacodynamics

A

refers to the physiological actions of drugs

88
Q

agonist drug

A

mimics neurotransmitter (high affinity to receptor) or increases prevalence/ effectiveness of natural neurotransmitters

89
Q

antagonist drug

A

blocks receptor to reduce effectiveness or decreases prevalence/ availability of natural neurotransmitter

90
Q

upregulation of receptors

A

increased receptors in postsynaptic neuron

91
Q

downregulation of receptors

A

decreased receptors in postsynaptic neuron
- chronic drug use can downregulate receptors = less sensitivity to the effects of NTs (tolerance)

92
Q

which DA receptors are excitatory?

A

D1 and D5

93
Q

which DA receptors are inhibitory?

A

D2, D3 and D4

94
Q

meso =

A

midbrain

95
Q

role of norepinephrine and epinephrine

A

promotes arousal and attention

96
Q

role of serotonin (5HT)

A

regulates mood, reduces anxiety

97
Q

role of acetylcholine (ACh)

A
  • arousal and attention
  • learning and memory
  • receptors - nicotinic and muscarinic
98
Q

endocannabinoids

A
  • produced by the body
  • involved in learning and memory
  • regulation of emotions
99
Q

processes involved in how drugs pass through the body (pharmacokinetics)

A

absorption
distribution
biotransformation
elimination

100
Q

what is the fastest route of drug administration?

A

intravenous
straight into the bloodstream

101
Q

bioavailability of drug

A

how much of the drug administered actually reaches its target (receptor)

102
Q

non-competitive antagonist

A

drug that does not bind to the same site as a neurotransmitter, but does prevent the neurotransmitter from activating the receptor

103
Q

competitive antagonist

A

drug that binds to the same site as a neurotransmitter, preventing a neurotransmitter from binding to the receptor

104
Q

non-competitive allosteric antagonist

A

means the chemicals no longer fit the receptor

105
Q

allosteric regulators

A
  • substance that binds to site on receptor and causes changes
  • non-competitive
  • can be agonist or antagonist
106
Q

positive allosteric modulator

A

substance that increases receptor affinity

107
Q

negative allosteric modulator

A

substance that decreases receptor affinity

108
Q

which receptors are common targets for positive or negative modulators?

A

GABA A receptors
- benzodiazepines enhance binding affinity for GABA, increasing the likelihood that NTs will bind (positive modulator)
- GABA is the primary inhibitory NT

109
Q

sensitisation in chronic drug use

A

adaptation that increases a drugs effects

110
Q

tolerance in chronic drug use

A

adaptation that reduces a drugs effects
- meaning higher doses are required to achieve desired effects

111
Q

pharmacokinetic tolerance (drug dispositional tolerance)

A
  • chronic use of a drug resulting in faster metabolism
  • reductions in the amount of drug reaching its action site
  • increased rate of drug to metabolites
112
Q

pharmacodynamic tolerance

A
  • reduced responsiveness at drug site of action
  • occurs due to change in number of receptors available to bind
113
Q

cross-tolerance

A

chronic use of one drug can result in tolerance of another drug with similar structure
- i.e. those addicted to heroin can tolerate a high dose of morphine

114
Q

biotransformation

A
  • what happens to a drug after they enter the bloodstream and before they leave the body
  • lipid-soluble drugs must be transformed into metabolites
115
Q

phase I biotransformation

A
  • cytochrome P450 enzymes catalyse reactions to biotransform the drug and make it less active and more hydrophilic
  • via oxidation, reduction or hydrolysis
116
Q

phase II biotransformation

A
  • conjunction
  • combining the drug with another molecule
  • often adding glucuronic acid
  • aim is to make the drug hydrophilic enough to be excreted
117
Q

where are the cytochrome P450 enzymes located?

A

in the hepatocytes in the liver and a few in the cells that line the GI tract
- these are the main system involved in drug metabolism

118
Q

do more lipid-soluble drugs get absorbed quicker than less lipid-soluble drugs?

A

yes

119
Q

half-life

A

time taken for the body to eliminate half the concentration of a drug

120
Q

cannabinoids

A

substances that act on cannabinoid receptors

121
Q

what is the psychoactive component in cannabis

A

THC

122
Q

endocannabinoids

A

naturally occurring, similar to cannabinoids

123
Q

what are endocannabinoids involved in?

A

learning, memory, emotional regulation and biological functioning
- which is why cannabinoids can effect these things

124
Q

how to cannabinoids influence dopamine?

A
  • activation of CB1 receptors in the brain and periphery leads to increased DA concentrations in the NAcc
  • this is indirect effect as they inhibit GABA neurons which then increases the activity of DA neurons, meaning they release more DA
125
Q

where does the reward during initial drug use come from?

A

comes from dopamine activity in the nucleus accumbens
- intense rewarding feeling so encoded as a strong memory

126
Q

what are the two components of the NAcc?

A

shell (liking) and core (wanting)

127
Q

what is the shell of the nucleus accumbens connected to?

A

VTA and hippocampus
- conditioning and learning

128
Q

what is the core of the nucleus accumbens connected to?

A

with the anterior cingulate cortex (ACC) and OFC
- motivation and goal-oriented behaviour

129
Q

direct dopamine agonists

A
  • trigger dopamine release
  • block dopamine reuptake
130
Q

drugs that are direct dopamine agonists

A

amphetamines
cocaine
MDMA

131
Q

indirect dopamine agonists

A
  • leads to dopamine release by activating other NT receptors
132
Q

examples of drugs that are indirect dopamine agonists

A

nicotine (acetylcholine)
alcohol (GABA)
THC (cannabinoid)

133
Q

examples of drugs that impact serotonin

A

amphetamines
cocaine
LSD

134
Q

examples of drugs that impact noradrenaline

A

amphetamines
cocaine

135
Q

examples of drugs that impact acetylcholine

A

nicotine (direct)
caffeine (lesser effect, indirect)

136
Q

pharmacokinetics

A

basic principles of drug absorption, distribution, metabolism, and excretion

137
Q
A

psychology stage 3 (1 decks)

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