2 - Addiction Flashcards

1
Q

what are the two classes of addiction?

A

substances
behavioural

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2
Q

what is the 3 stage course of alcohol/drug uses, misuse, addiction?

A
  • experimental use
  • increasingly regular use
  • spiralling dependence
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3
Q

drug abuse

A

when a substance is used in a manner that does not conform to social norms - do not have to be dependent or addicted

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4
Q

physical drug dependence

A

when an individual depends on drugs for normal physiological functioning and abstinence produces physical withdrawal reactions

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5
Q

psychological drug dependence

A

when acquiring or using drugs are a strong motivator of behaviour - compulsive use

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6
Q

drug addiction

A

the term typically used to emphasies psychological dependence - not a clinical diagnosis

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7
Q

how was drug misuse previously diagnosed? how is it diagnosed now?

A
  • previously substance dependence
  • now - substance use disorder
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8
Q

how is substance use disorder classified?

A

mild - 2-3 symptoms
moderate - 4-5 symptoms
severe - 6-7 symptoms

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9
Q

what area of the brain is the site of rewarding brain stimulation?

A

medial forebrain bundle

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10
Q

describe the experiment whereby the role of the medial forebrain bundle was discovered?

A
  • rat in box with lever
  • when lever pressed it shocked brain via electrode
  • when electrode was placed along medial forebrain bundle, it released dopamine
  • this was pleasurable for the rat, and so the rat picked the lever that delviered the shock, over the lever that delivered the food - even to the point of starvation
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11
Q

what is the acute effects of drugs of abuse on the nucleus accumbens?

A

substance use of amphetamines, cocaine, nicotine and morphine increase dopamine levels in the nucleus accumbens

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12
Q

where does the medial forebrain run between?

A

ventral tegmental area and nucleus accumbens
(VTA-NA pathway)

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13
Q

how does cocaine increase dopamine levels?

A

blocks the reuptake transporters on the post-synaptic neuron = increasing dopamine levels in synapse

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14
Q

how do opiates affect the GABA neurone?

A
  • inhibit GABA neuron
  • GABA itself has an inhibitory effect on dopamine system
  • acts as a double inhibition = initiation of nucleus accumbens
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15
Q

how does tolerance to drugs of abuse occur?

A
  • changes in endogenous dopamine release
  • decreased receptors, receptor densensitisation and down-regulation

mechanisms not fully understood

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16
Q

what is tolerance?

A

when an individual experiences a diminished response to a drug - there is a decreased effect or they need to take more for the same effect

17
Q

what are two common chronic effects of drug misuse?

A

tolerance
withdrawal

18
Q

what is withdrawal?

A
  • sudden cessation produces symptoms
  • changes to release and receptors means that functioning of pt depends on exogenous dopamine
  • without external stimulation - normal function is compromised
19
Q

why do some people become dependent on drugs?

A

GXE interaction
(genetics and environment)
- particularly changes in dopamine genes and availability of drugs

20
Q

what is the 3 stage clinical management of drug dependence?

A

acute - managment of withdrawal
medium term - harm reduction (short-term/long-term substitution)
long term - maintaining abstinence

21
Q

what proportion of people who undergo short term rehab/detox will relapse within 1 year of treatment?

22
Q

what 3 drugs can be used to prevent relapse in opiate dependency?

A
  • methadone - agonist
  • buprenorphine - partial agonist
  • naltrexone - antagonist
23
Q

when does fully developed withdrawal generally occur in drug dependent patients?

A

1-3 days after last use

25
many deaths in opiate addicts are accidental overdoses after detox - why does this occur?
* detox removes tolerance * when pt leaves detox facility and relapses, the quantity of the drug they take is too much for them now tolerance is gone
26
what is the aim of opiate maintenance treatments?
* aims to replace/substitute heroine through once daily dosing
27
why is opiate maintenance treatment beneficial?
* stops street use = reduces crime * oral administration so reduces IV risks, HIV * keeps pt in health care - easier to provide psychosocial treatment/support * easier withdrawal when ready due to flexible dosing
28
why is naltrexone not effective with pts?
* antagonist - blocks opiate receptor and leads to reduced dopamine activity * reduces cravings * but does not give pleasurable effect for pt, and so there is a real lack of adherence
29
what is a risk associated with opiates that we want to avoid with substitution pharmacotherapy?
respiratory depression
30
when might naltrexone be used clinically?
often only used in criminal justice system, where a person has to take it to avoid prison sentence
31
what are 3 main psychological treatments involved in opiate addictions?
* motivational interviewing * community reinforcement - pt can earn 'tokens'/money with clean urine samples * relapse prevention - CBT, skills training/practising saying no, alternative cognitions, lifestyle changes
32
how are drugs classified in the UK?
class A class B class C temporary drug classes - can be here for 1 year whilst they decide how it should be classified
33
what is drug decriminalisation?
when drug use and posession does not result in criminal charges - may be replaced with civil penalties such as referral to eduction or treatmnet programme
34
what was the findings of the 2010 lancet report into mortality and drugs?
alcohol was overall the most harmful drug when combining harm done to user and harm done to others
35
describe the 4 stages of cocaine addiction, with reference to postsynaptic receptors and the amount of DA in the synapes?
1. normal - normal DA and normal postsynaptic receptors 2. acute use - increased dopamine in synapes, cocaine blockade at reuptake 3. chronic use - normal DA in synapse, cocaine blockade at reuptake, decreased postsynaptic receptors 4. withdrawal - decreased DA in synapse, decreased postsynaptic receptors
36
Label this brain region that is involved in rewards and dopamine
37