Drug addiction Flashcards

1
Q

How is the reward pathway involved in addiction?

A

It reinforces the activity that caused activation of the pathway e.g. sex, food when hungry

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2
Q

How do amphetamines increase dopamine levels?

A

Directly stimulate transmission of dopamine

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3
Q

How does nicotine increase dopamine levels?

A

Stimulates dopamine neurons

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4
Q

How does cocaine increase dopamine levels?

A

Blocks the removal of dopamine from the synapse, so the brain receives constant messages of euphoria

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5
Q

How do alcohol, opioids and cannabis increase dopamine levels?

A

Suppress the action of GABA neurons and others that inhibit dopamine release

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6
Q

What is condition place preference?

A
  • Establish a side preference in the subject
  • Expose the subject to something pleasurable (e.g. a drug or food) when confined to one side
  • Test which side the subject prefers
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7
Q

What is the difference between crack cocaine and cocaine HCL?

A
  • Crack cocaine is free base of cocaine i.e. not water soluble so cannot inject or snort
  • Cocaine HCL is water soluble so can be snorted or injected
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8
Q

What do most highly addictive substances have in common in terms of route of administration and onset?

A

Most addictive substances have a fast onset and rapid decay - this is usually achieved via snorting or IV administration

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9
Q

Where does cocaine block dopamine reuptake?

A
  • Cocaine binds to DA transporter on the presynaptic terminal in the striatum (more specifically the nucleus accumbens)
  • Cocaine blocks the transporter from dopamine uptake
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10
Q

How do amphetamines increase dopamine release in the nucleus accumbens?

A
  • They mimic DA and get pumped into the presynaptic terminal into a vesicle, preventing DA from being pumped into the vesicle.
  • Thus leading to high levels of DA outside the synapse
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11
Q

How does this diagram demonstrate why cocaine is more likely to become addictive than methamphetamine?

A
  • Cocaine has a rapid uptake and rapid decay/clearance
  • Methamphetamine has a rapid uptake and slow clearance
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12
Q

How does nicotine stimulate dopamine release?

A
  • Through depolarisation of DA neurons.
  • Nicotinic channels are non-selective cation channels.
  • Calcium entry directly through receptor can supply enough calcium to trigger DA release
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13
Q

How is ethanol absorbed?

A

Rapidly (slowed by food), some metabolism in the gut, but most distributes to all tissues (inc. placenta –> FAS)

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14
Q

How is ethanol metabolised?

A
  • Via alcohol dehydrogenase (ADH) in the liver and gut.
  • Microsomal ethanol-oxidising enzyme (p450) kicks in above 0.1% blood ethanol i.e. when drunk
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15
Q

What are the 2 kinds of tolerance?

A
  • Metabolic (pharmacokinetic) tolerance
  • Functional (pharmacodynamic) tolerance
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16
Q

How are drugs like disulfram and antabuse supposed to stop alcoholics from wanting to drink?

A

They inhibit acetaldehyde dehydrogenase from converting acetaldehyde into acetic acid which causes nausea and vomiting (hangover symptoms)

17
Q

How does naltrexone work in alcohol and opioid dependence?

A
  • Blocks opioid receptors and blocks the effects of endogenous opioid peptides like dynorphin.
  • Dynorphin triggers drug seeking behaviours and decreases DA signalling in the nucleus accumbens
  • Thus naltrexone reduces the rewarding effects of alcohol and opioids
18
Q

How is acamprosate proposed to work as an anti-craving medication in alcoholism?

A
  • It is an anti-epileptic medication that may work by compensating for the increased excitability in the brains of alcoholics during withdrawal.
  • Thought to increase the activity of GABAa receptors while inhibiting glutamate receptor activity
19
Q

When would SSRIs be helpful in patients with alcoholism?

A

If they had co-morbid depression

20
Q

How is nalmefene proposed to work as an anti-craving medication in alcoholism?

A
  • Reduces craving presumably by antagonising the effects of endogenous opioid peptides.
  • Reduces the rewarding effects of alcohol.
  • Has a longer half-life than naltrexone, greater oral bioavailability and does not induce liver toxicity.
21
Q

What is the allostasis theory of addiction?

A
  • Starts with impulsive reward-seeking (drug experimentation)
  • With repeated exposure to the drug, pleasure effects diminish.
  • Thereafter compulsive drug use becomes dominant to avoid withdrawal.
  • Withdrawal causes negative reinforcement - “I need the drug because I feel sick” whereas before it was positive reinforcement, “I need the drug because it feels good”
22
Q

What are the 3 main stages of the addiction cycle?

A
  • Binge/intoxication - positive reinforcement
  • Withdrawal/ negative affect - negative reinforcement
  • Preoccupation/anticipation - craving