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PSY1016 Biological Psychology with Research Methods 1 > 5- Psychoactive Drugs > Flashcards

5- Psychoactive Drugs Flashcards

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1
Q

5 types of drugs that act on the dopamine system

A

L-DOPA
Antipsychotic drugs
Recreational drugs
Cocaine
Amphetamine

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2
Q

What does L-DOPA treat?

A

Parkinson’s disease

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2
Q

What is Parkinson’s caused by?

A

A loss of dopamine neurons

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2
Q

What do Parkinson’s patients have difficulty doing?

A

Initiating movements

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2
Q

How does L-DOPA treat Parkinson’s?

A

Compensates for the loss of neurons

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3
Q

What can L-DOPA do to make dopamine?

A

Cross the blood-brain barrier and enzymes in neurons convert precursor to dopamine

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4
Q

How does L-DOPA cause relief from Parkinson’s symptoms?

A

It increases in the brain

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5
Q

What side effects are common with L-DOPA?

A

Hallucinations, delusions, other psychotic symptoms

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6
Q

What do antipsychotic drugs treat?

A

Psychotic disorders

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7
Q

What is schizophrenia caused by?

A

An excess of dopamine- thought to be an excess of mesolimbic dopamine

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8
Q

How do antipsychotic drugs operate?

A

By interfering with dopamine receptors in the brain- acting as blockers

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9
Q

What receptor do antipsychotic drugs block?

A

D2

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10
Q

What do antipsychotic drugs reduce operation of?

A

The dopamine system

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11
Q

What does antipsychotic drugs efficacy hinge on?

A

Ability to bind to a D2 receptor

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12
Q

What is the side effect of antipsychotic drugs often binding to nigrostriatal pathways by mistake?

A

Can affect motor functions- very similar to Parkinson’s disease

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13
Q

Why is dopamine implicated in recreational drugs?

A

Dopamine is involved in producing reward and pleasure

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14
Q

What was cocaine previously used as?

A

As mental illness treatment and a coca-cola ingredient

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15
Q

When and why was cocaine banned?

A

In 1922 because people became aware of harmful effects

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16
Q

Short-term effects of cocaine use (7 points)

A
  • Increased energy levels
  • Decreased appetite
  • Mental alertness
  • Increased heart rate and blood pressure
  • Constricted blood vessels
  • Increased temperature
  • Dilated pupils
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17
Q

Long-term effects of cocaine use (5 points)

A
  • High risk of addiction
  • Irritability and mood disturbances
  • Restlessness
  • Paranoia
  • Auditory hallucinations
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17
Q

Medical consequences of cocaine use (4 points)

A
  • Cardiovascular (disturbances in heart rhythms, heart attacks)
  • Respiratory (chest pain, respiratory failure)
  • Neurological (strokes, seizures, headaches)
  • Gastrointestinal (abdominal pain, nausea)
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18
Q

How does cocaine increase dopamine levels?

A

By inhibiting reuptake

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19
Q

What happens when cocaine blocks the transporter opening?

A

It closes the passage and prevents the transporter from doing its job so dopamine remains high in the synapse

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20
Q

What are amphetamine effects similar to?

A

Cocaine effects

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21
Q

Amphetamine effects at low doses (7 points)

A
  • Energised and attentive
  • Mood improvement
  • Reduced appetite
  • Increased wakefulness
  • Improved reaction time
  • Fatigue resistance
  • Increased muscle strength
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22
Q

Amphetamine effects at higher doses (3 points)

A
  • Risk of psychosis
  • Addiction
  • Risk of seizure, stroke, coma, heart attack
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23
Q

What are amphetamines prescribed for?

A

ADHD, narcolepsy, obesity, depression

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24
Q

Why are amphetamines rarely prescribed now?

A

As there is a high risk of harm

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25
Q

What do amphetamines cause the neuron to do?

A

Release more dopamine

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26
Q

What do amphetamines disrupt?

A

Storage of dopamine into vesicles

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27
Q

With amphetamines, dopamine is released without…

A

Triggering an action potential

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28
Q

What is the difference between amphetamines and cocaine?

A

Amphetamines are less euphoric but more stimulating than cocaine

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29
Q

How are amphetamines similar to cocaine? (2 points)

A
  1. Increased dopamine signalling in the mesolimbic pathway
  2. Increased dopamine in the nigrostriatal pathway leads to enhanced basal ganglia and thalamic activity
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30
Q

3 types of drugs that act on the serotonin system

A
  1. Selective serotonin reuptake inhibitors (SSRIs)
  2. MDMA (ectasy)
  3. Hallucinogens
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31
Q

Example of an SSRI

A

Prozac

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32
Q

How do SSRIs inhibit reuptake of serotonin?

A

By blocking transporter

33
Q

What can more serotonin in the synapse exert influence on?

A

Other neurons

34
Q

Are all patients responsive to SSRIs?

A

No

35
Q

What is the half-life of fluoxetine (prozac)?

A

1-4 days

36
Q

What does MDMA trigger a neuron to do?

A

Release more serotonin

37
Q

How does MDMA enter a cell?

A

Via a passage of serotonergic transporter and triggers release of serotonin

38
Q

What can MDMA also have effects on?

A

Norepinephrine and dopamine transporters

39
Q

What does MDMA indirectly increase?

A

Hormones such as oxytocin

40
Q

What is the duration of MDMA action?

A

4-6 hours

41
Q

How long does it take for serotonin levels to normalise with MDMA?

A

Within 24-48 hours

42
Q

Do hallucinogens act as agonists or antagonists?

A

Agonists

43
Q

What can hallucinogens cause?

A

Distortion in a person’s perception of reality, and can cause changes in thoughts, moods and consciousness

44
Q

4 examples of hallucinogens

A

LSD
Psilocin
Mescaline
DMT

45
Q

What is the discussion regarding hallucinogens and SSRIs?

A

Whether hallucinogens should be used as a therapeutic treatment when people aren’t responsive to SSRIs

46
Q

What area does nicotine bind to nicotonic receptors and what does this lead to?

A

Ventral tegmental area, leads to neural activity that triggers release of dopamine in the mesolimbic pathway

47
Q

When is nicotine released?

A

By burning a cigarette

48
Q

What is smoking a major risk factor? (6 points)

A

Heart attacks
Strokes
Bronchitis
Cancers
High blood pressure
Alzheimer’s disease

49
Q

How addictive is nicotine?

A

Highly

50
Q

Effects nicotine has on the central nervous system (4 points)

A
  • Pleasure
  • Arousal and enhanced vigilance
  • Improved task performance
  • Anxiety relief
51
Q

Effects of nicotine on the cardiovascular system (5 points)

A
  • Increased heart rate
  • Increased cardiac output
  • Increased blood pressure
  • Coronary vasoconstriction
  • Cutaneous vasoconstriction
52
Q

Effects of nicotine on other systems (3 points)

A
  • Appetite suppression
  • Increased metabolic rate
  • Skeletal muscle relaxation
53
Q

What is the half-life of nicotine?

A

30 minutes

54
Q

3 individual differences in elimination of nicotine

A

Smokers metabolise faster
Gender differences
Genetic differences

55
Q

What is the most widely consumed stimulant?

A

Caffeine

56
Q

What is the caffeine molecule structurally similar to?

A

Adenosine

57
Q

What is adenosine?

A

An inhibitory neurotransmitter that suppresses CNS activities

58
Q

What does caffeine do to adenosine receptors?

A

Block them

59
Q

What can caffeine cause?

A

Increased release of other neurotransmitters

60
Q

Effects of caffeine in the cortex at normal doses (4 points)

A
  • Rewarding effect, feel competent
  • Alertness, sustained attention, faster thought
  • Reduced fatigue, lower need for sleep
  • Fine motor coordination, timing accuracy and arithmetic may be impaired
61
Q

Effects of caffeine with heavy doses (5 points)

A
  • Agitation
  • Anxiety
  • Tremors
  • Panting
  • Insomnia
62
Q

How long does it take for caffeine to be absorbed?

A

Within 45 minutes

63
Q

How is caffeine distributed?

A

Rapidly, circulating through body

64
Q

How big are caffeine molecules?

A

Small enough to cross the blood-brain barrier

65
Q

Why does the half-life of caffeine vary?

A

According to liver enzyme level

66
Q

Why are some people more sensitive to caffeine?

A

They have more efficient metabolism due to enzymes

67
Q

What is the major psychoactive ingredient in cannabis/marijuana?

A

Tetrahydrocannabinol

68
Q

What receptor does cannabis bind to?

A

The cannaboid CB1 receptor

69
Q

What does cannabis trigger?

A

The release of dopamine

70
Q

What does the mesolimbic dopamine release from cannabis lead to?

A

Feelings of euphoria

71
Q

2 potential medical benefits of cannabis

A

Can act as a painkiller for chronic pain
Can be as effective as opioids

72
Q

2 consequences of long-term habitual cannabis use

A

Associated with a decline in memory function
More brain tissue loss the longer cannabis is smoked regularly

73
Q

What is another word for alcohol?

A

Ethanol

74
Q

How is alcohol function at a cellular level understood?

A

Poorly

75
Q

How is alcohol a depressant?

A

It suppresses neural activities in the CNS

76
Q

What mechanism is involved in alcohol?

A

Alcohol triggers release of GABA and leads brain into a ‘sedation’ state

77
Q

What does alcohol increase release in?

A

Dopamine in the mesolimbic pathway

78
Q

2 things that alcohol decreases

A
  • Serotonin and noradrenaline: increases risk of depression
  • Glutamate: impaired memory
79
Q

3 things alcohol increases

A
  • Dopamine in the brain reward circuit
  • Endogenous opiates
  • GABA: sedation, motor impairments
80
Q

How does alcohol cross the blood-brain barrier?

A

Easily by diffusion

81
Q

How is alcohol metabolised?

A

By liver

82
Q

What is alcohol transformed to?

A

Water and CO2

83
Q

What is Korsakoff’s syndrome?

A

A chronic memory disorder

84
Q

2 consequences of Korsakoff’s syndrome

A
  • Persistent learning and memory problems (retrograde and anterograde amnesia)
  • Action coordination difficulty
85
Q

What is heavy alcohol use linked to in the brain?

A

Brain shrinkage particularly in prefrontal lobes

PSY1016 Biological Psychology with Research Methods 1 (34 decks)

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