Psychiatric disorders. drug action and drug addiction Flashcards

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1
Q

illegal drugs?

A

Cocaine, opiates, LSD

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2
Q

legal drugs?

A

Nicotine, alcohol, caffeine

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3
Q

Antagonist Drugs

A

Inhibit transmission at the synapse – a process that would normally work at the synapse is slowing down
So it is Blocking the neurotransmitter

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4
Q

Agonist Drugs

A

Facilitate transmission at the synapse – speeding up a process that would normally work at the synapse
Increase effects of neurotransmitter, or mimic the neurotransmitter

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5
Q

What does it mean if a drug has a high affinity for a receptor?

A

it binds to that receptor (but may not activate the receptor) – at the synapse you have nuerotransmitters that lock in and some drugs can work by binding to these receptors which coud cause these receptors to continue facilitating the process or block them – could be sitting on these neurotransmitters so that other neurotransmitters cant fit there

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6
Q

what does it mean if a drug has a high efficacy for a receptor?

A

it has a tendency to activate the receptor – whether it fits to them or not, if it activates it and causes a process to continue

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7
Q

What does the drug do?

A

Drug is causing → sustained bursts of dopamine (usually inhibitory) → inhibits GABA (inhibitory transmitter) → increases activity in nucleus accumbens

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8
Q

Stimulant - Amphetamine (Speed)

A

DOPAMINE AGONIST (increase the effects of dopamine) - Stimulates dopamine synapses by increasing the release of dopamine from presynaptic terminal – not mimicking it, its increasing the release at the presynaptic terminal before the synapse so it will affect processes at the synapse in that way

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9
Q

Stimulant - Cocaine

A
DOPAMINE AGONIST (increase the effects of dopamine) - Blocks the reuptake of dopamine, thus prolonging effects
= accumulation of dopamine in the synaptic cleft
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10
Q

What happens in the brain when dopamine agonists (speed and cocaine) are taken?

A

Widespread reduction in activity in most of the brain apart from the nucleus accumbens

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11
Q

Why is there increased arousal when taking cocaine? (excitement, confidence, alertness)

A
  • Decreases background noise (Mattay et al 1996)
  • Increases the clarity of signals and thoughts
  • focused on one thing and aren’t distracted by background noise
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12
Q

Why is the consumption of dopamine agonists (cocaine and speed) followed by a crash/downfall?

A

because the dopamine washes away and can’t be replaced quick enough because there hasn’t been the normal turnover of dopamine - causes them to feel worse than the did before

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13
Q

Opiates?

A

Morphine and Heroine

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14
Q

What happens when you take morphine or heroine?

A
  • increases relaxation
  • decreases sensitivity to pain (useful as medicine)
  • mimics endorphins (naturally occurring chemicals in the brain)
  • inhibits GABA which increases dopamine
  • blocks hindbrain area which releases norepinephrine (which thus reduces memory storage and reduces stress)
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15
Q

Marijuana?

A
  • contains cannabinoids
  • binds to specific cannabinoid receptors
  • inhibits GABA release (increased dopamine)
  • cannabinoid receptors abundant in hypothalamus ( increases appetite although not hungry)
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16
Q

Botox?

A

ANTAGONIST
Blocks the release of acetylcholine at neuromuscular junctions (where you have information being transferred and causing your core muscles to contract) so if you are blocking acetylcholine at the neuromuscular junctions it means the muscles cant work – this is how the bacteria are working, but when you consume it it causes the blocking and the junction which causes paralysis
BUT in small doses can be used to reduce muscle tremors and cosmetically – Waller et al (2006)

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17
Q

is there a difference between wanting, needing and liking something?

A

Yes,

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18
Q

Withdrawal

A

User learns that the drug relives distress associated with withdrawal, and so craves it more during future withdrawal
So you crave the drug more through withdrawal

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19
Q

Varenicline - CHAMPIX

A

stimulates and binds to the nicotine receptors, so it it partly increases dopamine (small amount) but it also binding so it means that nicotine is having less of an effect , because those receptors are being blocked, it means that nicotine cant sit there. So this pathway between the noctine and stimulation of nicotine receptors is being effected and is being inhibited and stopping nicotine from having a negative effect- advised to continue smoking whilst taking it so you learn that nicotine doesn’t have an effect anymore – cigarette feels less exciting

20
Q

Alcohol addiction

A

continued use of a substance when it interferes with your life

21
Q

Type 1 alcoholism

A

late onset (after 25), gradual onset, equal men and women, less severe – few relatives with alcoholism

22
Q

Type 2 alcoholism

A
early onset (before 25), rapid onset, more men than women, severe – more relatives with alcoholism 
suggests genetic basis
23
Q

do sons of alcoholic fathers show predispositions to alcoholism?

A

yes!

  • show less than average intoxication
  • show greater decrease of stress
  • slightly smaller amygdala (increased risk taking?)
24
Q

Psychiatric disorders - main issues

A
  • understanding psychiatric disorders from a biological perspective
  • contribution of genetics, environment and personal experience
25
Q

Depression

A
  • feelings of extreme sadness and helplessness
  • severe enough to interfere with daily life, and can last for weeks or months rather than days
  • more about the absence of happiness
  • twice as common in women than man
  • 5% of population
26
Q

Fu et al (2002)

A

moderate degree of heritability to depression - close relatives more likely to get depression
(BUT not just to do with depression, close relatives are also more likely to get other disorders like anxiety, bipolar etc.)

27
Q

Lyon et al (1998)

A

Depression is more common among relatives with early onset of depression (before 30) - heritability?

28
Q

serotonin

A

low serotonin turnover associated with aggression and depression

29
Q

Caspi et al (2003)

A
  • association between gene controlling the serotonin transporter protein (controls repute process) and depression
    gene seems to affect how people cope with life experiences
  • classic example of interaction between life experience, environment and biology
    -you have short and long types of these genes
  • those with two short forms of this gene are more likely to have depressive episodes in response to stressful events
30
Q

postnatal (postpartum) depression

A
  • depression after giving birth

- 20% women (but only 0.1% have long lasting)

31
Q

Murphy-Ebernez et al (2006)

A

– postnatal depression runs in families (therefore genetic propensity?)

32
Q

Hall et al (2006)

A
  • postnatal depression is a normal reaction to childbirth
  • Suggests that the 20% could be a normal reaction to child birth but the 0.1% needs to be revised as maybe a genetic influence?
33
Q

Unipolar Disorder

A

vary between normality (normal way of dealing with the world) and depression (depressive episodes)

34
Q

Bipolar disorder

A

varying between mania (a very excitable and aroused interpretation of the world) and depression
-Increased metabolism during manic phases – a lot of brain activity (PET scans)

35
Q

Genetic component of Bipolar Disorder

A

more common in monozygotic twins (identical twins) etc. but this seems to increase risk rather than cause it – more about the life events and how they handle it

36
Q

Seasonal Affective Disorder

A
  • Depression associated with one season (usually winter)
  • Common near the poles where the nights are long -can affect circadian rhythms/ sleep
  • Less severe than major depression
  • Light therapy as treatment (affects biological clock)
37
Q

Schizophrenia

A

SPLIT refers to a division between emotional and intellectual experiences and behaviour – social context is different to their behaviour
hallucinations, delusions, thought disorder, movement disorder

38
Q

Postive Symptoms of Schizophrenia

A
  • delusions
  • halluncinations
  • disorganized – odd emotional displays,
  • thought disorder (not being able understand an abstract concept)
39
Q

Negative Symptoms of Schizophrenia

A
  • poor social interaction
  • poor speech
  • absent facial expression
40
Q

Problems with Schizophrenia

A
  • not all patients exhibit all symptoms
  • Difficult to diagnose, often confused with other conditions - - - Difficult to pinpoint a specific brain area
  • BUT PET scans have found activation in thalamus, hippocampus and auditory cortex during hallucinations
41
Q

Demographics of Schizophrenia

A
  • More common in men
  • Earlier onset in men
  • Present in 1% of the population- - - Equal proportions in all cultures/populations (although more diagnosis in developed countries)
  • Implies there is a genetic basis and is something us about us being human because it is common across all cultures
42
Q

Crow (1995)

A

byproduct of language, genes that code for lateralization of the brain (organization of the brain in terms of hemispheres) have normal variation

43
Q

Genetics of Schizophrenia

A
  • More likely in closely related individuals
  • not all genes that your genetic make up is made of are necessarily active – somethings are not expressed in your behaviour or phenotype
  • May not be one gene but instead a combination of genes interacting with the environment
44
Q

Neurodevelopmental hypothesis

A

abnormalities in the development of the nervous system before birth (prenatal) and in the newborn, supported by evidence like:

  1. Infections, poor nutrition, complicated delivery BUT only increases chance of schizophrenia slightly
  2. Some slight brain abnormalities in patients, suggesting subtle changes during development – interaction process
45
Q

Brain abnormalities in Schizophrenia

A
  1. Ventricles (fluid-filled spaces in the brain) larger, so less space for brain cells - small
  2. Prefrontal cortex damaged (working memory impaired) e.g. korsakoff syndrome – confabulations - make up stories (trouble understanding abstract concepts)
  3. Cell bodies are smaller in the hippocampus and prefrontal cortex (responsible for memory consolidation and working memory) - social interaction
  4. Less lateralization than most people (right planum temporale is larger or equal to the left, usually it is the other way around – wernickes area (which is important for language)!) - more likely to be left handed
46
Q

what is happening at the synapse in schizophrenia?

A
  • Abused drugs are associated with an excess of dopamine, and can cause psychosis
  • Dopamine hypothesis of schizophrenia = excess activity of dopamine synapses – psychosis we see in schizophrenia could be similar to the psychosis we see in drug abuse
  • Schizophrenia patients have twice as many dopamine receptors than other people - same when measured directly
  • Schizophrenia is also associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex
    o Glutamate hypothesis of schizophrenia = deficient activity at glutamate synapses
    o Related to dopamine – dopamine inhibits glutamate release and glutamate activates neurons that inhibit dopamine – still related to dopamine
    o Phencyclidine (PCP, angel dust) inhibits glutamate receptors and produces simial symptoms to schizophrenia – add to the glutamate hypothesis and that it could be something to do with that (hallucinations, thought disorder, memory loss)