Psychiatric Disorders, Drug Action and Addiction Flashcards

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1
Q

What are drugs?

A

Tend to imitate substances already present in our nervous system, particularly those that affect transmission at the synapse

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2
Q

Why do drugs tend to imitate substances already present in our nervous system

A
  • Mainly from plants (e.g. nicotine - tobacco plant)
  • The plant produces these chemicals to attract insects, to stop being eaten etc., or for own processes
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3
Q

Name the 2 ways that drugs affect transmission at the synapsy

A
  • Antagonist
  • Agonist
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4
Q

Describe an Antagonistic drug

A
  • Inhibit transmission at the synapse
  • Block neurotransmitter
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5
Q

Describe an Agonistic drug

A
  • Facilitate transmission at the synapse
  • Increase effects of neurotransmitter, or mimic the neurotransmitter
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6
Q

How much affinity do drugs have?

A

Drug has a high affinity for a receptor if it binds to that receptor

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7
Q

How much efficacy do drugs have?

A

Drug has a high efficacy if it has a tendency to activate that receptor

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8
Q

What do most drugs stimulate?

A

Most drugs stimulate the release of dopamine

Particularly in the nucleus accumbens

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9
Q

Define the nucleus accumbens

A

small subcortical area rich in dopamine receptors

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10
Q

How do drugs work?

(diagram)

A
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11
Q

Name 2 stimulants?

A

> Amphetamine (Speed)

> Cocaine

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12
Q

What does Speed do?

A

Stimulates dopamine synapses by increasing the release of dopamine from presynaptic terminal

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13
Q

What does Cocaine do?

A

Blocks the reuptake of dopamine, thus prolonging effects

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14
Q

Why are stimulants followed by a crash?

A

Dopamine washes away, can’t be replaced quick enough

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15
Q

Name 2 Opiates

A

> Morphine

> Heroine

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16
Q

How do Opiates work?

A
  1. Inhibits GABA, so increases dopamine
  2. Also blocks a hindbrain area that usually releases norepinepherine
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17
Q

What does Marijuana consist of

A

> Contains cannabinoids

> Bind to specific cannabinoid receptors (widespread in the brain)

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18
Q

What does marijuana do to the brain?

A
  1. Inhibit GABA release (increase in dopamine release in nucleus accumbens) = perception of heightened awareness
  2. Cannabinoid receptors abundant in hypothalamus (feeding!) = increased appetite
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19
Q

How do the functioning of drugs relate to addiction?

A
  • Many addictive substances increase activity at dopamine synapses
  • Particularly in the nucleus accumbens
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20
Q

What is the difference between liking and wanting drugs?

A

Drugs increase ‘need’ for the substance even if the experience is not pleasant

  • Mice with increased dopamine production showed no more pleasure in food, but made more effort to get it
  • Mice with decreased dopamine production made less effort to get food, but ate just as much.

(Kalat)

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21
Q

How does the sensitization of the nucleus accumbens relate to drugs?

A

– Becomes more sensitive to substances after repeated use

– Increased ability to release dopamine in response to the substance

– Reduced sensitivity to other things

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22
Q

How does the withdrawal symptoms of drugs relate to addiction

A

– Cravings for the drug

– Relapse causes increased sensitivity

– User learns that the drug relieves distress associated with withdrawal, and so craves it more during future withdrawal

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23
Q

Name something that can counter addiction

A

Varenicline (CHAMPIX), treatment for smoking

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24
Q

What is the functio of valenicline

A

Partial nicotine receptor agonist.

Stimulates and binds the nicotine agonist

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25
Q

How does alcohol affect the brain?

A

Alcohol acts on many areas of the brain – mainly inhibitory effects

26
Q

State the 2 types of alcoholism

A

Type 1 and 2

27
Q

Describe Type 1 alcoholism

A

Late onset (after 25)

Gradual onset

Equal men and women

Less severe

28
Q

Describe Type 2 alcoholism

A

Early onset (before 25)

Rapid onset

More men than women

Severe

29
Q

Can Genes influence alcoholism?

A

Genes might influence alcoholism in many ways (not as simple as ‘a gene for alcoholism’

30
Q

Give an example of how genes may influence alcoholism

A
  1. Coding for an increase in risk taking behaviour
  2. Coding for an increased stress response = more likely to relapse after quitting
31
Q

Do sons of alcoholic fathers show predispositions to alcoholism?

A
  1. Show less than average intoxication – tolerance to alcohol
  2. Show greater decrease of stress when drinking
  3. Slightly smaller amygdala (therefore increased risk taking?)
32
Q

Define Clinical/Major 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

33
Q

Can Serotonin be a cause of depression?

A

low serotonin turnover associated with aggression AND depression

So genes controlling serotonin have been implicated

34
Q

What study supports the suggestion that serotonin might be a cause of depression

A

Caspi et al. (2003)

35
Q

What did Caspi et al. (2003) find?

A
  • gene controlling the serotonin transporter protein
  • this protein controls the ability of an axon to reabsorb serotonin (recycling)
36
Q

What types of depression genes are there, and how do they affect a person’s depression

A

Short and long types

If you have two short forms of the gene = more likely to have depression in response to stressful events

37
Q

Define Postnatal Depression (postpartum)

A

Depression after giving birth

38
Q

Define Unipolar Disorder

A

Varying between normality and depression

39
Q

Define Bipolar Disorder

A

Varying between mania and depression (formally manic depression)

40
Q

How is Bipolar disorder treated?

A

Treated with lithium salts - Block synthesis of arachidonic acid (associated with brain inflammation)

41
Q

What does SAD stand for?

A

Seasonal Affective Disorder (SAD)

42
Q

What is Seasonal Affective Disorder?

A
  • depression associated with one season (usually winter)
  • common near the poles where the nights are long (circadian rhythms!)
  • less severe than major depression
  • light therapy as treatment (affects biological clock)
43
Q

Define Schizophrenia

A

‘Split Mind’

the SPLIT refers to a division between emotional and intellectual experiences and behaviour

44
Q

What are the symptoms of schizophrenia

A

Some patients show inappropriate emotional expression that seems detached from current circumstances

Hallucinations, delusions, thought disorder, movement disorder

Can be acute or chronic

45
Q

Name the types of symptoms in schizophrenia

A

> Positive Symptoms (additions)

> Negative Symptoms (absences)

46
Q

Name the two types of positive symptoms in schizophrenia

A

Psychotic - delusions and halucinations

Disorganised - odd emotional and thought disorder

47
Q

Name the 3 types of negative symptoms of schizophrenia

A

> Poor social interaction

> Poor speech

> absent facial expression

48
Q

Name the problem with schizophrenia

A

Not all patients exhibit all symptoms

  • difficult to diagnose, often confused with other conditions
  • difficult to pinpoint a specific brain area
49
Q

What demographic data is there about schizophrenia

A

More common in men Earlier onset in men

Present in 1% of the population

Equal proportions in all cultures/populations

50
Q

What did Kalat find?

A

It is more likely to develop in closely related individuals (i.e. MZ twins or a child of two schizophrenic parents)

51
Q

What did Kalat’s findings suggest?

A

May not be one gene, but instead a combination of genes interacting with the environment

52
Q

Name 2 ways which are theorised to be the cause of development of schizophrenia?

A

Neurodevelopmental hypothesis

Brain abnormalities

53
Q

Define Neurodevelopmental hypothesis

A

abnormalities in the development of the nervous system before birth (prenatal) and in the newborn

54
Q

Explain the Neurodevelopmental hypothesis

A
  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
55
Q

Name Brain Abnormalities of Schizophrenic

A
  1. Ventricles larger, so less space for brain cells
  2. Prefrontal cortex damaged
  3. Cell bodies are smaller in the hippocampus and prefrontal cortex
  4. Less lateralisation than most people
56
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60
Q
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