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Year 1 Individual and Abnormal Psych > Abnormal - Martyn > Flashcards

Abnormal - Martyn Flashcards

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1
Q

What is a phobia?

A

An ‘irrational’ fear of an objectively ‘harmless’ stimulus or situation

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2
Q

Phobia example: Koumpounphobia

A
  • Fear of buttons
  • Surprisingly common (approx. 1 in 75.000)
  • Fear factor: hygiene, aesthetics
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3
Q

Classification of phobias in DSM-5

A

Type of anxiety disorder

3 broad categories of phobia:
Agoraphobia - public places/ outside home (complex)

Social phobia - being watched / appraised by others (complex)

Specific phobia - fear of a specific object/item or situation (simple)

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4
Q

What is agoraphobia

A
  • Complex disorder
  • Typically develops during adulthood (late 20s)
  • Often viewed as fear of open spaces but is more complicated
  • Better thought if as a fear of places which are difficult to escape is a panic attack is experienced (shopping malls, cinema etc.)
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5
Q

What is a social phobia?

A
  • Complex disorder
  • Typically develops during teenage years
  • Fear of embarrassment/humiliation in presence of others
  • Leads to avoidance of social situations (often comorbid with agoraphobia)
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6
Q

What are specific phobias?

A
  • Simple phobia
  • Fear of a particular object or situation
  • Occurs during childhood/teenage years

5 broad categories according to DSM-V:

  • Animals
  • Natural environment
  • Medical/injury related
  • Situational (e.g. airplane, driving, lifts)
  • Other types (clowns, vomiting, pope)
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7
Q

What causes a phobia?

Behavioural account

A
  • Acquired through experience of phobic stimulus paired with frightening/painful event
  • i.e. acquired through classical conditioning
  • ‘Little Albert’ most prominent example
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8
Q

Little Albert experiment

A

Watson & Rayner (1920)

  1. Albert presented with a rat (conditioned stimulus) and various other animals = no fear
  2. Albert presented with surprising loud noise (unconditioned stimulus) = fear (unconditioned response)
  3. Albert presented rat, this time paired with loud noise = fear
  4. Albert presented with rat = fear (conditioned response)
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9
Q

What is generalisation (phobias)

A

When stimuli similar to the phobic stimulus also produce a fear response

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10
Q

Social approach to the behavioural account of phobias

A
  • Bandura
  • Phobias can be learned from others not just the individual’s own experiences (vicarious learning)

Modelling - watching someone without phobia model behaviour with phobic stimulus can help those overcome fear

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11
Q

Problems with the behavioural account of phobia

A
  • Doesn’t always happen (getting a dog bite doesn’t always mean the person will have a phobia)
  • Many people with phobias can’t remember acquiring them
  • Small set of stimuli seem to form most phobias (spiders, snakes)
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12
Q

What causes a phobia?

Evolutionary explanation

A
  • Seligman (1971) introduced the preparedness theory of phobias
  • Agreed that conditioning was important
  • Suggested that evolution has rendered some stimuli more susceptible to phobias (spiders and snakes) than others (plug sockets, pylons)
  • Things that were dangerous to humans a while ago causes us to have more phobias towards them
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13
Q

Evolutionary evidence for phobias

A
  • Ohman et al, 1976
  • Paired images of neutral stimuli (flowers and mushrooms) and common phobias (spiders and snakes) with a mild electric shock
  • During an extinction phase spiders and snakes still produced fear, whilst flowers and mushrooms didn’t
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14
Q

Problems with the evolutionary account of phobias

A
  • Not all stimuli ‘prepared’ for learning actually pose a threat (e.g. small % of spiders actually harmful)
  • How do we determine the evolutionary origin of fears
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15
Q

What causes a phobia?

Cognitive account

A
  • We have faulty cognitions about a situation or object (Beck, 1976)
  • Overestimate the inherent danger in objects/situations
    We demonstrate an attentional bias to these stimuli
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16
Q

Treatments for phobias

A
  • Mostly behavioural
  • Systematic desensitisation
  • Flooding
  • Modelling
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17
Q

What is systematic desensitisation

A
  • Developed by Joseph Wolpe (1958) based on work with cats

Three key stages:
1. Relaxation training (using Jacobsonian progressive relaxation)

  1. Fear hierarchy - develop list of fearful situations (low-high)
  2. Counter-conditioning (pair phobic stimulus with relaxation)
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18
Q

What is flooding or implosion therapy

A
  • Extreme version of systematic desensitisation
  • Immediate/rapid exposure to either real (flooding) or imagines (implosion) version of phobic stimulus/situation
  • Phobic stimulus presented until maximum tolerable anxiety begins to diminish (patient habituates)
  • Rapid and effective according to Marks (1975) but can produce intense anxiety and induce panic attacks
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19
Q

What is modelling as a therapy

A
  • Social approach
  • Patient observes a therapist/peer ‘model’ successful interactions/behaviour with phobic stimulus
  • Bandura used his observations of those with snake phobias to form social learning theory (1977)
  • Mineka and Cook (1986) found that when young monkeys observed their parents display fear towards snakes, they too developed the fear
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20
Q

What is Schizophrenia?

A

A debilitating psychiatric condition which is characterised by the individual demonstrating a loss of contact with reality

21
Q

Early accounts of schizophrenia (Haslam)

A

John Haslam (1810)

  • Provided detailed notes of patient James Tilly Matthews
  • Patient believed he was being controlled by a mind machine, named ‘the air loom’
22
Q

Early accounts of schizophrenia (Morel)

A

Benedict Morel

  • Case of 13 year old boy whose previously brilliant intellect underwent rapid decay
  • Boy became withdrawn & displayed homicidal thoughts to his father
  • Termed the disorder “dementia praecox” (premature dementia)
  • Believed brain had degenerated –> hereditary
23
Q

Early accounts of schizophrenia (Kraepelin)

A

Emil Kraepelin

  • Described “dementia praecox” in detail
  • Believed mental deterioration in early life
  • Focused on aetiology –> suggested its hereditary
  • Considered physical abnormalities as signs of markers for conditions e.g. deformities of fingers and toes
24
Q

Early accounts of schizophrenia (Bleuler)

A

Eugen Bleuler

  • Disagreed with term “dementia praecox”
  • Believed it can appear before/after adolescence
  • Deterioration is not the only outcome
  • Focused on the psychological aspects of the condition and provided us with the diagnostic term ‘schizophrenia’
25
Q

Bleuler’s 4 fundamental psychological aspects of schizophrenia

A
  • Blunted affect (reduced emotional response to stimuli)
  • Loosening of associations (disordered/contradictory responses)
  • Ambivalence (unable to make decisions)
  • Loss of awareness of external events (preoccupied on internal world)
26
Q

Prevalence of schizophrenia

A
  • Affects approx. 1% of the population
  • Typically onset during 20-30
  • Affects men (tens/20s) and women equally (20s/30s)
27
Q

Positive symptoms of schizophrenia

A

An excess of experience (hearing thing that aren’t there)

  • Delusions (fixed beliefs that have no basis in fact)
  • Hallucinations (‘perceptions’ without external stimulus)
  • Disorganised thinking/speech/behaviour
28
Q

What are delusions in relation to schizophrenia

A

An erroneous belief held with conviction despite contradictory evidence

Different types of delusions e.g.:

  • Persecution (people plotting against individual)
  • Grandiose (person has great fame, power, wealth)

Very common approx. 90% diagnosed experience there (Cutting, 1995)

29
Q

What are hallucinations in relation to schizophrenia

A

A sensory experience without an external stimulus to provoke it

  • Auditory hallucinations are most common; approx. 70% (Sartorius, Shaprio & Jablensky, 1974)
  • Visual less common; approx. 40%
  • Other types approx. less than 10%

Not uncommon to hear voices at some point but not persistently (Crowe et al., 2011)

30
Q

Disordered thoughts, speech and behaviour (schizophrenia)

A

Thoughts: difficulty in concentrating - hard to complete tasks

Speech: difficulty in making sense - may jump around in conversation or appear to present logical sentences but have made up words (e.g. ‘air loom’). Sometimes may become a word salad

Behaviour: may dress oddly to others, demonstrates odd reactions

31
Q

Negative symptoms of schizophrenia

A

The absence of normal behaviour/experiences (appearing emotionless)

5 As

  • Blunted affect: reduced emotional response to stimuli
  • Alogia: diminished speech output, difficult to communicate with others
  • Anhedonia: inability to feel pleasure during enjoyable activities (emotionless)
  • Asociality: reduction in social initiative
  • Avolitation: inability to complete goal directed tasks due to lack of motivation or drive
32
Q

Cognitive symptoms of schizophrenia

A

Deficits in cognitive abilities (working memory, attention)

  • Difficulty in sustaining attention
  • Impaired working memory
  • Poor abstract thinking
  • Poor problem solving
  • Low psychomotor speed (e.g. reaction time tasks)
33
Q

What is the prodromal phase (schizophrenia)

A
  • Most (not all) go through a prodromal phase
  • Development of symptoms such as social withdrawal, loss of interest in normal activities
  • Occur before active-phase symptoms which marks the disturbance as schizophrenia
34
Q

What causes schizophrenia?

A
  • Genetics
  • Biology
  • Environment
  • Psychosocial factors
  • Gene x environment
35
Q

Role of genetics in schizophrenia

A

Greater % of genes share = greater risk of developing schizophrenia

  • 12.5% genes shared (3rd degree relatives e.g. cousins)
  • 25% genes shared (2nd degree relatives e.g. nieces, grandchildren, half siblings)
  • 50% genes shared (1st degree relatives e.g. siblings, parents)

MZ (identical) twins have concordance rates of 40-50%

  • Contenders for liability include DISC1, DTNBP1, NRG1 and RGS4 (Sullivan, 2005)
36
Q

Dopamine-hypothesis of schizophrenia

A
  • In 1950s, Chlorpromazine was used in clinical practice. Researchers noted tranquillising effect then noted anti-psychotic effect
  • Chlorpromazine prevents excess dopamine = reduce symptoms of disorder
  • L-Dopa given to Parkinson sufferers (linked with low levels of dopamine) = produce symptoms of schizophrenia
37
Q

Neurological damage with schizophrenia

A
  • Schizophrenics with negative and cognitive symptoms exhibit neurological damage
  • Enlarged ventricles commonly seen; correlated with decrease in volume of other areas e.g. Thalamus (Gaser et al., 2004)
38
Q

Neurological damage with schizophrenia - causes

A
  • Greater risk of schizophrenia if born in winter months
  • Greater risk of child experiencing schizophrenia if mother experiences influenza in 2nd trimester
  • Pregnancy complications: low birth weight, prolonged labour, umbilical cord around the neck
  • Maternal stress: High levels of stress to the mother during pregnancy = more likely to develop schizophrenia
  • Nutritional deficiency: lack of nutrients also implicated; those deprived of essential nutrients show greater rise of developing
39
Q

Psychosocial factors of schizophrenia: Family and emotional expression (EE)

A
  • Brown (1958) better to live alone or with siblings than parents or spouse after hospitalisation
  • Due to emotional expression = hospitality, criticism and emotional overinvolvement (based on interview with researcher)
  • Families with high EE = higher relapse (Vaughn & Jeff, 1976)
40
Q

Psychosocial factors of schizophrenia: Urban living

A
  • Pederson and Mortenson 2001
  • 1.9 mill Danish in sample
  • Registered on a national database which updates if they move
  • Children who lived in urban environments for their first 15 years were 2.17x more likely to develop schizophrenia
  • Unknown why urban living is bad in this contxt
41
Q

Psychosocial factors of schizophrenia: Immigration

A
  • Cantor-Grace and Selton 2005
  • First generation immigrants 2.7x more likely to develop schizophrenia
  • Second generation 4.5x greater risk
42
Q

Psychosocial factors of schizophrenia: Drug use

A
  • Certain drugs increase risk . of schizophrenia e.g. cannabis (amphetamines also induce symptoms of psychosis
  • A meta-analysis (Henquet et al., 2005) revealed that young heavy cannabis users were 2x as likely as non-users to develop schizophrenia
43
Q

Treatments for schizophrenia

A
  • Primarily treated as a biological disorder

Pharmacological approaches

  • Typical antipsychotics
  • Atypical antipsychotics

Psychosocial approaches

  • Family therapy
  • Social skills training
  • Cognitive remediation therapy
  • Cognitive behavioural therapy
44
Q

Pharmacological treatments for schizophrenia

A

Front line treatments consists of anti-psychotic drugs

2 main types:
- Typical anti-psychotics (first generation) developed during 1950s e.g. chlorpromazine; reduce positive symptoms

  • Atypical anti-psychotics (newer generation) developed during 1990s e.g. clozapine; reduce positive and negative symptoms
45
Q

Side effects of pharmacological treatment

A

Typical anti-psychotics - extrapyramidal side effects e.g. movement disorder such as tremor, facial movement

Atypical anti-psychotics - Reduction in extrapyramidal side effects, but weight gain

Non-adherence - issue with both treatments up to 74% of patients stop taking medication resulting in relapse

46
Q

Psychosocial treatments for schizophrenia: Family therapy

A
  • One of the most effective
  • As effective as anti-psychotics (McFarlane, 2016) in terms of preventing relapse
  • Includes elements of CBT
  • Family-patient partnership at heart of treatment; family act as collaborator (not the source of treatment)
  • Reduce levels of EE and educate about the disorder
  • Looks at coping skills
47
Q

Psychosocial treatments for schizophrenia: Social skills training

A
  • Social adjustment and obtaining employment are still low even with anti-psychotics
  • Goal is to provide training on improving social interactions
  • Uses some behaviour and modelling techniques with corrective feedback and role play
48
Q

Psychosocial treatments for schizophrenia: Cognitive remediation therapy

A
  • Cognitive performance tends to be poor over course of disorder thus aim is to provide training on improving cognitive performance
  • Teaches individual methods of strategic information processing
  • Individualises therapy and focuses on implementing strategies in the real world
  • Meta-analysis revealed that therapy not only produced effects in cognitive performance, but also in symptoms experienced and psychosocial functioning (McGurk et al., 2007)
49
Q

Psychosocial treatments for schizophrenia: Cognitive behavioural therapy

A
  • Not historically used but has been researched more recently
  • Goal is to explore nature of patient’s delusions and hallucinations and asses their validity
  • Evidence mixed, may help positive symptoms but not negative

Year 1 Individual and Abnormal Psych (4 decks)

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