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Year 1 Individual and Abnormal Psych > Abnormal Psychology - Heather > Flashcards

Abnormal Psychology - Heather Flashcards

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1
Q

Diathesis definition

A

An individual’s vulnerability toward having a particular abnormality or disease

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2
Q

Criteria for defining abnormal behaviour

A
  1. Personal distress - subjective experience of suffering
  2. Statistical rarity - has unusual behaviours (e.g. binge eating)
  3. Maladaptive behaviour - has impaired functioning (e.g. insomnia, poor reality testing)
  4. Violation of social norms - exhibits behaviour that is socially undesirable
  5. Danger to self or others - usually dangerous to self via poor judgement
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3
Q

Anhedonia definition

A

The condition of not being able to feel pleasure

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4
Q

Comorbidity definition

A

Meeting the diagnostic criteria for more than one disorder

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5
Q

Edwin Smith papyrus

A

Descriptions of treatment of wounds and surgical operations

Brain was described as the site of mental functions

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6
Q

Ebers papyrus

A

Treatment and magic to cure abnormal behaviour with no known cause - gave more detailed insight into psychopathology than edwin smith
Small section about psychiatry - separate from normal health. Described disorders relating to depression, concentration and emotions.

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7
Q

Indian scriptures that helped develop modern day psychology

A

Approx. 300 BC

Ramayana - gave clear explanations of depression and anxiety

Sharaka Samihaita - text on psychiatry e.g. personality disorders.

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8
Q

Historical perspectives of abnormal behaviour

A

Demonology (450-1000AD):

  • Possession by evil spirits
  • Exorcism
  • May have been a conflict between the gods that causes abnormal behaviour (Greeks and Romans)
  • Common in China, Babylon and Peru
  • China used acupuncture to treat abnormal behaviours
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9
Q

Philosophy and Medicine (Hippocrates)

A

Father of modern medicine

Believed that mental disorders had natural causes - organic nature
Can be heredity, can have a disposition towards a disorder or could have had a head injury - beginnings of psychology being a medical model.

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10
Q

Hippocrates’ 3 categories of mental disorders

A
  1. Melancholia - depression
  2. Mania - bipolar/manic episodes
  3. Phrenitis - inflammation of the brain
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11
Q

4 humors

A

Blood (sanguis) - optimistic, cheerful, unafraid

Phlegm - consistant, relaxed, compassionate.

Bile (choler) - energetic, passionate, bad-tempered

Black bile (melancholia) - thoughtful, depressed, reflective.

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12
Q

World views on treating mental illness

A

Greek - music and dance
Chinese - acupuncture
Roman - massages

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13
Q

Galen

A

First to suggest that blood flows through arteries
Drove forward the medical model
First to talk about the anatomy and the nervous system
Functions of the brain were the foremost causes of mental illnesses.

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14
Q

Medieval times (456-1450 AD)

A

Possession was the most common belief of abnormal traits

Treatments were beating out the devil and exorcisms performed by the church

First mental hospital was opened in Bhagdad in AD 792

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15
Q

Avicenna

A

Islamic physician between 980-1037 AD

Wrote the canon of medicine
Born in Uzbekistan
Made huge contributions to hysteria, mania, melancholia and epilepsy

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16
Q

Avicenna - Prince of Persia

A

Prince of Persia thought he was a cow and was very malnourished because he wouldn’t eat. Avicenna used reverse psychology and said he was the butcher but couldn’t kill the cow as it was too skinny. The prince started eating again and the delusions stopped.

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17
Q

Mass madness

A

Mania and hysteria

Persecution of 100,000 people, mostly women who were though to be witches (15th-17th century)

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18
Q

Salem Witch Trials

A

Spiritually mad were thought to be witches
1962 in Massachusetts
Hanging of 19 men and women
Epidemic of small-pox arised at this time
Disorder was caused by the stress of the threat of the disease

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19
Q

European and American Asylums

A

A humanitarian approach was taken to asylum reforms
Paracelsus (1490-1541) looked at madness as a disease
He believed in astral influences on behaviour (e.g. horoscopes)

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20
Q

Biological model of psychopathology

A
  • Medical model of psychology
  • Organic causes
  • Diseases like any physical disease
  • Pathology underlies symptoms
  • Wilhelm Greisinger (1817-1868), Emil Kraepelin (1856-1926)
  • Study of syphilis advanced the idea of a biological basis to psychopathology
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21
Q

Biological basis of abnormal behaviour

A
  • Psychopathology is the product of specific diseases

- A physical form of treatment will cure the problem e.g. ECT, drugs, hysterectomy

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22
Q

Achievements of the medical model of psychopathology

A
  • Progressively more humane treatments based on illness concepts
  • Mental health legislation
  • Classification system made by Kraepelin in 11883 is similar to that for physical diseases
  • Many technological advancements e.g. CT, MRI, PET and fMRI
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23
Q

Problems of the medical model of psychopathology

A
  • Organic factors can’t explain all psychopathologies
  • Abnormal behaviour can’t always be organised into discrete categories with biological explanations
  • Medication has side effects
  • Mental health legislation can be abused to limit the freedom of people with psychological problems
  • Marginalises non-biological specialities

Look at models of psychopathology powerpoint for more

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24
Q

Psychodynamic model of psychopathology

A
  • Sigmund Freud 1856-1939
  • Psychopathology due to psychological forces that unconsciously influence the mind
  • Behaviour is a result of conflicts between three psychic or mind structures (Id, Ego & Superego)
  • Interplay between these forces is referred to as ‘psychodynamics’ which try to defend the individual against anxieties and depression through repression
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25
Q

Where are Id, Ego and Super ego located?

A

Conscious - none
Preconscious - Ego (tries to control Id impulses)
Unconscious - Super ego (integrated learned values) and Id (Innate instinctive needs)

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26
Q

What is Id?

A
  • Present at birth
  • Operates by ‘pleasure principle’ e.g. immediate satisfaction of basic needs, relief of tension
  • A primary process e.g. thinking, images, fantasies; unconsciously driven
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27
Q

What is Ego?

A
  • Primarily conscious in its mode of activity
  • Reality orientated
  • Mediates between immediate gratification need of Id and what can be achieved in reality
  • Planning and decision making functions (secondary processes)
  • Relies on Id for energy therefore always in position of conflict between needs of reality and needs of Id
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28
Q

What is Super ego

A
  • Moral conscience
  • Develops throughout childhood
  • Grows out of the ego
  • Polices conflicts between Id and ego
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29
Q

Defence mechanisms in the psychodynamic approach

A
  • Psychodynamic conflict creates conscious or unconscious anxiety
  • Anxiety is controlled by defence mechanisms (repression, projection, denial, displacement, sublimation)
  • Role of ego and super ego often diminished by defence mechanisms
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30
Q

Achievements of psychodynamic approach

A
  • Discovery and role of unconscious mechanisms
  • Framework for understanding abnormal behaviour
  • ‘Talking cure’ for mental health practices
  • Importance of relationships at different stages of development
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31
Q

What is the conscious, preconscious and unconscious

A

Conscious - what we are constantly aware of

Preconscious - memories not in current awareness but we could if we focused on them e.g. phone number

Unconscious - largest part of the mind, brought to awareness only with difficulty. Holds our basic drives, impulses and instincts (mostly sexual)

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32
Q

Limitations of psychodynamic approach

A
  • Untestable hypothesis and little evidence for effectiveness
  • Infantile sexuality - no evidence, misconstrued in a social and cultural context
  • Psychoanalysis is too long and expensive
  • No longer part of mainstream clinical practice
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33
Q

Behaviourist model of psychopathology

A
  • John Watson 1878-1958 and B F Skinner 1904-1990
  • Followed from Pavlov’s work on conditioned reflexes
  • Behaviour is not the symptom but the problem
  • Certain abnormal behaviours can be learnt in childhood
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34
Q

Classical conditioning

A

conditioned stimulus –> unconditioned stimulus –> unconditioned response

bell –> food –> drool

bell –> drool/conditioned response

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35
Q

Operant conditioning

A

Behaviours increases with more positive reinforcement and diminish if followed by a punishment

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36
Q

Cognitive model of psychopathology

A
  • Aaron Beck and Albert Ellis
  • Meaning of events, more than the events themselves, that trigger anxiety
  • Same event can evoke a different emotional response in different people
  • Distorted thinking or schema
  • Less pathological
  • Many aspects of psychopathology are understandable errors of normal functioning
  • Emphasis placed on the continuity between normal and abnormal anxiety or emotions
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37
Q

Distorted thinking in the cognitive approach to psychopathology

A

Cognitive distortions are errors of thinking

  • Depressed people may have an overly negative view of the world
  • Exaggerate the significance of negative events - evaluation
  • Leads to maladaptive behaviour and emotional problems
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38
Q

Biopsychosocial perspective or psychopathology: integrative model

A
  • Increased incidence of certain psychological disorders in poor, some age groups, some genders, ethnic minorities
  • Interaction between genetics, environment and psychological factors
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39
Q

Stress-diathesis model (biopsychosocial perspective of psychopathology)

A

Diathesis:

  • A vulnerability or predisposition to develop a certain disorder
  • Relevant to a;; illness categories in physical and mental health domains

Stress:

  • Anything that can be seen as a stressor
  • Anything that exposes or exacerbates a vulnerable disposition

Genetic predisposition + environmental stressor = disorder

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40
Q

Interaction model of psychopathology

A
  • Exposure to a stressor can trigger a disorder in a person with vulnerability
  • A person can be protected from stressors that are likely to trigger a condition
  • Those with vulnerability need less stress to elicit a disorder
  • More susceptible to routine life stresses
  • Greater diatheses, less of a stressor needed to provoke a disorder
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41
Q

Emil Kraepelin in classification

A
  • First to publish a form of classification in 1883

- Studied the differences in dementia praecox and manic-depressive psychosis

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42
Q

What are the classification systems?

A

ICD:

  • International classification of mental & behavioural disorders (WHO)
  • Includes physical health issues
  • Europe and worldwide

DSM:

  • Diagnostic statistical manual
  • Psychiatric disorders only
  • USA
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43
Q

Comparison of ICD and DSM

A
  • ICD has no axes
  • 16 major categories in DSM-IV, 11 in ICD-10
  • ICD-10 categories are more general
  • Some categories e.g. sexual and gender identity appear in DSM-IV but not in ICD-10
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44
Q

Why do we need classification systems?

A
  • Improves the reliability of psychiatric diagnoses, an everlasting problem in psychiatry (Whaley, 2001)
  • Research and clinical purposes
  • USA: insurance companies require DSM diagnoses for reimbursement
  • Impose homogeneity, develop theories of causation
  • Aid communication between professionals
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45
Q

What is the multi-axial system in the DSM?

A
  • 5 dimensions or axes
  • Involves biological, psychological and social factors
  • Should enable a person-centred approach
  • Should help plan treatment
  • Should help predict outcome
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46
Q

What are the axes in the DSM?

A

Axis I: Clinical disorders, including major mental disorders, as well as developmental and learning disorders

Axis II: Underlying pervasive or personality conditions, as well as mental retardation

Axis III: Acute medical conditions and physical disorders

Axis IV: Psychosocial and environmental factors contributing to the disorder

Axis V: Global assessment of functioning or children’s global assessment scale for children under the age of 18 (on a scale from 100 to 0)

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47
Q

How is the DSM-5 different from previous editions?

A

Moved to a non-axial documentation of diagnosis (formerly axes I, II, III) with separate notations for important psychosocial and contextual factors (axis IV() and disability (axis V)

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48
Q

Why did the DSM-5 change?

A
  • To account for the last 2 decades of scientific and clinical advancement
  • To make sure the manual is useful to those who diagnose and treat individuals with mental illness, and to those being treated
49
Q

Criticisms of classification systems

A
  • Circular arguments (without bodily signs to confirm the presence of these ‘illnesses’, diagnoses are not an explanation)
  • Criteria can mislead people into thinking they have a disorder when they don’t
50
Q

Why is the reliability of the DSM criticised?

A
  • Level of reliability varies between disorders (less agreement about personality disorders)
  • Low inter-tester reliability
  • Poor reliability across clinical settings
  • Nature of diagnostic criteria is important because some are based on patient reports and some are based on clinical observations
  • It is always evolving and being refined
51
Q

Key difficulties with classification

A

Cross-cultural differences - most of the classification systems are based on the western view of what is ‘abnormal’, and therefore can be considered to represent ‘‘psychiatric imperialism”

Gender bias - argued that male-based assumptions influence what is included in DSM

There is no absolute cut-off between ‘well’ and ‘ill’

Criteria are all essentially subjective

There are no medical tests for psychiatric problems and no firm evidence for ‘biochemical imbalances’, or faulty genes

52
Q

Criticisms on the revision revision of the DSM-5

A
  • Unhealthy influence of the pharmaceutical industry: 67% of the task force had direct links to the pharmaceutical industry
  • Increasing tendency to ‘medicalise’ patterns of behaviour and mood that are not considered to be particularly extreme
53
Q

Risks of maintaining a medical model for psychiatry

A
  • Maintains view that difficulties lie ‘within’ the individual
  • Under estimates social and cultural role in psychological distress (i.e. power, abuse, neglect etc)
54
Q

Alternative to diagnosis

A

Psychological formulation - core skill for clinical psychologists and counselling psychologists

Instead of ‘What’s wrong with you?’ ask ‘What’s happened to you?’

55
Q

How the body responds to stress

A
  1. Forebrain and brain stem send action potentials to the hypothalamus
  2. Causes the hypothalamus to release corticotropin releasing hormone into the anterior pituitary
  3. Anterior pituitary releases adrenocorticotrophic hormone to the adrenal cortex
  4. This secrets cortisol which causes the body to react to stress and stops the body from producing more CRH and ACTH
56
Q

How do we define stress?

A
  • Psychological response to a trigger or stressor
  • Any uncomfortable ‘emotional experience accompanied by predictable biochemical, physiological and behavioural changes’ (Baum, 1990)
57
Q

Historical perspectives of PTSD

A

World war 1

  • Approx. 80,000 soldiers have shell shock
  • Associated with ‘going over the top’
  • Flashbacks, nightmares, desertion
  • War neurosis
  • Many were shot at dawn for cowardice
  • Did not appear in DSM until version 3, 1980
  • Was recognised 60 years earlier in WW1 and may even have been recognised as early as the American civil war, 1861-65 (irritable heart)

World war II

  • Americans coined the term ‘battle fatigue’
  • > 900,000 soldiers treated

Vietnam war

  • Combat stress
  • Increased post 1973; 20-30% of veterans
  • Later became known as PTSD
58
Q

Points of PTSD

A
  • Symptoms of PTSD shortly after a traumatic event recover
  • Green (1994) approx. 25% of those exposed to traumatic events develop PTSD
  • PTSD affects 1 in 12 adults at some time in their life (Kessler et al, 1995)
  • Trauma and disasters are related not only to PTSD but also to concurrent depression, other anxiety disorders, cognitive impairment, and substance abuse (Schnurr et al, 2002)
59
Q

Prevalence of PTSD

A
  • 1-3% of general population
  • 9% exposed to trauma

Depends on severity:

  • 3% physical assault
  • 20% wounded in combat
  • 50% of rape or serious sexual assault victims
  • 50% POWs
  • 7% New York City dwellers post 9/11
60
Q

What causes PTSD

A
  • Exposure to a traumatic event
  • Mugging, rape, kidnapping, torture, natural disasters, terrorism, combat
  • Theory of shattered assumptions (Janoff-Bulman 1992)
  • Develops through classical conditioning
  • Maintained through operant conditioning; Mowrer’s two factory theory, active avoidance
61
Q

PTSD risk factors

A
  • Type of trauma e.g. threat to life/self integrity
  • Being female = twice the risk of developing PTSD
  • Males experience different types of trauma e.g. combat, fighting, increased risk taking
  • Previous exposure to trauma
  • Pre-existing anxiety disorder, substance misuse
  • Sexual trauma - rape victims have high incidence
  • Poor social support
62
Q

What are the biological predispositions of PTSD?

A
  • Over sensitive noradrenalin system
  • Threat detection system
  • Increased levels of noradrenalin in PTSD
63
Q

Are there any signs of brain damage in PTSD?

A
  • Neuropsychological testing to probe hippocampal function in 26 Vietnam vets, 15 controls
  • Decreased immediate and delayed recall in vets
64
Q

Symptoms of PTSD

A

Intrusions

  • Flashbacks, nightmares, hallucinations
  • Distress at exposure to cues
  • Physiological response to cue exposure

Avoidance

  • Avoid thoughts, places, people linked to event
  • Diminished interest in social engagement
  • Loss of interest and pleasure
  • Sense of foreshortened future

Hyperarousal

  • Increased startle response
  • Hypervigilance
  • Insomnia
  • Irritability
  • Outbursts of anger
  • Lack of concentration
65
Q

Treatment approaches to PTSD

A
  • Medication
  • Psychological/therapeutic interventions
  • Cognitive behavioural therapy
  • Eye movement desensitisation reprocessing
  • Critical incident debriefing
66
Q

Medication for PTSD

A
  • Similar to treatments for other anxiety disorders
  • Medication: SSRIs, SNRIs
  • Psychotherapy: Behavioural modification, cognitive behavioural therapy, critical incident debriefing, eye movement desensitisation reprocessing
  • Comes second to trauma-based therapy
67
Q

Pros of drug therapy for PTSD

A
  • Antidepressants lessen sadness/depression that comes along with PTSD
  • Anti-anxiety meds can reduce symptoms of hyper arousal
  • Can have underlying mental health issues that need certain medications are able to help ease their hidden symptoms
68
Q

Cons of drug therapy for PTSD

A
  • Potential side effects
  • Examples: Nausea, dizziness, decrease . in sex drive, increased anxiety, weight changes etc.
  • Increased risk of depression/suicide
69
Q

CBT for PTSD: Emotional processing theory

A
  • Rauch & Foa, 2006

Traumatic events can lead to develop associations among objectively safe reminders of the event, meaning and responses. Changing these associations that lead to unhealthy functioning is the core of emotional processing

70
Q

CBT for PTSD: Social cognitive theory

A
  • Benight & Bandurra, 2004

Incorporating the experience of trauma into existing beliefs lead to unhelpful understandings of their experience and perceptions of control of self or the environment.

71
Q

What is eye movement desensitisation

A
  • Think about trauma whilst following therapists finger with eyes
  • Talk about negative thoughts
  • Replace them with positive thoughts with eye exercises
  • Resolve incomplete processing of the event
72
Q

What is critical incident debriefing

A
  • Immediate support within 72 hours
  • Visit the site of the event
  • Prevent PTSD and ASD occurring
73
Q

What is the nature of anxiety?

A
  • It is universal
  • Useful behaviour because it can energise behaviour and motivate
  • Disordered if intense and debilitating
74
Q

What is OCD?

A

The occurrence of unwanted and intrusive obsessive thoughts usually accompanied by compulsive behaviours used to neutralise the obsessive thoughts

75
Q

Prevalence and age of onset of OCD

A
  • 2% lifetime prevalence, 1% one year prevalence (1-2% in UK adults)
  • 98% cases show obsessions and compulsions
  • Equal across genders and cultures
  • Socio-economic drift noticeable
  • Onset late adolescence, early adulthood
  • Childhood onset more common in males (but only about 1%)
  • Fourth most common mental disorder after depression, alcohol and substance abuse, and social phobia
76
Q

Key features of OCD

A

Obsessions

  • Recurrent intrusive thoughts
  • Images
  • Experienced as disturbing or inappropriate

Compulsions

  • Used to get rid of or deal with obsessions; prevent distress
  • Repetitive behaviours (hand washing, checking)
  • Covert mental acts (counting, chanting, sayings)

Must be recognised by the sufferer as a product of their own mind

  • Not externally driven
  • Distinct from Schizophrenia

Degree of insight is variable

77
Q

How is OCD grouped in the DSM-5?

A
  • Grouped with related disorders
  • Disorders grouped in this new chapter have features in common such as an obsessive preoccupation and repetitive behaviours
OCD
Body dysmorphic disorder
Trichtillomania (hair pulling disorder) 
Hoarding disorder
Excoriation (skin-picking) disorder
78
Q

Co-morbidity of OCD

A
  • 80% experience depressive symptoms
  • 30% experience major depression

Co-occurs with other anxiety disorders

  • Panic
  • Social phobia
  • GAD
  • PTSD
  • High co-occurence with body dysmorphic disorder
79
Q

Characteristics of OCD

A
  • Intrusive thoughts happen to everyone e.g. did we lock the door?
  • Repetitive behaviours also normal e.g. checking we locked the door

Needs to be excessive, persistent, distressing, dysfunctional

  • Washing hands 45 times before leaving the house with a rigid sub-routine
  • Hands bleeding, raw skin, can’t get to work on time
80
Q

Typical obsessive thoughts (OCD)

A
  • Fear of contamination
  • Fear of harming self or others
  • Pathological doubt
  • Need for symmetry
  • Religious themes
  • Sexual obsessions
81
Q

What are the 5 main types of compulsion (OCD)?

A
  • Cleaning
  • Checking
  • Repeating
  • Ordering/arranging
  • Counting
82
Q

Other examples of compulsions

A

Primary obsessional slowness
- Performing every day acts such as dressing extremely slowly

Hoarding

  • 30-40% of sufferers
  • Failure to discard personal possessions
  • Cluttered and disorganised
  • Interfered with normal functioning
83
Q

Common elements of OCD

A
  • Anxiety is the affective symptom
  • Compulsions reduce anxiety in the short term
  • Majority of OCD sufferers fear being responsible for something terrible happening to themselves or others
  • Risk assessment is unrealistic
84
Q

Behavioural explanations of OCD: Mowrer’s two factor theory of avoidance

A
  1. Fear of neutral stimulus is acquired by classical conditioning
  2. Thought of stimulus causes anxiety
  3. Anxiety is reduced by performing act
  4. Performing act extensively reinforces behaviour
85
Q

Intrusive thoughts with OCD

A
  • Thought suppression increases intrusive thoughts in OCD sufferers
  • Re-bound effect
  • Helps to associate thought with negative mood state
86
Q

Biological explanations for OCD

A

Increased glucose metabolism in the orbitofrontal cortex

Brain basis of OCD:

  • Primitive urges arise in the orbitofrontal cortex e.g. sex, aggression, hygiene, danger
  • Urges usually filtered by basal ganglia before reaching thalamus and onto the rest of the cortex
  • Drugs that increases serotonin alleviate symptoms (50-70% patients show improvement and relapse rates are higher if discontinued)
  • Behavioural therapies are important
87
Q

Treatments for OCD

A
  • Behavioural therapy
  • Cognitive therapy
    (CBT - ERP)
  • Medication
  • Surgery
88
Q

Psychosurgery for intractable OCD

A
  • 10% of sufferers don’t improve with treatment

- Bilateral cingulotomy

89
Q

Outcome of bilateral cingulotomy (OCD)

A
  • Post-operation follow-up assessment of 44 patients
  • 32-45% showed improvement in OCD symptoms
  • N=1: seizure disorder
  • N=2: memory impairment, resolved within 6 months
  • N=1: suicide (but also a history of major depression)
90
Q

Drug treatments for OCD

A
  • Initial pharmacological treatment should be an SSRI
  • If effective, consider continuing for 12 months to prevent relapse then review with the patient
  • Consider prescribing a different a different SSRI if prolonged side effects
91
Q

CBT for OCD

A
  • Offer low intensity psychological treatments initially if functional impairment is mild and/or the person prefers a low intensity approach

Low intensity treatments include:

  • Brief individual CBT (including exposure and response prevention [ERP]) using structured self-help materials
  • Brief individual CBT (including ERP) by telephone
  • Group CBT (including ERP)
92
Q

What are mood disorders?

A

A group of disorders (DSM) which are categorised as such due to a disturbance in mood being the central feature

93
Q

What is depression?

A

A term used to describe symptoms and behaviours, not a diagnostic label

Biology, emotions, behaviours, and cognitions contribute to the etiology and maintenance of depression

94
Q

What is major depressive disorder?

A

Mood disorder characterised by one or more major depressive episodes (MDE) without a history of manic, mixed, or hypomanic episodes, but not due to a medical condition, medication or substance

95
Q

Prevalence of major depressive disorder

A
  • Common (more than bipolar)
  • Lifetime prevalence 10-20%
  • Marriage/cohabiting and a good socioeconomic position are associate with a lower risk of depression in both genders
  • Less common in children and presents differently
96
Q

Related conditions to depression

A
  • Dysthymia
  • Perinatal or postpartum depression
  • Seasonal affective disorder
  • Bipolar disorder
97
Q

Unipolar (depression) vs bipolar

A

Unipolar - recurrent episodes of lows

Bipolar - both low and high episodes outside of normal range

98
Q

What does depression feel like?

A
  • Muted and dull
  • Very low
  • Very slowed down
  • Including our thoughts and reactions
99
Q

What does mania feel like?

A
  • Full of energy
  • An extreme sense of well-being and optimism
  • Very happy and excites, irritated if other people who don’t share your optimistic outlook
  • Unable or unwilling to sleep
  • Full of new and exciting ideas
  • More important than usual
100
Q

Gender and major depressive disorder

A
  • More than twice prevalent in young women than men aged 14-25y (5.5% in females and 3.2% in males)
  • Biological and hormonal factors: variation in ovarian hormone levels and decreases in oestrogen may contribute to triggering depression
  • Socio-cultural factors: lack of choice, role overload, and competing social roles e.g. mothers who stay at home and are unemployed are increasingly less valued; power and abuse
  • 3x higher risk of depression in women who lost their own mothers before 11 years
101
Q

Suicide prevalence

A
  • 90% of suicide and attempts are associated with a psychiatric disorder
  • Highest rates of suicide associated with depressive disorders
  • 30,000 suicides in the USA per year are due to depression
  • 16% of survivors attempt suicide again within a year with 2% of repeat attempts being fatal
  • Socio-economic inequality in suicide risk - poor people approx. 10x more at risk
102
Q

Male suicide statistics

A
  • 3x more likely than women to die by suicide
  • High suicide rates in young men have received some public attention
  • Rates in middle aged men have been at a comparable level for 40 years and have recently become the age group at highest risk
  • Particularly those who are socio-economically disadvantaged
103
Q

Signs and symptoms of mood disorders (9)

A
  • Withdrawal
  • Feelings of hopelessness & pessimism
  • Fatigue
  • Sleep difficulties
  • Lack of energy
  • Feelings of guilt and worthlessness
  • Attention & concentration difficulties
  • Physical complaints (headaches/digestive problems)
  • Suicidal thoughts
104
Q

Major depressive disorder symptoms

A
  • Mood changes
    e. g. a long period of feeling worried or empty
  • Behavioural changes e.g being restless or irritable
105
Q

Genetic basis of major depressive disorder?

A
  • People who have a first-degree relative with depression appear to have a 2-3x greater risk of developing the condition than the general public
  • Serotonin transporter gene and short alleles linked to depression
106
Q

Biological factors of major depressive disorder

A

Schildkraut (1965):
Depression is caused by a functional deficit of monoamine transmitters (norepinephrine and/or serotonin); and depletion studies have shown a correlation between such deficiencies and depressive symptoms

107
Q

Biological factors of major depressive disorder (Stress hypothesis)

A
  • Depression results from exposure to chronic mild stressors
  • Causes over-activity in the hypothalamic-adrenocortical axis
  • Too much cortisol causes long term damage to some brain areas
108
Q

Personality factors of MDD

Neuroticism

A

Neuroticism (sensitivity to external factors)

  • Higher risk of experiencing stressful life-events
  • Heritable trait
  • Higher levels of neuroticism and lower levels of extroversion noted as risk factors
  • Social network, together with neuroticism, also showed strong association with depressive severity, independently from current depressive state
109
Q

Personality factors of MDD (Introversion)

A

Introversion (low positive affectivity)

  • Unenthusiastic, unenergtic, flat, bored
  • Vulnerable personalities (characterised by low extraversion, agreeableness and conscientiousness but higher neuroticism) linked to poorer treatment outcomes and longitudinal course of depression
110
Q

Beck’s cognitive triad and errors in logic

A

Errors in logic: depressed people draw illogical conclusions when they evaluate themselves

Cognitive triad: there are 3 forms of negative thinking that are typical of those with depression

111
Q

The cognitive triad

A
  • Negative views about the world
    “Everyone is against me because I’m worthless”
  • Negative views about the future
    “I’ll never be good at anything”
  • Negative views about oneself
    “I’m worthless and inadequate”
112
Q

Cognitive distortions (errors in logic)

A

Dichotomous reasoning
- If I can’t get a perfect score it is not worth trying

Selective abstraction
- Remembering only the negative points of an otherwise good day

Arbitrary inference
- Jumping to conclusions, something didn’t work today therefore it will never work

113
Q

Learned helplessness theory

A
  • Seligman 1975
  • Animals given unavoidable shocks
  • Become passive if they can’t escape
  • “Non-contingency” (subject’s perception of the uncontrollability of events) is the basis of human depression
114
Q

Hopelessness theory

A
  • Perception that a person has no control over what
    was going to happen
  • A certainty that an important bad outcome was going to occur or that a highly desired good outcome was not going to occur
115
Q

Psychological approaches to

A

Counselling

Psychodynamic psychotherapy: long-term, focused on past

Interpersonal psychotherapy: focuses on the connection between current symptoms and interpersonal/relationship problems

Cognitive therapy: Cognitive analytic therapy, acceptance, and commitment therapy (ACT), cognitive behavioural therapy, rational emotive behavioural therapy (REBT)

116
Q

Aims of CBT for depression

A
  • Targets understanding and identifying thoughts
  • Attempts to address underlying cognitions driving behaviour
  • Encourages challenging irrational thinking
  • Plans for relapse prevention
117
Q

CBT formats

A

Guided self-help in primary care:
- Some effect and cheaper, but low engagement/completion

Group work:

  • Reduces symptoms, but low on recovery
  • Not always economically efficient

Individual work:

  • Highest impact
  • More costly/time-consuming
118
Q

What does CBT for depression include?

A
  • Self help (mild to moderate)
  • Risk management
  • Activity scheduling
  • Diary ]- Cognitive restructuring
  • Behavioural experiments
  • Homework

Year 1 Individual and Abnormal Psych (4 decks)

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