Mental Health - MCT 1

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History of diagnostic concepts and systems, anxiety conditions, mood conditions.

Last updated 5:02 PM on 10/11/26
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1
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What did Karl Ludwig Kahlbaum do?

  • Tried to develop classification system that grouped mental diseases according to their course and outcome

  • Stressed importance of parental upbringing to prevent ‘Juvinile Madness’


2
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What did Emil Kraepelin do?

  • Wrote the Compendium of Psychiatry - used detailed case studies & methods such as clinical observation, psychological tests and psychopharmacology.

  • First described schizophrenia, which he called ‘dementia praecox’, and differentiated it from manic-depression and paranoia


3
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What did Helen Boyle do?

  • First female president of the Royal College of Psychiatrists

  • Focused on helping women living in poverty by offering free and low-cost mental health care at the Lady Chichester Hospital in Brighton

  • Set up to reduce amount of women ending up in asylums

  • Lady Chichester was the first faculty to offer early intervention systems


4
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What did Eugen Bleuler do?

  • Published Lehrbuch der Psychiatrie, which listed the fundamental symptoms of dementia praecox as
    - Ambivalence
    - Inappropriate affect
    - Loosening of associations
    - Autism
    And the accessory symptoms as
    - Hallucinations
    - Delusions


5
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What did Kurt Schneider do?

  • Distinguished between ‘form’ and ‘content’ of disorders

  • “Diagnosis looks for the ‘how’ (form) not the ‘what?’ (content)


6
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What did Karl Jaspers do?

  • Questioned popular understanding of mental illness and diagnostic criteria

  • Controversially stated abnormal experiences can occur through normal cognitive processes

  • Published General Psychopathology, which influences many current diagnostic criterea


7
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What is the evolution of the concept of bipolar disorder?

  • Kraepelin - Grouped all affective psychoses into a single category of manic-depression

  • Klaus Leohnard - observed some patients experience both manic and depressive episodes, some only depressive

  • By 1970s, it had become commonplace to distinguish between unipolar and bipolar disorder


8
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What lead to the development of the DSM?

  • At the end of WWII, seperate army, navy, airforce and civilian classifications were in use.

  • The APA formed a task force in 1948 to create new standardised system

  • DSM published in 1952


9
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What lead to the inclusion of psychiatric illnesses in the ICD?

  • In 1948, WHO tasked with creating an International List of Causes of Death

  • When creating ICD-6 in 1951, WHO added nonfatal diseases including psychiatric diagnoses.

  • In 1960s, APA began revising DSM-I to make it more consistent with ICD-8.


10
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Who suggested the criterion ‘reliability’ and ‘validity’ for evaluating diagnostic systems?

Spitzer and Fliess (1974)

11
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Define reliability

The extent to which diagnosticians can agree about who had what diagnosis

12
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Define validity

The extent to which the diagnostic system is useful for the purposes intended

13
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What was initially described as the ‘satisfactory’ Kappa score?

0.70

14
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What happened during DSM-III field trials?

Kappa values often failed to exceed 0.7

15
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What did Krueger et al. propose as an alternative model of classification?

The Hierarchical Taxonomy of Psychopathology (HiTOP) model

16
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What are some benefits of the HiTOP model?

  • Removes arbitrary boundaries between psychopathology and normality

  • Focus on symptoms as opposed to diagnosis

  • Easier to explain co-morbidity due to hierarchical structure

  • Higher test-retest reliability than traditional classification systems


17
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Limitations of HiTop model?

  • Created using simple structure factor analysis approach - does not accurately represent dimensional space of the symptoms of psychopathology

  • Dimensional ratings do not fix problems inherent to descriptive classification

  • No clinical evidence found suggesting clinicians using HiTOP have better clinical outcomes than those using DSM.


18
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The DSM-IV included an exclusion for which stressor when diagnosing depression?

Bereavement

19
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How did the DSM-V differ from DSM-IV?

Removed all exclusions for stressors

20
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What is the core symptom of a major depressive episode?

Depressed mood or loss of interest/pleasure (anhedonia)

21
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What are the other symptoms of a major depressive episode?

  1. Weight loss/gain

  2. Insomnia/hypersomnia

  3. Psychomotor agitation or retardation

  4. Fatigue

  5. Feelings of worthlessness or excessive guilt

  6. Difficulty thinking, concentrating or making decisions

  7. Recurrent thoughts of death or suicide ideation


22
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What are the conditions of a major depressive episode according to DSM 5?

  • 5 or more symptoms (including core symptom)

  • Symptoms present for at least 2-week period

  • Causing significant impair or distress

  • Not due to physiological effects of a medical condition


23
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What is major depressive disorder?

Has at least one major depressive episode, and no mania or hypomania before or during.

24
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What is persistent depressive disorder?

  • At least 2 years of consistent depressed mood, with no more than 2 month gaps

  • At least two symptoms like those of major depressive disorder

  • No mania or hypomania before or during

  • Over one year in children & adolescents


25
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What are three sub-type diagnoses of depression?

  • Anxious distress

  • Psychotic features

    • Seasonal pattern


26
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What is premenstrual dysphoria disorder?

Depression related to menstrual cycle, distinguished from typical premenstrual cycle, new addition to DSM 5.

27
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What is a concern regarding premenstrual dysphoria disorder?

Potential stigmatisation of typical menstrual cycle

28
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What exclusionary factor was removed from the DSM 5?

Grief

29
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Why was grief removed from DSM 5?

Considered fundamentally different from MDD, removed to prevent obstructing treatment.

30
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What % of adults in the UK have been diagnosed with depression?

19%

31
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What condition is highly co-morbid with depression?

Anxiety

32
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In what groups are depression rates highest?

People aged between 18-29, women

33
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Define relapse

Return of difficulties within a short timeframe

34
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Define recurrence

New episode of difficulties

35
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What are the biological factors associated with depression?

  • Genetic vulnerability

  • Neurotransmitters

  • Brain structure and functioning

  • Overactive Hypothalamic-Pituitary-Adrenal Axis


36
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How do genetics influence depression?

1st degree relative with depression = 2-3x more likely to also develop.

37
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How do neurotransmitter effect depression?

  • Monoamines including norepinephrine, serotonin, dopamine

  • Serotonin and norepinephrine synthesis, release or reception may be abnormal

  • HOWEVER recent review suggests no consistent evidence of serotonin theory of depression


38
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How does brain structure and functioning affect depression?

  • Pre-frontal cortex - reduced metabolic and brainwave activity, reduces grey matter.

  • Anterior cingulate - differing activity to non-depressed

  • Hippocampus - reduced volume, reduced metabolic activity

  • Amygdala - increased activity


39
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How does overactive HPA axis affect depression?

  • High levels of CRH and cortisol

  • Inhibits receptors for monoamine neurotransmitters

  • Impacts brain structures


40
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What psychological factors are associated with depression?

  • Behavioural theory

  • Cognitive theory

  • Reformulated learned helplessness theory

  • Cognitive factors involved in depression


41
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Behavioural theory of depression

Stress/negative event → depressive mood → less activity and withdrawal → fewer natural reinforcers → further depressed mood

42
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Cognitive theory of depression

  • Cognitive triad (negative view of life, world, future)

  • Early adverse experiences → core beliefs and cognitive vulnerabilities → activation of beliefs due to cognitive biases → depression


43
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Reformulated Learned Helplessness theory of depression

  • The understanding we form of our experiences can be associated with our mood

  • Internal vs External, Stable vs Unstable, Global vs Specific

  • Way of thinking = greater vulnerability to depression


44
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Cognitive factors involved in depression

  • Cognitive biases (ways of processing)

  • Cognitive emotion regulation strategies (rumination, distraction…)

  • Cognitive control on depression


45
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What social factors are associated with depression?

  • Social factors as triggers for depression → difficulties in interpersonal relationships precede depressive episodes

  • Social difficulties due to depression → higher likelihood of relationship conflict and social skill difficulties

  • Component of difficulties → elevated feedback seeking (positive and negative), perception of rejection from others


46
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Biopsychosocial theory of depression

knowt flashcard image
47
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What is the Matched Care Model?

  • Ensures most effective, least intrusive and least resource intensive treatments are delivered first.

  • Allows access to more intensive treatments if and when needed

  • Considers other factors (pt presentation, pt choices and preferences, previous tx)


48
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What are the categories for severity of depression?

  • Sub-threshold depression → <5 symptoms

  • Mild depression → 5 symptoms, minor functional impairment

  • Moderate depression → Symptoms or function impairment between ‘mild’ and ‘severe’

  • Severe depression → Most symptoms present, considerable impact on functioning


49
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What are the biological interventions for depression?

  • Antidepressants (MAO inhibitors, Tricyclic antidepressants, SSRIs, SNRIs)

  • Electroconvulsive therapy

  • Repetitive Transcranial Magnetic Stimulation


50
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How do monoamine oxidase inhibitors work?

Inhibits monoamine oxidase enzyme which breaks down neurotransmitters such as serotonin and dopamine

51
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How do tricyclic antidepressants work?

Block serotonin and norepinephrine reuptake within the presynaptic terminals

  • Differ from SNRIs as they are less selective and carry a higher risk of side effects


52
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How do SSRIs work?

Block serotonin reuptake within the presynaptic terminals

53
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How do SSNRIs work?

Block serotonin and norepinephrine reuptake within the presynaptic terminals

54
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How effective are antidepressants?

  • Relative equivalence in effectiveness between antidepressants

  • Approx 50-60% experience some improvements

  • Different side effects for different medications

  • When antidepressants compared to placebos, medication was found to be no better than placebo except in very severe depression


55
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What is ECT?

Inducing seizures by passing electrical current through the brain

56
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What are the side effects of ECT?

Memory loss, slowed response, difficulty learning new information

57
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Who is ECT reccomended to?

Individuals with severe or treatment-resistant depression

58
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What is RTMS?

Administering magnetic pulses to the brain, targeting the left prefrontal cortex.

Few known side effects and considered safe, however requires more evidence to evaluate.

Currently appears to have short-term efficacy

59
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What are the psychological interventions for depression?

  • Cognitive behavioural therapy

  • Behavioural activation

  • Mindfulness-based Cognitive Therapy


60
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What is Cognitive Behavioural Therapy?

Derived from the work of Beck et al. and formed of 2 main components:

  • Cognition → Changing negative thoughts and beliefs

  • Behaviour → Changing actions`


61
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What is behavioural activation?

Based on behaviour theory of depression: therapeutic focus of increasing activity.

Increasing activity levels allows for more positive reinforcement and a reduction in avoidant behaviours.

It also allows us to increase our understanding of our current behaviour by encouraging monitoring of daily activities and how they effect our mood, design personally meaningful goals and acts based on structure not based on mood.

62
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What is the ABC of functional analysis?

A - ANTECEDENTS - What is the situation?

B - BEHAVIOUR - What does the person do?

C - CONSEQUENCE - What happens as a result?

63
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What is mindfulness-based cognitive therapy?

  • Combines CBT and mindfulness-based stress reduction

  • Learning to observe as opposed to engage with depressive thoughts and feelings

  • Considered particularly helpful for recurrent depression


64
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What are the social interventions for depression?

  • Interpersonal therapy

  • Behavioural couples therapy


65
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What is interpersonal therapy?

Focuses on 4 general areas:

  • Grief about loss

  • Relationship conflict

  • Change relating to interpersonal roles

  • Social/communication skills


66
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What is behavioural couples therapy?

Specifically designed intervention to change the nature of interactions between the participants and develop a more supportive relationship with less conflict.

67
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Effectiveness of psychological interventions

  • Compared to controls, treatment effect appears moderate to large

  • Compared to antidepressants, treatment effect appears comparable

  • Compared to each other, treatment effects appear largely comparable

  • CBT associated with significant reductions in mental health problems

    • However, quality of evidence is limited


68
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What are the NICE recommended interventions for less severe depression?

  • Guided self-help

  • Therapy (inc. CBT, BA, IPT, mindfulness counselling)

  • Individual/group settings

  • Group exercise

  • SSRIs


69
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What are the NICE recommended interventions for more severe depression?

  • Combination therapy and medication

  • Individual therapy (CBT, BA, IPT, mindfulness counselling, individual problem-solving)

  • Medication (SSRIs, SNRIs or others based on clinical history)

  • Guided self-help

  • Group exercise


70
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What is the guidance on relapse prevention for depression?

Those with significant risk of relapse should be considered for continuation of support and development of relapse prevention skills.

71
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What are some physiological components of the fight or flight response?

Slowed digestion, pupil dilation, reduced saliva, fast breathing, increased heart-rate, decreased motility of the large intestine, epinephrine production

72
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How does anxiety differ from fear/panic?

  • Anxiety is an adaptive reaction that primes the individual for the fight/flight response

  • Anxiety is future-focused

  • Anxiety centralises on uncontrollability and future threats as opposed to actual danger


73
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At what point does anxiety become a disorder?

When it can be considered ‘maladaptive’ - impaired daily functioning, unmanageable levels of anxiety, unexpected onset of anxiety

74
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What 5 primary types of anxiety disorder does the DSM-5 recognise?

  • Specific phobia

  • Social anxiety disorder

  • Panic disorder

  • Generalized anxiety disorder

  • Agoraphobia


75
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What are the symptoms of a phobia?

  • A fear or anxiety about a specific object or situation, in which the fear or anxiety if out of proportion to the danger posed

  • The fear and anxiety or avoidance of the phobic object is persistent

  • Causes clinically significant distress or impairment


76
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What are some sub-types of phobias in the DSM-5 and DSM-5-TR?

  • Animals

  • Natural environments

  • Blood/injection/injury

  • Situational

  • Other



77
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What is the lifetime prevalence for phobias?

12%

78
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What is the age of onset for phobias?

Onset varies widely and persists over decades

79
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What are the gender differences in phobias?

More common in women than men, but the gender ratio depends on the type of phobia

80
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What has high co-morbidity with phobias?

Other anxiety disorders and mood and substance use disorders.

81
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What are the psychological causal factors of phobias?

  • Psychoanalytic theories

  • Learned behaviour (including vicarious conditioning, individual differences in learning, evolutionary preparedness)


82
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Psychoanalytic theory of phobias

Defence against anxiety that stems from repressed ‘id’ impulses, externalised as a defence mechanism

83
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Vicarious conditioning theory of phobias

Person-to-person observation of someone reacting to their phobia, or observation of a non-fearful person experiencing a fear-provoking event leads to development of phobia

84
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Individual differences in learning theory of phobias

Everyone has their own experiences and risk vs protective factors

85
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Evolutionary preparedness theory of phobias

Not innate but more easily acquired, where the conditioning to the fear-relevant stimuli is more effective

86
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Biological theories of phobias

  • Temperament

  • Genetic


87
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Temperament explanation for phobias

Behavioural inhibition (being shy, avoidant) personality type, starts early in childhood, shows motivation to avoid aversive outcomes.

88
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Genetic explanations for phobias

Modest heritability shown in twin studies, phobias more related to individual experiences and differences

89
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What types of exposure therapy are there?

  • Modelling

  • Flooding

  • Systematic desensitisation

  • Virtual reality exposure therapy (VRET)



90
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Modelling exposure therapy

Based on SLT, imitation based on behaviour helps gain coping skills and self efficacy

91
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Flooding exposure therapy

Emphasises habituation to the phobic stimuli. Single sessions of exposure have been found to be effective in phobic stimulus such as small animals and claustrophobia.

92
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New research on flooding exposure therapy

Knowles and Olatunji (2019) have suggested strengthening inhibitory association as opposed to habituation

93
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Systematic densensitisation exposure therapy

Focus on reducing sympathetic activity via relaxation training before gradual exposure to a fear hierarchy. Based on the premise that anxiety and relaxation cannot co-exist.

94
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Virtual reality exposure therapy

Combination of in vivo and imaginal exposure, Botella et al. (2017) found in a systematic review that the control, flexibility and safety of the individual were advantages however it is not equally effective in all patients

95
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What are the symptoms of social anxiety disorder?

  • A persistent fear or one or most social or performance situations

  • The person recognizes that the fear is unreasonable or excessive

  • The avoidance, anxious anticipation or distress interferes significantly with the person’s daily activities


96
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What is the lifetime prevalence of social anxiety?

12%

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What is the age of onset for social anxiety disorder?

Most common in adolescence and early adulthood

98
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Why may adolescence be a common time for social anxiety to develop?

The most rapid phase of human development, changes in cognition, body image and body dissatisfaction, emotional and sexual identity.

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What are the rates of co-morbidty in social anxiety?

90%

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What other conditions are regularly comorbid with social anxiety?

  • Specific phobias

  • Major depressive disorder

  • Alcohol use disorder

  • Eating disorders