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Psychopathology Flashcards

1
Q

Psychopathology

A

Definition: Study of mental disorders

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2
Q

Defining mental disorders: Infrequency

A
  1. Something is a mental disorder because the symptoms the person experiences are statistically infrequent (e.g. auditory and visual hallucinations)
  2. Doesn’t hold: While some mental disorders are statistically infrequent (schizophrenia), there are other conditions that are frequent (depression); 48% lifetime prevalence rate for having any DSM-5 mental disorder
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3
Q

Schizophrenia prevalence rate in general population

A

0.5-1.5%

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4
Q

Depression prevalence rates (men + women)

A
  1. 10-20% prevalence rate for women
  2. 5-12% for men
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5
Q

Defining mental disorders: Deviance

A
  1. Mental disorder as atypical behaviour for a particular context (normative/contextual deviance)
  2. Opponent of deviance definition: Thomas Szasz wrote a book arguing that society has defined what a mental disorder is without any real biological underpinnings (mental illness/mental health issues are a social construct)
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6
Q

Defining mental disorders: Distress

A
  1. Mental disorder defined by subjective distress
  2. Issues: Not applicable to all mental disorders, as it depends on individual’s degree of insight/self-awareness - mental disorders not always accompanied by distress (e.g. NPD)
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7
Q

Defining mental disorders: Disability or impairment

A
  1. Mental disorder defined by some impairment in functioning
  2. Issues: Individuals with mental disorders not always impaired (e.g. people with anxiety disorder who can still go to school and study)
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8
Q

Defining mental disorders: Danger

A
  1. Something is a mental disorder because it relates to harming themselves or others
  2. Issues: Not associated with every mental disorder, not frequent
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9
Q

Actual DSM-5 mental disorder definition:

A
  1. Associated with present distress or;
  2. Disability, or;
  3. With a significantly increased risk of suffering, death, pain, disability, or an important loss of freedom -and;
  4. Must not be an expectable and culturally sanctioned response to an event - and;
  5. Must be considered a manifestation of a behavioural, psychological, or biological dysfunction in the individual
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10
Q

Emil Kraepelin

A

Medical doctor who came up with first modern classification system of modern mental disorders (published in 1883)

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11
Q

History of the DSM-5

A
  1. Diagnostic and Statistical Manual of Mental Disorders (published by the APA in 1952)
  2. DSM-3 (1980): Push for it to be more descriptive and less theoretical (have a symptom checklist, certain number where you meet diagnostic criteria)
  3. 5th edition revised in 2022 (DSM-5)
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12
Q

Biomedical/biological treatment

A
  1. Consider mental illness a biological disease (disease of the brain and central nervous system)
  2. Medication can be used to remove or at least improve symptoms of disorder, brain surgery may be used but is highly unusual
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13
Q

Psychological treatment: Psychodynamic (a.k.a psychoanalytic) approaches

A
  1. Developed by Freud, tried to define what was “normal” and had no interest in defining what was problematic and how to intervene
  2. Strong emphasis on child development (sees psychological difficulties as stemming from unresolved childhood trauma/difficulties)
  3. Sees behaviour as driven by powerful unconscious inner forces
  4. Insight-oriented approach - goal of psychoanalysis is for patients to arrive at an insight for why they are having certain difficulties
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14
Q

Psychological treatment: Humanistic (a.k.a positive) approaches

A

Focus is on teaching the patient to seek fulfilment and reach their potential; goal is to help patient discover and then achieve their potential

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15
Q

Psychological treatment: Behavioural approaches

A
  1. Second oldest modality, largely a rejection of psychodynamic theory
  2. Focus on the present, rooted in principles of classical and operant conditioning
  3. Goal is to: Use techniques that counter essentially-conditioned punishments (e.g. phobia of dogs treated with exposure therapy), extinguish non-productive/upsetting behaviours, reinforce desirable behaviours
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16
Q

Psychological treatment: Cognitive-behavioural approaches

A
  1. Focuses on the way people think, argues that the way people think about their environment influences how they feel
  2. Goal is to identify maladaptive, dysfunctional thoughts leading to negative emotions and challenge these thoughts, replacing them with more positive ones
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17
Q

Psychological treatment: Integrated/eclectic treatments

A
  1. Therapist selects techniques from various types of therapy to design a treatment that best suits the case
  2. Goal: Meet individual needs of the patient, mix and match techniques to do so
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18
Q

Anxiety definition

A

Apprehension about an anticipated issue (future oriented)

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19
Q

Forms of therapy:

A
  1. Individual
  2. Couple
  3. Family
  4. Group - often linked by an underlying difficulty
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20
Q

Fear/panic

A

Apprehensive response to immediate threat or danger; reflexive or autonomic response to a stimulus

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21
Q

Three components of anxiety and fear:

A
  1. Cognitive/subjective (what you’re thinking about, source of your anxiety)
  2. Physiological (both anxiety and fear produce autonomic responses)
  3. Behavioural (produce avoidance a.k.a. as “flight”)
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22
Q

Fight/flight response

A
  1. Occurs when confronted with danger
  2. Sympathetic nervous system (sweat, shaking, heart-racing, shallow breathing)
  3. Automatic perception of threat (physical, social, thoughts)
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23
Q

Yerkes-Dodson Law

A

Optimal area of arousal for anxiety for peak performance (certain level of anxiety as a motivator)

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24
Q

Anxiety disorders: Diagnosis rate

A

Most common psychiatric diagnosis (28% of individuals in the U.S. diagnosed at some point in life)

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25
Q

Types of anxiety disorders:

A
  1. Phobias (specific phobias, social phobia [social anxiety disorder], agoraphobia)
  2. Panic Disorder
  3. Generalised Anxiety Disorder (GAD)
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26
Q

Previously considered anxiety disorders:

A
  1. Obsessive-Compulsive Disorder (OCD)
  2. Post-Traumatic Stress Disorder (PTSD)
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27
Q

Generalised Anxiety Disorder (GAD)

A
  1. Extensive amount of apprehension and worry that individual finds uncontrollable (consistent apprehensive expectation)
  2. Anxiety is generalised and persistent, not situational
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28
Q

Panic Disorder

A
  1. Discrete period of intense fear in the absence of any real danger, unpredictable
  2. Sudden onset, builds rapidly (reaches peak within minutes)
  3. Concern about future attacks leads to avoidance, otherwise relatively free of anxiety in between attacks
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29
Q

Agoraphobia

A
  1. Often goes with Panic Disorder (fear of going out and being embarassed by having a panic attack)
  2. Marked fear about at least two of: using public transport, being in open spaces, being in closed spaces, standing in line/being in a crowd, being outside of home alone
  3. Feared situations produce anxiety and either avoided, require a companion to enter, or endured with intense fear or anxiety
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30
Q

Social Anxiety Disorder (SAD)

A
  1. Fear or anxiety about one or more social situations where the individual is exposed to possible scrutiny by others
  2. Individual fears that they will act in a way that will be negatively evaluated by others
  3. Feared social situations are avoided or endured with intense fear or anxiety
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31
Q

Specific phobias

A
  1. Anxiety evoked by specific circumstances or situations
  2. Fear is out of proportion to the situation and beyond voluntary control
  3. Avoidance is a characteristic feature
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32
Q

Common features of obsessive-compulsive related disorders:

A

Repetitive thoughts and behaviours which cause distress, feel uncontrollable, and take up a lot of time

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33
Q

Co-morbidity of obsessive-compulsive related disorders:

A
  1. 1/3 BDD comorbid with OCD
  2. 1/4 HD comorbid with OCD
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34
Q

What are the obsessive-compulsive related disorders?

A
  1. Obsessive-Compulsive Disorder (OCD)
  2. Hoarding Disorder (HD)
  3. Body Dysmorphic Disorder (BDD)
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35
Q

Trauma and stressor related disorders:

A
  1. PTSD
  2. Acute Stress Disorder (more immediate reaction to trauma instead of delayed)
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36
Q

Features of OCD:

A
  1. Obsessions (intrusive and recurring throughts, images, or impulses that are persistent, uncontrollable, and irrational)
  2. Compulsions (repetitive, excessive behaviours or mental acts person does to reduce anxiety caused by obsessions or to prevent expected consequences) - 78% “insight” (recognise compulsions as irrational)
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37
Q

Most common OCD obsessions:

A
  1. Contamination
  2. Sexual or aggressive impulses
  3. Body problems
  4. Religion
  5. Symmetry or order
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38
Q

Common OCD compulsions:

A
  1. Cleanliness and orderliness
  2. Repetitive “magical” acts (e.g. tapping something a certain number of times in order to save family)
  3. Excessive checking
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39
Q

DSM-5 PTSD

A
  1. Exposure to actual or threatened death, serious injury, or sexual violence
  2. Presence of one or more intrusive symptoms
  3. Persistent avoidance of associated stimuli, by one or more: avoidance of actual or external triggers for memories, thoughts, feelings
  4. Presence of two or more negative alterations in cognition and mood
  5. Negative alterations in cognition and mood (two or more)
  6. Two or more marked alterations in arousal and reactivity
  7. Duration > 1 month (needs to be at least 1 month separated from traumatic event)
  8. Clinically significant distress or impairment, can’t be due to substance/medical condition
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40
Q

Intrusive symptoms of PTSD:

A
  1. Distressing memories
  2. Dreams
  3. Flashbacks
  4. Distress and/or arousal response to internal/external reminders
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41
Q

Negative alterations in cognition and mood for PTSD:

A
  1. Amnesia
  2. Negative beliefs
  3. Blame for cause/consequences
  4. Negative emotional state
  5. Loss of interest/pleasure
  6. Detachment/estrangement
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42
Q

Alterations in arousal and reactivity for PTSD:

A
  1. Irritable
  2. Reckless
  3. Hypervigilance
  4. Startle response
  5. Concentration
  6. Sleep
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43
Q

Aetiology of anxiety and related disorders:

A
  1. Fear conditioning (environmental learning), especially for specific phobias
  2. Cognitive (maladaptive/dysfunctional thoughts)
  3. Genetic vulnerability (especially OCD, PTSD)
  4. Neurobiology
  5. Personality
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44
Q

Psychological treatment for anxiety and related disorders (anxiety disorders among the most treatable):

A
  1. Relaxation (helps with physiological response)
  2. Cognitive restructuring (challenges maladaptive thoughts)
  3. Exposure therapy and behavioural experiments to challenge, habituate, and learn
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45
Q

Exposure therapy

A
  1. Works on the principle of habituation - the more a person is exposed to fear-provoking stimulus, the more accustomed they get to being around it
  2. Systematic desensitisation: imagine the stimulus (imaginal exposure) –> focus on relaxation techniques –> eventually be directly exposed to stimulus (in vivo exposure)
  3. Effective in 70-90% of cases
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46
Q

Major Depressive Episode (MDE)

A

Change in previous functioning (must include either depressed mood or loss of interest), clinically signifcant distress or impairment, and five or more of the following over 2 weeks:
1. Depressed mood most of the day
2. Markedly diminished interest or pleasure in most activities
3. Clinically significant weight loss or gain (> 5% change)
4. Insomnia or hypersomnia
5. Psychomotor agitation or retardation
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive/inappropriate guilt
8. Diminished ability to think or concentrate, indecisiveness
9. Recurrent thoughts of death, suicidal ideation, plan or attempt

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47
Q

DSM-5 depressive disorders

A
  1. Major Depressive Disorder (MDD): Characterised by multiple MDEs, higher prevalence for women than men and more prevalent overall than Dysthymia
  2. Persistent Depressive Disorder (Dysthymia): Milder than MDD but lasts longer, slightly higher prevalence in women and less prevalent overall than MDD
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48
Q

Aetiology of depressive disorders: Genetics (biological factor)

A

Heritability for depression at 37%

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49
Q

Aetiology of depressive disorders: Biochemical (biological factor)

A
  1. NTs: Low levels of norepinephrine (increases energy), serotonin (mood regulation), and dopamine (processing rewards in environment) linked to depression
  2. Hormones: Cortisol released through the Hypothalamic-Pituitary-Adrenal (HPA) axis in response to stress, chronically excessive cortisol linked to breaking down NTs such as serotonin
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50
Q

Cortisol production pathway

A

Stressor –> amygdala –> HPA axis –> cortisol

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51
Q

Aetiology of depressive disorders: Brain abnormalities (biological factors)

A
  1. Limbic system (composed of amygdala and hippocampus) sends signals through our serotonergic pathways to prefrontal cortex (where info comes to our awareness) –> less serotonin in body disrupts this
  2. Prefrontal cortex doesn’t function very well for individuals with MDE (can’t inhibit maladaptive emotional responses that well)
  3. Left-frontal hemisphere asymmetry linked to depression (left frontal lobe associated with more positive emotions)
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52
Q

Emotion regulation system

A
  1. Emotional importance: Amygdala
  2. Emotion regulation: Subgenual anterior cingulate, dorsolateral prefrontal cortex (inhibition of emotional responses), hippocampus (conjuring up memories)
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53
Q

Diathesis-Stress Model

A

Argues that there is an underlying biological vulnerability to the development of a disorder, but will not develop into a disorder without experiencing certain stressors

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54
Q

Psychological theories of depression: Cognitive theories

A
  1. One of the founders of cognitive theories of depression and cognitive therapy was Aaron Beck
  2. Way we perceive environment is what contributes to depression, as well as other mental disorders (hopelessness + rumination [thinking about negative events in one’s life] –> depression)
  3. Negative triad: negative thoughts about self, others, and the future –> depression
  4. Cognitive distortions: should-ing, over-generalisation, discounting positives, black-and-white thinking, unfair comparisons
  5. Integrative model of depression: biological + psychological vulnerability –> activation of stress hormones which affect NTs, maladaptive cognition, social issues —> mood disorder
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55
Q

Psychological treatment for depressive disorders: Beck’s Cognitive Therapy

A

Four phases (~20 sessions):
1. Increase activities and elevate mood (e.g. going on walks)
2. Challenge automatic thoughts
3. Identify negative thinking and biases
4. Change primary attitudes/schemas

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56
Q

Efficacy of cognitive restructuring:

A
  1. 75+ treatment studies
  2. Effective and reduced risk of relapse
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57
Q

Biological treatment for depressive disorders: Anti-depressant drugs

A
  1. Monoamine oxidase (MAO) inhibitors - last resort for treatment
  2. Tricyclics - can lead to significant nausea, reduced libido
  3. Selective serotonin reuptake inhibitors (SSRIs) - increase amount of serotonin in the synapse → better mood, less side effects
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58
Q

Biological treatment for depressive disorders: Electroconvulsive Therapy (ECT)

A
  1. Place electrodes on head and “buzz” patient
  2. Effective for severe depression, only used for treatment-resistant depression
  3. Can lead to significant memory less, relapse is common
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59
Q

Schizophrenia vs. psychosis:

A
  1. Psychosis refers to a cluster of symptoms that are related to a range of mental disorders
  2. Schizophrenia is the specific type of mental disorder, defined by a subset of psychotic symptoms
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60
Q

Three symptom clusters of psychosis:

A
  1. Positive symptoms: Symptoms that occur in excess of what is typical
  2. Negative symptoms: Symptoms that are absent, but would be present in a non-psychotic individual
  3. Disorganised symptoms: Disruptions in thought patterns and behaviour
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61
Q

DSM-5 schizophrenia

A
  1. Two or more of the following symptoms: Delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour, negative symptoms
  2. Social/occupational dysfunction and decline
  3. Continuous signs of the disorder for 6 months
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62
Q

Positive symptoms of psychosis: Delusions

A
  1. Defined as a fixed and irrational belief that a person holds despite evidence to the contrary
  2. May be of: Persecution (being conspired against), grandeur (special ability like flying), reference (believing that some source is trying to connect with them), erotomania (fixed belief that someone is in love with them), somatic (belief that there is something medically wrong with them), nihilistic (belief that the world is coming to an end)
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63
Q

Bizarre vs. non-bizarre delusions

A
  1. Bizarre delusions: Implausible, could not happen
  2. Non-bizarre delusions: Plausible, even if far-fetched
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64
Q

Positive symptoms of psychosis: Hallucinations

A
  1. Defined as sensory experiences that are not real
  2. May be: Auditory, visual, olfactory, gustatory, tactile
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65
Q

Disorganised symptoms of psychosis: Disorganised speech or thought

A
  1. Loose association (essentially speaking a stream of consciousness, sudden shifts in topic)
  2. Neologisms (words made up by the person)
  3. Clang associations (speaks in rhymes)
  4. Echolalia (repeats what other people are saying)
  5. Echopraxia (mimicking someone’s movements)
  6. Word salad (jumbled, random speech - more confusing than loose association)
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66
Q

Negative symptoms of psychosis:

A
  1. Affective flattening (shallow emotions, reduced or absent expression of affect)
  2. Alogia (poverty of speech)
  3. Thought blocking (when someone is speaking and then completely forgets what they were saying and starts talking about something else)
  4. Avolition (lack of drive/motivation)
  5. Anhedonia (inability to experience pleasure)
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67
Q

Downward drift

A

Symptoms emerge and worsen over time

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68
Q

Course of schizophrenia

A

Three phases:
1. Prodromal: Begin to experience negative symptoms (example: withdrawing from others), and begin to have pseudo-positive symptoms
2. Active: When person reaches the criteria for schizophrenia
3. Residual: Well-managed, begins to be more negative symptoms
Typically chronic

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69
Q

Schizophreniform Disorder

A

Shortened form of schizophrenia (1 month instead of at least 6 months), sometimes goes away

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70
Q

Schizoaffective Disorder

A
  1. Meets diagnostic criteria for schizophrenia, as well as a mood disorder
  2. Typically chronic
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71
Q

Mood disorder with psychotic features

A
  1. Some individuals with Bipolar Disorder or depression may develop psychotic symptoms
  2. Psychotic symptoms only occur in the context of an active mood episode (e.g. may have grandiose sense of self in a manic episode → grandiose delusions)
  3. NOT a psychotic disorder
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72
Q

Delusional Disorder

A
  1. Focuses specifically on the presence of delusion, but no other symptoms of psychosis
  2. Any hallucinations directly related to delusion
  3. Few or no negative symptoms
  4. Less observable impairment
  5. Rare
  6. Better prognosis
  7. Delusions for 1 month or longer
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73
Q

Data for schizophrenia

A
  1. About 0.7-1.5% of the population suffers from schizophrenia in their lifetime
  2. In 3⁄4 of cases, disorder occurs between 15-45 years
  3. Men’s first psychotic break usually between 18-25, women’s is usually betwen 25-35
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74
Q

Aetiology of schizophrenia: Prenatal environmental causes

A
  1. Birth-giver having viral infection during pregnancy may affect brain development of foetus - some studies suggest that children born in winter and spring more susceptible to developing schizophrenia than children born in other seasons (mirrors pattern of viral illness)
  2. Pregnancy and birth complications
  3. Maternal drug use
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75
Q

Aetiology of schizophrenia (one of the most heritable mental conditions): Genetics

A
  1. Study by Sullivan found that about 80% of the symptom variation associated with schizophrenia can be attributed to genetic effects, can be 95% confident that that number is between 70-90%
  2. Study from Denmark (roughly same population size as NZ) compared identical and fraternal twins with respect to concordance rate of schizophrenia, calculated that it was approximately 73% (Hilker et al., 2018)
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76
Q

Concordance rate

A

Statistical measure that describes the proportion of pairs of individuals that share an attribute, given that one already possesses this trait

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77
Q

Aetiology of schizophrenia: Molecular genetics

A
  1. Genes DTNBP1, NGR1 - linked to NTs (dopamine), white matter development
  2. Genes COMT, DDNF - linked to prefrontal functioning
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78
Q

Aetiology of schizophrenia: Brain abnormalities

A
  1. Enlarged ventricles (linked to lower brain volume), found that when looking at identical twins, could accurately identify 12/15 identical twins with schizophrenia (Suddath et al., 1990)
  2. Prefrontal hypometabolism (information that is processed in the prefrontal lobe tends to be slower, less prefrontal lobe activity)
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79
Q

The neurodegenerative hypothesis for schizophrenia:

A

Individuals with schizophrenia have lower brain volumes than individuals without it, have a faster deterioration of brain matter than individuals without it

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80
Q

Dopamine paradox in schizophrenia

A
  1. Excessive dopamine in the subcortical areas (limbic system) → positive psychotic symptoms
  2. Reduced dopamine in prefrontal cortex → negative psychotic symptoms
  3. Research suggests that this really involves different dopaminergic pathways - in prefrontal cortex, less dopamine; limbic system has more dopamine (more of an imbalance)
  4. Implications for a learning paradox (Millard et al., 2022): individuals with schizophrenia tend to condition rewards in the wrong things
81
Q

Biological treatment for schizophrenia

A
  1. 1st gen antipsychotics: Reduced positive symptoms, but had side effects (tardive dyskinesia [TD], neuroleptic malignant syndrome [NMS])
  2. 2nd gen antipsychotics (hoped to reduce side-effects), target both positive and negative symptoms of psychosis
82
Q

Cognitive treatment for schizophrenia: Cognitive rehabilitation

A
  1. Helps guide patient’s perceptual processes (research suggests that schizophrenic individuals pay attention to the wrong cues in the environment, tend to hyperfixate on things)
  2. Some tasks designed to help patients overcome hyperfixation (modify over- and under-attention)
83
Q

Cognitive treatment for schizophrenia: Cognitive restructuring

A
  1. Identify maladaptive and delusional beliefs, challenge them
  2. Psychoeducation: Help patients learn about their symptoms and manage them, help them take care of themselves, might give them social skills training
84
Q

Manic episode

A
  1. 1 week of elevated, expansive, or irritable mood
  2. Three (changes) of the following: grandiose self-esteem, lower need for sleep, overly talkative, racing thoughts, easily distracted, increased activity or agitation, engagement in high-risk activities
  3. Impairment to functioning, possible hospitalisation, or psychotic features
85
Q

Most common delusions in a manic episode:

A
  1. Delusions of grandeur
  2. Delusions that someone is “out to get them”
  3. May have hallucinations
86
Q

Hypomanic episode (HME; milder variant of manic episode)

A
  1. 4 days of elevated, expansive, or irritable mood
  2. Mood disturbance does not critically impair ability to work or maintain social responsibilities (far less than what you’d see in manic episode)
  3. Responses are uncharacteristic and observable by others
  4. NOT euthymia (normal, tranquil state of mood)
87
Q

List bipolar and related disorders:

A
  1. Bipolar I Disorder
  2. Bipolar II Disorder
  3. Cyclothymic Disorder
88
Q

Bipolar I Disorder

A

Defined as the presence of at least one MDE and at least one ME in the person’s lifetime; typically cyclical

89
Q

Bipolar II Disorder

A

Defined as the presence of at least one MDE and at least one HME in the person’s lifetime; depression gets as bad as it does for those with Bipolar I Disorder, but the mania rarely gets as severe

90
Q

Cyclothymic Disorder (mildest version)

A

Individual experiences persistent depressive symptoms/PDD and HME; ups and downs not as severe as in the other disorders, change gradually over time

91
Q

Data for Bipolar I Disorder (typically chronic)

A
  1. U.S.: 12-month prevalence rate is 1.6% of men, 1.5% of women
    Liftetime prevalence rate is 2.2% of men, 2% of women
  2. NZ: Lifetime prevalence rate is 3.8% for all bipolar disorders
    Māori more than twice as likely to meet diagnostic criteria for bipolar disorder in their lifetime (8.3%)
92
Q

Aetiology of bipolar disorders (one of the most heritable disorders): Genetics (biological factor)

A
  1. ~70-90% heritability according to meta-analysis (Smoller et al., 2004)
  2. Looked at 19,000+ same sex twins, found that heritability was 93% (Kieseppa et al., 2004)
93
Q

Bipolar vs. unipolar mood disorder: Genetics

A
  1. Genetic role in bipolar disorder is far greater than what you’d see in unipolar depression, despite there being a lot of similar symptoms
  2. Vulnerability for unipolar or bipolar mood disorder inherited separately
94
Q

Aetiology of bipolar disorders: Biochemical factors (biological)

A
  1. Low levels of serotonin (5HT) + higher levels of norepinephrine (NE) → mania
  2. Low levels of 5HT + low levels of NE → depression
  3. Excessive dopamine has been linked to mania, as well as psychotic symptoms (research not conclusive)
95
Q

What differentiates mania from depression in the biochemical context?

A

Regulation of norepinephrine (NE) - NE is related to energy, and when in a manic episode there is a lot more NE in the body (particularly in the synapses) than when depressed

96
Q

Aetiology of bipolar disorders: Ion activity (biological factor)

A

Ion activity disrupted → chemical misfirings, which may be related to mood changes

97
Q

Aetiology of bipolar disorders: Brain abnormalities (biological factor)

A
  1. Overly active striatum → leads to increased reward-seeking behaviour
  2. Deficits in membranes
  3. Deficits in basal ganglia and cerebellum (implicated in movement, balance)
98
Q

Treatment for bipolar disorders: Biological

A
  1. Psychotropic medication (first-line treatment bipolar disorders)
  2. Mood stabilisers (lithium)
  3. Anticonvulsants (mostly for seizure treatment, have also been effective as mood stabilisers for people with bipolar disorders): Valproic acid, carbamazepine
  4. Atypical antipsychotics (not just for psychotic symptoms, may be prescribed for calming effect and better sleep): Olanzapine, aripiprazole, clozapine
99
Q

Describe what lithium is

A
  1. Type of salt
  2. Most effective medication for reducing symptoms of bipolar disorder
  3. Will often be prescribed as a first method of treatment
  4. Issues: Side effects such as nausea, requires lots of monitoring (easy to overdose) - therapeutic effect of lithium close to the threshold of where it could be a fatal overdose
100
Q

Psychological treatment for bipolar disorders: Psychotherapy

A
  1. Can be helpful with psychoeducation (assisting patients with medication management, developing strategies for managing disorder)
  2. Focuses: Medication management, self-care, social skills, interpersonal relationships
  3. Adjunctive therapy (combining psychotherapy and medication) may:
    Reduce hospitalisation, improve social and occupational functioning
101
Q

Anorexia Nervosa data

A
  1. U.S. mortality rate is 10-15%, highest of any mental health disorder
  2. Highest levels of treatment-seeking, inpatient hospitalisation, suicide attempts
  3. U.S.: 12% of adolescents meet criteria for one or more eating disorders
102
Q

Symptoms of EDs

A
  1. Weight or shape concerns/body dissatisfaction (all EDs)
  2. Restrictive eating (all EDs)
  3. Binge-eating
  4. Purging/compensating
103
Q

Anorexia Nervosa (AN)

A
  1. Restriction of energy intake leading to a significantly low body weight (severity based on BMI)
  2. Intense fear of gaining weight
  3. Disturbance in the way in which one’s body weight or shape is experienced
104
Q

Two types of AN:

A
  1. Restricting Type (no bingeing or purging)
  2. Binge-Eating/Purging Type
105
Q

Bulimia Nervosa (BN)

A
  1. Recurrent binge eating with a sense of lost control
  2. Recurrent inappropriate compensatory behaviour in order to prevent weight gain
  3. Binge eating and compensatory behaviour occur at least once a week for 3 months
  4. Self-evaluation is unduly influenced by body shape and weight
  5. Severity depends on number of binges and compensatory behaviours per week
106
Q

Binge Eating Disorder (BED)

A
  1. Recurrent binges (twice a week, at least 6 months)
  2. Three or more of the following:
    Eating more rapidly than normal
    Eating until uncomfortably full
    Bingeing when not hungry
    Eating alone due to embarrassment
    Feeling disgusted, depressed, guilty after overeating
  3. Self-evaluation unduly influenced by body size and shape
  4. BED does not involve regular use of inappropriate compensatory behaviours
107
Q

Features associated with Bulimia Nervosa

A
  1. Individuals are usually within the normal or overweight range
  2. Individuals typically restrict caloric intake between binges
  3. Low self-esteem
  4. Low mood/depression
  5. High rates of smoking (reduces appetite)
  6. Higher rates of substance abuse (impulse control difficulties)
108
Q

Orthorexia

A

Specific and obsessive adherence to special forms of diets

109
Q

Cognitive restraint

A

Being obsessed with diets, “healthy eating”

110
Q

Muscle-building

A

Typically more “male” manifestation of eating disorder

111
Q

Aetiology of EDs: Genetics (biological factor)

A
  1. High concordance rates for both AN and BN
  2. Relatives of people with ED are six times more likely to develop ED
112
Q

Aetiology of EDs: NTs and hormones (biological factor)

A
  1. Lower levels of serotonin and norepinephrine linked to EDs
  2. AN linked to a deficiency in hypothalamus functioning; weight set point (some people can’t lose weight in the same way as others due to genetics; human body tries to maintain a certain weight)
113
Q

What are EDs in men often associated with?

A
  1. Steroid use
  2. Excessive exercise/weight lifting
  3. Mirror checking
  4. Strict diet
  5. Comparing themselves with other men
114
Q

Multidimensional risk perspective

A
  1. Biological factors
  2. Sociocultural factors
  3. Psychological factors
    More factors → greater risk
115
Q

Diet-Binge-Purge Cycle

A

Rigid dieting → slip → abstinence violation effect → bingeing → guilt, remorse (for BED, purging is skipped and individuals go straight to rigid dieting) → purging → cycle starts again

116
Q

Treatment for AN:

A
  1. Restoration of proper weight
  2. Sometimes hospitalisation for malnutrition
  3. Residential programs (need to be monitored)
  4. Cognitive Behavioral Therapy (CBT; underlying maladaptive thoughts that lead to that behaviour)
  5. Family Systems Therapy (due to influence of broader family dynamics)
117
Q

Treatment for BN and BED:

A
  1. CBT
  2. Medication
118
Q

Intellectual disability

A

Types (based on deficits): Mild, moderate, severe, profound - most individuals beyond the ‘mild’ type cannot function on their own

119
Q

Disorders that emerge in childhood:

A
  1. Neurodevelopmental disorders
  2. Behaviour disruptive disorders (a.k.a. externalising disorders)
  3. Mood and anxiety disorders
120
Q

Difficulties with diagnosing disorders in childhood:

A
  1. Children more likely to act out rather than seek help (not the same capacity for communication or self-awareness)
  2. Certain degree of deviance and irrational behaviour is typical (difficult to differentiate between what behaviour is typical and what behaviour is cause for concern)
  3. Some psychological disorders in children cause little/no conscious distress - might not have sufficient insight or awareness that they’re having mental health problems
121
Q

Intellectual disability

A
  1. Present at birth and persists throughout life (no real treatment)
  2. Diagnostic criteria:
    Onset before age 18
    Deficits in intellectual functioning - determined by intelligence testing and as appropriate for social and cultural context (white Western society)
    Deficits in adaptive functioning (communication, social, practical)
  3. Types (based on deficits): Mild, moderate, severe, profound - most individuals beyond the “mild” type cannot function on their own
122
Q

Aetiology of intellectual disabilities: Biological factors

A
  1. Genetics: Down Syndrome, Fragile X Syndrome
  2. Metabolic abnormalities: Phenylketonuria (PKU), Tay-Sachs Disease
  3. Prenatal and postnatal complications (drug exposure, anoxia at birth)
123
Q

Autism Spectrum Disorder (ASD)

A
  1. Deficits in social communication:
    Nonverbal/limited verbal behaviours
    Poor peer relations due to atypical communication
    Difficulty with social and emotional reprocity (issues with empathy)
  2. Restricted, repetitive behaviour patterns:
    Stereotypic, repetitive speech
    Excessive adherence to routines, rituals
    Very restricted interests, with abnormal focus (special interest)
    Hyper- or hypo-reactivity to sensory input
124
Q

ASD data

A
  1. Occurs in less than 1% of the population
  2. Symptoms are typically recognised during the second year of life (pre-school)
  3. Four times more common in boys than girls
  4. In most cases, there is no period of normal development - but developmental gains often occur in late childhood
125
Q

Aetiology of ASD: Genetics (biological factor)

A

Meta-analysis by Tick et al. 2016 found:
Heritability of ~90%
Identical twins concordance rate of ~98%

126
Q

Aetiology of ASD: Brain abnormalities (biological factor)

A
  1. Cerebellum (movement, balance), limbic system (empathy, perspective-taking), amygdala, white matter (information-processing)
  2. NT abnormalities
127
Q

Treatment for ASD

A
  1. Modelling and operant conditioning applied behaviour analysis - for individuals with a more “severe” case
  2. Communication training to the degree necessary
  3. Parent training (psychoeducation, helping parents understand; offering support)
  4. Community integration (schools)
128
Q

Behaviour disruptive disorders/externalising disorders:

A
  1. ADHD (also a neurodevelopmental disorder)
  2. Oppositional Defiant Disorder (ODD)
  3. Conduct Disorder (CD)
129
Q

ADHD

A
  1. Inattention (above and beyond what is typical, especially in childhood), hyperactivity, and impulsivity
  2. Three subtypes:
    Predominantly inattentive type, predominantly hyperactive-impulsive type, combined type
130
Q

Aetiology of ADHD: Genetics (biological factor)

A

60-80% heritability rate (Nikolas & Burt, 2010)

131
Q

Aetiology of ADHD: Structural and NT abnormalities (biological factor)

A
  1. Structural abnormalities: Under-responsive prefrontal and striate regions (dorsolateral part of prefrontal cortex particularly underfunctioning –> poor attention/executive functioning)
  2. NT abnormalities: Excess dopamine in the brain, more reward-seeking - difficult to inhibit response to something that brings them joy
132
Q

ADHD treatment: Biological

A
  1. Stimulant medications (e.g. Ritalin [most effective], Adderall, Concerta)
  2. Non-stimulant medications without addictive potential (Strattera [Atomoxetine])
133
Q

ADHD treatment: Psychological

A

Behaviour therapy based on operant conditioning

134
Q

Oppositional Defiant Disorder (ODD)

A
  1. Early onset
  2. Excessively argumentative
  3. Temper tantrums
  4. Behaviour tends to be fairly restrictive to authority figures
  5. Refusal to comply with rules
  6. Blame externalisation
  7. Anger and resentment
135
Q

Conduct Disorder (CD)

A
  1. More severe than ODD, more pervasive (not just reacting to particular authority figures)
  2. Aggression to people and animals
  3. Destruction of property
  4. Deceitfulness or theft
  5. Serious violation of rules
  6. Childhood-onset (before age 10); adolescent-onset (age 10 or later)
136
Q

Specifier that can be attached to a CD diagnosis: Limited Prosocial Emotions (callous or unemotional traits)

A

Shows two or more of the following characteristics persistently over at least 12 months and in more than one relationship or setting:
1. Lack of remorse or guilt
2. Callous
3. Unconcerned about performance
4. Shallow or deficient affect

137
Q

Aetiology of ODD and CD:

A
  1. Genetics: Genetic propensity towards externalising disorders ~50% (between 30-70%; Rhee et al., 2002; Waldman et al., 2021)
  2. Familial risk factors (child abuse, family conflict)
  3. Sociocultural risk factors (poverty, dangerous neighbourhoods, past antisocial behaviour)
  4. Peer groups and past antisocial behaviour in combination is best predictor
138
Q

Krueger et al. (2002)

A

Found that 81% of what all externalising disorders have in common can be attributed to a genetic vulnerability, but when you look at individual disorders there is a far greater environmental role (underlying genetic factors, but environment determines how it manifests)

139
Q

Treatment for ODD and CD:

A
  1. Family-focused: Multisystemic family therapy - focuses on full family system
  2. Child-focused: Behavioural (operant conditioning)
  3. Prevention-focused: Preventing full disorder development
140
Q

Alcohol data (NZ)

A
  1. 20% of adults drank alcohol in a way that could harm themselves or others in the last year
  2. Hazardous drinking rates higher in Māori (33%) than NZ European (20%); higher in men (27%) than women (12%)
  3. Highest in youth aged 18–24 years (33%)
  4. Adult drinkers in poor areas 1.7 times more likely to be hazardous drinkers
141
Q

Illicit drugs data (NZ)

A
  1. 12% of adults used cannabis in past year
  2. 1% used methamphetamine
    These rates are approximately double for Māori and 1⁄4 for Asian ethnicities
142
Q

Public health impact of substance use (U.S.)

A
  1. Annual cost to U.S. almost $500 billion
  2. 63% of all violent crime occurs during an intoxicated or drug-induced state
  3. Overall cost of substance use violence in U.S. per year is over $200 billion
143
Q

U.S. data on substance abuse

A

63% of all violent crime occurs during an intoxicated or drug-induced state

144
Q

Substance Use Disorder (SUD)

A
  1. Problematic pattern of use which impairs functioning, including two or more symptoms within a 1 year period:
  2. Diagnosis is substance-specific
  3. Classification: Use, intoxication, withdrawal (e.g. can be diagnosed with substance intoxication)
145
Q

Symptoms of SUD:

A
  1. Failure to meet obligations
  2. Repeated use in dangerous situations
  3. Repeated relationship problems
  4. Continued use despite problems caused
  5. Tolerance (need more drugs to have same effect)
  6. Withdrawal
  7. Substance taken for a longer time or in greater amounts than initially intended
  8. Efforts to reduce or control use ineffective
  9. Time spent acquiring substance
  10. Impairment to functioning
  11. Cravings
146
Q

Addiction definition

A

A severe SUD (six or more symptoms), requires both tolerance and withdrawal

147
Q

Depressants (alcohol, opioids)

A

Have a reducing effect on the brain, depresses functioning of prefrontal cortex (reduces inhibitions), depressing effect on central nervous system

148
Q

Stimulants (cocaine, methamphetamine)

A

Stimulate activity in the central nervous system, give person more energy

149
Q

Hallucinogens (LSD)

A

Induce an altered state of consciousness

150
Q

Cannabis (THC is the active ingredient)

A

Sort of depressant, can cause a state of calm

151
Q

Polysubstance Use

A

Meeting substance use criteria for at least three substances, especially with alcohol

152
Q

Sex differences in substance use

A
  1. Men more likely to use alcohol and psychoactive drugs overall
  2. Women more likely to misuse in response to stress or self-medicate
  3. Women have lower tolerance to alcohol than men
153
Q

Aetiology of substance use: Brain abnormalities (biological factor)

A
  1. Nucleus accumbens (related to the reward centre) feeds into the mesolimbic dopaminergic system (related to processing and conditioning of rewards in the environment)
  2. People with over-sensitive reward system → more prone to want to use
154
Q

Kendler et al. 2003

A

Found that there was a general genetic vulnerability to developing an externalising disorder, disorder-specific genetic factors for substance use dependence

155
Q

Treatment of substance abuse

A
  1. Biological: Antagonist therapy - taking medication that attenuates effects of substance, still feeds physiological addiction
  2. Psychological: Aversion therapy (behavioural principle) - punish substance use
    Motivational interviewing (effective to get people to engage in treatment, works through number of steps to come to terms with addiction)
    12-step programs
156
Q

DSM-5 Personality Disorder definition

A
  1. Inflexible and pervasive personality style that occurs across contexts
  2. Chronic and stable in duration
  3. Clinically significant distress and/or impairment in functioning
157
Q

History of Personality Disorders (PDs)

A
  1. Psychoanalytic theory, started out in early versions of the DSM (1952), DSM-II (1968) - tended to be defined through psychodynamic terms
  2. DSM-III and onwards: Descriptive checklist, stable measurement of aetiological, dynamic concepts - wanted to improve diagnostic reliability
158
Q

How do PDs affect therapeutic alliance?

A

Waldinger & Gunderson 1984: Found that patients with PDs tend to have a difficult time developing a therapeutic alliance with their therapist than those without PDs

159
Q

How do PDs affect the treatment of other mental disorders?

A

NZ research: Outcomes of treatment for the treatment of other mental disorders such as depression tend to be worse for individuals with a PD (Newton-Howes et al., 2014)

160
Q

U.S. stats on PDs:

A
  1. People with PDs have worse general health outcomes (Dixon-Gordon et al., 2015)
  2. People with PDs consume more psychiatric care resources than people with other mental disorders (Sansone et al., 2018)
161
Q

PDs fall into three general clusters:

A
  1. Cluster A (unusual thoughts or behaviours): Paranoid, schizoid, schizotypal
  2. Cluster B (dramatic, emotional, or erratic): Antisocial, borderline, histrionic, narcissistic
  3. Cluster C (anxious or fearful ): Avoidant, dependent, obsessive-compulsive
162
Q

Paranoid Personality Disorder

A
  1. Deep suspicion or mistrust of others
  2. Hypersensitivity, vigilance, and caution
  3. Control, anger/hostility
163
Q

Schizoid Personality Disorder

A
  1. Extreme social detachment
  2. Cold and disaffiliated emotional expression
164
Q

Schizotypal Personality Disorder (cross-sectioned with Schizophrenia Spectrum Disorders in DSM-5)

A
  1. Psychoticism, magical ideation; unusual beliefs - not to the degree of delusion
  2. Social anxiety and suspiciousness; social isolation - have some degree of awareness that their ideas are “eccentric”
165
Q

Similarity of Cluster A disorders to schizophrenia, treatment

A
  1. People with these disorders display behaviours similar to, but not as extensive as, schizophrenia - “schizophrenia-spectrum disorders”
  2. Little known about treatment
166
Q

Aetiology of Cluster A

A
  1. Schizotypal (conceptually) linked to positive symptoms of schizophrenia, but less severe
  2. Schizoid (conceptually) linked to negative symptoms of schizophrenia
167
Q

Cluster A PDs’ respective links to schizophrenia (Nigg & Goldsmith, 1994):

A
  1. Weak: Schizoid PD
  2. Medium: Paranoid PD
  3. Strong: Schizotypal PD
168
Q

Cluster B “dramatic” PDs

A
  1. Antisocial personality disorder (ASPD)
  2. Borderline personality disorder (BPD)
  3. Histrionic personality disorder
  4. Narcissistic personality disorder (NPD)
    All characterised by dramatic, emotional, or erratic behaviour - almost impossible to have satisfying relationships
169
Q

Antisocial personality disorder (ASPD)

A
  1. Disregard for social norms and standards
  2. Impulsivity and recklessness
  3. Irresponsibility
  4. Aggression
  5. Lack of remorse
170
Q

Borderline personality disorder (BPD)

A
  1. Extreme emotional dysregulation
  2. Identity and attachment disturbance
171
Q

Histrionic personality disorder

A

Extreme self-centeredness and need for attention; exhibitionism

172
Q

Narcissistic personality disorder (NPD)

A

Grandiose self-appraisal; entitlement and arrogance; needs admiration; self-obsession and lack of empathy

173
Q

Cluster C “anxious” PDs:

A
  1. Avoidant personality disorder
  2. Dependent personality disorder
  3. Obsessive-compulsive personality disorder
    All characterised by anxious and fearful behaviour
174
Q

Dependent personality disorder

A
  1. Separation anxiety, rely on others for decisions, high distress (self-aware)
  2. Extreme submissiveness
175
Q

Obsessive-compulsive personality disorder

A
  1. Rigid perfectionism, extreme need for order
  2. Excessive adherence to moral codes and standards
  3. Cold interpersonal style - not overtly emotional
176
Q

Avoidant personality disorder

A
  1. Most common PD, often diagnosed as social anxiety
  2. Pervasive social anxiety (fear of rejection and humiliation), significant self-doubt → significant social withdrawal
177
Q

What is the difference between the social withdrawal that characterises both schizoid PD and avoidant PD?

A

Individuals with schizoid PD are withdrawn socially but don’t care, while individuals with avoidant PD want social relationships but are highly fearful of them

178
Q

What is the diagnosis of BPD like in NZ?

A
  1. PDs not often diagnosed, but usually diagnosed as BPD when they are (Howes et al., 2021)
  2. Only disorder for which evidence-based treatments are available
179
Q

ASPD

A
  1. Needs to have three of seven symptoms
  2. Evidence of Conduct Disorder (CD) before age 15
  3. 50-80% of correctional inmates meet criteria for ASPD, although that number is lower with CD requirement
180
Q

What are the seven symptoms of ASPD?

A
  1. Disregard for social norms
  2. Reckless behaviour
  3. Impulsivity
  4. Irresponsibility
  5. Prone to anger/aggression
  6. Deceitfulness and manipulative
  7. Lack of guilt or remorse
181
Q

“Psychopathy” data

A

15-25% of prison population meet psychopathy requirements, as compared to 1% of general population

182
Q

Psychopathy symptoms (in addition to ASPD):

A
  1. Interpersonal deficits: Superficial charm, grandiosity, pathological lying
  2. Affective deficits: Shallow emotions, fearlessness, callous, lack of empathy, guilt, and remorse, inability to form deep relationships
183
Q

Two-process model for aetiology of psychopathy

A
  1. Affective/interpersonal: People with psychopathy have lower volume, reduced functioning in their amygdala – poor fear conditioning, inability to read distress cues
  2. Antisocial behaviour: Orbitofrontal cortex – disinhibition, poor emotional decision making
184
Q

BPD (border between neurosis and psychosis)

A
  1. Instability of self-image and relationships: Identity disturbance, intense interpersonal attachments, idolization vs. evaluation
  2. Affective instability: Dysphoria and chronic feelings of emptiness, prolonged/violent emotional outbursts, extreme emotional response to abandonment
  3. Impulsive, unpredictable, and destructive behaviour:
    Bouts of anger/violence, suicidal gestures, substance abuse, reckless behaviour
185
Q

Aetiology of BPD: Biopsychosocial theory (M. Linehan)

A

Genetic vulnerability to emotional dysregulation coupled with invalidating childhood environments (not learning from the environment to appropriately regulate their own emotions)

186
Q

Aetiology of BPD: Psychological

A

Psychodynamic → early parent relationships
1. Object-relations → lack of early acceptance by parents (attachment disturbance to other people; can’t form attachments to people in a safe manner)

187
Q

Treatment of BPD

A
  1. Dialectical behaviour therapy (DBT; initially designed to deal with extreme behaviours such as suicidality); DBT therapists on call for patients at all times
  2. Mentalization-Based Therapy (MBT): Psychodynamic, helping individuals develop an appropriate perspective
188
Q

Prevalence of BPD: Volkert et al. (2018) meta-analysis

A

Prevalence rate for at least one PD was 12.16%

189
Q

Ten-Year Course of BPD: Gunderson et al. (2010)

A

Found that if you studied individuals with BPD over time, they often remit - not as stable of a disorder as once thought

190
Q

Limitations within DSM-5 system for PD diagnoses:

A
  1. Excessive comorbidity (if you meet diagnostic threshold for at least one of these PDs, there’s at least 50% chance you’ll meet diagnostic threshold for another PD)
  2. Inadequate coverage - 40% of patients who meet general PD threshold don’t map onto any of these 10 PDs
  3. Excessive within-diagnosis heterogeneity - lots of different presentations in the same PD
  4. No clear boundary between normal and pathological personality
  5. Inadequate scientific base
  6. Marked temporal instability
191
Q

DSM-5 Section III Alternative Model (not adopted, placed in appendix): PDs

A
  1. Criterion A: Significant impairments in self (identity or self-direction) and interpersonal (empathy or intimacy) functioning
  2. Criterion B: Personality profile (five personality traits domains with three to seven facets each)
    Negative
    Affectivity
    Detachment
    Antagonism
    Disinhibition and compulsivity
    Psychoticism
  3. Six PDs, not 10
192
Q

DSM-5 Section III Alternative Model PDs:

A
  1. Antisocial
  2. Avoidant
  3. Borderline
  4. Narcissistic
  5. Obsessive-compulsive
  6. Schizotypal
193
Q

ICD-11 and PDs

A
  1. Published in 2018
  2. Approved for full acceptance by WHO member states in 2019, formal implementation by member states in January 2022
  3. PDs changed from categorical to dimensional
    (PD is a dimensional impairment continuum - personality traits can be used to characterise manifestation of PD)
194
Q

6D10 - PD (from ICD-11)

A

Severity gradient (how prevalent symptoms are across contexts, how are they impairing the individual), with different diagnoses for that severity

195
Q

6D10 PDs: Personality difficulty (no disorder/no real diagnosis)

A

Some disturbance in self-regulation or interpersonal functioning, but does not cause considerable subjective distress or impairment in functioning

196
Q

6D10 PDs: Mild PD

A

Disturbances affect some areas of personality functioning but not others, typically no harm to self or others, distress/impairment could be more circumscribed contexts or mild if in many

197
Q

6D10 PDs: Moderate PD

A

Disturbances affect some areas of personality functioning but not others, harm to self or others could be present, distress/impairment is marked across contexts, although functioning in some circumscribed contexts could be maintained

198
Q

6D10 PDs: Severe PD

A

Severe disturbance across contexts, functioning severely compromised, virtually all relationships and contexts are affected, often associated with self- and/or other harm, severe impairment in all or nearly all areas of life

199
Q

6D10 PDs: Trait qualifiers

A

Five personality trait qualifiers:
1. Negative affectivity (dispositional proclivity towards experiencing a wide range of negative emotions, emotional dysregulation, interpersonal difficulty/anxiety)
2. Detachment (extreme social withdrawal)
3. Dissociality (analogous to antagonism, disregard for others, self-focused, grandiose, etc.)
4. Disinhibition (impulsivity, risk-taking)
5. Anankastia (compulsivity, perfectionism)
6. Borderline pattern (initially not included) - personality disturbance characterised by a pervasive pattern of instability of interpersonal relationships, self-image, emotions, and marked impulsivity (as indicated by the nine symptoms of the traditional BPD diagnosis)

PSYC112 (4 decks)

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