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NMH BSc > Module 3: Part 3 > Flashcards

Module 3: Part 3 Flashcards

1
Q

What do MRI studies show of the pathogenesis of schizophrenia?

A
  • Decreased brain volume - Decreased size of hippocampus, amygdala & parahippocampal gyrus
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2
Q

What do PET studies show of the pathogenesis of schizophrenia?

A
  • Decreased activation of the frontal lobe - Increased activation of the temporal lobe
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3
Q

What is the dopamine hypothesis of schizophrenia?

A
  • Increased dopamine —> +ve symptoms - Decreased dopamine (in mesocortical areas) —> -ve symptoms - Amphetamine + Levodopa —> Increased dopamine —> +ve symptoms in non-schizophrenics - D2 receptor antagonists are effective antipsychotics
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4
Q

What is the serotonin hypothesis of schizophrenia?

A
  • Increased serotonin —> psychotic symptoms - 5HT receptor agonists (Psilocybin) —> +ve symptoms in non-schizophrenics - 5HT receptor antagonists —> -ve symptoms
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5
Q

What is the excitatory amino acid hypothesis?

A
  • Decreased EAAs or decreased receptors —> Schizophrenia - SCZ have low CSF glutamate & low glutamate receptors in temporal lobe - NMDA receptor antagonists —> +ve and -ve symptoms in non-schizophrenics
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6
Q

What is the phospholipid membrane hypothesis?

A
  • Abnormalities in phospholipid metabolism (neuronal membrane) —> Schizophrenia
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7
Q

What is the management of schizophrenia?

A
  • Antipsychotics - Talking therapies - ECT - Hormones (conflicting evidence)
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8
Q

What is the prognosis of schizophrenia?

A
  • Rule of 1/3 - 1/3 good outcomes - 1/3 have longer and repeated episodes - 1/3 chronic treatment resistance
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9
Q

What are some sex differences between males and females in schizophrenia?

A
  • Males have: - Earlier onset - More -ve symptoms - Poorer prognosis
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10
Q

What are some potential mechanisms for sex differences between males and females?

A
  • Higher incidence of birth injuries in boys - Buffer of early marriage in females (early marriage so more likely to have strong social relationships) - Sexually dimorphic brain anatomy - Differential effects of androgens and oestrogens
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11
Q

Describe the sexually dimorphic brain anatomy to explain sex differences in schizophrenia

A
  • Brain template is female - At 6 weeks of gestation, testosterone differentiates male characteristics
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12
Q

Describe the activational effects of oestrogen in schizophrenia (Later in life)?

A
  • Oestrogen may be protective against psychosis - Increased incidence after menopause, decreased psychosis during pregnancy and increased psychosis post-partum - Oestrogen antagonises dopamine receptors —> less positive symptoms - Oestrogen’s biphasic effects: effective in the short term but wears off - Oestrogen may up or down-regulate dopaminergic receptors - Oestrogen KO in mice —> Apoptosis of hypothalamic dopaminergic neurons (does not occur in females) - Variants in Oestrogen receptor alpha genes and mRNA (ESR1 variant associated with increased risk of psychosis)
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13
Q

What are the organisational effects of testosterone (Early in life)?

A
  • Perinatal organisation effects of sex hormones on sexual differentiation - During development: in males: Increased testosterone to masculinise hypothalamus (not in females) - Testosterone modulates pre-frontal cortex and amygdala (organisational effects)
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14
Q

How does testosterone and oestrogen affect the disruption of pre-pulse inhibition in schizophrenia?

A
  • Normally: loud noise —> startle response and quiet noise followed by loud noise —> decreased startle response - SCZ have disrupted startle PPI response so same startle response to loud and quiet + loud noise - Testosterone promotes disruption of pre-pulse inhibition - Oestrogen protects against disruption of pre-pulse inhibition
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15
Q

What domains do most child mental health problems fall into?

A
  • Emotional problems - Conduct problems - Developmental delays - Relationship difficulties
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16
Q

What is a framework for child mental health assessment?

A

SIRSE - Symptoms: What sort of problem is it? - Impact: How much distress or impairment is it causing? - Risks: What has initiated or maintained the problem? - Strengths: What assets are there to work with? - Explanatory model: what beliefs or expectations do the family or young person bring with them?

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17
Q

What is the epidemiology of Child/Adolescent Mental Health?

A
  • Overall prevalence of CYP disorder- 6.8% - In CYP, if there is a brain disorder, CYP disorders are 44% - Emotional disorders: Female and Male: 1:0.7 - Conduct disorder: Female and Male 1:4:
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18
Q

What is autism?

A
  • Triad of impairment 1) Communication 2) Social interactions 3) Restricted, repetitive and stereotypic patterns of behaviours - Spectrum - Strongly associated with Intellectual Disability but increasing prevalence now 70% have normal range IQ - Boys:Girls; 4:1 - ICD-10 - Regression 20-30%
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19
Q

Describe impairment in communication in Autism

A

Verbal - Speech delay - Stereotypic speech (utterances) Non-verbal - Poor gestures - Lack of varied spontaneous make-believe and creative play

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20
Q

Describe impairment in social interaction in Autism

A
  • Impaired reciprocal interaction - Miss social-emotional cues and lack reciprocity - Lacking ‘Theory of mind’ - Literal, concrete understanding - Failure to develop peer relationships - Lack of shared enjoyment and pleasure
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21
Q

Describe restricted, repetitive and stereotyped patterns of interests and behaviours

A
  • Tendency not to use objects in intended functional fashion (e.g. repetitive use, unusual sensory interests) - Little imaginative play - Stereotyped motor mannerisms (e.g. hand and finger/complex mannerisms) - Adherence to non functional routines/rituals - Unusual pre-occupations or circumscribed interests
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22
Q

What is Childhood Autism?

A
  • Triad of impaired communication, impaired social relationships and restricted, repetitive and stereotyped behaviour - Abnormal and/or impaired development before 3 years old - Non specific problems: fears/phobia, sleeping/eating disturbances, aggression, self-injury
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23
Q

What is Asperger’s Syndrome?

A
  • Autism BUT no delay in language or cognitive development - M > F - Strong tendency for abnormalities to persist into adolescence and adulthood
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24
Q

Describe development in Autism

A
  • A continual childhood process - Behaviours ‘normal’ at one age may be ‘abnormal’ at another - ASD has to be viewed developmentally for accurate diagnosis, assessment and intervention (deviance and/or delay) - Quality of social overture is more important in High Functional Autism and older children
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25
Q

What are examples of early age behaviours in autism?

A
  • Feeding problems - Dislike of physical contact/content to be alone ‘angel baby’ - Lack of social pointing and eye contact - Inability to play reciprocal games - Babbling limited in quantity and quality
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26
Q

What is the epidemiology of Autism?

A
  • Onset in early life - M > F - 1% of adult population - Associated with intellectual disability - Increasing prevalence? Improved diagnosis and increased awareness
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27
Q

Why is there increasing rates of Autism in migrant populations?

A
  • Viral infections - Consanguineous
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28
Q

What are the co-morbidities of Autism?

A
  • Intellectual disability (70%) - ADHD (30%) - Increasing rates of epilepsy
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29
Q

What are genetic factors of Autism?

A
  • Monozygotic twins in 36-60% concordance rates - Presumed X-linked due to M>F, but families some Male-to-Male transmission?
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30
Q

What are the environmental factors of Autism?

A
  • Obstetric complications (traumatic births) - Possible: ?Diet, Allergies, ?MMR Vaccine (now disproved)
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31
Q

What is the psychological hypothesis of Autism?

A
  • Evidence of persistent cognitive dysfunction in Autism - ?Less activation in pre-frontal cortex
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32
Q

What is the DDx of autism?

A
  • Language disorder - Expressive, receptive, both - Was development ever normal? - If yes then consider - Elective mutism - Disintegrative disorder - Schizophrenia - Severe psychological deprivation (e.g. Romanian orphans) —> Language delay, abnormal social behaviour, unusual habits - Deaf children: talk late, less socially skilled - Visual impairment: Autism is just a stage blind children go through due to issues with mother-infant relationships
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33
Q

What is included in the history and examination of Autism?

A
  • Wood’s light - Cafe-au-lait spots - Height, weight and head circumference (Rett’s) - Shape of the head IF INDICATED - Bloods - TORCH screen for prenatal infections - Toxoplasma - Rubella - Cytomegalo virus - Herpes simplex - Chromosomal karyotyping - CT or MRI
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34
Q

What are some diagnostic tools for Autism?

A
  • ADOS-2: Autism Diagnostic Observation Schedule (looking at the triad of impairment) - ADI-R: Autism Diagnostic Interview-Revised - DISCO: Diagnostic Interview for Social and Communication Disorders (Outdated) - 3di: The Developmental, Dimensional and Diagnostic Interview
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35
Q

What are some screening tests for Autism?

A
  • CHAT: Checklist for Autism in Toddlers - m CHAT - SCDC
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36
Q

What are the challenges of Autism diagnosis?

A
  • Cluster of symptoms important - Quality as well as presence or absence of phenomena - Comorbidity and other delay - Family styles - Behaviour patterns (and IQ) may change with increasing age
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37
Q

What does management of Autism involve?

A
  • No cure - Pharmacotherapy: Risperidone - Treat co-morbidities: Methylphenidate for co-morbid ADHD (30%) - Special needs education: Create a friendly environment - Speech and Language Therapist - Macaton: for non-verbal children, cards with symbols to help them communicate - Occupational therapy (for dyspraxia) - Behaviour management: reduce unwanted behaviours
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38
Q

What are specialist interventions for Autism?

A
  • Lovaas-behavioural technique- 20,000 pounds per year - applied behaviour analysis to treat Autism - PACT study: Pre-school Autism Communication Trial —> Decreased symptom severity at long-term follow up 6yr 12 month early intervention (vs TAU) to train child to interact socially, tell mother to act certain way
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39
Q

What is the prognosis of Autism?

A
  • Early symptoms tend to disappear with age - Social/Communication impairments may remain
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40
Q

What are the domains of development?

A
  • Emotional - Physical - Cognitive - Social
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41
Q

Describe social and emotional development between birth to 12 months

A
  • Birth to 3 months: Smiles/shows pleasure in response to interact, comforted by familiar adult - 3 to 6 months: initiates interaction, smile spontaneously, peek a boo - 6 to 9 months: differentiates emotions, distinguish friends/strangers, prefer familiar people - 9 to 12 months: separation anxiety, imitation, self regulation
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42
Q

Describe social and emotional development between 1 years to 4 years

A
  • 1 to 2 years: sense of self, assertive, direct others, pride and pleasure with accomplishments - 2 to 3 years: explore more, self help skills, self as good/bad etc., aware own feelings vs others - 3 to 4 years: more interested in other children, initiate/join, play with others, share toys
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43
Q

How does the brain develop in early years?

A
  • Child’s brain doubles in size in the first year - By age 3: reaches 80% of its adult volume - The back-and-forth interactions of babies and adults shape a baby’s brain architecture - Supports development of communication and social skills
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44
Q

What are emotions?

A
  • Feeling or state of mind - Generated from interaction with biochemical (internal) and/or environmental (external) factors - Positive or negative valence - Involves: - Physiological arousal - Expressive behaviours - Conscious experience
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45
Q

What is temperament?

A
  • How a young child acts and responds to different situations & individuals
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46
Q

What is an attachment?

A
  • Emotional bond between a child and caregiver
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47
Q

What is emotional regulation?

A
  • The ability of a child to control his or her emotions and reactions to the environment
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48
Q

What are social skills or social competence?

A
  • Ability to get along with others
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49
Q

How do basic emotions develop?

A
  • Joy (3 months) - Sadness (3 months) - Disgust (3 months) - Anger (2-6 months) - Surprise (first 6 months) - Fear (6-9 months)
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50
Q

How do self conscious emotions develop?

A
  • Empathy (1.5-2 years) - Jealousy (1.5-2 years) - Embarrassment (1.5-2 years) - Pride (2.5 years) - Shame (2.5 years) - Guilt (2.5 years)
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51
Q

What are the functions of early emotions?

A
  • Communicate needs - Solicit external response from a caregiver - Promote survival e.g. hunger - Relational - A way to engage in interactions with others and to understand others emotions
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52
Q

Describe the visual cliff experiment

A
  • If baby is encountering an insignificant situation, they will turn to the significant other (e.g. caregiver) and will respond depending on the significant other’s non-verbal cues
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53
Q

Describe temperament (in depth)

A
  • Individual differences or early dispositions - Simple, non-motivational, non-cognitive, stylistic characteristics that represent meaningful ways of describing individual differences (Rutter, 1987) - Child bring characteristics that contribute to his/her development - “Biological”, influence social/cognitive development, foundation for personality but different
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54
Q

Describe Thomas & Chess experiment

A

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55
Q

Describe Kagan’s temperament categories

A

Two types of temperament - Inhibited temperament (highly reactive): More reserved, more guarded and introverted - Uninhibited (low reactive): More outgoing, extroverted, very comfortable in social situations Characteristics —> influence later behaviour depending on how they interact with the environment

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56
Q

What are the origins of individual differences? (Temperament)

A

GENETICS - Behavioural genetics: Modest to high heritability esp. fearfulness - Molecular genetics: dopamine receptor gene, serotonin receptor gene, gene environment interaction, e.g. certain allele —> different outcome depending on maternal sensitivity EPIGENETICS - Preconception, pre- and perinatal influences: Maternal health, substance abuse, birth difficulties

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57
Q

How does temperament relate to stability?

A
  • Temperamental characteristics in first couple of years —> low correlation with supposedly comparable characteristics in adolescence - More consistency between between early school years and teenage period (correlations 0.3-0.5). - Consistency for extreme characteristics greater than for same characteristics in middle range.
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58
Q

What are the implications of temperament for psychopathology?

A
  • Temperament predicts development of later emotional and behaviour disorders in normal and high risk samples - Association between difficult temperament and higher rate of accidents, sleep difficulties and infantile colic - Predicts behavioural deviance at school - Increases psychiatric risk by altering others responses
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59
Q

Describe Bowlby’s Attachment theory

A

1) Children need their primary caregiver(s) to be: - A secure base for exploration - A safe haven for protection 2) Children’s perception of the caregiver form basis for “internal working models”: Of self, caregiver, others 3) As individuals grow to adulthood, internal working models influence interpersonal behaviour

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60
Q

Describe Mary Ainsworth’s Attachment theory

A
  • Strange situation procedure - Observation of child’s behaviour - Exploratory - Reaction to parent departures and return - Classification of child’s behaviour on parent’s return
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61
Q

Describe Mary Ainsworth’s 2nd Attachment theory

A
  • A) Insecure - avoidant: Infant is detached on separation, avoids parent on reunion, engages in displacement exploration that is devoid of true interest - B) Secure: infant engages in positive exploration, is upset by separation but gives a positive response to parent upon reunion, with a rapid return to exploration - C) Insecure - resistant/ambivalent: Infant is preoccupied with parent’s availability. Shows distress or separation and anger/ambivalence upon reunion and is difficult to comfort - D) Disorganised: Inconsistent contradictory behaviors, dysregulated in presence of caregiver
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62
Q

Describe stability/association/outcomes in attachment

A
  • Stability: longitudinal research mixed, methodologically complex - Stress response: cortisol increase in Strange Situation (Bernard et al 2010) - Secure attachment: none Disorganised and Insecure: present - Disorganised pattern strongest predictor for childhood psychopathology and adjustment - More: vulnerable to stress, difficulty regulating negative emotions, hostile, oppositional, aggressive behaviour - Early school years: internalizing /externalizing difficulties, self esteem, peer relations
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63
Q

What is emotional regulation?

A
  • The processes by which individuals influence which emotions they have, when they have them, and how they experience and express these emotions - During early development: dyadic - Becoming more capable of managing feelings, one of the most challenging tasks of development - Attention allocation important component - Impact of peers / stress on emotion regulation e.g. bullying & blunted cortisol response (Oellet-Morin et al 2011) - Adolescent impulsivity - Time of maximal maturity difference between subcortical and cortical brain structures - Adol’s better cognitive response inhibition than younger children - Difficulty suppressing reward related cues- ? Link with risk taking
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64
Q

What do twin studies for depression show us?

A
  • Monozygotic twins reared together show 76% concordance - Monozygotic twins reared apart show 67% concordance - Dizygotic twins reared together show 19% concordance
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65
Q

What are the environment risks of adolescent depression?

A
  • Parental depression - Family discord - Maltreatment - Peer victimisation - Bereavement
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66
Q

How does puberty occur?

A
  • Gonadal hormones —> ? Direct CNS effect mood, cognition, motivation - Rapid growth —> change in body shape/sexual maturation —> ? negative experience - Timing e.g. early or late developer - NB Mid puberty - Circadian rhythm changes
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67
Q

How does the brain develop during adolescent development changes?

A
  • Prefrontal cortex: grey matter thinning, synaptic pruning, myelination - Remodelling cortical and limbic circuits - Changes to face processing - Amygdala: PFC connectivity associated with: increased adolescent suicidal ideation/attempts (Alacron et al, 2019) - Positive parenting —> Decreased amygdala growth, increased cortical thinning (Whittle et al, 2013)
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68
Q

What are cognitive and emotional changes during adolescent development changes?

A
  • Cognitive changes Thoughts more logical, abstract, reasoning Alternative outcomes, consequences, ambiguity Ability to ruminate and ask ‘what if’? - Increased intensity of mood states - Changes to self-regulation - Establishment of identity Reflect on own thoughts and perspective in relation to others Sense of self across time Reputation with peers
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69
Q

What are social and relationship changes during adolescent development?

A
  • Family Relationships transformed Shift —> autonomy and independence Less time with family Cognitive changes —> discussion/arguments Question rules & values —> minor squabbles - Peers More times & more importance —> confidantes & models of behaviour Romantic & sexual relationships - Social world Autonomy —> Increased responsibility Increased exposure to media stereotypes ‘digital natives’ Experimentation tobacco, alcohol, drugs
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70
Q

What are the differences between normal adolescent angst and psychiatric disorders?

A
  • Normal adolescent angst: Mastering the tasks of development: physical, social, emotional, cognitive, moral - Psychiatric disorder: Symptoms —> serious suffering & impairment: impact on personal, family, peers, education/work
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71
Q

What is the epidemiology of adolescent depressive disorder?

A
  • Prevalence: 2-6% - Cumulative probability by late adol: 10-20% - Time trends: suggestions may be increasing over time
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72
Q

What are the differences of adolescent depressive disorders from that of adults?

A
  • Irritability instead of sadness/low mood especially in boys - Somatic complaints and social withdrawal are common - Psychotic symptoms are rare before mid-adolescence
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73
Q

What are associated problems with adolescent depressive disorders?

A
  • Increased risk of self harm - Associated with anxiety disorders, eating disorders, conduct problems - Familial aggregation (genetic and learning)
74
Q

What are the short term outcomes of adolescent depressive disorder?

A
  • High rates of persistence and recurrence (20% in 1 year)
75
Q

What are the long term outcomes of adolescent depressive disorder?

A
  • Significant continuity into adulthood —> 40-70% recurrence in adulthood —> 2-7x increased risk as an adult - Impairment relationships/education in adulthood
76
Q

What are interventions of adult depressive disorder?

A
  • Psychological CBT Interpersonal psychotherapy for adolescents Psychodynamic psychotherapy - Medication Antidepressants e.g. SSRIs: fluoxetine - For severe or persistent, combine medication + psychological intervention Consider family therapy if family factors prominent
77
Q

What are different types of specific anxiety disorders?

A
  • Separation anxiety disorder - Specific phobia - Social anxiety disorder - Generalised anxiety disorder (GAD) - Panic disorder - Agoraphobia
78
Q

What is separation anxiety disorder?

A
  • High distress with separation, tries to avoid separation, affects functioning
79
Q

What is specific phobia?

A
  • Marked, unreasonable fear, specific objects
80
Q

What is social anxiety disorder?

A
  • Fear of being perceived as foolish/stupid; focus of attention, eating or talking in public
81
Q

What is generalised anxiety disorder?

A
  • Variety of worries; schoolwork, appearance, future strive for perfection; strongly related to depression
82
Q

What is panic disorder?

A
  • Repeated experience of unprovoked panic attacks, intense fear, physical symptoms
83
Q

What is agoraphobia?

A
  • Extreme fear & avoidance of crowds, public places, independent travel
84
Q

What is OCD?

A
  • Repetitive and intrusive thoughts, images or urges - Often accompanied by repeated characteristic actions or behaviours with the goal of anxiety - The mental components commonly focus on some expected threat or danger (hence it is an anxiety disorder) - Often comorbid with other anxiety disorders, GAD, social phobia etc - Categorised as different to anxiety disorders - In DSM 5 (US classification system) in same chapter as - Body dysmorphic disorder - Hoarding disorder - Trichotillomania - Excoriation - skin picking disorder
85
Q

Why is OCD no longer anxiety disorder?

A
  • Compulsion - No avoidance
86
Q

What are the features of anxiety disorder?

A
  • Avoidance - Expectation of threat (worry, rumination. anxious anticipation, negative thoughts) - Affective component (shy) - Physical complaints e.g. SOB
87
Q

What are physical symptoms in anxiety?

A
  • Tension headaches - Dizziness - Hyperventilation - Lump in the throat - Chest pain - Abdominal pain
88
Q

What is the epidemiology of anxiety disorders?

A
  • 5% (Western populations) - F > M (2:1) - Age of Onset: Mid-childhood to Adolescence - Comorbidities: Anxiety disorders strongly comorbid with depression - 75% have more than one anxiety disorder - 80-90% have more than one disorder
89
Q

What is the course of anxiety disorders?

A
  • Among the most stable - Little spontaneous remission - Increased risk of adolescence - Anxiety and mood disorders - Increased risk of adulthood - Anxiety and mood disorders - Substance use - Suicide - No association with family size, parental marital status, educational attainment, intelligence
90
Q

Describe family transmission in anxiety disorders

A
  • Heritability 40% (twin studies) - No specific gene - potential: 5HTTLPR gene, 2 short alleles on 5HTT gene increase environmental responsiveness - High degree of specificity: 1st degree relatives have increased risk of anxiety disorders and mood disorders esp same disorder
91
Q

What are the 3 most important neurotransmitters in anxiety disorders?

A
  • GABA - Benzodiazepines exert effects via GABA receptor complex, reducing anxiety - Serotonin - Mediates anxiety and fear; serotonergic neurones emerge from raphe nuclei, with median raphe providing innervation to septohippocampal system & cortex. SSRI’s show benefit for anxiety disorders in children [RCT data] - Norepinephrine - NA neurones arise from locus coeruleus, which releases stores of NA; noradrenergic neurones serve diverse areas of brain. In adults increase or decrease of NA release associated with changes in anxiety [some evidence children]
92
Q

What does neuroimaging show in anxiety?

A
  • Increased amygdala activity during anxiety - Increase in pre-frontal cortex, striatum - Extinction - > ventromedial aspects PFC - Capture of attention by threats ventrolateral aspects PFC
93
Q

How do temperamental factors affect anxiety?

A
  • Best studied and most clearly established risk factor for anxiety - Withdrawal in face of novelty - Lack of smiling - Limited eye contact - Close proximity to attachment figure - Slowness to warm up to strangers or peers - Unwillingness to explore new situations - Inhibited preschool kids 2-4x more likely to have anxiety by middle childhood
94
Q

How do parent and family factors affect anxiety?

A
  • Parenting characteristics: Overprotection Intrusiveness Negativity - Parental modeling and communication of fear - Sexual abuse, physical abuse, family violence
95
Q

How do life events affect anxiety?

A
  • Increased negative life events - Greatest difference on dependent events - Bullying and teasing - Neglect and rejection by peers
96
Q

Describe cognitive biases and anxiety

A
  • Heightened threat beliefs and expectations - Specific to disorder type - Decrease with successful treatment - Bias in attention toward threat - Bias to interpret ambiguous info as threat
97
Q

How do we assess anxiety?

A
  • Questionnaires, diagnostic interview, behavioural observation - Identify motivation behind behaviors - Determine primary disorder and treat first
98
Q

What psychological treatments are relevant to anxiety?

A
  • CBT - Psychoeducation - Contingency management (rewarding) - Parent training - Relaxation - Exposure
99
Q

What pharmacological treatment for anxiety?

A
  • SSRI (always monitor suicide risk in young people) - Combination therapy (SSRI + CBT) > Monotherapy
100
Q

What can be done to prevent and intervene early in anxiety disorders?

A
  • Universal programs (broad emotional health, small but meaningful effect sizes) - Selective programs (increased risk but no diagnosis, moderate effect sizes) - Indicated programs (high score on risk factors like temperament, Cool Little Kids for high parent anxiety)
101
Q

What is the prognosis of anxiety?

A
  • Anxiety disorder in childhood —> increased risk of anxiety and mood disorders in adolescence and adulthood
102
Q

What is the difference between antisocial behaviour, delinquency and conduct disorder?

A
  • Antisocial behaviour: defined by society - Delinquency: defined by the Law - Conduct Disorder: defined by psychiatry
103
Q

What is the ICD-10 criteria for Conduct Disorder?

A
  • Repetitive and persistent (> 6 months) pattern of antisocial, aggressive or defiant behaviour - Frequency and severity beyond age appropriate norms - Violate other people’s expectations or rights
104
Q

What are the 4 domains of Conduct Disorder?

A
  • Aggression to people and animals: bullying, animal cruelty - Serious violation of rules: truancy, running way from home, crime - Deceitfulness or Theft: stealing, breaking into someone’s house - Destruction of property: fire-setting
105
Q

What is the mindset of Conduct Disorder?

A
  • Often touchy or easily annoyed by others - Often angry or resentful - Often spiteful or vindictive - Often blames others for their own mistakes or behaviours - Not connected to other’s pain
106
Q

What are the different types of conduct disorder?

A
  • F91.0: Conduct disorder confined to the family context - F91.1: Unsocialised conduct disorder - absence of lasting friendships/rejected by peers - F91.2: Socialized conduct disorder – presence of lasting friendships
107
Q

What is Oppositional Defiant Disorder? (ODD)

A
  • Similar to CD BUT much younger (< 10 years old) - not yet broken line of societal norms + not broken the Law - Characterised by persistently negative, defiant, disobedient behaviour to authority figures
108
Q

What is the epidemiology of Conduct Disorder?

A
  • Most common mental diagnosis in childhood and adolescence - M > F (2.5:1) - Risk factors: Male, Quality of Parenting, Low socioeconomic status - Prognostic factors: Symptom severity, symptom duration - Prognosis: 40% of 8 year olds with CD have Criminal Behaviour as Adults - Associated with: Unemployment, violence, mental health issues, poor parenting (intergeneration transmission)
109
Q

What are individual factors of Conduct Disorders?

A
  • Genetic predisposition: Parents with CD more likely to have children with CD - Personality: Callous-Unemotional Traits, failure to inhibit aggression in response to signs of distress to others e.g. lack of guilt, no empathy, grandiosity, shallow affect - Development problems: Autism Spectrum Disorder or ID may be comorbid with CD - Physical health issues
110
Q

What are familial factors of Conduct Disorders?

A
  • Bad parenting style: Poor supervision, harsh discipline, persistent criticism of child, child abuse - Domestic abuse - Parental mental health
111
Q

What are environmental factors of Conduct Disorders?

A
  • “Bad” school: poorly organised, run down - “Bad” neighbourhood: inner cities, high crime, high unemployment - Low socioeconomic status
112
Q

What is SAVRY?

A
  • Structured Assessment of Violence and Risk in Youth —> Historical RFs, Social RFs, Individual RFs, Protective Factors (/30)
113
Q

What are the main interventions (NICE guidelines) for Conduct Disorders?

A
  • Modify risk factors at an early age - School interventions - Parenting programs - Treat co-morbidities - Cognitive problem-solving skills - Multi-systemic therapy - Clinical services
114
Q

How do you modify risk factors at an early age for CD?

A
  • Social policies to reduce violence/tackle poverty
115
Q

Describe school interventions for CD

A
  • Educate teachers to manage disrupt behaviours
116
Q

Describe parenting programs for CD

A

e.g. Incredible Years - Quality time - Praise good behaviour - Set expectations

117
Q

What is the purpose of treating comorbidities of CD?

A
  • Manage underlying hyperactivity - Exclude DDx: ODD, ADHD, Mood Disorder, ASD
118
Q

Describe cognitive problem-solving skills training

A
  • Develop accurate perceptions of others’ emotions and responses, develop social skills
119
Q

What is multi-systemic therapy for CD?

A
  • Improving family functioning, 24/7 social support available for crises - Improve Parent-Teen relationship - Parenting skills - Less deviant peer associations - Develop support network
120
Q

What are the clinical services for CD?

A
  • CAMHS - Young Offending Services - Criminal Justice System - Forensic Inpatient Services
121
Q

What is intelligence?

A
  • Mental ability to judge and apart to any environmental context which involves ability to plan, solve problems, think abstractly, comprehend complex ideas, learn quickly and learn from experience
122
Q

What is Intelligence Quotient?

A
  • Index of how one performs in a standardised test - Wechsler Adult Intelligence Scale (WAIS) is the most commonly used IQ Test
123
Q

What is the WHO degree of ID?

A
  • Mild ID: IQ 50-70: Delay in developmental milestones, can communicate, can do unskilled/semi-skilled work - Moderate ID: IQ 35-50: Delay in developmental milestones, can communicate, can work with supervision - Severe ID: IQ 20-35: Development delay in every aspect, limited speech, partly independent but require supervision - Profound ID: IQ < 20: Unable to take care of themselves, non-verbal
124
Q

What IQ is ID?

A
  • IQ < 70
125
Q

What is mild ID most likely due to?

A
  • Socioeconomic causes
126
Q

What is severe ID most likely due to?

A
  • Pathology
127
Q

How do genetic factors play a role in IQ?

A
  • Monozygotic twins’ IQ more alike than Dizygotic twins (even when reared apart) - Adopted children’s IQ closer to biologically parents’ IQ - If intellectual disability —> relatives have a 2x increased risk of ID
128
Q

How do environmental factors play a role in IQ?

A
  • Foetal Growth - Intrauterine infections - Obstetric complications - School - Socioeconomic deprivation - Rearing in socially advantaged adoptive families associated with higher IQ - Prolonged education associated with IQ increments - Forced school closures (war) associated with IQ decrements
129
Q

What is the Order of Concordance in IQ?

A
  • Same person taking IQ test twice —> Monozygotic twins reared together —> Dizygotic twins reared together —> Biological siblings reared together —> Biological siblings reared apart
130
Q

Which medical conditions are associated with both ID and Autism?

A
  • Down’s syndrome: epicanthic folds, single palmar crease, Trisomy 21 (risk of AD), autistic features - Fragile X syndrome: large ears, connective tissue issues, risk of epilepsy, learning difficulties - Tuberous sclerosis: hypopigmentated skin lesions, risk of epilepsy, severity of learning disability linked to seizure severity, autistic
131
Q

How are ID and Psychiatric disorders associated?

A
  • Mild ID —> 30% associated with Emotional, Behavioural and Hyperactivity disorders - Severe ID —> 40-50% associated with Autistic Spectrum Disorders, severe hyperactivity
132
Q

Why is there an association between ID and Psychiatric disorders?

A
  • Biological: Genetic causes of ID + Psychiatric disorders | Epilepsy (in 30% of ID) | Sensory impairments (hearing, visual) - Psychological: Decreased capacity (learning, peer interactions, difficulties in school) | Family dysfunction | Parent’s mental health - Social: Social disadvantage | High rates of stressful events (inc. abuse) | School failure | Peer rejection
133
Q

Describe management of ID

A
  • Early detection - Parental genetic counselling and support - Early treatment e.g. for inborn errors of metabolism - Management of co-morbid physical disorders e.g. epilepsy - Helping parents manage challenging behaviours - Treatment of psychiatric disorders - behaviourally, medication etc - Education: special schools or mainstream with support
134
Q

What is the trial of symptoms in ADHD?

A
  • Inattention - Hyperactivity - Impulsivity
135
Q

What is the definition of hyperkinetic disorder ICD-10?

A
  • Symptoms > 6 months - Symptoms pervasive across different situations - Onset < 7 years (ADHD is a neurodevelopmental condition) - Significant distress or social impairment - Variable according to - Family culture (parents tend to exaggerate sibling difference) - Cultural influences - Clinical heterogeneity (no two children have the same symptoms
136
Q

What is Inattention?

A
  • 6+ of - Fails to sustain attention - Careless - Avoid task requiring mental effort - Losing things - Distracted - Forgetful
137
Q

What is Hyperactivity?

A
  • 3+ of - Fidgets - Difficulty sitting still - Excess running about - Leaves seat - Noisy - Restless
138
Q

What is Impulsivity?

A
  • 1+ of - Failure to wait in line - Interrupts others - Blurts out answers - Poor self-control - Risk-taking
139
Q

What are co-morbidities of ADHD?

A
  • Conduct disorder (25-50%) - Anxiety disorder (25%)/Depressive disorder (15) - Learning difficulties (30%) - Including specific reading difficulties - Tourette’s disorder - Soft neuro signs e.g. clumsiness - Alcohol and substance misuse - Offending (45% young adults in prison have hyperactivity)
140
Q

Why does ADHD cause co-morbidity?

A
  • Common neurodevelopment deficits contribute to ADHD and another condition (e.g. ASD) - Diagnostic criteria for ADHD may overlap with other conditions (e.g. inability to concentrate —> ?depression ?ADHD) - ADHD may cause another condition (e.g. ADHD are impulsive —> social issues —> Conduct disorder)
141
Q

What is the ADHD spiral?

A
  • ADHD Sx —> Failure at school (academically, socially) —> Low self-esteem/isolation/delinquent peer group —> Sx
142
Q

What is the epidemiology of ADHD?

A
  • Prevalance - 1.4% hyperkinetic disorder (ICD-10) - 3.4% ADHD (DSM-IV) - M:F 3:1 - Inner city/SES/Institutions
143
Q

Describe family studies of ADHD

A
  • 20% of hyper children (vs. 5% paediatric controls) had parent reporting childhood hyperactivity - but rely on retro history - 8x increased risk of child ADHD if parent meets ADHD criteria
144
Q

Describe adoption studies of ADHD

A
  • Biological parents of hyperactive child tend to have childhood hyperactivity
145
Q

Describe twin studies of ADHD

A
  • Monozygotic twins- 80% concordance rates - Dizygotic twins- 30% concordance rates - Heritability (proportion of variance due to genetic differences between individuals): 0.76
146
Q

Describe GWAS studies in ADHD

A
  • No gene variant over stat threshold - ? small sample size - Demontis et al 2017 - Implicated 12 genomic loci
147
Q

What candidate genes are implicated in ADHD?

A
  • ADHD possiblly due to decreased DA - DRD4 allele: Dopamine receptor prevalent in PFC, PFC affected in ADHD, ADHD drugs act in PFC to stimulate DRD4 - DAT allele: DA transporter affects basal ganglia size, BG is affected in ADHD, ADHD drugs target DAT1 to inhibit BG - Tyrosine hydroxylase (produces DA) - COMT - Dopamine beta hydroxylase (DA —> NA)
148
Q

How do genes and environment affect ADHD?

A
  • Combination of risky alleles (DRD4, DAT1) and smoking —> increased risk of ADHD
149
Q

What prenatal risk factors affect ADHD?

A
  • Maternal smoking - Maternal alcohol or substance misuse - Maternal stress
150
Q

What are perinatal risk factors in ADHD?

A
  • Pregnancy complications - Low birth weight
151
Q

What are post-natal risk factors in ADHD?

A
  • Exposure to Lead/Organophosphate poisoning - Nutritional deficiency (Zn, Mg) or surplus (sugar, additives)
152
Q

What are psychosocial family factors in ADHD?

A
  • Critical comments, decreased encouragement, decreased sensitivity to child’s needs, Maternal depression - Romanian orphanage: known for poor care giving, abuse and neglect - severe psychosocial deprivation - Those adopted from Romanian orphanages had increased inattention and over activity at 6 years (30% at 2 year, 10% at 6m)
153
Q

Describe the fronto-striatal/executive function hypothesis (ADHD)

A
  • Top-Down control by pre-frontal cortex to facilitate future orientated behaviour: planning, impulsivity, surpress actions - ADHD have difficulty in these domains/EF - Phineas Gage highlights role of pre-frontal cortex in executive function - ADHD do consistently poor on Executive function tests (Wisconsin Card Sorting Test, Stroop Test)
154
Q

What genes influence executive function?

A
  • COMT Val156Met polymorphism
155
Q

How is the PFC affected by ADHD? (Imaging)

A
  • Decrease in size (MRI) - Decreased blood flow/activity (fMRI) - Decreased white matter (MRI DTI) - However similar changes are seen in non-ADHD relatives
156
Q

What is the Down-Top Hypothesis? (ADHD)

A
  • Other brain areas (Posterior Parietal Cortex, Basal ganglia, Cerebellum) signal to PFC to tell what is happening - Posterior Parietal Cortex signals to PFC when competing stimuli require attention, in ADHD: decreased blood flow to PPC - BG & Cerebellum: adjusts behaviour to diff. context, learn what to expect and when (role of DA), signal to PFC when unexpected or competing event occurs, in ADHD: decreased volume and decreased blood flow of BG and Cerebellum
157
Q

Which ADHD hypothesis is correct?

A
  • Don’t know - ADHD is an umbrella term of a large variation of pathological and aetiological conditions
158
Q

How are children assessed for ADHD?

A
  • Hx + Collateral Hx (parents, child, school - Exclude DDx: Learning disabilities, hearing difficulties
159
Q

What are psychological therapies for ADHD?

A
  • Behavioural therapy - Psychoeducation - Diet
160
Q

Describe behavioural therapy for ADHD

A
  • 1st line - Parents to have realistic expectations - praise appropriately - have quality time with child
161
Q

Describe psychoeducation in ADHD

A
  • Explain disorder - Info leaflets - School interventions
162
Q

How does diet affect ADHD?

A
  • Small evidence base - Remove additives
163
Q

Describe pharmacotherapy for ADHD

A
  • Methylphenidate —> Increased DA, slow kinetics, S/E: decreased appetite, decreased growth - Dexamfetamine - Atomoxetine (NA reuptake inhibitor) - Guanfacine/Cloidine —> alpha-2 agonist - Drugs are more effective than psychotherapy but more S/E
164
Q

What is the prognosis of ADHD?

A
  • If untreated —> 90% Conduct disorder (ADHD spiral) - As adults: less hyperactivity and impulsivity (33% still Dx)
165
Q

What is the difference between eating disorder and disordered eating?

A
  • Disordered eating is a behaviour - Eating disorder is a cluster of behaviours
166
Q

What is the difference between feeding and eating?

A
  • Feed = to give food - Eat = Autonomous action of taking food
167
Q

What were the Eating Disorders classifications in DSM V?

A
  • Anorexia Nervosa - Bulimia Nervosa - Eating Disorder Not Otherwise Specified (EDNOS)
168
Q

What were the eating disorder classifications in ICD-10?

A
  • Anorexia Nervosa - Bulimia Nervosa - Atypical AN and BN
169
Q

What were feeding disorders according to the DSM IV and ICD-10?

A
  • Feeding Disorder of Infancy and Early Childhood - Pica - Rumination disorder: bringing food and reswallow
170
Q

Describe feeding disorders

A
  • Most feeding disorders classified under a single diagnosis of ‘Feeding disorder of infancy and early childhood’ - No internationally agreed subtypes - Ambiguity about ‘organic basis’ - Exclusion criterion criteria in DSM - Feeding problems not associated with weight loss did not qualify - Two commonest are selective eating and tube dependence - Age limitation (onset before age 6) - BUT does emphasise the importance of relationships around food
171
Q

How were eating disorder classifications changed in DSM 5?

A
  • Anorexia Nervosa - Removal of amenorrhoea criteria - Removal of specific weight criterion - “Markedly low weight defined as weight less than minimally normal - Persistent behaviours to avoid weight gain replacing fear of weight gain - Addition of binge eating disorder
172
Q

How were eating disorders and feeding disorders merged together in DSM 5?

A
173
Q

What is a definition of an eating disorder

A

A persistent disturbance of eating behaviour or behaviour intended to control weight, which significantly impairs physical health or psychosocial functioning

174
Q

What are disturbances of eating behaviour?

A
  • Binge eating
  • Restricted eating
175
Q

What are behaviours intended to control weight?

A
  • Restricted eating (fasting)
  • Self induced vomiting
  • Excessive exercise
  • Laxative, diuretic and other energy burning or appetite suppressing medications e.g. caffeine, smoking
176
Q

How do eating disorders impair physical health?

A
  • Impacts growth and development
  • Stop periods
  • Effects on the brain
  • Results in osteoporosis
  • High mortality
177
Q

How do eating disorders impact psychosocial functioning?

A
  • Impacts family relationships
  • Impacts peer relationships
  • Impacts intimate relationships
  • Interferes with education and work
  • Causes distress
178
Q

What is OSFED?

A

Other Specified Feeding or Eating Disorders

  • Atypical anorexia nervosa
  • Bulimia nervosa
  • Purging disorder
  • Night eating syndrome
179
Q

What is the diagnostic criteria of AN?

A
  • Persitently restricting energy intake which leads to significantly low body weight
  • An intense fear of gaining weight or becoming fat or persistently trying not to gain weight
  • The view of one’s body weight and shape is distorted and unable to recognise the seriousness of significantly low body weight
180
Q

What is the diagnostic criteria of BED?

A
  • Recurrent episodes of binge eating. [Definition of binge as before]
  • The binge eating episodes are associated with three or more of the following: • eating much more rapidly than normal • eating until feeling uncomfortably full • eating large amounts of food when not feeling physically hungry • eating alone because of feeling embarrassed by how much one is eating • feeling disgusted with oneself, depressed or very guilty afterward • Marked distress regarding binge eating is present
  • Binge eating occurs, on average, at least once a week for three months
  • Binge eating not associated with the recurrent use of inappropriate compensatory behaviours as in Bulimia Nervosa and does not occur exclusively during the course of Bulimia Nervosa, or Anorexia Nervosa
181
Q
A

NMH BSc (7 decks)

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