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Psyc 241 - Final Exam > Childhood and Adolescent Disorders > Flashcards

Childhood and Adolescent Disorders Flashcards

1
Q

historical perspective

A

early 19th century - inadequate parenting, insufficient moral discipline in upbringing
reflection of environments

end of 19th century - abnormal brain functioning

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2
Q

current issues in assessing and treating children and adolescents

A

must study age specific variations - dif symptoms based on cognitive stage

youth more influenced by environments - lack of autonomy

children cannot self report

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3
Q

general prevalence of childhood disorders

A

18-22% between ages 4-17
anxiety disorders most common

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4
Q

types of comorbidity

A

homotypic continuity - current diagnosis predictive of receiving the same diagnosis in the future - panic disorders, psychosis, verbal tics, ecopresis, enuresis

heterotypic continuity - predictive of receiving a different diagnosis in the future - depression to anxiety, ADHD to ODD

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5
Q

ADHD clinical description

A

persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development

early childhood onset, 1/3 maintain diagnosis into adulthood

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6
Q

inattention symptoms

A

making careless mistakes, difficulty with attention, easily distracted, side tracked, problems with organization, messy, losing things, forgetful

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7
Q

hyperactivity symptoms

A

fidgeting, running around at inappropriate times, not remaining seated, talking excessively, blurting things out

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8
Q

ADHD specifiers

A

ADHD-I: predominantly inattentive, ADHD-H: predominately hyperactive, ADHD-HI: combined

ADHD-I - more common in girls, associated with academic problems
ADHD-H, HI - three times more common in boys, higher rates of comorbid conduct problems - motor hyperactivity symptoms often decrease over time

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9
Q

comorbidity and ADHD

A
  • 50% have at least one other psychiatric disorder
  • ODD or CD 40-60%, learning disorders 25%, anxiety disorders 25%, depression 30%, substance use disorders 40%
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10
Q

ADHD prevalence

A

2% preschool aged, 6% in children and adolescents, 4% adults

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11
Q

ADHD developmental trajectory

A

increased risk for developing another psychiatric disorder

begin substance use earlier than youth who do not have ADHD

four times greater risk of serious injury - motor vehicle accidents

lower occupational attainment and greater academic problems

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12
Q

ADHD brain structure and function

A
  • 3-8% reduction in brain size
  • abnormalities of the prefrontal cortex and basal ganglia
  • marked delay when attaining peak thickness through cerebellum - 10.5 years ADHD, 7.5 years controls
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13
Q

genetics and ADHD

A
  • heritability as high as 70-80%
  • extensive study of genes responsible for the recycling and transportation of the neurotransmitter dopamine, genes implicated in developmental process
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14
Q

prenatal risk factors ADHD

A

prenatal toxin exposure - poor diet, exposure to antidepressants, antihypertensives, illicit drugs, alcohol, tobacco, caffeine, mercury, lead, pregnancy or delivery complications

exposure to manganese, organophosphates, phthalates - particularly problematic for boys

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15
Q

psychosocial risk factors ADHD

A
  • low socio-economic status, large family size, paternal criminality, poor maternal mental health, child maltreatment, foster care placement, family dysfunction
  • inattentive symptoms - influenced by psychosocial risk factors
  • hyperactive-impulsive symptoms - influenced by by biological risk factors
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16
Q

gene-environment interactions and ADHD

A

maternal smoking and genetic predisposition

dopamine receptor in prefrontal cortex and inconsistent parenting

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17
Q

ADHD assessment

A

reports from more than one informant using valid and reliable assessment tools

basic assessment - administering a rating to parents and teachers - self report in adolescence

clinical interview - developmental history, onset of problems, degree of impairment in different settings, differential psychiatric and medical diagnosis, psychosocial issues, family mental health history

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18
Q

pharmacological treatment ADHD

A

stimulant medication - effective in approximately 80% - increase release of dopamine and NE from storage sites and blocking their reuptake by inhibition of the dopamine transport system

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19
Q

types of ADHD medication

A
  • short or long action methylphenidate, dextroamphetamine, amphetamine - increase vigilance, reaction time, short term memory, learning of new material in children with ADHD
  • atomoxetine - act on noradrenaline and serotonin - additional benefits in reducing ODD and anxiety symptoms
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20
Q

ADHD medication side effects

A

side effects - decreased appetite, weight loss, trouble falling asleep, headaches, increases in pulse and blood pressure - sometimes more irritable or angry

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21
Q

psychoeducational interventions ADHD

A

adults responsible for the child educated about symptoms, disorder course, deficits associated with ADHD

importance of routines, physical exercise, supervised or planned activities

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22
Q

academic skill faciliation and remediation ADHD

A

scheduled breaks from classroom activities, the use of reward systems, appropriate positioning of desks, auditory vs written instructions, use of agendas

testing to identify challenges - specific interventions

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23
Q

behavioural parent training ADHD

A

parents learn techniques to help the child modify their own behaviour by providing consistent rewards and attention when the child completes a task or ceases a negative behaviour

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24
Q

other treatments ADHD

A
  • behavioural classroom management, behavioural peer intervention, organizational training
  • no evidence for family therapy, individual psychotherapy, social skills training
  • most effective - those that help children enhance their deficient self motivation and working memory
25
Q

oppositional defiant disorder

A

frequently argue with adults, temper tantrums, deliberately annoy others, angry and irritable, spiteful, blame others for outbursts, defiant to authority

generally diagnosed by age 8

26
Q

ODD three symptom categories

A

angry/irritable mood
argumentative/defiant behaviour
vindictiveness

27
Q

conduct disorder

A

behaviour that violates the basic rights of others or major societal norms, lack of remorse or guilt, callousness

aggression towards people and animals
destruction of propety
deceitfulness or theft
serious violation of rules

28
Q

CD classifications

A

onset in childhood, adolescence, unspecfied

mild, moderate, severe

29
Q

CD and ODD sex differences

A

boys 3-4x more likely for CD, girls more likely at a later age
slightly more boys diagnosed with ODD
assortative mating - females with CD tend to date males with CD

30
Q

ODD and CD comorbidity

A

92% with ODD met criteria for another disorder - mood, anxiety, impulse control, substance use

highly comorbid with ADHD

CD and substance abuse

CD and ODD share a genetic influence

31
Q

three pathways linked to internalizing disorders

A

failure model: engaging in externalizing behaviour increases probability of experiencing social failure - related to developing internalizing problems

acting out model: youth may mask their mood problems by behaving aggressively

reciprocal model: associations between externalizing problems and internalizing problems are reciprocal

32
Q

dysruptive mood dysregulation disorder

A

chornic and severe irriability manifested clinically by frequent temper outbursts, persistently angry or irriable mood

2-5% prevalence

onset before age 10

33
Q

ODD and CD prevalence

A

ODD in preschool - 9-12%, 3-6% adolescence

CD 8.1% boys, 2.8% girls

true prevalence hampered by changes in DSM criteria

34
Q

ODD and CD developmental trajectory

A

ODD -> CD -> ASPD
trajectory is robust - more concern for those diagnosied with ODD and CD than just CD

arguments that they are distinct
ODD linked to mood disorders, CD antisocial

35
Q

ODD and CD genetics

A

CD - 71%
strong genetic basis for antisocial behaviour
heritability estimates range from 44-72%

36
Q

ODD and CD neurobiology

A

aggression - decreased glucose metabolism in frontal lobe

damage to amygdala - impulsive aggressive behaviour

serotonin abnormalities, low norepinephrine

37
Q

hot executive functions

A

smaller brain structures and lower brain activity in these areas

motivation and affective cognitive processing associated with self management skills when emotions run high - anterior cingulate cortex, insular cortex, frontal cortex

38
Q

ODD and CD cognitive factors

A

poor executive functioning, low IQ, reading disorders, lack of empathy, poor social cognition

39
Q

ODD and CD prenatal risk factors

A

maternal smoking, substance use, pregnancy and birth complications - CD

most important is maternal stress and smoking during pregnancy

40
Q

ODD and CD psychosocial risk factors

A

poor parenting - low monitoring, harsh and inconsistent, discpline, abuse - externalizing difficulties

moderate relation with insecure attachemnt - strong relation to disorganized attachment

peer rejection, association with deviant peers, poverty

41
Q

ODD and CD gene environment interaction

A

MAOA - 80% with low activity version who were maltreated had a conduct disorder vs 40% with high activity

differential susceptibility theory and biological sensitivity context theory - sources of vulnerability can increase risk of poorer outcomes or better outcomes with supportive environments

42
Q

ODD and CD problem solving skills training

A

modelling and practice, role playing, reinforcement contingencies

try to reduce hostile attributions

never fully reach normal functioning

43
Q

ODD and CD pharmacological treatment

A

first consideration if there is comorbid ADHD

antipsychotic - moderate effect on disruptive and aggressive behaviour

lithium for short term anger management

44
Q

ODD and CD parent training

A

promote social behaviour while reducing negative behaviour

idea that parents can reinforce antisocial behaviour

45
Q

seperation anxiety disorder

A

distress when seperated from attachment figure, constant worry about caregiver, withdraw, timid, distress, worry about harm, nightmares about seperation

1/3 develop other anxiety or mood disorders

46
Q

three trajectories for seperation anxiety disorder

A

high increasing group - 15.5% - 16x more likely to meet criteria for social anxiety disorder in adulthood
moderate - 37.3%
low - 47.2%

47
Q

GAD in childhood

A

many worries, difficult to control worries, tired, restless, fatigued, irritable
6 months
1 physiological symptom

48
Q

anxiety disorders comorbidity

A

mood disorders

71% met criteria for depression and anxiety

1/3 with SAD present with GAD, another 1/3 will develop GAD

73% heterotypic comorbidity

49
Q

anxiety disorders prevalence

A

9% aged 4-11, 15% aged 12-17
equally common in boys and girls in youth

50
Q

anxiety disorders developmental trajectory

A

anxiety age 11 - predictive of anxiety age 15

SAD predicts SAD

anxiety in early childhood -> behavioural issues middle childhood -> depressive late childhood

51
Q

temperament and anxiety

A

anxious temperament in infancy
behavioural inhibition - withdrawal or fear in novel situations - persists throughout life, 2-4x more risk of anxiety disorders

52
Q

brain structure and function and anxiety

A

amygdala - prolonged activation can lead to anxiety

higher resting heart rates and blood pressure

53
Q

anxiety and genetics

A

38% of children with parents with an anxiety disorder had one

heritability 59%

genetic factors explain 68% stability in anxiety symptoms

54
Q

prenatal risk factors and anxiety

A

mother experiencing stress while pregnanct

elevated cortisol in mother on developing brain

55
Q

psychosocial risk factors and anxiety

A

genetic risk might be chanelled through environment

vicarious learning, operation and classical conditioning

relationship with poverty and psychoapthology

56
Q

gene environement interactions and anxiety

A

fear conditioning

anxiety following stressful life period

57
Q

cognitive behavioural treatment and anxiety

A

most evidence
helping parents learn to cope, gradual exposure to stimuli

58
Q

pharmacological treatment of anxiety

A

SSRIs
fluvoaxamine - reduction in 8 weeks
92% of those taking medication stayed well
combined SSRI and CBT - best results aged 7-17

Psyc 241 - Final Exam (4 decks)

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