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CPS Statements 2018-2020 > ADHD Parts 1-3 > Flashcards

ADHD Parts 1-3 Flashcards

1
Q

What is the definition of ADHD in the DSM-5

A

A persistent patter of inattention and or hyperactivity-impulsivity that’s interferes with functioning or development, and negatively impacts on social, academic, occupation activities

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2
Q

How common is ADHD

A

3rd most common mental health disorder

- 3.4% of children and youth

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3
Q

Why does the ICD-10 have a lower ADHD prevelance than the DSM-5

A

ICD-10 requires both inattention and hyperactivity criteria to be met

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4
Q

What adverse effects is ADHD associated with?

A
  1. Educational problems - lower rates of high school and post-secondary graduation rates
  2. Difficult peer relationships
  3. Increased MVA injuries
  4. Increased substance misuse - esp. if comorbid CD

**increases overall mortality risk

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5
Q

What are predictors of persistent ADHD

A
  1. Combined ADHD
  2. Increased symptom severity
  3. Comorbid MDD,
  4. High comorbidity (>3 DSM-5 diagnoses)
  5. Parental anxiety
  6. Parental ASPD
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6
Q

What are ADHD gene variants important for in development?

A
  1. Brain development
  2. Cell migration
  3. Encoding catecholamine receptor and transporter genes
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7
Q

What neurological factors are implicated in ADHD pathogens is

A
  1. Alcohol or tobacco exposure in uterus
  2. BW <2.5kg
  3. HIE
  4. Epilepsy disorders
  5. TBI
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8
Q

What environmental factors increase ADHD risk

A
  1. Lead
  2. Organophosphate pesticides
  3. Polychlorinated biphenyls
  4. Exceptional early deprivation
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9
Q

How does cortical maturation differ between ADHD and controls

A

Delayed maturation, with peak cortical thickness attained at 10y instead of 7y

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10
Q

What rating scales can be used in preschool children?

A

Conner’s Comprehensive Behaviour Rating scale

ADHD Rating scales IV

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11
Q

What is first line treatment of ADHD in preschool children?

A

Parent training programs

Help develop age-appropriate developmental expectations and specific management skills

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12
Q

Why is diagnosing ADHD in teens difficult?

A

Less consistent observation in schools - multiple teachers
Parents observe behaviors less often
Less likely to exhibit overt behaviors
Adolescent minimize problematic behaviors

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13
Q

What should be on the differential for ADHD in teens?

A

Substance use
Depression
Anxiety

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14
Q

What is the most effective practice for evaluating ADHD symptomatology

A

Clinical impressions and use of standardized scales

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15
Q

How are rating scales helpful in ADHD

A

Not diagnostic!

Subjective impressions to help quantify degree to which behaviour deviates from norm, and helps evaluate effects of interventions

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16
Q

Are the following required in ADHD diagnosis?

  1. Lab work
  2. Genetic testing
  3. EEG, neuroimaging
  4. Psychological, SLP assessments
  5. Psychological, executive function tests
A

No! Only if indicated by history and physical

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17
Q

What is the DSM-5 criteria for ADHD

A
  1. Symptoms are severe, persistent (i.e., present before 12 years of age and continuing >6 months), and inappropriate for the patient’s age and developmental level.
  2. Symptoms are associated with impairment in academic achievement, peer and family relations and adaptive skills.
  3. If there is a discrepancy of symptoms across settings, it is important to identify why the discrepancy exists.
  4. Specify the type of ADHD presentation as per the DSM-5:

i) Combined presentation
ii) Predominantly inattentive presentation
iii) Predominantly hyperactive-impulsive presentation

  1. Specify current severity (mild, moderate or severe) based on the symptoms and degree of functional impairment.
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18
Q

What conditions are commonly misdiagnosed as ADHD

A
  1. Learning disorder
  2. Sleep disorder
  3. ODD
  4. Anxiety disorder
  5. Intellectual disability
  6. Language disorder
  7. Mood disorder
  8. Tic disorder
  9. Conduct disorder
  10. ASD
  11. DCD
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19
Q

What are psychiatric disorders on the differential for ADHD

A
  1. Externalising disorders
    - ODD
    - IED
  2. Internalizing disorders
    - Anxiety
    - Depression
    - Bipolar
    - disruptive mood days regulation
  3. Trauma and stress related
    - reactive attachment disorder
    - adjustment disorders
    - PTSD
  4. Cognitive development
    - ID
    - superior intellectual function
    - specific learning disorder
  5. Neurodevelopmental disorders
    - ASD
    - Tic disorder, Tourette’s
    - Stereotypic movement disorder
  6. Other
    - personality disorders
    - SUD
  7. Medical
    - OSA
    - IBD
    - sensory impairments
    - chronic health conditions with ++school absenteeism
    - epilepsy
    - post concussion status
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20
Q

How is epilepsy associated with ADHD

A
  • ADHD 2-3x more prevalent in pt with seizure disorders
  • may be present prior to seizure or as a secondary cause
  • complicated epilepsy, higher seizure frequency and earlier age onset = higher ADHD risk
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21
Q

Which AEDs are associated with ADHD

A

PHB, PHY, VPA

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22
Q

What genetic conditions have higher prevalence of ADHD

A 
NF1
FXS
Turners
TSC
Noonan (22q11 deletion syndrome)
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23
Q

What are ADHD comorbidities

A
  1. ODD/CD - up to 90%
  2. Anxiety - up to 30%, more fears, in attention, poorer social skills,++ severity symptoms, more difficult engaging in CBT
  3. Mood disorders (including BD)
  4. SUD - ?self-medicating
  5. Tic disorder
  6. DCD
  7. ASD
  8. Specific learning disorder - up to 33% (1/3)
  9. Eating disorder
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24
Q

Why is a shared care model important for treatment of ADHD

A

Need a shared understanding of identified treatment goals, preferences and accurate understanding of underlying etiology

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25
Q

Under what age is parent behavior training first line?

A

<6 years old

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26
Q

What are nonpharmacologic interventions for ADHD

A
  1. Psychoeducation - provides accurate education and information for families, clears up misperceptions
  2. Shared decision making: share all info about dx and rx and identify treatment goals before implementing interventions
  3. Parent based training
  4. Classroom management
  5. Daily report card - to help with homework completion
  6. Behavioural peer interventions
  7. Organizational skills training - address executive functioning
  8. Exercise
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27
Q

What are potential non-pharmacological interventions

A
  1. Diet IF suspected deficiency, insufficiency, food allergy
  2. EEG neurofeedback
  3. Cognitive training
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28
Q

What intervention has not been proven effective for ADHD

A

Social skills training

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29
Q

Why are nonpharmacologic interventions helpful in ADHD

A
  • > 50% have psychiatric and developmental comorbid items

- help with compliance, academic performance, quality of life

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30
Q

When should medication be used in ADHD

A

Pt with ADHD who’s learning, academic performance are impaired by attention difficulties, or whose behaviours and social interactions are impaired by impulsivity, hyperactivity

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31
Q

What are the benefits of stimulant medications

A

Improved academic achievement
Improved QoL
Lower rates of comorbid anxiety, depression in adulthood
Improved function - decision making, handwriting, school productivity
Better evening driving performance
Better math and reading scores
Fewer injuries, and fewer ER visits
Reduced morbidity, mortality associated with MVAs

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32
Q

What is the impact in adulthood of persistent ADHD symptoms

A

Greater difficulties with educational and occupational adjustments
Risky sexual behaviours
Psychiatric disorders

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33
Q

How should ADHD symptoms be monitored?

A
  1. Set specific goals focused on symptom reduction and improved function to guide treatment
  2. Use checklists to monitor response based on the goals
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34
Q

What stimulation should be started?

A

Can start with either the MPH or DEX subclass using an extended release formulation appropriate based on age

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35
Q

How long after starting a medication do you have to wait to assess if its effective?

A

2-4 weeks after initiation

36
Q

Before deciding that a youth does not respond to stimulants what do you?

A

Switch to another medication in same subclass, or to the other subclass

37
Q

When should IR medications be used

A

If child cannot tolerate ER medication

Individuals with short-term attention and behavioural targets

38
Q

Should drug holidays be recommended?

A

No

39
Q

What is the benefit of taking ER stimulants 7 days a week?

A
  1. Reduced risky behaviors
  2. Improve family and peer relationships
  3. Better attention for homework
40
Q

How are ER stimulants taken

A

Once daily at breakfast.

Aim for effects to wean off at dinner time

41
Q

Why might stimulants need to be uptitrated?

A

Upregulation by liver leading to tachyphylaxis

42
Q

What are the most common adverse effects of stimulants

A 
Low appetite 
Sleep difficulties
Moodiness
Irritability
Tics (maybe...)
Peripheral vasculopathic symptoms - Raynaud’s 
Priapism 
Slight increase in HR and BP
43
Q

Who needs an ECG before starting a stimulant?

A

Youth at risk for stimulant-induced CVS adverse events based on H+P, FHx

44
Q

Is final height affected by stimulant use?

A

Minimally - up to 2.5cm difference

45
Q

How is BMI affected by stimulants

A

Slight overall reduction, especially if overweight when treatment started

46
Q

Do stimulants affect puberty?

A

Sometimes delay pubertal growth spurt timing

47
Q

What the two non stimulant medications approved by Health Canada for ADHD treatment? What age group are they approved in?

A

Atomoxetine
Guanfacine

6-17yo

48
Q

Other than ADHD benefits - what are the potential benefits of atomoxetine?

A

Lower risk for weight loss
Lower risk for tic exacerbation
Improved anxiety

49
Q

For individuals with ADHD and a history of SUD - what options are recommended, and why?

A

ER stimulant
Non-stimulant

Decreased risk for abuse and diversion

50
Q

In what scenario is guanfacine beneficial?

A

Treating ADHD and comorbid ODD/CD

51
Q

What are the adverse effects of

  1. Atomoxetine
  2. Guanfacine
A
  1. Appetite loss, upper abdominal pain, somnolence, HA, moodiness, irritability, slight increase in BP and HR, suicide related events, hepatic disorders
  2. Sedation, somnolence, fatigue, orthostatic hypotension, bradycardia, syncopated episodes

Raynaud’s can happen with both

Bother need BP and HR monitoring during treatment, esp. if dose increases UIKeyInputEnd

52
Q

How should atomoxetine be started?

A

Metabolized by CYP2D6 with a half-life of 5-22h
can have extensive or slow metabolizes due to polymorphism

SSRIs can slow the metabolism
Start at 0.5mg/kg/day x 2-4 weeks before increaeeing

Can take up to 3mo to see effects

53
Q

Can you stops guanfacine or clonidine immediately if its not working?

A

NO, risk of rebound HTN, tachycardia, HTNive encephalopathy

Taper dose by 1mg q3-7d

54
Q

Which stimulant medications are options if a young child cannot take pills?

A

Biphentin (beads) - 6-10h
Vyvanse (powder in a capsule) - 8-13h
Adderall (beads in capsule) - 6-8h

55
Q

Which stimulant medications are options if a older child cannot take pills?

A

Concerts (capsule) - 8-12h
Vyvanse (powder in a capsule) - 8-13h
Adderall (beads in capsule) - 6-8h

56
Q

What NDD can overlap or mimic ADHD?

A

ASD
ID
Prematurity

57
Q

How many children with ASD meet criteria for ADHD

A

> 50%

58
Q

How many children with ADHD have ASD traits

A

~50%

59
Q

What are similarities between ADHD and ASD?

A

High heritability
High comorbidity
More common in males
Early onset

60
Q

How do children with ASD+ADHD present?

A 
More cognitive function impairment
More severe behavior problems 
Greater psychopathology 
More pronounced ASD symptoms 
More difficulties with social and communication skills, self-care, adaptive and executive functioning 
More internalizing behaviors 
More common to have maladaptive disruptive behaviors, stereotypic or repetitive behaviors 
More comorbid psychiatric disorders 
More SLD
61
Q

What genetic syndromes have ASD+ADHD features

A

FXS
TSC
22q11 deletion
Williams

62
Q

What are the underlying genetics for ASD+ADHD

A

More common to have rare copy number variants, chromosomal deletions and duplications

Loci on chromosome 12, 16, 18 have been identified

16-25 single-nucleotide polymorphism identified

63
Q

How is ADHD+ASD treated?

A

Stimulants = 1st line
Psychical activity - alleviated ADHD symptoms, and improve social skills
No studies on the efficacy of nonpharmacological or behavioral managements
BUT should still implement them

64
Q

What are the most common adverse effects of stimulant medications in children?

A

Irritability with emotional outbursts
Increased stereotypic behaviours
Agitation
Dysphoria, psychotic symptoms

65
Q

Is there a role for nonstimulant medications in ASD+ADHD?

A

Atomoxetine - maybe, but takes longer time

Guanfacine - yes

66
Q

Is there a role for atypical antipsychotics or antidepressants in ASD+ADHD?

A

only if indicated by comorbidities

67
Q

How many children over 5yo have ID

A

2-3%

68
Q

How is ID characterized?

A

Developmental deficits in cognitive function, or in adaptive function such that the individual cannot meet standards for personal independence and social responsibility

IQ >2SD below the mean

Severity depends on level of adaptive functioning, NOT IQ

69
Q

What is the prevalence of ADHD in ID?

A

3-4x general population

70
Q

Why is diagnosing ADHD in ID difficult

A

Lower intellectual functioning can affect attention and behavior

71
Q

Are there rating scales for ADHD in special populations?

A

No

72
Q

How does ID+ADHD present?

A

ADHD symptoms tend to be more severe, and less likely to remit with age
Higher rates of agitation, aggressive and self-injurious behaviors, ASD traits, stereotypic behaviors, conduct problems
Impaired adaptive functioning

73
Q

What conditions are associated with ID+ADHD

A 
Klinefelters 
FXS
Turners
Aminoacidemias
Phenylketonuria
Galactosemia 
NF1
TSC
Myotonic dystrophy
74
Q

How is ID+ADHD treated

A

Optimize environment and academic interventions to meet needs
Use lowest dose medication possible -IR stimulants then nonstimulants
Physical exercise
Use atypical antipsychotic for behavioral problems

75
Q

Does ID+ADHD respond well to stimulants?

A

Response rate to IR MPH of 45-66%

76
Q

In ID+ADHD what predicts a poor response to stimulants?

A

IQ <50

77
Q

Define the following terms:

  1. VLBW
  2. ELBW
  3. VPT
  4. EPT
A
  1. <1.5kg
  2. <1kg
  3. <30wk
  4. <26wk
78
Q

Are premature infants surviving with more, the same or less rates of disability?

A

Less

79
Q

What sequelae of prematurity have increased?

A

Milder CI
NDD
Mental health difficulties

80
Q

What percent of EPT or ELBW have DD

A

~50%

81
Q

What factors affecting premature babies affect educational achievement later in childhood?

A

CI
ADHD
Internalizing behaviour disorders - anxiety, depression
Social interaction difficulties

82
Q

What is the most common disability in ELBW?

A

CI

  • 25% have IQ 1-2 SD below the mean
  • 20% have IQ 2 SD below the mean
83
Q

What is the association between GA/BNW and cognitive scores by school age?

A

As GA increases >26 - impairments decrease linearly until past 32wk

Past 32wk = mean remains 5 SD lower than for NBW peers

84
Q

What is the preterm behavioural phenotype

A

In VPT/EBLW - experience cluster of NDD and behaviours associated with:

  • ADHD
  • Internalizing disorders: anxiety, depression, withdrawal, somatic complaints
  • Social difficulties
85
Q

What is the rate of ADHD in ELBW children

A

2x

Also higher rates of anxiety, ID, and needs for IEP

86
Q

How do the rates of ADHD differ between later preterm and term infants

A

They don’t

87
Q

How should medications be used in prematurity and ADHD

A

The same - but pay attention to monitoring of treatment, and internalizing behaviour disorders

CPS Statements 2018-2020 (16 decks)

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