ADHD Flashcards

(61 cards)

1
Q

what is the definition of ADHD?

A

neurodevelopmental disorder defined by impairing levels of inattention, disorganisation, and/or hyperactivity-impulsivity

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2
Q

what does inattention and disorganisation of ADHD entail?

A

inability to stay on task, seeming not to listen, and losing materials, at a level that are inconsistent with age or developmental level

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3
Q

what does hyperactivity-impulsivity of ADHD entail?

A

overactivity, fidgeting, inability to stay seated, intruding into other people’s activities, and inability to wait - symptoms that are excessive for age or developmental level

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4
Q

what is the DSM 5 diagnosis criteria for ADHD?

A

A. a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development
B. several inattentive of hyperactive-impulsive symptoms were present prior to age 12
C. several inattentive-impulsive symptoms are present in two or more settings
D. there is clear evidence that the symptoms interfere with, or reduce the quality of, social, academic or occupational functioning
E. the symptoms do not occur exclusively during the course of schizophrenia, or another psychotic disorder and are not better explained by another mental disorder

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5
Q

what are the 3 subtypes of ADHD?

A
  1. inattentive
  2. hyperactive-impulsive
  3. combined
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6
Q

at what age do ADHD symptoms have to be present before in order to qualify for a diagnosis?

A

12

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7
Q

what are some risk factors for ADHD?

A

low birth weight/prematurity
exposure to smoking during pregnancy
family history of ADHD
perinatal stress
fetal alcohol syndrome
lead poisoning
traumatic brain injury
severe early oxygenation deprivation
adverse parent-child relationships

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8
Q

T or F
people with ADHD exhibit EEG abnormalities

A

true
90% do but not diagnostic

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9
Q

what is the pathophysiology of ADHD?

A

anatomical structures
- delay and rate of cortical thickening contributes to difficulty prioritizing tasks
- lack of connectivity between PFC is associated with lapses in attention and poor impulse control

DA and NE abnormalities
- deficit in DA reward pathway impairs brains ability to maintain attention to dull or repetitive tasks, postpone indulgence, regulate mood and arousal, resist distractions
- NE dysfunction leads to inability to modulate attention, arousal, and mood

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10
Q

dysfunction of which neurotransmitters are associated with ADHD?

A

dopamine and norepinephrine

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11
Q

what is the effect of too little DA and NE?

A

fatigue

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12
Q

what is the effect of too much DA and NE?

A

stressed

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13
Q

what are signs and symptoms of ADHD seen in infancy?

A
  • difficulty being soothed because irritability, fidgeting, crying and/or colic
  • feeding problems including poor sucking, crying during feedings
  • short periods of sleep or very little sleep
  • when crawling in constant motion
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14
Q

what are some s/sx of ADHD seen in school age children?

A
  • constantly “on the go”, unable to stay seated or play quietly
  • easily distracted, trouble completing tasks
  • impulsive, unable to wait turn, may blurt out answers, needs instant gratification
  • may appear accident prone due to hyperactivity and impulsivity
  • disorganised, forgetting or losing homework
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15
Q

what are s/sx of ADHD seen in adolescence?

A
  • dominant features include disorganisation, forgetfulness, inattention, overreaction
  • reckless driving and risky behaviour may occur
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16
Q

what are s/sx of ADHD seen in adulthood?

A
  • hyperactive symptoms include inability to sit through class/work meetings, excessive talking, needs to get to places quickly
  • impulsive symptoms include frequent job changes, low frustration tolerance, unstable interpersonal relationships
  • inattentive symptoms include poor time management, poor motivation and concentration, forgetfulness, excessive mistakes
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17
Q

which assessment tools are recommended by CADDRA for initial information gathering for suspected ADHD?

A

SNAP-IV 26 questionnaire and CADDRA teacher assessment form

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18
Q

what % of people diagnosed with ADHD in childhood have symptoms persisting into adulthood?

A

60%

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19
Q

what are the differences seen between boys and girls with ADHD?

A

boys present with hyperactivity/impulsive symptoms that are more noticeable
girls present with more inattentive symptoms

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20
Q

how do symptoms of ADHD change with age?

A

hyperactive symptoms begin to decline in adolescents but impulsive and inattention symptoms persist
inattentive symptoms become more prominent in adolescence and are the most common symptoms seen in adults

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21
Q

which symptoms of ADHD are associated with higher rates of bipolar/psychosis in adults?

A

hyperactive/impulsive

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22
Q

what are common co-morbidities seen with ADHD?

A

conduct or behavioural problems
anxiety
MDD
OCD
depression
oppositional defiant disorder
Tourette’s disorder
autism
epilepsy
substance use disorder
learning disorder

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23
Q

what is ODD?

A

oppositional defiant disorder
behavioural problem that is characterised by active confrontation of authority

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24
Q

what is CD?

A

conduct disorder
show a pattern of repeated aggression, lying, stealing, vandalizing, and skipping school

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25
what are the consequences of untreated ADHD?
decrease social, educational, vocational, and self-care functioning increased rates of accidental injury increase time and energy to cope with ADHD related challenges
26
what is the most effective treatment of ADHD?
behavioural therapies + medications
27
what are non-pharm treatments of ADHD?
- behavioural parent training - behavioural classroom management - behavioural peer interventions - CBT
28
what did the study of concerta vs atomoxetine conclude?
in treatment of ADHD without comorbidities (besides ODD) concerta is 1st line option ATX is second line option for concerta non-respondings
29
what is the MOA of methylphenidate?
inhibits the presynaptic reuptake of DA and NE by specifically blocking transport proteins - DA appears to have larger role than NE - leads to increased sympathomimetic activity in CNS - limited peripheral activity
30
what is the MOA of amphetamine?
increase the release of DA and NE into the presynaptic nerve terminal enhance release of NE in peripheral from adrenergic nerve terminals may stimulate the release of serotonin and act as a serotonin agonist (at higher doses) inhibit the reuptake of monoamines in extraneuronal space
31
what is the MOA of atomoxetine?
inhibits the presynaptic reuptake of NE in CNS
32
which antidepressant is atomoxetine similar in structure to?
fluoxetine
33
what are the 2 alpha-2 adrenergic receptor agonists used in treatment of ADHD?
guanfacine and clonidine
34
T or F clonidine is more selective for the alpha2a receptor than guanfacine?
false guanfacine is more selective
35
what does agonism of alpha 2a receptor result in?
leads to improvement in underlying working memory and behavioural functions
36
according to CADDRA guidelines, what is 1st, 2nd, and 3rd line treatment of ADHD?
1st line: long acting stimulants 2nd line: non-stimulants (atomoxetine, guanfacine XR), short/intermediate acting psychostimulants 3rd line: bupropion, clonidine, imipramine, modafinil; exceeding recommended max doses
37
what are examples of long acting stimulants?
Adderall XR Vyvanse Biphentin Concerta Foquest Quillivant
38
what is the efficacy of long-acting stimulants?
core ADHD symptoms reduced by 30-40% in 70%+ of treated patients
39
when is a response seen in treatment with long acting stimulants?
some response seen in 1st week for some, adequate trial 3-4 weeks
40
what is the next move is patient fails on a long acting stimulant?
try the other class before moving towards non-stimulant
41
what are the advantages of long acting stimulants over intermediate/short acting?
maintain privacy for patients and family in context of school, work, social situations may diminish diversion and rebound associated with better tolerability
42
what is the efficacy of atomoxetine?
core ADHD symptoms reduced by 25-30% in 60-70% treated
43
when is a response seen with non-stimulants?
onset 2 weeks max effect seen at 6-8 weeks
44
T or F non-stimulants take longer to show max effect than stimulants?
true
45
when are atomoxetine/guafacine treatments considered first line in ADHD?
if stimulants are CI intolerable a/e develop comorbid active SUD severe anxiety or tic disorders present parents hesitant to use a stimulant
46
when are short/intermediate acting psychostimulants used in ADHD?
to augment long-acting formulations early or late in day or early evening
47
when are 3rd line treatments used in ADHD?
treatment resistant cases and may require specialized care
48
what are the amphetamine based psychostimulants?
Adderall XR vyvanse dexedrine
49
what are the methylphenidate based psychostimulants?
biphentin concerta foquest quillivant ER Ritalin SR
50
which stimulants are in the formulary?
Dexedrine Concerta Ritalin SR require EDS: - Vyvanse - biphentin not covered: - Adderall XR - Foquest - Quillivant ER
51
what are the CIs and precautions with all ADHD medications?
CI: known hypersensitivity precaution: cardiac disease, bipolar, psychosis, pregnancy and lactation
52
what are CI and precautions with stimulants?
CI: treatment with MAOI (14 days), narrow angle glaucoma, untreated hyperthyroidism, moderate to severe HTN, pheochromocytoma, symptomatic CVD, history of mania or psychosis precaution: history of substance abuse, anxiety, renal impairment, tic disorders, epilepsy, peripheral vasculopathy
53
what are CI and precautions with atomoxetine?
CI: treatment with MAOI (14 days), narrow angle glaucoma, uncontrolled hyperthyroidism, pheochromocytoma, moderate to severe HTN, symptomatic CVD, severe CV disorders, advanced atherosclerosis precaution: asthma, CYP2D6 poor metabolisers, peripheral vasculopathy
54
what are CI and precautions with alpha2 agonists?
CI: inability for parents or pts to ensure regular daily dosage precaution: hepatic or renal impairment
55
why is adherence to alpha2 agonists to important?
risk of rebound hypertension when stopped abruptly
56
what are DIs with amphetamine based products?
acidifying agents (fruit juices) alkalizing agents opioids linezolid antidepressants: MAOIs (CI), SSRIs, SNRIs, TCAs alpha2 agonsits beta blockers antipsychotics decongestants
57
what are DI with methylphenidate based products?
linezolid warfarin phenobarb, phenytoin, primidone antidepressants: MAOI (CI), SSRI, SNRI, TCAs alpha2 agonists decongestants
58
what are AEs seen with stimulants?
increase BP and HR appetite suppression constipation/diarrhea dry mouth GI upset nausea/vomiting anxiety dizziness dysphoria/irritability headache initial insomnia somnolence tics decrease in weight skin reactions
59
what are some AEs seen with atomoxetine?
BP and HR increase appetite suppression constipation/diarrhea dry mouth GI upset nausea/vomiting anxiety dysphoria/irritability headache initial insomnia somnolence decrease is weight sexual dysfunction skin reactions
60
what are some AEs seen with alpha-2 agonists?
BP and HR decrease constipation/diarrhea dry mouth nausea/vomiting headache somnolence
61