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PHAR 358 > ADHD > Flashcards

ADHD Flashcards

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
Q

what are the consequences of untreated ADHD?

A

decrease social, educational, vocational, and self-care functioning
increased rates of accidental injury
increase time and energy to cope with ADHD related challenges

26
Q

what is the most effective treatment of ADHD?

A

behavioural therapies + medications

27
Q

what are non-pharm treatments of ADHD?

A
  • behavioural parent training
  • behavioural classroom management
  • behavioural peer interventions
  • CBT
28
Q

what did the study of concerta vs atomoxetine conclude?

A

in treatment of ADHD without comorbidities (besides ODD) concerta is 1st line option
ATX is second line option for concerta non-respondings

29
Q

what is the MOA of methylphenidate?

A

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
Q

what is the MOA of amphetamine?

A

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
Q

what is the MOA of atomoxetine?

A

inhibits the presynaptic reuptake of NE in CNS

32
Q

which antidepressant is atomoxetine similar in structure to?

A

fluoxetine

33
Q

what are the 2 alpha-2 adrenergic receptor agonists used in treatment of ADHD?

A

guanfacine and clonidine

34
Q

T or F
clonidine is more selective for the alpha2a receptor than guanfacine?

A

false
guanfacine is more selective

35
Q

what does agonism of alpha 2a receptor result in?

A

leads to improvement in underlying working memory and behavioural functions

36
Q

according to CADDRA guidelines, what is 1st, 2nd, and 3rd line treatment of ADHD?

A

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
Q

what are examples of long acting stimulants?

A

Adderall XR
Vyvanse
Biphentin
Concerta
Foquest
Quillivant

38
Q

what is the efficacy of long-acting stimulants?

A

core ADHD symptoms reduced by 30-40% in 70%+ of treated patients

39
Q

when is a response seen in treatment with long acting stimulants?

A

some response seen in 1st week for some, adequate trial 3-4 weeks

40
Q

what is the next move is patient fails on a long acting stimulant?

A

try the other class before moving towards non-stimulant

41
Q

what are the advantages of long acting stimulants over intermediate/short acting?

A

maintain privacy for patients and family in context of school, work, social situations
may diminish diversion and rebound
associated with better tolerability

42
Q

what is the efficacy of atomoxetine?

A

core ADHD symptoms reduced by 25-30% in 60-70% treated

43
Q

when is a response seen with non-stimulants?

A

onset 2 weeks
max effect seen at 6-8 weeks

44
Q

T or F
non-stimulants take longer to show max effect than stimulants?

A

true

45
Q

when are atomoxetine/guafacine treatments considered first line in ADHD?

A

if stimulants are CI
intolerable a/e develop
comorbid active SUD
severe anxiety or tic disorders present
parents hesitant to use a stimulant

46
Q

when are short/intermediate acting psychostimulants used in ADHD?

A

to augment long-acting formulations early or late in day or early evening

47
Q

when are 3rd line treatments used in ADHD?

A

treatment resistant cases and may require specialized care

48
Q

what are the amphetamine based psychostimulants?

A

Adderall XR
vyvanse
dexedrine

49
Q

what are the methylphenidate based psychostimulants?

A

biphentin
concerta
foquest
quillivant ER
Ritalin SR

50
Q

which stimulants are in the formulary?

A

Dexedrine
Concerta
Ritalin SR

require EDS:
- Vyvanse
- biphentin

not covered:
- Adderall XR
- Foquest
- Quillivant ER

51
Q

what are the CIs and precautions with all ADHD medications?

A

CI: known hypersensitivity

precaution: cardiac disease, bipolar, psychosis, pregnancy and lactation

52
Q

what are CI and precautions with stimulants?

A

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
Q

what are CI and precautions with atomoxetine?

A

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
Q

what are CI and precautions with alpha2 agonists?

A

CI: inability for parents or pts to ensure regular daily dosage

precaution: hepatic or renal impairment

55
Q

why is adherence to alpha2 agonists to important?

A

risk of rebound hypertension when stopped abruptly

56
Q

what are DIs with amphetamine based products?

A

acidifying agents (fruit juices)
alkalizing agents
opioids
linezolid
antidepressants: MAOIs (CI), SSRIs, SNRIs, TCAs
alpha2 agonsits
beta blockers
antipsychotics
decongestants

57
Q

what are DI with methylphenidate based products?

A

linezolid
warfarin
phenobarb, phenytoin, primidone
antidepressants: MAOI (CI), SSRI, SNRI, TCAs
alpha2 agonists
decongestants

58
Q

what are AEs seen with stimulants?

A

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
Q

what are some AEs seen with atomoxetine?

A

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
Q

what are some AEs seen with alpha-2 agonists?

A

BP and HR decrease
constipation/diarrhea
dry mouth
nausea/vomiting
headache
somnolence

61
Q
A

PHAR 358 (10 decks)

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