ADHD Flashcards
What is ADHD?
neurodevelopmental disorder defined by impairing levels of inattention, disorganization, and hyperactivity-impulsivity
What does the inattention and disorganization of ADHD entail?
inability to stay on task
seeming not to listen
losing materials
at levels that are inconsistent with age or developmental level
What does the hyperactivity-impulsivity of ADHD entail?
overactivity
fidgeting
inability to stay seated
intruding into other peoples activities
inability to wait
symptoms that are excessive for age or developmental level
Is ADHD only a disorder of children?
can persist into adulthood
-with resultant impairments of social, academic, and occupational functioning
What is the biomarker or imaging study that is diagnostic of ADHD?
there is no biological marker or imaging study that is diagnostic for ADHD
-a clinical diagnosis
What is the essential feature of ADHD?
persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development
Describe the diagnostic criteria for the inattention side of ADHD.
6+ sx persist for 6+ mo and inconsistent with development and impact social and occupational/academic activities
1. fails to pay attention to details or makes careless mistakes
2. difficulty sustaining attention
3. does not seem to listen when spoken to
4. does not follow through on instructions or tasks
5. difficulty organizing
6. dislikes/reluctant to tasks requiring mental effort
7. loses things
8. easily distracted by extraneous stimuli
9. often forgetful in daily activities
Describe the diagnostic criteria for the hyperactivity-impulsivity side of ADHD.
6+ sx persist for 6+ mo and inconsistent with development and impact social and occupational/academic activities
1. fidgety
2. leaves seat when seating expected
3. runs around when inappropriate
4. unable to engage in activities quietly
5. often “on the go”
6. often talks excessively
7. blurting answer before question is done
8. difficulty waiting for turn
9. interrupts or intrudes on others
What is key regarding the diagnosis of ADHD in regards to age and setting?
several inattentive or hyperactive-impulsive symptoms were present prior to age of 12 and are present in two or more settings
Describe the etiology of ADHD.
not entirely known
multifactorial:
-genetics (heritability, NT dysfunction - mainly DA & NE)
-non genetic factors (20-25%)
What are the risk factors for ADHD?
low birth weight/prematurity
exposure to smoking during pregnancy
family history of ADHD
perinatal stress
FAS
lead poisoning
traumatic brain injury
severe early oxygenation deprivation
adverse parent-child relationships
Describe the pathophysiology of ADHD.
anatomical structures
-delay and rate of cortical thickening contributes to difficulty prioritizing tasks
-lack of connectivity between prefrontal cortex is associated with lapses in attention & poor impulse control
EEG abnormalities
-90% with ADHD (not diagnostic)
DA and NE abnormalities
-DA: impairs brains ability to maintain attention to dull or repetitive tasks, postpone indulgence, regulate mood and arousal, resist distractions
-NE: inability to modulate attention, arousal, and mood
Describe the ability of the PFC when catecholamine levels fluctuate between low to high.
low: fatigued
moderate: alert
high: stressed
Which assessment forms are recommended for initial information gathering for children/adolescents suspected of ADHD?
SNAP-IV 26
CADDRA Teacher Assessment Form
What are some comorbidities often seen with ADHD?
conduct or behavioral problems
anxiety
MDD
OCD
SUD 2.5x more likely
learning disorders
epilepsy 2-3x more likely
autism
Tourettes
oppositional defiant disorder
What are the consequences of untreated ADHD?
decreased social, educational, vocational, and self-care functioning
increased rates of accidental injury
increased time and energy to cope with ADHD related challenges
What are the goals of therapy for ADHD?
eliminate or significantly decrease the core ADHD sx
improve behavioral, academic, and/or occupational performance
improve self-esteem
improve social functioning
minimize drug AEs
improve QoL
What should the treatment of ADHD be based on?
current evidence, family, and clinician preference
When can behavioral therapies be considered as the initial treatment of ADHD?
if symptoms are mild, diagnosis is unclear, or medication is not preferred by parents
What is the most effective treatment for ADHD?
behavioral therapies + medication
What are the non-pharm treatment options for ADHD?
family-focused interventions
-behavioral parent training
school-focused interventions
-behavioral classroom management
child-focused interventions
-behavior peer interventions
CBT
What should the meds target in ADHD?
the symptoms that cause impairment
What did the landmark study of atomoxetine vs Concerta find regarding adverse events?
similar in between groups
What is the bottom line of the landmark study of atomoxetine vs Concerta?
in treatment of ADHD without comorbidities (besides ODD), Concerta is 1st line option
-ATX is 2nd line option for Concerta non-responders
-however, if pts family is hesitant to start a stimulant then ATX is an option although not as effective as MPH
-also if pt doesnt respond to MPH than ATX could be an option
What was the MTA study?
second landmark ADHD study
RCT comparing behavioral therapy, intensive medication management, combination behavioral therapy + intensive med management
What were the results of the MTA study?
combined behavioral + pharm tx = pharm alone for core ADHD sx
pharm tx > behavioral tx for core ADHD tx
combined behavioral + pharm tx > pharm alone or behavioral alone for reducing oppositional behaviors/anxiety and improving social interactions/self-esteem
What are examples of ADHD medications?
stimulants:
-methylphenidate products
-amphetamine products
non-stimulants:
-atomoxetine
-guanfacine
-clonidine
-bupropion
What is the MOA of methylphenidate?
inhibits presynaptic reuptake of DA and NE by blocking transport proteins
-DA appears to have a larger role than NE
-leads to increased sympathomimetic activity in CNS
-limited peripheral activity
What is the MOA of amphetamines?
increase release of NE and DA into synapses from presynaptic nerve terminal
-enhance NE release in periphery from adrenergic nerve terminals
-may stimulate release of 5HT and act as a 5HT agonist (higher doses)
-inhibit the reuptake of monoamines in extraneuronal space
What is the MOA of atomoxetine?
inhibits the presynaptic reuptake of NE in CNS
What is the MOA of guanfacine and clonidine?
alpha-2 adrenergic receptor agonists
peripherally block sympathetic nerve impulses=decreased vasomotor tone (BP) and heart rate
How does guanfacines MOA differ from clonidines?
guanfacine more selective for alpha2a receptor than clonidine
-binds to postsynaptic alpha2a receptors in PFC –> improves delay related firing of PC neurons
-leads to improvements in underlying working memory and behavioral functions
What is the 1st line pharmacotherapy for ADHD?
long-acting stimulants
-Adderall XR, Concerta, Vyvanse, Biphentin, Foquest, Quillivant
What is the benefit of the 1st line drugs for ADHD?
reduces core ADHD sx by 30-40% in 70%+ of treated pts
When is response seen from the 1st line drugs for ADHD?
1 week in some but an adequate trial is 3-4 wks
Which stimulant is more efficacious for ADHD?
MPH and amphetamines are equally efficacious
What is the method used to predict which stimulant class a patient will respond to?
there is no method
What should be done after treatment failure on a stimulant?
try the other stimulant class before moving to non-stimulant
What is the benefit of sustained release products for the patient and family?
maintains privacy for patients and family in context of school, work, and social situations
What is the benefit of sustained release products when compared to IR products?
may diminish diversion and rebound
better tolerability
What is the 2nd line pharmacotherapy for ADHD?
non-stimulants
-guanfacine XR, atomoxetine
short/intermediate acting psychostimulants
-dextroamphetamine, dextroamphetamine Spansules, MPH, MPH SR
What is the benefit of atomoxetine for ADHD?
core ADHD sx reduced by 25-30% in 60-70% treated with atomoxetine
What is the onset of non-stimulants?
2 weeks
max effect seen at 6-8 weeks (slower than stimulants)
When are non-stimulants used 1st line for ADHD?
stimulant contraindicated
active substance use
intolerable AE develop to stimulants
severe anxiety or tic disorder
parents hesitant to use stimulant
What should be done if there is a partial response to non-stimulants?
combine with behavioral therapy or stimulant
What is the use of short/intermediate stimulants?
augment long-acting formulations early or late in day or early evening
dextroamphetamine products used to augment long-acting amphetamine products and lisdexamfetamine
MPH products used to augment MPH extended and controlled release products
What are the 3rd line pharmacotherapy options for ADHD?
bupropion, clonidine, imipramine, modafinil
AAPs for comorbidities commonly seen with ADHD
exceeding max doses may be considered after regular doses
agents who use is off-label, have higher risks, more AE’s, and/or lower efficacy profile
What is an important consideration if switching from brand to generic with ADHD meds?
advising patient/family of the switch and to watch for clinical changes in efficacy and tolerability
What is a contraindication to any ADHD med?
hypersensitivity or allergy to products
What are precautions for all ADHD meds?
cardiac disease
bipolar
psychosis
pregnancy and lactation
What are monitoring parameters for all ADHD meds?
ht and wt
new mood/anxiety/SUD/psychotic/manic sx
irritability/mood swings
sleep or appetite changes
suicidal behavior or ideation
aggressive behavior
What are contraindications to stimulants?
history of mania or psychosis
mod-severe HTN
symptomatic CVD
pheochromocytoma
untreated hyperthyroidism
narrow angle glaucoma
MAOI tx, up to 14 days after d/c
What are precautions to stimulants?
history of SUD
anxiety
renal impairment
epilepsy
tic disorder
Raynauds
What are some monitoring parameters specific to stimulants?
BP, HR
growth issues
Raynauds
priapism
What are the contraindications to atomoxetine?
MAOI tx, up to 14 days after d/c]
narrow angle glaucoma
mod-severe HTN
symptomatic CVD
severe CV disorders
uncontrolled hyperthyroidism
pheochromocytoma
advanced atherosclerosis
What are the precautions of atomoxetine?
asthma
CYP 2D6 poor metabolizers
Raynauds
What are some monitoring parameters specific to atomoxetine?
priapism and urinary retention
signs and sx of liver injury
growth retardation
Raynauds
What are the contraindications to alpha-2 agonists?
inability to take regular daily dosage
-risk of rebound HTN
What are the precautions to alpha-2 agonists?
hepatic impairment
kidney impairment
What are some monitoring parameters specific to alpha-2 agonsits?
BP (hypotension)
bradycardia, syncope
sedation and somnolence
increased BP and HR upon dc
QTc
What are some examples of drug interactions with amphetamines and MPH?
antidepressants
-increased risk of serotonin syndrome
-hypertensive crisis with MAOI
-CV and stimulatory effect increased with TCA
antihypertensives
-decreased hypotensive effect of antihypertensive
antipsychotics
-increased risk of psychosis, decreased effect of AMP
decongestants
-increased hypertensive and tachycardic effect of decongestant
What are the CV AE’s of ADHD meds?
increase BP and HR: stims, ATX, a2a if abrupt dc
decrease BP and HR: a2a
What are the GI AE’s of ADHD meds?
appetite suppression: stims, ATX
constipation/diarrhea: all
nausea/vomiting: all
dry mouth: all
GI upset: all
What are the CNS/psych AE’s of ADHD meds?
anxiety: stims, ATX
dizziness: all
dysphoria/irritability: stims, ATX
HA: all
initial insomnia: stims, ATX
somnolence: a2a
rebound effect: stims
tics: stims
Which ADHD meds cause decrease in weight?
stims and ATX
Which ADHD med can cause sexual dysfunction?
ATX
Which ADHD meds can cause skin reactions?
stims and ATX
How should ADHD meds be initiated?
start low and go slow
What are dose increases based upon in ADHD?
continue dose increases until reached desired goals of treatment, side effects occurring, or max dose reached
What is the optimal dose?
dose above which there is no further improvement
