ADHD Flashcards

1
Q

sx of ADHD in toddler, preschool, elementary school, and adolescent stages

A

tod: before age 4, excessive motor activity (but highly variable anyway)
pre: hyperactivity
elem: inattention becomes more prominent and impairing
early adolescence: fidgety, restless, impatient, inattentive, poor planning, impulsive; hyperactivity is less common

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2
Q

ADHD comorbidities

A

many: disruptive mood dysregulation d/o
common: specific learning d/o
minor: anxiety/MDD d/o, substance use, OCD, tic d/o, ASD, intellectual disabilities

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3
Q

non-pharm tx of ADHD

A

psychodynamic interventions: good for emotionally-based sx
family system: focus on connection b/t parent-child intxn and sx
behavioral-cognitive interventions including parent training to learn appropriate punishment and reinforcement
school behavioral intervention: target positive behaviors with stickers and rewards

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4
Q

actions of meds for ADHD

A

modify signal to noise ratio: increase signal by increasing NE, decrease noise by increasing DA

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5
Q

method of stimulants

A

increased signal attention in PFC (NE) and decrease noise from extraneous stimuli (DA)
*may cause over-focus

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6
Q

method of adrenergic agents

A

specifically increase signal (attention) by increased NE

*no effect on restlessness (inc noise) directly

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7
Q

stimulants for ADHD

A

first line; indirect sympathomimetics

methylphenidate, dexmethylphenidate, dextroamphetamine, lisdexamfetamine, mixed amphetamine salts, pemoline (off market)

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8
Q

non-stimulant meds for ADHD

A

2nd line: atomoxetine

3: TCAs, bupropion
4: a2 agonists (clonidine, guanfacine)

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9
Q

characteristics of stimulants

A

equal efficacy in reducing sx, but effective dose unpredictable
different DEA classes (amphetamines and methylphenidate are schedule 2), durations of action, adverse effects, and drug interactions

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10
Q

methylphenidate MOA and metabolism

A

inhibits reuptake of DA and NE by presynaptic terminals by blocking DAT and NET
metabolized by CYP 2D6
*schedule 2 d/t high abuse potential

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11
Q

ADRs of methylphenidate

A

anorexia, insomnia, tic d/o (transient or chronic), growth (take break when not in school), DA elevation may worsen psychosis, abuse potential (inc DA), drug interactions w CYP inhibitors or inducers

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12
Q

drug interactions with methylphenidate

A

CYP 2D6 inhibitors- fluoxetine, paroxetine
MAOIs- increase effect = medical emergency
TCAs- increase TCA effect
phenytoin- increase its effect
clonidine- cardiac arrhythmia, unknown MOA

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13
Q

amphetamine MOA

A

indirect sympathomimetic, inhibits reuptake of DA and NE by presynaptic neuron and enhances release of DA
*schedule 2

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14
Q

ADHD stimulants and cardiovascular risk

A

stimulants raise BP and HR; can cause MI, stroke, sudden death

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15
Q

antidepressants used in ADHD

A

bupropion
imipramine
desipramine

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16
Q

when a2-agonists are used in ADHD

A

children who are unusually insomniac, irritable, explosive, or labile

17
Q

atomoxetine MOA, metabolism, effectiveness

A

selective NE reuptake inhibitor (but more effective for ADHD than depression)
metabolized by CYP 2D6
more effective than placebo but less than stimulants
non-stimulant = less abuse potential, not a controlled substance

18
Q

atomoxetine ADR

A

GI upset, fatigue, decreased appetite, HTN, tachycardia, possible growth retardation
BBW: potential for severe liver dz, potential for suicidal ideation in children and adolescents

19
Q

long-term effects of pharmacologic treatment of ADHD

A

improvement in core symptoms but not academic achievement or social skills, but no conclusive evidence that long-term treatment is harmful (except dose-related ADRs, possible abuse potential)