Pharmacotherapy Exam 4 Adhd Flashcards
ADHD: Vayarin: MOA
Prescription medical food No evidence of efficacy Possibly helps with low levels EPA in patients with ADHD Fish oil supplements may work as well
ADHD: Natural products
Phosphatidylserine omega 3 Fatty Acids (Vayarin) Iron Zinc Sulfate
ADHD: Lithium/antiepileptics: role in therapy
Effective for explosive behavior, aggression, and impulsivity Not effective for inattentive type Often used for Bipolar dx
ADHD: Lithium/antiepileptics: Onset of therapy
1-2 weeks to therapeutic response
ADHD: Lithium/antiepileptics: Drugs
Lithium Valproate Carbamazepine
ADHD: Antipsychotics: ADEs
EPS Sedation Metabolic effects QTc prolongation
ADHD: Antipsycotics: role in therapy
May help with hyperactivity and impulsivity Negative effects on cognition and learning Help with severe aggression in refractory cases Adjunct Not FDA approved for ADHD
ADHD: TCAs: role in therapy
Last line, due to CV side effects and risk in overdose
ADHD: TCAs: ADEs
Anticholinergic effects Increased HR, Heart Block
ADHD: TCAs: Drugs
Imipramine Nortriptyline Desipramine: may help reduce tics
ADHD: TCAs: Kinetics
Onset is 2-4 weeks
ADHD: TCAs: MOA
Blocks reuptake of NE and serotonin
Bupropion: Therapy Considerations
Used off label Use in patients with co-existing depression Minimal to moderate improvement in ADHD
Bupropion: Monitoring
Weight loss, eating and sleeping patterns Psychiatric reaction: depression, SI, AX, Agitation, panic attacks, hostility BP and HR
Bupropion: Warnings/Precautions
Cognitive Impairment Hypertension Weight loss
Bupropion: Contraindications
Seizure disorders Hx anorexia/bulimia Patients undergoing abrupt discontinuation of ethanol Use MAO inhibitors within 14 days
Bupropion: Less common ADEs
Arrhythmia Hypertension Abdominal pain Skin rash Diarrhea
Bupropion common ADEs
Tachycardia Diaphoresis Weight loss Insomnia Headache Nausea Constipation Agitation Tremor
Bupropion: Drug Interactions
Additive seizure threshold lowering potential CYP2B6 inhibitors/inducers Inhibit CYP 2D6 substrates
Bupropion: Pharmacokinetics
IR Peak: within 2 hours 12 hr ER/SR Peak: within 3 hours 24 hr ER: 5-12 hours Half-life: 21 hours (Chronic); metabolite: up to 37 hours after a single dose Metabolism: Extensively hepatic via CYP2B6 Strong 2D6 inhibitor
Bupropion: Dose Adjustments
Renal Impairment: CrCl: 15-60 ml/min- consider max 150 mg/day CrCl: <15 ml/min: use alternative agent Hepatic impairment: use with caution
Bupropion XL Dosing
Initial Dose: 150 mg daily Max Dose: 450 mg daily
Bupropion ER Dosing
Initial Dose: 100 mg daily Max dose: 200 mg BID
Bupropion IR Dosing
Initial dose: 3 mg/kg/day in 2-3 divided doses Max dose: 6 mg/kg/day or 300 mg/day
Bupropion: Action
Takes up to 4 weeks to see max effects Less effective than stimulants; good option for comorbid depression
Bupropion: MOA
Monocyclic antidepressant that inhibits reuptake of NE and DA Not FDA approved- off label usage
Alpha-2 Adrenergic Agonists: Therapy considerations
Lacks abuse potential No head to head comparisons of guanfacine and clonidine Require tapering when D/C to avoid rebound hypertension May be used if stimulant intolerant or failure Adjunctive treatment to control disruptive behavior or alleviate insomnia May be an optimal choice for patients with tics
Alpha-2 Adrenergic Agonists: Monitoring
Evaluate BP and HR Assess mental status and sedation CV assessment Consider further evaluation (EKG) if any symptoms
Alpha-2 Adrenergic Agonists: Warning/Precautions
CNS effects: Sedation/drowsiness Hypotension, Bradycardia, syncope Cardiac induction abnormalities Rebound hypertension
Clonidine ER: ADEs
Somnolence Fatigue Irritability Nightmare Insomnia Constipation Dry mouth
Guanfacine: ADEs
Somnolence Fatigue Hypotension(Possibly dose limiting) Dizziness Lethargy Nausea Dry mouth
Guanfacine: Drug Interactions
3A4 inducers/inhibitors May increase VPA levels Additive CNS depressant effects Enhance hypotensive or bradycardic effects
Guanfacine: Pharmacokinetics
Time to peak: IR: 1-4 hours, ER: 5-8 hours Half-life: Children: 17 hours, Adults: 14-18 hours Metabolism: CYP3A4 (50% hepatic clearance) Clearance reduced in renal impairment
Guanfacine: Dose Adjustments
Renal Impairments: recommend lower dosing range Hepatic Impairment: use with caution
Guanfacine ER: Dosing
Initial Dose: 6-17 yo: 1 mg daily Titration: 1 mg/week; no more than 1 mg every 3-7 days Max Dose: 6-12 yo: 4 mg/day; 13-17 yo: 7 mg/day
Guanfacine IR: Dosing
Initial Dose: <45kg: 0.5 mg Qday; >45 kg: 1 mg daily Titration: every 3-4 days in 0.5 mg/day increments Max dose: 27-40.5kg: 2 mg/day; 40.5-45 kg: 3 mg/day; >45kg: 0.4 mg/day
Clonidine: Drug Interactions
Additive CNS depressant effects Enhance hypotensive or bradycardic effects Diminish hypertensive effects
Clonidine: Pharmacokinetics
Time to peak: IR: 1-3 hours, ER: 7-8 hours Half-life: Children: 5-7 hours, Adults: 12-16 hours Metabolism: Extensively hepatic to inactive metabolites
Clonidine: Transdermal patch: characteristics
Not FDA approved for ADHD 1-3 day overlap with oral, once optimal oral dose reached Change patch every 5-7 days Therapeutic levels persist ~8 hours after patch removal
Clonidine: Dose adjustments
Renal impairment: lower end dosage range recommended Hepatic impairment: no adjustment
Clonidine ER: Dosing
Initial Dose: 0.1 mg QHS Titration: 0.1 mg/week, no more than 0.1 mg every 3-7 days Max dose: 0.4 mg/day
Clonidine IR: Dosing
Initital Dose: <45kg: 0.05 mg QHS; >45kg: 0.1 mg QHS Titration: every 3-7 days-0.05 mg increments, over 1-2 weeks Max dose: 27-40.5 kg: 0.2 mg/day; 40.5-45 kg: 0.3 mg/day
Alpha-2 adrenergic Agonists: Efficacy
Less effective than stimulants Takes 2-4 weeks to see effect
Alpha-2 Adrenergic Agonists: Formulations
ER: Approved for ADHD Monotherapy or adjunct with stimulants IR used off label
Alpha-2 Adrenergic Agonists: MOA
Binds presynaptic and postsynaptic alpha-2 adrenoreceptors in the PFC: Works on NE Enhance daily related firing of PFC neurons- important for overcoming distraction and behavioral inhibition
Viloxazine ER: Characteristics
Unknown clear advantage over other ADHD options May potentially work quicker than atomoxetine (Onset 1 wk v. 2-4 weeks with IR) Very Expensive
Viloxazine: Monitoring
Assess Cardiac health prior to initiation Screen patients for personal/family hx of suicide, bipolar, and depression Monitor BP and HR: Baseline, following dose increases, and periodically Monitor LFTs, SCr, GFR
Viloxazine: Warnings/Precautions
CV effect: May increase BP, HR CNS: May cause fatigue, lethargy, sedation Suicidal thinking or behavior in pediatrics
Viloxazine: Contraindications
Concomitant use with or within 14 days of MAOIs Concomitant use of CYP1A2 substrates with a narrow therapeutic range
Viloxazine: Less Common ADEs
Abdominal pain Decreased appetite N/V Insomnia Irritability SI
Viloxazine: common ADEs
Increased DBP Drowsiness Headache
Viloxazine: Drug Interactions
Strong CYP 1A2 inhibitor Weak CYP2D6, 3A4 inhibitor Minor CYP2D6 substrate
Viloxazine: Pharmacokinetics
Time to peak: 5 hours (range 3-9) Half-life: 7 hours +/- (4.74hr) Metabolized by CYP2D6, UGT1A9, UGT2B15 High fat meal may decerase absorption
Viloxazine: Dosing adjustments
Renal impairment: Severe- max 200 mg/day Hepatic impairment: Not recommended
Viloxazine: Max dose
400 mg/day
Viloxazine: Dosing: 12-17 yo
200 mg Qday; may increase to 400 mg after 1 week
Viloxazine: Dosing: 6-11 yo
100 mg Qday; may titrate by 100 mg/week
Viloxazine: Atomoxetine comparison
Increased Intracellular NE, DA, and 5-HT levels in the PFC Less activity toward NET then atomoxetine More 5-HT functionality in the PFC then atomoxetine
Viloxazine: MOA
Selective NE reuptake inhibitor Antagonist toward 5-HT2B Agonist toward 5-HT2C No activity toward Ach or Histamine (No anticholinergic affect)
Viloxazine: FDA approval age
6-17 yo
Atomoxetine: Therapy considerations
Lacks abuse potential; Typically more expensive than other ADHD medications; Lack long term efficacy data; May be used as adjunct or if stimulant therapy fails
Atomoxetine: Monitoring
Evaluate need for dose adjustments at least monthly to start; Height, weight, growth, appetite, HR, BP, baseline, routine LFTs; Liver enzymes if symptoms of liver dysfunction; Cardiac eval if CV symptoms
Atomoxetine: BBW
Increased risk of suicidal Ideation in children/adolescents; Potential for severe liver damage, CV events, Priapism, hostile/aggressive behaviors, treatment-emergent psychotic or manic symptoms
Atomoxetine: Contrindications
Narrow angle Glaucoma, MOAI use currently or within last 14 days; Severe cardiac or Vascular disorders
Atomoxetine: ADEs
Headache; Insomnia; Xerostomia; Decreased Appetite; Nausea;Hyperhydrosis; Abdominal pain; ED
Atomoxetine: Drug Interactions
2D6 Inhibitors may increase concentration
Atomoxetine: Pharmacokinetics
Time to peak: 1-2 hours, delayed 3 hours by high fat meal; Half-life: 5 hours; Active metabolites: 6-8 hor; Metabolized via CYP2D6 and 2C19
Atomoxetine: Dosing: >6yo, >70 kg, Adults
40 mg/day; Target Dose: 1.2 mg/kg/day; Max Dose: 1.4 mg/kg/day
Atomoxetine: Dosing: Poor Metabolizers
1.2 mg/kg/day or 80 mg/day
Atomoxetine: Dosing: >6yo, <70kg
0.5 mg/kg/day; Target Dose: 1.2 mg/kg/day; Max dose 1.4 mg/kg/day or 100mg/day
Atomoxotine: Caution
Additive side effects with stimulants (can be added, just have to be careful)
Atomoxetine: Onset of action
2-4 weeks
Atomoxetine: Role in therapy
Second or third line
Atomoxetine: FDA approved age
Children and adults
Atomoxetine: MOA
Inhibits presynaptic reuptake of selective NE in CNS
ADHD: Non-stimulants: Characteristics
Less abuse potential, Less sleep disturbance, Overall, Lower Efficacy then stimulants; Used if stimulants are not effective or if side effects are intolerable
ADHD: Pharm Therapy: Non-stimulant drgs
Atomoxetine, Viloxazine, Clonidine(IR, ER), Guanfacine (IR, ER), Bupropion
Stimulants: Drug interactions
Other Psychostimulants Anti-hypertensive agents MAOIs TCAs: MPH can increase TCA concentration Antacids, PPIs, H2 receptor antagonists: Affect absorption of MPH Opioid analgesics and other sympathomimetics: may increase AMP concentrations
Stimulants: Patient education
Medication guide: reviews cardiac, psychiatric and peripheral circulation risks
Stimulants: Efficacy monitoring
Evaluate Q 2-4 weeks until stable dose, then every 3 months
Stimulants: Safety monitoring
Baseline and follow up: height, weight, appetite, sleep, BP EKG/Cardio consult Watch for chest pain, syncope, other signs of CV issues, cardiac eval
Stimulants: Contraindications
CV: CVD, Arrhythmias, HF, Recent MI Hyperthyroidism Glaucoma Hx drug abuse within 14 days of MAOI use Known hypersensitivity to stimulants
Stimulants: Precautions
HTN/Tachycardia Seizures Visual Disturbances/blurred vision Exacerbation of tics Peripheral vasculopathy Some drugs may contain lactose, sucrose, or phenylalanine
MPH Mydayis: Warning
Avoid in ESRD (Single amphetamine mixed salts)
MPH Suspension: Warning
Contains benzoic acid (metabolite of benzoyl alcohol), may cause allergic reaction
MPH Concerta: Warning
Avoid in patients with GI obstruction or severe GI narrowing
MPH Transdermal patch: Warning
Severe allergic contact sensitization Chemical Leukoderma: Permanent loss of skin color at application site
Stimulants: BBW
High Abuse potential (C-II) Sudden cardiac death, serious CV events Priapism after prolonged exposure, dose increase, or drug withdrawal
Stimulants: Cardiac ADEs
Sudden unexplained death Risk higher with stimulant use, but still low Screen for structural abnormalities, FH, ECG Discuss lowest dose possible with Physician
Stimulants: Psychiatric ADEs
Exacerbation of psychosis Induction of mania/mixed episodes with bipolar Treatment emergent psychotic or manic symptoms Aggressive or hostile behavior
Stimulants: Substance Abuse risk
ADHD is a known substance abuse risk factor Untreated adults with ADHD more likely to engage in drug abuse Earlier treatment may reduce risk Patients starting stimulant therapy with no hx of drug abuse are not at increased risk of abuse
Stimulants: ADE Management: Growth suppression
Stimulants may alter growth hormones, thyroxine, and suppress appetite and caloric intake Transient, typically resolves by mid adolescence Take drug holidays during winter and summer breaks to mitigate
Stimulants: ADE Management: Tics
Decrease dose Change to a different stimulant or a non-stimulant Stimulants can worsen existing tics
Stimulants: ADE Management: Irritability, dysphoria, agitation
Early onset (peak-related): Decrease dose or change to longer-acting stimulant Late onset (Withdrawal related): Change to longer acting stimulant Treat comorbidities as necessary
Stimulants: ADE Management: Headache
Decrease or divide dose Change to longer acting stimulant or non-stimulant
Stimulants: ADE Management: Insomnia
Move dose earlier in the day Discontinue late day dose Change to shorter acting formulation or non-stimulant Consider treatment for insomnia (melatonin)
Stimulants: ADE Management: GI upset/Nausea/Decreased appetite/Growth delay
Encourage high calorie breakfast and dinner Divide dose Change to short acting product or non-stimulant Drug holidays
Stimulants: ADEs
GI upset Nausea Decreased appetite Potential growth delay Insomnia Headache Irritability/aggitation Dysphoria Tics
Amphetamine IR to ER conversions
Same total daily dose taken once daily
Vyvanse: Kinetics
Dosing: 30-70 mg daily Duration: 10-12 hours Onset: Slower: 1.5-2.5 hours (longer duration than dextroamphetamine)
Vyvanse: Advantage
Only converted to active form if ingested; may limit abuse potential from snorting or IV injection
Vyvanse: MOA
Prodrug of Dextroamphetamine Converted to active drug via hydrolysis into D-amp and l-lysine
Vyvanse: Approval age
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Lisdexamfetamine: Brand name
Vyvanse (brand name only)
Mydayis: Kinetics
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Adderall XR: Kinetics
<html>Initial Dose: 5-10 mg Qday Max Dose: 30-60 mg/day Duration: 8-12 hours Peak: 7 hours 50% IR, 50% ER beads FDA Approval: <u>>6 yo</u></html>
Long Acting Amphetamine mixed salts: Drugs
Adderall XR Mydayis
Dyanavel XR: Kinetics
Initial Dose: 2.5-5 mg Qday Max Dose: 20 mg/day Duration: 8-10 hours, up to 13 hours Peak: 4 hours Liquid formulation Ion exchange resin- contains both IR and ER
Adzenys XR: Kinetics
Initial Dose: 6.3 mg Qday Max Dose: 18.8 mg/day Duration: 10-12 hours Peak: 5 hours 50% IR, 50% ER 3.1 mg equivalent to Adderall XR 5 mg
Long acting Amphetamine: Drugs
Adzenys XR, XR-ODT Dyanavel XR
Dextroamphetamine Spansule: Formulation
IR and DR beads in 1:1 ratio
Dextroamphetamine formulation
Has liquid formulation
Dextroamphetamine-Amphetamine formulation
D-amp : l-amp in 3:1 ratio
Amphetamine formulation
D-amp : l-amp in 1:1 ratio
Short acting AMP: FDA approved age
<html><u>></u><u>3 yo</u></html>
Short Acting AMP: Duration of Action
4-6 hours (8 hr for intermediate action)
Short Acting AMP: Max Dose
40 mg/day
Short Acting AMP: Initial Dose
5-10 mg BID
Short Acting AMP: Drug names
Amphetamine: Evekeo Dextroamphetamine-Amphetamine: Adderall Dextroamphetamine: Dexedrine, Procentra, Zenzedi Dextroamphetamine: Spansule (Intermediate-acting)
Amphetamines: Pharmacokinetics
Oral absorption: High fat meals may delay time to peak concentration Metabolism: 2 active metabolites Duration of action dependent on formulation
Amphetamines: MOA
Stimulant release of DA and NE into the presynaptic nerve terminal: May stimulate release of serotonin at high doses Dextro-AMP is more active compared to levo-AMP
MPH Patch conversion guidelines
Patients converting from another formulation to a patch should be initiated at 10 mg and titrated as needed Apply patch to hip 2 hours before needed Remove 9 hours after application; at least 3 hours before bedtime
MPH Conversions: IR MPH Dose: 45 mg/day
Daytrana patch size: 30 mg Concerta: 54 mg/day
MPH Conversions: IR MPH Dose: 30 mg/day
Daytrana patch size: 20 mg Concerta: 36 mg/day
MPH Conversions: IR MPH Dose: 22.5 mg/day
Daytrana patch size: 15 mg Concerta: 27 mg/day
MPH Conversions: IR MPH Dose: 15 mg/day
Daytrana patch size: 10 mg Concerta: 18 mg/day
MPH Conversions: IR MPH Dose: 20 mg 2-3 times daily
Concerta: 72 mg once daily Ritalin LA: Same total daily dose should be used
MPH Conversions: IR MPH Dose: 15 mg 2-3 times daily
Metadate ER: 60 mg daily Concerta: 54 mg daily Ritalin LA: Same total daily dose should be used
MPH Conversions: IR MPH Dose: 10 mg 2-3 times daily
Metadate ER: 40 mg daily Concerta: 36 mg daily Ritalin LA: Same total daily dose should be used
MPH Conversions: IR MPH dose: 5 mg 2-3 times daily
Metadate ER: 20 mg Daily Concerta: 18 mg daily Ritalin LA: Same total daily dose
Dexmethylphenidate: Initial dosage
1/2 daily dose of racemic methylphenidate
Dexmethylphenidate: Approved age
<html><u>></u><u>6 yo</u></html>
Dexmethylphenidate: MOA
D-isomer of methylphenidate More potent at NE and DA transporter than L isomer
Ritalin LA: Kinetics
Initial Dose: 20 mg Qday Max Dose: 60 mg/day Duration of Action: 6-8 hours Peak: ~2 and 7 hours Note: 50% IR and 50% ER beads Delayed release over 8-12 hours
Quillivant XR: Kinetics
Initial Dose: 20 mg Qday Max Dose: 60 mg/day Duration of Action: 12 hours Peak: ~4 hours Note: 20% IR and 80% DR
Quillichew ER: Kinetics
Initial Dose: 20 mg Qday Max Dose: 60 mg/day Duration of Action: 10-12 hours Peak: ~5 hours Note: 30% IR and 70% DR
Metadate CD: Kinetics
Initial Dose: 20 mg Qday Max Dose: 60 mg/day Duration of Action: 6-8 hours Peak: 1.5 and 4.5 hours Note: 30% IR and 70%ER Delayed release over 8-12 hours
Jornay PM: Kinetics
Initial Dose: 20 mg Qday Max Dose: 100 mg/day Peak: 14 hours Note: Given in evening; effect occurs in 8-10 hours Insomnia occurs in up to 41% of patients
Focalin XR (Dex-MPH): Kinetics
Initial Dose: 10 mg Qday Max Dose: 40 mg/day Duration of Action: 9-12 hours Peak: 1.5 and 6.5 hours Note: 50% IR and 50% ER beads; mimics BID dosing
Daytrana: Kinetics
Initial Dose: 10 mg Qday Max Dose: 30 mg/day Duration of Action: 10-12 hours Peak: 8-10 hours Note: Onset 2 hours after application Apply patch to hip continuous release over 9-12 hours Remove after 9 hours
Contempla: Kinetics
Initial dose: 17.3 mg Qday Max Dose: 51.8 mg/day Duration of Action: 12 hours Peak: 5 hours Note: 25% IR and 75% ER
Concerta: Kinetics
Initial Dose: 18 mg Qday Max Dose: 54-72 mg/day Duration: 10-12 hours Peak: 1 and 6 hours 22% IR and 78% ER beads; controlled release over 10-12 hours May leave shell in stool
Aptensio XR: Kinetics
Initial Dose: 10 mg Qday Max dose: 60 mg/day Duration: 12 hours Peak: 2 and 8 hours 40% IR and 60% ER beads; controlled release over 12 hours
Adhansia: Kinetics
Initial Dose: 25 mg Qday Max dose: 85 mg/day Duration: 12 hours Peaks: 2 hours, 10-12 hours 20% IR and 80% ER beads; controlled release over 16 hours
Adhansia: Disadvantage
Need to take early in the morning due to late peak time (12 hours)
MPH: Long acting: Drugs
Adhansia XR Aptensio XR Concerta Contempla XR-ODT Daytrana Focalin XR (Dex-MPH) Jornay PM Metadate CD Quillichew ER Quillivant XR (Solution) Ritalin LA
Metadate ER: FDA approval
<html><u>></u><u>6 yo</u></html>
Metadate ER: Kinetics
Initial Dose: 10 mg BID Max Dose: 60 mg/day Duration of Action: 3-8 hours Delayed onset May still need BID dosing
MPH Intermediate: Drug
Metadate ER
MPH Short acting: FDA approval
<html><u>></u><u> 6 yo</u></html>
Dexmethylphenidate IR: Kinetics
Initial Dose: 2.5 mg BID Max dose: 20 mg/day Duration of action: 3-5 hours (peak 1-1.5 hours)
Methylphenidate IR: Kinetics
Initial Dose: 5 mg BID (3-5 yo: 2.5 mg BID) Max dose: 60 mg/day (NTE 2 mg/kg/day) Duration of action: 3-6 hours (peak 1-2 hours)
MPH: Short acting: Drugs
Methylphenidate IR Dexmethylphenidate IR
MPH: Short acting Disadvantage
Rebound symptoms Potential for re-emerging ADHD symptoms
Methylphenidate (MPH): MOA
Selectively inhibits presynaptic reuptake of DA and NE- specifically blocks DA transport of carrier proteins Dex MPH is more active isomer compared to levo-MPH
Methylphenidate (MPH): Pharmacokinetics
Oral absorption: time to peak may be delayed by high fat meal AUC and Cmax increase for ER chewable or suspension Metabolism: Inactive Metabolites Duration of action dependent on each formulation
Stimulants: Extended acting: Kinetics
Duration: 8-12 hours
Stimulant: Intermediate acting: Kinetics
Onset: 60-90 minutes Duration: 3-8 hours
Stimulant: Short acting: Kinetics
Onset: within 30 minutes Duration: 3-6 hours
Stimulants: Control of core symptoms
May alleviate conduct and anxiety disorders Improve academic performance and improved cognition
Stimulants: Characteristics in ADHD
Most effective agents in treating ADHD Better control of core symptoms compared to behavioral interventions alone Block dopamine and NE reuptake Controlled substances
ADHD: Effect size review
Measures strength of effect or association: ((mean for active agent) - (mean for placebo))/Standard deviation (pooled) Effect size of 1: average person in experimental group is 1 SD above average person in control group 0.8 = large 0.2 = Small
ADHD: Second line treatment: Adults
NICE: Atomoxetine
ADHD: Second line treatment: 5-17 yo
NICE: Atomoxetine, guanfacine
ADHD: Second line treatment: 6-19 yo
AAP: atomoxetine, guanfacine XR, clonidine XR
ADHD: Second line treatment: 4-5 yo
AAP: MPH
ADHD: First line treatment: Adults
NICE: MPH or lisdexamfetamine
ADHD: First line treatment: 5-17 yo
NICE: MPH (if failure, consider lixdexamfetamine)
ADHD: First line treatment: 6-18 yo
AAP: MPH or AMP
ADHD: First line treatment: 4-5 yo
AAP: Behavioral therapy
ADHD: Treatment guidelines
Stimulants recommended as initial therapy: Response rates 65-75% --> increase to 90% with careful therapy management Methylphenidate and Amphetamines are generally equally efficacious (individual patients may have different responses) If one stimulant fails, try other class
ADHD: Multimodal treatment approach
Involve parents, teachers, & clinicians Screen for comorbidities Behavioral therapies for mild symptoms, uncertain dx, or medication not preferred Medication alone is better than behavioral intervention alone Medication + Behavioral therapy better for improving oppositional and aggressive behaviors
ADHD: Secondary treatment goals
Improve relationships with family, teachers, peers Decrease disruptive behavior in academic and social settings Improve academic performance Increase independence in activities Minimize undesirable adverse effects in therapy
ADHD: Primary Treatment goals
Improve behavior Increase attention/response inhibition
ADHD: Pathophysiology of the brain: Consequences
Difficulty prioritizing attention and tasks Lapses in attention and inhibitory control Negative effects on cognitive processing, motor planning, speed of processing, and other behavioral issues
ADHD: Pathophysiology of the brain
Prefrontal cortex, caudate, cerebellum may be primary areas affected Slower maturation of PFC or smaller volume and reduced activity Lower AD activity in the midbrain
ADHD: Pathophysiology: NE/DA dysfunction
Deficit in DA reward pathway impairs ability to maintain attention to dull or repetitive tasks, regulate mood and arousal NE dysfunction- inability to modulate attention, arousal, mood
ADHD: Pathophysiology
Disorder of self regulation or response inhibition Dysfunction of NE and Dopamine Difficulty maintaining self-control, resisting distractions, and concentrating on ideas
ADHD: Risk Factors: Environmental Factors
Lead poisoning Fetal alcohol syndrome Meningitis Maternal smoking Adverse parent-child relationships
ADHD: Risk factors: Genetic
>40% heritability; 4-8x increase risk with first degree relative
ADHD: Risk Factors: Substantial Comorbidity
30% of patients with ASD; 50-60% of patients with Tourette's
ADHD: Risk Factors
Genetic Substantial comorbidity Environmental Diet (possible, but unlikely)
ADHD: Adult Etiology
60% of childhood cases have symptoms persisting in adulthood More likely to develop conduct disorder or antisocial personality disorder in adulthood Typically see inattentive in adult patients
ADHD: Prevalence
Most prevalent neurodevelopmental disorder in childhood in US 6-11% of school age children 4% of adults Boys>Girls: 2:1 (Females more likely to have inattentive symptoms)
DSM-5 Criteria: Severe ADHD
Many more than 6 symptoms Symptoms are severe Social or school impairment is severe
DSM-5 Criteria: Moderate ADHD
Symptoms or impairment is between mild and severe
DSM-5 Criteria: Mild ADHD
6 or slightly more symptoms social or school function impairment in minor
<html>ADHD: DSM-5 Diagnostic Criteria: Impulsivity/Hyperactivity (<u><</u>17 yo)</html>
Must have 6 or more symptoms for at least 6 months: Fidgets with hands/feet, squirms in chair Frequently leaves chair when seating is expected Runs or climbs excessively Trouble playing/engaging in activities quietly Acts "on the go" and as if "driven by a motor" Talks excessively Blurts out answers before questions are completed Trouble waiting or taking turns Interrupts or intrudes on what others are doing
<html>ADHD: DSM-5 Diagnostic Criteria: Inattention (<u><</u>17 yo)</html>
Must have 6 or more symptoms for at least 6 months: Poor attention to detail Trouble sustaining attention Poor listening when spoken to directly Fails to follow instructions, fails to finish schoolwork Difficulty with organization Avoids or dislikes doing things that require sustained focus Loses things frequently Easily distracted by other things Forgets things
ADHD: Long Term Effect
Interferes with functioning
ADHD: Common Comorbidities
50-60% of patients have one or more comorbidities Oppositional Defiant disorder Conduct disorder
ADHD: DSM-5 diagnostic criteria
1. Inattentive 2. Hyperactivity/Impulsivity 3. Combined
ADHD: Clinical presentation: 4-18 years
Inattention Hyperactivity Impulsivity Academic Behavioral problems
ADHD: Symptoms in adults
Inattentive symptoms primarily persist
ADHD: Symptoms in Adolescence
Hyperactive symptoms decline Inattentive symptoms may be more prominent
ADHD: Symptoms in school age
Typically, initial diagnosis occurs
ADHD: Symptoms in Preschool age
Initial symptom onset: hyperactive/impulsive symptoms predominate
ADHD: Symptoms in Infancy
Delay in motor and language development