Pharmacotherapy Exam 4 Adhd Flashcards ionicons-v5-c

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: 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)

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: 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

<html>Initial Dose: 12.5 mg Qday Max Dose: 25-50 mg/day Duration: up to 16 hours FDA approval: <u>></u>13 yo Capsule contains 1:1:1 ratio of beads(pH dependent release) DR: proximal Small intestine release XR: Distal small intestine release</html>

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>

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

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Short Acting AMP: Duration of Action

4-6 hours (8 hr for intermediate action)

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

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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

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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 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

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: 5-17 yo

NICE: Atomoxetine, guanfacine

ADHD: Second line treatment: 6-19 yo

AAP: atomoxetine, guanfacine XR, clonidine XR

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: 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