ADHD Flashcards
pathogenesis of ADHD
- brain develops in normal pattern but is delayed on average by about 3 years.
what are the 4 phases of management of ADHD
- Counseling
- Titration
- Maintenance - schedule 2 drug so visits for refills
- Potential termination
- trial and error w/ these drugs is very crucial to find the optimum dose! They are cleared rapidly from the body and half lives are short so need frequent dosing or sustain release preparations.
What is the counseling phase?
parental educations to expected side effects and outlining evolution of drug dose and dosing schedule
- little overall difference btw agents in initial response
Major side effects of stimulant drugs
- appetite suppression - time meals when drug effect is minimal or worn off, eat breakfast prior to dosing
- delayed sleep onset - may want to decrease afternoon dosing, use good sleep hygiene, rarely consider 2nd agent
- Wearing off phenomenon - consider 4pm dose of short acting agent
- Tics - check for emergence of Tourette syndrome, simple tics are common, if bad stop drug
- Depression - check timing of symptoms and if correlates w/ drugs then stop or change drug
- Social withdrawal - uncommon effect of zombie like behvaior. decrease dose
MOA of amphetamines
release DA and NE
MOA Atomoxetine
SNRI centrally and peripherally
MOA dexmethyphenidate and methylphenidate
block reuptake of DA and NE
MOA Guanfacine and Clonidine
improved prefrontal cortical function via post-synaptic alpha 2 receptor agonist effect in PFC
MOA Haloperidol
blocks D2 receptor post-synaptically
When are short acting amphetamines usually used?
initial treatment in small kids (<16kg), need multiple dosing throughout day
What are some problems seen w/ longer acting amphetamines?
- evening appetite and sleep problems
DDI for Amphetamine and Dextroamphetamine
- Acetazolamide, NaHCO3 - basic urine reuptakes drug in kidneys –> increased drug levels
- NH4Cl - acidic urine favors elimination – lower levels
- Chlorpromazine, Haloperidol - diminish effects of drug
- Dextromethorphan - leads to impaired judgment, erratic euphoria
- Digoxin - increased arrhythmogenic effect
- MAOI - increased drug levels and toxicity
- CYP2D6 - changes levels of drug
ADE amphetamines
More common = ab pain, headache, insomnia, loss of appetitie
Less common = anxiety, emotional lability, nervousness, tachycardia, wt loss
DDI for Atomoxetine
- Albuterol - increases CV adverse effects
- Epi - further increase BP
- MAOI - increase toxicity - allow 2 week interval b/w drugs
- Ergotamine, pseudoephedrine - increase pressor agent effect on BP
- CYP2D6 - affect drug levels
DDI for Methylphenidate
- MAOI - increase tox - allow 2 wk interval btw drugs
- Alcohol- increase production of toxic metabolite
- Phenytoin - increases blood levels of phenytoin
- Ergotamine, pseudoephedrine - increase pressor agent effect on BP
- CYP2D6 - affects drug levels
ADE Atomoxetine
Dry mouth, headache, ab pain, decreased appetite, cough, somnolence, vomiting, insomnia
ADE methylphenidate
headache, insomnia, decrease appetite, N/V, ad pain
absolute contraindications for stimulants
- MAOI
- psychosis
- glaucoma - b/c cause transient mydriasis (increased ICP)
- underlying cardiac conditions - mild increases in pulse and BP
- existing liver disorders
- Hx of stimulant drug dependence
Treatment for Tourette syndrome’s tics?
1st choice - alpha 2 agonists improve tics and ADHD
2nd choice - stimulants affect the ADHD but not tics
3rd choice - methyphenidate + alpha 2 agonist combo
DDI for clonidine
cyclosporine - increases levels of interactant
- no CYP interactions
DDI guanfacine
Bupropion - grand mal seizures
- no CYP interactions
DDI haloperidol
-metabolized by glucoronidation and CYP 2D6 and 3A4. inhibition of one or more of these metabolic pathways may result in increased haloperidol concentrations and potential QT PROLONGATION
ADE clonidine and guanfacine
skin reactions, dry mouth, somnolence, headache, fatigue, drowisness, dizziness, anxiety, ab pain
clinical management of overdose for amphetamine/methyphenidate
- Amphetamine/methlyphenidate - toxicity is mainly neurological and CV but secondary complications involve other systems. GOAL for treatment is mainly supportive, maybe use BNZs
clinical management of overdose for atomoxetine
mild overdose. GOAL for treatment is supportive w/ focus on sedation and control of dyskinesias and seizures
clinical management of overdose for clonidine
- OD = short term HTN, usually hypotension
Treat: Nitroprusside for HTN
Atropine, DA for support of hypotension
clinical management of overdose for guanfacine
OD = mixed picture, depending on central and peripheral effects. Initially drowsiness, lethargy, dry mouth, diaphoresis. CV effects = hypotension or HTN
Treat: largely supportive w/ focus on support of BP
