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Psych Pharm > ADHD > Flashcards

ADHD Flashcards

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1
Q

pathogenesis of ADHD

A
  • brain develops in normal pattern but is delayed on average by about 3 years.
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2
Q

what are the 4 phases of management of ADHD

A
  1. Counseling
  2. Titration
  3. Maintenance - schedule 2 drug so visits for refills
  4. 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.
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3
Q

What is the counseling phase?

A

parental educations to expected side effects and outlining evolution of drug dose and dosing schedule
- little overall difference btw agents in initial response

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4
Q

Major side effects of stimulant drugs

A
  1. appetite suppression - time meals when drug effect is minimal or worn off, eat breakfast prior to dosing
  2. delayed sleep onset - may want to decrease afternoon dosing, use good sleep hygiene, rarely consider 2nd agent
  3. Wearing off phenomenon - consider 4pm dose of short acting agent
  4. Tics - check for emergence of Tourette syndrome, simple tics are common, if bad stop drug
  5. Depression - check timing of symptoms and if correlates w/ drugs then stop or change drug
  6. Social withdrawal - uncommon effect of zombie like behvaior. decrease dose
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5
Q

MOA of amphetamines

A

release DA and NE

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6
Q

MOA Atomoxetine

A

SNRI centrally and peripherally

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7
Q

MOA dexmethyphenidate and methylphenidate

A

block reuptake of DA and NE

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8
Q

MOA Guanfacine and Clonidine

A

improved prefrontal cortical function via post-synaptic alpha 2 receptor agonist effect in PFC

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9
Q

MOA Haloperidol

A

blocks D2 receptor post-synaptically

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10
Q

When are short acting amphetamines usually used?

A

initial treatment in small kids (<16kg), need multiple dosing throughout day

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11
Q

What are some problems seen w/ longer acting amphetamines?

A
  • evening appetite and sleep problems
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12
Q

DDI for Amphetamine and Dextroamphetamine

A
  1. Acetazolamide, NaHCO3 - basic urine reuptakes drug in kidneys –> increased drug levels
  2. NH4Cl - acidic urine favors elimination – lower levels
  3. Chlorpromazine, Haloperidol - diminish effects of drug
  4. Dextromethorphan - leads to impaired judgment, erratic euphoria
  5. Digoxin - increased arrhythmogenic effect
  6. MAOI - increased drug levels and toxicity
  7. CYP2D6 - changes levels of drug
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13
Q

ADE amphetamines

A

More common = ab pain, headache, insomnia, loss of appetitie

Less common = anxiety, emotional lability, nervousness, tachycardia, wt loss

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14
Q

DDI for Atomoxetine

A
  1. Albuterol - increases CV adverse effects
  2. Epi - further increase BP
  3. MAOI - increase toxicity - allow 2 week interval b/w drugs
  4. Ergotamine, pseudoephedrine - increase pressor agent effect on BP
  5. CYP2D6 - affect drug levels
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15
Q

DDI for Methylphenidate

A
  1. MAOI - increase tox - allow 2 wk interval btw drugs
  2. Alcohol- increase production of toxic metabolite
  3. Phenytoin - increases blood levels of phenytoin
  4. Ergotamine, pseudoephedrine - increase pressor agent effect on BP
  5. CYP2D6 - affects drug levels
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16
Q

ADE Atomoxetine

A

Dry mouth, headache, ab pain, decreased appetite, cough, somnolence, vomiting, insomnia

17
Q

ADE methylphenidate

A

headache, insomnia, decrease appetite, N/V, ad pain

18
Q

absolute contraindications for stimulants

A
  1. MAOI
  2. psychosis
  3. glaucoma - b/c cause transient mydriasis (increased ICP)
  4. underlying cardiac conditions - mild increases in pulse and BP
  5. existing liver disorders
  6. Hx of stimulant drug dependence
19
Q

Treatment for Tourette syndrome’s tics?

A

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

20
Q

DDI for clonidine

A

cyclosporine - increases levels of interactant

- no CYP interactions

21
Q

DDI guanfacine

A

Bupropion - grand mal seizures

- no CYP interactions

22
Q

DDI haloperidol

A

-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

23
Q

ADE clonidine and guanfacine

A

skin reactions, dry mouth, somnolence, headache, fatigue, drowisness, dizziness, anxiety, ab pain

24
Q

clinical management of overdose for amphetamine/methyphenidate

A
  1. Amphetamine/methlyphenidate - toxicity is mainly neurological and CV but secondary complications involve other systems. GOAL for treatment is mainly supportive, maybe use BNZs
25
Q

clinical management of overdose for atomoxetine

A

mild overdose. GOAL for treatment is supportive w/ focus on sedation and control of dyskinesias and seizures

26
Q

clinical management of overdose for clonidine

A
  • OD = short term HTN, usually hypotension
    Treat: Nitroprusside for HTN
    Atropine, DA for support of hypotension
27
Q

clinical management of overdose for guanfacine

A

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

Psych Pharm (7 decks)

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