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23 Cards in this Set

  • Front
  • Back
What is the etiology of ADHD?
Underactivity* of catecholamergic system mediated by dysregulation* of dopaminergic AND noradrenergic CNS systems
Dopamine neurotransmission pathways:

4 pathways?

What does each pathway do?
4 pathways: tuberoinfundibular, nigrostriatal, mesolimbic, mesocortical
tuberoinfundibular – involved w/ prolactin
nigrostriatal – controls movement via DA excess or deficit
mesolimbic – behavioral reinforcement; role in substance abuse
mesocortical – cell bodies arise in VTA and project to cerebral cortex (prefrontal cortex)
Dopamine neurotransmission functions:
DA enhances** signals → mediates arousal, involved in attention, aids concentration, mediates cognitive fxns (verbal fluency, executive fxns, etc.)
Noradrenergic neurotransmission pathway:
Cell bodies project from locus ceruleus to areas in prefrontal cortex, limbic brain (amygdala and hippocampus), cerebellum and brainstem
Noradrenergic neurotransmission function:
NE dampens** “noise” associated w/ ADHD → enhances executive operations and increases inhibition
1st line meds for ADHD (2):
stimulants: amphetamine formulations and methylphenidate
2nd line meds for ADHD (5):
1. atomoxetine
2. buproprion
3. clonidine
4. guanfacine
5. modafinal
Previously used meds for ADHD (2):
Why were they stopped?
1. magnesium pemoline – hepatic tox and liver damage
2. TCAs – cardiac tox, increased risk of death in overdose; need to check serum levels
Why are stimulants considered 1st line for ADHD?

How effective are they for ADHD?
Stimulants are effective in 70% of ADHD affected school-agers
MOA of methylphenidate and dextroamphetamine:

What effects does this have?
Blocks reuptake of DA and NE in presynaptic neurons thru inhibition of reuptake pump
1. increases available concentration of catecholamines in synaptic cleft
2. increases availability of catecholamines to interact w/ BOTH NE and DA postsynaptic neurons
3. regulates attention and impulse control in brain areas involved w/ ADHD
How do mechanisms of methylphenidate and amphetamines differ? (although same result)
1. methylphenidate more specifically inhibits reuptake pump
2. amphetamines more specifically affects NT release, reuptake, and storage
2 theories as to why stimlants work for ADHD:
1. ramp effect → shorter time to peak concentration, the more effective it is
2. concentration effect → higher peak concentration of the stimulant, the more effective it is
3 current formulation categories for stimulants:
What drugs go in these categories?
Who are they used for?
Which category uses both ramp and concentration effects?
1. immediate acting (2-4 hrs) – Adderall, Ritalin; preschooler
2. intermediate acting preps (6-8 hrs) – Ritalin LA; school age who does homework after school
3. long-acting preps (10-12 hrs) – Adderall XR and Concerta; school age kids who have after school activities
(long-acting preps use ramp and concentration effects)
3 most common S/Es of stimulants?
Decreased appetite, insomnia*, nervousness
Frequently seen or inquired about S/Es of stimulants (though not the most common):
1. tics – mainly motor
2. growth retardation (need to monitor)
Atomoxetine MOA:
Potent NE reuptake inhibiting antidepressant
Atomoxetine uses and S/Es:
1st line for patients w/ tics
headaches, mood instability, increased BP
Bupropion off-label use?
ADHD in kids
Bupropion S/Es:
Same as stimulants (insomnia) except increased risk of seizures at high doses
Clonidine and guanfacine MOA:
Alpha-agonist antihypertensive meds for adults
Clonidine and guanfacine uses:
Hyperacivity, impulsivity, impulsive aggression
1st line – Tourette’s or tic disorders
Clonidine and guanfacine common S/Es:
Sedation (used to initiate sleep), irritability, and low BP
Modafinil uses:
1. wake agent in nacroleptics
2. minimal evidence for ADHD in kids