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23 Cards in this Set

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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
Effects:
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