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amphetamine MOA
- release NE
- release DA
- release 5-HT
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4 AE of amphetamines
- CNS stimulation
- weight loss
- cardiovascular effects
- psychosis
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MOA of amphetamines for ADHD
Increasing attention span will decrease the random motor activity.
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MOA of amphetamines on DA release
- Amph is a substrate of DAT, secondary action of indirect competition.
- Once in the cell it inhibits MAO and also VMAT, DA isn't taken into the vesicles and accumultes intracellularly. DAT is reversible and the gradient causes the (primary action) of DA release extracellularly
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amphetamine action on wt loss
loss first 6-9 mo and then rebound wt. gain
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Tx of amphetamine tox in GI
activated charcoal
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Tx of amph. tox of sedation
BZDs - diazepam or phenothiazine
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Tx of amph tox of psychosis
chlorpromazine or haloperidol
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Tx of amph tox of HTN
alpha adrenergic blocker, b blocker not first line
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#1 drug therapy for ADHD
- CNS stimulant
- ritalin
- adderall
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#2 drug therapy for ADHD
- atomoxetine
- blocks NE reuptake - a2 agonist, decreases SNS outflow, little CV effects
- nonstimulant
- no abuse potential
- QD
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what two scenarios would atomoxetine be useful for ADHD
- amphetamine isn't workin
- causing excess excitability
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#3 drug therapy for ADHD
- antidepressants
- buproprion - wellbutrin
- little effect of impulsivity and inattention
- poses risk of seizures
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drug for wt loss
combo of phentermine/topiramate
Qysmia
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drug for wt loss
selective serotonin2C receptor agonist
extensively metabolized in the liver
lorcaserin - bleviq
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4 Xanthine alkaloids
- theophylline - coffee, tea
- aminophylline
- theorbromine - cocoa
- caffeine
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Xanthine MOA
- 1. reversible blockade of adenosine receptors
- 2. accumulation of cAMP secondary to inhibition of PPD
- 3. calcium permeability
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misc CNS stimulant
promotes wakefulness
ADHD
Tx of fatigue in MS
enhance NE & 5HT but not conventionally
modafinil - provigil
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Tx of strychnine poisoning
IV diazepam, general anesthesia or neuromuscular block
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