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45 Cards in this Set

  • Front
  • Back
methylphenidate
CNS stimulant
short-acting- Ritalin, Methylin
intermediate-acting- Ritalin SR, Methyln ER
long-acting- Ritalin LA, Concerta, Daytrana
dexmethylphenidate
CNS stimulant
short-acting-Focalin
long-acting-Focali XR
dextroamphetamine
CNS stimulant
short-acting-Dexetrine
long-acting- Dexetrine spansule
amphetamine mixture
CNS stimulant
short-acting- Adderall
long-term-Adderall XR
lisdexamfetamine dimesylate
CNS stimulant
long-acting- Vyvanse
CNS stimulants MOA
raise the level of norepinepherine, serotonin, and dopamine into the CNS
CNS stimulants USE
ADHD
Conduct disorder
CNS stimulants adverse effects
CNS stimulation, weight loss, cardivascular effects, psychotic manifestations, withdrawal reactions, hypersensitivity skin reaction to transdermal
CNS stimulants contraindications
substance abuse disorder, cardiovascular, severe anxiety, psychosis
CNS stimulants Interactions
MAOIs may cause hypertensive crisis, concurrent use of caffiene may increase CNS effects
methylphenidte inhibits metabolism of phenytoin, warfarin (Coumadin) and phenobarbital, leading to increased serum levels
OTC cold meds with sympathomimetic action can increase CNS stimulant effects
CNS stimulants Administration
transdermal meds- place patch on one hip daily in the morning and leave it in place no longer than 9 hr alternate hips daily
high potential for substance abuse disorder especially in adolescents
CNS stimulant effectiveness
improvement of ADHD manifestations
improved ability to stay awake
Norepinepherine Selective reuptake inhibitor
atomoxetine (Strattera)
NSRI MOA:
block reuptake of norepinepherine at synapses in the CNS, Atomoxetine is not a stimulant med
NSRI USE
ADHD
NSRI adverse
appetite suppression
GI effects
suicidal ideation
hepatoxicity
NSRI contraindications
cardiovascular disorders
NSRI interactions
MAOIs may cause hypertensive crisis
paroxetine (Paxil), floexetine (Prozac), inhibit hepatic metabolizing enzymes, thereby increasing levels of atomoxetine
NSRI admin
daily dose in the morning, or in two divided doses, morning and afternoon, with or without food
NSRI effectiveness
increase in ability to focus and complete tasks, and manage impulsitivity (ADHD manifestations)
TCAs
desipramine (Norpramin)
imipramine (Tofranil)
TCA
clomipramine (Anafranil)
TCA
TCA MOA:
block reuptake of monoamine neurotransmitters norepinepherine and serotonin in the synaptic space, thereby intensifying the effects that these neurotransmitters produce
TCA USE
depression, autism, ADHD, panic, school phobia, separation anxiety disorder, OCD
TCA adverse
orthostatic hypotension
anticholinergic effects
weight gain
sedation
toxicity resulting in cholinergic blockade and cardiac toxicity evidenced by dysrhythmias
decreased seizure threshold
excessive sweating
TCA Interactions
concurrent use of MAOI causes hypertension
antihistamines and other anticholinergic agents have additive anticholinergic effects
block uptake of epinepherine and NE in the synaptic space, leading to decreased intensity of effects
inhibit uptake of ephederine and amphetamine- leads to decreased responses of these meds
alcohol, benzodiazepines, opioids and antihistamines cause additive CNS depression
TCA admin
may take 1-3 weeks to experience therapeutic effects
full therapeutic effects may take 2-3 months
sudden discontinuation of the meds can result in relapse
TCA contraindications
seizure, diabetes, liver, kidney, and respiratory disorders
TCA effectiveness
improvement in mood
improved sleeping and eating habits
increased interaction with peers
decreased anger and compulsive behavior
less hyperactivity, greater ability to pay attention
alpha2-adrenergic agonists
guanfacine (Intuniv)
clonidine (Kapvay)
alpha adrenergic agonist
alpha adrenergic agonists MOA
known to activate presynaptic alpha adrenergic receptors within the brain
alpha adrenergic agonist Uses
ADHD
alpha adrenergic agonists Adverse
CNS effects, cardivascular effects, weight gain
alpha adrenergic agonist contraindications
clonidine is ccontraindicated for children less than 6 years old
clients who have cardiac disease
alpha adrenergic agonist interactions
cns depressants can increase CNS effects
antihypertensives can worsen hypotension
foods with high-fat content will increase guanfacine absorption
alpha adrenergic agonist administration
abrupt discontinuation can result in rebound hypertension
alpha adrenergic agonist effectiveness
improvement of manifestations of ADHD, such as an increase in ability to focus and complete tasks, interact with peers, and manage impulsitivity
antipsychotic-atypical
risperidone (Risperdal)
antipsychotic- atypical MOA
block serotonin, and to a lesser degree, dopamine receptors
also block norepinepherine, histamine, and acetylcholine
antipsychotic- atypical Uses
autism
conduct disorder
PTSD
relief of psychotic manifestations
antipsychotic- atypical adverse
new onset of diabetes, or loss of glucose control in clients who have diabetes
weight gain
hypercholesterolemia with increased risk for hypertension and other cardiovascular disease
orthostatic hypotension
anticholinergic effects
agitation, dizziness, sedation, and sleep disruption
mild extrapyramidial adverse effects, such as tremor
antipsychotics-atypical interactions
alcohol, opioids, and antihistamines cause additive CNS depressant effects
by activating dopamine receptors, levodopa counteracts effects of antipsychotic agents
TCAs amiodarone, and clarithromycin (Biaxin) prolong QT interval which increases risk of cardiac dysrhythmias
barbituates and phenytoin decrease drug levels of quetiapine
meds that inhibit CY3A4, such as fluconazole (Diflucan) inhibit hepatic drug metabolizing enzymes thereby increasing drug levels of aripprazole, queitiapine, and ziprasidone
antipsychotic-atypical effectiveness
reduction of hyperactivity and improvement in mood
decrease in aggressiveness
improvement in psychosis
improvement in ability to perform ADLs
improvement in ADHD manifestations