ADHD meds Flashcards
MOA of amphetamines
release DA and NE
moa of atomoxetine
selective NE reuptake inhibitor centrally and peripherally
dexmehtyphenidate
methylphenidate
block reuptake of DA and NE
clonidine and guanfacine
improved PFC function through post-synaptic alpha-2 receptor AGONIST effects in the PFC
moa of haloperidol
blocks post-synaptic D2 receptors
what are the six ADEs of stimulant ADHD drugs
- depression + withdrawal
- appetite suppression + delayed sleep onset
- wearing off + tics
management of ADHD is comprised of 4 phases what are they?
- counsel
- titrate
- maintenance
- potential termination
what are the more common amphetamine ADE?
HILA
Headache
Insomnia
Loss of appetite
Abdominal pain
less common ADE of amphetamines:
WANTEd
W-weight loss
A-anxiety
N- nervousness
T-tachycardia
E-emotional lability
D -
atomoxetine ADE
HID
SCAD
dry mouth
headache
abdominal pina
decreased appetite
cough
somonolence
vomiting
insomnia
methylphenidate ADE
HID N/V and AB pain
Headache
Abdominal pain
Decreased appetite(patch)
Insomina
N/V
what are the ABSOLUTE C/I in to stimulant use? (6 of them)
MAOI + psychosis
glaucoma + underlying caridac conditions: early arrhythimic death (mild increase in pulse and BP)
existing liver disease
history of stimulant drug dependance
effectof amphetamine with acetazolamine and NA bicarbonate?
alkaline urine favors reuptake of drug in renal tubules –> increse serum drug levels
amphetamine + ammonium chloride?
acidic urine favors renal elimination –>decrease serum drug levels
amphetamine + chlorpormazine +haloperidol?
dopamine receptor blockers DIMINISH effects of amphetamines
dextromethorphan + amphetamine
increased impaired judgement + erratic euphoria
dixogin + amphetamine
increase pro-arrhythmogenic effect
MAOIs + amphetamine
increase serum drug levels + toxicitiy
CYP2D6 ind/inh + amphetamines
serum drug levels increase or decrease
atomoxetine + albuterol
accentuate CV ADE
epinephrine + atomoxetine
further Increase in BP
MAOIs + atomoxetine + methylphenidate
increase toxicity; allow 2-week interval btw each drug
alcohol + methyphenidate
increase production of toxic metabolite. –>functional inability to concentrate(drive)
what is the MC comorbid condition in ppl w/tic s and tourette syndrome?
ADHD
which drugs are the 1st choice for ADHD+Tourettes?
2nd choice?
3rd choice?
1st choice: alpha-2 agonists significantly improve tics and ADHD
2nd choice: stimulants have rapid activity against ADHD but no activity against tis
3rd choice: methylphenidate + alpha-2 agonist combo
which drugs are the beset for reducing tic?
antipsychotic
what is the problem with using antipsychotics in to tx tics?
antipscychotics agents have a considerabl worse side-effect profile compared to alpha-2 agonist medications and behavioral therapy.
alpha-2 agonists demonstrated similar or slightly larger benefit in reducing tics but only among subjects with comorbid ADHD
note: alpha 2 agonsits do not really reduce tics in subjects w/out ADHD
clonidine guanfacine + cyclosporine
increase serum levels of interact
buproprion + clycosporine/guanfacine
grand mal seizures
do clonidine/guanfacine have CYP mediated interactions?
NOT really
Haloperidol -
how is it metalobized?
what is two ADEs?
- metabolized by CYP2D6 and CYP3A4
ADE: 1. prolong QT interval and hepatically mediated drug interactions
Amphetamine/methylphenidate tox is primarily pormientn neurological and cardiovascular effects, but secondary complications can involve renal, muscle, pulmonary and GI effects
how would you manage this?
management is supportive, with judicious use of BNZs
atomoxetine tox = generally mild
(drowsiness, agitation, hyperactivity, GI upset, tremor, hyperreflexia, tachycardia hypertension, and seizure)
how do you manage?
supportive w/focus on sedation, and control of dyskinesia and seizure
clonidine OD may produce paradoxical short term HTN, but usally hypotension. How do you manage this?
which drug for the HTN? for the support of hypotension?
HTN = atropine
support of hypotension = dopamine
guanfacine produces mixed picture, depending on central and peripheral effects
initaly presentation may be drowsienss, lethargy, dry mouth, diaphoresis.
CV effects may present as hyotension or HTN
-how do you manage?
management of guanfacine OD = largerly supportive with a focus on support of BP
