Pharmacology of ADHD medications
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24 Terms
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What is ADHD?
\-a neurodevelopment disorder
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What can be some symptoms of ADHD?
\-hyperactive/impulsive: excessive motor activity, fidgety, leaving seat, on the go, excessive talking, blurting out answers, interrupting or intruding on others
\-inattentive: difficulty concentrating, difficulty organizing tasks/activities, easily distracted
\-inattentive: difficulty concentrating, difficulty organizing tasks/activities, easily distracted
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What area of the brain is seen to be reduced in individuals with ADHD?
\-prefrontal cortex (PFC)
\-basal ganglia ( caudate, putamen, globus pallidus)
\-basal ganglia ( caudate, putamen, globus pallidus)
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What catecholamines are seen to be attributed to ADHD?
\-norepinephrine and dopamine
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How does norepinephrine and dopamine contribute to ADHD?
\-too little norepinephrine and dopamine can lead to symptoms
\-too much norepinephrine and dopamine which is caused by stressful conditions may impair cortical function.
\-too much norepinephrine and dopamine which is caused by stressful conditions may impair cortical function.
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Amphetamines
•Amphetamine (Adzenys XR-ODT, Dyanavel-XR)
•Mixed amphetamine salts (Adderall XR, others)
•Dextroamphetamine (Dexedrine)
•Lisdexamfetamine (Vyvanse)– is a prodrug
•Methamphetamine (Desoxyn)– half-life is longer than amphetamine
\-amphetamine is a racemic mixture
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What is the most potent isomer of amphetamine?
\-D-isomer
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What CYP enzymes can metabolize amphetamines?
\-CYPA3,2C9,2D6,3A4 which can lead to potential drug to drug interactions
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What is the duration of action for immediate release amphetamine formulations?
\-4-5 hrs.
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Methylphenidate
\-ritlan, methylin, metadate, concerta, daytrana, Quillivant XR
\-it is a racemic mixture
\-it is a racemic mixture
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What isomer of methylphenidate is the active isomer?
\-D isomer
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What is methylphenidate metabolized by?
\-esterases
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What is the duration of action for immediate release metylphenidate?
\-3-4 hrs.
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Dextromethylphenidate
\-Focalin
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What is the mechanism of action of amphetamine?
\-competes with norepinephrine for NET or with dopamine for DAT
\-reverse transporter direction for NET or DAT
\-this increases synaptic concentrations of norepinephrine or dopamine
\-reverses direction of vesicular transporter (VMAT), pushing norepinephrine or dopamine into the cytoplasm
\-inhibits MAO ( so catecholamines can not be degraded)
\-reverse transporter direction for NET or DAT
\-this increases synaptic concentrations of norepinephrine or dopamine
\-reverses direction of vesicular transporter (VMAT), pushing norepinephrine or dopamine into the cytoplasm
\-inhibits MAO ( so catecholamines can not be degraded)
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Which psychostimulant ADHD medication has a patch?
\-methylphenidate
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What is the mechanism of action of methyphenidate?
\-it blocks NET and DAT
\-this leads to an increase in synaptic concentration of norepinephrine or dopamine
\-this leads to an increase in synaptic concentration of norepinephrine or dopamine
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What happens postynaptically due to elevated NE from the action of amphetamine and methylphenidate in the prefrontal cortex?
\-norepinephrine actives alpha2a receptors postsynaptically in the prefrontal cortex which causes:
* decrease in cAMP :
* closure of ion channels (HCN channels) on dendritic spines of prefrontal cortex neurons
* this stops the efflux of positive ions in this dendritic area and facilitates inputs from dendrites to soma
* this results in strengthening of neuronal networks to improve ADHD symptoms
* decrease in cAMP :
* closure of ion channels (HCN channels) on dendritic spines of prefrontal cortex neurons
* this stops the efflux of positive ions in this dendritic area and facilitates inputs from dendrites to soma
* this results in strengthening of neuronal networks to improve ADHD symptoms
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What happens postynaptically due to elevated DA from the action of amphetamine and methylphenidate in the prefrontal cortex?
\-activation of D1 receptors postynaptically in the prefrontal cortex causes:
* increased cAMP which causes:
* activation and opening of ion channels ( HCN channels) that cause efflux of positive ions from dendritic spines of the prefrontal cortex neurons.
* this decreases inputs from dendrites to soma and weakens a specific type of neuronal firing for nonpreferred networks.
* this causes a reduced noise and weakening of neuronal firing for nonpreferred networks
* increased cAMP which causes:
* activation and opening of ion channels ( HCN channels) that cause efflux of positive ions from dendritic spines of the prefrontal cortex neurons.
* this decreases inputs from dendrites to soma and weakens a specific type of neuronal firing for nonpreferred networks.
* this causes a reduced noise and weakening of neuronal firing for nonpreferred networks
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What are some side effects of methylphenidate and amephetamine?
\-appetite suppression
\-insomnia
\-insomnia
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What are the non stimulants used to treat ADHD?
\-atomoxetine
\-guanfacine
\-clonidine
\-guanfacine
\-clonidine
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What is the mechanism of action for atomoxetine?
\-blocks NET and this causes an increase synaptic concentrations of norepinephrine
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What is the mechanism of action of guanfacine and clonidine?
\-agonists at alpha2A receptors located postsynaptically on prefrontal cortex neurons
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What happens as a result of therapy with atomoxetine, guanfacine and clonidine?
\-there is a decrease in cAMP:
* closure of HCN ion channels in dendritic spines of prefrontal cortex neurons
* increase of inputs from dendrites to soma
\-This results in improved attention, arousal, and working memory
* closure of HCN ion channels in dendritic spines of prefrontal cortex neurons
* increase of inputs from dendrites to soma
\-This results in improved attention, arousal, and working memory
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