1|Page
NR546 week 7 test your knowledge ||Verified Exam!!||
Most Recent Exam 2026 Actual Complete Real Exam
Questions And Correct Answers (Verified Answers)
Already Graded A+ || Newest Exam !!!
The PMHNP is considering treatment options for an 18-
year-old man with ADHD who has a history of alcohol and
marijuana abuse. Which of the following accurately
explains the effects of different stimulant formulations on
neuronal firing?
a. Tonic firing is the result of rapid receptor occupancy and
fast onset of action, as seen with extended-release
formulations
b. Immediate-release stimulants lead to tonic firing, which
can lead to euphoria and abuse.
c. Pulsatile stimulation amplifies undesirable phasic DA
and NE firing, which can lead to euphoria and abuse.
d. Extended-release stimulants result in phasic stimulation
of NE and DA signals, but this does not lead to euphoria
and abuse. - Answers-c. Pulsatile stimulation amplifies
undesirable phasic DA and NE firing, which can lead to
euphoria and abuse.
,2|Page
Rationale: Phasic firing is hypothetically associated with
reward, feelings of euphoria, and abuse potential.
Immediate-release stimulants rapidly increase DA and NE,
especially increasing phasic firing, not tonic firing.
Therefore, immediate-release stimulants have a higher
risk of abuse. Extended-release formulations of stimulants
lead to a gradual and sustained increase in NE and DA,
enhancing tonic firing, which is hypothetically linked to the
therapeutic effects of stimulants. They are amplifying tonic
NE and DA signals, which are thought to be low in ADHD.
The extended-release formulations occupy the NE
transporter in the prefrontal cortex with slow enough onset
and for long enough to enhance tonic NE and DA
signaling; however, they do not block DA transporters fast
or long enough in the nucleus accumbens to increase
phasic signaling, thus reducing abuse potential.
A 27-year-old bartender was diagnosed with ADHD at age
10. She has been on and off medication since then, first
on immediate-release methylphenidate, then on the
methylphenidate patch. She experimented with illicit drugs
during her late adolescence and is still a heavy drinker.
After a few years of self-medication with alcohol and
cigarettes, she is seeking medical attention again. You
decide to put her on 80 mg/day of atomoxetine, one of the
non-stimulant medications effective in ADHD.
,3|Page
Why does atomoxetine lack abuse potential?
a. Atomoxetine decreases norepinephrine levels in the
nucleus accumbens but not in the prefrontal cortex.
b. It increases dopamine levels in the prefrontal cortex but
not in the nucleus accumbens.
c. Atomoxetine modulates serotonin levels in the raphe
nucleus.
d. Atomoxetine increases dopamine in the striatum and
anterior cingulate cortex. - Answers-b. It increases
dopamine levels in the prefrontal cortex but not in the
nucleus accumbens.
Rationale: The prefrontal cortex lacks high concentrations
of dopamine transporters (DAT), so in this brain region, DA
gets inactivated by norepinephrine transporters (NET).
Therefore, inhibiting NET in the prefrontal cortex increases
both DA and NE. As only a few NET exist in the nucleus
accumbens, atomoxetine does not induce an increase in
DA and NE in the nucleus accumbens, the reward center
of the brain, thus atomoxetine does not have abuse
potential.
In the nucleus accumbens, there are only a few NE
neurons and NE transporters. Inhibiting NET in the
, 4|Page
nucleus accumbens will not lead to an increase in NE or
DA. Atomoxetine does not modulate serotonin levels. The
striatum and the anterior cingulate cortex are not brain
areas involved in reward.
Which neurotransmitters play a role in Attention-
deficit/hyperactivity disorder (ADHD)? - Answers-
Norepinephrine (NE) and dopamine (DA) play a role in the
symptoms and treatment of ADHD.
When is ADHD typically diagnosed? - Answers-ADHD is
typically diagnosed in childhood, many individuals
experience symptoms into adolescence and adulthood.
Prevalence of ADHD - Answers-
Symptoms of ADHD - Answers-- ADHD symptoms typically
start before the age of 12, though symptoms may begin to
appear as early as 3 years of age.
- ADHD presents as a constellation of symptoms related to
attention, hyperactivity, and impulsivity.
- Symptoms related to attention usually develop 2-4 years
after the emergence of hyperactive symptoms in
childhood.
NR546 week 7 test your knowledge ||Verified Exam!!||
Most Recent Exam 2026 Actual Complete Real Exam
Questions And Correct Answers (Verified Answers)
Already Graded A+ || Newest Exam !!!
The PMHNP is considering treatment options for an 18-
year-old man with ADHD who has a history of alcohol and
marijuana abuse. Which of the following accurately
explains the effects of different stimulant formulations on
neuronal firing?
a. Tonic firing is the result of rapid receptor occupancy and
fast onset of action, as seen with extended-release
formulations
b. Immediate-release stimulants lead to tonic firing, which
can lead to euphoria and abuse.
c. Pulsatile stimulation amplifies undesirable phasic DA
and NE firing, which can lead to euphoria and abuse.
d. Extended-release stimulants result in phasic stimulation
of NE and DA signals, but this does not lead to euphoria
and abuse. - Answers-c. Pulsatile stimulation amplifies
undesirable phasic DA and NE firing, which can lead to
euphoria and abuse.
,2|Page
Rationale: Phasic firing is hypothetically associated with
reward, feelings of euphoria, and abuse potential.
Immediate-release stimulants rapidly increase DA and NE,
especially increasing phasic firing, not tonic firing.
Therefore, immediate-release stimulants have a higher
risk of abuse. Extended-release formulations of stimulants
lead to a gradual and sustained increase in NE and DA,
enhancing tonic firing, which is hypothetically linked to the
therapeutic effects of stimulants. They are amplifying tonic
NE and DA signals, which are thought to be low in ADHD.
The extended-release formulations occupy the NE
transporter in the prefrontal cortex with slow enough onset
and for long enough to enhance tonic NE and DA
signaling; however, they do not block DA transporters fast
or long enough in the nucleus accumbens to increase
phasic signaling, thus reducing abuse potential.
A 27-year-old bartender was diagnosed with ADHD at age
10. She has been on and off medication since then, first
on immediate-release methylphenidate, then on the
methylphenidate patch. She experimented with illicit drugs
during her late adolescence and is still a heavy drinker.
After a few years of self-medication with alcohol and
cigarettes, she is seeking medical attention again. You
decide to put her on 80 mg/day of atomoxetine, one of the
non-stimulant medications effective in ADHD.
,3|Page
Why does atomoxetine lack abuse potential?
a. Atomoxetine decreases norepinephrine levels in the
nucleus accumbens but not in the prefrontal cortex.
b. It increases dopamine levels in the prefrontal cortex but
not in the nucleus accumbens.
c. Atomoxetine modulates serotonin levels in the raphe
nucleus.
d. Atomoxetine increases dopamine in the striatum and
anterior cingulate cortex. - Answers-b. It increases
dopamine levels in the prefrontal cortex but not in the
nucleus accumbens.
Rationale: The prefrontal cortex lacks high concentrations
of dopamine transporters (DAT), so in this brain region, DA
gets inactivated by norepinephrine transporters (NET).
Therefore, inhibiting NET in the prefrontal cortex increases
both DA and NE. As only a few NET exist in the nucleus
accumbens, atomoxetine does not induce an increase in
DA and NE in the nucleus accumbens, the reward center
of the brain, thus atomoxetine does not have abuse
potential.
In the nucleus accumbens, there are only a few NE
neurons and NE transporters. Inhibiting NET in the
, 4|Page
nucleus accumbens will not lead to an increase in NE or
DA. Atomoxetine does not modulate serotonin levels. The
striatum and the anterior cingulate cortex are not brain
areas involved in reward.
Which neurotransmitters play a role in Attention-
deficit/hyperactivity disorder (ADHD)? - Answers-
Norepinephrine (NE) and dopamine (DA) play a role in the
symptoms and treatment of ADHD.
When is ADHD typically diagnosed? - Answers-ADHD is
typically diagnosed in childhood, many individuals
experience symptoms into adolescence and adulthood.
Prevalence of ADHD - Answers-
Symptoms of ADHD - Answers-- ADHD symptoms typically
start before the age of 12, though symptoms may begin to
appear as early as 3 years of age.
- ADHD presents as a constellation of symptoms related to
attention, hyperactivity, and impulsivity.
- Symptoms related to attention usually develop 2-4 years
after the emergence of hyperactive symptoms in
childhood.
