ADHD, Dementia,
Impulsivity/Compulsivity, and Addiction
Questions with Answers & Rationales
Section 1: ADHD (Questions 1-30)
Question 1
The cortico-striatal-thalamic (CSTC) loop modulates motor activity through
connections from the prefrontal motor cortex to which structure?
• A. Caudate nucleus
• B. Putamen (lateral striatum)
• C. Globus pallidus interna
• D. Subthalamic nucleus
Rationale: The CSTC loop involved in motor activity (hyperactivity)
connects the prefrontal motor cortex to the putamen, then to the thalamus,
and back to the cortex.
Question 2
A 9-year-old boy is constantly fidgeting, leaves his seat in class, runs excessively,
and has trouble playing quietly. These symptoms are primarily mediated by
dysfunction in which brain pathway?
• A. Cortico-striatal-thalamic loop
• B. Mesolimbic dopamine pathway
• C. Mesocortical pathway
• D. Nigrostriatal pathway
Rationale: Hyperactivity symptoms in ADHD are modulated by the CSTC
loop from the prefrontal motor cortex to the putamen.
,Question 3
A child with ADHD has significant issues with distractibility, forgetfulness, and
fatigue. This presentation is most associated with deficiency of which
neurotransmitters?
• A. Serotonin and GABA
• B. Norepinephrine and dopamine
• C. Acetylcholine and histamine
• D. Glutamate and glycine
Rationale: ADHD involves dysregulation of dopamine and norepinephrine.
Low levels contribute to inattention and fatigue.
Question 4
The pathophysiology of ADHD is best described as:
• A. Excessive dopamine in the nucleus accumbens
• B. Overactivity of the default mode network
• C. Inefficient tuning of the prefrontal cortex by dysregulation of
dopamine and norepinephrine
• D. Decreased serotonin transmission in the raphe nuclei
Rationale: ADHD results from inefficient prefrontal cortex modulation due
to dysregulation of dopamine and norepinephrine, leading to inattention,
hyperactivity, and impulsivity.
Question 5
Which medication for ADHD is a non-stimulant that inhibits the norepinephrine
transporter (NET) in the prefrontal cortex?
• A. Methylphenidate
• B. Dextroamphetamine
• C. Atomoxetine
, • D. Guanfacine
Rationale: Atomoxetine (Strattera) selectively inhibits NET, increasing both
norepinephrine and dopamine in the PFC but not in the nucleus accumbens,
thus no abuse potential.
Question 6
A 15-year-old with ADHD has a history of substance misuse. Which medication is
preferred due to its lack of abuse potential?
• A. Mixed amphetamine salts
• B. Methylphenidate
• C. Atomoxetine
• D. Lisdexamfetamine
Rationale: Atomoxetine does not increase dopamine in the nucleus
accumbens (reward center), therefore it has no abuse potential, making it
ideal for patients with substance use history.
Question 7
A patient starting atomoxetine should be counseled about which potential adverse
effects?
• A. Priapism and liver injury
• B. Weight gain and diabetes
• C. QT prolongation and syncope
• D. Hypertensive crisis and stroke
Rationale: Atomoxetine carries black box warnings for priapism and severe
liver injury. Patients should report prolonged erections or jaundice.
Question 8
Atomoxetine requires a gradual buildup over time. Which statement about its onset
is correct?
• A. Immediate symptom relief within hours
, • B. Therapeutic effects take several weeks to develop
• C. Maximal effect after 24 hours
• D. It is a short-acting PRN medication
Rationale: Atomoxetine is not short-acting; it requires weeks of daily
dosing to achieve full therapeutic effect, unlike stimulants.
Question 9
Which medication combination is contraindicated with atomoxetine due to drug
interactions?
• A. Lisdexamfetamine and guanfacine
• B. Clonidine and methylphenidate
• C. Fluoxetine and risperidone
• D. Paroxetine and bupropion
Rationale: Atomoxetine should not be taken with strong CYP2D6 inhibitors
like paroxetine (Paxil) or bupropion (Wellbutrin) due to increased
atomoxetine levels and toxicity.
Question 10
Methylphenidate (Ritalin) exerts its therapeutic effect in ADHD by:
• A. Inhibiting monoamine oxidase
• B. Blocking dopamine and norepinephrine transporters (allosteric
modulation)
• C. Releasing stored catecholamines from vesicles
• D. Antagonizing serotonin receptors
Rationale: Methylphenidate binds to dopamine transporter (DAT) and
norepinephrine transporter (NET) as an allosteric modulator, preventing
reuptake and increasing synaptic dopamine/norepinephrine.