MCQ Quiz: Pharmacology of Drugs Used in ADHD

Attention-Deficit/Hyperactivity Disorder (ADHD) is a common neurodevelopmental disorder affecting both children and adults. The management of ADHD often involves a combination of behavioral therapy and pharmacotherapy. The pharmacology of drugs used in ADHD is a critical area of study for pharmacy students, as these medications form the cornerstone of treatment for many patients. This quiz will test your knowledge on the key pharmacological principles of both stimulant and non-stimulant medications. Understanding the mechanisms of action, pharmacokinetics, and pharmacodynamics of drugs like methylphenidate, amphetamines, atomoxetine, and alpha-2 adrenergic agonists is essential for ensuring safe and effective patient care, managing side effects, and advising on drug interactions. This quiz, designed for PharmD students, covers topics from the Patient Care VII: Brain and Behavior module to help reinforce your learning.

1. What is the primary mechanism of action of methylphenidate in the treatment of ADHD?

• a) Selective serotonin reuptake inhibition
• b) Inhibition of dopamine and norepinephrine reuptake
• c) Monoamine oxidase inhibition
• d) Alpha-2 adrenergic agonism Answer: b) Inhibition of dopamine and norepinephrine reuptake

2. Amphetamine-based stimulants primarily increase the synaptic levels of dopamine and norepinephrine by which mechanism?

• a) Blocking the reuptake transporters (DAT and NET)
• b) Promoting the release of these neurotransmitters from presynaptic vesicles
• c) Inhibiting the enzymatic breakdown by MAO
• d) Acting as a direct agonist on postsynaptic receptors Answer: b) Promoting the release of these neurotransmitters from presynaptic vesicles

3. Atomoxetine is a non-stimulant medication for ADHD that works by selectively inhibiting the reuptake of which neurotransmitter?

• a) Dopamine
• b) Serotonin
• c) Norepinephrine
• d) GABA Answer: c) Norepinephrine

4. Guanfacine and clonidine exert their therapeutic effects in ADHD by acting as agonists at which receptors?

• a) Dopamine D2 receptors
• b) Serotonin 5-HT2A receptors
• c) Alpha-2 adrenergic receptors
• d) NMDA receptors Answer: c) Alpha-2 adrenergic receptors

5. Which of the following is a key difference in the mechanism of action between methylphenidate and amphetamine?

• a) Methylphenidate primarily blocks reuptake, while amphetamine primarily promotes neurotransmitter release.
• b) Amphetamine has a higher affinity for serotonin transporters than methylphenidate.
• c) Methylphenidate is an MAO inhibitor, while amphetamine is not.
• d) Amphetamine blocks dopamine reuptake, while methylphenidate blocks norepinephrine reuptake. Answer: a) Methylphenidate primarily blocks reuptake, while amphetamine primarily promotes neurotransmitter release.

6. The therapeutic effect of alpha-2 adrenergic agonists like guanfacine in ADHD is thought to be mediated by strengthening regulation in which part of the brain?

• a) Cerebellum
• b) Hippocampus
• c) Prefrontal cortex
• d) Amygdala Answer: c) Prefrontal cortex

7. Why is there a black box warning for atomoxetine?

• a) Risk of severe liver injury
• b) Risk of suicidal ideation in children and adolescents
• c) High potential for abuse and dependence
• d) Risk of cardiovascular events Answer: b) Risk of suicidal ideation in children and adolescents

8. Which enzyme is primarily responsible for the metabolism of amphetamine?

• a) CYP2D6
• b) CYP3A4
• c) UGT1A1
• d) ALDH2 Answer: a) CYP2D6

9. Lisdexamfetamine is a prodrug that is converted to which active metabolite?

• a) Methylphenidate
• b) Dextroamphetamine
• c) Atomoxetine
• d) Guanfacine Answer: b) Dextroamphetamine

10. The conversion of lisdexamfetamine to its active form occurs primarily through the action of:

• a) Cytochrome P450 enzymes in the liver
• b) Hydrolysis by red blood cells
• c) First-pass metabolism in the gut wall
• d) Esterases in the small intestine Answer: b) Hydrolysis by red blood cells

11. Which pharmacological property of long-acting stimulant formulations is designed to provide symptom control throughout the day?

• a) Rapid absorption and elimination
• b) A biphasic release mechanism (immediate and delayed release)
• c) High protein binding
• d) Inhibition of its own metabolism Answer: b) A biphasic release mechanism (immediate and delayed release)

12. A common cardiovascular side effect of stimulant medications, such as increased heart rate and blood pressure, is due to their action on which system?

• a) The cholinergic system
• b) The sympathetic nervous system
• c) The serotonergic system
• d) The histaminergic system Answer: b) The sympathetic nervous system

13. The sedative effect often seen with clonidine and guanfacine is directly related to their:

• a) Dopaminergic blockade
• b) Alpha-2 adrenergic agonism
• c) Anticholinergic properties
• d) Serotonin reuptake inhibition Answer: b) Alpha-2 adrenergic agonism

14. What is a significant pharmacokinetic concern when co-administering methylphenidate with a MAO inhibitor?

• a) Reduced absorption of methylphenidate
• b) Accelerated metabolism of the MAO inhibitor
• c) Risk of hypertensive crisis
• d) Decreased efficacy of methylphenidate Answer: c) Risk of hypertensive crisis

15. Atomoxetine’s metabolism is heavily influenced by the genetic polymorphism of which enzyme, leading to “poor metabolizer” and “extensive metabolizer” phenotypes?

• a) CYP1A2
• b) CYP2C19
• c) CYP2D6
• d) CYP3A4 Answer: c) CYP2D6

16. The anorectic (appetite suppressant) effect of stimulant medications is primarily due to their action on:

• a) The prefrontal cortex
• b) The hippocampus
• c) The hypothalamus
• d) The cerebellum Answer: c) The hypothalamus

17. Why must clonidine and guanfacine be tapered upon discontinuation?

• a) To avoid severe withdrawal psychosis
• b) To prevent the risk of rebound hypertension
• c) To minimize the risk of liver toxicity
• d) To prevent sudden onset of seizures Answer: b) To prevent the risk of rebound hypertension

18. Which of the following drugs for ADHD is NOT classified as a controlled substance in the United States?

• a) Methylphenidate
• b) Dextroamphetamine
• c) Lisdexamfetamine
• d) Atomoxetine Answer: d) Atomoxetine

19. The abuse potential of stimulant medications is related to their ability to rapidly increase levels of which neurotransmitter in the brain’s reward pathway?

• a) Serotonin
• b) Dopamine
• c) Acetylcholine
• d) GABA Answer: b) Dopamine

20. Viloxazine, a newer non-stimulant for ADHD, has what primary mechanism of action?

• a) Dopamine agonist
• b) Selective norepinephrine reuptake inhibitor (SNRI)
• c) Alpha-2 adrenergic agonist
• d) NMDA receptor antagonist Answer: b) Selective norepinephrine reuptake inhibitor (SNRI)

21. The “d” and “l” isomers of amphetamine have different pharmacological activities. D-amphetamine is more potent in its effects on:

• a) The peripheral nervous system
• b) The central nervous system
• c) Serotonin release
• d) Histamine blockade Answer: b) The central nervous system

22. How does the consumption of acidic foods or juices affect the absorption of amphetamines?

• a) It increases absorption
• b) It has no effect on absorption
• c) It decreases absorption
• d) It converts it to an inactive metabolite Answer: c) It decreases absorption

23. The mechanism of action for stimulant-induced growth suppression is thought to be related to:

• a) Decreased appetite and caloric intake
• b) Direct effects on growth hormone secretion
• c) Inhibition of bone marrow development
• d) Both A and B are proposed mechanisms Answer: d) Both A and B are proposed mechanisms

24. Guanfacine is more selective than clonidine for which subtype of alpha-2 adrenergic receptors, potentially leading to less sedation?

• a) Alpha-2A
• b) Alpha-2B
• c) Alpha-2C
• d) Alpha-2D Answer: a) Alpha-2A

25. A patient taking atomoxetine who is a CYP2D6 poor metabolizer would be expected to have:

• a) Lower plasma concentrations and reduced efficacy
• b) Higher plasma concentrations and increased risk of side effects
• c) Faster drug clearance and shorter half-life
• d) No change in pharmacokinetic parameters Answer: b) Higher plasma concentrations and increased risk of side effects

26. The primary site of action for stimulants in improving attention and focus is believed to be the:

• a) Nucleus accumbens
• b) Prefrontal cortex and striatum
• c) Ventral tegmental area
• d) Locus coeruleus Answer: b) Prefrontal cortex and striatum

27. Methylphenidate exists as a racemic mixture. Which isomer is pharmacologically more active?

• a) Levo-methylphenidate
• b) Dex-methylphenidate
• c) Both are equally active
• d) Neither is active until metabolized Answer: b) Dex-methylphenidate

28. What is the primary reason for the development of prodrug stimulants like lisdexamfetamine?

• a) To increase potency
• b) To reduce the potential for abuse via non-oral routes
• c) To eliminate cardiovascular side effects
• d) To improve oral bioavailability Answer: b) To reduce the potential for abuse via non-oral routes

29. Abrupt cessation of a high dose of a stimulant medication can lead to:

• a) A hypertensive crisis
• b) Severe depression and fatigue (a “crash”)
• c) Serotonin syndrome
• d) Neuroleptic malignant syndrome Answer: b) Severe depression and fatigue (a “crash”)

30. Which of these ADHD medications has the longest time to reach maximal therapeutic effect, often taking several weeks?

• a) Immediate-release methylphenidate
• b) Lisdexamfetamine
• c) Atomoxetine
• d) Immediate-release amphetamine salts Answer: c) Atomoxetine

31. The pharmacological effect of stimulants on sleep is typically:

• a) Sedation
• b) Increased sleep latency and reduced total sleep time
• c) No effect on sleep patterns
• d) Increased REM sleep Answer: b) Increased sleep latency and reduced total sleep time

32. Co-administration of stimulants with tricyclic antidepressants can lead to what potential pharmacodynamic interaction?

• a) Decreased efficacy of the stimulant
• b) Increased risk of serotonin syndrome
• c) Potentiation of cardiovascular effects
• d) Antagonism of the antidepressant effect Answer: c) Potentiation of cardiovascular effects

33. The main difference between immediate-release (IR) and extended-release (ER) formulations of methylphenidate lies in their:

• a) Mechanism of action
• b) Peak plasma concentration and duration of action
• c) Chemical structure
• d) Route of elimination Answer: b) Peak plasma concentration and duration of action

34. A patient taking guanfacine ER should be advised to avoid which type of meal with their dose?

• a) A low-fat meal
• b) A high-fat meal
• c) A high-protein meal
• d) A meal rich in fiber Answer: b) A high-fat meal

35. How do alpha-2 adrenergic agonists help with symptoms of hyperactivity and impulsivity?

• a) By increasing the firing rate of neurons in the locus coeruleus
• b) By enhancing the signaling of the prefrontal cortex, which improves executive function
• c) By directly blocking dopamine receptors in the striatum
• d) By increasing levels of serotonin in the synaptic cleft Answer: b) By enhancing the signaling of the prefrontal cortex, which improves executive function

36. The transdermal patch formulation of methylphenidate (Daytrana) is applied to what part of the body?

• a) The upper arm
• b) The chest
• c) The hip
• d) The abdomen Answer: c) The hip

37. What pharmacological characteristic makes atomoxetine a suitable option for patients with a history of substance abuse?

• a) It has a very short half-life
• b) It does not significantly increase dopamine in the nucleus accumbens
• c) It is a potent dopamine agonist
• d) It can be administered intravenously Answer: b) It does not significantly increase dopamine in the nucleus accumbens

38. The main metabolic pathway for methylphenidate is:

• a) Glucuronidation
• b) CYP2D6 oxidation
• c) Hydrolysis by carboxylesterases to ritalinic acid
• d) N-demethylation Answer: c) Hydrolysis by carboxylesterases to ritalinic acid

39. A key counseling point for a patient starting an extended-release alpha-2 agonist like guanfacine ER or clonidine ER is the potential for:

• a) Immediate improvement in attention
• b) Increased appetite and weight gain
• c) Somnolence and dizziness
• d) Hypertensive crisis Answer: c) Somnolence and dizziness

40. The primary neurotransmitters implicated in the pathophysiology of ADHD are:

• a) Acetylcholine and GABA
• b) Dopamine and norepinephrine
• c) Serotonin and histamine
• d) Glutamate and glycine Answer: b) Dopamine and norepinephrine

41. Which non-stimulant medication for ADHD requires monitoring of liver function tests due to rare cases of hepatotoxicity?

• a) Guanfacine
• b) Clonidine
• c) Viloxazine
• d) Atomoxetine Answer: d) Atomoxetine

42. The “rebound effect” sometimes seen with short-acting stimulants refers to:

• a) The development of drug tolerance
• b) The worsening of ADHD symptoms as the medication wears off
• c) The onset of a new, unrelated side effect
• d) A paradoxical increase in hyperactivity while on the medication Answer: b) The worsening of ADHD symptoms as the medication wears off

43. Which of the following is an example of a methylphenidate-based product?

• a) Adderall
• b) Vyvanse
• c) Concerta
• d) Strattera Answer: c) Concerta

44. The pharmacological basis for using stimulants to treat ADHD involves improving which cognitive function?

• a) Long-term memory consolidation
• b) Emotional regulation
• c) Executive functions like sustained attention and inhibitory control
• d) Auditory processing Answer: c) Executive functions like sustained attention and inhibitory control

45. Why is a baseline EKG sometimes recommended before starting stimulant therapy in certain patients?

• a) To check for pre-existing seizure disorders
• b) To screen for underlying cardiac abnormalities that could be exacerbated
• c) To assess liver function
• d) To measure baseline cognitive function Answer: b) To screen for underlying cardiac abnormalities that could be exacerbated

46. The OROS (Osmotic Controlled-Release Oral Delivery System) technology is used in which ADHD medication to provide a controlled, ascending release profile?

• a) Adderall XR
• b) Vyvanse
• c) Concerta
• d) Focalin XR Answer: c) Concerta

47. A common side effect of atomoxetine that differs from stimulants is:

• a) Insomnia
• b) Decreased appetite
• c) Nausea and somnolence
• d) Increased heart rate Answer: c) Nausea and somnolence

48. What is the primary route of elimination for atomoxetine and its metabolites?

• a) Biliary excretion
• b) Renal excretion
• c) Pulmonary exhalation
• d) Excretion in sweat Answer: b) Renal excretion

49. The use of stimulants in patients with a history of psychosis is cautioned because they can:

• a) Induce sedation and worsen negative symptoms
• b) Exacerbate or precipitate psychotic symptoms
• c) Cause severe metabolic side effects
• d) Lead to rapid drug tolerance Answer: b) Exacerbate or precipitate psychotic symptoms

50. What is a key pharmacodynamic property of bupropion that allows for its off-label use in ADHD?

• a) It is a potent serotonin reuptake inhibitor
• b) It inhibits the reuptake of norepinephrine and dopamine
• c) It is a direct agonist at alpha-2 receptors
• d) It blocks muscarinic receptors Answer: b) It inhibits the reuptake of norepinephrine and dopamine