A thorough understanding of the etiology and pathophysiology of Attention-Deficit/Hyperactivity Disorder (ADHD) is crucial for pharmacists to effectively manage patients and provide evidence-based counseling. As a core topic in the Patient Care VII: Brain and Behavior course, the neurobiological underpinnings of ADHD provide the rationale for its pharmacotherapy. This quiz will test your knowledge on the key neurotransmitter systems, brain regions, and etiological factors implicated in ADHD, reflecting the foundational science taught in your PharmD curriculum.
1. The pathophysiology of ADHD is primarily associated with the dysregulation of which two neurotransmitters?
- A. Serotonin and Acetylcholine
- B. GABA and Glutamate
- C. Dopamine and Norepinephrine
- D. Histamine and Orexin
Answer: C. Dopamine and Norepinephrine
2. Which region of the brain, responsible for executive functions like attention, planning, and impulse control, is most implicated in the pathophysiology of ADHD?
- A. The cerebellum
- B. The brainstem
- C. The prefrontal cortex (PFC)
- D. The occipital lobe
Answer: C. The prefrontal cortex (PFC)
3. The “Etiology and Pathophysiology of ADHD” is a core lecture in which Patient Care course module?
- A. Module 5: Anxiety and Sleep-Wake Disorders
- B. Module 6: Epilepsy
- C. Module 7: Other Neuropsychiatric Disorders
- D. Module 2: Neurodegenerative Disorders
Answer: C. Module 7: Other Neuropsychiatric Disorders
4. What is the leading etiological factor for ADHD?
- A. High sugar intake
- B. Poor parenting
- C. A strong genetic component
- D. Excessive screen time
Answer: C. A strong genetic component
5. The therapeutic effect of stimulant medications like methylphenidate provides evidence for the ADHD pathophysiology by:
- A. Increasing serotonin levels.
- B. Blocking the reuptake of dopamine and norepinephrine, thereby increasing their availability in the synapse.
- C. Decreasing the levels of GABA.
- D. Acting as antagonists at dopamine receptors.
Answer: B. Blocking the reuptake of dopamine and norepinephrine, thereby increasing their availability in the synapse
6. Symptoms of inattention in ADHD are thought to be primarily linked to dysregulation of which neurotransmitter in the prefrontal cortex?
- A. Acetylcholine
- B. Norepinephrine
- C. Serotonin
- D. GABA
Answer: B. Norepinephrine
7. Symptoms of hyperactivity and impulsivity are thought to be primarily linked to dysregulation of which neurotransmitter pathway?
- A. The mesolimbic dopamine pathway
- B. The nigrostriatal pathway
- C. The cholinergic pathway
- D. The histaminergic pathway
Answer: A. The mesolimbic dopamine pathway
8. Which of the following is considered an environmental risk factor for the etiology of ADHD?
- A. Regular exercise
- B. A balanced diet
- C. Prenatal exposure to tobacco smoke or alcohol
- D. Reading books
Answer: C. Prenatal exposure to tobacco smoke or alcohol
9. The dopamine transporter (DAT) is a key protein in ADHD pathophysiology because it:
- A. Is the primary site of action for non-stimulant medications.
- B. Is responsible for clearing dopamine from the synapse and is a primary target of stimulant medications.
- C. Synthesizes dopamine in the presynaptic neuron.
- D. Is a type of dopamine receptor.
Answer: B. Is responsible for clearing dopamine from the synapse and is a primary target of stimulant medications
10. The mechanism of action of atomoxetine, a non-stimulant, supports the pathophysiology of ADHD by selectively targeting the:
- A. Serotonin transporter (SERT).
- B. Norepinephrine transporter (NET).
- C. Dopamine D2 receptor.
- D. GABA-A receptor.
Answer: B. Norepinephrine transporter (NET)
11. The concept that ADHD involves “sub-optimal” signaling in the prefrontal cortex means that:
- A. There is too much dopamine and norepinephrine activity.
- B. There is an inefficient or “low-level” signal of dopamine and norepinephrine, which stimulants help to optimize.
- C. Neurotransmitter levels are completely normal.
- D. The prefrontal cortex is larger than average.
Answer: B. There is an inefficient or “low-level” signal of dopamine and norepinephrine, which stimulants help to optimize
12. ADHD is officially classified as what type of disorder?
- A. A mood disorder
- B. A neurodevelopmental disorder
- C. A personality disorder
- D. An anxiety disorder
Answer: B. A neurodevelopmental disorder
13. The high heritability of ADHD suggests that genes involved in what processes are likely candidates in its etiology?
- A. Glucose metabolism
- B. Dopamine transport and receptor function
- C. Muscle contraction
- D. Bone development
Answer: B. Dopamine transport and receptor function
14. The pathophysiology of ADHD helps explain why patients often have difficulty with:
- A. Hearing and vision.
- B. Motor coordination only.
- C. Executive functions.
- D. Long-term memory storage.
Answer: C. Executive functions
15. How do alpha-2 adrenergic agonists like guanfacine and clonidine work to treat ADHD?
- A. They increase the release of dopamine.
- B. They are thought to strengthen prefrontal cortex regulation by modulating norepinephrine signaling at postsynaptic receptors.
- C. They block the dopamine transporter.
- D. They are potent serotonin reuptake inhibitors.
Answer: B. They are thought to strengthen prefrontal cortex regulation by modulating norepinephrine signaling at postsynaptic receptors
16. The “default mode network” (DMN) is a brain network that is active during rest. In ADHD pathophysiology, it is thought that:
- A. The DMN is underactive at all times.
- B. There is difficulty suppressing the DMN during tasks that require focus.
- C. The DMN is not involved in ADHD.
- D. The DMN is responsible for hyperactivity.
Answer: B. There is difficulty suppressing the DMN during tasks that require focus.
17. Which of the following is a common misconception about the etiology of ADHD?
- A. It has a strong genetic basis.
- B. It is caused by poor parenting or a chaotic home environment.
- C. It involves dysfunction in brain chemistry.
- D. It is a real medical condition.
Answer: B. It is caused by poor parenting or a chaotic home environment
18. The pharmacology of amphetamine differs slightly from methylphenidate in that amphetamine not only blocks dopamine/norepinephrine reuptake but also:
- A. Blocks serotonin reuptake.
- B. Promotes the release of dopamine and norepinephrine from presynaptic vesicles.
- C. Antagonizes dopamine receptors.
- D. Inhibits the MAO enzyme.
Answer: B. Promotes the release of dopamine and norepinephrine from presynaptic vesicles
19. An understanding of the pathophysiology of ADHD helps the pharmacist counsel patients that the goal of treatment is to:
- A. Cure the disorder.
- B. Manage symptoms to improve functioning.
- C. Eliminate the need for behavioral therapy.
- D. Only improve academic performance.
Answer: B. Manage symptoms to improve functioning
20. The “Assess” step of the PPCP for an ADHD patient would involve evaluating the effectiveness of their medication on:
- A. Their height and weight only.
- B. Their core symptoms of inattention, hyperactivity, and impulsivity.
- C. Their blood pressure only.
- D. Their mood only.
Answer: B. Their core symptoms of inattention, hyperactivity, and impulsivity
21. Brain imaging studies in individuals with ADHD have often shown:
- A. A larger-than-average prefrontal cortex.
- B. Differences in brain structure and function, including slightly smaller volume in certain areas like the prefrontal cortex.
- C. No differences compared to individuals without ADHD.
- D. Increased activity in all brain regions.
Answer: B. Differences in brain structure and function, including slightly smaller volume in certain areas like the prefrontal cortex
22. Which of the following is NOT considered a primary etiological factor for ADHD?
- A. Genetics
- B. Food additives and sugar
- C. Prenatal exposure to toxins
- D. Brain injury
Answer: B. Food additives and sugar
23. The “catecholamine hypothesis” of ADHD is another name for the theory involving which two neurotransmitters?
- A. Serotonin and GABA
- B. Dopamine and Norepinephrine
- C. Acetylcholine and Glutamate
- D. Histamine and Serotonin
Answer: B. Dopamine and Norepinephrine
24. The foundational knowledge on the normal function of dopamine and norepinephrine pathways is covered in which course?
- A. PHA5560 Pathophysiology and Patient Assessment I
- B. PHA5239 Applications of Pharmacy Law & Ethics
- C. PHA5176 Drug Delivery Systems
- D. PHA5222 Pharmacy Practice Management
Answer: A. PHA5560 Pathophysiology and Patient Assessment I
25. An understanding of ADHD’s pathophysiology explains why a common comorbidity is:
- A. Hypertension
- B. Diabetes
- C. Oppositional defiant disorder and conduct disorder.
- D. Asthma
Answer: C. Oppositional defiant disorder and conduct disorder.
26. The fact that symptoms of ADHD must be present before the age of 12 for diagnosis supports its classification as a(n):
- A. Adult-onset disorder
- B. Neurodevelopmental disorder
- C. Age-related cognitive decline
- D. Infectious disease
Answer: B. Neurodevelopmental disorder
27. The role of the norepinephrine transporter (NET) in the prefrontal cortex is unique because it is also responsible for clearing:
- A. Serotonin
- B. GABA
- C. Dopamine
- D. Acetylcholine
Answer: C. Dopamine
28. This anatomical and physiological fact explains why a selective norepinephrine reuptake inhibitor like atomoxetine can also increase ________ levels in the prefrontal cortex.
- A. Serotonin
- B. Dopamine
- C. GABA
- D. Acetylcholine
Answer: B. Dopamine
29. The symptoms of ADHD must be present in how many settings for a diagnosis to be made (e.g., home and school)?
- A. One setting
- B. Two or more settings
- C. Three or more settings
- D. The number of settings is not important.
Answer: B. Two or more settings
30. The “Plan” step of the PPCP for an ADHD patient involves selecting a therapy. The choice between a stimulant and non-stimulant is based on:
- A. Only the cost.
- B. Patient-specific factors like comorbidities (e.g., substance use history, cardiovascular risk) and side effect concerns.
- C. The pharmacist’s preference.
- D. A coin toss.
Answer: B. Patient-specific factors like comorbidities (e.g., substance use history, cardiovascular risk) and side effect concerns
31. The “Etiology” of a disorder refers to its:
- A. Signs and symptoms
- B. Treatment
- C. Causes and risk factors
- D. Prognosis
Answer: C. Causes and risk factors
32. The “Pathophysiology” of a disorder refers to the:
- A. Functional changes in the body that result from the disease process.
- B. The cost of treating the disease.
- C. The laws regulating treatment.
- D. The patient’s feelings about the disease.
Answer: A. The functional changes in the body that result from the disease process
33. The rewarding effects of stimulant misuse are related to their potent action on which neurotransmitter system?
- A. The norepinephrine system
- B. The mesolimbic dopamine system
- C. The serotonin system
- D. The cholinergic system
Answer: B. The mesolimbic dopamine system
34. Some theories suggest that the hyperactivity in ADHD may be a compensatory mechanism for:
- A. An overactive prefrontal cortex.
- B. An under-aroused or sub-optimally stimulated prefrontal cortex.
- C. Poor vision.
- D. Low blood sugar.
Answer: B. An under-aroused or sub-optimally stimulated prefrontal cortex.
35. The genetic basis for ADHD is best described as:
- A. A single gene mutation.
- B. An extra chromosome.
- C. Complex, involving multiple genes of small effect.
- D. Purely environmental with no genetic link.
Answer: C. Complex, involving multiple genes of small effect
36. A key part of the “Implement” step of the PPCP for ADHD management is counseling the patient or parent on:
- A. The neurobiology of the prefrontal cortex.
- B. The expected therapeutic effects and common side effects of the chosen medication.
- C. The history of ADHD diagnosis.
- D. The cost of all available medications.
Answer: B. The expected therapeutic effects and common side effects of the chosen medication
37. The pathophysiology of ADHD helps explain why __________ is a common comorbidity.
- A. Asthma
- B. A learning disability
- C. Hypertension
- D. Diabetes
Answer: B. A learning disability
38. The fact that ADHD symptoms persist into adulthood for many individuals demonstrates that it is not just a:
- A. Real disorder.
- B. Treatable disorder.
- C. Childhood disorder that is always outgrown.
- D. Genetic disorder.
Answer: C. Childhood disorder that is always outgrown
39. The “Follow-up: Monitor and Evaluate” step for ADHD management is crucial for:
- A. Titrating the medication to the optimal dose that maximizes benefits and minimizes side effects.
- B. Ensuring the patient never returns.
- C. Only checking the patient’s weight.
- D. Only asking if the patient likes the medication’s color.
Answer: A. Titrating the medication to the optimal dose that maximizes benefits and minimizes side effects
40. Understanding the pathophysiology of ADHD allows the pharmacist to:
- A. Diagnose ADHD.
- B. Provide a rationale to patients for why stimulant medications are not “uppers” but work to normalize brain function.
- C. Prescribe stimulant medications.
- D. Perform brain imaging scans.
Answer: B. Provide a rationale to patients for why stimulant medications are not “uppers” but work to normalize brain function
41. The prefrontal cortex dysfunction in ADHD leads to deficits in “working memory,” which is the ability to:
- A. Recall distant childhood memories.
- B. Hold and manipulate information for short periods to complete a task.
- C. Remember to take medication.
- D. Never forget a name.
Answer: B. Hold and manipulate information for short periods to complete a task
42. Which of the following is NOT a core symptom of ADHD?
- A. Inattention
- B. Hyperactivity
- C. Impulsivity
- D. Mania
Answer: D. Mania
43. A key etiological principle is that ADHD is a brain-based disorder, not a character flaw.
- A. True
- B. False
Answer: A. True
44. The pharmacology of stimulants, which target DA and NE transporters, directly supports the theory that ADHD pathophysiology involves:
- A. A surplus of serotonin.
- B. A dysfunction in monoamine signaling.
- C. A deficit in GABA.
- D. Overactive acetylcholine receptors.
Answer: B. A dysfunction in monoamine signaling
45. Which of the following best describes the etiology of ADHD?
- A. It is caused solely by genetics.
- B. It is caused solely by environmental factors.
- C. It is a complex interplay of genetic predisposition and environmental risk factors.
- D. The cause is completely unknown.
Answer: C. It is a complex interplay of genetic predisposition and environmental risk factors
46. The symptoms of ADHD can lead to significant impairment in which life domain?
- A. Academic or occupational functioning
- B. Social relationships
- C. Daily adaptive functioning
- D. All of the above
Answer: D. All of the above
47. Understanding that ADHD involves inefficient signaling helps explain why a patient might:
- A. Be able to focus perfectly on all tasks.
- B. Have difficulty sustaining attention on non-stimulating tasks but can “hyperfocus” on highly engaging activities.
- C. Never experience hyperactivity.
- D. Not respond to any medication.
Answer: B. Have difficulty sustaining attention on non-stimulating tasks but can “hyperfocus” on highly engaging activities.
48. The “Etiology and Pathophysiology of Migraine” is covered in the same module as the etiology and pathophysiology of ADHD, suggesting a focus on common __________ disorders.
- A. psychiatric
- B. cardiovascular
- C. neuropsychiatric
- D. gastrointestinal
Answer: C. neuropsychiatric
49. The therapeutic goal of ADHD pharmacotherapy, based on its pathophysiology, is to:
- A. Decrease DA and NE signaling.
- B. Increase DA and NE signaling to an optimal level.
- C. Block DA and NE receptors.
- D. Increase serotonin signaling.
Answer: B. Increase DA and NE signaling to an optimal level
50. An understanding of the pathophysiology of ADHD is essential for the pharmacist to combat stigma by explaining that ADHD is a:
- A. Real, brain-based medical condition.
- B. A sign of low intelligence.
- C. A result of laziness.
- D. A simple behavioral problem.
Answer: A. Real, brain-based medical condition
I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
Mail- Sachin@pharmacyfreak.com