Downloadable Test Bank – Stahl’s Essential Psychopharmacology, 5th edition

Test Bank: An Overview

Build regular question practice into your coursework with this downloadable test bank of 500+ psychopharmacology practice questions. It is intended for students in classes using Stahl’s Essential Psychopharmacology, 5th edition. Use the topics below to compare the resource with your syllabus and the material you are studying.

What’s Included

• Multiple choice questions for choosing between possible answers.
• True/false questions for checking your understanding of key statements.
• Short answer questions for explaining concepts in your own words.

Topics Covered in the Test Bank

The question bank covers the following areas of psychopharmacology:

• Chemical signaling between nerve cells and the roles of neurotransmitters.
• How psychiatric medicines interact with transport proteins, receptors, enzymes, and ion channels.
• Brain signaling in psychosis and schizophrenia, including dopamine, serotonin, and glutamate.
• How antipsychotic medicines act on dopamine and serotonin systems.
• Mood conditions, norepinephrine and GABA signaling, and the actions of antidepressants and mood-stabilizing medicines.
• Medication approaches to anxiety and trauma-related conditions.
• Drug treatment concepts for persistent pain.
• Sleep and alertness, including histamine and orexin pathways and medication approaches to sleep difficulties.
• Attention and hyperactivity difficulties and their medication management.
• Dementia, acetylcholine signaling, and medicines used to address symptoms.
• Impulsive behavior, compulsive behavior, and addiction.

Compare these topics with your assigned reading and class objectives to choose where to focus your practice.

Sample Practice Questions

Try these 15 multiple choice questions to preview the question style in the test bank

1. A GPCR produces 20 units of signaling in the absence of any ligand. An inverse agonist reduces this signal to 5 units. Ligand X binds reversibly to the same site, blocks agonist responses, and has no effect on the ligand-free signal when given alone. X is added at a concentration sufficient to occupy most receptors at equilibrium. What is the most likely result?
   1. Signaling remains near 5 units because X has no intrinsic efficacy.
   2. Signaling falls below 5 units because the two drugs have additive inhibitory effects.
   3. Signaling returns toward 20 units as X displaces the inverse agonist.
   4. Signaling rises toward the full-agonist maximum as X displaces the inverse agonist.
2. A patient with ADHD is switched from methylphenidate to atomoxetine. Which change in direct transporter inhibition best characterizes this switch?
   1. Inhibition of DAT and NET changes to predominantly NET inhibition.
   2. Inhibition of DAT and NET changes to predominantly DAT inhibition.
   3. Predominantly NET inhibition changes to inhibition of DAT and NET.
   4. Predominantly DAT inhibition changes to predominantly SERT inhibition.
3. In cultured cells, lithium reduces phosphorylation of beta-catenin at sites that target it for degradation, leading to beta-catenin accumulation. Inhibition of which enzyme most directly explains this finding?
   1. Inositol monophosphatase
   2. Glycogen synthase kinase 3
   3. Monoamine oxidase A
   4. Protein phosphatase 2A
4. Drugs P and Q compete reversibly for the same GPCR binding site. In a preparation with negligible receptor reserve, the reference full agonist P has an EC₅₀ of 20 nM and a maximum response of 100 units; Q has an EC₅₀ of 2 nM and a maximum response of 40 units. Responses are measured above the ligand-free baseline. While P is producing a near-maximal response, enough Q is added to occupy almost all receptors at equilibrium. Which response is expected?
   1. Approximately 0 units, because competition eliminates Q’s intrinsic efficacy.
   2. Approximately 40 units, because Q has lower efficacy despite greater potency.
   3. Approximately 100 units, because greater potency compensates for lower efficacy.
   4. Approximately 140 units, because the individual maximum responses are additive.
5. In isolated dopaminergic nerve terminals, Drug X enters through DAT, interacts with VMAT2, redistributes dopamine from vesicles toward the cytoplasm, and promotes dopamine efflux through DAT. Which drug best matches this mechanism?
   1. Cocaine
   2. Methylphenidate
   3. Tetrabenazine
   4. Amphetamine
6. Cells expressing a constitutively active Gi-coupled receptor are studied in the absence of endogenous or added agonist. Acute application of ligand X increases intracellular cAMP. This effect is absent in cells lacking the receptor and is prevented by a neutral antagonist at that receptor. Which mechanism best explains the findings?
   1. Direct inhibition of cAMP phosphodiesterase
   2. Competitive displacement of an endogenous agonist
   3. Inverse agonism that reduces constitutive Gi activation
   4. Full agonism that increases Gi activation
7. A patient with Alzheimer disease develops nausea and sinus bradycardia after a donepezil dose increase. Which mechanism best links these adverse effects to the drug’s intended action on cholinergic neurotransmission?
   1. Direct activation of muscarinic receptors in the brain, gut, and heart
   2. Increased choline uptake that accelerates presynaptic acetylcholine synthesis
   3. Inhibition of monoamine oxidase that prolongs acetylcholine availability
   4. Inhibition of acetylcholinesterase, prolonging acetylcholine signaling
8. Two patients receive the same daily dose of escitalopram, an active parent drug for which CYP2C19 is an important metabolic pathway. One is a CYP2C19 poor metabolizer and the other is a normal metabolizer. Assuming comparable adherence, organ function, and concomitant medications, which difference is most likely in the poor metabolizer?
   1. Reduced metabolic clearance and increased steady-state parent-drug exposure
   2. Increased metabolic clearance and reduced steady-state parent-drug exposure
   3. Reduced bioactivation and reduced exposure to the principal active drug
   4. Increased SERT binding affinity despite unchanged parent-drug exposure
9. A fixed amount of serotonin is added to the extracellular fluid surrounding isolated serotonergic nerve terminals. After an SSRI is added, extracellular serotonin disappears more slowly. Which mechanism most directly explains this observation?
   1. Inhibition of SERT-mediated uptake across the plasma membrane
   2. Inhibition of VMAT2-mediated uptake across the vesicular membrane
   3. Inhibition of monoamine oxidase-mediated degradation within mitochondria
   4. Activation of serotonin autoreceptors that suppress further transmitter release
10. After exposure to an irreversible monoamine oxidase inhibitor, unbound drug and active metabolites are cleared, but enzyme activity remains suppressed. Increasing substrate concentration does not restore activity. Which process is principally required for recovery?
    1. Displacement of the inhibitor by a sufficiently high substrate concentration
    2. Spontaneous dissociation of the inhibitor from the inactivated enzyme
    3. Reduction of the inhibitor’s plasma concentration by one additional half-life
    4. Synthesis of functional enzyme to replace the inactivated enzyme
11. A new ligand blocks agonist-induced signaling at a GPCR but has no effect when administered alone. The assay has no detectable constitutive receptor activity. A researcher concludes that the ligand is a neutral antagonist rather than an inverse agonist. Which follow-up experiment would best test this conclusion?
    1. Determine whether increasing agonist concentration overcomes the blockade.
    2. Measure the ligand’s receptor-binding affinity in the same preparation.
    3. Test the ligand alone in a preparation of the same receptor with measurable constitutive activity.
    4. Compare the degree of blockade at a lower agonist concentration in the original preparation.
12. In cells expressing dopamine D2 receptors, dopamine reduces cAMP formation. Haloperidol prevents this reduction but does not impair cAMP production when adenylyl cyclase is activated directly in the absence of dopamine. Which action best explains these findings?
    1. Inhibition of DAT-mediated dopamine uptake
    2. Inhibition of monoamine oxidase-mediated dopamine metabolism
    3. Antagonism of D2 receptor-mediated Gi/o signaling
    4. Direct inhibition of adenylyl cyclase catalytic activity
13. In isolated nerve terminals exposed to a fixed extracellular dopamine concentration, Na⁺/K⁺-ATPase inhibition raises intracellular Na⁺ and reduces DAT-mediated uptake. ATP remains available, and DAT abundance at the plasma membrane is unchanged. Which mechanism best explains the reduced uptake?
    1. Loss of ATP hydrolysis by DAT during each dopamine transport cycle
    2. Dissipation of the vesicular proton gradient used by DAT at the plasma membrane
    3. Reduced dopamine synthesis, leaving fewer extracellular molecules available for uptake
    4. Weakening of the sodium electrochemical gradient that helps drive DAT-mediated uptake
14. A patient whose genotype predicts normal CYP2D6 metabolism is stable on atomoxetine. After fluoxetine is added, atomoxetine exposure increases despite an unchanged atomoxetine dose and stable liver and kidney function. Which interpretation best explains why the genotype alone did not predict the new exposure?
    1. Fluoxetine induced CYP2D6, accelerating conversion of atomoxetine to metabolites.
    2. Fluoxetine inhibited CYP2D6, reducing atomoxetine clearance.
    3. Fluoxetine inhibited bioactivation of atomoxetine, an inactive prodrug.
    4. Fluoxetine increased renal elimination of unchanged atomoxetine.
15. Radiolabeled serotonin is added outside intact serotonergic nerve terminals and is later detected inside synaptic vesicles. Which sequence of transporter-mediated steps most directly explains its movement from extracellular fluid into the vesicle lumen?
    1. VMAT2 transports it into the cytoplasm; SERT transports it into vesicles.
    2. SERT transports it into the cytoplasm; VMAT2 transports it into vesicles.
    3. SERT transports it into the cytoplasm; GAT1 transports it into vesicles.
    4. GAT1 transports it into the cytoplasm; VMAT2 transports it into vesicles.

Question Development

The questions were written in collaboration with Savita Bhakta, MD, Clinical Professor of Psychiatry. The resource brings together three question formats for practice across the topics listed above.

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