NSG 552 Psychopharmacology Exam 1 - Modules 1-3 (Latest
2026/2027 Update) Pharmacokinetics, Antipsychotics,
Antidepressants, Mood Stabilizers | Q&A | Grade A | 100%
Correct (Verified Answers) – Nursing Program
Subject: Psychopharmacology – Neurobiology, Drug Mechanisms, Clinical Applications
Source: Evidence-based psychopharmacology / 2026-2027 curriculum
Format: Q&A Guide with Rationale – 100% Verified Answers + Clinical Explanations
1: What does pharmacokinetics study?
Correct Answer: How the body acts on the drug
1. Pharmacokinetics includes absorption, distribution, metabolism, and excretion (ADME) of drugs.
2. Understanding PK guides dosing, route selection, and adjustment for organ dysfunction.
3. Pharmacodynamics (wrong) studies how the drug acts on the body; PK is body on drug.
2: What does pharmacodynamics study?
Correct Answer: How the drug acts on the body
1. Pharmacodynamics involves drug-receptor binding, signal transduction, and therapeutic/ adverse
effects.
2. PD determines potency, efficacy, and side effect profiles.
3. Pharmacokinetics (wrong) is body on drug; PD is drug on body.
3: Describe first-generation antipsychotics (FGAs).
Correct Answer: First developed in 1950s, first available treatment for psychosis; aka typical
antipsychotics; increased risk for EPS and tardive dyskinesia; D2 blocker; 11 FDA-approved; differences
include potency and side effects; examples: Thorazine (chlorpromazine), Haldol (haloperidol), Prolixin
(fluphenazine), perphenazine (Trilafon)
1. FGAs antagonize D2 receptors in mesolimbic pathway (therapeutic) but also nigrostriatal (EPS).
2. High-potency FGAs (haloperidol) cause more EPS; low-potency (chlorpromazine) more
sedating/anticholinergic.
3. FGAs treat positive symptoms but may worsen negative symptoms; SGAs developed to improve this.
4: Describe second-generation antipsychotics (SGAs).
Correct Answer: Examples: Abilify (aripiprazole), Seroquel (quetiapine), Zyprexa (olanzapine), Risperdal
(risperidone), Clozaril (clozapine); lower risk of EPS; higher risk of metabolic side effects; serotonin-
dopamine receptor antagonists; aka atypical antipsychotics
1. SGAs block 5-HT2A and D2 receptors; rapid D2 dissociation reduces EPS risk.
2. Metabolic syndrome (weight gain, dyslipidemia, diabetes) is major concern with SGAs.
3. Clozapine is most effective for treatment-resistant schizophrenia but requires REMS monitoring.
,5: What is EPS (extrapyramidal symptoms)?
Correct Answer: Involuntary movements that occur as side effect to certain medications; aka drug-
induced movement disorder; includes tardive dyskinesia, dystonic reactions, parkinsonism, akathisia,
NMS, akinesia; can be acute or chronic; related to D2 blockade in nigrostriatal pathway
1. Nigrostriatal D2 antagonism impairs motor coordination, leading to EPS.
2. Acute EPS (dystonia, akathisia, parkinsonism) often reversible; tardive dyskinesia may be irreversible.
3. SGAs have lower EPS risk but not zero; monitoring required.
6: What is tardive dyskinesia (TD)?
Correct Answer: Characterized by involuntary movements in face and body; induced by long-term
antipsychotic use; also associated with antidepressants, lithium, antihistamines; more common with
FGAs; movements include writhing, mouth puckering, tongue rolling, lip smacking, pill rolling, tongue
protrusion
1. TD results from D2 receptor supersensitivity after chronic blockade; may persist after停药.
2. AIMS scale screening recommended every 3-6 months for patients on long-term antipsychotics.
3. FDA-approved treatments: valbenazine (Ingrezza) and deutetrabenazine (Austedo).
7: Define upregulation.
Correct Answer: Refers to activation of the nervous system; process by which a cell increases its response
to a substance or signal from outside to carry out a specific response
1. Upregulation increases receptor number or sensitivity in response to low neurotransmitter levels.
2. Chronic antagonist use can cause upregulation (e.g., dopamine supersensitivity after antipsychotics).
3. Downregulation (opposite) occurs with chronic agonist exposure.
8: Define downregulation.
Correct Answer: Refers to state of calm/relaxation within nervous system; characterized by decreased
response by a cell to a molecule or neurotransmitter
1. Downregulation decreases receptor numbers after prolonged high neurotransmitter exposure.
2. SSRIs cause downregulation of 5-HT receptors, contributing to therapeutic effect.
3. Tolerance often involves receptor downregulation.
9: Compare receptor profiles of FGA vs SGA.
Correct Answer: FGA: primarily D2 antagonism, also M2, H1, α1 antagonism. SGA: 5-HT2A & D2
antagonism, rapid D2 dissociation, 5HT2A agonism, also M2, H1, 5HT2C, α1 antagonism.
1. SGA's 5-HT2A blockade reduces EPS risk by allowing dopamine release in nigrostriatal pathway.
2. H1 blockade causes sedation and weight gain; α1 blockade causes orthostatic hypotension.
3. M2 (muscarinic) blockade causes anticholinergic effects: dry mouth, constipation, blurred vision.
10: Define binding in pharmacology.
Correct Answer: When a neurotransmitter binds to a receptor on a receiving cell, it causes ion channels
to open or close
1. Drug-receptor binding initiates signal transduction via G-proteins or ion channel modulation.
2. Affinity describes strength of binding; efficacy describes ability to activate receptor.
3. Antagonists bind but do not activate; agonists bind and activate.
,11: Define affinity.
Correct Answer: The property of a drug that describes its ability to bind to a receptor. Constant unique
for each drug-receptor pair depending on their structures.
1. High affinity means drug binds tightly even at low concentrations; low affinity requires higher doses.
2. Affinity is quantified by dissociation constant (Kd).
3. Selectivity depends on relative affinity for different receptor subtypes.
12: What is CYP450 and its clinical significance?
Correct Answer: Membrane-bound hemoproteins that play pivotal role in detoxification of xenobiotics,
cellular metabolism, homeostasis. Inhibition or induction is major mechanism of drug-drug interactions.
Inhibitor decreases drug metabolism (increases serum levels). Inducer increases hepatic metabolism
(decreases serum concentration). Grapefruit juice is an inhibitor.
1. CYP450 enzymes (e.g., 3A4, 2D6, 1A2) metabolize most psychotropics.
2. Inhibitors (fluoxetine, grapefruit) increase levels of substrates, risking toxicity.
3. Inducers (carbamazepine, rifampin) decrease levels, risking treatment failure.
13: List the four dopamine pathways and their clinical associations.
Correct Answer: Mesolimbic (positive symptoms), Mesocortical (negative symptoms), Nigrostriatal (EPS),
Tuberoinfundibular (prolactin elevation)
1. Mesolimbic hyperactivity contributes to positive symptoms; blockade treats psychosis.
2. Mesocortical hypoactivity contributes to negative symptoms; FGAs may worsen this.
3. Nigrostriatal blockade causes EPS; tuberoinfundibular blockade causes hyperprolactinemia.
14: What is metabolic syndrome and its antipsychotic association?
Correct Answer: Cluster of conditions increasing risk for T2DM and CVD (obesity, HTN, high triglycerides,
low HDL, insulin resistance). Increased risk found with some antipsychotics, primarily SGAs.
1. SGAs (clozapine, olanzapine) have highest metabolic risk; aripiprazole and ziprasidone have lower risk.
2. Mechanisms include H1, 5-HT2C, and M3 receptor blockade.
3. Baseline and quarterly monitoring of weight, glucose, lipids required.
15: Compare high potency vs low potency antipsychotics.
Correct Answer: High potency: higher risk for EPS/hyperprolactinemia, effective at lower doses (Haldol,
risperidone, Prolixin, olanzapine). Low potency: more sedating with more anticholinergic symptoms
(Thorazine, Seroquel, Clozaril, Geodon).
1. Potency refers to dose needed for effect, not efficacy.
2. High potency FGAs tighter D2 binding → more EPS.
3. Low potency FGAs more off-target (H1, α1, M1) → sedation, hypotension, anticholinergic effects.
16: What is Neuroleptic Malignant Syndrome (NMS)?
Correct Answer: Life-threatening reaction to dopamine receptor antagonists or dopaminergic medication
withdrawal. Symptoms begin within 2 weeks of starting or changing dose. Characterized by fever, AMS,
muscle rigidity, autonomic dysfunction. Dantrolene sodium is FDA approved treatment (muscle relaxant).
1. NMS triad: fever, rigidity, autonomic instability. CK elevated.
2. Immediate stop antipsychotic, supportive care, consider dantrolene or bromocriptine.
3. Mortality up to 10% if untreated; requires ICU management.
, 17: What is QTc interval and medication concern?
Correct Answer: Measurement of left ventricle's repolarization efficiency on ECG (normal 350-450 men,
360-460 women). Prolongation associated with life-threatening arrhythmias (torsade de pointes).
Antipsychotics and antidepressants can prolong QT interval.
1. QTc >500 ms or increase >60 ms from baseline increases arrhythmia risk.
2. High-risk drugs: ziprasidone, thioridazine, citalopram (>40 mg).
3. Obtain baseline ECG and monitor with other risk factors (electrolyte disturbances, bradycardia).
18: The study of the use of psychotropic medications in psychiatric disorders is called:
Correct Answer: Psychopharmacology
1. Psychopharmacology integrates neurobiology, pharmacology, and clinical psychiatry.
2. Distinguish from pharmacokinetics (body on drug) and pharmacodynamics (drug on body).
3. Foundational for PMHNP practice.
19: What is a CYP450 inhibitor?
Correct Answer: Increases serum levels of other drugs that are substrates of that enzyme
1. Inhibitors (fluoxetine, paroxetine, grapefruit juice) slow metabolism → higher drug levels → toxicity risk.
2. Important for narrow therapeutic index drugs (e.g., lithium, warfarin).
3. Inducers do the opposite (decrease levels).
20: What is a CYP inducer?
Correct Answer: Decreases serum levels of other drugs that are substrates of that enzyme
1. Inducers (carbamazepine, rifampin, St. John's wort) increase metabolism → lower drug levels →
treatment failure.
2. Dose adjustments often needed when adding inducers or inhibitors.
3. Auto-induction occurs with carbamazepine (increases its own metabolism).
21: Which brain structure regulates powerful emotions such as fear, rage, sexual desires?
Correct Answer: Amygdala
1. Amygdala is key for fear conditioning, aggression, and emotional memory.
2. Hyperactivity in anxiety/PTSD; part of limbic system.
3. Distinguish from hippocampus (memory) and hypothalamus (homeostasis).
22: The relay station for sensory information is the:
Correct Answer: Thalamus
1. Thalamus filters and relays sensory (except olfactory) and motor signals to cortex.
2. Damage can cause sensory deficits or central pain syndromes.
3. Hypothalamus regulates endocrine/autonomic; thalamus is gateway.
23: Essential for maintaining homeostasis, controls basic needs such as sleep-wake cycles:
Correct Answer: Hypothalamus
1. Hypothalamus controls temperature, hunger, thirst, circadian rhythms, and pituitary function.
2. Damage leads to dysregulation of these homeostatic systems.
3. Suprachiasmatic nucleus regulates sleep-wake cycles.
2026/2027 Update) Pharmacokinetics, Antipsychotics,
Antidepressants, Mood Stabilizers | Q&A | Grade A | 100%
Correct (Verified Answers) – Nursing Program
Subject: Psychopharmacology – Neurobiology, Drug Mechanisms, Clinical Applications
Source: Evidence-based psychopharmacology / 2026-2027 curriculum
Format: Q&A Guide with Rationale – 100% Verified Answers + Clinical Explanations
1: What does pharmacokinetics study?
Correct Answer: How the body acts on the drug
1. Pharmacokinetics includes absorption, distribution, metabolism, and excretion (ADME) of drugs.
2. Understanding PK guides dosing, route selection, and adjustment for organ dysfunction.
3. Pharmacodynamics (wrong) studies how the drug acts on the body; PK is body on drug.
2: What does pharmacodynamics study?
Correct Answer: How the drug acts on the body
1. Pharmacodynamics involves drug-receptor binding, signal transduction, and therapeutic/ adverse
effects.
2. PD determines potency, efficacy, and side effect profiles.
3. Pharmacokinetics (wrong) is body on drug; PD is drug on body.
3: Describe first-generation antipsychotics (FGAs).
Correct Answer: First developed in 1950s, first available treatment for psychosis; aka typical
antipsychotics; increased risk for EPS and tardive dyskinesia; D2 blocker; 11 FDA-approved; differences
include potency and side effects; examples: Thorazine (chlorpromazine), Haldol (haloperidol), Prolixin
(fluphenazine), perphenazine (Trilafon)
1. FGAs antagonize D2 receptors in mesolimbic pathway (therapeutic) but also nigrostriatal (EPS).
2. High-potency FGAs (haloperidol) cause more EPS; low-potency (chlorpromazine) more
sedating/anticholinergic.
3. FGAs treat positive symptoms but may worsen negative symptoms; SGAs developed to improve this.
4: Describe second-generation antipsychotics (SGAs).
Correct Answer: Examples: Abilify (aripiprazole), Seroquel (quetiapine), Zyprexa (olanzapine), Risperdal
(risperidone), Clozaril (clozapine); lower risk of EPS; higher risk of metabolic side effects; serotonin-
dopamine receptor antagonists; aka atypical antipsychotics
1. SGAs block 5-HT2A and D2 receptors; rapid D2 dissociation reduces EPS risk.
2. Metabolic syndrome (weight gain, dyslipidemia, diabetes) is major concern with SGAs.
3. Clozapine is most effective for treatment-resistant schizophrenia but requires REMS monitoring.
,5: What is EPS (extrapyramidal symptoms)?
Correct Answer: Involuntary movements that occur as side effect to certain medications; aka drug-
induced movement disorder; includes tardive dyskinesia, dystonic reactions, parkinsonism, akathisia,
NMS, akinesia; can be acute or chronic; related to D2 blockade in nigrostriatal pathway
1. Nigrostriatal D2 antagonism impairs motor coordination, leading to EPS.
2. Acute EPS (dystonia, akathisia, parkinsonism) often reversible; tardive dyskinesia may be irreversible.
3. SGAs have lower EPS risk but not zero; monitoring required.
6: What is tardive dyskinesia (TD)?
Correct Answer: Characterized by involuntary movements in face and body; induced by long-term
antipsychotic use; also associated with antidepressants, lithium, antihistamines; more common with
FGAs; movements include writhing, mouth puckering, tongue rolling, lip smacking, pill rolling, tongue
protrusion
1. TD results from D2 receptor supersensitivity after chronic blockade; may persist after停药.
2. AIMS scale screening recommended every 3-6 months for patients on long-term antipsychotics.
3. FDA-approved treatments: valbenazine (Ingrezza) and deutetrabenazine (Austedo).
7: Define upregulation.
Correct Answer: Refers to activation of the nervous system; process by which a cell increases its response
to a substance or signal from outside to carry out a specific response
1. Upregulation increases receptor number or sensitivity in response to low neurotransmitter levels.
2. Chronic antagonist use can cause upregulation (e.g., dopamine supersensitivity after antipsychotics).
3. Downregulation (opposite) occurs with chronic agonist exposure.
8: Define downregulation.
Correct Answer: Refers to state of calm/relaxation within nervous system; characterized by decreased
response by a cell to a molecule or neurotransmitter
1. Downregulation decreases receptor numbers after prolonged high neurotransmitter exposure.
2. SSRIs cause downregulation of 5-HT receptors, contributing to therapeutic effect.
3. Tolerance often involves receptor downregulation.
9: Compare receptor profiles of FGA vs SGA.
Correct Answer: FGA: primarily D2 antagonism, also M2, H1, α1 antagonism. SGA: 5-HT2A & D2
antagonism, rapid D2 dissociation, 5HT2A agonism, also M2, H1, 5HT2C, α1 antagonism.
1. SGA's 5-HT2A blockade reduces EPS risk by allowing dopamine release in nigrostriatal pathway.
2. H1 blockade causes sedation and weight gain; α1 blockade causes orthostatic hypotension.
3. M2 (muscarinic) blockade causes anticholinergic effects: dry mouth, constipation, blurred vision.
10: Define binding in pharmacology.
Correct Answer: When a neurotransmitter binds to a receptor on a receiving cell, it causes ion channels
to open or close
1. Drug-receptor binding initiates signal transduction via G-proteins or ion channel modulation.
2. Affinity describes strength of binding; efficacy describes ability to activate receptor.
3. Antagonists bind but do not activate; agonists bind and activate.
,11: Define affinity.
Correct Answer: The property of a drug that describes its ability to bind to a receptor. Constant unique
for each drug-receptor pair depending on their structures.
1. High affinity means drug binds tightly even at low concentrations; low affinity requires higher doses.
2. Affinity is quantified by dissociation constant (Kd).
3. Selectivity depends on relative affinity for different receptor subtypes.
12: What is CYP450 and its clinical significance?
Correct Answer: Membrane-bound hemoproteins that play pivotal role in detoxification of xenobiotics,
cellular metabolism, homeostasis. Inhibition or induction is major mechanism of drug-drug interactions.
Inhibitor decreases drug metabolism (increases serum levels). Inducer increases hepatic metabolism
(decreases serum concentration). Grapefruit juice is an inhibitor.
1. CYP450 enzymes (e.g., 3A4, 2D6, 1A2) metabolize most psychotropics.
2. Inhibitors (fluoxetine, grapefruit) increase levels of substrates, risking toxicity.
3. Inducers (carbamazepine, rifampin) decrease levels, risking treatment failure.
13: List the four dopamine pathways and their clinical associations.
Correct Answer: Mesolimbic (positive symptoms), Mesocortical (negative symptoms), Nigrostriatal (EPS),
Tuberoinfundibular (prolactin elevation)
1. Mesolimbic hyperactivity contributes to positive symptoms; blockade treats psychosis.
2. Mesocortical hypoactivity contributes to negative symptoms; FGAs may worsen this.
3. Nigrostriatal blockade causes EPS; tuberoinfundibular blockade causes hyperprolactinemia.
14: What is metabolic syndrome and its antipsychotic association?
Correct Answer: Cluster of conditions increasing risk for T2DM and CVD (obesity, HTN, high triglycerides,
low HDL, insulin resistance). Increased risk found with some antipsychotics, primarily SGAs.
1. SGAs (clozapine, olanzapine) have highest metabolic risk; aripiprazole and ziprasidone have lower risk.
2. Mechanisms include H1, 5-HT2C, and M3 receptor blockade.
3. Baseline and quarterly monitoring of weight, glucose, lipids required.
15: Compare high potency vs low potency antipsychotics.
Correct Answer: High potency: higher risk for EPS/hyperprolactinemia, effective at lower doses (Haldol,
risperidone, Prolixin, olanzapine). Low potency: more sedating with more anticholinergic symptoms
(Thorazine, Seroquel, Clozaril, Geodon).
1. Potency refers to dose needed for effect, not efficacy.
2. High potency FGAs tighter D2 binding → more EPS.
3. Low potency FGAs more off-target (H1, α1, M1) → sedation, hypotension, anticholinergic effects.
16: What is Neuroleptic Malignant Syndrome (NMS)?
Correct Answer: Life-threatening reaction to dopamine receptor antagonists or dopaminergic medication
withdrawal. Symptoms begin within 2 weeks of starting or changing dose. Characterized by fever, AMS,
muscle rigidity, autonomic dysfunction. Dantrolene sodium is FDA approved treatment (muscle relaxant).
1. NMS triad: fever, rigidity, autonomic instability. CK elevated.
2. Immediate stop antipsychotic, supportive care, consider dantrolene or bromocriptine.
3. Mortality up to 10% if untreated; requires ICU management.
, 17: What is QTc interval and medication concern?
Correct Answer: Measurement of left ventricle's repolarization efficiency on ECG (normal 350-450 men,
360-460 women). Prolongation associated with life-threatening arrhythmias (torsade de pointes).
Antipsychotics and antidepressants can prolong QT interval.
1. QTc >500 ms or increase >60 ms from baseline increases arrhythmia risk.
2. High-risk drugs: ziprasidone, thioridazine, citalopram (>40 mg).
3. Obtain baseline ECG and monitor with other risk factors (electrolyte disturbances, bradycardia).
18: The study of the use of psychotropic medications in psychiatric disorders is called:
Correct Answer: Psychopharmacology
1. Psychopharmacology integrates neurobiology, pharmacology, and clinical psychiatry.
2. Distinguish from pharmacokinetics (body on drug) and pharmacodynamics (drug on body).
3. Foundational for PMHNP practice.
19: What is a CYP450 inhibitor?
Correct Answer: Increases serum levels of other drugs that are substrates of that enzyme
1. Inhibitors (fluoxetine, paroxetine, grapefruit juice) slow metabolism → higher drug levels → toxicity risk.
2. Important for narrow therapeutic index drugs (e.g., lithium, warfarin).
3. Inducers do the opposite (decrease levels).
20: What is a CYP inducer?
Correct Answer: Decreases serum levels of other drugs that are substrates of that enzyme
1. Inducers (carbamazepine, rifampin, St. John's wort) increase metabolism → lower drug levels →
treatment failure.
2. Dose adjustments often needed when adding inducers or inhibitors.
3. Auto-induction occurs with carbamazepine (increases its own metabolism).
21: Which brain structure regulates powerful emotions such as fear, rage, sexual desires?
Correct Answer: Amygdala
1. Amygdala is key for fear conditioning, aggression, and emotional memory.
2. Hyperactivity in anxiety/PTSD; part of limbic system.
3. Distinguish from hippocampus (memory) and hypothalamus (homeostasis).
22: The relay station for sensory information is the:
Correct Answer: Thalamus
1. Thalamus filters and relays sensory (except olfactory) and motor signals to cortex.
2. Damage can cause sensory deficits or central pain syndromes.
3. Hypothalamus regulates endocrine/autonomic; thalamus is gateway.
23: Essential for maintaining homeostasis, controls basic needs such as sleep-wake cycles:
Correct Answer: Hypothalamus
1. Hypothalamus controls temperature, hunger, thirst, circadian rhythms, and pituitary function.
2. Damage leads to dysregulation of these homeostatic systems.
3. Suprachiasmatic nucleus regulates sleep-wake cycles.
