1. First-generation antipsychotics are grouped by chemical structure into classes including the phenothiazines, the butyrophenones, and the thioxanthenes. Which statement most precisely characterizes the butyrophenone class, of which haloperidol is the prototype?
A) Butyrophenones have the highest anticholinergic and sedative burden of all first-generation antipsychotics
B) Butyrophenones are uniformly low-potency agents requiring several hundred milligrams per day for therapeutic effect
C) Butyrophenones are among the most D2-selective first-generation agents, with limited off-target receptor activity at clinical doses and consequently high extrapyramidal-symptom risk
D) Butyrophenones are defined by meaningful blockade of serotonin 5-HT2A receptors, which classifies them as atypical agents
E) Butyrophenones lack any long-acting injectable formulation and are therefore unsuitable for adherence management
ANSWER: C
Rationale:
Butyrophenones such as haloperidol are among the most D2-selective compounds in the first-generation class, with very high D2 affinity and limited meaningful activity at histamine H1, muscarinic M1, or alpha-1 adrenergic receptors at clinical doses; this selectivity explains both their low sedative and anticholinergic burden and their high extrapyramidal-symptom (movement side effect) liability.
Option A: Option A is incorrect because the highest anticholinergic and sedative burden belongs to low-potency aliphatic and piperidine phenothiazines such as chlorpromazine and thioridazine, not the butyrophenones.
Option B: Option B is incorrect because butyrophenones are high-potency, effective at single-digit milligram doses, not low-potency agents.
Option D: Option D is incorrect because meaningful 5-HT2A blockade is the defining pharmacology of atypical agents and of loxapine's profile, not of the butyrophenones.
Option E: Option E is incorrect because haloperidol decanoate is an established long-acting injectable, so the class is well suited to adherence management.
2. The phenothiazines are subdivided into aliphatic, piperidine, and piperazine subgroups, and this subclassification tracks closely with potency. Which pairing of subgroup to potency and representative agent is correct?
A) The piperazine subgroup contains the highest-potency phenothiazines, including fluphenazine, trifluoperazine, and perphenazine
B) The aliphatic subgroup contains the highest-potency phenothiazines, including chlorpromazine
C) The piperidine subgroup contains the highest-potency phenothiazines, including thioridazine
D) All three phenothiazine subgroups are equivalent in potency and differ only in half-life
E) The piperazine subgroup contains the lowest-potency phenothiazines and carries the greatest anticholinergic burden
ANSWER: A
Rationale:
The piperazine phenothiazines — fluphenazine, trifluoperazine, and perphenazine — are the highest-potency members of the phenothiazine class, with high D2 affinity and relatively low anticholinergic burden.
Option B: Option B is incorrect because the aliphatic subgroup, represented by chlorpromazine, is among the lowest-potency phenothiazines with a heavy anticholinergic and sedative burden.
Option C: Option C is incorrect because the piperidine subgroup, represented by thioridazine, is low-potency with the highest anticholinergic burden of the commonly used agents.
Option D: Option D is incorrect because the subgroups differ substantially in potency and receptor profile, not merely in half-life.
Option E: Option E is incorrect because it inverts the relationship: piperazines are the highest-potency, lowest-anticholinergic subgroup, not the lowest-potency with the greatest anticholinergic burden.
3. Among the low-potency phenothiazines, chlorpromazine produces a characteristic set of adverse effects not shared to the same degree by other first-generation agents. Which adverse effect is most distinctively associated with long-term, high-dose chlorpromazine?
A) Pigmentary retinopathy leading to irreversible visual impairment
B) Torsades de pointes driven by potent cardiac potassium-channel blockade
C) Weight loss and metabolic neutrality
D) Photosensitivity reactions and a blue-grey discoloration of sun-exposed skin, with corneal and lenticular deposits
Chlorpromazine is distinctively associated with photosensitivity reactions and, with long-term high-dose use, a blue-grey discoloration of sun-exposed skin together with corneal and lenticular deposits detectable on slit-lamp examination; these pigmentary effects are dose- and duration-dependent.
Option A: Option A is incorrect because pigmentary retinopathy is the signature ocular toxicity of thioridazine at high doses, not of chlorpromazine.
Option B: Option B is incorrect because the most severe potassium-channel-mediated QTc prolongation and torsades risk belongs to thioridazine, although chlorpromazine can prolong the QTc to a lesser degree.
Option C: Option C is incorrect because chlorpromazine produces weight gain through histamine H1 blockade, not weight loss; metabolic neutrality is characteristic of molindone.
Option E: Option E is incorrect because mandatory monitoring for agranulocytosis is the hallmark of clozapine, a second-generation agent, not chlorpromazine.
4. Thioridazine, a piperidine phenothiazine, has been largely displaced from routine practice because of two distinctive toxicities that set it apart from other low-potency agents. Which pairing correctly identifies both?
A) Cholestatic jaundice and lowering of the seizure threshold
B) The most severe QTc prolongation in the class, from potent cardiac hERG potassium-channel blockade, and pigmentary retinopathy at doses above roughly 800 mg per day
C) Blue-grey skin discoloration and corneal-lenticular deposits
D) Agranulocytosis and myocarditis
E) Weight neutrality and a uniquely favorable cardiac safety profile
ANSWER: B
Rationale:
Thioridazine is distinguished by two toxicities: it is the most potent blocker of the cardiac hERG potassium channel among these agents, producing the most severe dose-dependent QTc prolongation with risk of torsades de pointes, and it causes pigmentary retinopathy at doses exceeding roughly 800 mg per day through melanin binding in the retinal pigment epithelium, with potential for irreversible visual impairment.
Option A: Option A is incorrect because cholestatic jaundice and prominent seizure-threshold lowering are more characteristic of chlorpromazine.
Option C: Option C is incorrect because blue-grey skin and corneal-lenticular deposits are the signature of chlorpromazine, not thioridazine.
Option D: Option D is incorrect because agranulocytosis and myocarditis are associated with clozapine, a second-generation agent.
Option E: Option E is incorrect because it inverts thioridazine's profile; thioridazine carries the worst cardiac risk in the class, not a favorable one, and weight neutrality is characteristic of molindone.
5. A large government-funded effectiveness trial in chronic schizophrenia compared the mid-to-high-potency first-generation agent perphenazine against several second-generation antipsychotics, using all-cause treatment discontinuation as its primary outcome. What is the most important clinical implication of that trial's finding for drug selection?
A) Perphenazine was clearly inferior to every second-generation agent and should be abandoned in chronic schizophrenia
B) Perphenazine eliminated the risk of tardive dyskinesia and therefore needs no movement monitoring
C) Perphenazine performed comparably to several second-generation agents on the primary outcome, supporting it as a pharmacoeconomically reasonable option in patients without a specific indication for a second-generation drug
D) Perphenazine was shown to be superior to all second-generation agents for negative symptoms and cognition
E) The result proved that potency, measured in milligrams, predicts clinical effectiveness across drug classes
ANSWER: C
Rationale:
The trial finding that perphenazine performed comparably to several second-generation antipsychotics on all-cause treatment discontinuation challenged the assumption that second-generation agents were categorically superior for chronic schizophrenia, and it supports perphenazine as a cost-effective, pharmacoeconomically reasonable option in patients without a specific indication for a second-generation drug.
Option A: Option A is incorrect because the finding was comparable effectiveness, not clear inferiority, and does not justify abandoning the agent.
Option B: Option B is incorrect because perphenazine, like other first-generation agents, carries tardive-dyskinesia risk and still requires movement monitoring.
Option D: Option D is incorrect because the trial did not establish perphenazine superiority for negative symptoms or cognition.
Option E: Option E is incorrect because the comparison concerned effectiveness across classes, not a demonstration that milligram potency predicts effectiveness.
6. The four major extrapyramidal syndromes (movement disorders from dopamine blockade) differ in time course and phenomenology. Which description correctly matches acute dystonia and distinguishes it from the others?
A) Motor restlessness with an inner urge to move, emerging over days to weeks, most responsive to propranolol
B) Bradykinesia, rigidity, and resting tremor emerging over days to weeks, dose-dependent and worse in the elderly
C) Involuntary orolingual movements emerging after months to years of exposure
D) Fever, lead-pipe rigidity, autonomic instability, and altered consciousness developing over 24 to 72 hours
E) Sudden, sustained, often painful muscle contractions such as oculogyric crisis or torticollis, emerging within hours to about five days of starting or increasing the drug, with highest risk in young antipsychotic-naive males
ANSWER: E
Rationale:
Acute dystonia consists of sudden, sustained, often painful muscle contractions producing abnormal postures such as oculogyric crisis (forced upward eye deviation) and torticollis (neck spasm), and it is the earliest extrapyramidal syndrome, emerging within hours to about five days of starting or increasing a first-generation agent, with the highest risk in young antipsychotic-naive males.
Option A: Option A is incorrect because that describes akathisia.
Option B: Option B is incorrect because that describes drug-induced parkinsonism.
Option C: Option C is incorrect because involuntary orolingual movements after months to years describe tardive dyskinesia.
Option D: Option D is incorrect because fever with lead-pipe rigidity, autonomic instability, and altered consciousness describes neuroleptic malignant syndrome, a systemic emergency rather than an isolated dystonic posture.
7. A clinician must distinguish akathisia from drug-induced parkinsonism, two extrapyramidal syndromes that both emerge over days to weeks but require different management. Which statement correctly captures akathisia and its preferred pharmacological treatment?
A) Akathisia is a syndrome of motor restlessness with a subjective inner urge to move, often mistaken for agitation, and the most evidence-supported pharmacological treatment is propranolol, a non-selective beta-adrenergic blocker
B) Akathisia is characterized by bradykinesia, rigidity, and resting tremor, and the preferred treatment is an anticholinergic such as benztropine
C) Akathisia is a sudden sustained muscle spasm best treated with intramuscular diphenhydramine
D) Akathisia consists of involuntary orolingual movements best treated with a VMAT2 inhibitor
E) Akathisia is a febrile emergency requiring dantrolene and discontinuation of the antipsychotic
ANSWER: A
Rationale:
Akathisia is a syndrome of motor restlessness with a distressing subjective inner urge to move; it is commonly mistaken for psychomotor agitation or worsening psychosis, and the most evidence-supported pharmacological treatment, after considering dose reduction, is propranolol, particularly for the subjective restlessness component.
Option B: Option B is incorrect because bradykinesia, rigidity, and tremor describe drug-induced parkinsonism, and anticholinergics are less consistently effective for akathisia than for parkinsonism or dystonia.
Option C: Option C is incorrect because sudden sustained spasm describes acute dystonia, the syndrome treated with intramuscular diphenhydramine or benztropine.
Option D: Option D is incorrect because involuntary orolingual movements describe tardive dyskinesia, the indication for VMAT2 inhibitors.
Option E: Option E is incorrect because a febrile emergency requiring dantrolene describes neuroleptic malignant syndrome, not akathisia.
8. Drug-induced parkinsonism can be difficult to distinguish from idiopathic Parkinson disease because the motor features overlap. Which clinical clue most reliably favors drug-induced parkinsonism over the idiopathic disease?
A) A unilateral resting tremor that remains confined to one limb for years
B) Progressive worsening despite stopping the offending drug
C) An onset strictly limited to patients younger than 40 years
D) Symptoms that are bilateral and roughly symmetric from the outset and that improve within weeks to months of dose reduction or drug discontinuation
E) The presence of Lewy bodies on imaging that confirm the diagnosis at the bedside
ANSWER: D
Rationale:
Drug-induced parkinsonism is typically bilateral and roughly symmetric from the outset and improves within weeks to months once the offending drug is reduced or stopped, whereas idiopathic Parkinson disease characteristically begins asymmetrically and progresses despite drug changes; these two features are the most useful bedside discriminators.
Option A: Option A is incorrect because a persistent unilateral, asymmetric tremor favors idiopathic Parkinson disease, not the drug-induced form.
Option B: Option B is incorrect because progression despite withdrawal of the drug points away from a reversible drug-induced cause.
Option C: Option C is incorrect because drug-induced parkinsonism is in fact more common in the elderly, owing to reduced nigrostriatal reserve, not confined to the young.
Option E: Option E is incorrect because Lewy bodies are a neuropathological finding and are not identified on routine bedside imaging to make this distinction.
9. Distinguishing neuroleptic malignant syndrome from serotonin syndrome is clinically important because their precipitants and management differ. Which set of features most reliably identifies neuroleptic malignant syndrome rather than serotonin syndrome?
A) Hyperreflexia and clonus with onset within hours of a precipitating drug
B) Lead-pipe rigidity with reduced reflexes (bradyreflexia), onset over roughly 24 to 72 hours, and a markedly elevated creatine kinase often exceeding 10,000 units per liter
C) Flaccid paralysis with absent muscle enzyme elevation and a normal temperature
D) Prominent diarrhea and gastrointestinal hyperactivity with little rigidity
E) Rapid onset of dilated pupils and seizures without temperature change
ANSWER: B
Rationale:
Neuroleptic malignant syndrome is characterized by lead-pipe muscle rigidity with reduced reflexes (bradyreflexia), a relatively slow onset over roughly 24 to 72 hours, and markedly elevated creatine kinase (a muscle enzyme released by muscle injury) often exceeding 10,000 units per liter, reflecting the rigidity-driven muscle breakdown.
Option A: Option A is incorrect because hyperreflexia and clonus with onset within hours are the hallmark of serotonin syndrome, not neuroleptic malignant syndrome.
Option C: Option C is incorrect because neuroleptic malignant syndrome produces rigidity with high fever and elevated creatine kinase, not flaccid paralysis with normal temperature.
Option D: Option D is incorrect because prominent diarrhea and gastrointestinal hyperactivity point toward serotonin syndrome rather than the rigidity-dominant neuroleptic malignant syndrome.
Option E: Option E is incorrect because rapid pupillary dilation and seizures without temperature change do not capture the defining fever, rigidity, and altered consciousness of neuroleptic malignant syndrome.
10. Tardive dyskinesia has a mechanism and a clinically deceptive temporal pattern that distinguish it from the acute extrapyramidal syndromes. Which statement correctly characterizes both?
A) It results from acute cholinergic excess and resolves within minutes of an anticholinergic injection
B) It results from a sudden fall in striatal dopamine and appears within hours of the first dose
C) It results from dopamine receptor supersensitivity developing during chronic D2 blockade, and it may first appear or worsen when the antipsychotic dose is reduced because dose reduction unmasks the supersensitive receptors
D) It results from beta-adrenergic overactivity and is best prevented by propranolol
E) It results from an idiosyncratic immune reaction and is accompanied by fever and rigidity
ANSWER: C
Rationale:
Tardive dyskinesia arises from dopamine receptor supersensitivity that develops in the striatum in response to chronic D2 blockade, with postsynaptic D2 receptors upregulating in density and sensitivity over time; it characteristically first becomes apparent or worsens when the dose is reduced or discontinued, because dose reduction unmasks the supersensitivity that ongoing blockade had been concealing (the withdrawal-emergent or unmasking pattern).
Option A: Option A is incorrect because acute cholinergic excess relieved rapidly by an anticholinergic describes acute dystonia.
Option B: Option B is incorrect because a sudden dopamine fall with onset within hours describes the acute, not the tardive, syndrome.
Option D: Option D is incorrect because beta-adrenergic mechanisms and propranolol responsiveness relate to akathisia.
Option E: Option E is incorrect because an idiosyncratic reaction with fever and rigidity describes neuroleptic malignant syndrome, not tardive dyskinesia.
11. Which statement most precisely describes the only drug class specifically approved for the treatment of tardive dyskinesia and its mechanism?
A) Vesicular monoamine transporter 2 (VMAT2) inhibitors, valbenazine and deutetrabenazine, which deplete presynaptic dopamine stores and thereby reduce dopamine release at supersensitive receptors
B) Anticholinergic agents, benztropine and trihexyphenidyl, which block central muscarinic receptors to restore dopaminergic-cholinergic balance
C) Dopamine agonists, bromocriptine and amantadine, which directly stimulate postsynaptic dopamine receptors
D) Beta-adrenergic blockers, propranolol and metoprolol, which reduce noradrenergic drive
E) Skeletal muscle relaxants, dantrolene, which act on the ryanodine receptor to reduce rigidity
ANSWER: A
Rationale:
Valbenazine and deutetrabenazine are selective VMAT2 inhibitors and are the agents specifically approved for tardive dyskinesia; by inhibiting the transporter that loads dopamine into presynaptic storage vesicles, they deplete presynaptic dopamine stores and reduce dopamine release, lessening the excessive stimulation at the supersensitive receptors that drive the involuntary movements.
Option B: Option B is incorrect because anticholinergics treat dystonia and parkinsonism and can worsen tardive dyskinesia rather than treat it.
Option C: Option C is incorrect because dopamine agonists are used to restore dopaminergic tone in neuroleptic malignant syndrome and would tend to aggravate dyskinetic movements.
Option D: Option D is incorrect because beta-blockers are the treatment for akathisia, not tardive dyskinesia.
Option E: Option E is incorrect because dantrolene reduces rigidity and hyperthermia in neuroleptic malignant syndrome and has no approved role in tardive dyskinesia.
12. A patient develops an unexpectedly high burden of extrapyramidal side effects on a standard dose of haloperidol. Genotyping shows the patient is a poor metabolizer at the liver enzyme CYP2D6, which is responsible for breaking down haloperidol and perphenazine. What is the expected pharmacokinetic consequence?
A) Plasma haloperidol concentrations will be far lower than in extensive metabolizers, requiring a dose increase
B) CYP2D6 status has no effect on haloperidol; only smoking-induced CYP1A2 changes matter for this drug
C) The patient will convert haloperidol entirely to an inactive metabolite, abolishing its effect
D) Poor-metabolizer status accelerates elimination, shortening the half-life and reducing side effects
E) Plasma haloperidol concentrations will be roughly two to three times higher than in extensive metabolizers at the same dose, with proportionally increased extrapyramidal and other adverse effects
ANSWER: E
Rationale:
Poor metabolizers at CYP2D6 clear haloperidol and perphenazine slowly, so at a given dose they reach plasma concentrations roughly two to three times higher than extensive metabolizers, with proportionally greater extrapyramidal and other adverse effects — exactly the unexpectedly high side-effect burden described.
Option A: Option A is incorrect because poor metabolism raises rather than lowers concentrations, so a dose increase would worsen toxicity.
Option B: Option B is incorrect because CYP2D6 is specifically relevant to haloperidol and perphenazine; the smoking-CYP1A2 interaction applies chiefly to chlorpromazine, clozapine, and olanzapine.
Option C: Option C is incorrect because impaired CYP2D6 activity reduces metabolism rather than driving complete conversion to an inactive metabolite.
Option D: Option D is incorrect because poor-metabolizer status slows elimination and prolongs exposure, increasing rather than reducing adverse effects.
13. Cigarette smoking strongly induces the liver enzyme CYP1A2, which metabolizes chlorpromazine and is even more important for clozapine and olanzapine. A patient stabilized on a CYP1A2-metabolized antipsychotic is admitted to a smoke-free inpatient unit and abruptly stops smoking. What change should the clinician anticipate?
A) No change, because CYP1A2 induction by smoking is clinically negligible
B) A fall in plasma drug concentration as the enzyme remains maximally induced
C) A rise in plasma drug concentration, because loss of enzyme induction slows metabolism, potentially producing toxicity unless the dose is adjusted
D) Conversion of the antipsychotic into a more potent active metabolite, enhancing efficacy without risk
E) Accelerated renal elimination of the drug, lowering its concentration
ANSWER: C
Rationale:
Smoking induces CYP1A2, so heavy smokers metabolize CYP1A2-substrate antipsychotics faster and run lower plasma levels; when a patient stops smoking on a smoke-free unit, the induction is lost over days, metabolism slows, and plasma concentrations rise, which can produce toxicity unless the dose is reduced.
Option A: Option A is incorrect because the smoking-CYP1A2 interaction is substantial, reducing levels of these substrates by roughly 30 to 50 percent in heavy smokers.
Option B: Option B is incorrect because stopping smoking removes the inducer, so the enzyme activity falls and levels rise rather than fall.
Option D: Option D is incorrect because loss of induction slows breakdown rather than generating a more potent metabolite.
Option E: Option E is incorrect because the interaction operates through hepatic enzyme induction, not renal elimination.
14. Which statement about haloperidol decanoate, the long-acting injectable (depot) formulation of haloperidol, is most accurate?
A) It alters the underlying receptor-binding profile of haloperidol, so a patient who had extrapyramidal symptoms on the oral form will not experience them on the depot
B) It is administered approximately every four weeks, reaches steady-state plasma concentrations only after about three to four months of monthly injections, and produces a smaller peak-to-trough fluctuation than oral dosing, but does not change the drug's receptor profile or adverse-effect type
C) It reaches steady state within 48 hours of the first injection, allowing immediate dose finalization
D) It is water-soluble and rapidly absorbed, producing peak levels within minutes like the intramuscular lactate form
E) It eliminates the need for any dose optimization because the depot guarantees a fixed therapeutic level in all patients
ANSWER: B
Rationale:
Haloperidol decanoate is an oil-based depot given roughly every four weeks; because it is released slowly from the injection site, steady-state plasma concentrations are reached only after about three to four months of monthly injections, and the peak-to-trough fluctuation is smaller than with oral dosing, giving more stable exposure. Crucially, the depot changes only the delivery kinetics, not the drug's receptor-binding profile or adverse-effect type.
Option A: Option A is incorrect because the depot does not alter the receptor profile, so a patient prone to extrapyramidal symptoms on oral haloperidol remains prone to them on the depot at equivalent exposure.
Option C: Option C is incorrect because steady state takes months, not 48 hours, which is why oral tolerability is established first.
Option D: Option D is incorrect because the decanoate ester is lipophilic and slowly absorbed, unlike the rapidly absorbed intramuscular lactate.
Option E: Option E is incorrect because careful dose optimization is still required, and the long washout makes dose-related adverse effects slower to resolve.
15. Several first-generation antipsychotics have indications beyond schizophrenia in which their dopamine-blocking action is directly therapeutic. Which pairing of agent to non-schizophrenia indication is correct?
A) Chlorpromazine is the agent of choice for suppressing motor tics in Tourette syndrome
B) Thioridazine is first-line for chemotherapy-induced nausea because of its favorable cardiac profile
C) Fluphenazine decanoate is used for procedural sedation and postoperative nausea at sub-antipsychotic doses
D) Low-dose haloperidol or pimozide is used to suppress tics in Tourette syndrome, droperidol is used for procedural sedation and postoperative nausea and vomiting at sub-antipsychotic doses, and prochlorperazine and promethazine are used as antiemetics through dopamine blockade in the chemoreceptor trigger zone
E) Molindone is the standard antiemetic in emergency medicine because of its strong action at the chemoreceptor trigger zone
ANSWER: D
Rationale:
Several first-generation agents have dopamine-mediated indications beyond schizophrenia: low-dose haloperidol or pimozide (a highly D2-selective diphenylbutylpiperidine) suppresses tics in Tourette syndrome; droperidol, a short-acting butyrophenone, is used for procedural sedation and postoperative nausea and vomiting at sub-antipsychotic doses; and prochlorperazine and promethazine act as antiemetics through dopamine blockade in the chemoreceptor trigger zone.
Option A: Option A is incorrect because haloperidol or pimozide, not chlorpromazine, are the agents used for Tourette tics.
Option B: Option B is incorrect because thioridazine has the worst cardiac profile in the class and is not an antiemetic of choice.
Option C: Option C is incorrect because fluphenazine decanoate is a maintenance depot for schizophrenia, not a procedural sedation or antiemetic agent.
Option E: Option E is incorrect because molindone is a niche antipsychotic noted for weight neutrality, not a standard antiemetic.
16. Each extrapyramidal syndrome and its related emergency has a characteristic first-line pharmacological treatment. Which option correctly matches every syndrome to its first-line agent?
A) Acute dystonia is treated with propranolol; akathisia with benztropine; neuroleptic malignant syndrome with a VMAT2 inhibitor; tardive dyskinesia with dantrolene
B) Acute dystonia is treated with a VMAT2 inhibitor; akathisia with dantrolene; neuroleptic malignant syndrome with diphenhydramine; tardive dyskinesia with propranolol
C) Acute dystonia is treated with dantrolene; akathisia with a VMAT2 inhibitor; neuroleptic malignant syndrome with propranolol; tardive dyskinesia with benztropine
D) All four are treated identically with an intramuscular anticholinergic, because they share a single mechanism
E) Acute dystonia is treated with an intramuscular anticholinergic or antihistamine (benztropine or diphenhydramine); akathisia with propranolol; neuroleptic malignant syndrome with discontinuation plus dantrolene and a dopamine agonist such as bromocriptine; tardive dyskinesia with a VMAT2 inhibitor such as valbenazine
ANSWER: E
Rationale:
The first-line treatments differ by syndrome: acute dystonia responds rapidly to an intramuscular anticholinergic or antihistamine such as benztropine or diphenhydramine; akathisia is best treated with propranolol after considering dose reduction; neuroleptic malignant syndrome requires discontinuation of the antipsychotic with supportive care plus dantrolene to reduce rigidity and a dopamine agonist such as bromocriptine to restore dopaminergic tone; and tardive dyskinesia is treated with a VMAT2 inhibitor such as valbenazine.
Option A: Option A is incorrect because it scrambles the matches, assigning propranolol to dystonia and dantrolene to tardive dyskinesia.
Option B: Option B is incorrect because it misassigns a VMAT2 inhibitor to acute dystonia and propranolol to tardive dyskinesia.
Option C: Option C is incorrect because it misassigns dantrolene to dystonia and propranolol to neuroleptic malignant syndrome.
Option D: Option D is incorrect because the four syndromes have distinct mechanisms and are not treated identically; anticholinergics in particular can worsen tardive dyskinesia.
This Web-based pharmacology and disease-based integrated teaching site is based on reference materials that are believed reliable and consistent with standards accepted at the time of development.
Possibility of error and on-going research and development in medical sciences do not allow assurance that the information contained herein is in every respect accurate or complete.
Users should confirm the information contained herein with other sources.
This site should only be considered as a teaching aid for undergraduate and graduate biomedical education and is intended only as a teaching site.
Information contained here should not be used for patient management and should not be used as a substitute for consultation with practicing medical professionals.
Users of this website should check the product information sheet included in the package of any drug they plan to administer to be certain that the information contained in this site is accurate and that changes have not been made in the recommended dose or in the contraindications for administration.
Medical or other information thus obtained should not be used as a substitute for consultation with practicing medical or scientific or other professionals.