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Pharmacology — Step 1 practice questions
268 questions in this area, with an explanation for every answer choice.
Three samples below, free and without an account.
How this shows up on Step 1
Pharmacology is examined as mechanism, effect and adverse effect, rarely as dosing. Drugs appear in clinical vignettes, so recognising the class from its consequences matters more than recalling a list. Autonomic pharmacology underlies a surprising number of questions across every system.
Sample questions
Sample question 1
A patient with metastatic melanoma harboring a BRAF V600E mutation is considered for targeted therapy. Which of the following best describes the rationale for combining a BRAF inhibitor with a MEK inhibitor?
Explanations
A. MEK inhibitors act on an unrelated pathway with additive toxicity only
MEK lies immediately downstream of BRAF in the same pathway.
B. The combination eliminates the need for any monitoring
Monitoring for toxicity and resistance remains essential.
C. BRAF inhibition is only effective in melanomas lacking the V600E mutation
Efficacy requires the activating mutation.
D. Combined blockade at two points in the MAP kinase pathway improves response duration and reduces paradoxical pathway activation causing secondary squamous cell carcinomas · correct
BRAF V600E constitutively activates the MAP kinase pathway (RAS-RAF-MEK-ERK) driving proliferation in roughly half of cutaneous melanomas. BRAF inhibitors such as vemurafenib produce rapid responses but resistance emerges quickly, and paradoxical pathway activation in BRAF-wild-type cells causes secondary squamous cell carcinomas and keratoacanthomas. Adding a MEK inhibitor blocks the pathway downstream, improving response duration and REDUCING those secondary lesions. Checkpoint inhibitors are the other pillar of advanced melanoma treatment.
E. BRAF inhibitors are effective regardless of BRAF mutation status
BRAF inhibitors require the mutation and can be harmful without it.
Sample question 2
A 25-year-old has a first generalized tonic-clonic seizure with a normal neurologic examination, normal MRI, normal EEG, and no provoking factors. Which of the following is the most appropriate management?
Explanations
A. Begin two antiepileptic drugs to maximize protection
Monotherapy is standard when treatment is indicated.
B. No counseling or follow-up is needed
Safety counseling is essential.
C. Begin lifelong antiepileptic therapy in all patients after a first seizure
Treatment is individualized rather than universal after one seizure.
D. Recommend permanent driving prohibition regardless of jurisdiction
Restrictions are typically time-limited and jurisdiction-specific.
E. Counsel about driving and safety precautions, and generally defer antiepileptic therapy after a single unprovoked seizure with normal workup, since recurrence risk is relatively low · correct
After a FIRST unprovoked seizure with a normal examination, imaging, and EEG, recurrence risk is roughly 30–40%, and treatment reduces short-term recurrence without improving long-term seizure-free outcomes — so therapy is often deferred with shared decision-making. Treatment is favored when recurrence risk is high: an epileptiform EEG, structural lesion on imaging, nocturnal seizure, or abnormal examination. All patients require counseling about driving restrictions per local law, swimming, bathing, heights, and sleep and alcohol as triggers.
Sample question 3
A patient with prostate cancer is started on continuous leuprolide (a GnRH agonist) therapy. Which of the following best explains why this suppresses testosterone despite GnRH normally stimulating gonadotropin release?
Explanations
A. Leuprolide has no effect on the HPG axis
Leuprolide has a significant, well-established effect on the HPG axis, which is precisely its therapeutic mechanism.
B. Leuprolide destroys the testes directly
Leuprolide does not directly destroy testicular tissue; it works via central suppression of the HPG axis.
C. Leuprolide only works when given in a pulsatile fashion, identical to normal physiology
The therapeutic effect specifically relies on CONTINUOUS (non-pulsatile) administration, the opposite of normal physiologic pulsatile GnRH release.
D. Leuprolide directly blocks the androgen receptor
This describes androgen receptor antagonists (e.g., bicalutamide), a different drug class, not the primary mechanism of leuprolide.
E. Continuous, non-pulsatile GnRH receptor stimulation causes receptor downregulation and desensitization, ultimately suppressing FSH/LH and testosterone · correct
Continuous (non-pulsatile) GnRH agonist exposure, unlike the body's normal pulsatile GnRH release, causes downregulation and desensitization of pituitary GnRH receptors, paradoxically suppressing FSH/LH release and consequently testosterone production over time (after an initial transient "flare").
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