Pharmacology USMLE Practice Questions
Drug mechanisms, interactions, and clinical applications.
5 free pharmacology practice questions
Pick an answer and check it. After each question you get the same explanation StepGenie students see: the stem decoded clue by clue, the reasoning chain with its infographic, why every wrong option is wrong, and the trap the question was built around. Step 1 questions test mechanism; Step 2 CK questions ask for the next step.
A 58-year-old man presents with a 6-month history of depressed mood, poor concentration at work, daytime sleepiness, and fatigue. He reports early-morning awakening with difficulty returning to sleep, loss of interest in previously enjoyable activities such as fishing with his son, decreased appetite, and an unintentional 5-kg (11-lb) weight loss during this period. He denies suicidal ideation. He has no significant past medical history and takes no medications. He drinks several alcoholic beverages on weekends and lives with his girlfriend. He is diagnosed with major depressive disorder, and initiation of sertraline therapy is recommended. This patient is at greatest risk for which of the following adverse effects?
Correct answer · C
Delayed ejaculation
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Clinical picture (depressed mood, anhedonia, sleep/appetite changes, >2 weeks) → Major depressive disorder diagnosis.
Step 2 of 5
MDD first-line pharmacologic treatment → SSRIs such as sertraline due to safety and tolerability profile.
Step 3 of 5
SSRIs increase synaptic serotonin by blocking its reuptake, improving mood over several weeks.
Step 4 of 5
Increased serotonergic activity in spinal cord sexual pathways frequently → sexual dysfunction (delayed ejaculation, anorgasmia, decreased libido).
Step 5 of 5
Among given options, the classic SSRI adverse effect is delayed ejaculation, making this the greatest risk for this patient starting sertraline.
Why not the others?
A. Postural hypotension
This option implies alpha-1 blockade, typical of tricyclic antidepressants and some antipsychotics, BUT SSRIs like sertraline have minimal effect on vascular alpha receptors.
B. Serotonin syndrome
This option implies excess serotonergic activity, usually from drug interactions (SSRI + MAOI, linezolid, triptans), BUT this patient is starting monotherapy with no interacting meds mentioned.
D. Urinary retention
This option implies anticholinergic effects, classically from TCAs or antihistamines, BUT SSRIs have very little anticholinergic activity and rarely cause significant urinary retention.
E. Increased suicidality
This option reflects the black-box warning in children/young adults starting antidepressants, BUT this patient is 58 years old, where this risk is not significantly increased.
F. Hypertensive crisis
This option implies tyramine reaction in patients on MAOIs who eat aged cheeses/wine, BUT sertraline is an SSRI and does not cause this interaction.
G. Priapism
This option implies alpha-1 blockade effect seen with trazodone, BUT sertraline is not known for priapism; its main sexual effect is delayed ejaculation/anorgasmia.
Exam trap
Students may overfocus on the well-known antidepressant suicidality warning and pick increased suicidality, but age >25 and classic SSRI sexual dysfunction point to delayed ejaculation instead.
The bottom line
SSRIs (eg, sertraline) commonly cause sexual dysfunction (delayed ejaculation, anorgasmia, ↓libido) in patients treated for major depressive disorder.
A 32-year-old woman presents to the emergency department with a 3-hour history of severe nausea, vomiting, tremor, and anxiety. She recently began taking a new medication but cannot recall its name. Her medical history is significant for major depressive disorder treated with fluoxetine. Her temperature is 38.9°C (102.1°F), pulse is 132/min, respirations are 22/min, and blood pressure is 152/94 mm Hg. She appears confused and diaphoretic. Neurologic examination reveals an ataxic gait and markedly hyperactive (4+) patellar reflexes bilaterally. This patient's condition is most likely due to which of the following medications?
Correct answer · B
Sumatriptan
Decoding the stem
Step-by-step reasoning
Step 1 of 6
Patient is on chronic fluoxetine, an SSRI that increases synaptic serotonin by blocking reuptake.
Step 2 of 6
She recently started a new medication and now acutely develops fever, confusion, autonomic instability, tremor, and marked hyperreflexia.
Step 3 of 6
The triad of mental status changes, autonomic hyperactivity, and neuromuscular hyperactivity (hyperreflexia, clonus, ataxia) is characteristic of serotonin syndrome.
Step 4 of 6
Serotonin syndrome is commonly triggered by combining multiple serotonergic agents (e.g., SSRIs with MAOIs, linezolid, tramadol, or triptans).
Step 5 of 6
Sumatriptan is a 5-HT1B/1D agonist used for migraine; when combined with an SSRI like fluoxetine, it can precipitate serotonin syndrome.
Step 6 of 6
Other listed drugs do not significantly increase central serotonin and would not explain the specific triad of findings.
Why not the others?
A. Amiodarone
This option implies class III antiarrhythmic toxicity, which causes thyroid dysfunction, pulmonary fibrosis, liver toxicity, and skin changes, BUT it does not cause acute hyperthermia, hyperreflexia, and neuromuscular hyperactivity in the context of SSRI use.
C. Scopolamine
This option implies anticholinergic toxicity (dry skin, mydriasis, urinary retention, decreased bowel sounds), BUT this patient is diaphoretic, hyperreflexic, and febrile with SSRI use—more consistent with serotonin syndrome than anticholinergic syndrome.
D. Haloperidol
This option implies neuroleptic malignant syndrome (rigidity, bradyreflexia, lead-pipe tone, very high CK), BUT the hallmark here is hyperreflexia and clonus, not rigidity; also no history of antipsychotic initiation.
E. Succinylcholine
This option implies depolarizing neuromuscular blocker toxicity (hyperkalemia, malignant hyperthermia with certain anesthetics), BUT there is no perioperative setting, muscle rigidity, or exposure to anesthesia agents; and it does not cause the classic serotonin triad with SSRI use.
Exam trap
The high fever and confusion may push you toward NMS or malignant hyperthermia, but the question hinges on hyperreflexia/clonus + SSRI + new serotonergic drug (triptan) → serotonin syndrome.
The bottom line
Serotonin syndrome: serotonergic drug (triptan) added to SSRI (fluoxetine) → hyperthermia, agitation, hyperreflexia, clonus, autonomic instability.
A 43-year-old woman presents with a 2-week history of new, intensely pruritic plaques on her scalp and on the extensor surfaces of her elbows and knees. She was diagnosed with psoriasis 10 years ago and has been using topical calcipotriene as her only medication. Physical examination reveals well-demarcated, symmetrical, erythematous plaques with overlying silvery scale and nail pitting on all fingers. She is started on a high-potency topical medication that inhibits NF-κB and phospholipase A2. Long-term use of this agent is most likely to result in which of the following adverse effects?
Correct answer · D
Dermal collagen loss
Decoding the stem
Step-by-step reasoning
Step 1 of 5
The patient has classic plaque psoriasis (extensor plaques, silvery scale, nail pitting).
Step 2 of 5
Treatment escalation from calcipotriene to a high-potency topical agent suggests a strong topical corticosteroid.
Step 3 of 5
Corticosteroids inhibit NF-κB and phospholipase A2, decreasing inflammatory cytokines and eicosanoid synthesis → anti-inflammatory effect.
Step 4 of 5
Chronically, steroids decrease fibroblast activity and collagen synthesis in the dermis.
Step 5 of 5
Loss of dermal collagen causes skin atrophy: thinning, striae, telangiectasias, easy bruising → due to dermal collagen loss.
Why not the others?
A. Dysplastic nevi
This option implies atypical melanocytic lesions with melanoma risk, which are related to UV exposure and genetics, BUT topical steroids do not induce dysplastic nevi formation.
B. Nonblanchable pinpoint macules
This option implies petechiae from platelet disorders or vascular fragility, BUT while steroids can thin skin, they classically cause atrophy and striae, not isolated petechiae as the main chronic adverse effect tested here.
C. Decreased sebum production
This option implies effects on sebaceous glands (e.g., isotretinoin), which reduces sebum, BUT topical corticosteroids mainly affect dermal collagen and epidermal thickness, not sebum output.
E. Hair growth on upper lip
This option implies hirsutism from systemic androgen or corticosteroid excess, BUT localized high-potency topical steroids are more associated with local skin atrophy than prominent facial hirsutism as the key exam-tested toxicity.
Exam trap
The stem emphasizes NF-κB and PLA2 inhibition, tempting recall of systemic steroid side effects; the exam instead targets the classic local effect of chronic topical steroids—skin atrophy from dermal collagen loss.
The bottom line
Chronic high-potency topical corticosteroids inhibit NF-κB and PLA2, causing skin atrophy from dermal collagen loss and striae, especially on thin skin.
A 63-year-old man presents with a 4-hour history of severe right knee pain. He reports progressive swelling and difficulty moving the joint due to pain. His temperature is 38.0°C (100.1°F). Examination shows an erythematous, edematous, and warm right knee with markedly limited range of motion secondary to pain. Arthrocentesis yields cloudy synovial fluid with a leukocyte count of 24,000/mm³ (74% segmented neutrophils). Polarized light microscopy reveals needle-shaped, negatively birefringent crystals. Five hours after initiation of therapy, he develops abdominal cramping, diarrhea, and vomiting. The patient was most likely treated with a drug that predominantly acts on which of the following parts of the cell?
Correct answer · D
Cytoskeleton
Decoding the stem
Step-by-step reasoning
Step 1 of 7
The hot, swollen, erythematous knee with severe pain and limited motion indicates an acute inflammatory monoarthritis.
Step 2 of 7
Synovial fluid shows 24,000 WBCs/mm³ with neutrophil predominance, indicating an inflammatory rather than purely septic process (often >50,000 in septic arthritis).
Step 3 of 7
Polarized light microscopy demonstrating needle-shaped, negatively birefringent crystals confirms gout due to monosodium urate deposition.
Step 4 of 7
Acute gout is treated first-line with NSAIDs; colchicine is a classic alternative/adjunct, especially tested pharmacologically.
Step 5 of 7
Colchicine inhibits microtubule polymerization in leukocytes, disrupting the cytoskeleton and impairing neutrophil chemotaxis and phagocytosis.
Step 6 of 7
Microtubule disruption in rapidly renewing GI cells explains the abdominal cramping, diarrhea, and vomiting soon after therapy.
Step 7 of 7
Therefore, the drug used predominantly acts on the cytoskeleton.
Why not the others?
A. Cell wall
This option implies cell wall–active antibiotics (e.g., beta-lactams, vancomycin), which treat septic arthritis, BUT the crystal findings and classic GI toxicity point to gout treated with colchicine, not infection.
B. Cytosolic enzyme
This option implies drugs like allopurinol or febuxostat (xanthine oxidase inhibitors), which lower uric acid chronically, BUT they are not used for acute gout flares and do not classically cause acute severe GI symptoms within hours.
C. Nucleus
This suggests drugs acting on DNA/RNA synthesis (e.g., methotrexate, azathioprine, glucocorticoid receptor in nucleus). Steroids can treat gout, BUT the question highlights the classic microtubule and GI profile of colchicine instead.
E. Membrane transporter
This implies drugs like probenecid (uricosuric), which inhibit renal tubular transporters to increase uric acid excretion, BUT those are for chronic management and not associated with rapid-onset GI toxicity as emphasized here.
Exam trap
The stem clearly shows gout; many students jump to chronic urate-lowering mechanisms. The key is the acute GI side effects, which specifically point to colchicine’s microtubule (cytoskeleton) inhibition, not xanthine oxidase or uricosurics.
The bottom line
Acute gout treated with colchicine, which inhibits microtubule polymerization in the cytoskeleton, causing GI side effects (abdominal cramping, diarrhea, vomiting).
A 54-year-old man comes to the physician for follow-up one week after being treated in the emergency department for chest pain, palpitations, and dyspnea. As part of his management, he was started on a medication that irreversibly inhibits the synthesis of thromboxane A2 and prostaglandins. Which of the following is the most likely adverse effect of this medication?
Correct answer · E
Gastrointestinal hemorrhage
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Irreversible inhibition of TXA2 and prostaglandins = aspirin, which acetylates and irreversibly inhibits COX-1 and COX-2.
Step 2 of 5
In platelets, COX-1 inhibition → ↓TXA2 → ↓platelet aggregation → antithrombotic effect (used in chest pain/ACS).
Step 3 of 5
In GI mucosa, COX-1–derived prostaglandins usually promote mucus and bicarbonate secretion and maintain mucosal blood flow.
Step 4 of 5
Aspirin’s COX-1 inhibition → ↓protective prostaglandins in stomach/duodenum → mucosal injury and ulcer formation.
Step 5 of 5
Ulceration plus impaired platelet aggregation → increased risk of gastrointestinal hemorrhage.
Why not the others?
A. Chronic rhinosinusitis
This option implies chronic inflammatory sinonasal disease, which is not a classic direct toxicity of aspirin. Aspirin can cause aspirin-exacerbated respiratory disease (asthma, nasal polyps, eosinophilia), BUT the stem focuses on the medication’s COX inhibition and most common serious adverse effect, which is GI bleeding, not isolated chronic rhinosinusitis.
B. Acute interstitial nephritis
This option implies an idiosyncratic hypersensitivity reaction to NSAIDs, which can occur, BUT at low, cardioprotective aspirin doses in a short course for chest pain, the most tested and likely adverse effect is GI bleeding due to prostaglandin inhibition and platelet dysfunction.
C. Gout attack
This option implies low-dose aspirin inhibiting uric acid secretion and precipitating gout, BUT the question emphasizes irreversible TXA2/PG inhibition and asks the most likely adverse effect—GI bleeding is far more common and high-yield than gout flares in this context.
D. Tinnitus
This option implies salicylate toxicity (often at higher doses) causing tinnitus, vertigo, and potential respiratory alkalosis/metabolic acidosis, BUT the vignette suggests standard post–chest pain aspirin dosing, where GI hemorrhage is the most relevant and common adverse effect.
F. Hepatic encephalopathy
This option implies severe liver failure with ammonia buildup, which is not a typical aspirin toxicity. Aspirin can cause Reye syndrome in children with viral illness, BUT in this adult man treated for chest pain, the key and most likely adverse effect is GI bleeding, not liver failure leading to encephalopathy.
Exam trap
The stem never says “aspirin,” only describes its mechanism (irreversible TXA2/PG inhibition). If you don’t first identify aspirin, you might scan for generic NSAID or unrelated toxicities instead of the classic GI hemorrhage risk from COX-1 inhibition in platelets and gastric mucosa.
The bottom line
Aspirin irreversibly inhibits COX → ↓TXA2/PGs, impairing platelet aggregation and mucosal protection, causing GI bleeding as a key adverse effect.
Source: StepGenie question bank. Questions are written by StepGenie, not taken from NBME or USMLE materials, and are chosen for this page by how students actually performed on them (first-attempt accuracy on StepGenie). Selection last refreshed September 5, 2026.
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Are the pharmacology practice questions on this page free?
Yes. The 5 questions above come from StepGenie's question bank and can be answered here without an account, with the full explanation shown after each one. From the link under the set you can try three more Pharmacology questions in the dashboard preview, also without an account; a free account is what lets you choose the system and keep going.