USMLE Step 1 Pharmacology Questions with Answers (87 High-Yield MCQs)

These 87 USMLE Step 1 pharmacology practice questions cover the drug mechanisms, side effects and interactions that appear again and again on the exam. They are organized by organ system so you can study one topic at a time. Every question includes the correct answer and a short explanation.

Written by Dr. Ray Makar, MD, author of the Repeated USMLE Questions eBook series.

Prefer video? Watch daily USMLE case questions on MedFocus by Dr. Ray on YouTube.

How to use this page: read the question, pick your answer, then click Show Answer and Explanation. Read the explanation even when you are right — repeated question types are common on the real exam.

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Cardiovascular and Hematology Drugs

Question 1. A patient with heart failure is prescribed a drug that inhibits the Na⁺/K⁺-ATPase pump, increasing intracellular calcium in cardiac myocytes. Which one of the following drugs is most likely responsible?

A- Amiodarone
B- Digoxin
C- Diltiazem
D- Verapamil

B- Digoxin- Digoxin inhibits the Na⁺/K⁺-ATPase pump, increasing intracellular sodium. This reduces Na⁺/Ca²⁺ exchange, leading to increased intracellular calcium and stronger cardiac contraction (positive inotropy).

 

Question 2. A patient taking an ACE inhibitor has developed a persistent cough. Which one of the following mediators is most responsible for this complaint?

A- Bradykinin
B- Histamine
C- Leukotriene B4
D- Serotonin

A- Bradykinin- ACE inhibitors such as lisinopril reduce the breakdown of bradykinin, resulting in its accumulation. Elevated bradykinin contributes to dry cough and, in rare cases, angioedema.

 

Question 3. A patient treated for severe hypertension develops lupus-like syndrome, reflex tachycardia, and fluid retention. Which mechanism best describes his medication?

A- Alpha-1 receptor blockade
B- Calcium channel blockade
C- Direct arteriolar vasodilation
D- Muscarinic antagonism

C- Direct arteriolar vasodilation- Lupus-like syndrome, reflex tachycardia, and fluid retention are classic adverse effects of hydralazine. It directly relaxes the arteriolar smooth muscle, reducing afterload. Hydralazine is a favorite USMLE clue. 📘 Want More Pharmacology Practice? Continue practicing with 300 Pharmacology MCQs for Medical and Pharmacy Students by Dr. Ray Makar. Each question includes the correct answer and a concise explanation. 📘 Get 300 Pharmacology MCQs on Amazon

 

Question 4. A patient with chronic angina is treated with ranolazine. What is the primary mechanism responsible for its antianginal effect?

A- Decreased heart rate via beta blockade
B- Inhibition of late sodium current in cardiac cells
C- Increased coronary artery dilation
D- Stimulation of nitric oxide release

B- Inhibition of late sodium current in cardiac cells – Ranolazine blocks the late inward sodium current in cardiac myocytes, reducing intracellular calcium overload and improving myocardial relaxation and oxygen efficiency.

 

Question 5. A patient with atrial fibrillation is treated with dofetilide. Which electrophysiologic effect explains the antiarrhythmic action of this drug?

A- Decreased phase 0 depolarization
B- Increased refractory period by potassium channel blockade
C- Inhibition of calcium influx in AV node
D- Sodium channel blockade during depolarization

B- Increased refractory period by potassium channel blockade- Dofetilide is a Class III antiarrhythmic that blocks delayed rectifier potassium channels, prolonging repolarization and the action potential duration, which increases the refractory period and prevents reentry arrhythmias.

 

Question 6. A patient treated with verapamil develops constipation and bradycardia. What class of drug does verapamil belong to?

A- Beta-blockers
B- Calcium channel blockers
C- Potassium channel blockers
D- Sodium channel blockers

B- Calcium channel blockers- Verapamil blocks L-type calcium channels, decreasing cardiac conduction and contractility while also relaxing vascular smooth muscle.

 

Question 7. Thiazide diuretics increase digoxin toxicity primarily through which electrolyte disturbance?

A- Hypercalcemia
B- Hyponatremia
C- Hypomagnesemia
D- Hypokalemia

D- Hypokalemia- Potassium competes with digoxin for the same binding site on Na+/K+-ATPase. Thiazide-induced hypokalemia reduces this competition, allowing digoxin to bind more effectively and worsening toxicity.

 

Question 8. A patient treated with a nonselective beta blocker develops hypoglycemia that is difficult to recognize. What explains the masking of hypoglycemia symptoms?

A- Alpha receptor blockade
B- Beta-1 receptor stimulation
C- Beta-2 receptor blockade
D- Muscarinic receptor blockade

C- Beta-2 receptor blockade- Nonselective beta blockers inhibit β₂-mediated glycogenolysis and mask adrenergic warning symptoms like tachycardia, making hypoglycemia harder to detect.

 

Question 9. A patient with hypertension is treated with clonidine. What is the primary mechanism by which this drug lowers blood pressure?

A- Alpha-1 receptor blockade
B- Central alpha-2 receptor stimulation
C- Inhibition of angiotensin II receptors
D- Sodium channel blockade

B- Central alpha-2 receptor stimulation- Clonidine activates α₂ receptors in the brainstem, reducing sympathetic outflow and lowering peripheral vascular resistance and blood pressure.

 

Question 10. A patient who is taking a high dose of niacin for hyperlipidemia develops hyperglycemia. What explains this effect?

A- Decreased insulin secretion
B- Decreased peripheral glucose uptake
C- Increased hepatic gluconeogenesis
D- Increased pancreatic glucagon release

C- Increased hepatic gluconeogenesis- Niacin can impair glucose tolerance by increasing hepatic glucose production and reducing insulin sensitivity, leading to hyperglycemia.

 

Question 11. A patient with heart failure is started on sacubitril/valsartan. What is the primary pharmacologic action of sacubitril?

A- Angiotensin II receptor blockade
B- Inhibition of neprilysin
C- Inhibition of renin release
D- Stimulation of natriuretic peptide receptors

B- Inhibition of neprilysin- Sacubitril inhibits neprilysin, the enzyme that degrades natriuretic peptides, leading to increased vasodilation, natriuresis, and reduced cardiac remodeling. It is combined with valsartan to block RAAS activation.

 

Question 12. A patient with atrial fibrillation is prescribed sotalol. Which additional pharmacologic property does this drug possess?

A- Alpha-1 blockade
B- Beta-adrenergic blockade
C- Calcium channel blockade
D- Sodium channel blockade

B- Beta-adrenergic blockade- Sotalol is both a nonselective beta blocker and a Class III antiarrhythmic that prolongs repolarization by blocking potassium channels.

 

Question 13. A patient taking warfarin is given vitamin K. What is the primary effect of vitamin K administration?

A- Decreases synthesis of clotting factors II, VII, IX, X
B- Increases synthesis of clotting factors II, VII, IX, X
C- Inhibits platelet aggregation
D- Prevents fibrin degradation

B- Increases synthesis of clotting factors II, VII, IX, X- Vitamin K reverses warfarin by restoring gamma-carboxylation of vitamin K–dependent clotting factors.

 

Question 14. A patient receiving heparin develops thrombocytopenia and thrombosis. What is the underlying mechanism?

A- Antibody formation against heparin–platelet factor 4 complex
B- Bone marrow suppression
C- Direct platelet destruction by heparin
D- Inhibition of platelet cyclooxygenase

A- Antibody formation against heparin–platelet factor 4 complex – HIT is immune-mediated and paradoxically causes thrombosis despite low platelets.

 

Question 15. A patient with asthma is prescribed propranolol and develops worsening shortness of breath. What explains this effect?

A- Alpha-1 receptor blockade
B- Beta-1 receptor stimulation
C- Beta-2 receptor blockade
D- Muscarinic receptor activation

C- Beta-2 receptor blockade- Nonselective beta blockers like propranolol block β₂ receptors in the lungs, causing bronchoconstriction in asthmatic patients.

 

Question 16. Which medication reduces platelet aggregation by irreversibly inhibiting cyclooxygenase (COX)?

A- Aspirin
B- Clopidogrel
C- Dipyridamole
D- Warfarin

A- Aspirin- Aspirin irreversibly inhibits COX-1, decreasing thromboxane A₂ synthesis and platelet aggregation for the life of the platelet.

 

Question 17. A patient with heart failure is started on an ACE inhibitor. Which physiologic change contributes to its beneficial effect?

A- Decreased aldosterone secretion
B- Decreased heart rate
C- Increased preload
D- Increased sympathetic tone

A- Decreased aldosterone secretion- ACE inhibitors reduce angiotensin II and aldosterone, leading to decreased sodium and water retention and improved cardiac remodeling.

 

Question 18. Which antiarrhythmic drug is classified as a Class III agent?

A- Amiodarone
B- Lidocaine
C- Propranolol
D- Verapamil

A- Amiodarone- Class III antiarrhythmics block potassium channels, prolonging repolarization and action potential duration, making them effective in treating both atrial and ventricular arrhythmias.

 

Question 19. A patient with hyperlipidemia is prescribed ezetimibe. What is the primary mechanism of action of this drug?

A- Decreased bile acid reabsorption
B- Increased lipoprotein lipase activity
C- Inhibition of cholesterol synthesis
D- Inhibition of intestinal cholesterol absorption

D- Inhibition of intestinal cholesterol absorption- Ezetimibe blocks the NPC1L1 transporter in the small intestine, reducing dietary and biliary cholesterol absorption.

 

Question 20. A patient receiving heparin therapy develops a sudden drop in platelet count. What is the underlying mechanism?

A- Bone marrow suppression
B- Decreased platelet production
C- Direct platelet toxicity
D- Immune-mediated platelet activation

D- Immune-mediated platelet activation- Heparin-induced thrombocytopenia (HIT) is caused by antibodies against heparin–platelet factor 4 complexes, leading to thrombosis despite low platelets.

 

Question 21. A 60-year-old man with benign prostatic hyperplasia (BPH) and hypertension is prescribed terazosin. Which of the following adverse effects should he be warned about?

A- constipation
B- Orthostatic hypotension
C- Reflex bradycardia
D- Sedation

B- Orthostatic hypotension- α₁-blockers like terazosin cause relaxation of vascular smooth muscle, leading to postural hypotension, especially after the first dose.

 

Question 22. A 26-year-old man presents with muscle pain and dark urine after starting simvastatin. Which enzyme system metabolizes this drug?

A- CYP1A2
B- CYP2C9
C- CYP2D6
D- CYP3A4

D- CYP3A4- Most statins (like simvastatin) are metabolized by CYP3A4; inhibitors (e.g., macrolides, azoles) increase toxicity risk, such as myopathy and rhabdomyolysis.

 

Question 23. A 55-year-old man with atrial fibrillation is taking warfarin. He is started on trimethoprim-sulfamethoxazole for a urinary tract infection. What is the most likely outcome of this drug interaction?

A- Decreased anticoagulant effect
B- Enhanced metabolism of warfarin
C- Increased risk of bleeding
D- No significant effect

C- Increased risk of bleeding- Sulfonamides inhibit warfarin metabolism (CYP2C9 inhibition), leading to higher plasma levels and increased bleeding risk.

 

Question 24. A 60-year-old man with atrial fibrillation is started on amiodarone. Which adverse effect is most commonly associated with this medication?

A- Hyperkalemia
B- Hypoglycemia
C- Nephrotoxicity
D- Pulmonary fibrosis

D- Pulmonary fibrosis- Amiodarone can cause pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal deposits, and skin discoloration (“blue-gray”).

 

Question 25. A 28-year-old woman develops a dry cough after beginning treatment for hypertension. Which drug is most likely responsible?

A- Amlodipine
B- Lisinopril
C- Losartan
D- Propranolol

B- Lisinopril- ACE inhibitors (like lisinopril) cause a persistent dry cough due to increased bradykinin levels.

 

Question 26. A 60-year-old patient with chronic heart failure is started on digoxin. Which electrolyte imbalance increases the risk of digoxin toxicity?

A- Hyperkalemia
B- Hypocalcemia
C- Hypokalemia
D- Hyponatremia

C- Hypokalemia- Low potassium enhances digoxin binding to the Na⁺/K⁺-ATPase, increasing the risk of toxicity (arrhythmias, visual disturbances).

 

Question 27. A patient with atrial fibrillation is prescribed warfarin. Which of the following factors will increase the anticoagulant effect of warfarin?

A- Vitamin K deficiency
B- Rifampin therapy
C- Liver disease
D- Chronic alcohol use

C- Liver disease- Warfarin’s effect is enhanced when clotting factor synthesis is decreased, as seen in liver disease. Rifampin and chronic alcohol induce metabolism (decreasing effect), while vitamin K opposes warfarin’s action.

 

Antimicrobials

Question 28. A patient treated with amoxicillin develops a rash after taking the medication. What type of reaction is most likely?

A- Type I hypersensitivity
B- Type II hypersensitivity
C- Type III hypersensitivity
D- Type IV hypersensitivity

A- Type I hypersensitivity- Penicillin allergies commonly involve IgE-mediated reactions such as rash, urticaria, or anaphylaxis.

 

Question 29. A patient taking daptomycin for a resistant infection develops muscle pain and elevated creatine kinase levels. What is the mechanism of action of this drug?

A- Binds D-alanine in bacterial cell walls
B- Blocks bacterial DNA gyrase
C- Creates membrane pores causing depolarization
D- Inhibits bacterial ribosomal protein synthesis

C- Creates membrane pores causing depolarization – Daptomycin inserts into the bacterial cell membrane and forms pores, leading to potassium efflux, membrane depolarization, and rapid bacterial cell death.

 

Question 30. Isoniazid-induced peripheral neuropathy is caused by deficiency of which vitamin?

A- Vitamin B6
B- Vitamin B12
C- Vitamin B1
D- Folate

A- Vitamin B6- Isoniazid increases pyridoxine excretion and inhibits its activation, causing a functional B6 deficiency that leads to peripheral neuropathy. This is prevented by co-administering pyridoxine.

 

Question 31. A patient receiving trimethoprim-sulfamethoxazole develops megaloblastic anemia. Which mechanism explains this adverse effect?

A- Folate metabolism inhibition
B- Hemoglobin oxidation
C- Inhibition of erythropoietin synthesis
D- Vitamin B12 malabsorption

A- Folate metabolism inhibition- Trimethoprim inhibits dihydrofolate reductase, and sulfamethoxazole blocks dihydropteroate synthase, impairing folate metabolism and potentially causing megaloblastic anemia.

 

Question 32. A patient with tuberculosis treated with rifampin develops decreased effectiveness of multiple medications. What pharmacologic property of rifampin causes this effect?

A- CYP450 enzyme inhibition
B- CYP450 enzyme induction
C- Decreased intestinal absorption
D- Renal excretion competition

B- CYP450 enzyme induction- Rifampin strongly induces hepatic cytochrome P450 enzymes, accelerating metabolism of many drugs such as oral contraceptives, warfarin, and antiretrovirals.

 

Question 33. A patient treated with vancomycin develops acute kidney injury. Which concurrent medication increases this risk most significantly?

A- Amoxicillin
B- Azithromycin
C- Gentamicin
D- Metronidazole

C- Gentamicin- Both vancomycin and aminoglycosides are nephrotoxic; concurrent use significantly increases the risk of acute tubular injury.

 

Question 34. A patient taking linezolid develops thrombocytopenia after prolonged therapy. What is the underlying mechanism?

A- Direct platelet destruction
B- Immune complex deposition
C- Mitochondrial protein synthesis inhibition
D- Vitamin K antagonism

C- Mitochondrial protein synthesis inhibition- Linezolid inhibits the 50S ribosomal subunit but can also affect mitochondrial ribosomes, leading to bone marrow suppression and thrombocytopenia with long-term use.

 

Question 35. A patient treated with ciprofloxacin develops tendon pain and swelling. What is the most likely complication?

A- Achilles tendon rupture
B- Aplastic anemia
C- Cardiomyopathy
D- Hemolytic anemia

A- Achilles tendon rupture – Fluoroquinolones increase risk of tendinitis and tendon rupture, especially the Achilles tendon.

 

Question 36. Which medication is most likely to cause photosensitivity as a side effect?

A- Amoxicillin
B- Doxycycline
C- Erythromycin
D- Vancomycin

B- Doxycycline- Tetracyclines commonly cause photosensitivity reactions, leading to exaggerated sunburn.

 

Question 37. A patient treated with gentamicin develops renal impairment. What is the primary mechanism of this adverse effect?

A- Accumulation in proximal tubule cells
B- Acute interstitial nephritis
C- Decreased renal blood flow
D- Immune-mediated glomerulonephritis

A- Accumulation in proximal tubule cells- Aminoglycosides concentrate in proximal tubular epithelial cells, causing cellular damage and acute tubular necrosis, leading to nephrotoxicity.

 

Question 38. Which of the following antifungal medications inhibits ergosterol synthesis by blocking fungal cytochrome P450 enzymes?

A- Amphotericin B
B- Fluconazole
C- Flucytosine
D- Terbinafine

B- Fluconazole- Azoles inhibit fungal CYP450 enzymes, decreasing ergosterol synthesis and disrupting cell membrane integrity.

 

Question 39. A patient treated with erythromycin develops QT prolongation on ECG. What is the main mechanism behind this effect?

A- Beta-adrenergic blockade
B- Calcium channel inhibition
C- Potassium channel blockade
D- Sodium channel blockade

C- Potassium channel blockade- Macrolides like erythromycin block cardiac potassium channels, delaying repolarization and increasing the risk of QT prolongation and torsades de pointes

 

Question 40. A patient treated for latent tuberculosis develops elevated liver enzymes. Which drug is most likely responsible?

A- Cycloserine
B- Ethambutol
C- Isoniazid
D- Streptomycin

C- Isoniazid- Isoniazid commonly causes hepatotoxicity and peripheral neuropathy due to vitamin B6 deficiency.

 

Question 41. A 25-year-old woman is taking oral contraceptive pills (OCPs). Which antibiotic can decrease the effectiveness of her contraceptive therapy?

A- Amoxicillin
B- Azithromycin
C- Ciprofloxacin
D- Rifampin

D- Rifampin- Rifampin induces hepatic enzymes, increasing the metabolism of estrogen and progestin, thus reducing OCP efficacy.

 

Question 42. A 40-year-old man is treated with chloramphenicol for a severe infection. Later, he develops pancytopenia. What is the most likely mechanism of this adverse effect?

A- Immune-mediated hemolysis
B- Irreversible aplastic anemia
C- Megaloblastic anemia due to folate deficiency

B- Irreversible aplastic anemia- Chloramphenicol can cause idiosyncratic, irreversible aplastic anemia that is not dose-dependent. Dose-dependent reversible suppression may also occur.

 

Question 43. Which of the following drugs is most likely to cause ototoxicity and nephrotoxicity, especially when combined with loop diuretics?

A- Amoxicillin
B- Azithromycin
C- Ceftriaxone
D- Gentamicin

D- Gentamicin- Aminoglycosides (like gentamicin) can cause dose-dependent nephrotoxicity and irreversible ototoxicity, especially when combined with furosemide.

 

Question 44. Which of the following drugs inhibits bacterial folate synthesis by blocking dihydropteroate synthase?

A- Ciprofloxacin
B- Isoniazid
C- Trimethoprim
D- Sulfamethoxazole

D- Sulfamethoxazole- Sulfonamides inhibit dihydropteroate synthesis. Trimethoprim inhibits dihydrofolate reductase.

 

Question 45. Which one of the following antibiotics is most associated with tendinitis and tendon rupture?

A- Ciprofloxacin
B- Azithromycin
C- Doxycycline
D- Amoxicillin

A- Ciprofloxacin- Fluoroquinolones such as ciprofloxacin impair collagen synthesis and increase the risk of tendon rupture, specifically in older patients or those on corticosteroids.

 

CNS, Psychiatry and Neuromuscular Drugs

Question 46. A patient with Parkinson’s disease is treated with selegiline. What is the primary mechanism of this drug?

A- Inhibition of catechol-O-methyltransferase
B- Inhibition of monoamine oxidase B
C- Stimulation of dopamine receptors
D- Stimulation of muscarinic receptors

B- Inhibition of monoamine oxidase B- Selegiline inhibits MAO-B in the brain, decreasing dopamine breakdown and increasing dopamine availability.

 

Question 47. A patient with hyperlipidemia is treated with cholestyramine. What is the primary mechanism by which this drug lowers cholesterol?

A- Decreases hepatic cholesterol synthesis
B- Inhibits intestinal cholesterol absorption
C- Increases bile acid excretion in stool
D- Stimulates lipoprotein lipase

C- Increases bile acid excretion in stool- Cholestyramine binds bile acids in the intestine, preventing their reabsorption. The liver then uses more cholesterol to synthesize new bile acids, lowering LDL levels.

 

Question 48. A patient treated with morphine develops constipation. What is the primary mechanism responsible?

A- Decreased intestinal secretion
B- Decreased intestinal motility
C- Increased fluid absorption
D- Increased smooth muscle tone

B- Decreased intestinal motility- Opioids reduce GI peristalsis by acting on μ-receptors in the gut, leading to constipation.

 

Question 49. A patient with epilepsy is started on carbamazepine. Which laboratory abnormality should be monitored?

A- Hypercalcemia
B- Hyponatremia
C- Hypokalemia
D- Hypomagnesemia

B- Hyponatremia- Carbamazepine can cause SIADH, leading to dilutional hyponatremia.

 

Question 50. A patient taking phenelzine develops severe hypertension after eating aged cheese. What is the underlying cause of this reaction?

A- Excess dopamine release
B- Increased norepinephrine levels
C- Inhibition of acetylcholinesterase
D- Reduced serotonin reuptake

B- Increased norepinephrine levels- Tyramine in aged foods increases norepinephrine release, which cannot be broken down in patients taking MAO inhibitors, causing hypertensive crisis.

 

Question 51. A 29-year-old woman treated with lithium presents with tremor, polyuria, and confusion. Which laboratory finding is most likely present?

A- Hypercalcemia
B- Hypoglycemia
C- Hypokalemia
D- Hyponatremia

A- Hypercalcemia- Lithium can cause hyperparathyroidism, leading to elevated calcium levels, in addition to nephrogenic diabetes insipidus.

 

Question 52. A patient develops muscle weakness and respiratory failure after receiving a neuromuscular blocker during surgery. Which drug was most likely used?

A- Atracurium
B- Succinylcholine
C- Pancuronium
D- Rocuronium

B- Succinylcholine- Succinylcholine is a depolarizing neuromuscular blocker that can cause prolonged paralysis and hyperkalemia, especially in susceptible patients.

 

Question 53. A patient taking metoclopramide develops restlessness and involuntary muscle movements. This adverse effect is due to blockade of which receptor?

A- Dopamine receptors
B- Histamine receptors
C- Muscarinic receptors
D- Serotonin receptors

A- Dopamine receptors- Metoclopramide blocks D2 receptors in the CNS, which can cause extrapyramidal symptoms such as akathisia and dystonia.

 

Question 54. Which of the following is the mechanism of action of botulinum toxin at cholinergic nerve terminals?

A- Activates muscarinic receptors directly
B- Inhibits acetylcholine release by preventing SNARE protein function
C- Blocks acetylcholine reuptake
D- Blocks acetylcholine synthesis by inhibiting choline acetyltransferase
E- Stimulates excessive acetylcholine release at the neuromuscular junction

B- Inhibits acetylcholine release by preventing SNARE protein function- Botulinum toxin cleaves SNARE proteins (such as SNAP-25), which are required for vesicle fusion and acetylcholine release at cholinergic nerve terminals. This leads to flaccid paralysis. Other options do not describe its true mechanism.

 

Question 55. A 32-year-old man presents with dry mouth, blurred vision, and urinary retention after taking an over-the-counter cold medication. Which component is most likely responsible for these symptoms?

A- Dextromethorphan
B- Diphenhydramine
C- Guaifenesin
D- Phenylephrine

B- Diphenhydramine- First-generation antihistamines like diphenhydramine have strong anticholinergic effects, causing dry mouth, blurred vision, and urinary retention.

 

Question 56. A 50-year-old man with Parkinson’s disease is started on levodopa–carbidopa. After several months, he develops involuntary movements of his limbs and face. What is this side effect called?

A- Akathisia
B- Chorea
C- Dystonia
D- Tardive dyskinesia

B- Chorea- Long-term levodopa therapy can lead to dyskinesias (chorea-like movements) due to fluctuating dopamine levels in the basal ganglia.

 

Question 57. A 25-year-old man develops muscle rigidity, hyperthermia, and autonomic instability after receiving haloperidol. Which drug can be used to treat this condition?

A- Atropine
B- Dantrolene
C- Physostigmine
D- Propranolol

B- Dantrolene- Dantrolene is used to treat neuroleptic malignant syndrome and malignant hyperthermia by reducing muscle calcium release.

 

Question 58. A patient taking haloperidol develops muscle rigidity, high fever, and confusion. What is the best initial management step?

A- Administer dantrolene
B- Give epinephrine
C- Start propranolol
D- Stop the antipsychotic

D- Stop the antipsychotic- Neuroleptic malignant syndrome (NMS) is a medical emergency. The first step is to stop the offending drug, followed by supportive care and possibly dantrolene or bromocriptine

 

Question 59. A 35-year-old woman with generalized anxiety disorder is started on buspirone. Which of the following statements about this drug is correct?

A- It acts as a partial agonist at 5-HT₁A receptors
B- It causes dependence and withdrawal effects
C- It has sedative and muscle relaxant properties
D- It provides rapid relief of anxiety symptoms

A- It acts as a partial agonist at 5-HT₁A receptors- Buspirone is a non-benzodiazepine anxiolytic that works as a 5-HT₁A partial agonist. It has no sedation or dependence, but takes 1–2 weeks for effect.

 

Question 60. Which of the following drugs is a reversible cholinesterase inhibitor used in the management of myasthenia gravis?

A- Atropine
B- Neostigmine
C- Pralidoxime
D- Succinylcholine

B- Neostigmine- Neostigmine is a reversible acetylcholinesterase inhibitor that increases acetylcholine at the neuromuscular junction, improving muscle strength in myasthenia gravis.

 

Endocrine and Renal Drugs

Question 61. A patient taking metformin develops lactic acidosis. Which condition increases this risk?

A- Hypertension
B- Liver failure
C- Obesity
D- Smoking

B- Liver failure- Impaired lactate metabolism due to liver failure increases the risk of lactic acidosis in patients taking metformin.

 

Question 62. A patient treated with acetazolamide develops metabolic acidosis. What is the mechanism responsible for this effect?

A- Decreased ammonium excretion
B- Increased bicarbonate excretion
C- Increased hydrogen ion secretion
D- Inhibition of aldosterone release

B- Increased bicarbonate excretion- Acetazolamide inhibits carbonic anhydrase in the proximal tubule, preventing bicarbonate reabsorption and causing bicarbonate loss in urine, resulting in metabolic acidosis.

 

Question 63. Furosemide-induced ototoxicity results from disrupted ion transport in which structure?

A- Organ of Corti hair cells
B- Vestibular apparatus
C- Stria vascularis of the cochlea
D- Auditory nerve

C- Stria vascularis of the cochlea- Loop diuretics inhibit the Na-K-2Cl cotransporter in the stria vascularis, disrupting the endolymph ionic gradient and causing usually reversible ototoxicity, especially with high-dose or rapid IV administration.

 

Question 64. Tamoxifen increases endometrial cancer risk because it acts as a partial estrogen agonist in which tissue?

A- Breast
B- Bone
C- Endometrium
D- Liver

C- Endometrium- As a selective estrogen receptor modulator (SERM), tamoxifen antagonizes estrogen receptors in breast tissue but acts as a partial agonist in the endometrium, raising the risk of endometrial hyperplasia and cancer.

 

Question 65. A patient receiving long-term glucocorticoid therapy develops osteoporosis. What is the main mechanism responsible for this effect?

A- Decreased calcium absorption and increased bone resorption
B- Decreased osteoclast activity
C- Increased vitamin D activation
D- Increased calcium reabsorption in bone

A- Decreased calcium absorption and increased bone resorption- Glucocorticoids decrease intestinal calcium absorption and increase osteoclast activity, leading to bone loss and osteoporosis.

 

Question 66. A patient with metastatic prostate cancer is treated with leuprolide. Shortly after therapy begins, his bone pain temporarily worsens. What explains this phenomenon?

A- Direct androgen receptor activation
B- Initial surge in luteinizing hormone and testosterone
C- Inhibition of adrenal steroid synthesis
D- Increased prolactin secretion

B- Initial surge in luteinizing hormone and testosterone- GnRH agonists like leuprolide initially stimulate LH and FSH release, causing a temporary rise in testosterone before receptor downregulation suppresses hormone production.

 

Question 67. A patient taking spironolactone develops breast enlargement and sexual dysfunction. What is the mechanism behind this adverse effect?

A- Androgen receptor stimulation
B- Antiandrogen effect
C- Calcium channel blockade
D- Serotonin receptor activation-

B- Antiandrogen effect – Spironolactone blocks androgen receptors, decreasing the effects of testosterone, which can cause gynecomastia and decreased libido.

 

Question 68. A patient with type 2 diabetes is started on acarbose. What is the mechanism of action of this drug?

A- Decreases hepatic gluconeogenesis
B- Delays intestinal carbohydrate absorption
C- Increases insulin secretion
D- Improves insulin sensitivity

B- Delays intestinal carbohydrate absorption- Acarbose inhibits intestinal α-glucosidases, slowing carbohydrate digestion and reducing postprandial glucose spikes.

 

Question 69. A 55-year-old woman with osteoporosis is prescribed a bisphosphonate. Which instruction is most important to prevent esophageal irritation?

A- Remain upright for 30 minutes after ingestion
B- Take at bedtime
C- Take with milk
D- Use with a proton pump inhibitor

A- Remain upright for 30 minutes after ingestion- Bisphosphonates can cause esophagitis and ulceration; patients must remain upright after taking the medication.

 

Question 70. A 45-year-old woman treated with methimazole for hyperthyroidism develops fever and sore throat. What is the most appropriate next step?

A- Add propranolol
B- Administer prednisone
C- Continue the medication
D- Stop the drug and check WBC count

D- Stop the drug and check WBC count- Methimazole can cause agranulocytosis. The drug should be discontinued immediately, and a CBC obtained to confirm neutropenia.

 

Question 71. A 70-year-old woman with hypertension and type 2 diabetes is started on a thiazide diuretic. Which electrolyte imbalance is most likely to occur?

A- Hyperkalemia
B- Hypernatremia
C- Hypocalcemia
D- Hypokalemia

D- Hypokalemia- Thiazides increase sodium and chloride excretion but promote potassium loss, leading to hypokalemia and metabolic alkalosis.

 

Immunosuppressants, Chemotherapy and Gout Drugs

Question 72. A patient treated with tacrolimus after kidney transplantation develops nephrotoxicity. What is the primary molecular mechanism of tacrolimus?

A- Blocks IL-2 transcription by inhibiting calcineurin
B- Inhibits dihydrofolate reductase
C- Inhibits inosine monophosphate dehydrogenase
D- Stimulates T-cell apoptosis directly

A- Blocks IL-2 transcription by inhibiting calcineurin – Tacrolimus binds FKBP and inhibits calcineurin, preventing activation of T-cells by decreasing IL-2 transcription.

 

Question 73. A patient treated with mycophenolate mofetil develops leukopenia. What is the primary molecular target of this drug?

A- Dihydrofolate reductase
B- Inosine monophosphate dehydrogenase
C- Thymidylate synthase
D- Xanthine oxidase

B- Inosine monophosphate dehydrogenase – Mycophenolate inhibits IMP dehydrogenase, blocking de novo guanine nucleotide synthesis in lymphocytes, which depend heavily on this pathway, leading to immunosuppression and bone marrow suppression.

 

Question 74. A patient with acute gout is treated with colchicine. What is the primary mechanism of this drug?

A- Inhibition of uric acid synthesis
B- Inhibition of xanthine oxidase
C- Inhibition of neutrophil microtubule formation
D- Increased renal uric acid secretion

C- Inhibition of neutrophil microtubule formation- Colchicine disrupts microtubule polymerization, reducing neutrophil migration and inflammatory response to urate crystals.

 

Question 75. Leucovorin rescues normal cells from methotrexate toxicity by bypassing inhibition of which enzyme?

A- Thymidylate synthase
B- Dihydrofolate reductase
C- Ribonucleotide reductase
D- DNA polymerase

B- Dihydrofolate reductase- Methotrexate inhibits dihydrofolate reductase, blocking folate activation needed for DNA synthesis. Leucovorin is a reduced folate that bypasses this block, rescuing normal cells from toxicity.

 

Question 76. A patient taking allopurinol for gout should be closely monitored for which serious adverse effect?

A- Aplastic anemia
B- Hepatotoxicity
C- Severe hypersensitivity reaction
D- Thrombocytopenia

C- Severe hypersensitivity reaction- Allopurinol can cause a life-threatening hypersensitivity syndrome characterized by rash, fever, eosinophilia, and organ involvement.

 

Question 77. A patient treated with cisplatin develops hearing loss. What is the mechanism of this adverse effect?

A- Accumulation in cochlear hair cells
B- Autoimmune inner ear inflammation
C- Decreased cerebral perfusion
D- Inhibition of prostaglandin synthesis

A- Accumulation in cochlear hair cells- Cisplatin accumulates in inner ear hair cells, leading to dose-dependent ototoxicity and irreversible hearing loss.

 

Question 78. A patient receiving chemotherapy develops neutropenia. Which drug is used to stimulate neutrophil production?

A- Aminocaproic acid
B- Epoetin alfa
C- Filgrastim
D- Romiplostim

C- Filgrastim- Filgrastim is a granulocyte colony-stimulating factor (G-CSF) that increases neutrophil production and reduces infection risk in chemotherapy patients.

 

Respiratory, GI, Autonomic and Toxicology

Question 79. A patient taking NSAIDs develops decreased kidney function. What is the mechanism of this effect?

A- Decreased prostaglandin synthesis
B- Increased aldosterone secretion
C- Increased renin release
D- Increased sodium reabsorption

A- Decreased prostaglandin synthesis- NSAIDs reduce prostaglandins that maintain renal blood flow, leading to decreased GFR.

 

Question 80. A patient with asthma is started on montelukast. What is the mechanism of action of this medication?

A- Blocks leukotriene receptors
B- Inhibits cyclooxygenase
C- Stimulates beta-2 receptors
D- Stimulates muscarinic receptors

A- Blocks leukotriene receptors – Montelukast blocks CysLT1 receptors, reducing bronchoconstriction and inflammation in asthma.

 

Question 81. A patient on long-term NSAID therapy develops gastric ulcers. Which mechanism is responsible?

A- Decreased leukotriene production
B- Direct bacterial injury
C- Increased gastric acid secretion
D- Inhibition of prostaglandin synthesis

D- Inhibition of prostaglandin synthesis- NSAIDs inhibit COX enzymes, reducing prostaglandins that normally protect the gastric mucosa by increasing mucus, bicarbonate secretion, and mucosal blood flow.

 

Question 82. A patient with chronic obstructive pulmonary disease (COPD) is prescribed tiotropium. What is the mechanism of action of this drug?

A- β₂-adrenergic agonism
B- Leukotriene receptor blocker
C- Muscarinic receptor antagonism
D- Phosphodiesterase inhibition

C- Muscarinic receptor antagonism- Tiotropium blocks M3 receptors in airway smooth muscle, reducing bronchoconstriction and mucus secretion, leading to long-acting bronchodilation in COPD.

 

Question 83. Which drug is most appropriate for the acute management of anaphylaxis?

A- Albuterol
B- Diphenhydramine
C- Epinephrine
D- Hydrocortisone

C- Epinephrine- Epinephrine is first-line therapy for anaphylaxis because it causes rapid vasoconstriction (α₁), bronchodilation (β₂), and increased cardiac output (β₁), reversing life-threatening hypotension and airway compromise.

 

Question 84. Which medication decreases gastric acid secretion by irreversibly inhibiting the H⁺/K⁺ ATPase pump?

A- Famotidine
B- Misoprostol
C- Omeprazole
D- Sucralfate

C- Omeprazole- Proton pump inhibitors irreversibly block the H⁺/K⁺ ATPase in parietal cells, producing profound and long-lasting acid suppression.

 

Question 85. A 25-year-old man presents with tremors, tachycardia, and anxiety after taking an excessive amount of caffeine. Which of the following drugs has a similar mechanism of action to caffeine?

A- Chlorpromazine
B- Diazepam
C- Metoprolol
D- Theophylline

D- Theophylline- Theophylline, like caffeine, inhibits phosphodiesterase → increases cAMP → bronchodilation. It also antagonizes adenosine receptors.

 

Question 86. Which of the following drugs is used as an antidote for acetaminophen overdose?

A- Atropine
B- Flumazenil
C- N-acetylcysteine
D- Naloxone

C- N-acetylcysteine- N-acetylcysteine replenishes glutathione, helping detoxify toxic acetaminophen metabolites.

 

Question 87. A patient with asthma develops tremor and tachycardia after using his inhaler. Which of the following drugs is most likely responsible?

A- Albuterol
B- Ipratropium
C- Beclomethasone
D- Montelukast

A- Albuterol- Albuterol is a short-acting β₂-agonist that can cause tremor and tachycardia due to some β₁ stimulation.

 

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