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Immunology — Step 1 practice questions
99 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
Examined as mechanism throughout: which cell, which signal, which step. Hypersensitivity reactions, immunodeficiencies and transplant rejection recur, and the same concepts reappear inside blood, respiratory and rheumatology questions.
Sample questions
Sample question 1
A patient develops fever, urticaria, arthralgia, and lymphadenopathy 10 days after receiving an antivenom for a snake bite. Which of the following best describes the underlying mechanism?
Explanations
A. IgE-mediated immediate hypersensitivity
This delayed onset (about 1-2 weeks) is inconsistent with an immediate IgE-mediated reaction.
B. Immune complex deposition (type III hypersensitivity) from antibodies against the foreign (often animal-derived) proteins in the antivenom · correct
Serum sickness results from immune complex formation between host antibodies and the foreign (often animal-derived) proteins in products like antivenom or antitoxin, with subsequent complement activation and tissue deposition, causing fever, urticaria, arthralgia, and lymphadenopathy roughly 1-2 weeks after exposure — a classic type III hypersensitivity reaction.
C. Direct toxin-mediated organ damage from the snake venom itself, unrelated to the antivenom
This presentation, and its timing, is related to the immune response against the antivenom itself, not direct venom toxicity (which would present much more acutely, immediately after the bite).
D. T-cell mediated delayed hypersensitivity exclusively
While some T-cell involvement can occur in various reactions, the classic, defining mechanism of serum sickness is immune complex (type III) mediated.
E. Complement deficiency
This is not a complement deficiency state; if anything, complement is being actively consumed/activated in this process.
Sample question 2
A 28-year-old woman has had an episode of optic neuritis 2 years ago and now has new numbness and weakness in one leg lasting weeks. MRI shows periventricular white matter lesions of differing ages. Which of the following best describes the diagnostic principle?
Explanations
A. Demyelinating lesions disseminated in SPACE and TIME, supported by MRI and oligoclonal bands in cerebrospinal fluid · correct
Multiple sclerosis is diagnosed by demonstrating central nervous system demyelination DISSEMINATED IN SPACE (lesions in multiple characteristic locations — periventricular, juxtacortical, infratentorial, spinal cord) and DISSEMINATED IN TIME (lesions of differing ages, or new lesions over time, or oligoclonal bands). Relapses last DAYS TO WEEKS rather than minutes, distinguishing them from transient ischemic attacks. It affects young adults, more women than men, and is more common at higher latitudes. Suggestive features include optic neuritis, internuclear ophthalmoplegia, and worsening with heat (Uhthoff phenomenon).
B. A single lesion is sufficient for diagnosis regardless of history
Dissemination in both space and time is required.
C. Symptoms lasting minutes are characteristic
Very brief symptoms suggest other processes.
D. Cerebrospinal fluid oligoclonal bands exclude the diagnosis
Oligoclonal bands SUPPORT the diagnosis.
E. The diagnosis requires positive serum autoantibodies
No specific serum autoantibody defines the disease.
Sample question 3
A child develops migratory polyarthritis, carditis, and subcutaneous nodules several weeks after a Group A Streptococcus pharyngitis infection. Which of the following best explains this presentation?
Explanations
A. Simple viral arthritis unrelated to the prior infection
This presentation, following a documented strep infection with this classic symptom complex, is specifically explained by post-streptococcal rheumatic fever, not a coincidental unrelated viral process.
B. Normal post-infectious recovery with no pathology
This represents a significant pathologic complication, not normal recovery.
C. Direct bacterial invasion of the joints and heart
This is an immune-mediated (not direct bacterial invasion) process affecting the heart/joints, occurring after the acute infection has often already resolved.
D. Acute rheumatic fever, an immune-mediated complication from molecular mimicry between streptococcal antigens and host tissues · correct
Acute rheumatic fever is a delayed, immune-mediated complication of Group A Streptococcus pharyngitis, thought to result from molecular mimicry (antibodies against streptococcal M protein cross-reacting with host tissues in the heart, joints, skin, and brain), causing the classic Jones criteria features including migratory polyarthritis, carditis, and subcutaneous nodules.
E. A coincidental, unrelated autoimmune condition
This is a well-established, direct causal relationship (not coincidental) between the preceding strep infection and this delayed immune complication.
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