, Question 1
A patient develops urticaria, wheezing, and hypotension within minutes of
receiving IV penicillin. Which pathophysiologic sequence best explains these
findings?
A. IgG-mediated complement activation with neutrophil chemotaxis
B. IgE cross-linking on mast cells causing preformed and newly
synthesized mediator release
C. Antigen-antibody immune complex deposition in vascular
endothelium
D. T-cell-mediated cytotoxicity against drug-haptenated hepatocytes
Correct Answer: B - IgE cross-linking on mast cells causing
preformed and newly synthesized mediator release
RATIONALE
This is a Type I immediate hypersensitivity reaction: drug-specific IgE
binds mast cells, and antigen cross-linking triggers degranulation and
release of histamine, tryptase, leukotrienes, and prostaglandins,
producing vasodilation, bronchoconstriction, and urticaria. The other
options describe Type II, III, and IV mechanisms, which do not
produce this rapid clinical picture.
Question 2
Which laboratory pattern most strongly supports a diagnosis of systemic lupus
erythematosus (SLE) in a patient with malar rash and arthralgias?
A. Positive anti-histone antibodies and high C3/C4 levels
B. Positive anti-dsDNA and anti-Smith antibodies with low C3/C4
C. Positive c-ANCA and elevated CRP
D. Positive anti-CCP and rheumatoid factor
Correct Answer: B - Positive anti-dsDNA and anti-Smith
antibodies with low C3/C4
Page 2
, RATIONALE
Anti-dsDNA and anti-Smith are highly specific for SLE, and
complement consumption (low C3/C4) reflects active immune
complex-mediated disease. Anti-histone antibodies are associated with
drug-induced lupus (with normal complements), while c-ANCA and
anti-CCP point to vasculitis and rheumatoid arthritis, respectively.
Question 3
In a patient with myasthenia gravis, which mechanism best explains fatigable
muscle weakness?
A. Antibodies against presynaptic voltage-gated calcium channels
B. Antibodies against acetylcholine receptors causing
complement-mediated destruction
C. Antibodies against muscle-specific kinase (MuSK) enhancing receptor
clustering
D. T-cell-mediated destruction of lower motor neurons
Correct Answer: B - Antibodies against acetylcholine receptors
causing complement-mediated destruction
RATIONALE
Myasthenia gravis is caused by IgG autoantibodies against
postsynaptic nicotinic acetylcholine receptors, leading to
complement-mediated damage and accelerated receptor degradation,
which reduces neuromuscular transmission and causes fatigable
weakness. Anti-VGCC antibodies cause Lambert-Eaton, anti-MuSK is
a less common MG subtype but does not enhance clustering, and
motor neuron destruction is seen in ALS.
Question 4
A patient with rheumatoid arthritis is started on adalimumab. Which statement
best reflects the rationale for screening for latent tuberculosis before therapy?
A. TNF- inhibition impairs granuloma formation and can reactivate latent
Page 3
, infection
B. Adalimumab directly kills Mycobacterium tuberculosis
C. TNF- enhances viral replication and increases TB risk
D. The drug induces CYP450 enzymes that inactivate anti-TB drugs
Correct Answer: A - TNF- inhibition impairs granuloma
formation and can reactivate latent infection
RATIONALE
TNF- is critical for granuloma formation and containment of latent
TB; adalimumab neutralizes TNF-, increasing the risk of reactivation.
Adalimumab does not directly kill mycobacteria, does not enhance
viral replication, and does not induce CYP450 enzymes.
Question 5
Which finding best distinguishes hyperacute from acute transplant rejection?
A. Hyperacute rejection is mediated by preformed antibodies and occurs
within minutes to hours
B. Hyperacute rejection is a T-cell-mediated process occurring days to
weeks after transplant
C. Acute rejection is caused by preformed antibodies and occurs within
minutes
D. Acute rejection is characterized by graft arteriosclerosis months to
years later
Correct Answer: A - Hyperacute rejection is mediated by
preformed antibodies and occurs within minutes to hours
RATIONALE
Hyperacute rejection is caused by preformed recipient antibodies
against donor antigens, leading to immediate complement activation,
thrombosis, and graft necrosis within minutes to hours. Acute
rejection is T-cell-mediated and occurs days to weeks, while chronic
rejection manifests months to years with graft arteriosclerosis.
Page 4
A patient develops urticaria, wheezing, and hypotension within minutes of
receiving IV penicillin. Which pathophysiologic sequence best explains these
findings?
A. IgG-mediated complement activation with neutrophil chemotaxis
B. IgE cross-linking on mast cells causing preformed and newly
synthesized mediator release
C. Antigen-antibody immune complex deposition in vascular
endothelium
D. T-cell-mediated cytotoxicity against drug-haptenated hepatocytes
Correct Answer: B - IgE cross-linking on mast cells causing
preformed and newly synthesized mediator release
RATIONALE
This is a Type I immediate hypersensitivity reaction: drug-specific IgE
binds mast cells, and antigen cross-linking triggers degranulation and
release of histamine, tryptase, leukotrienes, and prostaglandins,
producing vasodilation, bronchoconstriction, and urticaria. The other
options describe Type II, III, and IV mechanisms, which do not
produce this rapid clinical picture.
Question 2
Which laboratory pattern most strongly supports a diagnosis of systemic lupus
erythematosus (SLE) in a patient with malar rash and arthralgias?
A. Positive anti-histone antibodies and high C3/C4 levels
B. Positive anti-dsDNA and anti-Smith antibodies with low C3/C4
C. Positive c-ANCA and elevated CRP
D. Positive anti-CCP and rheumatoid factor
Correct Answer: B - Positive anti-dsDNA and anti-Smith
antibodies with low C3/C4
Page 2
, RATIONALE
Anti-dsDNA and anti-Smith are highly specific for SLE, and
complement consumption (low C3/C4) reflects active immune
complex-mediated disease. Anti-histone antibodies are associated with
drug-induced lupus (with normal complements), while c-ANCA and
anti-CCP point to vasculitis and rheumatoid arthritis, respectively.
Question 3
In a patient with myasthenia gravis, which mechanism best explains fatigable
muscle weakness?
A. Antibodies against presynaptic voltage-gated calcium channels
B. Antibodies against acetylcholine receptors causing
complement-mediated destruction
C. Antibodies against muscle-specific kinase (MuSK) enhancing receptor
clustering
D. T-cell-mediated destruction of lower motor neurons
Correct Answer: B - Antibodies against acetylcholine receptors
causing complement-mediated destruction
RATIONALE
Myasthenia gravis is caused by IgG autoantibodies against
postsynaptic nicotinic acetylcholine receptors, leading to
complement-mediated damage and accelerated receptor degradation,
which reduces neuromuscular transmission and causes fatigable
weakness. Anti-VGCC antibodies cause Lambert-Eaton, anti-MuSK is
a less common MG subtype but does not enhance clustering, and
motor neuron destruction is seen in ALS.
Question 4
A patient with rheumatoid arthritis is started on adalimumab. Which statement
best reflects the rationale for screening for latent tuberculosis before therapy?
A. TNF- inhibition impairs granuloma formation and can reactivate latent
Page 3
, infection
B. Adalimumab directly kills Mycobacterium tuberculosis
C. TNF- enhances viral replication and increases TB risk
D. The drug induces CYP450 enzymes that inactivate anti-TB drugs
Correct Answer: A - TNF- inhibition impairs granuloma
formation and can reactivate latent infection
RATIONALE
TNF- is critical for granuloma formation and containment of latent
TB; adalimumab neutralizes TNF-, increasing the risk of reactivation.
Adalimumab does not directly kill mycobacteria, does not enhance
viral replication, and does not induce CYP450 enzymes.
Question 5
Which finding best distinguishes hyperacute from acute transplant rejection?
A. Hyperacute rejection is mediated by preformed antibodies and occurs
within minutes to hours
B. Hyperacute rejection is a T-cell-mediated process occurring days to
weeks after transplant
C. Acute rejection is caused by preformed antibodies and occurs within
minutes
D. Acute rejection is characterized by graft arteriosclerosis months to
years later
Correct Answer: A - Hyperacute rejection is mediated by
preformed antibodies and occurs within minutes to hours
RATIONALE
Hyperacute rejection is caused by preformed recipient antibodies
against donor antigens, leading to immediate complement activation,
thrombosis, and graft necrosis within minutes to hours. Acute
rejection is T-cell-mediated and occurs days to weeks, while chronic
rejection manifests months to years with graft arteriosclerosis.
Page 4
