, Question 1
A patient with recurrent pyogenic infections and poor wound healing is found
to have normal T-cell function but absent respiratory burst activity on
dihydrorhodamine testing. Which molecular defect best explains this pattern?
A. Deficiency of adenosine deaminase causing toxic purine accumulation
in lymphocytes
B. Mutation in the gp91phox subunit of NADPH oxidase impairing
superoxide generation
C. Defective CD40 ligand expression preventing immunoglobulin class
switching
D. Absence of C5-C9 complement components blocking membrane
attack complex formation
Correct Answer: B - Mutation in the gp91phox subunit of
NADPH oxidase impairing superoxide generation
RATIONALE
Chronic granulomatous disease results from NADPH oxidase defects
(commonly gp91phox), preventing superoxide production and causing
recurrent catalase-positive infections; the normal DHR test is
abnormal in CGD. Adenosine deaminase deficiency causes SCID
(T-cell defect), CD40L defect causes hyper-IgM syndrome, and C5-C9
defects cause recurrent Neisseria infections, none matching the
respiratory burst pattern.
Question 2
Which statement most accurately distinguishes the immunopathogenesis of
type II from type III hypersensitivity reactions?
A. Type II is IgE-mediated mast cell degranulation; type III is T-cell
mediated cytotoxicity
B. Type II involves IgG/IgM binding to fixed tissue antigens; type III
involves deposition of circulating antigen-antibody immune complexes
C. Type II is delayed and cell-mediated; type III is immediate and
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, complement-independent
D. Type II requires sensitized T lymphocytes; type III requires only
complement activation without antibody
Correct Answer: B - Type II involves IgG/IgM binding to fixed
tissue antigens; type III involves deposition of circulating
antigen-antibody immune complexes
RATIONALE
Type II hypersensitivity is antibody-mediated against antigens fixed
on cell surfaces or matrix (e.g., Goodpasture, hemolytic transfusion
reactions), whereas type III results from soluble circulating immune
complexes depositing in tissues (e.g., SLE, serum sickness). Options
A, C, and D misassign IgE (type I), T-cell mechanisms (type IV), or
omit antibody entirely, which is incorrect.
Question 3
A kidney transplant recipient develops rising creatinine and a biopsy showing
mononuclear interstitial infiltrate with tubulitis two weeks post-transplant.
Which mechanism predominates?
A. Preformed donor-specific antibodies causing hyperacute rejection
B. T-cell mediated recognition of donor MHC alloantigens initiating acute
cellular rejection
C. Immune complex deposition from chronic antigenemia causing
membranous nephropathy
D. Ischemia-reperfusion injury with neutrophil infiltration independent of
alloimmunity
Correct Answer: B - T-cell mediated recognition of donor MHC
alloantigens initiating acute cellular rejection
Page 3
A patient with recurrent pyogenic infections and poor wound healing is found
to have normal T-cell function but absent respiratory burst activity on
dihydrorhodamine testing. Which molecular defect best explains this pattern?
A. Deficiency of adenosine deaminase causing toxic purine accumulation
in lymphocytes
B. Mutation in the gp91phox subunit of NADPH oxidase impairing
superoxide generation
C. Defective CD40 ligand expression preventing immunoglobulin class
switching
D. Absence of C5-C9 complement components blocking membrane
attack complex formation
Correct Answer: B - Mutation in the gp91phox subunit of
NADPH oxidase impairing superoxide generation
RATIONALE
Chronic granulomatous disease results from NADPH oxidase defects
(commonly gp91phox), preventing superoxide production and causing
recurrent catalase-positive infections; the normal DHR test is
abnormal in CGD. Adenosine deaminase deficiency causes SCID
(T-cell defect), CD40L defect causes hyper-IgM syndrome, and C5-C9
defects cause recurrent Neisseria infections, none matching the
respiratory burst pattern.
Question 2
Which statement most accurately distinguishes the immunopathogenesis of
type II from type III hypersensitivity reactions?
A. Type II is IgE-mediated mast cell degranulation; type III is T-cell
mediated cytotoxicity
B. Type II involves IgG/IgM binding to fixed tissue antigens; type III
involves deposition of circulating antigen-antibody immune complexes
C. Type II is delayed and cell-mediated; type III is immediate and
Page 2
, complement-independent
D. Type II requires sensitized T lymphocytes; type III requires only
complement activation without antibody
Correct Answer: B - Type II involves IgG/IgM binding to fixed
tissue antigens; type III involves deposition of circulating
antigen-antibody immune complexes
RATIONALE
Type II hypersensitivity is antibody-mediated against antigens fixed
on cell surfaces or matrix (e.g., Goodpasture, hemolytic transfusion
reactions), whereas type III results from soluble circulating immune
complexes depositing in tissues (e.g., SLE, serum sickness). Options
A, C, and D misassign IgE (type I), T-cell mechanisms (type IV), or
omit antibody entirely, which is incorrect.
Question 3
A kidney transplant recipient develops rising creatinine and a biopsy showing
mononuclear interstitial infiltrate with tubulitis two weeks post-transplant.
Which mechanism predominates?
A. Preformed donor-specific antibodies causing hyperacute rejection
B. T-cell mediated recognition of donor MHC alloantigens initiating acute
cellular rejection
C. Immune complex deposition from chronic antigenemia causing
membranous nephropathy
D. Ischemia-reperfusion injury with neutrophil infiltration independent of
alloimmunity
Correct Answer: B - T-cell mediated recognition of donor MHC
alloantigens initiating acute cellular rejection
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