NR507 Advanced Pathophysiology Midterm
Exam 2026/2027 - Grade A Questions & 100%
Correct Verified Answers for Chamberlain
University
Module 1: Cellular, Genetic & Immunologic Mechanisms
1. A 3-year-old patient presents with severe, recurrent bacterial infections. Lab work
reveals markedly elevated IgE levels and eosinophilia. Genetic testing confirms a
STAT3 mutation. Which pathophysiological mechanism best explains this clinical
picture?
A) Defective NADPH oxidase in phagocytes, impairing respiratory burst.
B) Failure of thymic development and T-cell deficiency.
C) Dysregulated JAK-STAT signaling leading to impaired Th17 differentiation and
poor antimicrobial defense.
D) Deficiency in complement C1 esterase inhibitor causing recurrent
angioedema.
Correct Answer: C
Correct Answer Text: Dysregulated JAK-STAT signaling leading to impaired Th17
differentiation and poor antimicrobial defense.
Rationale: This describes Hyper-IgE Syndrome (Job syndrome). The STAT3
mutation disrupts JAK-STAT signaling, critical for Th17 cell differentiation. Th17
cells are essential for mucosal and systemic defense against fungi and certain
bacteria. The lack of this response leads to recurrent infections, elevated IgE
(from dysregulated cytokine production), and eosinophilia. Option A describes
Chronic Granulomatous Disease. Option B describes severe combined
immunodeficiency (SCID) or DiGeorge syndrome. Option D describes Hereditary
Angioedema.
2. In a patient with chronic, poorly controlled hypertension, renal biopsy shows
arteriolar hyalinosis and glomerular sclerosis. The primary mechanism leading to
this glomerular injury is:
A) Direct toxic injury to podocytes from inflammatory cytokines.
B) Deposition of immune complexes within the glomerular basement membrane.
C) Sustained intraglomerular hypertension causing mechanical stress and
endothelial dysfunction.
, D) Ischemic atrophy due to renal artery stenosis.
Correct Answer: C
Correct Answer Text: Sustained intraglomerular hypertension causing
mechanical stress and endothelial dysfunction.
Rationale: Hypertensive nephrosclerosis is characterized by sustained high
pressure transmission to the glomeruli. This causes endothelial injury, increased
permeability, and mesangial cell proliferation, leading to sclerosis. It is a
hemodynamic injury, not primarily immune (B) or toxic (A). Renal artery stenosis
(D) causes a different pattern of ischemic injury and is not the most common
mechanism in essential hypertension.
3. A 28-year-old woman presents with photosensitive malar rash, joint pain, and
proteinuria. Anti-dsDNA antibodies are positive. Which immunologic mechanism
causes the renal injury in this disease?
A) Deposition of IgA immune complexes in the mesangium, activating
complement and mesangial proliferation.
B) Formation of immune complexes containing nuclear antigens, deposited in
subendothelial space, activating complement and attracting inflammatory cells.
C) Direct cytotoxic T-cell attack on podocytes, causing foot process effacement.
D) Activation of alternative complement pathway due to factor H deficiency,
leading to membranoproliferative pattern.
Correct Answer: B
Correct Answer Text: Formation of immune complexes containing nuclear
antigens, deposited in subendothelial space, activating complement and
attracting inflammatory cells.
Rationale: Systemic lupus erythematosus (SLE) nephritis is mediated by immune
complexes of anti-dsDNA with DNA fragments, deposited in glomeruli
(subendothelial or subepithelial), activating classical complement and recruiting
neutrophils/macrophages, leading to proliferative glomerulonephritis. Option A
describes IgA nephropathy. Option C is not the primary mechanism in SLE.
Option D describes atypical hemolytic uremic syndrome.
Module 2: Integrated System Pathophysiology
4. A patient with long-standing Crohn's disease develops numbness, paresthesias,
and a macrocytic anemia. Which pathophysiological sequence best explains
these neurological findings?
A) Chronic inflammation → ileal resection → vitamin B12 malabsorption →
impaired myelin synthesis (demyelination of dorsal columns).
Exam 2026/2027 - Grade A Questions & 100%
Correct Verified Answers for Chamberlain
University
Module 1: Cellular, Genetic & Immunologic Mechanisms
1. A 3-year-old patient presents with severe, recurrent bacterial infections. Lab work
reveals markedly elevated IgE levels and eosinophilia. Genetic testing confirms a
STAT3 mutation. Which pathophysiological mechanism best explains this clinical
picture?
A) Defective NADPH oxidase in phagocytes, impairing respiratory burst.
B) Failure of thymic development and T-cell deficiency.
C) Dysregulated JAK-STAT signaling leading to impaired Th17 differentiation and
poor antimicrobial defense.
D) Deficiency in complement C1 esterase inhibitor causing recurrent
angioedema.
Correct Answer: C
Correct Answer Text: Dysregulated JAK-STAT signaling leading to impaired Th17
differentiation and poor antimicrobial defense.
Rationale: This describes Hyper-IgE Syndrome (Job syndrome). The STAT3
mutation disrupts JAK-STAT signaling, critical for Th17 cell differentiation. Th17
cells are essential for mucosal and systemic defense against fungi and certain
bacteria. The lack of this response leads to recurrent infections, elevated IgE
(from dysregulated cytokine production), and eosinophilia. Option A describes
Chronic Granulomatous Disease. Option B describes severe combined
immunodeficiency (SCID) or DiGeorge syndrome. Option D describes Hereditary
Angioedema.
2. In a patient with chronic, poorly controlled hypertension, renal biopsy shows
arteriolar hyalinosis and glomerular sclerosis. The primary mechanism leading to
this glomerular injury is:
A) Direct toxic injury to podocytes from inflammatory cytokines.
B) Deposition of immune complexes within the glomerular basement membrane.
C) Sustained intraglomerular hypertension causing mechanical stress and
endothelial dysfunction.
, D) Ischemic atrophy due to renal artery stenosis.
Correct Answer: C
Correct Answer Text: Sustained intraglomerular hypertension causing
mechanical stress and endothelial dysfunction.
Rationale: Hypertensive nephrosclerosis is characterized by sustained high
pressure transmission to the glomeruli. This causes endothelial injury, increased
permeability, and mesangial cell proliferation, leading to sclerosis. It is a
hemodynamic injury, not primarily immune (B) or toxic (A). Renal artery stenosis
(D) causes a different pattern of ischemic injury and is not the most common
mechanism in essential hypertension.
3. A 28-year-old woman presents with photosensitive malar rash, joint pain, and
proteinuria. Anti-dsDNA antibodies are positive. Which immunologic mechanism
causes the renal injury in this disease?
A) Deposition of IgA immune complexes in the mesangium, activating
complement and mesangial proliferation.
B) Formation of immune complexes containing nuclear antigens, deposited in
subendothelial space, activating complement and attracting inflammatory cells.
C) Direct cytotoxic T-cell attack on podocytes, causing foot process effacement.
D) Activation of alternative complement pathway due to factor H deficiency,
leading to membranoproliferative pattern.
Correct Answer: B
Correct Answer Text: Formation of immune complexes containing nuclear
antigens, deposited in subendothelial space, activating complement and
attracting inflammatory cells.
Rationale: Systemic lupus erythematosus (SLE) nephritis is mediated by immune
complexes of anti-dsDNA with DNA fragments, deposited in glomeruli
(subendothelial or subepithelial), activating classical complement and recruiting
neutrophils/macrophages, leading to proliferative glomerulonephritis. Option A
describes IgA nephropathy. Option C is not the primary mechanism in SLE.
Option D describes atypical hemolytic uremic syndrome.
Module 2: Integrated System Pathophysiology
4. A patient with long-standing Crohn's disease develops numbness, paresthesias,
and a macrocytic anemia. Which pathophysiological sequence best explains
these neurological findings?
A) Chronic inflammation → ileal resection → vitamin B12 malabsorption →
impaired myelin synthesis (demyelination of dorsal columns).
