NURS6501 Advanced Pathophysiology Cumulative
Final Exam - Complete Review & Test Bank -
Walden University MSN Program
60 items | Mechanistic & integrative reasoning | Pathway-model rationales
Section 1: Cellular, Genetic & Immunologic Mechanisms (15 Q)
Q1
Foundation: RA patient develops scleritis & elbow nodules.
Question: Extra-articular manifestations PRIMARILY attributed to which process?
A. Local pannus invasion
B. Systemic immune-complex deposition in small vessels
C. Secondary bacterial infection
D. Identical T-cells attacking skin/eye
Correct: B
Rationale: Circulating rheumatoid immune complexes deposit in small vessels → Type
III hypersensitivity → vasculitis & nodules. Local pannus (A) destroys cartilage but does
not reach distant organs.
Q2
,Foundation: Tumor shows high telomerase activity.
Question: MOST directly enables which cancer hallmark?
A. Sustained proliferation via oncogenes
B. Immortalization / evasion of replicative senescence
C. Angiogenesis induction
D. Tissue invasion & metastasis
Correct: B
Rationale: Telomerase rebuilds telomeres → limitless divisions. Other hallmarks use
different pathways (VEGF for C; proteases for D).
Q3
Foundation: Germ-line mutation in BRCA1 (truncating) → loss of DNA break repair.
Question: Which cellular stress is MOST likely to initiate carcinogenesis in these cells?
A. Hypoxia
B. Double-strand DNA breaks
C. Telomere shortening
D. Mild heat shock
Correct: B
,Rationale: BRCA1 is essential for homologous recombination repair; unrepaired
double-strand breaks accumulate mutations → carcinogenesis. Hypoxia (A) promotes
existing tumors but is not the initiating event here.
Q4
Foundation: Patient with C1 esterase inhibitor deficiency presents with facial swelling
after dental work.
Question: Which complement-derived mediator is PRIMARILY responsible for the
edema?
A. C3a
B. C5a
C. Bradykinin (via factor XIIa–kallikrein pathway)
D. C5b-9 membrane attack complex
Correct: C
Rationale: C1-INH normally inhibits factor XIIa & kallikrein; deficiency → unchecked
bradykinin generation → vascular permeability & angioedema. C3a/C5a (A,B) are
anaphylatoxins but not the main driver in HAE.
Q5
Foundation: HIV patient with CD4 50 cells/µL develops fever, weight loss,
hepatosplenomegaly; bone marrow shows acid-fast bacilli within macrophages.
Question: Which macrophage receptor is MOST critical for Mycobacterium avium
uptake?
, A. TLR-4
B. Mannose receptor (CD206)
C. Fc-gamma receptor
D. NOD-like receptor
Correct: B
Rationale: Mycobacterial cell-wall mannans bind mannose receptor → phagocytosis;
TLR-4 (A) signals but does not mediate uptake. NOD (D) senses peptidoglycan
cytosolically after uptake.
Q6
Foundation: Young woman with anti-dsDNA antibodies presents with photosensitive
rash & proteinuria.
Question: Which type of hypersensitivity reaction underlies lupus nephritis?
A. Type I (IgE-mediated)
B. Type II (cytotoxic)
C. Type III (immune-complex mediated)
D. Type IV (delayed T-cell)
Correct: C
Rationale: DNA-anti-DNA complexes deposit in glomeruli → complement activation →
inflammation (Type III). Type IV (D) contributes to skin lesions but not nephritis.
Q7
Final Exam - Complete Review & Test Bank -
Walden University MSN Program
60 items | Mechanistic & integrative reasoning | Pathway-model rationales
Section 1: Cellular, Genetic & Immunologic Mechanisms (15 Q)
Q1
Foundation: RA patient develops scleritis & elbow nodules.
Question: Extra-articular manifestations PRIMARILY attributed to which process?
A. Local pannus invasion
B. Systemic immune-complex deposition in small vessels
C. Secondary bacterial infection
D. Identical T-cells attacking skin/eye
Correct: B
Rationale: Circulating rheumatoid immune complexes deposit in small vessels → Type
III hypersensitivity → vasculitis & nodules. Local pannus (A) destroys cartilage but does
not reach distant organs.
Q2
,Foundation: Tumor shows high telomerase activity.
Question: MOST directly enables which cancer hallmark?
A. Sustained proliferation via oncogenes
B. Immortalization / evasion of replicative senescence
C. Angiogenesis induction
D. Tissue invasion & metastasis
Correct: B
Rationale: Telomerase rebuilds telomeres → limitless divisions. Other hallmarks use
different pathways (VEGF for C; proteases for D).
Q3
Foundation: Germ-line mutation in BRCA1 (truncating) → loss of DNA break repair.
Question: Which cellular stress is MOST likely to initiate carcinogenesis in these cells?
A. Hypoxia
B. Double-strand DNA breaks
C. Telomere shortening
D. Mild heat shock
Correct: B
,Rationale: BRCA1 is essential for homologous recombination repair; unrepaired
double-strand breaks accumulate mutations → carcinogenesis. Hypoxia (A) promotes
existing tumors but is not the initiating event here.
Q4
Foundation: Patient with C1 esterase inhibitor deficiency presents with facial swelling
after dental work.
Question: Which complement-derived mediator is PRIMARILY responsible for the
edema?
A. C3a
B. C5a
C. Bradykinin (via factor XIIa–kallikrein pathway)
D. C5b-9 membrane attack complex
Correct: C
Rationale: C1-INH normally inhibits factor XIIa & kallikrein; deficiency → unchecked
bradykinin generation → vascular permeability & angioedema. C3a/C5a (A,B) are
anaphylatoxins but not the main driver in HAE.
Q5
Foundation: HIV patient with CD4 50 cells/µL develops fever, weight loss,
hepatosplenomegaly; bone marrow shows acid-fast bacilli within macrophages.
Question: Which macrophage receptor is MOST critical for Mycobacterium avium
uptake?
, A. TLR-4
B. Mannose receptor (CD206)
C. Fc-gamma receptor
D. NOD-like receptor
Correct: B
Rationale: Mycobacterial cell-wall mannans bind mannose receptor → phagocytosis;
TLR-4 (A) signals but does not mediate uptake. NOD (D) senses peptidoglycan
cytosolically after uptake.
Q6
Foundation: Young woman with anti-dsDNA antibodies presents with photosensitive
rash & proteinuria.
Question: Which type of hypersensitivity reaction underlies lupus nephritis?
A. Type I (IgE-mediated)
B. Type II (cytotoxic)
C. Type III (immune-complex mediated)
D. Type IV (delayed T-cell)
Correct: C
Rationale: DNA-anti-DNA complexes deposit in glomeruli → complement activation →
inflammation (Type III). Type IV (D) contributes to skin lesions but not nephritis.
Q7
