NUR 3120 – Pathophysiology Final Exam |
2025/2026 Verified Questions with Detailed
Rationales
Question 1: Inflammation
A 45-year-old male presents with acute appendicitis. Histology shows neutrophil infiltration and edema.
What is the primary mediator driving this acute inflammatory response?
A. Interleukin-10 (anti-inflammatory cytokine)
B. Tumor necrosis factor-alpha (TNF-α) from macrophages
C. Transforming growth factor-beta (TGF-β) for fibrosis
D. Eosinophil cationic protein
Correct Answer: B
Rationale: In acute inflammation, such as appendicitis, resident macrophages detect bacterial PAMPs via
TLRs, releasing TNF-α, which induces vascular permeability (via histamine from mast cells) and
chemotaxis of neutrophils through endothelial adhesion molecules (E-selectin, ICAM-1). This leads to
exudation and phagocytosis. IL-10 (A) dampens response; TGF-β (C) is chronic/fibrotic; eosinophil
protein (D) is allergic.
Question 2: Inflammation
A 30-year-old female with rheumatoid arthritis has synovial inflammation. What chronic inflammatory
cell predominates and contributes to pannus formation?
A. Neutrophils for acute response
B. Lymphocytes and plasma cells with autoantibody production
C. Eosinophils for parasitic defense
D. Basophils for immediate hypersensitivity
Correct Answer: B
,Rationale: Chronic inflammation in RA involves CD4+ T-cell activation and B-cell differentiation to
plasma cells producing RF/ACPA, forming immune complexes that activate complement and
macrophages, leading to cytokine storm (IL-1, TNF-α) and synovial hyperplasia/pannus eroding cartilage.
Neutrophils (A) are acute; eosinophils (C)/basophils (D) type I.
Question 3: Inflammation
A patient with burns develops systemic inflammatory response syndrome (SIRS). What mechanism
explains capillary leak and hypotension?
A. Increased hydrostatic pressure
B. Endothelial glycocalyx degradation by heparanase
C. Lymphatic obstruction
D. Venous stasis
Correct Answer: B
Rationale: Burn-induced DAMPs (HMGB1) activate endothelial TLR4/NF-κB, upregulating heparanase
and ADAMTS13, shedding glycocalyx and exposing junctions, allowing protein-rich fluid extravasation,
reducing intravascular volume, and causing distributive shock. Hydrostatic (A) is cardiogenic; lymphatic
(C) lymphedema; stasis (D) thrombotic.
Question 4: Inflammation
In sepsis, a patient exhibits coagulopathy. What inflammatory mediator bridges inflammation and
thrombosis?
A. Antithrombin III deficiency
B. Tissue factor expression on monocytes
C. Protein C activation
D. Fibrinolytic excess
Correct Answer: B
Rationale: Sepsis LPS/TLR4 induces TF on monocytes/endothelium via NF-κB, initiating extrinsic
coagulation (VIIa-TF to Xa), thrombin generation, and DIC with microthrombi, while inhibiting
fibrinolysis (PAI-1 upregulation). ATIII (A)/protein C (D) are consumed/inhibited; fibrinolytic (D)
opposite.
,Question 5: Inflammation
A 55-year-old with gout has joint pain from monosodium urate crystals. What inflammatory pathway is
activated?
A. NLRP3 inflammasome leading to IL-1β release
B. JAK-STAT for cytokine signaling
C. Complement classical pathway
D. Fc receptor cross-linking
Correct Answer: A
Rationale: Urate crystals phagocytosed by macrophages activate NLRP3/caspase-1, cleaving pro-IL-1β
to active IL-1β, amplifying neutrophil recruitment and pyroptosis, causing acute gouty arthritis.
JAK-STAT (B) downstream; complement (C) secondary; Fc (D) immune complex.
Question 6: Inflammation
A child with asthma exacerbation shows bronchial edema. What vascular change underlies this?
A. Vasoconstriction from leukotrienes
B. Increased permeability via histamine H1 receptors
C. Platelet aggregation
D. Smooth muscle hypertrophy
Correct Answer: B
Rationale: Mast cell degranulation in type I hypersensitivity releases histamine, binding H1 on venules,
activating RhoA/MLC phosphatase inhibition, causing gap formation and plasma exudation, contributing
to airway narrowing. Leukotrienes (A) bronchoconstrict; platelets (C) vascular; hypertrophy (D) chronic.
Question 7: Inflammation
Post-MI, a patient develops pericarditis. What is the pathophysiologic basis?
A. Autoimmune reaction to myocardial antigens
B. Dressler's syndrome with anti-myocardial antibodies
C. Direct bacterial invasion
D. Viral myocarditis extension
, Correct Answer: B
Rationale: Dressler's (post-MI autoimmune pericarditis) involves molecular mimicry where damaged
myocardium releases antigens, eliciting IgG against myosin/sarcolemma, forming immune complexes that
deposit in pericardium, activating complement and causing sterile inflammation 2-6 weeks post-MI.
Acute (A) earlier; bacterial (C)/viral (D) infectious.
Question 8: Inflammation
A patient with IBD has granulomatous inflammation. What macrophage-derived factor drives this?
A. IL-4 for Th2 response
B. IFN-γ for Th1 activation
C. IL-17 for neutrophil recruitment
D. IL-10 for suppression
Correct Answer: B
Rationale: In Crohn's (granulomatous IBD), dysregulated Th1 cells release IFN-γ, activating
macrophages to form epithelioid/giant cells via STAT1, containing antigens in non-caseating granulomas
to limit spread. IL-4 (A) Th2; IL-17 (C) psoriasis; IL-10 (D) regulatory.
Question 9: Inflammation
In wound healing, a diabetic patient has delayed granulation. What cytokine imbalance?
A. Excess VEGF for angiogenesis
B. Reduced TGF-β for fibroblast migration
C. High IL-6 for proliferation
D. Low TNF-α for debridement
Correct Answer: B
Rationale: Hyperglycemia impairs TGF-β/Smad signaling in fibroblasts, reducing ECM synthesis
(collagen via α-SMA) and migration, stalling proliferative phase and causing non-healing ulcers. VEGF
(A) impaired too but secondary; IL-6 (C)/TNF-α (D) pro-inflammatory.
Question 10: Inflammation
2025/2026 Verified Questions with Detailed
Rationales
Question 1: Inflammation
A 45-year-old male presents with acute appendicitis. Histology shows neutrophil infiltration and edema.
What is the primary mediator driving this acute inflammatory response?
A. Interleukin-10 (anti-inflammatory cytokine)
B. Tumor necrosis factor-alpha (TNF-α) from macrophages
C. Transforming growth factor-beta (TGF-β) for fibrosis
D. Eosinophil cationic protein
Correct Answer: B
Rationale: In acute inflammation, such as appendicitis, resident macrophages detect bacterial PAMPs via
TLRs, releasing TNF-α, which induces vascular permeability (via histamine from mast cells) and
chemotaxis of neutrophils through endothelial adhesion molecules (E-selectin, ICAM-1). This leads to
exudation and phagocytosis. IL-10 (A) dampens response; TGF-β (C) is chronic/fibrotic; eosinophil
protein (D) is allergic.
Question 2: Inflammation
A 30-year-old female with rheumatoid arthritis has synovial inflammation. What chronic inflammatory
cell predominates and contributes to pannus formation?
A. Neutrophils for acute response
B. Lymphocytes and plasma cells with autoantibody production
C. Eosinophils for parasitic defense
D. Basophils for immediate hypersensitivity
Correct Answer: B
,Rationale: Chronic inflammation in RA involves CD4+ T-cell activation and B-cell differentiation to
plasma cells producing RF/ACPA, forming immune complexes that activate complement and
macrophages, leading to cytokine storm (IL-1, TNF-α) and synovial hyperplasia/pannus eroding cartilage.
Neutrophils (A) are acute; eosinophils (C)/basophils (D) type I.
Question 3: Inflammation
A patient with burns develops systemic inflammatory response syndrome (SIRS). What mechanism
explains capillary leak and hypotension?
A. Increased hydrostatic pressure
B. Endothelial glycocalyx degradation by heparanase
C. Lymphatic obstruction
D. Venous stasis
Correct Answer: B
Rationale: Burn-induced DAMPs (HMGB1) activate endothelial TLR4/NF-κB, upregulating heparanase
and ADAMTS13, shedding glycocalyx and exposing junctions, allowing protein-rich fluid extravasation,
reducing intravascular volume, and causing distributive shock. Hydrostatic (A) is cardiogenic; lymphatic
(C) lymphedema; stasis (D) thrombotic.
Question 4: Inflammation
In sepsis, a patient exhibits coagulopathy. What inflammatory mediator bridges inflammation and
thrombosis?
A. Antithrombin III deficiency
B. Tissue factor expression on monocytes
C. Protein C activation
D. Fibrinolytic excess
Correct Answer: B
Rationale: Sepsis LPS/TLR4 induces TF on monocytes/endothelium via NF-κB, initiating extrinsic
coagulation (VIIa-TF to Xa), thrombin generation, and DIC with microthrombi, while inhibiting
fibrinolysis (PAI-1 upregulation). ATIII (A)/protein C (D) are consumed/inhibited; fibrinolytic (D)
opposite.
,Question 5: Inflammation
A 55-year-old with gout has joint pain from monosodium urate crystals. What inflammatory pathway is
activated?
A. NLRP3 inflammasome leading to IL-1β release
B. JAK-STAT for cytokine signaling
C. Complement classical pathway
D. Fc receptor cross-linking
Correct Answer: A
Rationale: Urate crystals phagocytosed by macrophages activate NLRP3/caspase-1, cleaving pro-IL-1β
to active IL-1β, amplifying neutrophil recruitment and pyroptosis, causing acute gouty arthritis.
JAK-STAT (B) downstream; complement (C) secondary; Fc (D) immune complex.
Question 6: Inflammation
A child with asthma exacerbation shows bronchial edema. What vascular change underlies this?
A. Vasoconstriction from leukotrienes
B. Increased permeability via histamine H1 receptors
C. Platelet aggregation
D. Smooth muscle hypertrophy
Correct Answer: B
Rationale: Mast cell degranulation in type I hypersensitivity releases histamine, binding H1 on venules,
activating RhoA/MLC phosphatase inhibition, causing gap formation and plasma exudation, contributing
to airway narrowing. Leukotrienes (A) bronchoconstrict; platelets (C) vascular; hypertrophy (D) chronic.
Question 7: Inflammation
Post-MI, a patient develops pericarditis. What is the pathophysiologic basis?
A. Autoimmune reaction to myocardial antigens
B. Dressler's syndrome with anti-myocardial antibodies
C. Direct bacterial invasion
D. Viral myocarditis extension
, Correct Answer: B
Rationale: Dressler's (post-MI autoimmune pericarditis) involves molecular mimicry where damaged
myocardium releases antigens, eliciting IgG against myosin/sarcolemma, forming immune complexes that
deposit in pericardium, activating complement and causing sterile inflammation 2-6 weeks post-MI.
Acute (A) earlier; bacterial (C)/viral (D) infectious.
Question 8: Inflammation
A patient with IBD has granulomatous inflammation. What macrophage-derived factor drives this?
A. IL-4 for Th2 response
B. IFN-γ for Th1 activation
C. IL-17 for neutrophil recruitment
D. IL-10 for suppression
Correct Answer: B
Rationale: In Crohn's (granulomatous IBD), dysregulated Th1 cells release IFN-γ, activating
macrophages to form epithelioid/giant cells via STAT1, containing antigens in non-caseating granulomas
to limit spread. IL-4 (A) Th2; IL-17 (C) psoriasis; IL-10 (D) regulatory.
Question 9: Inflammation
In wound healing, a diabetic patient has delayed granulation. What cytokine imbalance?
A. Excess VEGF for angiogenesis
B. Reduced TGF-β for fibroblast migration
C. High IL-6 for proliferation
D. Low TNF-α for debridement
Correct Answer: B
Rationale: Hyperglycemia impairs TGF-β/Smad signaling in fibroblasts, reducing ECM synthesis
(collagen via α-SMA) and migration, stalling proliferative phase and causing non-healing ulcers. VEGF
(A) impaired too but secondary; IL-6 (C)/TNF-α (D) pro-inflammatory.
Question 10: Inflammation
