NR507/ NR 507 Final Exam (2026/2027) Advanced
Pathophysiology Ques & Ans - to Pass the Exam, 100% Verified -
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CATEGORIES
Cellular Injury, Inflammation, and Immune Mechanisms
Cardiovascular and Hematologic Pathophysiology
Respiratory, Acid-Base, and Pulmonary Disorders
Renal, Fluid, Electrolyte, and Acid-Base Balance
Endocrine, Neurologic, and Multisystem Pathophysiology
STUVIAACTUALEXAM
, Section 1: Cellular Injury, Inflammation, and Immune Mechanisms
Question 1
A 54-year-old man with longstanding hypertension develops progressive left-ventricular hypertrophy. Myocardial
biopsy demonstrates enlarged myocytes with hyperchromatic nuclei. The pathologist attributes these changes to a
specific form of cellular adaptation. Which adaptive process best explains the increase in cell size observed in this
patient's myocardium?
A. Hypertrophy driven by increased mechanical workload and trophic signals
B. Hyperplasia resulting from proliferation of cardiac stem cells
C. Metaplasia converting contractile myocytes into fibroblastic cells
D. Atrophy caused by chronic ischemic underperfusion of the ventricle
Correct Answer: A
Rationale: Hypertrophy is the increase in cell size in response to increased workload; adult cardiac myocytes have limited
proliferative capacity, so hyperplasia is not the primary mechanism. Metaplasia and atrophy represent different adaptive responses
not consistent with the histologic findings.
Question 2
A 32-year-old woman develops acute swelling, erythema, and pain at the site of a recent insect bite. Histologic
examination of the tissue shows dilated vessels, extravasated neutrophils, and protein-rich edema fluid. Which
chemical mediator is primarily responsible for the early increase in vascular permeability that produces the edema?
A. Histamine released from mast cells causing immediate endothelial gap formation
B. Interleukin-10 acting to suppress endothelial activation and reduce leakage
C. Transforming growth factor-beta promoting fibrosis and vessel stabilization
D. Nitric oxide exclusively mediating late-phase sustained permeability changes
Correct Answer: A
Rationale: Histamine is a key early mediator of increased vascular permeability in acute inflammation, producing rapid endothelial
contraction and gap formation. IL-10 and TGF-beta are largely anti-inflammatory or pro-fibrotic, and nitric oxide contributes more to
sustained effects than to the immediate response.
Question 3
A patient with a severe burn injury develops extensive tissue necrosis. Microscopic examination reveals cellular
swelling, membrane disruption, and nuclear pyknosis progressing to karyolysis. Which form of cell death is
characterized by these morphologic features and is typically associated with inflammation?
A. Necrosis resulting from irreversible injury and loss of membrane integrity
B. Apoptosis occurring through orderly caspase-mediated programmed pathways
C. Autophagy involving lysosomal degradation of cellular components without inflammation
D. Anoikis triggered solely by detachment from the extracellular matrix
Correct Answer: A
Rationale: Necrosis is the form of cell death that produces membrane rupture, inflammation, and the nuclear changes described.
Apoptosis is programmed and typically non-inflammatory; autophagy and anoikis represent distinct pathways not matching the
morphologic description of coagulative or liquefactive necrosis.
Question 4
A 28-year-old woman with systemic lupus erythematosus develops a malar rash and rising anti-double-stranded DNA
titers. Immune-complex deposition is detected in skin and kidney biopsy samples. Which type of hypersensitivity
reaction is primarily responsible for the tissue injury in this autoimmune disease?
A. Type III hypersensitivity mediated by circulating immune complexes
B. Type I hypersensitivity driven by IgE and mast-cell degranulation
C. Type II hypersensitivity caused by antibody binding to cell-surface antigens
D. Type IV hypersensitivity mediated exclusively by cytotoxic T lymphocytes
Correct Answer: A
Rationale: SLE is the classic example of type III hypersensitivity, in which immune complexes deposit in tissues and activate
complement and inflammation. Type I is immediate allergic; type II involves antibodies directed against fixed cell-surface antigens;
type IV is delayed cell-mediated.
NR507 Advanced Pathophysiology | 2026/2027 Page 2