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NGR 5149 Advanced Pathophysiology Final Exam 2026 | Cellular Injury, Inflammation, Reperfusion Injury, Cytokines | Verified Questions & Rationales

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Prepare for the NGR 5149 Advanced Pathophysiology Final Exam 2026 with this verified practice question set, covering cellular injury mechanisms, ATP-dependent sodium-potassium pump failure, hypoxia-induced cellular swelling, ischemia-reperfusion injury, reactive oxygen species, oxidative stress, acute and chronic inflammation, mononuclear cell infiltration, histologic features, tissue fibrosis, systemic inflammatory response syndrome (SIRS), TNF-alpha, IL-4, IL-10, and TGF-beta cytokine signaling. Each question includes correct answers and rationales, helping graduate nursing students, DNP students, and advanced practice nurses enhance their critical thinking, pathophysiology knowledge, and NGN exam preparation strategies.

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NGR 5149 ADVANCED PATHOPHYSIOLOGY
FINAL EXAM ACTUAL QUESTIONS AND
ANSWERS - LATEST AND COMPLETE UPDATE
WITH VERIFIED SOLUTIONS – ASSURED PASS
WITH INSTANT DOWNLOAD PDF.
1. A hospitalized patient develops cellular swelling after prolonged hypoxia.
Which intracellular process is the primary cause of this change?
A. Increased lysosomal membrane stability
B. Failure of ATP-dependent sodium-potassium pumps
C. Increased protein synthesis
D. Activation of apoptosis
Rationale: Hypoxia leads to decreased ATP production, impairing Na⁺/K⁺-
ATPase function and causing intracellular sodium and water accumulation,
resulting in cellular swelling.
2. Which mechanism best explains reperfusion injury following ischemia?
A. Restoration of normal mitochondrial ATP production
B. Decreased neutrophil activation
C. Generation of reactive oxygen species and inflammatory mediators
D. Suppression of cytokine release
Rationale: Reperfusion introduces oxygen that generates free radicals and
triggers inflammation, worsening tissue damage rather than reversing it.
3. A patient with chronic inflammation is most likely to demonstrate which
histologic feature?
A. Neutrophilic predominance
B. Mononuclear cell infiltration
C. Fibrin deposition

, D. Extensive edema
Rationale: Chronic inflammation is characterized by macrophages,
lymphocytes, plasma cells, tissue destruction, and fibrosis rather than acute
neutrophil dominance.
4. Which cytokine plays a central role in systemic inflammatory response
syndrome (SIRS)?
A. IL-4
B. IL-10
C. Tumor necrosis factor-alpha (TNF-α)
D. Transforming growth factor-β
Rationale: TNF-α is a key pro-inflammatory cytokine responsible for fever,
hypotension, capillary leak, and shock in systemic inflammation.
5. A mutation affecting the p53 gene increases cancer risk primarily because
p53 normally:
A. Enhances angiogenesis
B. Induces cell cycle arrest and apoptosis after DNA damage
C. Promotes cellular differentiation
D. Stimulates telomerase activity
Rationale: p53 functions as a tumor suppressor by halting the cell cycle and
triggering apoptosis when DNA damage is detected.
6. Which characteristic distinguishes malignant tumors from benign tumors?
A. Encapsulation
B. Slow growth rate
C. Ability to metastasize
D. Uniform cell morphology
Rationale: Metastatic potential is a defining feature of malignant tumors
and is absent in benign growths.

,7. An adult patient presents with edema, hypotension, and hypoalbuminemia
due to capillary leak. Which pathophysiologic process best explains this
finding?
A. Increased plasma oncotic pressure
B. Increased vascular permeability
C. Decreased hydrostatic pressure
D. Enhanced lymphatic drainage
Rationale: Inflammation increases endothelial permeability, allowing
albumin and fluid to escape into the interstitial space.
8. In type II hypersensitivity reactions, tissue injury primarily results from:
A. Immune complex deposition
B. Antibody-mediated cell destruction
C. T-cell cytotoxicity
D. IgE-mediated mast cell degranulation
Rationale: Type II reactions involve IgG or IgM antibodies targeting cell
surface antigens, leading to complement activation or phagocytosis.
9. A patient with systemic lupus erythematosus is experiencing renal injury.
Which mechanism is most responsible?
A. Direct antibody-dependent cytotoxicity
B. Immune complex deposition in glomeruli
C. Delayed T-cell hypersensitivity
D. Mast cell activation
Rationale: SLE is a classic type III hypersensitivity disorder characterized
by immune complex deposition causing inflammation and tissue damage.
10.Which laboratory finding best supports a diagnosis of acute bacterial
infection?
A. Lymphocytosis

, B. Neutrophilia with left shift
C. Eosinophilia
D. Decreased C-reactive protein
Rationale: Acute bacterial infections stimulate neutrophil production, often
with immature forms (“left shift”).
11.A patient develops autoantibodies against acetylcholine receptors. Which
condition is most likely?
A. Guillain-Barré syndrome
B. Lambert-Eaton syndrome
C. Myasthenia gravis
D. Multiple sclerosis
Rationale: Myasthenia gravis results from antibodies blocking acetylcholine
receptors at the neuromuscular junction.
12.Which physiologic change is expected in an aging adult?
A. Increased renal concentrating ability
B. Decreased baroreceptor sensitivity
C. Increased alveolar surface area
D. Enhanced immune responsiveness
Rationale: Aging reduces baroreceptor responsiveness, increasing
susceptibility to orthostatic hypotension.
13.A patient with septic shock has persistent hypotension despite adequate fluid
resuscitation. This is most directly related to:
A. Increased systemic vascular resistance
B. Decreased nitric oxide production
C. Pathologic vasodilation and capillary leak
D. Enhanced myocardial contractility

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