NSG 530 Exam 1, 2, 3 & 4 | Advanced Pathophysiology – Wilkes | 2026/2027 Verified Questions & Answers | PDF

NSG 530 EXAM 1, 2, 3 & 4 | ADVANCED PATHOPHYSIOLOGY –
WILKES | 2026/2027 VERIFIED QUESTIONS & ANSWERS | PDF


NSG 530: Advanced Pathophysiology — Comprehensive Examination (Exams 1–4 Bundle)

Course: NSG 530 — Advanced Pathophysiology (Wilkes University Graduate Nursing
Program)

Academic Year:

Format: Multiple-Choice (MCQ), Short-Answer, and Clinical Case Scenarios with Answers &
Rationales

Table of Contents

1. Introduction & Examination Guidelines

2. Section I: Exam 1 — Cellular Biology, Inflammation, Immunity, Genetics & Acid-Base
(Questions 1–25)

3. Section II: Exam 2 — Hematologic, Cardiovascular & Respiratory Pathophysiology
(Questions 26–50)

4. Section III: Exam 3 — Renal, Gastrointestinal & Endocrine Pathophysiology (Questions
51–75)

5. Section IV: Exam 4 — Neurological, Musculoskeletal & Multisystem Pathophysiology
(Questions 76–100)

6. Section V: Applied Clinical Scenarios & Complex Synthesis (Questions 101–105)
7. Comprehensive Answer Key & Detailed Rationales

1. Introduction & Examination Guidelines

This comprehensive exam bank is designed for graduate nursing students enrolled in NSG 530:
Advanced Pathophysiology. It synthesizes core concepts across all four primary exam domains
of the curriculum:

• Exam 1 Content: Cellular adaptation, cellular injury, apoptosis/necrosis, inflammation,
hypersensitivity, innate/adaptive immunity, genetics, fluid/electrolytes, and acid-base
disturbances.

• Exam 2 Content: Hematologic disorders, cardiovascular dynamics, myocardial
infarction, heart failure, vascular pathology, and restrictive/obstructive pulmonary
pathophysiology.

, • Exam 3 Content: Renal hemodynamic regulation, acute/chronic kidney disease,
gastrointestinal ulcerative and inflammatory disorders, hepatic failure, and endocrine
dysfunction (thyroid, adrenal, pancreatic).

• Exam 4 Content: Central and peripheral nervous system pathology, neurodegenerative
diseases, neuromuscular junction disorders, musculoskeletal conditions, and multisystem
dysfunction.

2. Section I: Exam 1 — Cellular Biology, Inflammation, Immunity, Genetics & Acid-Base

Question 1 (MCQ)

Which cellular adaptation occurs as a direct result of chronic increased mechanical workload in
non-dividing cardiac myocytes, leading to increased protein synthesis and organelle size?

• A) Hyperplasia

• B) Hypertrophy

• C) Metaplasia
• D) Dysplasia

Question 2 (MCQ)

A cervical Pap smear report demonstrates "cervical dysplasia." Which cellular description best
characterizes this alteration?

• A) Reversible conversion of one mature epithelial cell type to another mature cell type

• B) Increase in the total number of normal parenchymal cells driven by growth factors

• C) Disorganized, atypical cell growth with variable size, shape, and loss of normal
architectural orientation
• D) Programmed, energy-dependent cell suicide without plasma membrane disruption

Question 3 (MCQ)

During hypoxic cell injury, which biochemical event immediately triggers cellular swelling
(cloudy swelling)?

• A) Influx of extracellular potassium into the cytoplasm

• B) Failure of the 𝑁𝑎+ /𝐾 + ATPase pump leading to intracellular sodium accumulation

• C) Rapid upregulation of mitochondrial ATP synthase

• D) Efflux of calcium ions out of the endoplasmic reticulum

Question 4 (MCQ)

,Which form of tissue necrosis is characteristically seen in ischemic injury to the central nervous
system (brain tissue)?

• A) Coagulative necrosis
• B) Liquefactive necrosis

• C) Caseous necrosis

• D) Fat necrosis

Question 5 (MCQ)

Which chemical mediator is primarily responsible for generating the systemic and localized pain
sensation during acute inflammation by directly stimulating nociceptors?

• A) Histamine

• B) Leukotriene 𝐵4

• C) Bradykinin

• D) Factor XII (Hageman factor)

Question 6 (MCQ)

Which leukocyte is the primary early responder recruited to the extravascular space within 6 to
12 hours of acute tissue injury?

• A) Monocyte

• B) Lymphocyte

• C) Neutrophil

• D) Eosinophil
Question 7 (MCQ)

A patient with a history of severe allergies presents with wheezing and laryngeal tightness.
Histamine released during this Type I hypersensitivity reaction binds to 𝐻1 receptors on
bronchial smooth muscle, causing:

• A) Bronchodilator relaxation

• B) Smooth muscle contraction and bronchoconstriction

• C) Inhibition of mucosal secretions

• D) Decreased vascular permeability

Question 8 (MCQ)

, In Type III hypersensitivity reactions (such as Systemic Lupus Erythematosus), tissue injury is
primarily driven by:

• A) IgE-mediated mast cell degranulation
• B) Direct cytotoxic T-cell destruction of target parenchymal cells

• C) Deposition of circulating soluble antigen-antibody immune complexes in
microvascular walls, activating complement

• D) Complement-independent antibody neutralization of cell surface receptors

Question 9 (MCQ)

Which immune cell type is predominantly responsible for the cell-mediated delayed
hypersensitivity response seen in contact dermatitis (e.g., poison ivy)?

• A) Plasma cells producing IgE

• B) Sensitized 𝑇𝐻 1 and cytotoxic T-lymphocytes

• C) Basophils and eosinophils

• D) Circulating immune complexes with neutrophils

Question 10 (MCQ)

Alloimmunity is best illustrated by which of the following clinical scenarios?

• A) Development of anti-double-stranded DNA antibodies in SLE

• B) An acute hemolytic transfusion reaction occurring after receiving ABO-mismatched
packed red blood cells

• C) Development of contact dermatitis after wearing nickel-plated jewelry

• D) IgE-mediated anaphylactic reaction to peanut exposure

Question 11 (MCQ)

A patient's arterial blood gas (ABG) displays: pH 7.28, 𝑃𝑎𝐶𝑂2 58 mmHg, 𝐻𝐶𝑂3− 26 mEq/L.
Which primary acid-base disorder is present?

• A) Metabolic acidosis

• B) Metabolic alkalosis

• C) Respiratory acidosis

• D) Respiratory alkalosis

Question 12 (MCQ)