A+
HERZING UNIVERSITY VERIFIED
NSG 120 Exam 2 V3
Nursing Pathophysiology — Actual Q&A with Rationale
50 4 100%
QUESTIONS OPTIONS EACH W I T H R AT I O N A L E
W H AT T H I S C O V E R S
Cellular adaptation and injury Inflammation and tissue repair
Fluid, electrolyte, and acid–base Hemodynamics and perfusion
Immune function and hypersensitivity Neoplasia and tumor biology
Cardiopulmonary pathophysiology Renal and hepatic pathophysiology
Neurologic and neuromuscular disorders Endocrine pathophysiology
ABOUT THIS ASSESSMENT
This assessment is an original, educationally focused question set written for nursing students preparing for the
second examination in NSG 120 Nursing Pathophysiology. It is not affiliated with, endorsed by, or derived from
any official examination, and no institution-issued exam content is reproduced. Every item is freshly authored in
the style and depth of the course.
Each question is followed by a clearly marked correct answer and a concise, evidence-informed rationale that
reinforces the underlying mechanism. The set emphasizes the high-yield domains most likely to appear on a
pathophysiology examination: cellular adaptation, inflammation and repair, fluid–electrolyte and acid–base
balance, hemodynamics, neoplasia, and the pathophysiology of major organ systems.
Students should use this material as a guided review tool rather than a memorization drill — the rationales
explain why an answer is correct and why the distractors are plausible, building the conceptual foundation
needed to translate pathophysiology into safe clinical nursing practice.
STUVIA ACTUAL EXAM
,NSG 120 EXAM 2 V3 Page 1
NSG 120 EXAM 2 V3 — ACTUAL Q&A WITH RATIONALE
Read each item carefully. Select the single best option. The correct answer and a rationale follow each question.
1. A patient with chronic atrophic gastritis develops parietal cell loss. Which pathophysiologic
consequence is most expected?
A. Hypersecretion of gastrin with Zollinger–Ellison syndrome.
B. Increased gastric acid secretion with peptic ulcer disease.
C. Decreased intrinsic factor with subsequent vitamin B12 malabsorption.
D. Iron overload due to increased iron absorption.
CORRECT ANSWER: C. Decreased intrinsic factor with subsequent vitamin B12 malabsorption.
RATIONALE
Parietal cells secrete both hydrochloric acid and intrinsic factor. In chronic atrophic gastritis (often autoimmune), loss
of parietal cells reduces intrinsic factor, impairing B12 absorption and producing megaloblastic anemia. Acid secretion
decreases (not increases), and Zollinger–Ellison is driven by a gastrinoma, not parietal cell loss.
2. Which cellular adaptation is best characterized by reversible substitution of one differentiated cell
type for another in response to chronic irritation?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Hypertrophy
CORRECT ANSWER: B. Metaplasia
RATIONALE
Metaplasia is the reversible substitution of one adult cell type for another, exemplified by squamous metaplasia in the
bronchi of smokers or Barrett esophagus in chronic reflux. Hypertrophy is size increase; hyperplasia is number
increase; dysplasia is disordered growth that may be a precursor to neoplasia.
3. Tissue hypoxia at the cellular level most directly initiates injury by:
A. Increasing intracellular pH and activating acid-base buffering.
B. Impairing adenosine triphosphate (ATP) production and failure of Na+/K+-ATPase.
C. Directly destroying the cellular nuclear membrane.
D. Stimulating ribosomal protein synthesis.
CORRECT ANSWER: B. Impairing adenosine triphosphate (ATP) production and failure of
Na+/K+-ATPase.
RATIONALE
Hypoxia reduces oxidative phosphorylation, depleting ATP. Loss of ATP fails the Na+/K+-ATPase, causing
intracellular Na+ and water accumulation (cellular swelling) and ultimately Ca2+ influx that activates phospholipases,
proteases, and endonucleases, producing irreversible injury. Ribosomal protein synthesis decreases (not increases)
under hypoxia.
Original educational study material — not affiliated with any institution STUVIA ACTUAL EXAM
, NSG 120 EXAM 2 V3 Page 2
4. A patient develops a pulmonary embolism. The most immediate pathophysiologic consequence at
the alveolar level is:
A. Increased diffusion capacity due to recruitment.
B. Left-to-right intracardiac shunt.
C. Increased V/Q ratio with subsequent hypoxemia.
D. Decreased V/Q ratio producing hypercapnia alone.
CORRECT ANSWER: C. Increased V/Q ratio with subsequent hypoxemia.
RATIONALE
A pulmonary embolus obstructs pulmonary blood flow, producing ventilated but non-perfused alveoli (increased dead
space, high V/Q). The result is hypoxemia from low end-capillary O2 and shunt through poorly perfused regions.
Hypercapnia is typically modest because minute ventilation increases. The other options describe non-embolic
physiology.
5. During acute inflammation, which mediator is most responsible for the pain and vascular
permeability observed at the site of injury?
A. Albumin only
B. Prostaglandins and bradykinin
C. Interleukin-10 only
D. Insulin
CORRECT ANSWER: B. Prostaglandins and bradykinin
RATIONALE
Bradykinin stimulates pain receptors and increases vascular permeability; prostaglandins (PGE2) sensitize
nociceptors and amplify vasodilation/permeability. NSAIDs relieve inflammatory pain by inhibiting cyclo-oxygenase,
blocking prostaglandin synthesis. IL-10 is anti-inflammatory; albumin and insulin are not primary inflammatory
mediators.
6. The predominant leukocyte in the acute phase (first 24 hours) of acute bacterial infection is the:
A. Eosinophil
B. Macrophage
C. Lymphocyte
D. Neutrophil
CORRECT ANSWER: D. Neutrophil
RATIONALE
Neutrophils (PMNs) are the first responders in acute bacterial infection, arriving within hours and predominating in the
first 24–48 hours. Macrophages dominate later (subacute/chronic inflammation). Lymphocytes predominate in viral
and chronic inflammation. Eosinophils predominate in parasitic infestation and allergic reactions.
7. Which finding is the hallmark of type I (immediate) hypersensitivity reactions?
A. IgG-mediated complement activation against cell surface antigens.
B. Formation of circulating immune complexes depositing in tissues.
C. T-cell mediated delayed-type hypersensitivity.
D. IgE-mediated release of histamine from mast cells.
CORRECT ANSWER: D. IgE-mediated release of histamine from mast cells.
RATIONALE
Type I hypersensitivity is IgE-mediated; cross-linking of IgE on mast cells by antigen triggers degranulation of
histamine and other mediators, producing urticaria, bronchospasm, and anaphylaxis. Type II is IgG/complement
against cells; Type III is immune-complex deposition (e.g., SLE); Type IV is T-cell mediated (e.g., tuberculin reaction,
contact dermatitis).
Original educational study material — not affiliated with any institution STUVIA ACTUAL EXAM
HERZING UNIVERSITY VERIFIED
NSG 120 Exam 2 V3
Nursing Pathophysiology — Actual Q&A with Rationale
50 4 100%
QUESTIONS OPTIONS EACH W I T H R AT I O N A L E
W H AT T H I S C O V E R S
Cellular adaptation and injury Inflammation and tissue repair
Fluid, electrolyte, and acid–base Hemodynamics and perfusion
Immune function and hypersensitivity Neoplasia and tumor biology
Cardiopulmonary pathophysiology Renal and hepatic pathophysiology
Neurologic and neuromuscular disorders Endocrine pathophysiology
ABOUT THIS ASSESSMENT
This assessment is an original, educationally focused question set written for nursing students preparing for the
second examination in NSG 120 Nursing Pathophysiology. It is not affiliated with, endorsed by, or derived from
any official examination, and no institution-issued exam content is reproduced. Every item is freshly authored in
the style and depth of the course.
Each question is followed by a clearly marked correct answer and a concise, evidence-informed rationale that
reinforces the underlying mechanism. The set emphasizes the high-yield domains most likely to appear on a
pathophysiology examination: cellular adaptation, inflammation and repair, fluid–electrolyte and acid–base
balance, hemodynamics, neoplasia, and the pathophysiology of major organ systems.
Students should use this material as a guided review tool rather than a memorization drill — the rationales
explain why an answer is correct and why the distractors are plausible, building the conceptual foundation
needed to translate pathophysiology into safe clinical nursing practice.
STUVIA ACTUAL EXAM
,NSG 120 EXAM 2 V3 Page 1
NSG 120 EXAM 2 V3 — ACTUAL Q&A WITH RATIONALE
Read each item carefully. Select the single best option. The correct answer and a rationale follow each question.
1. A patient with chronic atrophic gastritis develops parietal cell loss. Which pathophysiologic
consequence is most expected?
A. Hypersecretion of gastrin with Zollinger–Ellison syndrome.
B. Increased gastric acid secretion with peptic ulcer disease.
C. Decreased intrinsic factor with subsequent vitamin B12 malabsorption.
D. Iron overload due to increased iron absorption.
CORRECT ANSWER: C. Decreased intrinsic factor with subsequent vitamin B12 malabsorption.
RATIONALE
Parietal cells secrete both hydrochloric acid and intrinsic factor. In chronic atrophic gastritis (often autoimmune), loss
of parietal cells reduces intrinsic factor, impairing B12 absorption and producing megaloblastic anemia. Acid secretion
decreases (not increases), and Zollinger–Ellison is driven by a gastrinoma, not parietal cell loss.
2. Which cellular adaptation is best characterized by reversible substitution of one differentiated cell
type for another in response to chronic irritation?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Hypertrophy
CORRECT ANSWER: B. Metaplasia
RATIONALE
Metaplasia is the reversible substitution of one adult cell type for another, exemplified by squamous metaplasia in the
bronchi of smokers or Barrett esophagus in chronic reflux. Hypertrophy is size increase; hyperplasia is number
increase; dysplasia is disordered growth that may be a precursor to neoplasia.
3. Tissue hypoxia at the cellular level most directly initiates injury by:
A. Increasing intracellular pH and activating acid-base buffering.
B. Impairing adenosine triphosphate (ATP) production and failure of Na+/K+-ATPase.
C. Directly destroying the cellular nuclear membrane.
D. Stimulating ribosomal protein synthesis.
CORRECT ANSWER: B. Impairing adenosine triphosphate (ATP) production and failure of
Na+/K+-ATPase.
RATIONALE
Hypoxia reduces oxidative phosphorylation, depleting ATP. Loss of ATP fails the Na+/K+-ATPase, causing
intracellular Na+ and water accumulation (cellular swelling) and ultimately Ca2+ influx that activates phospholipases,
proteases, and endonucleases, producing irreversible injury. Ribosomal protein synthesis decreases (not increases)
under hypoxia.
Original educational study material — not affiliated with any institution STUVIA ACTUAL EXAM
, NSG 120 EXAM 2 V3 Page 2
4. A patient develops a pulmonary embolism. The most immediate pathophysiologic consequence at
the alveolar level is:
A. Increased diffusion capacity due to recruitment.
B. Left-to-right intracardiac shunt.
C. Increased V/Q ratio with subsequent hypoxemia.
D. Decreased V/Q ratio producing hypercapnia alone.
CORRECT ANSWER: C. Increased V/Q ratio with subsequent hypoxemia.
RATIONALE
A pulmonary embolus obstructs pulmonary blood flow, producing ventilated but non-perfused alveoli (increased dead
space, high V/Q). The result is hypoxemia from low end-capillary O2 and shunt through poorly perfused regions.
Hypercapnia is typically modest because minute ventilation increases. The other options describe non-embolic
physiology.
5. During acute inflammation, which mediator is most responsible for the pain and vascular
permeability observed at the site of injury?
A. Albumin only
B. Prostaglandins and bradykinin
C. Interleukin-10 only
D. Insulin
CORRECT ANSWER: B. Prostaglandins and bradykinin
RATIONALE
Bradykinin stimulates pain receptors and increases vascular permeability; prostaglandins (PGE2) sensitize
nociceptors and amplify vasodilation/permeability. NSAIDs relieve inflammatory pain by inhibiting cyclo-oxygenase,
blocking prostaglandin synthesis. IL-10 is anti-inflammatory; albumin and insulin are not primary inflammatory
mediators.
6. The predominant leukocyte in the acute phase (first 24 hours) of acute bacterial infection is the:
A. Eosinophil
B. Macrophage
C. Lymphocyte
D. Neutrophil
CORRECT ANSWER: D. Neutrophil
RATIONALE
Neutrophils (PMNs) are the first responders in acute bacterial infection, arriving within hours and predominating in the
first 24–48 hours. Macrophages dominate later (subacute/chronic inflammation). Lymphocytes predominate in viral
and chronic inflammation. Eosinophils predominate in parasitic infestation and allergic reactions.
7. Which finding is the hallmark of type I (immediate) hypersensitivity reactions?
A. IgG-mediated complement activation against cell surface antigens.
B. Formation of circulating immune complexes depositing in tissues.
C. T-cell mediated delayed-type hypersensitivity.
D. IgE-mediated release of histamine from mast cells.
CORRECT ANSWER: D. IgE-mediated release of histamine from mast cells.
RATIONALE
Type I hypersensitivity is IgE-mediated; cross-linking of IgE on mast cells by antigen triggers degranulation of
histamine and other mediators, producing urticaria, bronchospasm, and anaphylaxis. Type II is IgG/complement
against cells; Type III is immune-complex deposition (e.g., SLE); Type IV is T-cell mediated (e.g., tuberculin reaction,
contact dermatitis).
Original educational study material — not affiliated with any institution STUVIA ACTUAL EXAM
