NUR 555 QUIZ 5
Questions and Answers with Complete Solutions
2026 Update | Southern New Hampshire University
Gastrointestinal, Musculoskeletal, Integumentary, and Reproductive Pathophysiology
Differential Diagnosis and Evidence-Based Management
Total Questions: 40 | Total Points: 100 | Time Limit: 90 Minutes
Cognitive Distribution: 30% Recall | 50% Application | 20% Analysis
,NUR 555 Quiz 5 | Advanced Pathophysiology | 2026 Update | SNHU 40 Questions | 100 Points Total
Section 1: Gastrointestinal & Hepatic Pathophysiology (Questions 1-10)
Q1. [2.5 pts] Which pathophysiological mechanism is most responsible for the development of
gastroesophageal reflux disease (GERD)?
A. Hypersecretion of gastric acid by parietal cells driven by gastrin overproduction
B. Transient lower esophageal sphincter (LES) relaxations unaccompanied by swallowing,
allowing retrograde flow of gastric contents [CORRECT]
C. H. pylori-induced chronic gastritis causing gastric mucosal atrophy and increased intragastric
pressure
D. Delayed gastric emptying with consequent pyloric sphincter spasm forcing contents superiorly
Correct Answer: B
Transient LES relaxations (TLESRs) are the dominant mechanism in GERD pathophysiology. Unlike
swallow-induced relaxations, TLESRs occur without a peristaltic trigger and are mediated by vagal afferent
pathways from gastric distension. Option A describes Zollinger-Ellison syndrome, not GERD. Option C reflects
H. pylori-associated gastritis, which is actually inversely correlated with GERD severity in some populations.
Option D describes gastroparesis, a less common contributor to reflux.
Q2. [2.5 pts] A 45-year-old patient presents with epigastric burning pain that improves with meals.
Endoscopy reveals a 1.5-cm gastric ulcer. Testing confirms H. pylori infection. Which virulence factor of
H. pylori is most directly responsible for mucosal injury in this patient?
A. Urease production, which elevates gastric pH and promotes bacterial colonization
B. CagA protein injection via a type IV secretion system, inducing cytoskeletal rearrangement
and pro-inflammatory signaling in gastric epithelial cells [CORRECT]
C. Flagellin-mediated motility enabling penetration of the submucosal layer
D. Biofilm formation on the ulcer crater surface, preventing antibiotic penetration
Correct Answer: B
The CagA cytotoxin is the key virulence factor directly causing epithelial damage. Once injected into gastric
epithelial cells via a type IV secretion system, CagA is phosphorylated and disrupts tight junctions, activates
NF-kB-mediated inflammation, and promotes apoptosis. Urease (Option A) is important for bacterial survival but
does not directly injure mucosa. Flagellin (Option C) aids motility in the mucus layer, not submucosal invasion.
Biofilm formation (Option D) is not a primary H. pylori pathogenic mechanism in gastric ulceration.
Q3. [2.5 pts] A 28-year-old woman presents with chronic bloody diarrhea, tenesmus, and urgency.
Colonoscopy reveals continuous mucosal inflammation and ulceration extending from the rectum to the
splenic flexure. Biopsy shows crypt abscesses and mucosal depletion of goblet cells. Which cytokine
profile is most characteristic of the pathophysiology of this condition?
A. Th1-dominant with elevated IFN-gamma and IL-2, driving transmural granulomatous
inflammation
B. Th2-dominant with elevated IL-4 and IL-5, promoting eosinophilic infiltration
C. Th17-dominant with elevated IL-17 and IL-23, driving neutrophilic mucosal inflammation
[CORRECT]
D. Treg-dominant with elevated TGF-beta and IL-10, causing immune suppression
Correct Answer: C
This patient has ulcerative colitis (UC), characterized by continuous mucosal inflammation beginning in the
rectum. The immunopathogenesis of UC is driven by a Th17/IL-23 axis, with IL-17 recruiting neutrophils that
form crypt abscesses and IL-23 sustaining Th17 cell survival. Option A describes Crohn disease (transmural,
granulomatous, skip lesions). Option B describes eosinophilic gastroenteritis. Option D describes a regulatory
phenotype, which is actually deficient in IBD, contributing to unchecked inflammation.
Page 2
, NUR 555 Quiz 5 | Advanced Pathophysiology | 2026 Update | SNHU 40 Questions | 100 Points Total
Q4. [2.5 pts] A patient with biopsy-proven Crohn disease involving the terminal ileum presents with
fatigue and pallor. Laboratory studies reveal a hemoglobin of 9.2 g/dL, MCV of 72 fL, and ferritin of 15
ng/mL. The pathophysiology of this anemia is best explained by which mechanism?
A. Chronic disease anemia due to hepcidin-mediated iron sequestration in enterocytes and
macrophages
B. Iron deficiency anemia secondary to impaired iron absorption in the inflamed terminal
ileum where DMT1 transporters are downregulated [CORRECT]
C. Vitamin B12 malabsorption due to loss of intrinsic factor-producing parietal cells in the gastric
body
D. Hemolytic anemia from autoimmune antibodies generated against erythrocyte membranes in the
setting of chronic inflammation
Correct Answer: B
Crohn disease of the terminal ileum impairs dietary iron absorption because the duodenum and proximal jejunum
(primary iron absorption sites) may be functionally compensated, but the terminal ileum contributes significantly
to iron uptake via DMT1, and chronic inflammation here reduces absorptive surface area and downregulates iron
transporters. The microcytic anemia (low MCV) and low ferritin confirm iron deficiency, not anemia of chronic
disease (which would have normal/high ferritin, Option A). Vitamin B12 malabsorption (Option C) causes
macrocytic anemia, not microcytic. Hemolytic anemia (Option D) is not a feature of Crohn disease.
Q5. [2.5 pts] A 58-year-old man with compensated cirrhosis develops ascites, asterixis, and confusion.
Serum ammonia is elevated at 185 mcg/dL. Which statement best describes the pathophysiological
cascade of hepatic encephalopathy in this patient?
A. Portal hypertension shunts blood around the liver, allowing ammonia to reach the systemic
circulation and cross the blood-brain barrier, where astrocytes convert it to glutamine, causing
cerebral edema [CORRECT]
B. Hepatocyte necrosis releases intracellular ammonia directly into the hepatic vein, overwhelming
the urea cycle in remaining functional hepatocytes
C. Accumulation of bilirubin in the brain parenchyma causes kernicterus, which directly depresses
neuronal function and consciousness
D. Decreased hepatic albumin synthesis reduces plasma oncotic pressure, leading to cerebral
vasogenic edema and increased intracranial pressure
Correct Answer: A
In hepatic encephalopathy, portosystemic shunting (collateral vessels opening due to portal hypertension)
bypasses the liver, so ammonia is not metabolized to urea. Ammonia crosses the blood-brain barrier and is taken
up by astrocytes, which convert it to glutamine via glutamine synthetase, causing astrocyte swelling and cerebral
edema. This explains the asterixis and confusion. Option B incorrectly describes the mechanism as hepatocyte
lysis rather than shunting. Option C describes bilirubin encephalopathy (kernicterus), a distinct entity seen in
neonates, not cirrhotic adults. Option D describes the mechanism of peripheral edema and ascites, not
encephalopathy.
Q6. [2.5 pts] Which laboratory pattern is most consistent with alcoholic cirrhosis as opposed to viral
hepatitis-induced cirrhosis?
A. AST:ALT ratio greater than 2:1 with both enzymes less than 500 IU/L [CORRECT]
B. ALT greater than AST with both enzymes greater than 1000 IU/L
C. Elevated alkaline phosphatase and GGT with minimally elevated transaminases
D. Predominantly elevated GGT with normal AST and ALT levels
Correct Answer: A
Alcoholic liver disease characteristically produces an AST:ALT ratio greater than 2:1, because alcohol induces
Page 3
Questions and Answers with Complete Solutions
2026 Update | Southern New Hampshire University
Gastrointestinal, Musculoskeletal, Integumentary, and Reproductive Pathophysiology
Differential Diagnosis and Evidence-Based Management
Total Questions: 40 | Total Points: 100 | Time Limit: 90 Minutes
Cognitive Distribution: 30% Recall | 50% Application | 20% Analysis
,NUR 555 Quiz 5 | Advanced Pathophysiology | 2026 Update | SNHU 40 Questions | 100 Points Total
Section 1: Gastrointestinal & Hepatic Pathophysiology (Questions 1-10)
Q1. [2.5 pts] Which pathophysiological mechanism is most responsible for the development of
gastroesophageal reflux disease (GERD)?
A. Hypersecretion of gastric acid by parietal cells driven by gastrin overproduction
B. Transient lower esophageal sphincter (LES) relaxations unaccompanied by swallowing,
allowing retrograde flow of gastric contents [CORRECT]
C. H. pylori-induced chronic gastritis causing gastric mucosal atrophy and increased intragastric
pressure
D. Delayed gastric emptying with consequent pyloric sphincter spasm forcing contents superiorly
Correct Answer: B
Transient LES relaxations (TLESRs) are the dominant mechanism in GERD pathophysiology. Unlike
swallow-induced relaxations, TLESRs occur without a peristaltic trigger and are mediated by vagal afferent
pathways from gastric distension. Option A describes Zollinger-Ellison syndrome, not GERD. Option C reflects
H. pylori-associated gastritis, which is actually inversely correlated with GERD severity in some populations.
Option D describes gastroparesis, a less common contributor to reflux.
Q2. [2.5 pts] A 45-year-old patient presents with epigastric burning pain that improves with meals.
Endoscopy reveals a 1.5-cm gastric ulcer. Testing confirms H. pylori infection. Which virulence factor of
H. pylori is most directly responsible for mucosal injury in this patient?
A. Urease production, which elevates gastric pH and promotes bacterial colonization
B. CagA protein injection via a type IV secretion system, inducing cytoskeletal rearrangement
and pro-inflammatory signaling in gastric epithelial cells [CORRECT]
C. Flagellin-mediated motility enabling penetration of the submucosal layer
D. Biofilm formation on the ulcer crater surface, preventing antibiotic penetration
Correct Answer: B
The CagA cytotoxin is the key virulence factor directly causing epithelial damage. Once injected into gastric
epithelial cells via a type IV secretion system, CagA is phosphorylated and disrupts tight junctions, activates
NF-kB-mediated inflammation, and promotes apoptosis. Urease (Option A) is important for bacterial survival but
does not directly injure mucosa. Flagellin (Option C) aids motility in the mucus layer, not submucosal invasion.
Biofilm formation (Option D) is not a primary H. pylori pathogenic mechanism in gastric ulceration.
Q3. [2.5 pts] A 28-year-old woman presents with chronic bloody diarrhea, tenesmus, and urgency.
Colonoscopy reveals continuous mucosal inflammation and ulceration extending from the rectum to the
splenic flexure. Biopsy shows crypt abscesses and mucosal depletion of goblet cells. Which cytokine
profile is most characteristic of the pathophysiology of this condition?
A. Th1-dominant with elevated IFN-gamma and IL-2, driving transmural granulomatous
inflammation
B. Th2-dominant with elevated IL-4 and IL-5, promoting eosinophilic infiltration
C. Th17-dominant with elevated IL-17 and IL-23, driving neutrophilic mucosal inflammation
[CORRECT]
D. Treg-dominant with elevated TGF-beta and IL-10, causing immune suppression
Correct Answer: C
This patient has ulcerative colitis (UC), characterized by continuous mucosal inflammation beginning in the
rectum. The immunopathogenesis of UC is driven by a Th17/IL-23 axis, with IL-17 recruiting neutrophils that
form crypt abscesses and IL-23 sustaining Th17 cell survival. Option A describes Crohn disease (transmural,
granulomatous, skip lesions). Option B describes eosinophilic gastroenteritis. Option D describes a regulatory
phenotype, which is actually deficient in IBD, contributing to unchecked inflammation.
Page 2
, NUR 555 Quiz 5 | Advanced Pathophysiology | 2026 Update | SNHU 40 Questions | 100 Points Total
Q4. [2.5 pts] A patient with biopsy-proven Crohn disease involving the terminal ileum presents with
fatigue and pallor. Laboratory studies reveal a hemoglobin of 9.2 g/dL, MCV of 72 fL, and ferritin of 15
ng/mL. The pathophysiology of this anemia is best explained by which mechanism?
A. Chronic disease anemia due to hepcidin-mediated iron sequestration in enterocytes and
macrophages
B. Iron deficiency anemia secondary to impaired iron absorption in the inflamed terminal
ileum where DMT1 transporters are downregulated [CORRECT]
C. Vitamin B12 malabsorption due to loss of intrinsic factor-producing parietal cells in the gastric
body
D. Hemolytic anemia from autoimmune antibodies generated against erythrocyte membranes in the
setting of chronic inflammation
Correct Answer: B
Crohn disease of the terminal ileum impairs dietary iron absorption because the duodenum and proximal jejunum
(primary iron absorption sites) may be functionally compensated, but the terminal ileum contributes significantly
to iron uptake via DMT1, and chronic inflammation here reduces absorptive surface area and downregulates iron
transporters. The microcytic anemia (low MCV) and low ferritin confirm iron deficiency, not anemia of chronic
disease (which would have normal/high ferritin, Option A). Vitamin B12 malabsorption (Option C) causes
macrocytic anemia, not microcytic. Hemolytic anemia (Option D) is not a feature of Crohn disease.
Q5. [2.5 pts] A 58-year-old man with compensated cirrhosis develops ascites, asterixis, and confusion.
Serum ammonia is elevated at 185 mcg/dL. Which statement best describes the pathophysiological
cascade of hepatic encephalopathy in this patient?
A. Portal hypertension shunts blood around the liver, allowing ammonia to reach the systemic
circulation and cross the blood-brain barrier, where astrocytes convert it to glutamine, causing
cerebral edema [CORRECT]
B. Hepatocyte necrosis releases intracellular ammonia directly into the hepatic vein, overwhelming
the urea cycle in remaining functional hepatocytes
C. Accumulation of bilirubin in the brain parenchyma causes kernicterus, which directly depresses
neuronal function and consciousness
D. Decreased hepatic albumin synthesis reduces plasma oncotic pressure, leading to cerebral
vasogenic edema and increased intracranial pressure
Correct Answer: A
In hepatic encephalopathy, portosystemic shunting (collateral vessels opening due to portal hypertension)
bypasses the liver, so ammonia is not metabolized to urea. Ammonia crosses the blood-brain barrier and is taken
up by astrocytes, which convert it to glutamine via glutamine synthetase, causing astrocyte swelling and cerebral
edema. This explains the asterixis and confusion. Option B incorrectly describes the mechanism as hepatocyte
lysis rather than shunting. Option C describes bilirubin encephalopathy (kernicterus), a distinct entity seen in
neonates, not cirrhotic adults. Option D describes the mechanism of peripheral edema and ascites, not
encephalopathy.
Q6. [2.5 pts] Which laboratory pattern is most consistent with alcoholic cirrhosis as opposed to viral
hepatitis-induced cirrhosis?
A. AST:ALT ratio greater than 2:1 with both enzymes less than 500 IU/L [CORRECT]
B. ALT greater than AST with both enzymes greater than 1000 IU/L
C. Elevated alkaline phosphatase and GGT with minimally elevated transaminases
D. Predominantly elevated GGT with normal AST and ALT levels
Correct Answer: A
Alcoholic liver disease characteristically produces an AST:ALT ratio greater than 2:1, because alcohol induces
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