,NSG 530 Exam 3 Advanced Pathophysiology Questions And Answers
2026/2027 Wilkes University
Q1. Loss of gastric parietal cells most directly interferes with
intestinal absorption of which nutrient?
A) Folate
B) Vitamin B12
C) Vitamin C
D) Vitamin K
Correct Answer: B) Vitamin B12
Rationale: Parietal cells produce intrinsic factor, which binds vitamin B12
and permits its absorption in the terminal ileum. Significant loss of intrinsic
factor can therefore cause vitamin B12 deficiency and ultimately
megaloblastic anemia and neurologic dysfunction.
Q2. Gastroesophageal reflux develops most directly when which
protective mechanism becomes inadequate?
A) Gastric pepsin secretion
B) Small-intestinal segmentation
C) Pancreatic bicarbonate secretion
D) Lower esophageal sphincter barrier function
Correct Answer: D) Lower esophageal sphincter barrier function
Rationale: The lower esophageal sphincter normally limits movement of
acidic gastric contents into the esophagus. Reduced sphincter pressure or
inappropriate transient relaxation allows reflux, exposing esophageal mucosa
to acid and causing inflammation and characteristic burning discomfort.
Q3. Helicobacter pylori contributes to peptic ulcer formation
primarily through which mechanism?
A) Chronic mucosal inflammation that disrupts gastroduodenal defenses
B) Complete inhibition of gastric acid secretion
C) Permanent closure of the pyloric sphincter
D) Increased synthesis of protective prostaglandins
, Correct Answer: A) Chronic mucosal inflammation that disrupts
gastroduodenal defenses
Rationale: H. pylori colonization promotes chronic mucosal inflammation
and alters mechanisms regulating acid secretion and mucosal protection.
The resulting imbalance between aggressive factors and protective defenses
increases susceptibility to gastric and duodenal ulceration.
Q4. Long-term nonsteroidal anti-inflammatory drug use increases
peptic ulcer risk because these drugs reduce synthesis of what
substance?
A) Gastrin
B) Histamine
C) Protective prostaglandins
D) Intrinsic factor
Correct Answer: C) Protective prostaglandins
Rationale: Prostaglandins support gastric mucosal blood flow, bicarbonate
secretion, and mucus production. NSAID-mediated cyclooxygenase inhibition
reduces prostaglandin synthesis, weakening these defenses and increasing
susceptibility to mucosal injury and ulceration.
Q5. An infant has progressive projectile nonbilious vomiting several
weeks after birth. Which mechanism best explains the disorder?
A) Failure of intestinal villi to develop
B) Hypertrophy of the pyloric musculature producing gastric outlet
obstruction
C) Absence of pancreatic enzymes
D) Malrotation of the colon
Correct Answer: B) Hypertrophy of the pyloric musculature producing
gastric outlet obstruction
Rationale: Infantile hypertrophic pyloric stenosis involves progressive
thickening of pyloric smooth muscle. Gastric contents cannot pass effectively
into the duodenum, causing forceful nonbilious vomiting and eventually
dehydration, weight loss, and characteristic metabolic abnormalities.
2026/2027 Wilkes University
Q1. Loss of gastric parietal cells most directly interferes with
intestinal absorption of which nutrient?
A) Folate
B) Vitamin B12
C) Vitamin C
D) Vitamin K
Correct Answer: B) Vitamin B12
Rationale: Parietal cells produce intrinsic factor, which binds vitamin B12
and permits its absorption in the terminal ileum. Significant loss of intrinsic
factor can therefore cause vitamin B12 deficiency and ultimately
megaloblastic anemia and neurologic dysfunction.
Q2. Gastroesophageal reflux develops most directly when which
protective mechanism becomes inadequate?
A) Gastric pepsin secretion
B) Small-intestinal segmentation
C) Pancreatic bicarbonate secretion
D) Lower esophageal sphincter barrier function
Correct Answer: D) Lower esophageal sphincter barrier function
Rationale: The lower esophageal sphincter normally limits movement of
acidic gastric contents into the esophagus. Reduced sphincter pressure or
inappropriate transient relaxation allows reflux, exposing esophageal mucosa
to acid and causing inflammation and characteristic burning discomfort.
Q3. Helicobacter pylori contributes to peptic ulcer formation
primarily through which mechanism?
A) Chronic mucosal inflammation that disrupts gastroduodenal defenses
B) Complete inhibition of gastric acid secretion
C) Permanent closure of the pyloric sphincter
D) Increased synthesis of protective prostaglandins
, Correct Answer: A) Chronic mucosal inflammation that disrupts
gastroduodenal defenses
Rationale: H. pylori colonization promotes chronic mucosal inflammation
and alters mechanisms regulating acid secretion and mucosal protection.
The resulting imbalance between aggressive factors and protective defenses
increases susceptibility to gastric and duodenal ulceration.
Q4. Long-term nonsteroidal anti-inflammatory drug use increases
peptic ulcer risk because these drugs reduce synthesis of what
substance?
A) Gastrin
B) Histamine
C) Protective prostaglandins
D) Intrinsic factor
Correct Answer: C) Protective prostaglandins
Rationale: Prostaglandins support gastric mucosal blood flow, bicarbonate
secretion, and mucus production. NSAID-mediated cyclooxygenase inhibition
reduces prostaglandin synthesis, weakening these defenses and increasing
susceptibility to mucosal injury and ulceration.
Q5. An infant has progressive projectile nonbilious vomiting several
weeks after birth. Which mechanism best explains the disorder?
A) Failure of intestinal villi to develop
B) Hypertrophy of the pyloric musculature producing gastric outlet
obstruction
C) Absence of pancreatic enzymes
D) Malrotation of the colon
Correct Answer: B) Hypertrophy of the pyloric musculature producing
gastric outlet obstruction
Rationale: Infantile hypertrophic pyloric stenosis involves progressive
thickening of pyloric smooth muscle. Gastric contents cannot pass effectively
into the duodenum, causing forceful nonbilious vomiting and eventually
dehydration, weight loss, and characteristic metabolic abnormalities.
