,NSG530/NSG 530 Exam 3 Advanced
Pathophysiology | Wilkes University | Q&A|
1. Which enzyme is primarily responsible for the chemical digestion of carbohydrates in the small
intestine?
A) Amylase
B) Lipase
C) Pepsin
D) Trypsin
Correct Answer: Amylase
Rationale: Amylase, secreted by the pancreas and salivary glands, hydrolyzes starch into smaller
sugars like maltose. Lipase digests fats, pepsin digests proteins in the stomach, and trypsin digests
proteins in the small intestine. Amylase is the principal carbohydrate-digesting enzyme.
2. Intrinsic factor, secreted by gastric parietal cells, is essential for the absorption of which vitamin?
A) Vitamin B6
B) Vitamin B9 (folate)
C) Vitamin B12
D) Vitamin C
Correct Answer: Vitamin B12
Rationale: Intrinsic factor binds to vitamin B12, facilitating its absorption in the terminal ileum. A
deficiency leads to pernicious anemia. B6, folate, and C do not require intrinsic factor for absorption.
3. In the cephalic phase of gastric secretion, which nervous system pathway primarily stimulates acid
production?
A) Sympathetic nervous system
B) Parasympathetic nervous system via the vagus nerve
C) Somatic nervous system
D) Enteric nervous system independently
Correct Answer: Parasympathetic nervous system via the vagus nerve
,Rationale: The cephalic phase is triggered by the sight, smell, or thought of food, activating the
parasympathetic nervous system through the vagus nerve, which stimulates gastric acid secretion.
The sympathetic system inhibits digestion.
4. Which hormone, released from the duodenum in response to acidic chyme, inhibits gastric acid
secretion?
A) Gastrin
B) Secretin
C) Cholecystokinin
D) Motilin
Correct Answer: Secretin
Rationale: Secretin is released by S cells in the duodenum when acidic chyme enters, inhibiting gastric
acid secretion and stimulating pancreatic bicarbonate release. Gastrin stimulates acid, CCK stimulates
gallbladder contraction, and motilin regulates migrating motor complexes.
5. A patient with a history of chronic NSAID use develops a gastric ulcer. Which pathophysiological
mechanism is most directly responsible?
A) Increased gastric acid hypersecretion
B) Decreased mucosal prostaglandin synthesis
C) Helicobacter pylori overgrowth
D) Reduced gastric emptying
Correct Answer: Decreased mucosal prostaglandin synthesis
Rationale: NSAIDs inhibit cyclooxygenase-1, reducing prostaglandin synthesis, which diminishes
mucosal protective factors like mucus and bicarbonate. While H. pylori is a common cause, NSAIDs act
through this specific prostaglandin-dependent mechanism, not primarily by increasing acid or slowing
emptying.
6. In Zollinger-Ellison syndrome, which cell type is responsible for the excessive secretion of gastrin?
A) Gastric G cells
B) Pancreatic alpha cells
C) Gastrin-secreting tumor (gastrinoma)
D) Duodenal S cells
, Correct Answer: Gastrin-secreting tumor (gastrinoma)
Rationale: Zollinger-Ellison syndrome is caused by a gastrinoma, a neuroendocrine tumor, usually in
the pancreas or duodenum, that secretes excessive gastrin. This leads to severe peptic ulcer disease.
Gastric G cells are the normal source but are not the cause of this syndrome.
7. Which complication of gastroesophageal reflux disease (GERD) is characterized by the replacement
of stratified squamous epithelium with columnar epithelium in the esophagus?
A) Esophageal stricture
B) Barrett esophagus
C) Esophagitis
D) Adenocarcinoma
Correct Answer: Barrett esophagus
Rationale: Barrett esophagus is a metaplastic change where the normal squamous epithelium is
replaced by intestinal-type columnar epithelium as a protective response to chronic acid reflux. It is a
premalignant condition. Stricture, esophagitis, and adenocarcinoma are other potential complications
but not this specific cellular change.
8. In the pathophysiology of acute pancreatitis, which enzyme is prematurely activated within the
pancreas, leading to autodigestion?
A) Amylase
B) Lipase
C) Trypsin
D) Elastase
Correct Answer: Trypsin
Rationale: Premature activation of trypsinogen to trypsin within the pancreatic acinar cells initiates a
cascade of digestive enzyme activation, causing autodigestion of pancreatic tissue. Amylase and lipase
are also released but are downstream effects, and elastase is activated later.
9. A patient with liver cirrhosis develops ascites. Which combination of pathophysiological factors
primarily contributes to this condition?
A) Portal hypertension and hypoalbuminemia
B) Hepatic encephalopathy and hyperammonemia
Pathophysiology | Wilkes University | Q&A|
1. Which enzyme is primarily responsible for the chemical digestion of carbohydrates in the small
intestine?
A) Amylase
B) Lipase
C) Pepsin
D) Trypsin
Correct Answer: Amylase
Rationale: Amylase, secreted by the pancreas and salivary glands, hydrolyzes starch into smaller
sugars like maltose. Lipase digests fats, pepsin digests proteins in the stomach, and trypsin digests
proteins in the small intestine. Amylase is the principal carbohydrate-digesting enzyme.
2. Intrinsic factor, secreted by gastric parietal cells, is essential for the absorption of which vitamin?
A) Vitamin B6
B) Vitamin B9 (folate)
C) Vitamin B12
D) Vitamin C
Correct Answer: Vitamin B12
Rationale: Intrinsic factor binds to vitamin B12, facilitating its absorption in the terminal ileum. A
deficiency leads to pernicious anemia. B6, folate, and C do not require intrinsic factor for absorption.
3. In the cephalic phase of gastric secretion, which nervous system pathway primarily stimulates acid
production?
A) Sympathetic nervous system
B) Parasympathetic nervous system via the vagus nerve
C) Somatic nervous system
D) Enteric nervous system independently
Correct Answer: Parasympathetic nervous system via the vagus nerve
,Rationale: The cephalic phase is triggered by the sight, smell, or thought of food, activating the
parasympathetic nervous system through the vagus nerve, which stimulates gastric acid secretion.
The sympathetic system inhibits digestion.
4. Which hormone, released from the duodenum in response to acidic chyme, inhibits gastric acid
secretion?
A) Gastrin
B) Secretin
C) Cholecystokinin
D) Motilin
Correct Answer: Secretin
Rationale: Secretin is released by S cells in the duodenum when acidic chyme enters, inhibiting gastric
acid secretion and stimulating pancreatic bicarbonate release. Gastrin stimulates acid, CCK stimulates
gallbladder contraction, and motilin regulates migrating motor complexes.
5. A patient with a history of chronic NSAID use develops a gastric ulcer. Which pathophysiological
mechanism is most directly responsible?
A) Increased gastric acid hypersecretion
B) Decreased mucosal prostaglandin synthesis
C) Helicobacter pylori overgrowth
D) Reduced gastric emptying
Correct Answer: Decreased mucosal prostaglandin synthesis
Rationale: NSAIDs inhibit cyclooxygenase-1, reducing prostaglandin synthesis, which diminishes
mucosal protective factors like mucus and bicarbonate. While H. pylori is a common cause, NSAIDs act
through this specific prostaglandin-dependent mechanism, not primarily by increasing acid or slowing
emptying.
6. In Zollinger-Ellison syndrome, which cell type is responsible for the excessive secretion of gastrin?
A) Gastric G cells
B) Pancreatic alpha cells
C) Gastrin-secreting tumor (gastrinoma)
D) Duodenal S cells
, Correct Answer: Gastrin-secreting tumor (gastrinoma)
Rationale: Zollinger-Ellison syndrome is caused by a gastrinoma, a neuroendocrine tumor, usually in
the pancreas or duodenum, that secretes excessive gastrin. This leads to severe peptic ulcer disease.
Gastric G cells are the normal source but are not the cause of this syndrome.
7. Which complication of gastroesophageal reflux disease (GERD) is characterized by the replacement
of stratified squamous epithelium with columnar epithelium in the esophagus?
A) Esophageal stricture
B) Barrett esophagus
C) Esophagitis
D) Adenocarcinoma
Correct Answer: Barrett esophagus
Rationale: Barrett esophagus is a metaplastic change where the normal squamous epithelium is
replaced by intestinal-type columnar epithelium as a protective response to chronic acid reflux. It is a
premalignant condition. Stricture, esophagitis, and adenocarcinoma are other potential complications
but not this specific cellular change.
8. In the pathophysiology of acute pancreatitis, which enzyme is prematurely activated within the
pancreas, leading to autodigestion?
A) Amylase
B) Lipase
C) Trypsin
D) Elastase
Correct Answer: Trypsin
Rationale: Premature activation of trypsinogen to trypsin within the pancreatic acinar cells initiates a
cascade of digestive enzyme activation, causing autodigestion of pancreatic tissue. Amylase and lipase
are also released but are downstream effects, and elastase is activated later.
9. A patient with liver cirrhosis develops ascites. Which combination of pathophysiological factors
primarily contributes to this condition?
A) Portal hypertension and hypoalbuminemia
B) Hepatic encephalopathy and hyperammonemia
