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NSG 530 – Exam III Advanced Pathophysiology | Wilkes University | 2024/2025 | Verified Questions and Answers | Grade A+

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NSG 530 – Exam III Advanced Pathophysiology | Wilkes University | 2024/2025 | Verified Questions and Answers | Grade A+

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NSG 530 – Exam III Advanced Pathophysiology |
Wilkes University | 2024/2025 | Verified Questions
and Answers | Grade A+

GASTROINTESTINAL PATHOPHYSIOLOGY
1. The stomach is impermeable to water but can absorb which of the following
substances due to their lipid solubility?
• A. Vitamin B12 and intrinsic factor
• B. Alcohol and aspirin
• C. Glucose and amino acids
• D. Electrolytes and minerals
Answer: B
Rationale: The stomach is impermeable to water but can absorb lipid-soluble
substances such as alcohol and aspirin. These substances are absorbed through
the gastric mucosa due to their ability to cross lipid bilayers. Absorption is not the
primary function of the stomach, which is mainly for digestion and mixing.


2. A patient with chronic gastritis is at risk for pernicious anemia due to a
deficiency of which substance?
• A. Pepsin
• B. Intrinsic factor
• C. Gastroferritin
• D. Secretin

,Answer: B
Rationale: Intrinsic factor is produced by parietal cells in the stomach and is
essential for the absorption of vitamin B12 in the terminal ileum. Deficiency of
intrinsic factor results in pernicious anemia. Chronic gastritis can damage parietal
cells, leading to reduced intrinsic factor production.


3. A patient with a history of alcoholism presents with confusion, altered mental
status, and asterixis. Lab results show elevated serum ammonia. What is the
most likely pathophysiological mechanism?
• A. Impaired urea cycle due to hepatocellular injury
• B. Decreased renal excretion of ammonia
• C. Increased dietary protein intake
• D. Hyperammonemia due to urea cycle disorder
Answer: A
Rationale: Hepatic encephalopathy results from impaired ammonia metabolism in
the liver. Ammonia is produced by bacteria in the GI tract and normally cleared by
the liver via the urea cycle. In chronic liver disease or cirrhosis, impaired ammonia
metabolism leads to accumulation of ammonia, causing neurotoxicity and
symptoms like confusion and asterixis.


4. A patient with liver cirrhosis develops esophageal varices. Which
pathophysiological mechanism is responsible for this complication?
• A. Decreased hepatic synthesis of clotting factors
• B. Portal hypertension causing collateral circulation
• C. Direct invasion of esophageal tissue by cancer
• D. Obstruction of the hepatic artery

, Answer: B
Rationale: Portal hypertension occurs when there is increased resistance to blood
flow from the portal vein due to liver fibrosis/cirrhosis. This causes veins draining
into the portal system (gastric, esophageal, splenic) to become engorged, leading
to the formation of collateral vessels (varices) that bypass the liver. Esophageal
varices are a life-threatening complication of portal hypertension.


5. What is the primary function of intrinsic factor in the gastrointestinal tract?
• A. Enhances gastric acid secretion
• B. Protects the gastric mucosa from acid
• C. Binds vitamin B12 for absorption in the ileum
• D. Activates pepsinogen to pepsin
Answer: C
Rationale: Intrinsic factor is a glycoprotein secreted by gastric parietal cells. It
binds to vitamin B12, protecting it from digestion and facilitating its absorption in
the terminal ileum. Without intrinsic factor, vitamin B12 cannot be absorbed,
leading to pernicious anemia.


6. A patient presents with jaundice, clay-colored stools, and failure to thrive.
Which congenital condition should be suspected in an infant?
• A. Meckel diverticulum
• B. Intussusception
• C. Biliary atresia
• D. Hirschsprung's disease
Answer: C
Rationale: The cardinal symptoms of biliary atresia are jaundice, clay-colored
stools, and failure to gain weight. This condition involves obstruction or absence of

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