Question

A 45-year-old woman diagnosed with Crohn disease 3 years ago comes to the office due to recurrent right upper quadrant abdominal pain. The pain is graded 5/10 in intensity, is characterized as dull, and occasionally radiates to the right shoulder. It typically occurs after eating fatty meals and is associated with nausea. The patient has no fever, vomiting, melena, or hematochezia. She currently takes infliximab for Crohn disease and atorvastatin for hyperlipidemia. Vital signs and abdominal examination are normal. Abdominal ultrasonography reveals multiple mobile calculi within the gallbladder.

Which of the following processes is most likely responsible for the development of gallstones in this patient?

A. Gallbladder hypomobility

B. Increased bile acid wasting

C. Increased intestinal oxalate absorption

D.Medication side effect

E. Red blood cell destruction

Correct Answer: B. Increased bile acid wasting

🔍 Step 1: Patient History Points to Gallstone-Related Pain

• Clue: Pain post fatty meals + RUQ location → Suggests gallbladder issue.

• Metaphor: Gallbladder as a "traffic light" controlling bile flow for fat digestion. Blocked traffic (gallstones) causes congestion (pain).

🔍 Step 2: Linking Crohn Disease to Gallstone Formation

• 🧠 Key Insight: Crohn disease affects the terminal ileum → Impaired bile acid absorption.

⚙️ Mechanism Flow (Using Metaphor of Soap and Grease):

• Bile acids act like soap to dissolve cholesterol (grease).

• Crohn disease → Less soap (bile acids)

  • ↓ Soap → Cholesterol builds up → Gallstones.

Crohn's Disease (Terminal Ileum Involvement)
🧠 Terminal ileum as a "recycling center" for bile acids.
⬇️
Recycling center disrupted by inflammation or surgery
⬇️
⚙️ Result: ↓ Bile acids → Less cholesterol breakdown.
⬇️
Gallbladder bile becomes oversaturated with cholesterol (like grease without enough soap).
⬇️
Gallstones form
🧠 Explains postprandial RUQ pain after fatty meals.

Explanation of Other Answers

⚖️ Option A: Gallbladder Hypomobility

• ⚙️ Mechanism: Like a pump that isn’t working → bile stagnates → stones.

• 🧠 Key Insight: This is not supported in the scenario (no fasting, no chronic stasis issues).

⚖️ Option C: Increased Oxalate Absorption

• ⚙️ Mechanism: Oxalate builds up due to calcium binding issues (like too much lime in water).

• 🧠 Key Insight: Oxalate impacts kidneys → kidney stones, not gallstones.

⚖️ Option D: Medication Side Effect

• Statins or infliximab? 🧠 No evidence these "ingredients" directly add to gallstones.

⚖️ Option E: Red Blood Cell Destruction (Hemolysis)

• ⚙️ Mechanism: Burst red cells release pigment (like a dye in water) → pigment stones.

• 🧠 Key Insight: No "bursting" seen here (no anemia, jaundice, or hemolysis signs).

Flashcards

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