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Gastrointestinal Physiology — Step 1 practice questions
37 questions in this area, with an explanation for every answer choice.
Three samples below, free and without an account.
How this shows up on Step 1
Physiology questions in this section combine two things the exam tests separately elsewhere. Physiology questions can be reasoned rather than recalled, which makes them the best return on study time. GI is a pathology-heavy section.
Sample questions
Sample question 1
A patient with gallstones develops obstruction of the cystic duct, causing acute cholecystitis. Which of the following mechanisms explains the gallbladder inflammation in this scenario?
Explanations
A. Direct bacterial invasion is always the primary initiating event
While secondary bacterial infection often occurs, the INITIATING event in acute cholecystitis is typically mechanical obstruction/chemical irritation, not primary bacterial invasion.
B. This is purely an autoimmune process unrelated to the stone
This is a mechanically/chemically triggered inflammatory process, not an autoimmune one.
C. Gallstones have no relationship to gallbladder inflammation
Gallstones are the classic and most common precipitating cause of acute cholecystitis via this obstructive mechanism.
D. Obstruction causes bile stasis and increased intraluminal pressure, leading to gallbladder wall inflammation, which may become secondarily infected · correct
Cystic duct obstruction by a gallstone causes bile stasis and increased intraluminal pressure, triggering gallbladder wall inflammation (initially chemical/mechanical), which frequently becomes secondarily infected by enteric bacteria.
E. The pancreas directly causes this inflammation
This is a gallbladder process, not primarily pancreatic.
Sample question 2
A patient with cirrhosis develops confusion and asterixis after a large protein meal. Which of the following is the most appropriate first-line treatment?
Explanations
A. Lactulose · correct
Lactulose is first-line treatment for hepatic encephalopathy; colonic bacteria metabolize it to acidic byproducts, trapping ammonia as ammonium for fecal excretion.
B. IV mannitol
Mannitol is used for cerebral edema, not hepatic encephalopathy.
C. Protein restriction as the sole intervention long-term
Chronic protein restriction is no longer recommended as a primary strategy (risks malnutrition); adequate protein intake with lactulose/rifaximin is preferred.
D. Naloxone
Naloxone reverses opioids, unrelated to hepatic encephalopathy.
E. Flumazenil routinely
Flumazenil is not routine therapy for hepatic encephalopathy (it has a narrow, specific use in some benzodiazepine-related presentations).
Sample question 3
A patient with achalasia is being considered for treatment options. Which of the following interventions directly addresses the underlying LES dysfunction?
Explanations
A. Pneumatic dilation or surgical myotomy of the LES · correct
Pneumatic dilation (mechanically disrupting the LES) or surgical (Heller) myotomy directly address the impaired LES relaxation and are standard interventions for achalasia, unlike acid-suppression therapies which do not target the underlying motor disorder.
B. Antihistamines
Antihistamines are not a treatment for achalasia.
C. H2 blockers alone
H2 blockers, like PPIs, address acid production, not the motility disorder itself.
D. Proton pump inhibitors alone
PPIs reduce acid production but do not address the fundamental motility/LES relaxation problem in achalasia.
E. Antibiotics
Achalasia is not an infectious process (except in secondary Chagas-related cases, where the underlying organism is not treated by antibiotics targeting typical bacterial infections).
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