Gastroenterology USMLE Practice Questions

A. Neutrophilic inflammation of the crypts

This option implies acute cryptitis/crypt abscesses, which occur in both Crohn disease and ulcerative colitis, BUT it is not specific for Crohn and thus doesn’t uniquely confirm the diagnosis.

B. Inflammation of the terminal ileum

This option implies ileitis, which is common in Crohn disease, BUT ileal inflammation alone is not specific (e.g., infection, NSAID enteropathy); the question asks for the most specific histologic finding.

C. Intranuclear and cytoplasmic inclusion bodies

This option implies viral infection (e.g., CMV colitis), which causes inclusions, BUT the patient’s negative stool studies and segmental transmural disease pattern fit IBD, not primary viral colitis.

D. Inflammation limited to the mucosa and submucosa

This option implies ulcerative colitis, which is classically mucosal/submucosal, BUT this patient has transmural mural thickening and skip lesions, which argue against UC and for Crohn disease.

E. Neutrophil-rich pseudomembranes

This option implies pseudomembranous colitis (C. difficile), which presents with recent antibiotic use and positive stool toxin, BUT this patient’s stool studies are negative and imaging shows segmental transmural ileocolitis instead.

F. Poorly differentiated gland-forming cells with desmoplasia

This option implies adenocarcinoma, which would present with mass lesion, obstruction, or overt bleeding, BUT the CT shows inflammatory mural thickening/fat stranding and the clinical course is inflammatory, not malignant.

A. Increased stool pH

This option implies less acid in stool. In carbohydrate malabsorption (like lactose intolerance), bacteria ferment sugars to acids, lowering stool pH, not raising it.

B. Decreased urinary D-xylose concentration

This option implies mucosal damage or decreased absorption (e.g., celiac). D-xylose absorption is normal in isolated lactase deficiency, so urinary D-xylose remains normal.

C. Increased serum glucose concentration

This option implies efficient carbohydrate digestion/absorption. In lactase deficiency, lactose is not split to absorbable monosaccharides, so serum glucose does not rise appropriately after lactose load.

E. Decreased fecal fat content

This option implies improved fat absorption. Lactase deficiency is a carbohydrate-specific brush-border enzyme defect; it does not improve or reduce fat malabsorption, and fecal fat is typically normal.

F. Decreased breath hydrogen content

This option implies less bacterial fermentation. In lactose intolerance, unabsorbed lactose is fermented by colonic bacteria, which increases breath hydrogen, not decreases it.

A. CT angiography

This option implies concern for acute mesenteric ischemia or vascular catastrophe, which causes severe pain often out of proportion to exam. BUT this patient has classic pancreatitis pain, markedly elevated lipase, and no atrial fibrillation-related embolic signs; imaging does not precede stabilization with fluids.

B. Calcium gluconate therapy

This option implies treatment of symptomatic hypocalcemia (tetany, seizures, arrhythmias). The patient’s calcium is low from pancreatitis saponification, BUT there are no neuromuscular or cardiac symptoms; initial priority in pancreatitis is volume resuscitation, not empiric calcium replacement.

C. Fomepizole therapy

This option implies toxic alcohol (eg, methanol, ethylene glycol) ingestion, which presents with high anion gap metabolic acidosis, visual changes, or oxalate crystals. BUT this patient’s presentation is classic for alcoholic pancreatitis with elevated lipase and no ingestion history or severe acidosis.

D. Laparotomy

This option implies surgical abdomen (perforation, peritonitis, necrotizing infection). BUT exam shows tenderness with guarding but no rebound or peritoneal signs, stable vitals, and labs consistent with uncomplicated acute pancreatitis, which is managed nonoperatively initially with fluids and supportive care.

E. Endoscopic retrograde cholangio-pancreatography

This option implies gallstone pancreatitis with cholangitis/obstruction (jaundice, elevated bilirubin/ALP). BUT this patient has normal bilirubin and ALP, no RUQ pain or jaundice; his risk factor is alcohol, so urgent ERCP is not indicated.

F. Insulin infusion

This option implies DKA or hyperosmolar state, which present with marked hyperglycemia, acidosis, and often altered mental status. The modest hyperglycemia here is stress-related from pancreatitis, BUT there is no acidosis or DKA picture; insulin is not the immediate priority—fluid resuscitation is.

A. Sphingomyelin

This option implies Niemann-Pick disease, which causes neurodegeneration, cherry-red macula, hepatosplenomegaly, BUT typically presents later in infancy and is not linked to acute onset after milk feeding or neonatal cataracts.

B. Uric acid

This option implies Lesch-Nyhan syndrome or gout-related pathology, which causes self-mutilation, neurologic deficits, and hyperuricemia, BUT not neonatal jaundice, cataracts, or milk-triggered decompensation.

C. Branched-chain amino acids

This option implies Maple syrup urine disease, which presents with vomiting, poor feeding, lethargy, and sweet-smelling urine, BUT does not cause cataracts or marked jaundice/hepatomegaly from galactose toxicity.

E. Limit dextrins

This option implies a debranching enzyme deficiency (Cori disease), which causes fasting hypoglycemia and hepatomegaly, BUT does not produce neonatal cataracts or clear milk-triggered symptoms; also usually presents a bit later.