Free USMLE Step 2 CK Gastroenterology and Hepatology practice questions

A microcytic anemia with a ferritin below 45 ng/mL confirms iron deficiency. In a man or a postmenopausal woman, iron deficiency is presumed to be from occult GI blood loss, and GI malignancy must be excluded, even without symptoms, overt bleeding or a positive stool test. Her diet is adequate, she has no other source of blood loss, and celiac disease has been screened. The AGA recommends bidirectional endoscopy (colonoscopy plus upper endoscopy) rather than either test alone. Colonoscopy looks for colorectal cancer and large polyps, especially right-sided lesions that bleed occultly. Upper endoscopy looks for gastric cancer, ulcers, erosions in a hiatal hernia (Cameron lesions), angiodysplasia and celiac disease (with duodenal biopsies). Synchronous upper and lower lesions occur in a meaningful minority of patients. Iron replacement is started at the same time but never replaces the evaluation. If both studies are unrevealing, capsule endoscopy evaluates the small bowel.

A. Treating with iron alone and attributing the anemia to diet risks missing a cancer; new iron deficiency in a postmenopausal woman is GI cancer until proven otherwise. C. Colonoscopy alone misses upper GI sources, which account for a substantial share of iron deficiency anemia. D. A fecal immunochemical test is a screening test for average-risk asymptomatic adults; it detects only lower GI blood loss, and a negative result would not end the workup of documented iron deficiency. E. Capsule endoscopy evaluates the small bowel only after EGD and colonoscopy are negative.

An isolated alkaline phosphatase elevation, with normal aminotransferases and bilirubin, may come from the liver or from bone (and, in pregnancy, the placenta). Before starting a hepatobiliary workup, the first step is to confirm the source. A raised GGT (or 5'-nucleotidase) means the ALP is hepatic and points to cholestasis; a normal GGT means a nonhepatic source. ALP isoenzyme fractionation is an alternative.

Here the clues point to bone: a long-standing thigh ache with femoral bowing in an older adult suggests Paget disease of bone, which commonly causes isolated, often marked ALP elevation with normal calcium. If the GGT is normal, the next steps are plain radiographs of the symptomatic area and a bone scan, not liver imaging. If the GGT is raised, the evaluation moves to a right upper quadrant ultrasound to look for duct dilation.

B. Right upper quadrant ultrasound is the first test for confirmed hepatic cholestasis, but ordering it before establishing that the ALP is hepatic may lead to an unnecessary hepatobiliary workup. C. Antimitochondrial antibody is the test for primary biliary cholangitis once a hepatic cholestatic pattern with nondilated ducts is established; she also lacks the typical pruritus and fatigue. D. MRCP is used for dilated ducts or suspected primary sclerosing cholangitis, both downstream of confirming a hepatic source and an ultrasound. E. Liver biopsy is reserved for unexplained hepatic cholestasis after serologic and imaging evaluation and is invasive and premature here.

This patient has cirrhosis, so he remains at risk for hepatocellular carcinoma (HCC) even after HCV cure, which is why he is in a 6-month ultrasound surveillance program. Surveillance has now found a new nodule of at least 1 cm. In cirrhosis, any new nodule 1 cm or larger is presumed to be possible HCC and must be characterized with multiphase contrast-enhanced CT or MRI (arterial, portal venous and delayed phases). The reason is that HCC can be diagnosed noninvasively: a nodule of 1 cm or more with nonrim arterial-phase hyperenhancement and washout on later phases is LI-RADS 5, which establishes HCC without tissue. A normal AFP does not lower the need for imaging, because many HCCs do not secrete AFP, and AFP is neither required for nor able to exclude the diagnosis. Nodules smaller than 1 cm, by contrast, are too small to characterize reliably and are followed with repeat ultrasound in 3 to 6 months.

A. Percutaneous biopsy is wrong as a first step: multiphase imaging may already be diagnostic, and biopsy carries bleeding risk and needle-tract seeding. Biopsy is reserved for indeterminate lesions (LI-RADS 4 or LI-RADS M) or a noncirrhotic liver. B. Repeat ultrasound in 3 months is the plan for a nodule under 1 cm; delaying characterization of a 1.6 cm nodule risks missing an early, curable cancer. D. FDG PET-CT is insensitive for well-differentiated HCC and has no role in initial characterization. E. Repeating AFP delays diagnosis; a normal AFP is common in early HCC and does not change the need for imaging.

Painless obstructive jaundice with pruritus and weight loss in an older adult suggests a malignant biliary obstruction, and the ultrasonography tells you its level. The intrahepatic ducts are dilated in both lobes while the common bile duct is normal and the gallbladder is collapsed, so the blockage sits at the hepatic duct confluence, above the cystic duct. That pattern is the signature of a perihilar (Klatskin) cholangiocarcinoma, the most common location of bile duct cancer.

His background adds a strong risk factor: years of eating raw freshwater fish in northeastern Thailand, the classic setting for chronic infection with the liver fluke Opisthorchis viverrini (Clonorchis sinensis in other parts of East Asia). Chronic biliary inflammation from flukes, like primary sclerosing cholangitis and choledochal cysts, drives cholangiocarcinoma. The elevated CA 19-9 supports but does not prove the diagnosis. Next steps are MRI with MRCP to map the tumor and ERCP for brushings and drainage.

A and D. Tumors of the pancreatic head or the ampulla obstruct the distal duct, so the common bile duct and the gallbladder are distended (a palpable, nontender gallbladder is the Courvoisier sign). B. Gallbladder carcinoma usually arises with long-standing stones and presents with a gallbladder mass invading the liver, not an isolated hilar obstruction with a collapsed gallbladder. C. Choledocholithiasis typically causes colicky pain and a dilated common bile duct down to the stone, without weight loss.

Sudden pain, hemodynamic instability, a falling hemoglobin, and a pseudocyst that has rapidly enlarged and filled with clot indicate bleeding into the cyst from a pseudoaneurysm. Pancreatic enzymes erode the wall of an adjacent artery; the splenic artery is most often involved, followed by the gastroduodenal and pancreaticoduodenal arteries. Untreated, the bleeding can be massive and fatal, either into the cyst, into the peritoneum, or through the pancreatic duct into the duodenum (hemosuccus pancreaticus).

Once the patient responds to initial resuscitation, the next step is CT angiography, which rapidly localizes the pseudoaneurysm and maps the vessel. It is followed by catheter angiography with coil embolization, the first-line treatment with high success rates; surgery is the backup if embolization fails or is unavailable. A patient who remains unstable despite resuscitation may go directly to catheter angiography.

A. Upper endoscopy is the first test for hematemesis or melena from a mucosal source; the clear aspirate and cyst findings point to bleeding within the pseudocyst, and endoscopy cannot treat a pseudoaneurysm. B. Puncturing a cyst that contains an arterial bleed risks catastrophic hemorrhage and does not identify the vessel. D. A tagged red blood cell scan detects slow intermittent lower GI bleeding and lacks the anatomic detail needed to guide embolization. E. Waiting to reimage in a patient with an active arterial bleed is dangerous.

About one third of patients with necrotizing pancreatitis develop infection of the necrosis, typically after the first 7 to 10 days and most often in weeks 2 to 4. The clues are clinical deterioration after initial improvement, with new fever, a rising leukocyte count, and new or worsening organ failure (here, hypotension), together with gas bubbles within a necrotic collection on CT, which is nearly diagnostic in the absence of a prior procedure or fistula. This is infected pancreatic necrosis. Image-guided fine-needle aspiration is rarely needed. Management is an antibiotic that penetrates necrotic tissue, usually a carbapenem (or a fluoroquinolone with metronidazole), continued enteral nutrition, and organ support, with drainage postponed when possible until the collection walls off at about 4 weeks, followed by a step-up approach of endoscopic transmural drainage and, only if needed, necrosectomy. Early surgical debridement of unencapsulated necrosis increases mortality.

B. Sterile necrosis can cause fever from inflammation, but new septic physiology in week 3 with gas in the collection indicates infection. C. A pseudocyst is a collection of fluid without solid necrotic material that follows interstitial pancreatitis; a collection containing necrotic debris after necrotizing pancreatitis is an acute necrotic collection or walled-off necrosis. D. Cholangitis requires biliary obstruction with jaundice; her bilirubin is normal. E. A catheter infection can cause fever and bacteremia, but the clean site and the gas-containing necrotic collection point to the pancreas as the source.

This woman has a strong pretest probability of celiac disease: chronic diarrhea and bloating, low BMI, iron-deficiency anemia refractory to oral iron, and coexisting autoimmune thyroid disease. Her tTG-IgA is undetectable, but her total IgA is also absent, and her recurrent sinopulmonary infections fit selective IgA deficiency, which is 10 to 15 times more common in celiac disease than in the general population. Any IgA-based antibody test is falsely negative when the patient cannot make IgA, which is why total IgA is measured with tTG-IgA. The 2023 ACG guideline recommends IgG-based testing in IgA deficiency: deamidated gliadin peptide IgG (DGP-IgG) or tTG-IgG. A positive IgG-based test, or high clinical suspicion even with a negative one, should lead to upper endoscopy with duodenal biopsies while she is still eating gluten. Duodenal biopsy remains the confirmatory test.

A. Repeating tTG-IgA will be undetectable again, because she makes no IgA. B. Endomysial antibody is also IgA-based and fails for the same reason. C. HLA-DQ2/DQ8 typing has excellent negative predictive value but poor positive predictive value, because about 30 to 40% of the population carries these alleles; it is used mainly to exclude celiac disease in patients already on a gluten-free diet or with equivocal results, not as the next test here. E. A gluten-free trial before testing would make later serology and biopsy falsely negative and does not establish the diagnosis.

A man in his early forties has a right-sided, poorly differentiated, lymphocyte-rich colon cancer with few polyps, and his family has endometrial cancer at 47 and colon cancer at 52 across two generations. Tumor immunohistochemistry shows loss of MSH2 and MSH6, which signals a mismatch-repair-deficient (microsatellite-unstable) tumor. Together these findings point to Lynch syndrome, the most common inherited colorectal cancer syndrome, caused by an autosomal dominant germline mutation in a mismatch-repair gene (MLH1, MSH2, MSH6, PMS2) or EPCAM. Endometrial cancer is the most common extracolonic cancer, followed by ovarian, gastric, small-bowel, urothelial, and hepatobiliary cancers. All colorectal cancers should undergo universal MMR or MSI testing; an abnormal result leads to germline testing with genetic counseling. If confirmed, he needs colonoscopy every 1 to 2 years, and his relatives should be offered cascade testing, with colonoscopy from age 20 to 25 for carriers.

B. Attenuated FAP causes 10 to 100 adenomas and cancers with intact mismatch-repair proteins. C. MUTYH-associated polyposis is autosomal recessive, usually causes multiple adenomas, and does not cause MMR protein loss or vertical transmission across generations. D. Peutz-Jeghers syndrome features hamartomatous polyps and mucocutaneous pigmentation, which he lacks. E. Sporadic MSI-high cancers usually arise from MLH1 promoter hypermethylation and show loss of MLH1 and PMS2, often in older patients with BRAF V600E mutations; isolated MSH2 and MSH6 loss is almost always germline.