American Board of Internal Medicine Certification (ABIM Board Certification) Gastroenterology & Hepatology Syllabus

What serologic test is the best initial screen for celiac disease, and what must the patient be doing?

Tissue transglutaminase IgA (tTG-IgA) with total IgA level; the patient must be on a gluten-containing diet.

What is the gold-standard confirmatory test and classic histology for celiac disease?

Duodenal biopsy showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis.

Which HLA haplotypes are associated with celiac disease (and useful for ruling it out)?

HLA-DQ2 and HLA-DQ8; their absence has a high negative predictive value.

What skin condition is pathognomonic for celiac disease?

Dermatitis herpetiformis - pruritic vesicular rash on extensor surfaces, treated with dapsone and gluten-free diet.

At what age does average-risk colorectal cancer screening now begin, per USPSTF/ACS?

Age 45 years for average-risk adults.

What is the surveillance colonoscopy interval after removal of 1-2 small (<10 mm) tubular adenomas?

Repeat colonoscopy in 7-10 years.

What polyp findings on colonoscopy warrant a shorter 3-year surveillance interval?

Advanced adenoma (>=10 mm, villous histology, or high-grade dysplasia) or 3-10 adenomas.

How does diverticular disease typically cause lower GI bleeding, and what is its usual course?

Painless, often brisk hematochezia from a ruptured vasa recta; the majority stop spontaneously.

What is the first-line diagnostic test for acute, brisk lower GI bleeding in a hemodynamically stable patient?

Colonoscopy after rapid bowel prep; CT angiography if bleeding is too brisk for prep or for localization.

What is the modern outpatient management of uncomplicated acute diverticulitis in selected patients?

Observation with or without antibiotics; antibiotics can be omitted in mild uncomplicated cases per recent guidelines.

What two diagnostic criteria (of three) are needed to diagnose acute pancreatitis?

Two of: characteristic epigastric pain radiating to back; lipase/amylase >3x upper limit normal; characteristic imaging findings.

What are the two most common causes of acute pancreatitis?

Gallstones and alcohol.

What is the cornerstone of early management of acute pancreatitis?

Aggressive goal-directed IV fluid resuscitation (lactated Ringer's), pain control, and early enteral nutrition.

What imaging findings characterize chronic pancreatitis?

Pancreatic calcifications, ductal dilatation/irregularity, and parenchymal atrophy (best seen on CT/MRCP).

What triad of complications results from advanced chronic pancreatitis?

Steatorrhea (exocrine insufficiency), diabetes (endocrine insufficiency), and chronic abdominal pain.

What is the classic presentation and stone type of cholelithiasis causing biliary colic?

Postprandial RUQ pain (especially after fatty meals) lasting <6 hours; most stones are cholesterol stones.

What clinical findings define ascending cholangitis (Charcot's triad and Reynolds' pentad)?

Charcot: fever, RUQ pain, jaundice. Reynolds pentad adds hypotension and altered mental status.

What is the management of acute cholangitis from choledocholithiasis?

IV antibiotics, fluid resuscitation, and urgent biliary decompression via ERCP.

What tumor marker and classic imaging finding suggest pancreatic adenocarcinoma?

CA 19-9 elevation; "double duct sign" (dilated common bile and pancreatic ducts) on imaging, usually in the pancreatic head.

What painless physical finding suggests malignant biliary obstruction from pancreatic head cancer?

Courvoisier's sign - a palpable, nontender, distended gallbladder with jaundice.

Compare transmission routes of hepatitis A through E.

HAV and HEV: fecal-oral. HBV, HCV, HDV: blood/body fluids (parenteral, sexual, perinatal); HDV requires HBV co-infection.

Which viral hepatitides cause chronic infection, and which are typically self-limited?

HBV, HCV, and HDV can become chronic; HAV and HEV are acute/self-limited (HEV severe in pregnancy).

How do you interpret HBsAg+, anti-HBc IgG+, HBeAg+, with high HBV DNA?

Chronic active hepatitis B with high replication/infectivity (immune-active phase).

What serologic marker indicates immunity to hepatitis B from vaccination versus prior infection?

Vaccination: anti-HBs positive ONLY. Prior natural infection: anti-HBs positive AND anti-HBc (total) positive.

What is the calculation and use of the MELD score in cirrhosis?

Based on bilirubin, INR, creatinine (and sodium in MELD-Na); it predicts 90-day mortality and prioritizes liver transplant allocation.

What is the diagnostic ascitic fluid criterion for spontaneous bacterial peritonitis, and its treatment?

Ascitic PMN count >=250 cells/mm3; treat with IV third-generation cephalosporin (cefotaxime) plus albumin.

What SAAG value indicates ascites due to portal hypertension?

Serum-ascites albumin gradient >=1.1 g/dL indicates portal hypertension.

What is first-line treatment for hepatic encephalopathy?

Lactulose (titrated to 2-3 soft stools/day) with rifaximin added for recurrent episodes.

How is MASLD (formerly NAFLD) defined and what is its progressive form?

Hepatic steatosis (>=5% fat) with >=1 cardiometabolic risk factor and no other cause; MASH (steatohepatitis) is the progressive inflammatory form that can lead to fibrosis/cirrhosis.

What antibody and demographic characterize primary biliary cholangitis, and its first-line treatment?

Anti-mitochondrial antibody (AMA) in middle-aged women with cholestatic (high alkaline phosphatase) pattern; treat with ursodeoxycholic acid.

What disease is associated with primary sclerosing cholangitis, and what is the cholangiographic finding?

Inflammatory bowel disease (especially ulcerative colitis); MRCP shows multifocal strictures with "beads-on-a-string" appearance; increased cholangiocarcinoma risk.

What defines acute liver failure?

Severe acute liver injury with coagulopathy (INR >=1.5) and encephalopathy in a patient without preexisting cirrhosis, within ~26 weeks of onset.