Gastroenterology Pearls: Digestive Tract in 7 Major Parts
As previously mentioned, the Gastroenterology and Hepatology section of the ABIM Internal Medicine exam comprises of about 9% of the entire exam – that means out of 240 total questions (4 sections of 60 questions each), we can expect about 20 questions to be geared towards our liver and GI tract. For the Internal Medicine Shelf Exam, Gastroenterology comprises 7-13% of the exam.
Overall, the digestive system is fascinating (the liver itself is the largest organ in the body and performs over 500 functions! ) yet quite simple (think of it this way – food goes in to the mouth, down the esophagus and in to the stomach, through 26 feet of small intestine in to the colon. Then out.)
To simplify for the ABIM exam, let’s divide the digestive tract in to 7 major parts and discuss a couple important topics in each – Esophagus, Stomach, Pancreas, Biliary Tract, Small Bowel, Colon, and Liver.
A favorite topic of boards is GERD and the development of Barrett esophagus. GERD is caused by a decrease in the physiologic antireflux barriers at the GE junction, resulting in gastric contents being released in to the esophagus. Surprisingly, the major cause of GERD is not hypersecretion of gastric contents, but rather an inappropriate relaxation of the lower esophageal sphincter.
- A 4-week empiric trial of a PPI has a high sensitivity for the diagnosis of GERD
- Patients presenting with weight loss, dysphagia, odynophagia, or are refractory to medical therapy should undergo further testing
- Ambulatory esophageal pH monitoring is the most accurate means to confirm the diagnosis of GERD
The development of Barrett esophagus is a feared complication of GERD due to the increased risk for esophageal adenocarcinoma (remember, squamous cell carcinoma arises in the upper portion of the esophagus and adenocarcinoma arises distally, closer to the GE junction).
- Histologically, Barrett esophagus has specialized intestinal metaplasia with mucin containing goblet cells
- Dysplasia found during EGD:
- none -> surveillance EGD should be repeated in 1 year, then every 5 years if negative
- low grade -> surveillance in 6 months for 1 year, then yearly
- high grade -> surveillance every 3 months for focal dysplasia vs. surgical or endoscopic management for multifocal dysplasia
Given the large number of hospitalizations and deaths from peptic ulcer disease every year, it is not surprising that this remains a major topic tested on the boards. The most common causes remain H. pylori infection and NSAIDs.
- H. pylori is associated with the development of gastric adenocarcinoma as well as MALT (mucoa-associated lymphoid tissue) lymphoma
- Treatment for H. pylori consists of triple therapy – PPI, Amoxicillin, and Clarithromycin (Metronidazole in Clarithromycin resistant areas)
- Urea breath test and fecal antigen test are both sensitive for the detection of H. pylori
Be able to recognize a patient with a perforated peptic ulcer! Look for a patient who is hypotensive and tachycardic with absent bowel sounds and severe rebound tenderness and guarding. Imaging will show free intraperitoneal air. Stat surgical consultation is required!
The prevalence of pancreatitis continues to rise in the Western world, and thus remains a favorite for the ABIM boards. Although alcohol and gallstones remain the major cause of acute pancreatitis, metabolic (hyperlipidemia, hypercalcemia), infectious (CMV, EBV, parasites), and autoimmune causes should be considered.
- Diagnosis of acute pancreatitis can be made without imaging, but contrast-enhanced CT scan is used if there is concern for necrotizing pancreatitis
- If necrotizing pancreatitis is suspected, prophylactic antibiotics should be used – Imipenem, cephalosporins, and fluoroquinolones
- ERCP is used if there is evidence of gallstone pancreatitis and suspected biliary obstruction
- Consider a deficiency in fat-soluble vitamins (A, D, E, K) in chronic pancreatitis
Look for CA 19-9 as a tumor marker for pancreatic cancer. Better yet, be able to recognize the whole table of important tumor markers discussed in the oncology section of Knowmedge.
The prevalence of gallstones is high in the United States, and thus should be considered as part of a differential for a patient presenting with abdominal pain. Be able to recognize and know how to treat acute cholecystitis, but also know when to expect and how to treat acalculous cholecystitis.
- Consider acalculous cholecystitis in patients with serious comorbidities, including trauma, burns, or prolonged states of fasting
- Management is similar to that of acute calculous cholecystitis, but patients with severe illness may require percutaneous drainage if unable to tolerate surgery
If choledocholithiasis is suspected, broad-spectrum antibiotics covering enteric gram-negative bacteria should be started. Fluoroquinolones are usually a good initial choice.
Another favorite boards topic – diarrhea. Diarrhea can of course be divided multiple ways – acute vs. chronic, secretory vs. osmotic vs. inflammatory, small-bowel vs. large-bowel diarrhea. Be able to easily distinguish the two main types of Inflammatory diarrhea, Ulcerative colitis vs. Crohn’s. Since this was already discussed in the last GI blog, I’ll just address some key words for each.
- Ulcerative colitis – Crampy pain. Mucosa and submucosa. Pseudopolyps. HLA-B27. Ankylosing spondylitis. Pyoderma gangrenosum. Primary sclerosing cholangitis. Toxic megacolon. Adenocarcinoma.
- Crohn’s disease – Colicky pain. Transmural. Lymphocytes. Granulomas. Rectal sparing. Skip lesions. Fistulas. Strictures. B12 deficiency.
Both conditions usually present with diarrhea on the boards, so be able to quickly recognize these key words for some easy points. Don’t forget, both of these conditions have an increased risk of colon cancer estimated to be 1-2% per year after 8 years of disease. Thus surveillance colonoscopy should be started in patients with IBD for 8 years or longer.
Colorectal cancer is the second leading cause of cancer death in the United States. According to the CDC, every year about 140,000 Americans are diagnosed with colorectal cancer and over 500,000 die from it. That being said, it should come as no surprise that colon cancer is a major GI topic in the ABIM exam.
Remember these Autosomal Dominant conditions and their management:
- Familial adenomatous polyposis (FAP) – caused by a mutation in the APC gene
- annual flex sig beginning at age 10-12, and colectomy should be considered when polyposis is detected
- Hereditary nonpolyposis colorectal cancer (HNPCC), or Lynch syndrome – caused by a mutations in the MLH1 and MSH2 mismatch repair genes
- colonoscopy every 1 to 2 years starting at age 20-25 years or 10 years before the age at diagnosis of the youngest family member diagnosed with colon cancer
- Puetz-Jeghers syndrome – caused by a germ line mutation in the STK11 gene
- Juvenile polyposis syndrome – caused by a germ line mutation of the SMAD4 gene
Know the who, how, and when of colorectal cancer screening!
Last but definitely not least of the major parts of the digestive tract – the liver. This organ, weighing in at about 3 lbs, is the second largest organ (after the skin) and affects nearly every physiologic process of the human body.
For the ABIM board exam, be able to interpret Hepatitis B serologies and have a good understanding of the difference between acute and chronic infection.
- The goal of therapy in chronic Hepatitis B is suppression of viral replication, seroconversion of HBeAg, and decrease in hepatic inflammation (as evidenced by an improvement in liver enzymes)
- Once a patient is found to have a chronic Hepatitis B infection, surveillance should be undertaken to prevent the development of cirrhosis and HCC by ultrasound and a-fetoprotein level every 6-12 months
In addition to viral hepatitis, several other causes of hepatitis need to be considered. Be able to distinguish between hepatocellular injury and cholestatic injury.
- Hepatocellular – elevation in ALT and AST released from injured hepatocytes
- viral hepatitis, alcoholic hepatitis, drug-induced hepatitis, NASH, ischemic hepatitis, autoimmune hepatitis (look for ASMA!), hemochromatosis, Wilson disease, a1-antitrypsin deficiency
- Cholestatic – elevation in alkaline phosphatase occurs due to a decrease in the flow of bile
- primary biliary cirrhosis (look for antimitochondial antibodies!), primary sclerosing cholangitis, drug-induced cholestasis
Dr. Ruchi Bhatia is currently an internal medicine resident at St. Louis University. She is interested in Gastroenterology.