MKSAP 16 Sample - Gastroenterology

gastroenterology and hepatology

Gastroenterology and Hepatology

Medical Knowledge Self-Assessment Program

Gastroenterology and Hepatology All New Content, Including 96 Multiple-Choice Questions

150591010

14 AMA PRA Category 1 Credits™ available until July 31, 2015.

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Table of Contents

Disorders of the Esophagus

Disorders of the Pancreas

Symptoms of Esophageal Disorders. . . . . . . . . . . . . . . . . . . . . 1 Dysphagia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Reflux . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Chest Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Odynophagia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Globus Sensation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Nonmalignant Disorders of the Esophagus . . . . . . . . . . . . . . . 3 Esophageal Motility Disorders . . . . . . . . . . . . . . . . . . . . . 3 Infectious, Pill-Induced, and Eosinophilic Esophagitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Gastroesophageal Reflux Disease . . . . . . . . . . . . . . . . . . . 7 Metaplastic and Neoplastic Disorders of the Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Barrett Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Esophageal Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . 11

Acute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 23 Prognostic Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Chronic Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 25 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Pancreatic Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . 26 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Diagnosis and Staging . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Autoimmune Pancreatitis and IgG4 Disease . . . . . . . . . . . . . 27 Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 28 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Cystic Neoplasms of the Pancreas . . . . . . . . . . . . . . . . . . . . . 28 Pancreatic Neuroendocrine Tumors . . . . . . . . . . . . . . . . . . . 29

Disorders of the Stomach and Duodenum Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Clinical Features, Diagnosis, and Complications. . . . . . . 12 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Dyspepsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . . . . . . 13 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Helicobacter pylori Infection. . . . . . . . . . . . . . . . . . . . . . . . . 13 Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Diagnostic Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Eradication Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Gastrointestinal Complications of NSAIDs . . . . . . . . . . . . . . 15 Epidemiology and Risk Factors . . . . . . . . . . . . . . . . . . . 15 Prevention of NSAID-Induced Injury . . . . . . . . . . . . . . 16 Gastroparesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Gastric Polyps and Submucosal Lesions. . . . . . . . . . . . . . . . . 19 Gastric Polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Gastric Subepithelial Masses. . . . . . . . . . . . . . . . . . . . . . 19 Gastric Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Epidemiology and Risk Factors . . . . . . . . . . . . . . . . . . . 20 Screening and Surveillance. . . . . . . . . . . . . . . . . . . . . . . 20 Clinical Manifestations and Diagnosis . . . . . . . . . . . . . . 20 Complications of Gastric Surgical Procedures . . . . . . . . . . . . 20 Bariatric Surgery Complications. . . . . . . . . . . . . . . . . . . 20 Other Gastric Resection Complications . . . . . . . . . . . . . 22 viii

Disorders of the Small and Large Bowel Diarrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Characterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Evaluation and Management . . . . . . . . . . . . . . . . . . . . . 30 Malabsorption. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Malabsorption Syndromes . . . . . . . . . . . . . . . . . . . . . . . 32 Inflammatory Bowel Disease. . . . . . . . . . . . . . . . . . . . . . . . . 34 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . . . . . . 35 Extraintestinal Manifestations . . . . . . . . . . . . . . . . . . . . 36 Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Health Care Maintenance for the Patient with Inflammatory Bowel Disease . . . . . . . . . . . . . . . . . . . . . 38 Microscopic Colitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Constipation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Irritable Bowel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Diverticular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Ischemic Bowel Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Acute Mesenteric Ischemia . . . . . . . . . . . . . . . . . . . . . . 43 Chronic Mesenteric Ischemia. . . . . . . . . . . . . . . . . . . . . 44 Colonic Ischemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Colorectal Neoplasia Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Environmental Exposures . . . . . . . . . . . . . . . . . . . . . . . 45 Predisposing Conditions . . . . . . . . . . . . . . . . . . . . . . . . 46 Nonsyndromic Family History. . . . . . . . . . . . . . . . . . . . 46 Hereditary Colorectal Cancer Syndromes . . . . . . . . . . . 46 Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Average Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Increased Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Surveillance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Postpolypectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Post–Colorectal Cancer Treatment . . . . . . . . . . . . . . . . 52 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Diagnosis and Staging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Chemoprevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

Disorders of the Liver Approach to the Patient with Abnormal Liver Chemistry Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Viral Hepatitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Hepatitis A . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Hepatitis B . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Hepatitis C . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 Hepatitis D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Hepatitis E . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Alcohol- and Drug-Induced Liver Disease. . . . . . . . . . . . . . . 57 Alcohol-Induced Liver Disease . . . . . . . . . . . . . . . . . . . 57 Drug- and Toxin-Induced Liver Disease . . . . . . . . . . . . 57 Autoimmune Hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Metabolic Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Nonalcoholic Fatty Liver Disease . . . . . . . . . . . . . . . . . . 58 Hereditary Hemochromatosis . . . . . . . . . . . . . . . . . . . . 59 α1-Antitrypsin Deficiency . . . . . . . . . . . . . . . . . . . . . . . 59 Wilson Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Cholestatic Liver Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 Primary Biliary Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . 60 Primary Sclerosing Cholangitis . . . . . . . . . . . . . . . . . . . 60 Complications of Liver Disease . . . . . . . . . . . . . . . . . . . . . . . 61 Portal Hypertension and Gastroesophageal Varices. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Ascites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 Spontaneous Bacterial Peritonitis . . . . . . . . . . . . . . . . . . 63 Hepatic Encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . 63 Hepatorenal Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . 64 Hepatopulmonary Syndrome. . . . . . . . . . . . . . . . . . . . . 64 Portopulmonary Hypertension . . . . . . . . . . . . . . . . . . . 64 Hepatocellular Carcinoma . . . . . . . . . . . . . . . . . . . . . . . 65 Fulminant Hepatic Failure. . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Liver Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 Hepatic Tumors, Cysts, and Abscesses. . . . . . . . . . . . . . . . . . 67

Hepatic Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67 Focal Nodular Hyperplasia. . . . . . . . . . . . . . . . . . . . . . . 67 Hepatic Adenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67 Hepatic Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Liver Abscesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Amebiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Pregnancy-Related Liver Disease . . . . . . . . . . . . . . . . . . . . . . 68 Health Care Maintenance of the Patient with Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69 Metabolic Bone Disease. . . . . . . . . . . . . . . . . . . . . . . . . 69 Immunizations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69 Medications to Avoid . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Nutrition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Vascular Disorders of the Liver . . . . . . . . . . . . . . . . . . . . . . . 70 Budd-Chiari Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . 70 Portal Vein Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . 71

Disorders of the Gallbladder and Bile Ducts Asymptomatic Gallstones . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 Biliary Colic and Acute Cholecystitis . . . . . . . . . . . . . . . . . . . 71 Epidemiology and Clinical Manifestations . . . . . . . . . . . 71 Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 Acalculous Cholecystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 Common Bile Duct Stones and Cholangitis . . . . . . . . . . . . . 72 Biliary Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 Gallbladder Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 Cholangiocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 Ampullary Adenocarcinoma. . . . . . . . . . . . . . . . . . . . . . 73 Biliary Cysts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Gastrointestinal Bleeding Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Upper Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . 74 Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Lower Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . 77 Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Obscure Gastrointestinal Bleeding. . . . . . . . . . . . . . . . . . . . . 79 Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . . . . . 85 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 ix

Gastroenterology and Hepatology

Dysphagia

difficulty in the initial phase of swallowing, in which the bolus is formed in the mouth and is transferred from the mouth through the pharynx to the esophagus. Esophageal dysphagia is characterized by difficulty in passage of the bolus through the esophagus. Defining the area of involvement (oropharyngeal or esophageal) often affects assessment, differential diagnosis, and treatment options. Causes of dysphagia are described in Table 1.

Dysphagia is defined as difficulty in swallowing. Patients typically describe a sensation of obstruction or difficulty passing food and/or liquid through the mouth, pharynx, or esophagus. Oropharyngeal or transfer dysphagia is characterized by

Oropharyngeal Dysphagia Causes of oropharyngeal dysphagia may be either neuromuscular or anatomic. Patients may have associated symptoms that

Disorders of the Esophagus Symptoms of Esophageal Disorders

TA B L E 1 .

Causes of Dysphagia

Condition

Diagnostic Clues

Oropharyngeal Dysphagia Structural disorders Cervical osteophytes Cricoid webs Pharyngoesophageal (Zenker) diverticulum

High dysphagia High dysphagia Presents with aspiration, neck mass, and regurgitation of foul-smelling food

Thyromegaly Neurologic/myogenic disorders Amyotrophic lateral sclerosis Central nervous system tumor Stroke Muscular dystrophy Myasthenia gravis Parkinson disease Dementia Sjögren syndrome

Presents with upper and lower motor neuron signs; fasciculations Neurologic deficits Proximal muscle weakness Weakness with repetitive activity Bradykinesia, tremor Dry mouth, dry eyes

Esophageal Dysphagia Structural disorders Dysphagia lusoria (vascular dysphagia) Epiphrenic/traction diverticulum Esophageal strictures Eosinophilic esophagitis Esophageal webs or rings Neoplasms

Intermittent dysphagia, especially for solid food; history of reflux Rings, strictures Usually incidental finding; may be associated with iron deficiency anemia Rapidly progressive dysphagia for solids then liquids; anorexia; weight loss

Motility disorders Achalasia Diffuse esophageal spasm Scleroderma

Concomitant liquid and solid dysphagia; chest pain Chest pain Tight skin, telangiectasias

1

Disorders of the Esophagus

provide clues to the underlying diagnosis, such as coughing (caused by aspiration), nasal regurgitation (caused by dysfunction of the soft palate in neurologic disorders), or other neurologic symptoms such as dysphonia, diplopia, and muscular weakness. Recurrent pneumonia may signal chronic aspiration. The diagnostic test of choice is videofluoroscopy (also referred to as a modified barium swallow), in which the oropharyngeal phase of swallowing is assessed with foods of different consistencies. Any indication of an intraluminal structural cause should prompt additional endoscopic evaluation. The management of functional disorders should include dietary and postural measures to improve swallowing and reduce the risk of aspiration; consultation with a speech pathologist can be helpful in this regard.

Esophageal Dysphagia Patients with esophageal dysphagia often report a sensation of food “sticking” in the esophagus. Esophageal dysphagia tends to occur after the initiation of the swallow. The sensation of dysphagia at the lower portion of the esophagus (particularly near the gastroesophageal junction) may accurately reflect a lower-esophageal pathology; however, the sensation of dysphagia at the upper portion of the esophagus (especially near the upper sternum) has poor specificity. Esophageal dysphagia often has an intraluminal cause, such as strictures, Schatzki rings, or masses (Figure 1). Progressive solid-food dysphagia may indicate a mechanical cause of obstruction; concomitant liquid and solid dysphagia may indicate a motility disorder such as achalasia. Associated symptoms such as reflux (indicating a possible peptic stricture), chest pain (indicating achalasia or diffuse esophageal spasm), or weight loss (concerning for malignancy) may help in narrowing the differential diagnosis. The diagnostic test of choice for esophageal dysphagia is upper endoscopy, which can be both diagnostic (allowing biopsy and visualization of the mucosa) and therapeutic (allowing dilation to be performed if indicated). Management depends on the underlying cause detected during evaluation, as described in later sections.

Reflux Typical symptoms of reflux are heartburn and acid regurgitation. Heartburn (or pyrosis) is defined as retrosternal burning pain or discomfort that is improved by therapy with antacids. Regurgitation occurs when a bitter- or sour-tasting fluid comes up into the throat or mouth. Almost 20% of the U.S. population experiences heartburn and/or regurgitation at least once per week. These symptoms are approximately 70% to 80% sensitive and specific for gastroesophageal reflux disease (GERD), as assessed by upper endoscopy or ambulatory pH studies. However, symptom severity does not correlate well with the severity of reflux. Factors that may precipitate or worsen reflux are listed in Table 2. For diagnosis and treatment of reflux, see Gastroesophageal Reflux Disease.

2

Chest Pain Chest pain caused by esophageal disorders can be difficult to distinguish from cardiac chest pain because of the anatomic proximity and common innervation of the esophagus and the

F I G U R E 1 . Barium esophagography showing a Schatzki ring TA B L E 2 .

Factors Associated with Reflux

Category

Factor

Lifestyle

Cigarette smoking

Eating habits

Eating large meals Eating late at night

Foods and beverages

Alcohol Chocolate Citrus fruits and juices Coffee Fatty and fried foods Onions Peppermint

Medications

Anticholinergic agents Aspirin and other NSAIDs Calcium channel blockers Nitrates Progesterone

Body position

Bending over, exercising (both result in increased intra-abdominal pressure)

This self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefully before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice questions. The American College of Physicians is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

The American College of Physicians designates MKSAP 16 Gastroenterology and Hepatology for a maximum of 14 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Earn “Same-Day” CME Credits Online For the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You can submit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of your MKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test and earn a score of at least 50% correct (number of correct answers divided by the total number of questions). Take any of the following approaches: ➢ Use the printed answer sheet at the back of this book to record your answers. Go to mksap.acponline.org, access the appropriate online answer sheet, transcribe your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ➢ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ➢ Pay a $10 processing fee per answer sheet and submit the printed answer sheet at the back of this book by mail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheet to 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physicians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope provided in your MKSAP 16 slipcase. You will need your 10-digit order number and 8-digit ACP ID number, which are printed on your packing slip. Please allow 4 to 6 weeks for your score report to be emailed back to you. Be sure to include your email address for a response.

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CME credit is available from the publication date of July 31, 2012, until July 31, 2015. You may submit your answer sheets at any time during this period.

85

Self-Assessment Test

Gastroenterology and Hepatology Self-Assessment Test

Each of the numbered items is followed by lettered answers. Select the ONE lettered answer that is BEST in each case.

Item 1 A 36-year-old woman is evaluated during a routine examination. She is generally healthy and has no gastrointestinal problems. She would like to discuss colorectal cancer screening recommendations. Her family history is as follows: Father Mother Paternal aunt Paternal uncle Brother

Colorectal cancer, age 52 years No known cancers or precancerous lesions Endometrial cancer, age 37 years Large (2.5-cm) colorectal adenoma (ascending colon), age 42 years Colorectal cancer, age 48 years

Physical examination, including cardiopulmonary examination, is normal.

Which of the following is the most appropriate management strategy?

(A) Colonoscopy now (B) Colonoscopy at age 40 years (C) Colonoscopy at age 50 years (D) CT colonography at age 40 years (E) Stool DNA test at age 40 years

Item 2 A 42-year-old man is evaluated in follow-up for elevated liver chemistry tests. He is asymptomatic. He has a 6-year history of type 2 diabetes mellitus, hyperlipidemia, and hypertension. His current medications are metformin, simvastatin, and lisinopril. He does not drink alcohol.

On physical examination, temperature is 37.0 °C (98.6 °F), blood pressure is 130/74 mm Hg, pulse rate is 82/min, and respiration rate is 14/min. BMI is 32.

Abdominal examination discloses mild hepatomegaly and active bowel sounds.

Laboratory studies: Alkaline phosphatase Alanine aminotransferase Aspartate aminotransferase Total bilirubin LDL cholesterol Hemoglobin A1c Iron Total iron-binding capacity Hepatitis B surface antigen Antibody to hepatitis B surface antigen Hepatitis C virus antibody

90 units/L 120 units/L 85 units/L 1.1 mg/dL (18.8 µmol/L) 100 mg/dL (2.59 mmol/L) 7.2% 75 µg/dL (13 µmol/L) 300 µg/dL (54 µmol/L) Negative Positive Negative

Abdominal ultrasound reveals increased hepatic echotexture consistent with hepatic steatosis. Hepatic configuration is otherwise normal.

In addition to weight loss, which of the following is the most appropriate management?

(A) Discontinue simvastatin (B) Initiate entecavir (C) Phlebotomy (D) Serial monitoring of aminotransferases

Item 3 A 45-year-old man is admitted to the hospital for a 2-day history of fever and abdominal pain. His medical history is notable for cirrhosis due to chronic hepatitis C, esophageal varices, ascites, and minimal hepatic encephalopathy. His medications are furosemide, spironolactone, nadolol, lactulose, zinc, vitamin A, and vitamin D. On physical examination, temperature is 36.5 °C (97.7 °F), blood pressure is 100/50 mm Hg, pulse rate is 84/min, and respiration rate is 20/min. BMI is 28.

Abdominal examination discloses distention consistent with ascites. The abdomen is nontender to palpation.

Laboratory studies: Hemoglobin 10 g/dL (100 g/L) Leukocyte count 3500/µL (3.5 × 109/L) Platelet count 70,000/µL (70 × 109/L) INR 1.5 (normal range, 0.8-1.2) Albumin 2.5 g/dL (25 g/L) Alkaline phosphatase 220 units/L Alanine aminotransferase 30 units/L Aspartate aminotransferase 40 units/L Total bilirubin 4 mg/dL (68.4 µmol/L) Creatinine 1.8 mg/dL (159 µmol/L) Urinalysis Normal Abdominal ultrasound discloses cirrhosis, splenomegaly, and ascites. The portal and hepatic veins are patent, and there is no hydronephrosis. Diagnostic paracentesis discloses a cell count of 2000/µL with 20% neutrophils, a total protein level of 1 g/dL (10 g/L), and an albumin level of 0.7 g/dL (7 g/L), consistent with spontaneous bacterial peritonitis.

Which of the following is the most appropriate treatment?

(A) Cefotaxime (B) Cefotaxime and albumin (C) Furosemide and spironolactone (D) Large-volume paracentesis

Item 4 A 34-year-old woman is evaluated in an urgent care clinic for a 1-day history of watery diarrhea and mild abdominal cramps. She is having four watery stools per day. She has not had fever or blood in her stool. Although she has felt mildly nauseated, she has been able to stay hydrated with oral intake.

She works as a banker, and colleagues at work have had similar gastrointestinal symptoms over recent weeks. She has no history of recent hospitalization, antibiotic use, or medication changes. She has no risk factors for HIV infection.

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Self-Assessment Test

Directions

Answers and Critiques Answer:

A

Educational Objective: Manage colorectal cancer surveillance in a patient with hereditary nonpolyposis colorectal cancer syndrome (Lynch syndrome).

The most appropriate management strategy is a colonoscopy now. This patient’s family history meets the Amsterdam criteria II, supporting a possible hereditary nonpolyposis colorectal cancer (HNPCC) kindred. The Amsterdam criteria II can be remembered by the “3-2-1 rule” (3 affected members, 2 generations, 1 under age 50 years). HNPCC (or Lynch syndrome) is an autosomal dominant syndrome that carries an 80% lifetime risk for colon cancer. HNPCC is the most common of the hereditary colon cancer syndromes, accounting for 2% to 3% of all colorectal adenocarcinomas. Colorectal adenomas develop at a relatively young age (by age 20 to 30 years) and are thought to progress to colorectal cancer more quickly than sporadic adenomas. HNPCC-associated extracolonic cancers include uterine cancer (40% to 60% lifetime risk) and ovarian cancer (10% to 12% lifetime risk). Colorectal evaluation should be initiated by age 20 to 25 years or 10 years prior to the earliest age of colorectal cancer diagnosis in the family, whichever comes first. Colonoscopy is the test of choice. In addition, gynecologic (transvaginal ultrasound or endometrial aspirate) and genitourinary (urine cytology) cancer screening should be performed.

Colonoscopy at age 40 years would be an acceptable option for a patient with a nonsyndromic family history of colorectal cancer in a first-degree relative but not in a patient with a possible hereditary nonpolyposis colorectal cancer syndrome.

Colonoscopy at age 50 years is one of several endorsed options for average-risk colorectal cancer screening, but it is not appropriate for this patient who is in a high-risk category.

Neither stool DNA testing nor CT colonography is currently endorsed for colorectal cancer screening/ surveillance among patients at increased risk because of family history.

KEY POINT

• In patients with hereditary nonpolyposis colorectal cancer syndrome (Lynch syndrome), colonoscopy should be initiated by age 20 to 25 years or 10 years prior to the earliest age of colorectal cancer diagnosis in the family, whichever comes first.

Item 2

Answer:

D

Educational Objective: Manage nonalcoholic steatohepatitis.

The most appropriate management is serial monitoring of aminotransferases, in addition to weight loss through dietary and lifestyle changes. There is no definitive treatment for nonalcoholic fatty liver disease. The reduction of underlying risk factors is essential. Weight loss, exercise, and aggressive control of plasma glucose, lipids, and blood pressure are the mainstays of treatment. Nonalcoholic fatty liver disease has become a leading cause of liver disease in the Western world, along with hepatitis C and alcoholic liver disease. When hepatic steatosis is associated with liver inflammation, as is seen in this patient with elevated hepatic aminotransferases, nonalcoholic steatohepatitis (NASH) is diagnosed. The association of NASH with the metabolic syndrome (obesity, dyslipidemia, hypertension, insulin resistance) is well established. Although most cases of nonalcoholic fatty liver disease are seen in patients who are overweight, the condition has also been described in patients who have a normal BMI. The cornerstone of management of NASH is typically weight loss through diet and lifestyle modification. Monitoring of hepatic aminotransferases is appropriate to confirm that weight loss results in improved markers of liver inflammation. Associated medical conditions such as dyslipidemia should be treated, and statins such as simvastatin should not be discontinued in this setting. The risks of hepatoxicity due to the use of medications such as simvastatin are usually outweighed by the benefits derived from these medications in regard to cardiovascular risk reduction.

This patient’s hepatitis B serologies indicate immunity to hepatitis B virus; therefore, an antiviral medication such as entecavir is not appropriate.

This patient’s iron stores are not elevated, with a transferrin saturation (iron/total iron binding capacity) of less than 45%; therefore, phlebotomy is not warranted as a treatment in this setting.

KEY POINT

• Weight loss, exercise, and aggressive control of plasma glucose, lipids, and blood pressure are the mainstays of treatment for nonalcoholic steatohepatitis; monitoring of hepatic aminotransferases is appropriate to confirm that weight loss results in improved markers of liver inflammation.

Bibliography

Bibliography Goodenberger M, Lindor NM. Lynch syndrome and MYH-associated polyposis: review and testing strategy. J Clin Gastroenterol.

2011;45(6):488-500. [PMID: 21325953]

Perlemuter G, Bigorgne A, Cassard-Doulcier AM, Naveau S. Nonalcoholic fatty liver disease: from pathogenesis to patient care. Nat Clin Pract Endocrinol Metab. 2007;3(6):458-469. [PMID: 17515890]

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Answers and Critiques

Item 1