Gastroenterology and Hepatology

150591010

Gastroenterology and HepatologyAll New Content, Including 96 Multiple-Choice Questions

14 AMA PRA Category 1 Credits™

available until July 31, 2015.

gastro

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Medical Knowledge Self -Assessment Program®

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Table of Contents

Disorders of the PancreasAcute Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 23Prognostic Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

Chronic Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 25Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

Pancreatic Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . 26Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . 27Diagnosis and Staging . . . . . . . . . . . . . . . . . . . . . . . . . . 27

Autoimmune Pancreatitis and IgG4 Disease . . . . . . . . . . . . . 27Clinical Presentation and Diagnosis . . . . . . . . . . . . . . . . 28Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Cystic Neoplasms of the Pancreas . . . . . . . . . . . . . . . . . . . . . 28Pancreatic Neuroendocrine Tumors . . . . . . . . . . . . . . . . . . . 29

Disorders of the Small and Large BowelDiarrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

Characterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Evaluation and Management . . . . . . . . . . . . . . . . . . . . . 30

Malabsorption. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Malabsorption Syndromes . . . . . . . . . . . . . . . . . . . . . . . 32

Inflammatory Bowel Disease. . . . . . . . . . . . . . . . . . . . . . . . . 34Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . . . . . . 35Extraintestinal Manifestations . . . . . . . . . . . . . . . . . . . . 36Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37Health Care Maintenance for the Patient withInflammatory Bowel Disease . . . . . . . . . . . . . . . . . . . . . 38Microscopic Colitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

Constipation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39Irritable Bowel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Diverticular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42Ischemic Bowel Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

Acute Mesenteric Ischemia . . . . . . . . . . . . . . . . . . . . . . 43Chronic Mesenteric Ischemia. . . . . . . . . . . . . . . . . . . . . 44Colonic Ischemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Disorders of the EsophagusSymptoms of Esophageal Disorders. . . . . . . . . . . . . . . . . . . . . 1

Dysphagia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Reflux . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Chest Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Odynophagia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Globus Sensation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Nonmalignant Disorders of the Esophagus . . . . . . . . . . . . . . . 3Esophageal Motility Disorders . . . . . . . . . . . . . . . . . . . . . 3Infectious, Pill-Induced, and Eosinophilic Esophagitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6Gastroesophageal Reflux Disease . . . . . . . . . . . . . . . . . . . 7

Metaplastic and Neoplastic Disorders of the Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Barrett Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Esophageal Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . 11

Disorders of the Stomach and DuodenumPeptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Clinical Features, Diagnosis, and Complications. . . . . . . 12Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Dyspepsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . . . . . . 13Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Helicobacter pylori Infection. . . . . . . . . . . . . . . . . . . . . . . . . 13Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Diagnostic Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Eradication Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Gastrointestinal Complications of NSAIDs . . . . . . . . . . . . . . 15Epidemiology and Risk Factors . . . . . . . . . . . . . . . . . . . 15Prevention of NSAID-Induced Injury . . . . . . . . . . . . . . 16

Gastroparesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Gastric Polyps and Submucosal Lesions. . . . . . . . . . . . . . . . . 19Gastric Polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Gastric Subepithelial Masses. . . . . . . . . . . . . . . . . . . . . . 19

Gastric Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Epidemiology and Risk Factors . . . . . . . . . . . . . . . . . . . 20Screening and Surveillance. . . . . . . . . . . . . . . . . . . . . . . 20Clinical Manifestations and Diagnosis . . . . . . . . . . . . . . 20

Complications of Gastric Surgical Procedures . . . . . . . . . . . . 20Bariatric Surgery Complications. . . . . . . . . . . . . . . . . . . 20Other Gastric Resection Complications . . . . . . . . . . . . . 22

Colorectal NeoplasiaEpidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

Environmental Exposures . . . . . . . . . . . . . . . . . . . . . . . 45Predisposing Conditions . . . . . . . . . . . . . . . . . . . . . . . . 46Nonsyndromic Family History. . . . . . . . . . . . . . . . . . . . 46Hereditary Colorectal Cancer Syndromes . . . . . . . . . . . 46

Screening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48Average Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48Increased Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51

Surveillance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51Postpolypectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51Post–Colorectal Cancer Treatment . . . . . . . . . . . . . . . . 52

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52Diagnosis and Staging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52Chemoprevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

Disorders of the LiverApproach to the Patient with Abnormal Liver Chemistry Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53Viral Hepatitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

Hepatitis A . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54Hepatitis B . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54Hepatitis C . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55Hepatitis D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56Hepatitis E . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56

Alcohol- and Drug-Induced Liver Disease. . . . . . . . . . . . . . . 57Alcohol-Induced Liver Disease . . . . . . . . . . . . . . . . . . . 57Drug- and Toxin-Induced Liver Disease . . . . . . . . . . . . 57

Autoimmune Hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Metabolic Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

Nonalcoholic Fatty Liver Disease . . . . . . . . . . . . . . . . . . 58Hereditary Hemochromatosis . . . . . . . . . . . . . . . . . . . . 59α1-Antitrypsin Deficiency . . . . . . . . . . . . . . . . . . . . . . . 59Wilson Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

Cholestatic Liver Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . 60Primary Biliary Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . 60Primary Sclerosing Cholangitis . . . . . . . . . . . . . . . . . . . 60

Complications of Liver Disease . . . . . . . . . . . . . . . . . . . . . . . 61Portal Hypertension and Gastroesophageal Varices. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61Ascites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62Spontaneous Bacterial Peritonitis . . . . . . . . . . . . . . . . . . 63Hepatic Encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . 63Hepatorenal Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . 64Hepatopulmonary Syndrome. . . . . . . . . . . . . . . . . . . . . 64Portopulmonary Hypertension . . . . . . . . . . . . . . . . . . . 64Hepatocellular Carcinoma . . . . . . . . . . . . . . . . . . . . . . . 65

Fulminant Hepatic Failure. . . . . . . . . . . . . . . . . . . . . . . . . . . 65Liver Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66Hepatic Tumors, Cysts, and Abscesses. . . . . . . . . . . . . . . . . . 67

Hepatic Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Focal Nodular Hyperplasia. . . . . . . . . . . . . . . . . . . . . . . 67Hepatic Adenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Hepatic Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . 68Liver Abscesses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68Amebiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

Pregnancy-Related Liver Disease . . . . . . . . . . . . . . . . . . . . . . 68Health Care Maintenance of the Patient with Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

Metabolic Bone Disease. . . . . . . . . . . . . . . . . . . . . . . . . 69Immunizations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69Medications to Avoid . . . . . . . . . . . . . . . . . . . . . . . . . . 70Nutrition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70

Vascular Disorders of the Liver . . . . . . . . . . . . . . . . . . . . . . . 70Budd-Chiari Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . 70Portal Vein Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . 71

Disorders of the Gallbladder and Bile DuctsAsymptomatic Gallstones . . . . . . . . . . . . . . . . . . . . . . . . . . . 71Biliary Colic and Acute Cholecystitis . . . . . . . . . . . . . . . . . . . 71

Epidemiology and Clinical Manifestations . . . . . . . . . . . 71Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Acalculous Cholecystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72Common Bile Duct Stones and Cholangitis . . . . . . . . . . . . . 72Biliary Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Gallbladder Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Cholangiocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Ampullary Adenocarcinoma. . . . . . . . . . . . . . . . . . . . . . 73Biliary Cysts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Gastrointestinal BleedingOverview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74Upper Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . 74

Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Lower Gastrointestinal Bleeding . . . . . . . . . . . . . . . . . . . . . . 77Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

Obscure Gastrointestinal Bleeding. . . . . . . . . . . . . . . . . . . . . 79Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81

Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . . . . . 85

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155

ix

Gastroenterology and Hepatology

difficulty in the initial phase of swallowing, in which the bolusis formed in the mouth and is transferred from the mouththrough the pharynx to the esophagus. Esophageal dysphagiais characterized by difficulty in passage of the bolus throughthe esophagus. Defining the area of involvement (oropharyn-geal or esophageal) often affects assessment, differential diag-nosis, and treatment options. Causes of dysphagia aredescribed in Table 1.

Oropharyngeal DysphagiaCauses of oropharyngeal dysphagia may be either neuromus-cular or anatomic. Patients may have associated symptoms that

Disorders of theEsophagusSymptoms of EsophagealDisordersDysphagiaDysphagia is defined as difficulty in swallowing. Patients typ-ically describe a sensation of obstruction or difficulty passingfood and/or liquid through the mouth, pharynx, or esopha-gus. Oropharyngeal or transfer dysphagia is characterized by

1

TABLE 1 . Causes of Dysphagia

Condition Diagnostic Clues

Oropharyngeal Dysphagia

Structural disorders

Cervical osteophytes High dysphagia

Cricoid webs High dysphagia

Pharyngoesophageal (Zenker) diverticulum Presents with aspiration, neck mass, and regurgitation of foul-smelling food

Thyromegaly

Neurologic/myogenic disorders

Amyotrophic lateral sclerosis Presents with upper and lower motor neuron signs; fasciculations

Central nervous system tumor

Stroke Neurologic deficits

Muscular dystrophy Proximal muscle weakness

Myasthenia gravis Weakness with repetitive activity

Parkinson disease Bradykinesia, tremor

Dementia

Sjögren syndrome Dry mouth, dry eyes

Esophageal Dysphagia

Structural disorders

Dysphagia lusoria (vascular dysphagia)

Epiphrenic/traction diverticulum

Esophageal strictures Intermittent dysphagia, especially for solid food; history of reflux

Eosinophilic esophagitis Rings, strictures

Esophageal webs or rings Usually incidental finding; may be associated with iron deficiency anemia

Neoplasms Rapidly progressive dysphagia for solids then liquids; anorexia; weight loss

Motility disorders

Achalasia Concomitant liquid and solid dysphagia; chest pain

Diffuse esophageal spasm Chest pain

Scleroderma Tight skin, telangiectasias

2

provide clues to the underlying diagnosis, such as coughing(caused by aspiration), nasal regurgitation (caused by dys-function of the soft palate in neurologic disorders), or otherneurologic symptoms such as dysphonia, diplopia, and mus-cular weakness. Recurrent pneumonia may signal chronicaspiration. The diagnostic test of choice is videofluoroscopy(also referred to as a modified barium swallow), in which theoropharyngeal phase of swallowing is assessed with foods ofdifferent consistencies. Any indication of an intraluminalstructural cause should prompt additional endoscopic evalu-ation. The management of functional disorders shouldinclude dietary and postural measures to improve swallowingand reduce the risk of aspiration; consultation with a speechpathologist can be helpful in this regard.

Esophageal DysphagiaPatients with esophageal dysphagia often report a sensation offood “sticking” in the esophagus. Esophageal dysphagiatends to occur after the initiation of the swallow. The sensa-tion of dysphagia at the lower portion of the esophagus (par-ticularly near the gastroesophageal junction) may accuratelyreflect a lower-esophageal pathology; however, the sensationof dysphagia at the upper portion of the esophagus (especiallynear the upper sternum) has poor specificity. Esophageal dys-phagia often has an intraluminal cause, such as strictures,Schatzki rings, or masses (Figure 1). Progressive solid-fooddysphagia may indicate a mechanical cause of obstruction;concomitant liquid and solid dysphagia may indicate a motil-ity disorder such as achalasia. Associated symptoms such asreflux (indicating a possible peptic stricture), chest pain (indi-cating achalasia or diffuse esophageal spasm), or weight loss(concerning for malignancy) may help in narrowing the dif-ferential diagnosis. The diagnostic test of choice foresophageal dysphagia is upper endoscopy, which can be bothdiagnostic (allowing biopsy and visualization of the mucosa)and therapeutic (allowing dilation to be performed if indi-cated). Management depends on the underlying causedetected during evaluation, as described in later sections.

RefluxTypical symptoms of reflux are heartburn and acid regurgita-tion. Heartburn (or pyrosis) is defined as retrosternal burn-ing pain or discomfort that is improved by therapy withantacids. Regurgitation occurs when a bitter- or sour-tastingfluid comes up into the throat or mouth. Almost 20% of theU.S. population experiences heartburn and/or regurgitationat least once per week. These symptoms are approximately70% to 80% sensitive and specific for gastroesophageal refluxdisease (GERD), as assessed by upper endoscopy or ambula-tory pH studies. However, symptom severity does not corre-late well with the severity of reflux. Factors that may precipi-tate or worsen reflux are listed in Table 2. For diagnosis andtreatment of reflux, see Gastroesophageal Reflux Disease.

Disorders of the Esophagus

Chest PainChest pain caused by esophageal disorders can be difficult todistinguish from cardiac chest pain because of the anatomicproximity and common innervation of the esophagus and the

F I G U R E 1 . Barium esophagography showing a Schatzki ring

TABLE 2 . Factors Associated with Reflux

Category Factor

Lifestyle Cigarette smoking

Eating habits Eating large mealsEating late at night

Foods and beverages AlcoholChocolateCitrus fruits and juicesCoffeeFatty and fried foodsOnionsPeppermint

Medications Anticholinergic agentsAspirin and other NSAIDsCalcium channel blockersNitratesProgesterone

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

Self-

Ass

essm

ent T

est

Gastroenterology and Hepatology Self-Assessment TestThis self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefullybefore answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choicequestions. The American College of Physicians is accredited by the Accreditation Council for Continuing MedicalEducation (ACCME) to provide continuing medical education for physicians.

The American College of Physicians designates MKSAP 16 Gastroenterology and Hepatology for a maximum of14 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of theirparticipation in the activity.

Earn “Same-Day” CME Credits OnlineFor the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You cansubmit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of yourMKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test andearn a score of at least 50% correct (number of correct answers divided by the total number of questions). Takeany 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-dayCME credits. There is no additional fee for this service.

➢ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, andsubmit 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 bymail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheetto 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physi-cians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope pro-vided 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 backto you. Be sure to include your email address for a response.

If you do not have a 10-digit order number and 8-digit ACP ID number or if you need help creating a usernameand password to access the MKSAP 16 online answer sheets, go to mksap.acponline.org or email custserv@acponline.org.

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

85

Item 1A 36-year-old woman is evaluated during a routine exami-nation. She is generally healthy and has no gastrointestinalproblems. She would like to discuss colorectal cancer screen-ing recommendations. Her family history is as follows:

Father Colorectal cancer, age 52 yearsMother No known cancers or precancerous

lesionsPaternal aunt Endometrial cancer, age 37 yearsPaternal uncle Large (2.5-cm) colorectal adenoma

(ascending colon), age 42 yearsBrother Colorectal cancer, age 48 years

Physical examination, including cardiopulmonaryexamination, is normal.

Which of the following is the most appropriate man-agement 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 2A 42-year-old man is evaluated in follow-up for elevatedliver chemistry tests. He is asymptomatic. He has a 6-yearhistory of type 2 diabetes mellitus, hyperlipidemia, andhypertension. His current medications are metformin, sim-vastatin, 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 is82/min, and respiration rate is 14/min. BMI is 32.Abdominal examination discloses mild hepatomegaly andactive bowel sounds.Laboratory studies: Alkaline phosphatase 90 units/LAlanine aminotransferase 120 units/LAspartate aminotransferase 85 units/LTotal bilirubin 1.1 mg/dL (18.8 µmol/L)LDL cholesterol 100 mg/dL (2.59 mmol/L)Hemoglobin A1c 7.2%Iron 75 µg/dL (13 µmol/L)Total iron-binding 300 µg/dL (54 µmol/L)

capacityHepatitis B surface antigen NegativeAntibody to hepatitis B Positive

surface antigenHepatitis C virus antibody Negative

Abdominal ultrasound reveals increased hepatic echo-texture consistent with hepatic steatosis. Hepatic configu-ration is otherwise normal.

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

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

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

Item 3A 45-year-old man is admitted to the hospital for a 2-dayhistory of fever and abdominal pain. His medical history isnotable for cirrhosis due to chronic hepatitis C, esophagealvarices, ascites, and minimal hepatic encephalopathy. Hismedications are furosemide, spironolactone, nadolol, lactu-lose, 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 is84/min, and respiration rate is 20/min. BMI is 28.Abdominal examination discloses distention consistent withascites. 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/LAlanine aminotransferase 30 units/LAspartate aminotransferase 40 units/LTotal 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 thereis no hydronephrosis. Diagnostic paracentesis discloses a cellcount of 2000/µL with 20% neutrophils, a total protein levelof 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 4A 34-year-old woman is evaluated in an urgent care clinic fora 1-day history of watery diarrhea and mild abdominalcramps. She is having four watery stools per day. She has nothad fever or blood in her stool. Although she has felt mildlynauseated, she has been able to stay hydrated with oral intake.She works as a banker, and colleagues at work have had sim-ilar gastrointestinal symptoms over recent weeks. She has nohistory of recent hospitalization, antibiotic use, or medicationchanges. She has no risk factors for HIV infection.

Item 1 Answer: AEducational Objective: Manage colorectal cancersurveillance in a patient with hereditary nonpolypo-sis colorectal cancer syndrome (Lynch syndrome).

The most appropriate management strategy is acolonoscopy now. This patient’s family history meets theAmsterdam criteria II, supporting a possible hereditarynonpolyposis colorectal cancer (HNPCC) kindred. TheAmsterdam criteria II can be remembered by the “3-2-1rule” (3 affected members, 2 generations, 1 under age 50years). HNPCC (or Lynch syndrome) is an autosomaldominant syndrome that carries an 80% lifetime risk forcolon cancer. HNPCC is the most common of the heredi-tary colon cancer syndromes, accounting for 2% to 3% of allcolorectal adenocarcinomas. Colorectal adenomas developat a relatively young age (by age 20 to 30 years) and arethought to progress to colorectal cancer more quickly thansporadic adenomas. HNPCC-associated extracolonic can-cers include uterine cancer (40% to 60% lifetime risk) andovarian cancer (10% to 12% lifetime risk). Colorectal eval-uation should be initiated by age 20 to 25 years or 10 yearsprior to the earliest age of colorectal cancer diagnosis in thefamily, whichever comes first. Colonoscopy is the test ofchoice. In addition, gynecologic (transvaginal ultrasound orendometrial aspirate) and genitourinary (urine cytology)cancer screening should be performed.

Colonoscopy at age 40 years would be an acceptableoption for a patient with a nonsyndromic family history ofcolorectal cancer in a first-degree relative but not in apatient with a possible hereditary nonpolyposis colorectalcancer syndrome.

Colonoscopy at age 50 years is one of several endorsedoptions for average-risk colorectal cancer screening, but it isnot 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 offamily history.

K E Y P O I N T

• In patients with hereditary nonpolyposis colorectal cancer syndrome (Lynch syndrome),colonoscopy should be initiated by age 20 to25 years or 10 years prior to the earliest age ofcolorectal cancer diagnosis in the family,whichever comes first.

BibliographyGoodenberger M, Lindor NM. Lynch syndrome and MYH-associated

polyposis: review and testing strategy. J Clin Gastroenterol.2011;45(6):488-500. [PMID: 21325953]

Item 2 Answer: DEducational Objective: Manage nonalcoholicsteatohepatitis.

The most appropriate management is serial monitoring ofaminotransferases, in addition to weight loss through dietaryand lifestyle changes. There is no definitive treatment fornonalcoholic fatty liver disease. The reduction of underlyingrisk factors is essential. Weight loss, exercise, and aggressivecontrol of plasma glucose, lipids, and blood pressure are themainstays of treatment. Nonalcoholic fatty liver disease hasbecome a leading cause of liver disease in the Western world,along with hepatitis C and alcoholic liver disease. Whenhepatic steatosis is associated with liver inflammation, as isseen in this patient with elevated hepatic aminotransferases,nonalcoholic steatohepatitis (NASH) is diagnosed. Theassociation of NASH with the metabolic syndrome (obesity,dyslipidemia, hypertension, insulin resistance) is well estab-lished. Although most cases of nonalcoholic fatty liver dis-ease are seen in patients who are overweight, the conditionhas also been described in patients who have a normal BMI.The cornerstone of management of NASH is typicallyweight loss through diet and lifestyle modification. Moni-toring of hepatic aminotransferases is appropriate to confirmthat weight loss results in improved markers of liver inflam-mation. Associated medical conditions such as dyslipidemiashould be treated, and statins such as simvastatin should notbe discontinued in this setting. The risks of hepatoxicity dueto the use of medications such as simvastatin are usually out-weighed by the benefits derived from these medications inregard to cardiovascular risk reduction.

This patient’s hepatitis B serologies indicate immunityto hepatitis B virus; therefore, an antiviral medication suchas entecavir is not appropriate.

This patient’s iron stores are not elevated, with a trans-ferrin saturation (iron/total iron binding capacity) of lessthan 45%; therefore, phlebotomy is not warranted as atreatment in this setting.

K E Y P O I N T

• Weight loss, exercise, and aggressive control ofplasma glucose, lipids, and blood pressure are themainstays of treatment for nonalcoholic steato-hepatitis; monitoring of hepatic aminotransferasesis appropriate to confirm that weight loss resultsin improved markers of liver inflammation.

BibliographyPerlemuter G, Bigorgne A, Cassard-Doulcier AM, Naveau S. Nonal-

coholic fatty liver disease: from pathogenesis to patient care. NatClin Pract Endocrinol Metab. 2007;3(6):458-469. [PMID:17515890]

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