Practical Gastroenterology and Hepatology Board Review Toolkit E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 2438

Veröffentlichungsjahr: 2016

Beschreibung

Packed with Board-focused hints, case studies and an online Board-standard MCQ test offering CME credits, this fantastic book covers every gastroenterology disease and symptom you’re likely to encounter and is the perfect tool to prepare for Board exams and certification.

Leseprobe

Practical gastroenterology and hepatology board review toolkit

Editor-in-Chief

Nicholas J. Talley

Section Editors

Kenneth R. DeVault Michael B. Wallace Bashar A. Aqel Keith D. Lindor

Second Edition

This edition first published 2016 © 2016 by John Wiley & Sons, Ltd

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Library of Congress Cataloging-in-Publication Data

Names: Talley, Nicholas Joseph, editor. | Aqel, Bashar A., editor. | Lindor, Keith D., editor. | DeVault, Ken, editor. | Wallace,    Michael B. (Michael Bradley), editor. Title: Practical gastroenterology and hepatology board review toolkit / editor-in-chief, Nicholas J. Talley ; section editors, Bashar A.    Aqel, Keith Lindor, Kenneth DeVault, Michael Wallace. Description: Second edition. | Chichester, West Sussex ; Hoboken, NJ : John Wiley & Sons Inc., 2016. | Preceded by three works    originally published in 2010 as individual volumes: Practical gastroenterology and hepatology. Esophagus and stomach,    Practical gastroenterology and hepatology. Liver and biliary disease, and Practical gastroenterology and hepatology. Small and large    intestine and pancreas. | Includes bibliographical references and index. Identifiers: LCCN 2016000004 | ISBN 9781118829066 (pbk.) | ISBN 9781118829080 (epub) | ISBN 9781118829073 (Adobe PDF) Subjects: | MESH: Digestive System Diseases | Diagnostic Techniques, Digestive System Classification: LCC RC801 | NLM WI 140 | DDC 616.3/30076--dc23 LC record available at http://lccn.loc.gov/2016000004

A catalogue record for this book is available from the British Library.

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Cover image: Getty/Ugreen

Contents

List of Contributors

Foreword

Preface

About the Companion Website

Section I How to Ace the Boards in Gastroenterology and Hepatology

1 Introduction and Overview of the Gastroenterology Boards

What to Expect at the Test Center

The Examination

Maintenance of Certification Changes

Specific Tips and Recommendations for the Gastroenterology Board Examination

Reference

Section II Esophagus and Stomach

Part 1 Pathobiology of the Esophagus and Stomach

2 Anatomy, Embryology, and Congenital Malformations of the Esophagus and Stomach

Summary

Anatomy

Embryology

Congenital Malformations of the Esophagus and Stomach

References

3 Esophageal and Gastric Motor Function

Summary

Esophageal Motor Function

Gastric Motor Function

References

Part 2 Other Diagnostic Modalities

4 Radiologic Approach to Diagnosis

Esophagus

Stomach

References

5 Esophageal Motility Disorders

Summary

Introduction

Achalasia

Chagas Disease

EGJ

Non-Achalasia Esophageal Motility Disorders

Disorders with Absent, Weak, or Frequent Failed Peristalsis

References

6 Gastric Motility Testing

Summary

Introduction

Gastric Motility Testing

References

Part 3 Problem-Based Approach to Diagnosis and Differential Diagnosis

7 General Approach to History-Taking and Physical Examination of the Upper Gastrointestinal Tract

Summary

Setting the Stage

Heartburn

Dysphagia

Nausea/Vomiting

Abdominal Pain

Diarrhea

Finishing the Visit

References

8 Heartburn, Regurgitation, and Chest Pain

Heartburn and Regurgitation

Chest Pain

References

9 Dysphagia

Summary

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

Prognosis

References

10 Miscellaneous Upper Gastrointestinal Symptoms

Belching (Eructation) and Aerophagia

Summary

Halitosis

Summary

Hiccups

Summary

Rumination

Summary

References

11 Dyspepsia

Summary

Introduction

Dyspepsia

Functional Dyspepsia

References

12 Nausea and Vomiting

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

References

13 Hematemesis

Summary

Initial Approach to the Patient

History

Physical Examination

Laboratory Studies

Nasogastric Aspiration

Triage

Medical Therapy

Acknowledgements

References

Part 4 Diseases of the Esophagus

14 Gastroesophageal Reflux Disease

Summary

Definition and Epidemiology

Key Terms

Pathophysiology

Clinical Features

Diagnosis of GERD and Extraesophageal Reflux

Therapeutic Approach

References

15 Barrett's Esophagus

Summary

Definition

Epidemiology, Genetics, Environmental Influence, and Natural History

Predictors of Progression

Screening

Endoscopic Surveillance

Evaluation

Management

Non-dysplastic Barrett's Esophagus

Barrett's Low-Grade Dysplasia

Barrett's High-Grade Dysplasia and Intramucosal Adenocarcinoma

References

16 Eosinophilic Esophagitis

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

17 Strictures, Rings, and Webs

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Treatment

References

Part 5 Diseases of the Stomach

18 Peptic Ulcer Disease

Summary

Background and Epidemiology

Etiologies

Clinical Features

Diagnosis

Therapeutics

References

19

Helicobacter pylori

Summary

Bacteriology

Epidemiology and Transmission

Pathogenesis and Disease Associations

Diagnosis

Treatment

Controversies in Management

References

20 Gastritis

Summary

Definitions

Assessment

Basic Morphology

Classification

Main Forms of Gastritis

References

21 Gastroparesis

Summary

Etiology

Clinical Presentation

Evaluation of Patients with Suspected Gastroparesis

Treatment

References

22 Non-variceal Upper Gastrointestinal Bleeding

Summary

Etiology

Initial Assessment and Management

Endoscopy

Peptic Ulcer Bleeding

Variceal Bleeding

Esophagitis

Stress Ulcers

Dieulafoy Lesion

Mallory–Weiss Tear

Cameron Erosions

Upper GI Malignancy

Gastric Antral Vascular Ectasia

Portal Hypertensive Gastropathy

Hemobilia

Hemosuccus Pancreaticus

Post-ERCP Sphincterotomy Bleeding

Aortoenteric Fistula

Angiomas

References

23 Other Gastric Tumors (Benign and Malignant)

Summary

Mucosal Tumors

Submucosal Tumors

Biopsy of Submucosal Tumors

References

24 Eosinophilic Gastroenteritis

Summary

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

References

25 Esophageal and Gastric Involvement in Systemic and Cutaneous Diseases

Connective-Tissue Diseases

Endocrine and Metabolic Diseases

Inflammatory Diseases

Neuromuscular Diseases

Cutaneous Syndromes

References

Part 6 Functional Disease of the Esophagus and Stomach

26 Functional Esophageal Disorders

Summary

Definitions

Epidemiology

Pathophysiology

Clinical Features and Diagnosis

Differential Diagnosis

Therapeutics

References

Section III Intestine and Pancreas

Part 1 Pathobiology of the Intestine and Pancreas

27 Clinical Anatomy, Embryology, and Congenital Anomalies

Small and Large Intestine

Pancreas

References

28 Small-Intestinal Hormones and Neurotransmitters

Introduction

Specific Peptides

Gastropancreatic Neuroendocrine Tumors

References

29 Mucosal Immunology of the Intestine

Mucosal and Epithelial Barrier

Innate Immune System

Antigen Uptake and Induction of a Mucosal Immune Response

Adaptive Immune System

Humoral Response and Secretory IgA

Tolerance and Regulatory T Cells

Commensal Flora

References

30 Motor and Sensory Function

Neuromuscular Apparatus

Gut Sensation: Neurobiology

Gut Motility

Motor Activity of the Anorectum

Intestinal Microbiota in Motility and Sensation

References

31 Neoplasia

Definition and Epidemiology

Clinical Features

Pathophysiology

Diagnosis

Treatment

Acknowledgements

References

Part 2 Problem-Based Approach to Diagnosis and Differential Diagnosis

32 General Approach to Relevant History-Taking and Physical Examination

Introduction to History Taking

Patient Concerns

Physical Examination

Conclusion

Acknowledgments

References

33 Acute Diarrhea

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Treatment

References

34 Chronic Diarrhea

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis and Differential Diagnosis

Therapeutics

Prognosis

References

35 Loss of Appetite and Loss of Weight

Introduction

History and Physical Exam

Causes of Unintentional Weight Loss

Evaluation of Unintentional Weight Loss

Nutrition Management of Unintentional Weight Loss

References

36 Gastrointestinal Food Allergy and Intolerance

Overview of Food Allergies and Food Intolerances

Are There Predisposing Factors in Food Allergies?

Immune-Mediated GI Adverse Reactions to Food

Non-Immune-Mediated GI Adverse Reactions to Food

Diagnosis

Management of Adverse Reactions to Foods

References

37 Obesity: Presentations and Management Options

Definitions and Epidemiology

GI Comorbidities

Management Options

Conclusion

References

38 Hematochezia

Definition and Epidemiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

39 Obscure Gastrointestinal Bleeding

Definition and Epidemiology

Clinical Features

Diagnosis

Differential Diagnosis

Management

Prognosis

References

40 Constipation

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapy

Prognosis

References

41 Perianal Disease

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

Management

References

42 Fecal Incontinence

Definition and Epidemiology

Etiology

Mechanisms of Normal Fecal Continence

Pathophysiology

Clinical Features

Diagnostic Testing

Management

Conclusion

References

43 Colorectal Cancer Screening

Introduction

Review of Screening Methods

Discussion of the Guidelines

Conclusion

References

44 Endoscopic Palliation of Malignant Obstruction

Equipment and Review of Technology

How to Place SEMS

Malignant Dysphagia

Malignant Gastric Outlet Obstruction

Colonic Obstruction

Enteral Tubes

References

Part 3 Diseases of the Small Intestine

45 Crohn's Disease

Definition and Epidemiology

Pathophysiology

Clinical Features

Disease Severity

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

46 Small-Bowel Tumors

Introduction

Benign Tumors of the Small Intestine

Malignant Small Bowel Tumors

Clinical Features

Diagnosis

Therapy

References

47 Small-Intestinal Bacterial Overgrowth

Definition and Epidemiology

Pathophysiology

Clinical Manifestations

Diagnosis

Treatment

References

48 Celiac Disease and Tropical Sprue

Celiac Disease

Tropical Sprue

References

49 Whipple's Disease

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

50 Short-Bowel Syndrome

Definition and Epidemiology

Pathophysiology

Clinical Features

Differential Diagnosis

Therapeutics

Prognosis

References

51 Protein-Losing Gastroenteropathy

Pathophysiology

Etiology

Clinical Features

Diagnosis

Therapy

Monitoring

References

52 Acute Mesenteric Ischemia and Chronic Mesenteric Insufficiency

Acute/Chronic Mesenteric Ischemia

Vascular Anatomy/Function Mesenteric Circulation

Mesenteric Vascular Physiology

Acute Mesenteric Ischemia

Chronic Mesenteric Insufficiency

References

53 Intestinal Obstruction and Pseudo-obstruction

Intestinal Obstruction

Intestinal Pseudo-obstruction

References

Part 4 Diseases of the Colon and Rectum

54 Ulcerative Colitis

Definition

Epidemiology

Risk Factors

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

References

55

Clostridium difficile

Infection and Pseudomembranous Colitis

Definition and Epidemiology

Pathophysiology

Clinical Features of

C. difficile

Infection

Diagnosis

Differential Diagnosis

Treatment

Prognosis

References

56 Colonic Ischemia

Epidemiology

Pathophysiology

Pharmacologic-Induced Colon Injury

Clinical Manifestations

Therapy

References

57 Acute Diverticulitis

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Medical Management

Surgery

References

58 Acute Colonic Pseudo-obstruction

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

Prognosis

References

59 Colonic Polyps and Colorectal Cancer

Definition and Epidemiology

Pathophysiology

Young-Onset CRC

Prevention

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

60 Pregnancy and Luminal Gastrointestinal Disease

Esophagus and Stomach

Small Intestine and Colon

References

61 Consequences of Human Immunodeficiency Virus Infection

Definition and Epidemiology

Pathogenesis

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

Part 5 Diseases of the Pancreas

62 Acute Pancreatitis and (Peri)pancreatic Fluid Collections

Introduction

Definitions

Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

63 Chronic Pancreatitis and Pancreatic Pseudocysts

Chronic Pancreatitis

Pseudocysts

References

64 Pancreatic Cancer and Cystic Pancreatic Neoplasms

Pancreatic Cancer

Cystic Pancreatic Neoplasms

References

Part 6 Functional Diseases of the Small and Large Intestine

65 Irritable Bowel Syndrome

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

Prognosis

References

66 Chronic Functional Constipation and Dyssynergic Defecation

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis and Differential Diagnosis

Management

References

67 Chronic Functional Abdominal Pain

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Differential Diagnosis

Therapeutics

Prognosis

References

68 Abdominal Bloating and Visible Distension

Epidemiology

Patient Evaluation

Pathophysiology of Bloating and Distension

Treatment

References

Part 7 Transplantation

69 Gastrointestinal Complications of Solid Organ and Hematopoietic Cell Transplantation

Introduction

Infections in the GI System Following SOT or HCT

GI Malignancies after SOT and HCT

GI Adverse Drug Events

General GI Complications

Special Topics

Note

References

Section IV Liver and Biliary Tract

Part 1 Diagnostic Approaches in Liver Disease

70 Approach to History-Taking and Physical Examination in Liver and Biliary Disease

Introduction

History-Taking

Physical Examination

Acknowledgements

References

71 Acute Liver Failure

Introduction

Definition

Etiology

Pathophysiology

Diagnostic Evaluation

Management

General Supportive Care

Treatment of Intracranial Hypertension

Seizure Management in ALF

Liver Support Devices

Prognostic Scoring Systems

Liver Transplantation

References

72 Imaging of the Liver and Bile Ducts: Radiographic and Clinical Assessment of Findings

Introduction

Liver Cysts

Hemangioma

Focal Nodular Hyperplasia

Hepatic Adenoma

Nodular Regenerative Hyperplasia

Miscellaneous Benign Lesions

Hepatocellular Carcinoma

Other Malignant Liver and Biliary Tumors

Cholelithiasis/Choledocholithiasis

Primary Sclerosing Cholangitis

References

73 Assessment of Liver Fibrosis: Liver Biopsy and Other Techniques

Liver Biopsy

Technique and Safety

Complications and Risks of Liver Biopsy

Preprocedure Assessment and Equipment

Technique

Postbiopsy Monitoring

Interpretation

Alternatives to Assessment of Liver Fibrosis

Serum Biomarkers

Ultrasound-Based Elastography

Magnetic Resonance Elastography

Evaluation of Portal Hypertension

References

74 Endoscopic Techniques Used in the Management of Liver and Biliary Tree Disease: ERCP and EUS

Equipment and Review of Technology

How to Perform ERCP and EUS

Role of EUS and ERCP in the Diagnosis and Management of Hepatobiliary Disease

Miscellaneous Uses of EUS

Complications of EUS and ERCP

References

Part 2 Diseases of the Liver

75 Acute Viral Hepatitis: Hepatitis A, Hepatitis E, and Other Viruses

Hepatitis A

Hepatitis E

Other Viruses

References

76 Chronic Hepatitis B and D

Hepatitis B Virus

Hepatitis Delta Virus

References

77 Hepatitis C

Diagnosis and Evaluation

When and Who to Treat

Treatment

Genotype 1

Genotype 2

Genotype 3

Genotype 4

Genotypes 5 and 6

Conclusion

References

78 Bacterial and Other Non-viral Infections of the Liver

Pyogenic Liver Abscess

Pylephlebitis

Amebic Liver Abscess

Acute Cholangitis

Granulomatous Hepatitis

Bacterial Infections of the Liver

Protozoa

Fungi

Helminths

References

79 Alcoholic Liver Disease

Introduction

Definition and Epidemiology

Pathophysiology

Metabolic Mechanisms

Genetic and Hereditary Factors

Clinical Features

Diagnosis

Differential Diagnosis

Prognosis

Management

Liver Transplantation

References

80 Drug-Induced Liver Injury

Definition and Epidemiology

Clinical Presentation and Clinical Evaluation

Diagnosis and Causality Assessment

Risk Factors

Prognosis

Management

References

81 Autoimmune Liver Diseases

Autoimmune Hepatitis

Primary Biliary Cholangitis

Celiac Disease

References

82 Vascular Diseases of the Liver

Budd–Chiari Syndrome

Hematopoietic Stem Cell Transplantation

Sinusoidal Obstruction Syndrome

References

83 Metabolic Syndrome and Non-alcoholic Fatty Liver Disease

Definition and Epidemiology

Pathophysiology

Clinical Features

Assessment of Disease Severity

Diagnosis

Differential Diagnosis

Prognosis

Treatment

References

84 Hemochromatosis, Wilson's Disease, and Alpha-1-Antitrypsin Deficiency

Hereditary Hemochromatosis

Wilson's Disease

Alpha-1-Antitrypsin Deficiency

References

85 Hepatic Manifestations of Systemic Diseases

Cardiovascular Disorders

Pulmonary Disorders

Renal Disorders

Endocrine Disorders

Rheumatologic Disorders

Gastroenterologic Disorders

Hematologic Disorders

Infiltrative Systemic Disorders

Miscellaneous Disorders

References

86 Diseases of the Biliary Tract and Gallbladder

Gallstone Disease and Cholecystitis

Choledocholithiasis and Cholangitis

Gallbladder Polyps

Biliary Flukes

Cancer of the Gallbladder and Biliary Tree

Cholangiocarcinoma

Primary Sclerosing Cholangitis

References

87 Portal Hypertension

Introduction

Diagnosis of Portal Hypertension

Varices

Ascites

Spontaneous Bacterial Peritonitis

Hepatorenal Syndrome

Hepatic Encephalopathy

Hepatopulmonary Syndrome and Portopulmonary Hypertension

References

88 TIPS

Equipment and Review of Technology

Application

Diagnostic Methods

Evidence-Based Therapeutics

Complications

References

89 Primary Carcinoma of the Liver

Hepatocellular Carcinoma

Cholangiocarcinoma

References

90 Pregnancy and Liver Disease

Definition and Epidemiology

Pathophysiology

Clinical Features

Diagnosis

Therapeutics

Prognosis and Recurrence of Disease in Future Pregnancies

References

91 Pediatric Liver Disease

Biliary Atresia

Cystic Fibrosis

Alpha-1-Antitrypsin Deficiency

Progressive Familial Intrahepatic Cholestasis

Benign Recurrent Intrahepatic Cholestasis

Alagille Syndrome

Dubin–Johnson Syndrome

Crigler–Najjar Syndrome

Urea Cycle Defects

Glycogen Storage Diseases

Inborn Errors of Mitochondrial Fatty Acid Oxidation

Liver Transplantation in Children

References

Part 3 Liver Transplantation

92 Indications and Selection of Patients for Liver Transplantation

Prognosis and Allocation

Indication and Timing of Liver Transplantation Evaluation

General Assessment of the Potential Liver Transplant Candidate

Deceased versus Living Donor Liver Transplantation

Listing for Simultaneous Liver–Kidney Transplantation

Disease-Specific Considerations

Conclusion

References

93 What Every Hepatologist Should Know about Liver Transplantation

Introduction

Liver Allocation

Future Trends in Organ Allocation

Donor Selection

Surgical Anatomy of the Liver

Techniques of Liver Transplantation

Phases of Liver Transplantation

Surgical Complications of Liver Transplantation

Living Donor Liver Transplantation

Conclusion

References

94 Immunosuppression Used in Liver Transplantation

Immunosuppressive Drugs

Induction Antibodies

Rescue Treatment for Episodes of Acute Rejection

Immunosuppressive Strategies to Minimize Long-Term Adverse Effects

References

95 Medical Management of the Liver Transplant Patient

Immunosuppression

Medical Complications

References

96 Organ Allocation Policy: Practical Issues and Challenges to the Gastroenterologist

Introduction

Allocation

Distribution

Modifications in Distribution Scheme

MELD Exceptions

Practical Challenges

Conclusion

Acknowledgement

References

97 Endoscopic Ultrasound

Introduction

Pancreatic EUS

Small-Bowel EUS

Colorectal EUS

Complications of EUS

References

Index

EULA

List of Tables

Chapter 1

Table 1.1

Chapter 2

Table 2.1

Chapter 3

Table 3.1

Chapter 4

Table 4.1

Chapter 6

Table 6.1

Chapter 9

Table 9.1

Table 9.2

Table 9.3

Table 9.4

Table 9.5

Chapter 10

Table 10.1

Table 10.2

Table 10.3

Table 10.4

Table 10.5

Table 10.6

Table 10.7

Chapter 11

Table 11.1

Table 11.2

Chapter 12

Table 12.1

Table 12.2

Table 12.3

Chapter 13

Table 13.1

Chapter 14

Table 14.1

Table 14.2

Table 14.3

Chapter 15

Table 15.1

Table 15.2

Table 15.3

Chapter 16

Table 16.1

Table 16.2

Chapter 17

Table 17.1

Table 17.2

Table 17.3

Table 17.4

Table 17.5

Table 17.6

Chapter 18

Table 18.1

Table 18.2

Table 18.3

Chapter 19

Table 19.1

Chapter 20

Table 20.1

Table 20.2

Table 20.3

Chapter 21

Table 21.1

Table 21.2

Table 21.3

Chapter 22

Table 22.1

Table 22.2

Chapter 23

Table 23.1

Table 23.2

Chapter 24

Table 24.1

Chapter 25

Table 25.1

Table 25.2

Table 25.3

Table 25.4

Table 25.5

Table 25.6

Chapter 26

Table 26.1

Chapter 27

Table 27.1

Chapter 28

Table 28.1

Table 28.2

Chapter 31

Table 31.1

Table 31.2

Chapter 32

Table 32.1

Table 32.2

Table 32.3

Table 32.4

Table 32.5

Table 32.6

Table 32.7

Table 32.8

Table 32.9

Table 32.10

Table 32.11

Table 32.12

Table 32.13

Table 32.14

Table 32.15

Table 32.16

Chapter 33

Table 33.1

Chapter 34

Table 34.1

Table 34.2

Chapter 35

Table 35.1

Chapter 37

Table 37.1

Table 37.2

Table 37.3

Chapter 38

Table 38.1

Table 38.2

Chapter 39

Table 39.1

Table 39.2

Chapter 40

Table 40.1

Table 40.2

Table 40.3

Table 40.4

Chapter 41

Table 41.1

Chapter 42

Table 42.1

Table 42.2

Table 42.3

Chapter 43

Table 43.1

Table 43.2

Chapter 44

Table 44.1

Table 44.2

Chapter 45

Table 45.1

Table 45.2

Table 45.3

Chapter 46

Table 46.1

Chapter 47

Table 47.1

Chapter 48

Table 48.1

Table 48.2

Table 48.3

Chapter 49

Table 49.1

Table 49.2

Chapter 50

Table 50.1

Table 50.2

Chapter 51

Table 51.1

Chapter 53

Table 53.1

Table 53.2

Table 53.3

Table 53.4

Table 53.5

Table 53.6

Chapter 54

Table 54.1

Chapter 55

Table 55.1

Table 55.2

Chapter 56

Table 56.1

Chapter 57

Table 57.1

Table 57.2

Table 57.3

Table 57.4

Chapter 58

Table 58.1

Table 58.2

Table 58.3

Table 58.4

Table 58.5

Table 58.6

Chapter 59

Table 59.1

Table 59.2

Table 59.3

Table 59.4

Table 59.5

Chapter 60

Table 60.1

Table 60.2

Chapter 61

Table 61.1

Table 61.2

Chapter 62

Table 62.1

Table 62.2

Chapter 63

Table 63.1

Table 63.2

Chapter 64

Table 64.1

Table 64.2

Table 64.3

Chapter 65

Table 65.1

Table 65.2

Table 65.3

Table 65.4

Table 65.5

Table 65.6

Chapter 66

Table 66.1

Table 66.2

Table 66.3

Chapter 67

Table 67.1

Table 67.2

Table 67.3

Table 67.4

Table 67.5

Chapter 68

Table 68.1

Table 68.2

Chapter 69

Table 69.1

Chapter 70

Table 70.1

Table 70.2

Chapter 71

Table 71.1

Table 71.2

Table 71.3

Table 71.4

Table 71.5

Chapter 73

Table 73.1

Table 73.2

Chapter 75

Table 75.1

Table 75.2

Table 75.3

Chapter 76

Table 76.1

Table 76.2

Table 76.3

Chapter 77

Table 77.1

Table 77.2

Table 77.3

Chapter 78

Table 78.1

Table 78.2

Table 78.3

Chapter 81

Table 81.1

Table 81.2

Table 81.3

Chapter 82

Table 82.1

Table 82.2

Table 82.3

Table 82.4

Table 82.5

Chapter 83

Table 83.1

Table 83.2

Table 83.3

Table 83.4

Chapter 84

Table 84.1

Table 84.2

Table 84.3

Chapter 85

Table 85.1

Chapter 86

Table 86.1

Table 86.2

Table 86.3

Table 86.4

Chapter 87

Table 87.1

Table 87.2

Table 87.3

Table 87.4

Chapter 88

Table 88.1

Table 88.2

Table 88.3

Chapter 89

Table 89.1

Chapter 90

Table 90.1

Table 90.2

Table 90.3

Chapter 91

Table 91.1

Chapter 92

Table 92.1

Table 92.2

Table 92.3

Table 92.4

Chapter 94

Table 94.1

Table 94.2

Table 94.3

Chapter 95

Table 95.1

Table 95.2

Table 95.3

Chapter 96

Table 96.1

Table 96.2

Table 96.3

List of Illustrations

Chapter 3

Figure 3.1

Esophageal motility: example of high-resolution motility tracing to demonstrate the progression of a bolus through the esophagus. With swallowing, there is rapid transit through the UES/pharyngeal region. The bolus continues to move relatively rapidly through the striated muscle and then transitions into slower transit in the smooth muscle. The LES actually relaxes with the initiation of swallowing and remains relaxed until the bolus passes into the stomach.

Figure 3.2

Gastric motility. See text for details, but in brief gastric function can be divided into what happens in the proximal stomach (receptive relaxation and fundic empting) and what happens in the corpus and distal stomach (mixing, peristalsis, and emptying). In addition, there is a gastric pacemaker that helps to coordinate not only gastric motility, but the motility of the upper small intestine. The pylorus provides resistance to emptying, which aids mixing, and opens to allow the bolus to pass into the duodenum.

Chapter 4

Figure 4.1

Schatzki ring (arrow).

Figure 4.2

Narrowing of the distal third of the esophagus and subtle rings resulting from eosinophilic esophagitis.

Figure 4.3

Normal Nissen fundoplication. The barium-filled esophageal lumen (arrowhead) is slightly narrowed as it passes through the wrap, represented by the soft-tissue density in the gastric fundus (small arrows). Note that the wrap is located entirely below the diaphragmatic hiatus (large arrows) and no hiatal hernia or any portion of the gastric fundus is seen above the wrap.

Figure 4.4

Disrupted Nissen fundoplication. Barium filling a bizarrely shaped paraesophageal hernia (arrows) located above the diaphragmatic hiatus (arrowheads) adjacent to the esophagus (E). Note the absence of the normal soft-tissue density in the gastric fundus, indicating herniation of the disrupted wrap through the hiatus into the chest.

Figure 4.5

Intrathoracic herniation of fundoplication. This patient experienced severe dysphagia several months after laparoscopic Nissen fundoplication. Endoscopy and barium studies showed an intact wrap. This sagittal MR image through the diaphragmatic hiatus demonstrates the fundoplication (large arrow) to be located above the diaphragm (small arrows). Source: Lord

et al.

, 2000 [8].

Figure 4.6

RYGBP with a large area of breakdown in the staple line between the gastric pouch (P) and the bypassed portion of the stomach (BP-S).

Figure 4.7

This band is too tight, causing gross esophageal dilation.

Figure 4.8

(a) LAGB on plain film. (b) Slipped LAGB. Almost no stomach is seen above the band in normal cases.

Chapter 5

Figure 5.1

Barium of achalasia: this is the typical appearance of achalasia on a barium esophagogram. The esophagus is usually (but not always) dilated, with a smooth tapering into what has been described as a “bird-beak” appearance. Secondary achalasia due to a malignancy at the esophagogastric junction may have an appearance identical to that of idiopathic achalasia and must be excluded with endoscopic visualization.

Figure 5.2

Manometry of achalasia: HRM tracing from a patient with type 2 achalasia. The two swallows can be seen to begin normally in the upper esophageal sphincter area, but the esophageal body has only simultaneous, repetitive, low-pressure contractions and there is minimal evidence of relaxation of the LES.

Figure 5.3

Distal esophageal spasm (DES): this is the classic appearance of esophageal spasm on barium testing. The diagnosis of DES cannot be made on barium alone and must be confirmed with manometry, showing a mixture of 20% or more simultaneous contractions with some normally propagated contractions.

Figure 5.4

Nutcracker esophagus is defined as a statistically determined increase in peristaltic pressures in the distal esophagus (>180 mmHg). Many feel this “diagnosis” to be more a marker of anxiety than anything else, but an occasional patient has very high pressures that seem to be a marker of underlying neuropathy. This example shows a distal pressure of >500 mmHg in a patient with severe chest pain with swallowing.

Chapter 6

Figure 6.1

Scintigraphic assessment of gastric emptying rate. The presence of the radiolabeled meal is quantified in a region of interest, representing the stomach (upper panels). The presence of the label in the stomach region of interest over time is plotted, allowing quantification of the gastric half-emptying time and lag phase.

Figure 6.2

(a) The principle of antroduodenojejunal manometry, which uses a catheter with manometry ports in the stomach and different parts of the small intestine. (b) Example of interdigestive motility as recorded via catheter in the antrum (A channels), duodenum (D channel), and jejunum (J channels).

Chapter 8

Figure 8.1

Schematic representation of the mechanisms involved in the generation of heartburn. These mechanisms and pathways include activation of chemoreceptors by acid, weak acid, and bile refluxates and mechanoreceptors. Dilated intercellular spaces (DISs) may facilitate the activation of these receptors. Afferent signaling and perception can be enhanced by sensitization of affluent sensory neurons, central brain processing, psychological factors, and stress. Source: Ang 2008. Reproduced with permission of the Nature Publishing Group.

Figure 8.2

Proposed diagnostic evaluation of patients with non-cardiac chest pain. NCCP, non-cardiac chest pain; PPI, proton pump inhibitor; GERD, gastroesophageal reflux disease.

Chapter 10

Figure 10.1

Manometric differences between gastric (left) and supragastric (right) belching. During the gastric belch, air moves in a proximal direction. During the supragastric belch, air enters the esophagus from a proximal direction and is immediately expelled in a retrograde direction. Source: Bredenoord 2007 [2]. Reproduced with permission of Elsevier.

Figure 10.2

Treatment algorithm for halitosis.

Figure 10.3

Anatomic representation of the diaphragm, lungs, and glottis in inhalation and exhalation during hiccups.

Figure 10.4

Algorithm for treating hiccups.

Figure 10.5

GI manometric tracing and distal esophageal pH in a rumination patient. Note the concurrence of regurgitation (arrows) with decreases in pH and R or simultaneous waves, consistent with increased intra-abdominal pressure. * Two R waves that are not associated with regurgitation or a decrease in intraesophageal pH. Source: O'Brien 1995. Reproduced with permission of Elsevier.

Figure 10.6

Three manometric variants of rumination, as measured by combined ambulatory manometry and pH impedance monitoring. Source: Boudewijn 2014 [14]. Reproduced with permission of Macmillan Publishers.

Chapter 12

Figure 12.1

Management algorithm. Adapted with permission from reference [13].

Chapter 14

Figure 14.1

Esophageal and extraesophageal manifestations of GERD. Esophageal syndromes include typical and atypical chest pain syndromes and reflux esophagitis, stricture, Barrett's esophagus, and adenocarcinoma. Extraesophageal syndromes include pharyngitis, laryngitis, dental erosions, cough, asthma, and pulmonary fibrosis. Source: Patel 2013 [23]. Reproduced with permission of Elsevier.

Figure 14.2

Pathophysiology of GERD: aggressive and defensive factors.

Figure 14.3

Various grades of esophagitis, according to the modified LA classification. Source: Nayar 2004 [24]. Reproduced with permission of Elsevier.

Figure 14.4

Suggested algorithm for the evaluation and treatment of suspected GERD and suspected gastroesophageal reflux laryngitis.

Chapter 15

Figure 15.1

The left-hand panel reveals the

in situ

hybridization image of the hr-HPV genome in Barrett's esophagus, Barrett's dysplasia, and EAC cells but not the squamous epithelium, raising the concept of viral tropism for esophageal glandular tissue. The panel on the right demonstrates a novel RNA

in situ

hybridization targeting hr-HPV 16 and 18 E6/E7 messenger RNA transcripts in esophageal dysplastic/adenocarcinoma cells. Source: Courtesy Professor S. Rajendra & Dr. B. Wang.

Figure 15.2

Endoscopic Barrett's esophagus: Prague C&M criteria. Patient with 5 cm-long Barrett's, distal 2 cm-circumferential and proximal 3 cm in the form of a tongue: Barrett's: C2M5. Source: Courtesy Professor P. Sharma.

Figure 15.3

Intramucosal Barrett's adenocarcinoma (T1) subclassification. Lymph node metastasis in intramucosal cancer is 1–2%, and that involving the upper third of the submucosa is between 0 and 20%.

Chapter 16

Figure 16.1

Mucosal tear post-dilation in EoE.

Figure 16.2

Management algorithm for adults with EoE.

Chapter 17

Figure 17.1

(a) Anastomotic stricture after esophageal resection with gastric tube interposition, treated with incisional therapy with needle-knife electrocautery. (b) Wide-open anastomosis following incisional therapy.

Figure 17.2

(a) Anastomotic stricture in the proximal esophagus, for which a (b) self-expanding biodegradable stent was placed.

Chapter 18

Figure 18.1

Management of peptic ulcer bleeding.

Chapter 19

Figure 19.1

Histology of

H. pylori

infection: (a) normal mucosa (H&E 100×); (b) active gastritis with HP (H&E 250×); (c) numerous HP bacilli (Toludene blue stain 500×).

Chapter 20

Figure 20.1

Biopsy protocol sampling in the routine assessment of gastritis. Biopsy samples from antral (A1, A2), oxyntic (B1, B2), and incisura angularis (A3) mucosa should be obtained. Antral specimens (including incisura angularis) can be placed in one vial and the corpus biopsies in another.

Figure 20.2

Extensive intestinal metaplasia, seen endoscopically. The pattern of irregular pink patches within a white, often velvety background is typical of intestinal metaplasia. When extensive, both the white and the pink mucosa typically show intestinal metaplasia histologically.

Chapter 22

Figure 22.1

Algorithm for an approach to upper GI bleeding.

Figure 22.2

Active arterial bleeding peptic ulcer.

Figure 22.3

Non-bleeding visible vessel in peptic ulcer.

Figure 22.4

Adherent clot in peptic ulcer.

Figure 22.5

Clean-based peptic ulcer.

Figure 22.6

Dieulafoy lesion in proximal stomach. Note the bleeding site without adjacent ulceration or mass.

Figure 22.7

Mallory–Weiss tear at the gastroesophageal junction (GEJ).

Figure 22.8

Cameron erosions caused by mucosal trauma from a hiatus hernia pinch.

Chapter 23

Figure 23.1

Endoscopic image demonstrating a fundic gland polyp (GFP). Notice the smooth borders and uniform “pits” on the surface.

Figure 23.2

Endoscopic image of a typical hyperplastic polyp.

Figure 23.3

Endoscopic image of an ulcerated mass along the lesser curvature of the stomach. This patient presented with melena. Biopsies confirmed a diagnosis of a MALT lymphoma.

Figure 23.4

EUS image of the lesion in Figure 23.3. Note the extension of the mass through the muscularis propria.

Figure 23.5

Endoscopic image demonstrating a submucosal mass in the antrum, with smooth, superficial mucosa.

Figure 23.6

EUS image of the lesion in Figure 23.5. A hypoechoic mass measuring 36 × 38 mm arising from the muscularis propria is seen.

Figure 23.7

EUS guided fine-needle aspiration (FNA) of the lesion described in Figure 23.6.

Figure 23.8

EUS image of gastric lipoma, demonstrating that it is relatively hyperechoic and found within the submucosa.

Figure 23.9

Endoscopic image of a gastric carcinoid with mucosal extension.

Figure 23.10

(a) Endoscopic image of a submucosal gastric carcinoid. (b) EUS image of the same gastric carcinoid, demonstrated to be in the submucosal layer. (c) Endoscopic image demonstrating clean endoscopic resection.

Figure 23.11

Endoscopic image showing a submucosal nodule with central dimpling. Biopsies confirmed the diagnosis of a pancreatic rest.

Chapter 24

Figure 24.1

(a) CT enterography demonstrating thickened jejunal folds from eosinophilic gastroenteritis. (b) CT abdomen illustrating gastric-wall edema and hyperenhancement of the gastric mucosa from eosinophilic gastritis.

Figure 24.2

(a) Small-bowel biopsy from the jejunum, demonstrating dense eosinophilic infiltration involving the submucosa and the serosa. Note the dense “sheet-like” configuration of the eosinophils within the submucosa. (b) Higher-magnification view of the subserosa, demonstrating the significant submucosal accumulation of eosinophils. Source: Courtesy of Dr Thomas C. Smyrk, Mayo Clinic College of Medicine.

Chapter 25

Figure 25.1

Pressure topography from high-resolution esophageal manometry in (a) an asymptomatic volunteer with normal esophageal peristalsis and (b) a patient with systemic scleroderma (SSc) who has very diminished lower esophageal sphincter (LES) pressure and absent esophageal peristalsis. Note that the pressures of the upper esophageal sphincter (UES) and proximal esophagus are preserved in SSc.

Figure 25.2

Papular scaly lesions over the knuckles (Gottren's signs) in a patient with dermatomyositis. Source: Courtesy of Dr. Jeff Callen, University of Louisville, Louisville, KY.

Figure 25.3

Endoscopic findings in a patient with Crohn's disease complaining of dysphagia. (a) Prominent scaring without active ulceration in the mid-esophagus. (b) Diffuse, non-specific granularity in the stomach. Source: Courtesy of Dr. Gerald Dryden, University of Louisville, Louisville, KY.

Figure 25.4

Sarcoid inflammatory infiltration of the larynx, identified during upper endoscopy.

Figure 25.5

(a) Endoscopic finding and (b) barium esophagram in a patient with megaesophagus from chronic

Trypanosoma cruzi

infection (Chagas' disease). Source: Courtesy of Dr. Paulo Sakai, University of Sao Paulo Medical School, Sao Paulo, Brazil.

Figure 25.6

Rectal biopsy in a patient with amyloidosis. (a) Low-power and (b) high-power fields of light microscopy shows the pink, homogeneous protein deposit in the submucosa using routine hematoxylin and eosin staining. Source: Courtesy of Dr. Walter Jones, Floyd Memorial Hospital, New Albany, IN.

Figure 25.7

Oral ulceration and buccal mucositis in a patient with pemphigus vulgaris. Source: Courtesy of Dr. Jeff Callen, University of Louisville, Louisville, KY.

Chapter 27

Figure 27.1

Schematic illustration of embryology of normal pancreas and pancreas divisum. Source: Kamisawa 2004 [6]. Reproduced with permission of Springer Science+Business Media.

Chapter 29

Figure 29.1

CD4

+

helper T cells differentiate along different pathways and assume various protective or harmful roles. IFN, interferon; IL, interleukin; TGF, transforming growth factor.

Chapter 30

Figure 30.1

Fasting motor activity in the human antrum (top three tracings) and small intestine (lower three tracings). Note irregular activity (phase 2) recorded at all sites, culminating in a burst of rhythmic activity (phase 3), which slowly traverses the segment and is followed by quiescence (phase 1) of the next cycle.

Figure 30.2

Fed motor pattern, from the same recording sites as Figure 30.1. The migrating motor complex (MMC) has been abolished and is replaced by intense, irregular activity at all sites.

Figure 30.3

Colonic motor activity. (a) Motor activity prior to and following waking. Note the immediate increase in motor activity on waking, which includes a high-amplitude propagating contraction (HAPC) in the more distal sites. (b) Fed motor response. Note the immediate increase in motor activity. Source: Bampton 2001. Reproduced with permission of Nature Publishing Group.

Chapter 31

Figure 31.1

Depiction of colorectal tumor progression in sporadic and high-risk genetic syndromes. The general paradigm is that a tumor is initiated from a normal colonocyte stem cell that has sustained genetic damage over time from the local environment and any germline genetic mutation that may have been inherited. The damaged DNA provides a growth advantage that drives tumor progression as successive clonal outgrowths are generated, ultimately forming carcinoma. In familial adenomatous polyposis (FAP), tumor initiation is accelerated by the inheritance of a germline

APC

mutation, and in Lynch syndrome, tumor progression is accelerated by the hypermutable phenotype that occurs with loss of DNA mismatch repair. Photomicrographs depict, in order, normal colon, tubular adenoma, high-grade dysplasia, and cancer.

Chapter 32

Figure 32.1

Four quadrants of the abdomen.

Figure 32.2

Nine segments of the abdomen. Source: Courtesy of Matthew Sara, MD.

Chapter 33

Figure 33.1

Approach to the treatment of acute diarrhea.

Chapter 34

Figure 34.1

Initial diagnostic approach to chronic diarrhea. OTC, over-the-counter; Rx, prescription; AIDS, acquired immunodeficiency syndrome; Ig, immunoglobulin; WBC, white blood cell. Source: Fine 1999. Reproduced with permission of the American Gastroenterological Association.

Figure 34.2

Algorithmic evaluation of subtypes of chronic diarrhea. CT, computed tomography; TSH, thyroid-stimulating hormone; ACTH, adrenocorticotropic hormone. Source: Fine 1999. reproduced with permission of the American Gastroenterological Association.

Chapter 37

Figure 37.1

Standard bariatric surgery procedures: (a) Roux-en-Y gastric bypass (RYGB), (b) laparoscopic adjustable gastric banding, (c) sleeve gastrectomy, (d) biliopancreatic diversion, (e) biliopancreatic diversion with duodenal switch. Source: Bardley 2012 [37]. Reproduced with permission of Elsevier.

Chapter 38

Figure 38.1

Algorithm for the diagnosis of hematochezia.

Chapter 39

Figure 39.1

   Treatment algorithm for OGIB.

Chapter 40

Figure 40.1

Management algorithm for chronic constipation. Source: Bharucha 2013 [5]. Reproduced with permission of Elsevier.

Chapter 41

Figure 41.1

(a) Complex fistula. (b) Simple fistula.

Figure 41.2

Proposed mechanism for fistula development: fistula beginning as an abscess.

Figure 41.3

Proposed mechanism for fistula development: fistula beginning as an ulcer.

Figure 41.4

Management algorithm for fistulas. EUS, endoscopic ultrasound; MRI, magnetic resonance imaging; TNF, tumor necrosis factor.

Chapter 42

Figure 42.1

Simplified algorithm for managing FI. The choice of investigations is guided by the clinical features, as detailed in the text, and by the response to conservative measures, particularly management of bowel disturbances. Thereafter, further measures (e.g., pelvic floor retraining) may be necessary. EMG, electromyography. Source: Stoker 2008 [17]. Fig 6.2.8. Reproduced with permission of Springer Science + Business Media.

Chapter 44

Figure 44.1

Expandable esophageal stent placement for unresectable tumor at the gastroesophageal junction (GEJ). (a) Endoscopic retroflexed view in the stomach, showing obstructing mass. (b) Endoscopic view from the esophagus immediately after placement of a covered self-expanding metal stent (SEMS).

Figure 44.2

Endoscopic palliation of malignant gastric outlet obstruction (GOO) and malignant biliary obstruction. Radiographic image shows a duodenal stent and biliary stent. Contrast is still visible in the biliary tree.

Figure 44.3

Palliation of malignant rectal stricture. (a) Endoscopic view of an obstructive mass, with predeployed stent visible. (b) Endoscopic view taken immediately after stent placement, With widely patent lumen inside the stent visible.

Chapter 45

Figure 45.1

Mechanisms of Crohn's disease.

Figure 45.2

Colonoscopy showing discrete patchy erythema involving the ascending colon and distal ileum in a skip pattern.

Figure 45.3

Biopsy showing chronic colitis with crypt distortion, cryptitis, and non-caseating granulomas.

Figure 45.4

Algorithm for the management of Crohn's disease.

Chapter 47

Figure 47.1

Mechanisms that maintain normal gut microflora.

Figure 47.2

Effects of bacteria on gut mucosa and clinical consequences of SIBO.

Figure 47.3

Schematic for hydrogen breath-testing. Source: Saad 2007 [32]. Reproduced with permission of Elsevier.

Figure 47.4

Algorithm for the treatment of SIBO. ATBs, antibiotics.

Chapter 48

Figure 48.1

   Algorithm for the detection of celiac disease.

Chapter 50

Figure 50.1

Management of SBS. TPN, total parenteral nutrition; MCT, medium-chain triglycerides; PPI, proton pump inhibitor; ESLD, end-stage liver disease. Source: Buchman 2003 [1]. Reproduced with permission of Elsevier.

Chapter 51

Figure 51.1

Denuded jejunal mucosa in PLGE, caused by chronic intestinal ischemia.

Figure 51.2

Jejunal biopsy with surface atrophy and regenerating crypts characteristic of ischemia. Source: Courtesy of Dr. Jerrold Turner.

Figure 51.3

Mechanisms of PLGE.

Chapter 52

Figure 52.1

View of the small bowel and colon mesenteric vasculature. The arc of Riolan and marginal artery of Drummond are mesenteric major collaterals. Source: Rosenblum 1997 [4]. Reproduced with permission of Elsevier.

Figure 52.2

Etiologies of acute mesenteric ischemia (AMI). SMA, superior mesenteric artery.

Figure 52.3

Algorithm for investigation of suspected AMI. CT, computed tomography. Source: AGA Guideline 2000 [1]. Reproduced with permission of Elsevier.

Figure 52.4

Algorithm for treatment of AMI. SMA, superior mesenteric artery. Source: AGA Guideline 2000 [1]. Reproduced with permission of Elsevier.

Figure 52.5

Outcome of AMI.

Chapter 53

Figure 53.1

Plain abdominal radiographs of a patient with acute colonic pseudo-obstruction. Note the marked colonic dilatation.

Figure 53.2

Algorithm outlining a management strategy in suspected bowel obstruction.

Figure 53.3

Plain, supine abdominal radiograph showing diffusely dilated small bowel. Note the presence of residual barium in a decompressed colon.

Figure 53.4

Upright abdominal radiograph showing dilated loops of small bowel and air–fluid levels in a patient with a partial small-bowel obstruction.

Figure 53.5

Lateral upright abdominal radiograph in a patient unable to stand. Note the presence of several air–fluid levels.

Figure 53.6

Patient presenting with recurrent episodes of abdominal pain, nausea, and vomiting. Note the presence of surgical clips and dilated loop of small bowel in the left upper quadrant.

Figure 53.7

Two CT images showing areas of narrowing and multiple loops of dilated bowel. Note the presence of contrast in a non-dilated colon. At laparotomy, this patient was determined to have an internal hernia causing a partial obstruction.

Figure 53.8

CT image of a patient with prior colonic resection for chronic ulcerative colitis presenting with nausea and vomiting. Note the dilated loops of bowel in the left pelvis compared to the decompressed loops of bowel in the right pelvis. At laparotomy, an adhesive stricture was found.

Figure 53.9

CT enterography showing a narrowed anastomosis in a patient with Crohn's disease and prior ileocolonic resection. Note the hypodense contrast in the bowel lumen compared to the higher density from IV contrast in the bowel wall. This patient was managed conservatively, without surgery.

Chapter 54

Figure 54.1

Diagnostic algorithm for UC. BM, bowel movement; IBD, inflammatory bowel disease; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; pANCA, perinuclear antineutrophil cytoplasmic antibody; ASCA, anti-

Saccharomyces cerevisiae

antibody; OmpC, antibody to

E. coli

outer membrane protein C; CBir-1, antibody to CBir1 flagellin.

Figure 54.2

Sequential therapies for UC and indeterminate colitis. TNF, tumor necrosis factor.

Chapter 55

Figure 55.1

Endoscopic image of pseudomembranous colitis in patient with

Clostridium difficile

infection (CDI).

Figure 55.2

Algorithm for the suggested management of CDI.

Chapter 56

Figure 56.1

Intestinal ischemic syndromes.

Figure 56.2

Outcomes of colonic ischemia.

Figure 56.3

Mesenteric ischemia: colonic distribution (frequency).

Figure 56.4

Colon ischemia: hemorrhagic phase.

Figure 56.5

Diagnostic algorithm for colonic ischemia. IV, intravenous; AMI, acute mesenteric ischemia. Source: AGA Guideline 2000 [1]. Reproduced with permission of Elsevier.

Chapter 57

Figure 57.1

Diverticulum seen during colonoscopy, with vasa recta vessels visible.

Figure 57.2

Colovesical fistula. The presence of air in the bladder is pathognomonic for this diagnosis.

Figure 57.3

Colovesicular fistula. Air in the bladder with thickening of the bladder wall.

Figure 57.4

Pandiverticulosis with transverse colon diverticulitis.

Figure 57.5

Pelvic abscess.

Figure 57.6

Supravesicular abscess.

Figure 57.7

Intramural abscess.

Chapter 58

Figure 58.1

Plain abdominal radiograph of a patient with acute colonic pseudo-obstruction (ACPO), demonstrating marked colonic dilation mimicking mechanical obstruction. Varying degrees of small-intestinal dilation are evident.

Figure 58.2

Management algorithm for ACPO. R/O, rule out; IV, intravenous.

Figure 58.3

Colonic decompression tube with guidewire and side holes.

Figure 58.4

Plain abdominal radiograph of a patient with ACPO with a colonic decompression tube placed into the right colon.

Chapter 59

Figure 59.1

Adenoma-to-carcinoma sequence and associated molecular alterations in colon cancer development. Source: Abeloff 2008 [9]. Reproduced with permission of Elsevier.

Chapter 61

Figure 61.1

Management algorithm. MAC,

Mycobacterium avium-intracellulare

complex; EGD, esophagogastroduodenoscopy.

Chapter 62

Figure 62.1

(a) Axial contrast-enhanced computed tomography (CT) image obtained in a 44-year-old female, showing subtotal necrosis of the pancreatic gland, with acute fluid collections in the anterior pararenal space. (b) Axial contrast-enhanced CT image obtained 4 weeks later, showing walled-off pancreatic and extrapancreatic necrosis.

Figure 62.2

Interstitial pancreatitis. Axial contrast-enhanced CT image obtained in a 39-year-old female, showing mild swelling of the pancreatic gland but normal enhancement. Note acute fluid collections in the anterior pararenal space.

Figure 62.3

Necrotizing pancreatitis. Axial contrast-enhanced CT image obtained in a 38-year-old female, showing necrosis of the pancreatic gland with acute fluid collections in the anterior pararenal space.

Figure 62.4

Extrapancreatic fluid collection. Axial contrast-enhanced CT image obtained in a 49-year-old male with necrotizing pancreatitis, showing pancreatic necrosis and the presence of extrapancreatic walled-off necrosis.

Figure 62.5

Pseudocyst. Axial contrast-enhanced CT image obtained in a 39-year-old female 6 weeks following an episode of interstitial pancreatitis, showing a 6 cm well-defined homogenous low-density fluid collection.

Figure 62.6

Walled-off pancreatic and peripancreatic necrosis. (a) Axial contrast-enhanced CT image obtained in a 63-year-old female with necrotizing pancreatitis, showing pancreatic necrosis and the presence of extrapancreatic walled-off necrosis. (b) Axial contrast-enhanced MRI obtained in the same patient 5 days later, better illustrating the heterogeneous appearance of the extrapancreatic necrosis.

Figure 62.7

Management algorithm for treatment of acute pancreatitis. *Treat organ failure, start enteral feeding.

Chapter 63

Figure 63.1

New pseudocyst in the body of the pancreas.

Figure 63.2

Transpapillary drainage of pseudocyst with stents in the main pancreatic duct (traversing the cyst) and in the pseudocyst.

Chapter 64

Figure 64.1

Contrast-enhanced CT scan of a pancreatic mass involving the stomach.

Figure 64.2

EUS-FNA of a hypoechoic pancreatic mass.

Figure 64.3

Fluoroscopic image at ERCP in a patient with metastatic cancer to the pancreas, demonstrating a classic double-duct sign. Strictures are present in both the pancreatic and bile ducts, with upstream dilatation. Incidental note is made of clips from a prior cholecystectomy.

Figure 64.4

Proposed management algorithm for suspected carcinoma of the pancreas. CT, computed tomography; MRI, magnetic resonance imaging; EUS-FNA, endoscopic ultrasound-guided fine-needle aspiration; ERCP, endoscopic retrograde cholangiopancreaticography.

Figure 64.5

Endoscopic image of a classic fish-mouth deformity, secondary to mucin overproduction and extrusion, which is pathognomonic for intraductal papillary mucinous neoplasm (IPMN).

Figure 64.6

Proposed algorithm for the management of cystic lesions of the pancreas. EUS-FNA, endoscopic ultrasound-guided fine-needle aspiration.

Chapter 65

Figure 65.1

Both “brain”- and “gut”-related mechanisms, as well as their interactions, are being explored in IBS. IBS patients show an enhanced responsiveness of this system, manifesting in altered modulation of GI motility and secretion and enhanced perception of visceral events. IBS, irritable bowel syndrome; CNS, central nervous system; CRF, corticotropin-releasing factor; HPA, hypothalamic–pituitary–adrenal.

Figure 65.2

Treatment algorithm for IBS. A non-pharmacologic approach is recommended initially, and the use of medication should not preclude trials of non-pharmacologic therapies: a combination of both may be required. IBS, irritable bowel syndrome; GI, gastrointestinal.

Chapter 66

Figure 66.1

Four types (type I–IV) of dyssynergic defecation seen with high-resolution anorectal manometry, with normal finding as the comparison.

Figure 66.2

Pathological mechanisms underlying normal defecation, constipation, and dyssynergic defecation. PR, puborectalis; EAS, external anal sphincter; IAS, internal anal sphincter.

Figure 66.3

Diagnostic and management algorithm for chronic functional constipation and dyssynergic defecation. IBS-C; constipation-predominant irritable bowel syndrome, MRI; magnetic resonance imaging.

Chapter 67

Figure 67.1

Model showing the interaction of peripheral and central processing with factors that affect symptom severity in IBS and FAPS. Source: Adapted from Sperber 2011. Reproduced with permission of Wiley.

Chapter 71

Figure 71.1

Pathophysiology of cerebral edema in ALF. In the early stages, an increase in cerebral blood flow (CBF) coupled with the impact of ammonia and other noxious stimuli (i.e., cytokines, hypoxia) on vascular endothelial cells can lead to a loss of the blood–brain barrier (BBB) and fluid accumulation in the brain. The conversion of glutamate to glutamine by astrocytes can lead to further fluid retention in the brain and worsening cerebral edema. In advanced grades of encephalopathy, a loss of intracranial autoregulation of CBF is frequently noted, which may eventually culminate in uncal herniation of the brain tissue into the foramen magnum due to the rising intracranial pressure (ICP). Source: Data provided by Will Lee, personal communication.

Figure 71.2

Management of ALF. A rapid determination of the etiology and severity of ALF is required so that patients with unfavorable prognostic features can be transferred to a liver transplant center. In addition, disease-specific treatments should be initiated as soon as possible, along with supportive intensive care unit (ICU) care for infectious, bleeding, and hemodynamic complications of ALF. An accurate assessment of the presence and severity of cerebral edema is critical, so that specific interventions to lower intracranial pressure (ICP)_can be implemented. Despite supportive care, many ALF patients require emergency liver transplantation, with generally favorable 1-year outcomes. However, 10–20% of ALF patients listed for liver transplantation die from complications of ALF, due to the organ donor shortage [29].

Chapter 72

Figure 72.1

Biliary cystadenoma. MRI image demonstrates thickened cyst walls (arrows) with focal biliary dilation and displacement of a vessel.

Figure 72.2

Hemangioma. (a) Arterial phase and (b) portal phase CT images demonstrate hemangioma (arrows) adjacent to a confluence of right and middle hepatic veins with inferior vena cava. (c) Delayed image showing persistent hyperenhancement relative to surrounding liver. (d) T2-weighted imaging showing hemangioma with hyperintensity approaching that of cysts.

Figure 72.3

Right lobe hemangioma. Top: T2-weighted MRI image. Bottom: T1-weighted image.

Figure 72.4

Focal nodular hyperplasia (FNH). Note slight enhancement from retained contrast on 1 hour-delayed (postgadolinium) image, with prominent central scar (arrow).

Figure 72.5

99m

Tc-labeled sulfur colloid scan. Note prominent left lobe uptake (arrow) by FNH, distinguishing it from adenoma, which would have appeared as a void.

Figure 72.6

Hepatic adenoma. T1-weighted MRIs sowing medial left lobe adenoma (a) with subtle hyperintensity on in-phase sequence and (b) with progressive hypointensity on the fat-saturated sequence. (c) After contrast, the mass appears heterogeneously hypervascular on arterial phase image. (d) Delayed-phase imaging, demonstrating relative washout.

Figure 72.7

Hepatocellular carcinoma (HCC). (a) Arterial-phase contrast-enhanced MRI demonstrating heterogeneous hypervascular mass. (b) Portal-venous-phase MRI showing washout and a surrounding pseudocapsule.

Figure 72.8

Cholangiocarcinoma (CCA). (a) MRCP image demonstrating dilated right and left biliary ducts terminating abruptly in hilum (arrows). (b) T2-weighted image of same ducts, showing ductal occlusion. (c) Contrast-enhanced image demonstrating the irregular enhancement pattern of tumor.

Figure 72.9

Cholelithiasis. (a) Non-enhanced CT without evidence for gallstones, as most are radio-opaque. (b) Corresponding T2-weighted MRI showing numerous small gallstones (arrowheads) and a single, larger stone (arrow). (c) Ultrasound from the same patient, demonstrating numerous, layering stones (arrows) and distal shadowing (larger arrows).

Chapter 73

Figure 73.1

Example of the use of biomarkers and elastography in the assessment of fibrosis. Source: Adapted from Castera 2012 [2].

Chapter 74

Figure 74.1

Stone in the common bile duct (CBD).

Figure 74.2

Stone on ERCP fluoro.

Figure 74.3

Stone sweep on ERCP.

Figure 74.4

Endoscopic view of a stone.

Figure 74.5

EUS FNA of a mass.

Chapter 75

Figure 75.1

Relevant clinical, viral, and serologic events in hepatitis A. Source: Bacon 2006 [8]. Reproduced with permission of Elsevier.

Figure 75.2

Algorithm for the management of acute viral hepatitis. HAV, HBV, HCV, HDV, HEV, hepatitis A–E virus; HSV, herpes simplex virus; CMV, cytomegalovirus; EBV, Epstein–Barr virus.

Figure 75.3

Relevant clinical, viral, and serologic events in hepatitis E. Source: Bacon 2006 [8]. Reproduced with permission of Elsevier.

Chapter 76

Figure 76.1

Natural course of chronic HBV infection. Source: Lok 2007 [16]. Reproduced with permission of Elsevier.

Chapter 77

Figure 77.1

Current prevalence of HCV infection in the United States. Source: Ditah 2014 [2]. Reproduced with permission of Elsevier.

Figure 77.2

Diagnostic algorithm for investigating the presence of cirrhosis in patients with chronic liver disease.

Chapter 78

Figure 78.1

CT scan showing pyogenic liver abscess in the left lobe.

Figure 78.2

Amebic liver abscess. The wall of the abscess is on the left, with adjacent purulent inflammation. The center, though necrotic, is largely acellular. The inset shows

E. histolytica

. H&E ×200 and ×1000.

Figure 78.3

Granulomatous hepatitis. This lesion is from an immunocompromised patient with acute leukemia. There is a centrally necrotic, well-defined lesion with a granulomatous rim in the hepatic parenchyma. The inset shows fungi with budding and a thin capsule most consistent morphologically with

Histolyticum capsulatum

. Central necrosis is common in infectious granulomas. H&E ×40; periodic acid–Schiff ×400.

Figure 78.4

Granulomatous hepatitis. Non-caseating granuloma from sarcoidosis in liver. In contrast to many infectious granulomas, the granuloma is tightly formed, with no necrosis. H&E ×40 and ×200.

Figure 78.5

Echinococcal cyst. This 48-year-old was found to have an “incidental” liver cyst on CT and ultrasonography when being evaluated for gallbladder disease. This cyst was calcified with a thick fibrous rim. The organisms are no longer present. The unilocularity, thick fibrous rim with calcification, and layered acellular internal debris (inset) suggest the etiology. H&E ×20 and ×200.

Figure 78.6

Hepatolithiasis. Liver resection from a patient with recurrent pyogenic cholangitis, showing multiple stones within large intrahepatic bile ducts. No organisms are present. The inset shows a destroyed biliary ductule with impacted stone material and dense surrounding chronic active inflammation. H&E ×200.

Figure 78.7

Hepatic schistosomiasis. Some intact hepatic parenchyma is visible at the extreme bottom of the photograph, but most of the liver is unidentifiable, replaced by fibrous tissue with granulomas. The inset demonstrates a granuloma, with the remains of pigmented egg and eosinophils in the upper right corner. H&E ×40 and ×400.

Chapter 79

Figure 79.1

Mechanisms of alcoholic liver disease (ALD).

Figure 79.2

Algorithm for the management of ALD.

Chapter 82

Figure 82.1

Algorithm for the assessment of patients with abdominal pain, liver biochemical abnormalities, hepatomegaly, and/or weight gain following hematopoietic stem cell transplantation (HSCT). AST, aspartate aminotransferase; ALT, alanine aminotransferase; AP, alkaline phosphatase; CT, computed tomography; US, ultrasound; GVHD, graft-versus-host disease; DIH, drug-induced hepatotoxicity; SOS, sinusoidal obstructive syndrome; ATG, antithymocyte globulin; UDCA, ursodeoxycholic acid; tPA, tissue plasminogen activator.

Figure 82.2

Hematoxylin and eosin stain of a liver biopsy in which the central vein is obliterated by fibrin deposition and the sinusoids are dilated and congested, consistent with SOS (20× magnification). Source: Courtesy of Dora Lam-Hamlin MD.

Chapter 83

Figure 83.1

Prevalence of features of the metabolic syndrome in NAFLD [13]. Source: Data from Angulo 2007 [13].

Figure 83.2

(a) Liver biopsy showing bland steatosis (H&E ×100). (b) Liver biopsy showing NASH with steatosis, inflammatory infiltrate, Mallory hyaline, and hepatocyte ballooning (H&E ×100). (c) Liver biopsy showing pericellular and perisinusoidal fibrosis in zone 3 (Masson trichrome ×400). (d) Liver biopsy showing cirrhotic-stage NAFLD (Masson trichrome ×100).

Chapter 84

Figure 84.1

Increased hepcidin production promotes binding and internalization of ferroportin, leading to decreased iron absorption from the gut and release from macrophages. TF, transferrin; DMT-1, divalent metal transporter-1; TfR2, transferrin receptor 2; HJV, hemojuvelin.

Figure 84.2

Normal physiology in states of iron deficiency. Hepcidin production is decreased, facilitating iron absorption from the gut and release from macrophages. TF, transferrin; DMT-1, divalent metal transporter-1; TfR2, transferrin receptor 2; HJV, hemojuvelin.

Figure 84.3

Diagnostic algorithm for the diagnosis of hereditary hemochromatosis. HIC, hepatic iron concentration. Source: Bacon 2011 [1].

Chapter 86

Figure 86.1

EUS image showing a shadowing gallstone within the common bile duct.

Figure 86.2

ERCP with sphincterotomy and stone removal for symptomatic choledocholithisis.

Figure 86.3

Cholangiogram in PSC, showing segmental bile duct fibrosis with saccular dilation of normal intervening areas, resulting in the characteristic “beads on a string” appearance.

Figure 86.4

MRCP showing characteristic findings in PSC.

Chapter 88

Figure 88.1

(a) Balloon occlusion catheter in the right hepatic vein. CO

2

is injected through the catheter to opacify the portal vein. This can be used to help target the portal vein for needle puncture. (b) After successful puncture of the portal vein from the hepatic vein, contrast is injected to assess varices and to allow stent graft deployment planning. Portal pressures are also measured. (c) Following placement of the stent graft, blood is shunted through the covered stent, with decreased filling of the intrahepatic portal vein branches. In this example, an extra stent was placed to extend the shunt near the hepatic vein/inferior vena cava confluence.

Figure 88.2

Balloon occlusion retrograde CO

2

portogram from a peripheral location, resulting in capsular liver perforation and intraperitoneal extravasation of CO

2

. Note the short tract defining the hepatic injury. Though capsular perforation can be life-threatening, this patient exhibited no hemodynamic changes.

Figure 88.3

(a) TIPS venogram from a patient with bare metal stent TIPS, showing narrowing near the mid portion of the shunt. Hemodynamic significance is suggested by prominent filling of the intrahepatic portal vein branches and the coronary vein. (b) The bare stent after re-lining with a Viatorr stent. The stenosis resolved with reduction in the portal pressure and resolution of the varices.

Chapter 89

Figure 89.1

Simplified schematic representation of HCC pathogenesis. NASH, non-alcoholic steatohepatitis; ROS, reactive oxygen species; HCC, hepatocellular carcinoma.

Figure 89.2

Algorithm for the evaluation of nodules found on ultrasound surveillance in patients with cirrhosis. US, ultrasound; CT, computed tomography; MRI, magnetic resonance imaging; HCC, hepatocellular carcinoma.

Figure 89.3

Treatment options for patients with HCC, based on BCLC staging. BCLC, Barcelona Clinic Liver Cancer; PS, performance status; CP, Child–Pugh class; HCC, hepatocellular carcinoma; HTN, hypertension; RFA, radiofrequency ablation; PVT, portal vein thrombosis; TACE, transarterial chemoembolization; TARE, transarterial radioembolization.

Figure 89.4

The anatomic landmarks that help classify CCA.

Figure 89.5

(a) MRI of liver with arterial enhancement. (b) Venous washout of the same lesion. (c) MRI liver demonstrating atrophy–hypertrophy with biliary ductal dilation of the left hepatic lobe.

Figure 89.6

Treatment algorithm for patients with cholangiocarcinoma. CCA, cholangiocarcinoma; EUS, endoscopic ultrasound.

Chapter 92

Figure 92.1

Patient and graft survival after liver transplantation in the United States between 1999 and 2008. Source: Thuluvath 2010 [1]. Reproduced with permission of

American Journal of Transplantation

.

Chapter 93

Figure 93.1

UNOS regions. Region 1: Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, Eastern Vermont. Region 2: Delaware, District of Columbia, Maryland, New Jersey, Pennsylvania, West Virginia, Northern Virginia. Region 3: Alabama, Arkansas, Florida, Georgia, Louisiana, Mississippi, Puerto Rico. Region 4: Oklahoma, Texas. Region 5: Arizona, California, Nevada, New Mexico, Utah. Region 6: Alaska, Hawaii, Idaho, Montana, Oregon, Washington. Region 7: Illinois, Minnesota, North Dakota, South Dakota, Wisconsin. Region 8: Colorado, Iowa, Kansas, Missouri, Nebraska, Wyoming. Region 9: New York, Western Vermont. Region 10: Indiana, Michigan, Ohio. Region 11: Kentucky, North Carolina, South Carolina, Tennessee, Virginia. Source: http://optn.transplant.hrsa.gov/converge/members/regions.asp.

Figure 93.2

Hepatic segmental anatomy.

Figure 93.3

Classic “piggyback” technique. The Barcelona modification includes the right hepatic vein to the outflow anastomosis, to reduce hepatic congestion. Source: By permission of Mayo Foundation for Medical Education and Research. All rights reserved.

Figure 93.4

Biliary reconstruction with T-tubes. Source: By permission of Mayo Foundation for Medical Education and Research. All rights reserved.

Chapter 97

Figure 97.1

Algorithm for an EUS-guided approach to a suspected pancreatic mass. CT, computed tomography; CBD, common bile duct; PD, pancreatic duct; EGD, esophagogastroduodenoscopy; EUS, endoscopic ultrasound; FNA, fine-needle aspiration.

Figure 97.2

Algorithm for EUS-guided management of rectal cancer. Flex Sig, flexible sigmoidoscopy; EUS, endoscopic ultrasound; LN, lymph node.

Guide

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