Full Download Sleisenger and Fordtran S Gastrointestinal and Liver Disease Review and Assessment Expert Consult Online and Print 9e 9th Edition Anthony J. Dimarino MD PDF

Get ebook downloads in full at ebookname.
com
Sleisenger and Fordtran s Gastrointestinal and

Liver Disease Review and Assessment Expert Consult
Online and Print 9e 9th Edition Anthony J.
Dimarino Md
https://ebookname.com/product/sleisenger-and-fordtran-s-
gastrointestinal-and-liver-disease-review-and-assessment-
expert-consult-online-and-print-9e-9th-edition-anthony-j-
dimarino-md/
OR CLICK BUTTON
DOWNLOAD EBOOK
Explore and download more ebook at https://ebookname.com

Instant digital products (PDF, ePub, MOBI) available
Download now and explore formats that suit you...
Sleisenger and Fordtran s Gastrointestinal and Liver

Disease 9th Edition Mark Feldman Md
https://ebookname.com/product/sleisenger-and-fordtran-s-
gastrointestinal-and-liver-disease-9th-edition-mark-feldman-md/
Review of Orthopaedics Expert Consult Online and Print

6e 6th Edition Mark D. Miller Md
https://ebookname.com/product/review-of-orthopaedics-expert-
consult-online-and-print-6e-6th-edition-mark-d-miller-md/
Assisted Ventilation of the Neonate Expert Consult

Online and Print Expert Consult Title Online Print 5th
Edition Jay P. Goldsmith Md
https://ebookname.com/product/assisted-ventilation-of-the-
neonate-expert-consult-online-and-print-expert-consult-title-
online-print-5th-edition-jay-p-goldsmith-md/
Java Precisely third edition Peter Sestoft
https://ebookname.com/product/java-precisely-third-edition-peter-
sestoft/
Parameterization Schemes Keys to Understanding
Numerical Weather Prediction Models Stensrud
https://ebookname.com/product/parameterization-schemes-keys-to-
understanding-numerical-weather-prediction-models-stensrud/
Disgust and its disorders theory assessment and

treatment implications 1st ed Edition American
Psychological Association.
https://ebookname.com/product/disgust-and-its-disorders-theory-
assessment-and-treatment-implications-1st-ed-edition-american-
psychological-association/
Polymer Morphology Principles Characterization and

Processing 1st Edition Qipeng Guo
https://ebookname.com/product/polymer-morphology-principles-
characterization-and-processing-1st-edition-qipeng-guo/
Everyday Surveillance Vigilance And Visibility In

Postmodern Life 2nd Edition Edition William G. Staples
https://ebookname.com/product/everyday-surveillance-vigilance-
and-visibility-in-postmodern-life-2nd-edition-edition-william-g-
staples/
Handbook of Neurocritical Care 1st Edition Wendy C.

Ziai (Auth.)
https://ebookname.com/product/handbook-of-neurocritical-care-1st-
edition-wendy-c-ziai-auth/
Technomics The Theory of Industrial Evolution 1st
Edition H. Lee Martin (Author)
https://ebookname.com/product/technomics-the-theory-of-
industrial-evolution-1st-edition-h-lee-martin-author/
Sleisenger and Fordtran’s
Gastrointestinal
and Liver Disease
REVIEW AND ASSESSMENT
r e v i e w a n d a ss e ss m e n t
This page intentionally left blank
Sleisenger and Fordtran’s Ninth Edition
Gastrointestinal
and Liver Disease
REVIEW AND A S S E S S MENT
9th
Edited by
Anthony J. DiMarino, Jr., MD
William Rorer Professor of Medicine
Chief, Division of Gastroenterology and Hepatology
Thomas Jefferson University and Hospital
Philadelphia, Pennsylvania
Robert M. Coben, MD
Associate Professor of Medicine
Academic Coordinator, GI Fellowship Program
Division of Gastroenterology and Hepatology
Anthony Infantolino, MD
Associate Professor of Medicine
Director, Endoscopic Ultrasound
Division of Gastroenterology and Hepatology
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
Sleisenger and Fordtran’s GASTROINTESTINAL AND ISBN: 978-1-437-70730-4

LIVER DISEASE: REVIEW AND ASSESSMENT
Copyright © 2010 by Saunders, an affiliate of Elsevier Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, recording, or any information storage and
retrieval system, without permission in writing from the publisher. Details on how to seek
permission, further information about the Publisher’s permissions policies, and our
arrangements with organizations such as the Copyright Clearance Center and the Copyright
Licensing Agency, can be found at our website: www.elsevier.com/permissions.
Notice
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional practices,
or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described
herein. In using such information or methods they should be mindful of their own safety
and the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to
check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or
formula, the method and duration of administration, and contraindications. It is the
responsibility of practitioners, relying on their own experience and knowledge of their
patients, to make diagnoses, to determine dosages and the best treatment for each individual
patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or
editors, assume any liability for any injury and/or damage to persons or property as a matter
of products liability, negligence or otherwise, or from any use or operation of any methods,
products, instructions, or ideas contained in the material herein.
The Publisher
Previous editions copyrighted 2007, 1999, 1996
Library of Congress Cataloging-in-Publication Data

Sleisenger and Fordtran’s gastrointestinal and liver disease review and assessment / [edited by]
Anthony J. DiMarino Jr., Robert Coben, Anthony Infantolino—9th ed.
â•…â•… p. ; cm.
â•… Other title: Gastrointestinal and liver disease
â•… Rev. ed. of: Sleisenger & Fordtran’s gastrointestinal and liver disease / edited by Mark
Feldman, Lawrence S. Friedman, Lawrence J. Brandt. 8th ed. c2006.
â•… Includes bibliographical references and index.
â•… ISBN 978-1-4377-0730-4
â•… 1.â•‡ Gastrointestinal system—Diseases—Examinations, questions, etc.â•… I.â•‡ DiMarino, Anthony
J.â•… II.â•‡ Coben, Robert.â•… III.â•‡ Infantolino, Anthony.â•… IV.â•‡ Sleisenger, Marvin H.â•… V.â•‡ Sleisenger &
Fordtran’s gastrointestinal and liver disease.â•… VI.â•‡ Title: Gastrointestinal and liver disease.
â•… [DNLM:â•… 1.â•‡ Gastrointestinal Disease.â•… 2.â•‡ Liver Diseases.â•‡ WI 140 S6321 2010]
â•… RC801.G384 2010 Suppl.
â•… 616.3′3—dc22
â•…â•…â•…â•…â•…â•… 2010005185
Acquisitions Editor: Druanne Martin

Developmental Editor: Virginia Wilson
Senior Project Manager: David Saltzberg Working together to grow
Design Direction: Steve Stave
libraries in developing countries
Printed in the United States of America. www.elsevier.com | www.bookaid.org | www.sabre.org
Last digit is the print number: 9â•… 8â•… 7â•… 6â•… 5â•… 4â•… 3â•… 2â•… 1â•…
Dedicated to medical students, residents, fellows, and faculty who have a continuing
quest for new knowledge in the field of gastroenterology and hepatology. Special
appreciation to co-editors Robert Coben and Anthony Infantolino and to the section
leaders—Cuckoo Choudhary, Sidney Cohen, Steven Herrine, David Kastenberg,
Howard Kroop, David Loren, and Satish Rattan—and to our gastroenterology fellows,
who participated in this project and raised many important questions and topics.
Recognition is given to Donna Collins and Patricia Shaughnessy for their invaluable
help in making this book a success.
Anthony J. DiMarino, Jr., MD

Contributors
Jeffrey A. Abrams, MD Steven M. Greenfield, MD
Clinical Assistant Professor of Medicine, Division of Gas- Assistant Professor of Medicine, Division of Gastroenterol-
troenterology and Hepatology, Department of Medicine, ogy and Hepatology, Department of Medicine, Thomas
Thomas Jefferson University, Philadelphia, Pennsylvania Jefferson University, Philadelphia, Pennsylvania
Kristin Braun, MD Hie-Won L. Hann, MD
Fellow, Division of Gastroenterology and Hepatology, Professor of Medicine; Director, Liver Disease Prevention
Department of Medicine, Thomas Jefferson University, Center, Division of Gastroenterology and Hepatology,
Philadelphia, Pennsylvania Department of Medicine, Thomas Jefferson University,
Cuckoo Choudhary, MD
Assistant Professor of Medicine, Division of Gastroenterol- Nikroo Hashemi, MD
ogy and Hepatology, Department of Medicine, Thomas Fellow, Advanced Hepatology, Division of Gastroenterol-
Jefferson University, Philadelphia, Pennsylvania ogy and Hepatology, Department of Medicine, Thomas
Jefferson University, Philadelphia, Pennsylvania
Robert M. Coben, MD
Associate Professor of Medicine; Academic Coordinator, Christine M. Herdman, MD
GI Fellowship Program, Division of Gastroenterology Fellow, Division of Gastroenterology and Hepatology,
and Hepatology, Department of Medicine, Thomas Department of Medicine, Thomas Jefferson University,
Jefferson University, Philadelphia, Pennsylvania Philadelphia, Pennsylvania
Sidney Cohen, MD Steven K. Herrine, MD
Professor of Medicine; Director of Research Program, Divi- Professor of Medicine; Associate Director, Fellowship
sion of Gastroenterology and Hepatology, Department Program; Associate Medical Director, Liver Transplant
of Medicine, Thomas Jefferson University, Philadelphia, Program, Division of Gastroenterology and Hepatology,
Pennsylvania Department of Medicine, Thomas Jefferson University;
Assistant Dean, Academic Affairs, Jefferson Medical
Mitchell Conn, MD, MBA College, Philadelphia, Pennsylvania
Associate Professor of Medicine; Medical Director, GI/
Transplant Service Line, Division of Gastroenterology Anthony Infantolino, MD, AGAF, FACG, FACP
and Hepatology, Department of Medicine, Thomas Associate Professor of Medicine; Director, Endoscopic
Jefferson University, Philadelphia, Pennsylvania Ultrasound, Division of Gastroenterology and Hepatol-
ogy, Department of Medicine, Thomas Jefferson Univer-
Anthony J. DiMarino, Jr. MD sity, Philadelphia, Pennsylvania
William Rorer Professor of Medicine; Chief, Division
of Gastroenterology and Hepatology, Division of David Kastenberg, MD, FACP, AGAF
Gastroenterology and Hepatology, Department of Associate Professor of Medicine, Division of Gastroenter-
Medicine, Thomas Jefferson University, Philadelphia, ology and Hepatology, Department of Medicine, Thomas
Pennsylvania Jefferson University, Philadelphia, Pennsylvania
Michael C. DiMarino, MD, MMS Leo C. Katz, MD
Clinical Assistant Professor of Medicine, Division of Assistant Professor of Medicine, Division of Gastroenterol-
Gastroenterology and Hepatology, Department of ogy and Hepatology, Department of Medicine, Thomas
Medicine, Thomas Jefferson University, Philadelphia, Jefferson University, Philadelphia, Pennsylvania
Pennsylvania
Bryan Kavanaugh, MD
Bob Etemad, MD Fellow, Division of Gastroenterology and Hepatology,
Medical Director of Endoscopy, Main Line GastroenÂ� Department of Medicine, Thomas Jefferson University,
terology Associates PC, Main Line Health System, Philadelphia, Pennsylvania
Wynnewood, Pennsylvania
Thomas Kowalski, MD
Jonathan M. Fenkel, MD Associate Professor of Medicine; Director, Gastrointestinal
Fellow, Division of Gastroenterology and Hepatology, Endoscopy, Division of Gastroenterology and Hepatol-
Department of Medicine, Thomas Jefferson University, ogy, Department of Medicine, Thomas Jefferson UniÂ�
Philadelphia, Pennsylvania versity, Philadelphia, Pennsylvania
Mara Goldstein-Posner, MD Patricia Kozuch, MD
Fellow, Division of Gastroenterology and Hepatology, Assistant Professor of Medicine, Division of Gastroenterol-
Department of Medicine, Thomas Jefferson University, ogy and Hepatology, Department of Medicine, Thomas
Philadelphia, Pennsylvania Jefferson University, Philadelphia, Pennsylvania
vii
viii Contributors
Howard S. Kroop, MD Susie Rivera, MD

Clinical Associate Professor of Medicine, Division of Gas- GI Motility Coordinator, Division of Gastroenterology and
troenterology and Hepatology, Department of Medicine, Hepatology, Department of Medicine, Thomas Jefferson
Thomas Jefferson University, Philadelphia, Pennsylva- University, Philadelphia, Pennsylvania
nia; Chief, Division of Gastroenterology, Department of
Medicine, Underwood Memorial Hospital, Woodbury, Jason N. Rogart, MD
New Jersey Fellow, Advanced Endoscopy, Division of Gastroenterol-
ogy and Hepatology, Department of Medicine, Thomas
David Loren, MD Jefferson University, Philadelphia, Pennsylvania
Assistant Professor of Medicine; Director of Endoscopic
Research, Division of Gastroenterology and Hepatology, Simona Rossi, MD
Department of Medicine, Thomas Jefferson University, Assistant Professor of Medicine, Division of Gastroenterol-
Philadelphia, Pennsylvania ogy and Hepatology, Department of Medicine, Thomas
Aarati Malliah, MD
Fellow, Division of Gastroenterology and Hepatology, Emily Rubin, RD, BS
Department of Medicine, Thomas Jefferson University, Clinical Dietician, Division of Gastroenterology and
Philadelphia, Pennsylvania Hepatology, Department of Medicine, Thomas Jefferson
University, Philadelphia, Pennsylvania
Victor J. Navarro, MD
Professor of Medicine, Pharmacology and Experimental Ivan Rudolph, MD
Therapeutics; Medical Director, Liver Transplantation, Clinical Assistant Professor of Medicine; Director, Gastro-
Division of Gastroenterology and Hepatology, Depart- enterology Clinic, Division of Gastroenterology and
ment of Medicine, Thomas Jefferson University, Phila- Hepatology, Department of Medicine, Thomas Jefferson
delphia, Pennsylvania University, Philadelphia, Pennsylvania
Nicholas T. Orfanidis, MD Bridget Jennings Seymour, MD

Fellow, Division of Gastroenterology and Hepatology, Fellow, Division of Gastroenterology and Hepatology,
Department of Medicine, Thomas Jefferson University, Department of Medicine, Thomas Jefferson University,
Philadelphia, Pennsylvania Philadelphia, Pennsylvania; Gastroenterologist/Hepa-
tologist, Department of Medicine, Merrimack Valley
Jorge A. Prieto, MD Hospital, Haverhill, Massachusetts; Gastroenterologist/
Clinical Assistant Professor of Medicine, Division of Gas- Hepatologist, Department of Medicine, Anna Jaques
troenterology and Hepatology, Department of Medicine, Hospital, Newburyport, Massachusetts
Thomas Jefferson University, Philadelphia, Pennsylvania
Maya Spodik, MD
Satish Rattan, DVM Fellow, Division of Gastroenterology and Hepatology,
Professor of Medicine; Director of Basic Research, Divi- Department of Medicine, Thomas Jefferson University,
sion of Gastroenterology and Hepatology, Department of Philadelphia, Pennsylvania
Medicine, Thomas Jefferson University, Philadelphia,
Pennsylvania
Marianne Ritchie, MD
Assistant Professor of Medicine, Division of Gastroenterol-
ogy and Hepatology, Department of Medicine, Thomas
Preface
The Division of Gastroenterology and Hepatology at Jefferson Medical College and Thomas Jefferson University Hospital
is honored to once again be given the opportunity to prepare this self-assessment text that accompanies the ninth edition
of Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. We are pleased to have worked with Mark Feldman,
MD; Lawrence S. Friedman, MD; Lawrence J. Brandt, MD; and the publisher, Elsevier Inc., to update the self-assessment
companion text.
We hope that the readers will find the questions stimulating. We are happy to receive questions, comments, or
critiques related to the content and hope that this text contributes to the lifelong commitment of obtaining new
knowledge that improves the care of patients with gastrointestinal and liver disease.
ix
Contents
CHAPTER 1 CHAPTER 8
Biology of the Gastrointestinal Tract and Liver 151
Liver Disease 1 Steven K. Herrine, Jonathan M. Fenkel,
Satish Rattan and Christine M. Herdman Hie-Won L. Hann, Nikroo Hashemi,
Questions 1 Victor J. Navarro, and Simona Rossi
Answers 4 Questions 151
Answers 167
CHAPTER 2
Nutrition in Gastroenterology 9 CHAPTER 9
David Kastenberg, Leo C. Katz, Emily Rubin, Small and Large Intestine 199
and Maya Spodik Anthony Infantolino, Jeffrey A. Abrams,
Questions 9 Mitchell Conn, Michael C. DiMarino,
Answers 12 Steven M. Greenﬁeld, Patricia Kozuch, and
Nicholas T. Orfanidis
CHAPTER 3 Questions 199
Topics Involving Multiple Organs 19 Answers 236
Cuckoo Choudhary, Aarati Malliah, Marianne Ritchie,
Ivan Rudolph, and Bridget Jennings Seymour CHAPTER 10
Questions 19 Palliative, Complementary, and Alternative
Answers 43 Medicine 306
David Kastenberg, Leo C. Katz, Emily Rubin,
CHAPTER 4 and Maya Spokik
Esophagus 66 Questions 306
Sidney Cohen, Anthony J. DiMarino, Jr., Answers 307
Mara Goldstein-Posner, Christine M. Herdman,
and Susie Rivera Illustration Credits 309
Questions 66
Answers 74
CHAPTER 5
Stomach and Duodenum
Howard S. Kroop, Kristin Braun, Robert M. Coben,
and Jorge A. Prieto
81
Video Contents
Questions 81
Answers 89 Videos available at www.expertconsult.com
CHAPTER 6 Ascaris lumbricoides in the colon
Pancreas 98
David Loren, Bob Etemad, Bryan Kavanaugh, Clonorchis sinensis exiting the ampulla during
Thomas Kowalski, and Jason N. Rogart endoscopic retrograde cholangiopancreatography
Questions 98
Answers 113 Enterobius vermicularis in the colon
CHAPTER 7 Taenia saginata seen on video capsule endoscopy
Biliary Tract 126 Taenia solium seen on colonoscopy
David Loren, Bob Etemad, Bryan Kavanaugh,
Thomas Kowalski, and Jason N. Rogart All videos correspond to chapter 110—“Intestinal
Questions 126 Worms”—from Sleisenger and Fordtran’s Gastrointestinal
Answers 140 and Liver Disease, 9e.
xi
CHAPTER
1â•…
Biology of the Gastrointestinal
Tract and Liver Disease
Questions 5 The Wnt pathway is important in which of the fol-

lowing processes?
A. Programmed cell death (apoptosis)
1 Several pathways play a role in gastrointestinal
B. Senescence
(GI) tumors. Recently this pathway has been recog-
C. Intestinal epithelial cell (IEC) proliferation
nized as a key regulator in prostaglandin synthesis
D. Pancreatic acinar cell proliferation
that is induced in inflammation and neoplasia. No
mutations have been identified, but inhibition 6 Adrenergic neurons originate in ganglia of the auto-
with aspirin and nonsteroidal anti-inflammatory nomic nervous system and synapse with enteric
drugs is associated with reduced risk of colorectal neurons. Adrenergic neurons only contain which
adenoma and cancer. What is the pathway? of the following?
A. Cyclooxygenase-2 (COX-2) A. Norepinephrine
B. Nuclear factor-κB B. Acetylcholine
C. P13K/Akt C. Neuropeptide Y and somatostatin
D. RAF D. A and C
2 What is the major function of glucagon and gluca- 7 Which of the following neuromodulators has the
gon-like peptide? following characteristics: a potent vasodilator that
A. As a neurotransmitter increases blood flow in the GI tract and causes
B. Mediator of satiety and food intake smooth muscle relaxation and epithelial cell secre-
C. To produce pancreatic fluid and pancreatic tion; is expressed primarily in neurons of the
secretion peripheral/enteric and central nervous systems;
D. To regulate glucose homeostasis has effects on many organ systems, although in
the GI tract stimulates fluid and electrolyte secre-
3 Which of the following is the most populous cell tion from intestinal epithelium and bile duct chol-
of the lamina propria mononuclear cells? angiocytes; causes relaxation of gastric smooth
A. Macrophages muscle and therefore is an important modulator of
B. Dendritic cells sphincters in the GI tract?
C. Immunoglobulin A–positive (IgA+) plasma A. Acetylcholine
cells B. Somatostatin
D. Tumor necrosis factor (TNF)–secreting T cells C. CCK
D. Gastrin
4 During a meal, nutrients interact with cells in the E. Vasoactive intestinal polypeptide
mouth and GI tract to regulate hunger and satiety.
Which of the following does not play a major role 8 T cell differentiation is influenced by the microen-
in this complex interaction? vironment of the gut. This will influence develop-
A. Cholecystokinin (CCK) ment of cells and promotion of cytokines, thereby
B. Glucagon-like peptide 1 promoting or suppressing inflammation. Which of
C. Ghrelin the following cytokines play a role in IgA secretion?
D. Leptin A. Interleukin (IL)-12
E. Lipase B. IL-4
1
2 Biology of the Gastrointestinal Tract and Liver Disease
C. IL-5 C. Large potentially antigenic macromolecules are

D. IL-6 degraded so that potentially immunogenic
E. A and B substances are rendered nonimmunogenic.
F. C and D D. Th3 cells that are activated in Peyer patches
9 CCK and somatostatin are both hormones that are 16 Patients who have celiac disease may have a disrup-
released in the GI tract. They may work as which tion in their oral tolerance. Which of the following
of the following? does not affect the induction of oral tolerance?
A. Endocrine agent A. Genetic factors
B. Paracrine agent B. Nature of the antigen
C. Neurocrine agent C. Ethnicity
D. All of the above D. Age
E. Tolerogen dose
10 The analog of which one of the following is used
to treat conditions of hormone excess produced by 17 Point mutations in this gene have been identified
endocrine tumors (including acromegaly, carcinoid in esophageal squamous carcinoma and adeno-
tumors, islet tumors, and gastrinomas)? carcinoma, gastric carcinoma, pancreatic adeno-
A. Somatostatin carcinoma, hepatocellular carcinoma, and sporadic
B. Gastrin colon cancers. Interestingly, mutations are rarely
C. CCK identified in colonic adenomas. What is the gene?
D. Secretin A. SMAD4
B. TP53
11 Which of the following genes is deleted or mutated C. APC
in pancreatic adenocarcinoma? D. MLH1
A. TP53
B. SMAD4 18 The gut is the largest lymphoid organ in the body.
C. APC It contains billions of organisms. Significant inflam-
D. MLH1 mation is not present in the intestine. What is this
phenomenon known as?
12 What is the phenomenon known as epithelial mes- A. Oral tolerance
enchymal transition? B. The intestinal barrier
A. Polarized epithelial cells no longer recognize C. Relative chemotaxis
boundaries of adjacent epithelial cells and D. Controlled/physiologic inflammation
adopt features of migratory mesenchymal cells.
B. Degradation of the basement membrane folÂ� 19 This gene is found on chromosome 5q and is associ-
lowed by migration into perivascular stroma ated with Gardner’s syndrome. Both somatic and
and creating capillary sprout germline mutations appear in this gene and contrib-
C. Clonal expansion after formation of a metaÂ� ute to the development of polyps.
static focus A. TP53
D. Genetic pathway used to modulate Wnt B. Multiple endocrine neoplasia (MEN1)
pathway C. E-cadherin1 (CDH1)
D. Adenomatous polyposis coli (APC)
13 Obesity has become an epidemic in the United
States. Much research has been targeted to identify 20 All GI peptides are synthesized via gene transcrip-
the mediators of satiety. Which one of the following tion of DNA into messenger RNA and subsequent
may be the major mediator of satiety and food intake? translation of messenger RNA into precursor pro-
A. Somatostatin teins known as preprohormones. The peptides that
B. Acetylcholine are destined to be secreted begin as proteins that
C. Gastrin are cleaved and the prepropeptide is then prepared
D. CCK for structural modifications. Modifications of the
peptide hormone for the full biological activity
14 The nature and form of the antigen play a large role in occur in which organelle of the cell?
oral tolerance. Which of the following represents an A. Mitochondria
antigen that is most effective at inducing tolerance? B. Golgi apparatus
A. Large amount of soluble carbohydrate C. Endoplasmic reticulum
B. Large amount of aggregate lipids D. Cytoplasm
C. Moderate amount of soluble protein
D. Moderate amount of aggregate protein 21 Which antibody is most abundant in mucosal
secretions?
15 Which of the following statements describes the A. IgA
major contributing mechanism behind the con- B. IgM
trolled inflammation in the gut? C. IgG
A. Lamina propria lymphocytes respond poorly D. IgE
when activated via their T cell receptor, failing
to proliferate and providing a state of activaÂ� 22 This test can be performed on archived colon
tion without expansion. tumor tissue and can be helpful in identifying those
B. Antigen-specific nonresponse to antigens individuals with colon cancer in the setting of
administrated orally hereditary nonpolyposis colorectal cancer.
Biology of the Gastrointestinal Tract and Liver Disease 3
A. Stool DNA for TP53 B. Activation of nuclear factor-κB by IL-18

B. Germline DNA analysis for PTEN C. Ability of intraepithelial lymphocytes to
C. Microsatellite instability testing secrete cytokines such as IL-7
D. Direct DNA sequencing D. All of the above
23 Which of the following seems to be overexpressed 30 Ras genes are the most commonly detected onco-
in patients with inflammatory bowel disease and genes in the GI tract cancers. The highest frequency
may contribute to activate T lymphocytes? of mutation (90%) is found in which of the follow-
A. Major histocompatibility complex class II ing tumors?
molecules A. Colon cancer
B. Toll-like receptors B. Exocrine pancreas
C. Peroxisome proliferator activated receptor-γ C. Gastric cancer
D. All of the above D. Colon adenoma
24 All of the following are tumor suppressor genes 31 Chemokines are secreted by IECs and they aid
except: in the regulation of inflammation. Chemokines
A. APC attract which of the following cells to sites of
B. TP53 interest?
C. SMAD4 A. Lymphocytes
D. C-Myc B. Macrophages
C. Dendritic cells
25 IECs are derived from the basal crypts and have many D. A and B
roles. Which of the following is not a role of the IECs? E. All of the above
A. Antigen trafficking
B. Secretion of cytokines and chemokines to conÂ� 32 What modulator is released from the extrinsic and
trol the spread of infection once a pathogen has intrinsic nerves and from the mucosal enterochro-
been recognized mophin cells of the gut? It is important in epithe-
C. Binding of antigens and then transporting to lial secretion, bowel motility, nausea, and emesis.
Peyer patches Identification of this hormone-specific receptor
D. Expression of Toll-like receptors subtype has led to the development of selective
E. IECs play a role in all of the above. agonists and antagonists for the treatment of irri-
table bowel syndrome and chronic constipation
26 Which of the following characteristics is not associ- and diarrhea.
ated with inherited GI cancer syndromes? A. Norepinephrine
A. Individuals are at risk of tumors outside the GI B. Acetylcholine
tract. C. Serotonin
B. Tumors carry a higher mortality. D. Histamine
C. Multiple primary tumors develop within the
target tissue. 33 Two pathways trigger cell apoptosis. One is
D. Tumors in affected individuals typically mediated by activation of TP53 and the other is
appear at a younger age. mediated through death receptors. Which of the
E. Tumor often develops in the absence of predisÂ� following is not a death receptor?
posing environmental factors. A. TNF receptor
B. DR5
27 The PP/PYY/NPY (pancreatic polypeptide/peptide C. Fas
tyrosine tyrosine/neuropeptide Y) family of pep- D. Caspase receptor
tides function as which type of transmitter?
A. Endocrine 34 In animal models, deletion of which of the follow-
B. Paracrine ing leads to colitis?
C. Neurocrine A. TNF
D. All of the above B. IL-6
E. None of the above C. IL-10
D. Transforming growth factor-β
28 Environmental factors play a role in tumorigenesis. E. A and B
Dietary and viral agents play a role in tumor. Which F. C and D
of the following viruses has been linked to gastric
lymphoepithelial malignancies? 35 Polio vaccine is one of the few orally administered
A. Human papillomavirus vaccines that induces active immunity in the gut.
B. Hepatitis B virus Which of the following may contribute to why this
C. Cytomegalovirus oral vaccine provides immunity?
D. Epstein-Barr virus A. The virus binds to IECs.
B. The virus binds to microfold cells (M cells).
29 The lamina propria mononuclear cells and lamina C. Disrupts tight junctions allowing antigen to
propria lymphocytes (LPLs) are involved in several pass into paracellular space
pathways. Which pathway may be defective in D. Activation of regulatory T cells
Crohn’s disease?
A. Resistance of the LPLs to undergo apoptosis 36 True or false: Somatic mutations lead to the expres-
when activated inappropriately sion of a gene in all cells within a tissue.
A. True A. Ulcerative colitis

B. False B. Crohn’s disease
C. Celiac disease
37 All of the following are gene mutations that can D. Carcinoid
lead to colon cancer and can be tested for by immu-
nohistochemistry except: 41 Which of the following is the principal regulator
A. MSH2 of cell cycle progression or movement from
B. MLH1 G2 to M phase and G1 to S phase in the cell
C. MYH cycle?
D. LKB1 A. Cyclin
B. Retinoblastoma protein
38 Pain pathways within the GI tract are complex. C. P21
Which of the following participate in pain path- D. Cyclin dependent kinase
ways and modulate inflammation? E. All of the above
A. Substance P F. A and D
B. Calcitonin gene–related peptide
C. Acetylcholine 42 A genetically unstable environment contributes to
D. None of the above the development of cancer. Microsatellite instabil-
E. All of the above (A, B, C) ity involves which of the following?
A. Frequent alterations in smaller tracts of
39 The primary origin of TNF is in the following cell microsatellite DNA
types: B. Aneuploidy
A. Macrophages, Th1, dendritic, endothelial C. Chromosomal deletions
B. Macrophages only D. Chromosomal duplication
C. Th2
D. Epithelial 43 All of the following are oncogenes except:
A. K-ras
40 Nuclear oligomerization domain 2 (NOD2)/CARD15 B. C-Src
polymorphisms are associated with which of the C. β-Catenin
following? D. P53
hormone to have arexigenic effects. Lipase is an

Answers enzyme released from the pancreas and does not
seem to regulate hunger and satiety.
1 A (S&F, ch3)
The COX-2 pathway plays an important role in GI 5 C (S&F, ch3)
tumors. The enzyme COX-2 is a key regulator of The Wnt pathway is one important example of a
prostaglandin synthesis that is induced in inflam- signaling pathway that regulates the cell cycle
mation and neoplasia. Although no mutations machinery to control the proliferation of IECs (see
of COX-2 have been described, overexpression of figure).
COX-2 in colon adenomas and cancers is associated
with tumor progression and angiogenesis, primarily
6 D (S&F, ch1)
through the induction of synthesis of prostaglandin
A single type of neuron contains and releases dif-
E2. Inhibition of COX-2 with a variety of agents
ferent chemical substances (e.g., adrenergic neurons
(aspirin, nonsteroidal anti-inflammatory drugs, and of the enteric nervous system contain not only nor-
COX-2 selective inhibitors) is associated with a epinephrine but also neuropeptide Y and soma-
reduced risk of colorectal adenomas and cancer. tostatin to modulate the smooth muscle intestinal
contraction or secretion).
2 D (S&F, ch1)
Glucagon and glucagon-like peptides are synthe-
sized and released from the cells of the pancreas, 7 E (S&F, ch1)
ileum, and colon and are not neurotransmitters. Vasoactive intestinal peptide has broad signifi-
cance in the GI tract, which is represented by the
3 C (S&F, ch2) listed characteristics.
Lamina propria mononuclear cells are a heteroge-
neous group of cells. The most populous cell type 8 F (S&F, ch2)
is the IgA+ plasma cell, but there are more than 50% IL-5 induces B cells expressing surface IgA to dif-
T and B cells, macrophages, and dendritic cells. ferentiate into IgA-producing plasma cells. IL-6
causes an increase in IgA secretion with little effect
4 E (S&F, ch1) on either IgM or IgG synthesis.
CCK is one of the most studied satiety hormones.
CCK reduces food intake in animals. Glucagon- 9 D (S&F, ch1)
like peptide 1 is produced by the ileum and the CCK and somatostatin are typical examples of
colon. Glucagon-like peptide 1 receptors are found chemical substances that can be released as hor-
in parts of the brain that are important in the regula- mones by the endocrine cells and transported to the
tion of hunger. Leptin is considered a long-term target cells. In addition, these substances may also
regulator of energy balance. Ghrelin is the only GI be released by the nearby cells and quickly act on
Wnt
Frz
β-catenin Frz
DSH
-P
GSK-3β
GSK-3β
Figure for answer 5 Axin
β-catenin Axin
β-catenin APC
APC β-catenin
P β-catenin
β-catenin
+
c-Myc
cyclin D1
β-catenin TCF-4 VEGF
Nucleus
Degradation
the neighboring cells and also be released as neu- 13 D (S&F, ch1)

rotransmitters. Somatostatin is a classic paracrine CCK has a major role in gallbladder contraction. It
hormone, but, depending on where in the GI tract stimulates pancreatic secretion and has been shown
it is released, it can exert endocrine and neural to delay gastric emptying. Low levels of CCK have
effects. been noted in individuals with celiac disease and
bulimia nervosa.
10 A (S&F, ch1)
Because of its varied physiologic effects, somatosta- 14 C (S&F, ch2)
tin has several clinically important pharmacologic Protein antigens are the most tolerogenic, whereas
uses. Many endocrine cells possess somatostatin carbohydrates and lipids are less effective at induc-
receptors and are sensitive to inhibitory regulation. ing tolerance. The way in which the antigen is
Therefore, somatostatin and its analogs are used to delivered is also critical. For example, a protein
treat conditions of hormone excess produced by delivered in soluble form is quite tolerogenic,
endocrine tumors, including acromegaly, carcinoid whereas aggregation of this protein reduces its
tumors, and islet cell tumors. Its ability to reduce potential to induce tolerance. The dose of antigen
splanchnic blood flow and portal venous pressure administered is critical to the form of oral tolerance
led to somatostatin analogs being useful in treating generated; too little or too much is often not the
esophageal variceal bleeding. The inhibitory effects correct dose to induce tolerance.
on secretion have been exploited by using soma-
tostatin analogs to treat some forms of diarrhea and 15 A (S&F, ch2)
reduce fluid output from pancreatic fistulas. Many The failure to produce GI pathology despite the
endocrine tumors express abundant somatostatin activation state of intestinal lymphocytes is prob-
receptors, making it possible to use radiolabeled ably the consequence of regulatory mechanisms.
somatostatin analogs, such as octreotide, to localize The failure of LPLs to generate “normal” antigen
even small tumors throughout the body. receptor-mediated responses is an important factor
in controlled inflammation. LPLs respond poorly
11 B (S&F, ch3) when activated via their T cell receptor, failing to
SMAD4, also designated the deleted in pancreas proliferate, although they still can produce cyto-
cancer 4 gene, is a tumor suppressor gene located kines. This is key to the maintenance of controlled
on chromosome 18q and is deleted or mutated in inflammation. Answers B and C describe the
most pancreatic adenocarcinomas and a subset of concept behind oral tolerance, in which Th3 cells
colon cancers. are thought to play a role.
12 A (S&F, ch3) 16 C (S&F, ch2)

Epithelial mesenchymal transition may be what Factors affecting the induction of oral tolerance are
promotes tumor progression. Clonal expansion the age of the host, genetic factors, the nature of
after metastasis is a “survival of the fittest” model antigen, and the tolerogen’s form and dose. The
in which the metastatic focus proliferates. The Wnt state of the intestinal barrier affects oral tolerance,
pathway is an example of a signaling pathway that and when barrier function is reduced, oral tolerance
regulates the cell cycle machinery to control the decreases as well. Oral tolerance is difficult to
proliferation of IECs. achieve in the neonate, but early on, the intestinal
flora and the limited diet likely play a beneficial role 24 D (S&F, ch3)
in preventing a vigorous response to food antigen. The c-Myc protein product is involved in critical
cellular functions such as proliferation, differentia-
17 B (S&F, ch3) tion, apoptosis, transformation, and transcriptional
TP53 is the gene responsible for the p53 protein. activation of key genes. Frequently, c-Myc is over-
The p53 protein was detected in tumors as the expressed in many GI cancers.
product of a mutated gene that was mapped to
chromosome 17p. Point mutations in TP53 have 25 C (S&F, ch2)
been identified in 50% to 70% of sporadic colon Microfold cells bind antigens and transport them to
cancers but only a small subset of colon adenomas. Peyer patches. In addition to their function as a
Mutations in TP53 have also been found in esopha- physical barrier in the gut-associated lymphoid
geal squamous carcinoma and adenocarcinoma, tissue, IECs contribute to both innate and adaptive
gastric carcinoma, pancreatic adenocarcinoma, and immunity in the gut and may play a key role in
hepatocellular carcinoma. maintaining intestinal homeostasis. Classic anti-
gen-presenting cells in the systemic immune system
18 D (S&F, ch2) possess the innate capacity to recognize compo-
nents of bacteria and viruses called pathogen-
19 D (S&F, ch3) associated molecular patterns. Receptors for
Genetic linkage analysis revealed markers on chro- these pathogen-associated molecular patterns are
mosome 5q21 that were tightly linked to polyp expressed both on the cell surface (e.g., Toll-like
development in affected members of kindreds with receptors) and inside the cell. After invasion and
familial adenomatous polyposis and Gardner’s syn- engagement of Toll-like receptor 5, the IECs are
drome. The gene responsible for familial adenoma- induced to secrete cytokines and chemokines that
tous polyposis is the adenomatous polyposis coli attract inflammatory cells to the local environment
(APC) gene. to control spread of infection.
20 B (S&F, ch1) 26 B (S&F, ch3)

For most of the peptides, including CCK, the final Despite the variation in the type of tumor found
modification of the molecule (e.g., sulfation) occurs in different inherited cancer syndromes, a number
in the Golgi apparatus. The endoplasmic reticulum of features are common to all inherited GI cancer
plays a critical role in the formation of the peptide; syndromes. Most importantly, the marked increase
however, further modification occurs in the Golgi in risk of a particular tumor is found in the
apparatus. absence of other predisposing environmental
factors. Multiple primary tumors often develop
21 A (S&F, ch2) within the target tissue, and tumors in these
Secretory IgA is the hallmark of mucosa-associated affected members typically arise at a younger
lymphoid tissue/gut-associated lymphoid tissue age. Finally, affected individuals are sometimes
immune responses. Although IgG is the most abun- at risk of some types of tumors outside the
dant isotype in the systemic immune system, IgA GI tract.
is the most abundant antibody in mucosal secre-
tions. In fact, given the numbers of IgA+ plasma 27 D (S&F, ch1)
cells and the size of the mucosa-associated lym- PP is the founding member of the PP family. The
phoid tissue, IgA turns out to be the most abundant PP family of peptides includes NPY and PYY. PP
antibody in the body. is stored and secreted from specialized pancreatic
endocrine cells (PP cells), whereas NPY is a prin-
22 C (S&F, ch3) cipal neurotransmitter found in the central and
The microsatellite instability test can be performed peripheral nervous systems. PYY has been local-
on archived colon tumor samples and serves as a ized to enteroendocrine cells throughout the GI
useful screening test to identify individuals whose tract but is found in greatest concentrations in the
colon cancers may have developed as a manifesta- ileum and colon. The PP/PYY/NPY family of pep-
tion of Lynch syndrome. Loss of hMSH (human tides functions as endocrine, paracrine, and neu-
Mut S homolog) 2, hMLH1, or hMSH6 protein by rocrine transmitters in the regulation of a number
immunohistochemical staining may provide similar of actions. PP inhibits pancreatic exocrine secre-
information. Emerging data suggest that the micro- tion, gallbladder contraction, and gut motility.
satellite instability status of a colon tumor may be PYY inhibits vagally stimulated gastric acid secre-
predictive of the response to 5-fluorouracil–based tion. NPY is one of the most abundant peptides in
chemotherapy. the central nervous system and, in contrast to
PYY, is a potent stimulant of food intake. Peripher-
23 A (S&F, ch2) ally, NPY affects vascular and GI smooth muscle
Increased expression of major histocompatibility function.
complex class II molecules by IECs has been
reported in patients with irritable bowel disease. 28 D (S&F, ch3)
Such overexpression would be expected to increase Viral agents can lead to disruption of normal genes
their potential to activate T lymphocytes. Drugs by entry into the host genome, which may disrupt
used to treat patients with irritable bowel disease the normal gene sequence. HPV has been linked to
such as 5-aminosalicylic acid preparations may squamous cell cancers of the esophagus and anus.
reduce major histocompatibility complex class II Hepatitis B virus has been linked to hepatocellular
expression on IECs. carcinoma.
29 A (S&F, ch2) increase in the bax-to-bcl-2 ratio. Both pathways

LPLs are more prone to undergo apoptosis com- converge to disrupt mitochondrial integrity and
pared with their peripheral counterparts. This may release of cytochrome c.
be a regulatory mechanism limiting the potentially
inflammatory effects of activated lymphocytes. A 34 F (S&F, ch2)
major defect reported in Crohn’s disease is the TNF and IL-6 are considered to be proinflamma-
resistance of LPLs to undergo apoptosis when acti- tory, while IL-10 and transforming growth factor-β
vated inappropriately. The mechanism underlying are anti-inflammatory.
this apoptotic phenomenon possibly relates to
engagement of the death receptor Fas and its ligand 35 B (S&F, ch2)
on activated LPLs and by the imbalance between Oral tolerance may also be associated with the
the intracellular anti-apoptotic and proapoptotic cells serving as the antigen-presenting cells as well
factors Bcl2 and Bax. Defects in this proapoptotic as the site of antigen uptake. Poliovirus binds to
balance have been reported in patients with Crohn’s M cells, which may account for its ability to stimu-
disease. late active immunity in the gut. The evidence of
this comes from studies in mice. Orally adminis-
30 B (S&F, ch3) tered reovirus type 3 is taken up in mice by M
Virtually all ras mutations in GI malignancies that cells expressing reovirus type 3–specific receptors.
have been identified occur in the K-ras oncogene. This epithelial uptake by M cells induces an active
The highest frequency is found in tumors of the IgA response to the virus. Reovirus type 1 infects
exocrine pancreas; more than 90% of these tumors IECs adjacent to M cells, and this uptake induces
possess mutations in the K-ras gene. Ras genes have tolerance to the virus. Thus, the route of entry
been identified in approximately 50% of colonic (M cell vs. IEC) of a specific antigen may dictate
cancers as well as large benign colon polyps. Less the type of immune response generated (IgA vs.
than 10% of colon adenomas smaller than 1 cm tolerance).
have K-ras mutations.
36 B (S&F, ch3)
31 E (S&F, ch2) Whereas germline mutations may lead to altered
Many of the chemokines secreted in the gut-associ- expression of a gene in all cells within a tissue,
ated lymphoid tissue are produced by IECs. This is subsequent additional somatic mutations generally
especially true in inflammatory bowel diseases in occur only in a small, largely random subpopula-
which the secretion of IEC-derived chemokines and tion of cells.
cytokines is increased, contributing to the augmen-
tation of mucosal inflammation. The chemokines 37 D (S&F, ch3)
have the capacity to attract inflammatory cells, such Immunohistochemistry can determine the presence
as lymphocytes, macrophages, and dendritic cells. or absence of a gene product in a tissue sample.
Gene LKB1 is detected in Peutz-Jeghers syndrome.
32 C (S&F, ch1) Loss of MSH2, MYH, and MLH1 protein can be
The GI tract contains more than 95% of the total detected by immunohistochemical staining.
body serotonin, and serotonin is important in a
variety of processes, including epithelial secretion, 38 E (S&F, ch1)
bowel motility, nausea, and emesis. Serotonin is Bipolar neurons that project to the mucosa and
synthesized from tryptophan and is converted to myenteric plexus act as sensory neurons and
its active form in nerve terminals. Most plasma contain the hormones listed.
serotonin is derived from the gut, where it is found
in mucosal enterochromaffin cells and the enteric 39 A (S&F, ch2)
nervous system. Serotonin mediates its effects by TNF is a cytokine that has its primary origin in
binding to a specific receptor. There are seven dif- macrophages, T cells, dendritic cells, and mesen-
ferent serotonin receptor subtypes (5-HT1 to 5-HT7) chymal cells. It functions to increase apoptosis and
found on enteric neurons, enterochromaffin cells, nuclear factor.
and GI smooth muscle. Serotonin can cause
smooth muscle contraction through stimulation of 40 B (S&F, ch2)
cholinergic nerves or relaxation by stimulating The significance of the ability of IECs to recognize
inhibitory nitric oxide–containing neurons. Sero- pathogen-associated molecular patterns via surface
tonin released from mucosal cells stimulates Toll-like receptors or via intracellular nuclear
sensory neurons, initiating a peristaltic reflex, oligomerization domains 1 and 2 (NOD1, NOD2)
secretion (via 5-HT4 receptors), and the serotonin has been increasingly recognized over the past
released modulates sensation through activation of decade. The latter ability has been shown to con-
5-HT3 receptors. tribute to intestinal inflammation because approxi-
mately 25% of patients with Crohn’s disease have
33 D (S&F, ch3) mutations in the NOD2/CARD15 gene, interfering
One pathway is mediated through membrane- with their ability to mount an appropriate immune
bound death receptors, which include TNF recep- response to bacterial stimuli.
tors, Fas, and DR5, whereas the other pathway
involves activation of TP53 expression by environ- 41 F (S&F, ch3)
mental insults such as ionizing radiation, hypoxia, Regulation of cell cycle progression seems to be
and growth factor withdrawal with the subsequent achieved principally by cyclins and cyclin-
dependent kinase activity at the G1/S and G2/M diploid or near-diploid on a chromosomal level but
phase transitions. Dysregulation can promote harbor frequent alterations in smaller tracts of microÂ�
neoplasia. satellite DNA.
42 A (S&F, ch3) 43 D (S&F, ch3)

Chromosomal instability results in tumor cells that More than 80 oncogenes have been isolated. Most
display frequent aneuploidy, large chromosomal of these genes are widely expressed in many differ-
deletions, and chromosomal duplications. Tumors ent types of tumor cells. Multiple oncogenes are
that display microsatellite instability are often commonly found within a single tumor.
CHAPTER
2â•…
Nutrition in Gastroenterology
A. Marginal ulcer
Questions B. Internal hernia
C. Intestinal obstruction
44 Which of the following is considered protective D. Dumping syndrome
against childhood obesity? E. Cholelithiasis/biliary colic
A. Maternal gestational diabetes
B. Maternal smoking during pregnancy
48 A 30-year-old female executive has frequent lunch
C. Breast-feeding
meetings during which she typically chooses salads
D. Reduced nighttime sleep for young children
and other low-calorie options. However, once a
month, she returns home late at night and con-
45 Human proteins are comprised of amino acids. There
sumes several pints of ice cream, boxes of cookies,
are 20 different amino acids, some of which are
and several cans of soda. Immediately afterward,
considered essential because their carbon skeletons
she becomes very anxious, takes several laxatives,
cannot be synthesized by the body. Which of the fol-
and forces herself to vomit. This pattern has been
lowing amino acids are considered to be essential?
repeating itself for the past 5 years. She is 5 feet 5
A. Histidine
inches tall and weighs 130 pounds. Her diagnosis
B. Glycine
is most likely
C. Serine
A. Bulimia nervosa
D. Alanine
B. Night-eating syndrome
C. Anorexia nervosa
46 A 3-year-old boy presents with crampy abdominal
D. Binge-eating disorder
pain and diarrhea occurring within an hour of eating.
He has a poor appetite and is in the 15th percentile
for height and weight. Both a food-specific immuno- 49 Protein requirements are affected by the adequacy
globulin E (IgE) antibody skin prick test and serum of essential amino acids in the protein source.
food-specific IgE antibody test are performed, and What proportion of total protein requirements
the results are positive. He is diagnosed as having a should be provided in the form of essential amino
gastrointestinal allergy due to IgE-mediated hyper- acids?
sensitivity. Eliminating which of the following A. 5% to 10%
group of foods would most likely reduce this child’s B. 15% to 20%
symptoms? C. 30% to 40%
A. Milk, egg, peanuts D. More than 50%
B. Barley, beef, lamb
C. Soy, wheat, potato 50 A 32-year-old woman is considering bariatric surÂ�
D. Shellfish, potato, wheat gery. Which of the following would usually be rec-
ommended as part of her preoperative evaluation?
47 A 50-year-old woman lost 60 pounds during the A. CT scan of the abdomen and pelvis
first four months after gastric bypass surgery for B. Abdominal ultrasonography
obesity. She now presents with new epigastric pain C. Esophagogastroduodenoscopy/upper
that begins about 30 minutes after a meal and is not endoscopy
relieved with antacids. What is the most likely D. Colonoscopy
explanation for this patient’s symptoms? E. Esophageal manometry
9
10 Nutrition in Gastroenterology
51 Which of the following statements regarding calÂ� C. Dietary protein-induced enteropathy

cium absorption is most accurate? D. Whipple’s disease
A. Calcium absorption occurs primarily in the
distal small intestine. 56 Orlistat (Xenical), an orally administered weight reÂ�
B. Calcium absorption occurs primarily in the duction agent, prevents the absorption of fats from
proximal small intestine. the diet, thereby reducing caloric intake. Which of
C. Calcium absorption occurs throughout the the following statements regarding orlistat is true?
length of the small intestine. A. The mechanism of action is inhibition of panÂ�
D. Calcium absorption occurs primarily in the creatic lipase.
colon. B. It is available in the United States by prescripÂ�
tion only.
52 Diarrhea in a chronically malnourished population C. Side effects are mostly related to excellent
is often caused by a combination of factors, includ- absorption of the drug via the GI tract.
ing increased GI secretions, decreased intestinal D. It is effective whether taken before, during, or
transit time, and osmotic stimulation of water secre- after a meal.
tion by unabsorbed contents of the food stream. The
somatostatin analog octreotide acetate (Sandostatin) 57 A 50-year-old woman presents to a primary care
may be used in the management of diarrhea in mal- physician for a routine physical examination. Her
nourished patients. Which of the following state- medical history is significant for hypertension and
ments regarding this medication is most accurate? diet-controlled diabetes. Her BMI is 42. What is her
A. It decreases stool volume, sodium, and chloÂ� weight classification?
ride output. A. Ideal weight
B. It decreases small intestinal transit time in B. Overweight
patients with short gut syndrome. C. Obese
C. It improves absorption of macronutrients and D. Morbidly obese
micronutrients.
D. It is typically administered by continuous 58 A 17-year-old girl with a history of binging and
infusion. purging is diagnosed with bulimia nervosa. She
reports to her dentist symptoms of heartburn, teeth
53 An 18-year-old girl with bulimia nervosa has a discoloration, and sensitivity to extreme tempera-
body mass index (BMI) of 15. She reports early tures. The dentist observes rounded teeth and some
satiety and postprandial abdominal pain and vomits dents. Which of the following best describes this
twice daily. Over the past two months, she has been complication of bulimia nervosa?
hospitalized twice for these symptoms and has lost A. Dentinogenesis imperfecta
5 pounds. Endoscopy reveals scant food debris in B. Gingivitis
the stomach. Treatment with a proton pump inhibi- C. Bruxism
tor results in minimal clinical improvement. Which D. Perimolysis
diagnostic test would be most helpful at this time?
A. Breath test for bacterial overgrowth 59 A 40-year-old man with a history of rhinoÂ�
B. Computed tomography scan of the abdomen conjunctivitis, asthma, and atopic dermatitis preÂ�
C. Gastric emptying scan sents with heartburn and dysphagia. Twice daily
D. Esophageal manometry treatment with a proton pump inhibitor for six
weeks does not improve his symptoms. Endoscopy
54 A 50-year-old alcoholic man has been homeless for reveals mucosal rings, ulcerations, and strictures
several months. He is evaluated in an emergency throughout the esophagus. What is his most likely
department and found to be confused and ataxic diagnosis?
and to have abnormal eye movements. A computed A. Reflux esophagitis
tomography scan of the head reveals no acute B. Allergic eosinophilic esophagitis
abnormalities, and the results of a drug and alcohol C. Bile reflux
screen are negative. Which of the following vitamin D. Candidal esophagitis
deficiencies best explains these symptoms?
A. Vitamin C deficiency 60 Undernutrition in children differs from that in
B. Riboflavin deficiency adults because it affects growth and development.
C. Niacin deficiency Which of the following is the most distinguishing
D. Pantothenic acid deficiency feature appreciated during physical examination of
E. Thiamine deficiency a child with kwashiorkor compared with a child
with marasmus?
55 A 2-month-old male infant presents with protracted A. Short stature
vomiting and diarrhea. The infant was initially B. Small head circumference
begun on a cow-milk formula and was then switched C. Low weight
to a soy-based formula, which he tolerated for two D. Peripheral edema
days before his symptoms recurred. A small intes-
tine biopsy specimen shows edema and an increased 61 Aggressive nutritional support will not benefit
number of lymphocytes, eosinophils, and mast every acutely ill patient. For which clinical sce-
cells. What is this infant’s most likely diagnosis? nario in a hospitalized patient would aggressive
A. Dietary protein-induced enterocolitis nutritional support be most beneficial?
syndrome A. Acute cholecystitis in an obese but otherwise
B. Celiac disease healthy 45-year-old woman
Nutrition in Gastroenterology 11
B. Acute alcoholic hepatitis in a 45-year-old man C. Ingest large volumes of fluids with meals.
without any other known medical problems D. Start a prokinetic agent.
C. Acute coronary syndrome in a 60-year-old man
with a history of hypertension 68 A 65-year-old woman with a history of diabetes and
hypertension is admitted to the hospital with severe
62 A 26-year-old woman with a recent diagnosis of nausea, vomiting, and abdominal pain. Acute cho-
diabetes mellitus and a BMI of 43 is referred by her lecystitis is diagnosed based on physical examina-
gynecologist for treatment of obesity. An evaluation tion, imaging, and laboratory studies. Her weight is
for infertility has led to a diagnosis of polycystic 150 pounds and her height is 5 feet 6 inches. Follow-
ovarian syndrome. Which of the following agents ing cholecystectomy, the patient suggests that had
would be most optimal for treating this patient? her weight been lower she would not have devel-
A. Orlistat oped gallbladder disease. Based on her BMI of 24.2,
B. Metformin how would you best describe her nutritional status?
C. Prozac A. Moderately malnourished
D. Wellbutrin B. Normal
C. Overweight
63 Which of the following agents is approved by the D. Obese
U.S. Food and Drug Administration (FDA) for long-
term use in the pharmacologic treatment of obesity? 69 A 45-year-old woman presents for a “health main-
A. Amphetamine tenance” visit to your office. Based on her height
B. Orlistat and weight obtained by your medical assistant, you
C. Fenfluramine calculate her BMI to be 37. The patient informs you
D. Phentermine that she is extremely interested in losing weight
with your help. Which of the following statements
64 A 30-year-old woman with a history of irritable regarding weight reduction agents is correct?
bowel syndrome is seen in a dermatology clinic for A. Fluoxetine is approved by the FDA for weight
evaluation of a papulovesicular rash on her elbows. reduction.
A biopsy is performed and dermatitis herpetiformis B. Fluoxetine is a good option for a long-term
is diagnosed. Her rash is likely to improve by exclud- weight loss.
ing which of the following foods from her diet? C. Wellbutrin has data to support off-label use for
A. Wheat, soy, and dairy short-term weight loss.
B. Wheat, soy, and peanuts D. Topiramate is ineffective for weight reduction.
C. Wheat, rye, and barley
D. Wheat, corn, and peanuts 70 A 19-year-old ballet dancer with a 10-year history
of anorexia nervosa presents to the emergency
65 A continuous supply of energy is required for department with confusion, headache, and diffuse
normal organ function, maintenance of metabolic weakness one day after a performance. The patient
homeostasis, heat production, and performance of severely restricts her daily intake, keeping to a low-
mechanical work. What is the largest contributor to calorie diet for one week before each performance.
the total (daily) energy expenditure (TEE)? Immediately after each performance, she quickly
A. Resting energy expenditure liberalizes her diet and starts eating a lot more calo-
B. Energy expenditure of physical activity ries in the form of carbohydrates. Her height is 5
C. Thermic effect of feeding feet 6 inches, and she weighs 100 pounds. The
emergency department staff suspects refeeding syn-
66 A 48-year-old woman with esophageal cancer has drome. Which laboratory result is most commonly
been undergoing chemotherapy and receives nutri- seen with refeeding syndrome?
tion via a percutaneously placed gastrostomy tube. A. Hyperphosphatemia
She was recently hospitalized for 5 days for treat- B. Hypophosphatemia
ment of pneumonia and subsequently developed C. Hypercalcemia
severe diarrhea. Which one of the following is the D. Hypocalcemia
best treatment for this patient’s diarrhea?
A. Change the enteral feeding formula 71 A 66-year-old man underwent a bariatric surgical
B. Change the gastrostomy tube to a jejunostomy procedure 8 years ago and now presents with
tube fatigue, anemia, and diarrhea in addition to a
C. Metronidazole greater than expected weight loss. Which of the
D. Ciprofloxacin following bariatric surgical procedures is most
likely to lead to serious complications due to
67 A 42-year-old man with a history of antrectomy and excessive malabsorption?
vagotomy for recalcitrant peptic ulcer disease preÂ� A. Biliopancreatic diversion/duodenal switch
sents with recurrent episodes of nausea, cramping, B. Roux-en-Y gastric bypass
diaphoresis, and palpitations after meals. Upper C. Laparoscopic adjustable gastric banding
endoscopy reveals normal postoperative findings D. Partial and sleeve gastrectomy
without obstruction or peptic ulcer disease. Which
interÂ�vention is most likely to improve this patient’s 72 Sibutramine (Meridia), an orally administered
symptoms? agent for the treatment of obesity, suppresses appe-
A. Ingest frequent small meals. tite. Which of the following statements regarding
B. Ingest simple sugars with meals. sibutramine is true?
A. It has no side effects. Which of the following statements is the most

B. It acts directly on serotonin receptors in the accurate?
brain. A. The stimulation of α1-adrenergic receptors
C. It is a selective inhibitor of serotonin uptake. increases food intake.
D. It is not considered effective for maintenance B. The stimulation of serotonin receptors in the
of weight loss. brain reduces fat intake, with little or no effect
on the intake of protein or carbohydrates.
73 Protein energy malnutrition affects nearly every C. The stimulation of β2 receptors in the brain
organ system. Which of the following abnormalities increases food intake.
is found in the GI tract of a malnourished patient? D. The stimulation of the H1 receptor in the
A. Proliferation of intestinal villi central nervous system increases food intake.
B. Increased volume of gastric secretions
C. Increased number of facultative and anaerobic 77 A cachectic 56-year-old schizophrenic man has
bacteria in the small bowel been living on the streets for several months and is
D. Increased volume of bile admitted to the hospital with pneumonia. He is
treated with intravenous antibiotics, and total par-
74 A 76-year-old man with a history of biliary obstruc- enteral nutrition is started. He initially demon-
tion due to cholangiocarcinoma presents to his strates clinical improvement but then becomes
primary care physician with fatigue and shortness short of breath despite an improved chest radio-
of breath. He has a long-term indwelling external graph. Which of the following deficiencies best
biliary drain that is functioning well. There is no explains his dyspnea?
scleral icterus. The serum bilirubin level is normal, A. Phosphorous
but the patient is noted to have a severe hypochro- B. Calcium
mic microcytic anemia. Which micronutrient defi- C. Copper
ciency best explains this patient’s anemia? D. Selenium
A. Selenium deficiency E. Zinc
B. Zinc deficiency
C. Copper deficiency 78 Hormonal disturbances may occur with eating
D. Iodine deficiency disorders. In patients with anorexia nervosa and
bulimia nervosa, elevation of which specific
75 An 18-year-old female college freshman is evalu- hormone is most closely associated with secretion
ated at the student health center because she has of growth hormone, stimulation of appetite and
never had a menstrual cycle. An aspiring gymnast, intake, induction of adiposity, and signaling to
she has been preoccupied with maintaining a low the hypothalamic nuclei involved in energy
weight for much of her life. The patient periodi- homeostasis?
cally diets by consuming only vegetables and fruit A. Leptin
for several days. Her current weight is 100 pounds, B. Serotonin
and her height is 5 feet 8 inches. What is her most C. Cholecystokinin
likely diagnosis? D. Ghrelin
A. Bulimia nervosa
B. Purging disorder 79 A 60-year-old woman living in an assisted care
C. Anorexia nervosa facility is admitted to the hospital with a hip frac-
D. Binge-eating disorder ture. During this hospitalization, the patient is
observed to have hyperglycemia. Which micronu-
76 The central nervous system plays an important role trient deficiency best explains this problem?
in regulating food intake by receiving and process- A. Chromium deficiency
ing information from the environment and internal B. Manganese deficiency
milieu. A number of neurotransmitter systems, C. Copper deficiency
including monoamines, amino acids, and neuro- D. Iron deficiency
peptides, are involved in modulating food intake. E. Selenium deficiency
Answers 45 A (S&F, ch4)

Histidine, isoleucine, leucine, lysine, methionine,
44 C (S&F, ch6) phenylalanine, threonine, tryptophan, valine, and
Several factors are linked to postnatal weight and possibly arginine are considered to be essential
lifetime weight gain. Among the risks for obesity amino acids because their carbon skeletons cannot
are maternal smoking and gestational diabetes. be synthesized by the human body. The remaining
Infants who are breast-fed for more than three amino acids (glycine, alanine, serine, cysteine,
months may have a reduced risk of future obesity. cystine, tyrosine, glutamine, glutamic acid, aspara-
Children who get more sleep tend to weigh less gine, and aspartic acid) are nonessential in most
when they enter school than do those who sleep circumstances because they can be made from
less. endogenous precursors or essential amino acids.
46 A (S&F, ch9) 52 A (S&F, ch4)

Milk, eggs, and peanuts are the most common The somatostatin analog octreotide acetate (Sand-
foods associated with food allergy due to IgE- ostatin) can decrease small intestine secretions.
mediated hypersensitivity. Symptoms may develop Therapy with octreotide has been shown to decrease
within minutes to two hours of consuming an ostomy or stool volume, decrease sodium and chlo-
implicated food and consist of nausea, abdominal ride output, and prolong small intestine transit
pain, vomiting, and diarrhea. The other food time in patients with short bowel syndrome.
choices are associated with non–IgE-mediated food Octreotide therapy, however, usually does not
hypersensitivities. improve absorption of macronutrients and other
minerals; in fact, it may exacerbate the degree of fat
47 E (S&F, ch7) malabsorption, presumably by inhibiting pancre-
Cholelithiasis is very commonly associated with atic secretions. In addition, octreotide is expensive,
rapid weight loss and occurs in as many as diminishes protein synthesis in the intestinal epi-
one third of patients after weight loss surgery. thelium and exocrine pancreas, and may decrease
Although marginal ulcers may occur and cause appetite and increase the risk of gallstones. It is
postoperative pain in this patient population, cho- usually administered subcutaneously, often several
lelithiasis is much more common and does not times per day.
respond to antacid therapy. Most experts recom-
mend prophylactic treatment with ursodiol for the 53 C (S&F, ch8)
first six months postoperatively to prevent this Gastroparesis is associated with bulimia nervosa
complication. and anorexia nervosa, and presents with early
satiety and postprandial abdominal pain. Upper
48 A (S&F, ch8) endoscopy excluded structural abnormalities, but
Bulimia nervosa is a recurrent binge-eating disor- the finding of food in the stomach did suggest gas-
der accompanied by inappropriate behaviors to troparesis. Therefore, the gastric emptying scan
control weight or purge calories. These behaviors would be the most helpful test at this point (see
may include using laxatives or diuretics, vomiting, table at end of chapter).
and excessive exercise. Binge-eating disorder is
characterized by excessive intake of calories within 54 E (S&F, ch5)
a discrete period of time, without associated inÂ� Thiamine is important for energy transformation as
appropriate compensatory behaviors to prevent well as membrane and nerve conduction. Thiamine
weight gain. Anorexia nervosa is characterized by deficiency may cause Wernicke’s encephalopathy,
an unwillingness to maintain normal weight. Com- which is characterized by altered mental status,
monly, this is described as a failure to exceed 85% ataxia, and abnormal eye movements. Although
of the expected body weight in association with a common in alcoholic patients, this condition may
fear of weight gain. Night-eating syndrome is occur in any severely malnourished patient. Treat-
defined as recurrent bouts of overeating during ment consists of immediate administration of
nighttime awakening, without necessarily binging. thiamine.
The syndrome is not associated with inappropriate
compensatory behaviors to prevent weight gain. 55 A (S&F, ch9)
Dietary protein-induced enterocolitis syndrome
49 B (S&F, ch4) occurs in infants between one and three months
Proteins containing low amounts of essential amino of age, presents with protracted vomiting and diar-
acids are considered to be of low biologic quality. rhea (mild to moderate steatorrhea in ~80%), and
The total protein requirement is higher when the may result in dehydration and poor weight gain.
protein source is of low biologic quality. In normal Cow’s milk sensitivity is the most frequent cause
adults, approximately 15% to 20% of the total of this syndrome, but it also has been associated
protein requirement should be in the form of essen- with sensitivities to soy, eggs, wheat, rice, chicken,
tial amino acids. and fish. Loss of protein sensitivity, with resultant
reduction in clinical reactivity, occurs frequently.
50 C (S&F, ch7) In this case, a rice-based formula would be rec-
Upper endoscopy is generally recommended for ommended. During breast-feeding, infants virtu-
all patients who will be undergoing bariatric ally never develop this syndrome. Celiac disease
surgery. A high percentage of patients considering is due to an immunologic reaction to gliadin,
bariatric surgery will have clinically significant which is found in wheat, rye, and barley. The
findings on endoscopy. The other listed options biopsy typically has an infiltrate limited to lym-
are only indicated for the evaluation of specific phocytes and may demonstrate villous atrophy.
symptoms. A colonoscopy is a reasonable screen- Whipple’s disease is a rare infectious disease
ing test for colon and rectal cancer but is not part resulting in weight loss, incomplete breakdown
of the routine preoperative evaluation for a young of carbohydrates and fats, and immune system
patient. dysfunction. Whipple’s disease is treated with
antibiotics.
51 C (S&F, ch5)
Calcium absorption occurs throughout the length of 56 A (S&F, ch6)
the entire small intestine and is vitamin D depen- Orlistat is taken three times daily and specifically
dent. During periods of restricted calcium intake, before meals. In the United States, orlistat is avail-
the colon may become more involved in calcium able in two strengths: a prescription dose of 120Â€mg
homeostasis by increasing its absorption. (Xenical) and an over-the-counter dose of 60Â€ mg
(Alli). Orlistat is poorly absorbed and acts by inhib- management of polycystic ovarian syndrome. It
iting the enzymatic action of pancreatic lipase. reduces hepatic glucose production, decreases
Subsequently, its side effects are those associated glucose absorption from the GI tract, and enhances
with maldigestion of fats including fecal inconti- insulin sensitivity. As compared to sulfonylureas,
nence, anal leakage, bloating, and borborygmi. clinical trials have demonstrated weight loss with
metformin.
57 A (S&F, ch6)
Over the past 50 years, there has been a steady rise 63 B (S&F, ch6)
in the incidence of obesity. A useful tool for study- Two agents are approved by the FDA for long-term
ing this trend is the BMI, defined as the weight (W) treatment of obesity—sibutramine and orlistat. As
in kilograms divided by the height (H) in meters monotherapy, both agents can produce weight loss
squared (W/H2). A BMI greater than 30 provides a of 8% to 10%. Orlistat promotes weight reduction
useful operating definition of obesity. by inhibiting the enzymatic action of pancreatic
lipase. Sibutramine promotes satiety and possibly
BMI <18 Underweight increases energy expenditure by blocking the
BMI 18-26.5 Ideal weight reduction in metabolic rate that accompanies
weight loss. Fenfluramine increases serotonin
BMI 26.6-29 Overweight
levels, resulting in a sense of fullness and loss of
BMI 30-40 Obese appetite. Phentermine acts on the hypothalamus
BMI >40 Morbidly obese to release norepinephrine and reduces hunger.
Outside the brain, phentermine causes release of
58 D (S&F, ch8) epinephrine, which acts to break down fat in
Chronic vomiting, a feature of bulimia nervosa, adipose tissue, and reduces hunger. Fenfluramine,
may cause dental erosions or perimolysis. Neither and a combination agent consisting of fenfluramine
gingivitis (irritation of the gums) nor bruxism and phentermine (“fen-phen”), were withdrawn
(teeth grinding) is associated with bulimia nervosa from the market after being shown to cause pulmo-
or typically presents with dental erosions. Den- nary hypertension and heart valve abnormalities.
tinogenesis imperfecta is a genetic disorder of
tooth development that causes the teeth to be dis- 64 C (S&F, ch9)
colored (most often a blue-gray or yellow-brown Dermatitis herpetiformis is a chronic blistering
color) and translucent and is not a feature of skin disorder associated with a gluten-sensitive
bulimia nervosa. enteropathy (celiac disease). It is characterized
by a chronic, intensely pruritic, papulovesicular
59 B (S&F, ch9) rash symmetrically distributed over the extensor
The most likely diagnosis is allergic eosinophilic surfaces and buttocks. Although many patients
esophagitis. A biopsy specimen demonstrating a have minimal or no GI symptoms, biopsy of the
high number of eosinophils would be helpful in small bowel generally confirms intestinal involve-
establishing a diagnosis. The symptoms may be ment. Elimination of gliadin, the alcohol-soluble
confused with those of reflux. Endoscopic findings portion of gluten found in wheat, rye, and barley,
include mucosal rings, ulcerations, and strictures. from the diet generally leads to resolution of
The absence of clinical improvement despite proton skin symptoms and normalization of intestinal
pump inhibitor therapy makes reflux esophagitis findings over several months. An increased inci-
less likely. The clinical presentation and endo- dence of celiac disease in individuals previously
scopic findings are not suggestive of bile reflux or diagnosed with irritable bowel syndrome has been
candidal esophagitis. shown.
60 D (S&F, ch4) 65 A (S&F, ch4)

The presence of peripheral edema distinguishes Total (daily) energy expenditure (TEE) is composed
children with kwashiorkor from those with maras- of three components: the resting energy expendi-
mus and nutritional dwarfism. ture (~70% of TEE), the energy expenditure of
physical activity (~20% of TEE), and the thermic
61 B (S&F, ch4) effect of enteral or parenteral nutrition (~10% of
The prevalence of moderate to severe protein TEE).
energy malnutrition is so high among patients
admitted for acute alcoholic hepatitis and other 66 C (S&F, ch5)
forms of decompensated alcoholic liver disease that The most common cause of diarrhea in patients
it is best to assume that all such patients are mal- receiving enteral feeds is Clostridium difficile (C.
nourished. Furthermore, patients with acute alco- difficile)–induced colitis due to concurrent antiÂ�
holic hepatitis usually fall far short of their biotics. Metronidazole is usually an effective treat-
nutritional needs when allowed to eat ad libitum. ment for this infection. Changing the route of
Clinical trials demonstrate that the rates of morÂ� feeding to the jejunum would likely worsen this
bidity and mortality and the speed of recovery are patient’s diarrhea. Another acceptable option that
improved with prompt institution of enteral or par- was not included as an answer choice is oral van-
enteral nutrition in these patients. comycin. Some patients have diarrhea after antibi-
otic therapy without C. difficile infection. This
62 B (S&F, ch6) subset of patients may improve with probiotic
Metformin is a biguanide that is approved for the supplementation after withdrawal of the original
treatment of diabetes mellitus and often used in antibiotic.
67 A (S&F, ch5) complications. All of the other choices, commonly

This patient has symptoms of dumping syndrome, performed in bariatric centers, are reasonable alter-
which is common in patients who have had a gas- natives that are associated with fewer postopera-
trectomy and vagotomy. These symptoms are tive problems.
caused by hypertonic gastric contents emptying
rapidly into the small intestine. This causes a sig- 72 C (S&F, ch6)
nificant amount of the plasma volume to be shifted Sibutramine (Meridia) selectively inhibits reup-
to the small intestine with resultant symptoms due take of serotonin and norepinephrine into neurons
mostly to hypovolemia. Nutritional therapy of this but does not act on any known receptors. Sibutra-
condition aims to deliver a lower osmolarity to the mine promotes satiety but may also increase
small intestine by frequent ingestion of small meals energy expenditure by blocking the reduction in
with limited simple sugars. Fluid intake should be metabolic rate that normally accompanies weight
restricted while eating solid food to avoid rapid loss.
gastric transit.
73 C (S&F, ch4)
68 B (S&F, ch4) Malnutrition is associated with structural and
This patient’s BMI based on her height and weight functional changes within the GI tract. Marked
is 24.2. According to the table, she is considered blunting of the intestinal villi, usually associated
normal (see table at end of chapter). with loss of some or all of the brush border hydro-
lases, is often seen. There is a reduction in gastric
69 C (S&F, ch6) and pancreatic secretions in association with lower
Fluoxetine is a selective serotonin reuptake inhiÂ� concentrations of acid and digestive enzymes,
bitor that blocks serotonin transporters, thus respectively. In addition, the volume of bile, and
prolonging the action of serotonin. Fluoxetine is the concentration of conjugated bile acids within
approved by the FDA for the treatment of depres- the bile, is reduced. Increased numbers of faculta-
sion. Approximately 50% of initial weight loss tive and anaerobic bacteria are found in the proxi-
associated with fluoxitine is regained during the mal small intestine, and this probably explains the
second six months of treatment, making this drug increased proportion of free bile acids within the
inappropriate for long-term treatment of obesity. intestinal lumen.
Bupropion is approved for the treatment of depres-
sion and as an adjunctive agent for smoking 74 C (S&F, ch5)
cessation. Two multicenter clinical trials, one in Copper is necessary for iron utilization, hemoglo-
obese subjects with depressive symptoms and bin formation and production, and survival of
one in uncomplicated overweight patients, evalu- erythrocytes. Copper is excreted in the bile, and
ated the effectiveness of buproprion for weight therefore patients with external biliary drainage are
loss. Nondepressed subjects may respond with at high risk of copper deficiency. The daily copper
more weight loss than those with depressive requirement is 1.5 to 3Â€µg/day.
symptoms. Topiramate, an antiepileptic drug, was
associated with weight loss in clinical trials for 75 C (S&F, ch8)
epilepsy. Anorexia nervosa is characterized by an unwilling-
ness to maintain normal weight. Commonly, this
70 B (S&F, ch8) is described as failure to exceed 85% of expected
Patients with anorexia nervosa are at risk of body weight in association with fear of gaining
refeeding syndrome, a potentially life-threatening weight and amenorrhea. Bulimia nervosa is defined
condition characterized by fluid and electrolyte as recurrent binge eating accompanied by a variety
disorders including hypophosphatemia, hypomag- of inappropriate purging behaviors, including lax-
nesemia, and hypokalemia. This syndrome typi- atives, excessive exercise, diuretics, or vomiting to
cally occurs within four days of introducing a control weight gained during a binge. These behav-
healthy diet to a patient with anorexia nervosa. iors must occur twice weekly for at least 3 months
As a shift from fat to carbohydrate metabolism to meet diagnostic criteria. Binge-eating disorder
occurs, insulin levels increase, leading to increased is characterized by excessive intake of calories
cellular uptake of phosphate. Associated with within a discrete period of time but is not associ-
intracellular movement of electrolytes is a decrease ated with recurrent inappropriate compensatory
in the serum electrolytes, particularly phosphate, behaviors to prevent weight gain. Purging disorder
potassium, magnesium, glucose, and thiamine. is defined by recurrent purging or elimination
Alteration in serum calcium levels is not com- using laxatives, exercise, diuretics, or vomiting in
monly associated with refeeding syndrome (see the absence of clinically significant binge-pattern
table from answer 53). eating.
71 A (S&F, ch7) 76 B (S&F, ch6)

Biliopancreatic diversion/duodenal switch may Stimulation of α1-adrenergic receptors reduces
result in serious complications due to excessive all food intake, whereas stimulation of serotonin
malabsorption resulting in malnutrition and a receptors in the brain selectively reduces fat intake,
variety of vitamin deficiencies. This may present with little or no effect on the intake of protein or
as excessive weight loss, anemia, and even diar- carbohydrate. Stimulation of β2 receptors in the
rhea. This procedure has thus fallen out of favor brain decreases food intake, and stimulation of the
because there are several other options that are H1 receptor in the central nervous system reduces
highly effective with fewer long-term nutritional feeding.
77 A (S&F, ch5) secretion of growth hormone. Leptin is associated

Phosphorous deficiency may occur in malnour- with longer-term regulation of body fat stores
ished patients who abruptly begin adequate nutri- and affects satiety through its binding to the ven-
tion. In these patients, the delivery of a glucose load tromedial nucleus of the hypothalamus, an area
after a period of starvation causes an increased known as the “satiety center.” Altered serotonin
serum insulin level. Insulin drives phosphorous, function contributes to dysregulation of appetite
magnesium, and potassium into cells, with resul- as well as mood and impulse control in eating
tant very low serum levels of these electrolytes. disorders. This abnormality persists after recovery
This disorder is called refeeding syndrome, and from anorexia nervosa and bulimia nervosa,
may be life-threatening. Severe hypophosphatemia suggesting possible premorbid vulnerability. In
causes skeletal muscle dysfunction, and this effect bulimia nervosa, a blunted postprandial cholecys-
may be most evident in the chest leading to tokinin (CCK) response impairs satiety. The find-
hypoventilation and eventual tissue hypoxia. ings regarding a relationship between pre- and
Severely malnourished patients should initially postprandial CCK levels and anorexia nervosa are
receive a reduced glucose load at a slow rate with inconsistent.
close monitoring of all serum electrolytes.
79 A (S&F, ch5)
78 D (S&F, ch8) Chromium is necessary for the synthesis of glucose
Ghrelin affects all of these regulatory functions tolerance factor, a cofactor for insulin action. A
and is elevated in anorexia nervosa and bulimia deficiency in chromium can thus lead to glucose
nervosa. The other hormones listed do not affect intolerance and elevated glucose levels.
Tables
Table for answer 53 Selected Clinical Features and Complications of Behaviors in Patients with Eating Disorders
CLINICAL FEATURE OR COMPLICATION
ASSOCIATED WITH WEIGHT LOSS AND ASSOCIATED WITH PURGING OR REFEEDING

FOOD RESTRICTION OR BINGE-EATING IN BEHAVIORS IN ANOREXIA NERVOSA, BULIMIA
SYSTEM AFFECTED ANOREXIA NERVOSA NERVOSA, OR EDNOS
Cardiovascular Arrhythmia Ventricular arrhythmia
Bradycardia Cardiomyopathy (with ipecac use)
Congestive heart failure (in refeeding syndrome) Prolonged QT interval
Decreased cardiac size Orthostasis
Diminished exercise capacity Syncope
Dyspnea
Hypotension
Mitral valve prolapse
Orthostasis
Prolonged QT interval
QT dispersion
Syncope
Dermatologic Brittle hair Russell’s sign (knuckle lesions from repeated
Dry skin scraping against the incisors)
Hair loss
Hypercarotenemia
Lanugo
Oral, pharyngeal Cheilosis Dental erosion and caries
Sialadenosis
Pharyngeal and soft palatal trauma
Angular cheilitis
Perimolysis
Vocal fold pathology
Gastrointestinal* Anorectal dysfunction Abdominal pain
Delayed gastric emptying Acute gastric dilatation
Elevated liver enzyme levels Barrett’s esophagus
Elevated serum amylase levels Bloating
Gastroesophageal reflux Constipation
Hepatic injury Delayed gastric emptying
Pancreatitis Diarrhea
Prolonged whole-gut transit time Dysphagia
Rectal prolapse Elevated liver enzyme levels
Slow colonic transit Elevated serum amylase levels
Superior mesenteric artery syndrome Esophageal bleeding
Esophageal ulcers, erosions, stricture
Gastroesophageal reflux
Mallory-Weiss tear
During refeeding:
Acute gastric dilatation, necrosis, and perforation Gastroesophageal reflux
Elevated liver enzyme levels Gastric necrosis and perforation
Hepatomegaly Hematemesis
Pancreatitis Pancreatitis
Prolonged intestinal transit time
Rectal bleeding
Rectal prolapse
Continued
Table for answer 53 Selected Clinical Features and Complications of Behaviors in Patients with Eating Disorders—Cont’d
CLINICAL FEATURE OR COMPLICATION
ASSOCIATED WITH WEIGHT LOSS AND ASSOCIATED WITH PURGING OR REFEEDING

FOOD RESTRICTION OR BINGE-EATING IN BEHAVIORS IN ANOREXIA NERVOSA, BULIMIA
SYSTEM AFFECTED ANOREXIA NERVOSA NERVOSA, OR EDNOS
Endocrine and Amenorrhea Hypercholesterolemia
metabolic Euthyroid sick syndrome Hyperphosphatemia
Hypercholesterolemia Hypochloremia
Hypocalcemia Hypoglycemia
Hypoglycemia Hypokalemia
Hyponatremia Hypomagnesemia
Hypothermia Hyponatremia
Low serum estradiol, low serum testosterone Hypophosphatemia
levels Metabolic acidosis
Osteopenia, osteoporosis Metabolic alkalosis
Pubertal delay, arrested growth Secondary hyperaldosteronism
As part of the refeeding syndrome:
Hypomagnesemia
Hypophosphatemia
Acute kidney injury Abnormal menses
Genitourinary and Amenorrhea Azotemia
reproductive Atrophic vaginitis Pregnancy complications (including low birth weight
Breast atrophy infant)
Infertility
Pregnancy complications (including low birth
weight, premature birth, and perinatal death)
Neurologic Cognitive changes Stroke (associated with ephedra use)
Cortical atrophy Neuropathy (with ipecac use)
Delirium (in refeeding syndrome) Reduced or absent gag reflex
Peripheral neuropathy
Ventricular enlargement
Hematologic Anemia
Leukopenia
Neutropenia
Thrombocytopenia
EDNOS, eating disorder, not otherwise specified.
*Gastrointestinal complications associated with binge pattern eating in any of the eating disorders, are not all listed, and include weight gain,
acute gastric dilatation, gastric rupture, gastroesophageal reflux, increased gastric capacity, and increased stool volume.
Table for answer 68 Classiﬁcation of Nutritional Status by Body Mass Index in Adults
BODY MASS INDEX (KG/M2) NUTRITIONAL STATUS

<16.0 Severely malnourished
16.0-16.9 Moderately malnourished
17.0-18.4 Mildly malnourished
18.5-24.9 Normal
25.0-29.9 Overweight
30.0-34.9 Obese (class I)
35.0-39.9 Obese (class II)
≥40 Obese (class III)
CHAPTER
3â•…
Topics Involving
Multiple Organs
Questions 84 A 20-year-old white woman who had hematochezia

when she was five days old is seeking a second
opinion. She has multiple cutaneous vascular
80 A 32-year-old nurse presents with symptoms of
lesions that have been present since five days of
dizziness, jittery behavior, and headaches before
age. She has received blood transfusions on three
meals. Which of the following supports the diagno-
occasions after hematochezia episodes. An emer-
sis of factitious hypoglycemia?
gent exploratory laparotomy showed a large pelvic
A. Elevated sulfonylurea levels
vascular malformation, which was not treated. On
B. Normal proinsulin levels
physical examination, she is asthenic and appears
C. Normal C-peptide levels
pale but in no distress. She has multiple, bluish,
D. Plasma insulin-to-glucose ratio <0.3
nodular, soft, compressible, nontender lesions on
E. All of the above
her face, soft palate, arms, legs, hands, and trunk.
No abdominal or rectal abnormalities are found on
81 Foreign bodies and/or food boluses can lodge in the
examination, and she is not orthostatic. All of the
esophagus in any of the following four areas of
following statements about this young woman’s
narrowing except:
diagnosis are true except:
A. Hiatal hernia
A. Gastrointestinal (GI) bleeding is a rare feature
B. Upper esophageal sphincter
of this condition.
C. Level of the aortic arch
B. Intussusception may be a presenting feature.
D. Level of the mainstem bronchus
C. It can be transmitted in an autosomal
E. Gastroesophageal junction
dominant fashion.
D. The cutaneous nodules are venous
82 Hypoproteinemia and edema are the principal
malformations, for which no treatment is
clinical manifestations of protein-losing gastroen-
needed.
teropathy. Hypoproteinemia, the most common
clinical sequela, manifests as a decrease in serum
levels of albumin, fibrinogen, lipoproteins, α1- 85 All of the following statements about eosinophilic
antitrypsin, transferrin, and ceruloplasmin, and the gastroenteritis are true except:
following gamma globulins except: A. It commonly presents between 20 and 60 years
A. Immunoglobulin A (IgA) of age.
B. IgM B. Peripheral eosinophilia is present in a majority
C. IgE of patients.
D. IgG C. It most commonly affects the stomach and
small bowel, but also can extend to the
83 Which of the following is the most common com- esophagus, colon, and rectum.
plication after colonoscopy with polypectomy? D. It affects primarily mucosa and pyloric
A. Perforation of the hollow viscus obstruction and usually indicates alterative
B. Infection disease.
C. Immediate postoperative bleeding
D. Cardiorespiratory complications 86 Which of the following statements regarding hepa-
E. Delayed postoperative bleeding titis B infection in pregnancy is true?
19
20 Topics Involving Multiple Organs
A. Most women of childbearing age with chronic panel, thyroid-stimulating hormone level, or pro-
hepatitis B have a high risk of the developÂ� thrombin time/partial thromboplastin time. He
ment of complications of their disease during reports taking 81Â€mg of aspirin daily for cardiopro-
gestation. tective reasons and enalapril (Vasotec) for control
B. Maternal-fetal transmission is responsible for of mild hypertension. Colonoscopy is performed to
most cases of hepatitis B worldwide. the cecal tip without difficulty and shows scattered
C. Mothers who test negative for the hepatitis B diverticula in the left and transverse colon and
e-antigen cannot transmit the virus to their a lesion in the cecum (see figure). Which of the
fetuses. following is a true statement about this lesion?
D. Women with hepatitis B can be treated with A. It should be treated with a heater probe to
interferon during pregnancy. prevent occurrence of lower GI bleeding.
E. Women with hepatitis B should not be treated B. It indicates that the patient should undergo
with lamivudine during pregnancy. angiography after the colonoscopy to confirm
that he does not have other similar lesions.
87 Typhlitis can be the presenting manifestation of or C. It indicates that the patient should be offered
be associated with hormonal therapy.
A. Yersinia infection D. It should be treated with argon plasma coaguÂ�
B. Acute leukemia lation because this kind of lesion is a common
C. Crohn’s disease cause of recurrent lower GI bleeding.
D. Cecal superinfection with cytomegalovirus E. It does not require any treatment because the
(CMV) risk of bleeding from this lesion is very small.
E. B and D
88 All of the following statements about esophaÂ�

geal dilation during upper endoscopy are true
except:
A. Patients with eosinophilic esophagitis (EE)
should not undergo dilation because they are
at very high risk of perforation.
B. The esophageal stricture should always be
dilated to the size of an uninvolved lumen for
symptom relief.
C. The greatest risk of esophageal dilation is
perforation.
D. The type of dilator used during the procedure
is a very important determinant of the risk of
perforation.
E. Proximal esophageal strictures are more likely
to perforate than mid or distal strictures. Figure for question 91
89 Early mucosa-associated lymphoid tissue (MALT)

lymphomas of the stomach can be difficult to dis- 92 A 54-year-old man who has undergone bilateral
tinguish from marked Helicobacter pylori gastritis. lung transplantation presents with midepigastric
Histologic features of the mucosa to assist the pain and nausea. He takes high-dose glucocorti-
differentiation include which of the following? coids and cyclosporine for acute rejection as well
A. Follicular colonization and invasion of germiÂ� as a proton pump inhibitor (PPI). Which one of the
nal centers of lymphoid follicles following studies should be performed next?
B. Destruction of gastric folds by lymphoid infilÂ� A. Upper GI series
trate (lymphoepithelial lesion) B. Upper endoscopy
C. Presence of plasma cells with Dutcher bodies C. Computed axial tomography (CAT) scan of the
(periodic acid–Schiff–positive intranuclear abdomen
inclusions) D. Gastric-emptying scan
D. All of the above
93 In polymyositis and dermatomyositis
90 In a patient with a history of food bolus impaction, A. Involvement is limited to skeletal muscle
symptoms of retrosternal chest pain can localize fibers.
the level of impaction to the middle of the B. Perforation of the esophagus and duodenal
esophagus. diverticulosis are frequent complications.
A. True C. Dermatomyositis is associated with an
B. False increased prevalence of malignancy.
D. Malabsorption and pseudo-obstruction occur
91 A 54-year-old white man presents for a screening commonly.
colonoscopy. He has not noticed any change in his E. The pathology is a result of antibodies against
bowel habits or any blood in the stool. He does not smooth muscle fibers.
have any GI symptoms. His family history is signifi-
cant for his father having colon cancer at 75 years 94 A 21-year-old man presents to the hospital emer-
of age. His laboratory test results show no abnor- gency department with food impaction while eating
mality in his complete blood count, metabolic a steak dinner. As upper endoscopy is performed,
Topics Involving Multiple Organs 21
the bolus spontaneously passes. EsophagogastroÂ� 98 All of the following statements regarding hyper-
duodenoscopy (EGD) shows no stenosis but longi- emesis gravidarum are true except:
tudinal furrows in the distal esophagus with A. It occurs in >15% of all pregnancies.
punctate white patches scattered over the mucosal B. It is defined by the presence of ketonuria and a
surface. There is no history of preceding heartburn, 5% decrease in prepregnancy weight.
but he has had multiple allergies in the past. All of C. As many as 20% of affected patients will have
the following statements about his diagnosis are symptoms until delivery.
true except: D. Symptoms may be exacerbated by higher
A. Dilation of the distal esophagus can be readily levels of human chorionic gonadotropin (HCG)
performed to prevent further impaction. such as with multiple gestations, trophoblastic
B. Biopsy specimens of the distal and midesophÂ� disease, and trisomy 21.
agus are expected to show >15 eosinophils E. Symptomatic treatment and hydration are the
per high-power field. mainstays of therapy.
C. Treatment with swallowed fluticasone should
be effective. 99 Which of the following treatments is the least
D. There is a personal history of atopy in 50% of appropriate treatment of gastroesophageal reflux
these patients. disease (GERD) in a pregnant patient?
A. Pantoprazole
95 A 32-year-old woman of Ashkenazi Jewish descent B. Omeprazole
who is 15 weeks pregnant was just admitted by the C. Ranitidine
high-risk obstetrics group because of multiple skin D. Sucralfate
lesions and odynophagia. She denies abdominal E. Lifestyle modifications
pain, but has had nausea for two weeks. She has
some constipation but has not noticed any blood in 100 When considering GI bacterial infections in patients
the stool. She states that she “was doing fine till with acquired immunodeficiency syndrome (AIDS),
three weeks ago when the skin lesions started.” Her all of the following are true except:
medical history is significant for appendectomy. A. Small bowel bacterial overgrowth is common
She is otherwise healthy and takes prenatal vita- in AIDS patients.
mins. On physical examination, she is afebrile. B. Salmonella, Shigella, and Campylobacter have
There are multiple erosions and pustules over the higher rates of bacteremia and antibiotic
skin on the arms, chest, abdomen, and thighs. resistance.
Similar lesions are seen in the oral cavity and C. They are more frequent and more virulent in
gingiva. All of the following statements about this human immunodeficiency virus (HIV)–infected
illness are true except: patients.
A. A definitive diagnosis of this condition is D. The most common bacterial infection is
made by biopsy and demonstration of antibody Clostridium difficile.
and complement in the basement membrane E. Mycobacterial infection most commonly
zone by immunofluorescence. involves the duodenum and may be suspected
B. Intravenous IgG has been used in the treatment at endoscopy by the presence of yellow
of this disorder. mucosal nodules, seen in the clinical setting of
C. Patients with serum IgG and IgA antibodies are malabsorption, bacteremia, and systemic
less likely to respond to medications. infection.
D. Oral ulcerations are present in 100% of
patients with this condition. 101 All of the following are useful in the staging of
E. Glucocorticoid medications, both topical and MALT lymphoma except:
systemic, have been used to treat this A. Endoscopic ultrasonography
condition. B. CT scan of the chest and abdomen
C. Upper airway examination
96 A 38-year-old woman who has been on oral contra- D. Bone marrow biopsy
ceptive pills for 18 years presents with abdominal E. Positron emission tomography
pain. A computed tomography (CT) scan shows
peritoneal nodules, and laparoscopy reveals mul- 102 All of the following statements about the relation-
tiple small, rubbery nodules along the peritoneum. ship between somatostatin and carcinoid tumors
What is the most appropriate treatment? are true except:
A. Hormone withdrawal A. Somatostatin and its analogs inhibit synthesis
B. Chemotherapy and release of peptides produced by carcinoid
C. Surgical debulking tumors.
D. Radiation B. They do not block the effects of amines and
peptides on target tissue.
97 Which of the following is/are true regarding esoph- C. Their role in carcinoid heart disease is
ageal strictures resulting from caustic ingestion? unclear.
A. They commonly develop two months after D. They have several side effects and are not very
injury. well tolerated by patients.
B. Primary treatment is frequent dilation. E. They are not effective in the treatment of
C. As many as 50% eventually need operative abdominal pain due to carcinoid tumor.
intervention.
D. A and B 103 A 46-year-old woman with type 2 diabetes, hyper-
E. All of the above tension, and gastroparesis was recently started on
22 Topics Involving Multiple Organs
nifedipine by her physician. She now presents with which she has started taking pain medication. She
a vague feeling of epigastric distress and worsening has no significant medical history, and before this,
early satiety. Her physical examination findings her only routine medication was a prenatal vitamin.
are unremarkable. An endoscopy performed two On physical examination, she is alert and oriented
months earlier for dyspepsia showed no abnormali- but appears uncomfortable and has a temperature
ties, but an upper GI series with barium contrast of 99.6°F. She has multiple lace-like lesions in
shows a gastric-filling defect. What is the most her oral cavity with overlying ulcerations and small
likely diagnosis? to medium, flat-topped pruritic and violaceous
A. Gastric ulcer papules all over her skin. All of the following state-
B. Gastric cancer ments about her condition are true except:
C. Lymphoma A. Upper GI endoscopy will likely show
D. Pharmacobezoar erythema, ulcers, and webs in the proximal
E. None of the above esophagus.
B. The condition should be treated with topical
104 A 60-year-old man is four months post–orthotopic and systemic glucocorticoids.
liver transplantation (OLT). He presents with C. The condition is associated with an increased
fever, malaise, myalgia, and an occasional cough. prevalence of chronic liver disease.
He is found to have elevated liver enzymes. D. Treatment of this condition will decrease the
His only medication is mycophenolate mofetil risk of the development of esophageal cancer.
(MMF). Which treatment should be started for his
condition? 108 A fragile, underweight 70-year-old woman is
A. Valgancyclovir brought to the emergency department with right
B. Ganciclovir lower abdominal pain. An obstructive series sug-
C. Acyclovir gests small bowel obstruction. An astute resident
D. Voriconazole notes that her pain is felt into the medial aspect of
the thigh with associated paresthesias. Hip flexion
105 A 16-year-old college student presents with symp- improves the pain, whereas extension of the hip
toms of abdominal pain, vomiting, and sporadic and medial rotation increase the pain. What is her
diarrhea. He has a serum albumin level of 2.3Â€g/dL most likely diagnosis?
and a creatinine level of 0.9Â€ mg/dL. His blood A. Unrecognized hip fracture
smear shows microcytosis and peripheral eosino- B. Femoral hernia
philia. The stool specimen will most likely show C. Obturator hernia
which of the following? D. Sciatic foramen hernia
A. C. difficile toxin
B. Charcot-Leyden crystals 109 What is the most common gastric lesion causing
C. Giardia severe protein loss?
D. Ova and parasites A. Ménétrier’s disease
B. H. pylori gastritis
106 A consult is requested on a hospitalized 24-year- C. Allergic gastroenteropathy
old white man with anemia and stools positive D. Systemic lupus erythematosus
for occult blood. He had been admitted to the gastroenteropathy
hospital because of a nonhealing ulcer over the
left medial malleolus that had not improved after 110 Which one of the following diseases causes
surgery for varicose veins on the left leg three constipation?
years ago. His medical history is significant for A. Addison’s disease
recurrent ulcer over the left medial malleolus, and B. Hyperparathyroidism
the patient’s parents report that he walks with a C. Hyperthyroidism
limp. On physical examination, there are multiple D. Medullary carcinoma of the thyroid
varicose veins over the left lower limb. There is
predominant left lower limb hypertrophy, with the 111 True statements regarding the relationship between
left limb being longer and larger. An x-ray shows carcinoid tumor of the gut and urine levels of
distinct soft tissue and osteohypertrophy of the 5-hydroxyindoleacetic acid (5-HIAA) include all of
left lower limb. A duplex scan of the left lower the following except:
limb shows massive superficial venous varicosities A. Urine excretion rates of 5-HIAA of
and multiple anastomoses between the superficial >25Â€mg/24Â€hr are diagnostic.
and deep venous systems. An angiogram shows B. The excretion rate of 5-HIAA in the urine
multiple arteriovenous fistulas. What is the most corresponds well with a carcinoid tumor mass.
likely diagnosis? C. Midgut carcinoid tumors are associated with
A. Klippel-Trénaunay syndrome an increased excretion rate of 5-HIAA in urine.
B. Blue rubber bleb nevus syndrome D. Foregut carcinoids may be associated with
C. Parkes Weber syndrome normal urinary levels of 5-HIAA.
D. Diffuse intestinal hemangiomatosis E. All of these statements are true.
E. None of the above
112 Which of the following statements regarding man-
107 A 29-year-old white woman who is 24 weeks preg- agement of carcinoid syndrome is most accurate?
nant presents with dysphagia and odynophagia that A. Serotonin antagonists such as methysergide,
started about a week ago and have progressed in ondansetron, and cyproheptadine provide
severity. She has pruritus and severe oral pain, for excellent control of flushing episodes.
Discovering Diverse Content Through
Random Scribd Documents
The Project Gutenberg eBook of The queen of the isle
This ebook is for the use of anyone anywhere in the United States
and most other parts of the world at no cost and with almost no
restrictions whatsoever. You may copy it, give it away or re-use it
under the terms of the Project Gutenberg License included with this
ebook or online at www.gutenberg.org. If you are not located in the
United States, you will have to check the laws of the country where
you are located before using this eBook.
Title: The queen of the isle

A novel
Author: May Agnes Fleming
Release date: February 2, 2024 [eBook #72860]
Language: English
Original publication: New York: G. W. Dillingham, Publisher, 1886
Credits: Al Haines
*** START OF THE PROJECT GUTENBERG EBOOK THE QUEEN OF

THE ISLE ***
THE
QUEEN OF THE ISLE.
A Novel.
BY
MAY AGNES FLEMING.

AUTHOR OF
"GUY EARLSCOURT'S WIFE," "THE ACTRESS' DAUGHTER,"
"A WONDERFUL WOMAN," "LOST FOR A WOMAN,"
"SILENT AND TRUE," "ONE NIGHT'S MYSTERY,"
"A TERRIBLE SECRET," "A MAD MARRIAGE,"
ETC., ETC.
NEW YORK:
COPYRIGHT, 1886.
G. W. Dillingham, Publisher,
SUCCESSOR TO G. W. CARLETON & Co.
LONDON: S. LOW, SON & CO.
MDCCCLXXXVI.
CONTENTS.
Chapter
I. Campbell's Isle
II. The Magic Mirror
III. The Maniac's Curse
IV. The Haunted Room
V. The Midnight cry
VI. "Off with the Old Love, and on with the New."
VII. The Heart's Struggle
VIII. The Triumph of Passion
IX. The Vision of the Isle
X. One of Fortune's Smiles
XI. The Storm—The Wreck
XII. Sibyl's Return to the Isle
XIII. The Meeting
XIV. Jealousy
XV. Self-Torture
XVI. Falsehood and Deceit
XVII. A Lull Before the Tempest
XVIII. The Fatal Note
XIX. That Day
XX. What Came Next
XXI. That Night
XXII. Next Morning
XXIII. Morning in the Island
XXIV. Christie
XXV. The Maniac's Story
XXVI. Remorse
XXVII. The Widowed Bridegroom
XXVIII. The Thunderbolt Falls
XXIX. The Devotion of Love
XXX. Sibyl's Doom
XXXI. The Bankrupt Heart
XXXII. Another Storm Within and Without
XXXIII. The Dead Alive
XXXIV. Explanations
XXXV. Meetings and Partings
THE QUEEN OF THE ISLE;

OR,
A HASTY WOOING.
CHAPTER I.
CAMPBELL'S ISLE.
"The island lies nine leagues away,
Along its solitary shore
Of craggy rock and sandy bay
No sound but ocean's roar,
Save where the bold, wild sea-bird makes her home,
Her shrill cry coming through the sparkling foam."—R. H. DANA.
About six miles from the mainland of M——, with its rock-bound coast
washed by the waters of the broad Atlantic, was an islet known in the days
of which I write as Campbell's Isle.
The island was small—about two miles in length and the same in
breadth, but fertile and luxurious. The dense primeval forest, which as yet
the destroying ax had scarcely touched, reared itself high and dark in the
northern part of the island. A deep, unbroken silence ever reigned here, save
when some gay party from the opposite coast visited the island to fish or
shoot partridges. Sometimes during the summer, pleasure parties were held
here, but in the winter all was silent and dreary on the lonely, isolated little
spot.
This island had been, from time immemorial, in the possession of a

family named Campbell, handed down from father to son. The people of the
surrounding country had learned to look upon them as the rightful lords of
the soil, "to the manner born." The means by which it had first come into
their possession were seldom thought of, or if thought of, only added to
their reputation as a bold and daring race. The legend ran, that long before
Calvert came over, a certain Sir Guy Campbell, a celebrated freebooter and
scion of the noble Scottish clan of that name, who for some reckless crime
had been outlawed and banished, and in revenge had hoisted the black flag
and become a rover on the high seas, had, in his wanderings, discovered
this solitary island, which he made the place of his rendezvous. Here, with
his band of dare-devils—all outlaws like himself—he held many a jolly
carousal that made the old woods ring.
In one of his adventures he had taken captive a young Spanish girl,

whose wondrous beauty at once conquered a heart all unused to the tender
passion. He bore off his prize in triumph, and without asking her consent,
made her his wife at the first port he touched. Soon, however, tiring of her
company on shipboard, he brought her to his island home, and their left her
to occupy his castle, while he sailed merrily away. One year afterward, Sir
Guy the Fearless, as he was called, was conquered by an English sloop-of-
war; and, true to his daring character, he blew up the vessel, and, together
with his crew and captors, perished in the explosion.
His son and successor, Gasper, born on the isle, grew up tall, bold, and
handsome, with all his father's daring and undaunted courage, and his
mother's beauty, and torrid passionate nature. He, in the course of time, took
to himself a wife of the daughters of the mainland; and, after a short, stormy
life, passed away in his turn to render an account of his works, leaving to
his eldest son, Hugh, the bold spirit of his forefathers, the possession of
Campbell's Isle, and the family mansion known as Campbell's Lodge.
And so, from one generation to another, the Campbells ruled as lords of
the isle, and became, in after years, as noted for their poverty as their pride.
A reckless, improvident race they were, caring only for to-day, and letting
to-morrow care for itself; quick and fierce to resent injury or insult, and
implacable as death or doom in their hate. Woe to the man who would dare
point in scorn at one of their name! Like a sleuth-hound they would dog his
steps night and day, and rest not until their vengeance was sated.
Fierce alike in love and hatred, the Campbells of the Isle were known
and dreaded for miles around. From sire to son the fiery blood of Sir Guy
the Fearless passed unadulterated, and throbbed in the veins of Mark
Campbell, the late master of the lodge, in a darker, fiercer stream than in
any that had gone before. A heavy-browed, stern-hearted man he was, of
whose dark deeds wild rumors went whispering about, for no one dared
breathe them aloud, lest they should reach his vindictive ears, and rouse the
slumbering tiger in his breast. At his death, which took place some two or
three years previous to the opening of our story, his son Guy, a true
descendant of his illustrious namesake, became the lord and master of the
isle, and the last of the Campbells.
Young Guy showed no disposition to pass his days in the spot where he
was born. After the death of his father, Guy resolved to visit foreign lands,
and leave Campbell's Lodge to the care of an old black servant, Aunt Moll,
and her son Lem, both of whom had passed their lives in the service of the
family, and considered that in some sort the honor of the house lay in their
hands.
Vague rumors were current that the old house was haunted. Fishermen
out, casting their nets, avowed that at midnight, blue, unearthly lights
flashed from the upper chambers—where it was known Aunt Moll never
went—and wild, piercing shrieks, that chilled the blood with horror, echoed
on the still night air. The superstitious whispered that Black Mark had been
sent back by his master, the Evil One, to atone for his wicked deeds done in
the flesh, and that his restless spirit would ever haunt the old lodge—the
scene, it was believed, of many an appalling crime. Be that as it may, the
old house was deserted, save by Aunt Moll and her hopeful son; and young
Guy, taking with him his only sister, spent his time in cruising about in a
schooner he owned, and—it was said, among the rest of the rumors—in
cheating the revenue.
Besides the lodge, or Campbell's Castle, as it was sometimes called, the

island contained but one other habitation, occupied by a widow, a distant
connection of the Campbells, who, after the death of her husband, had come
here to reside. The cottage was situated on the summit of a gentle elevation
that commanded an extensive view of the island; for Mrs. Tomlinson—or
Mrs. Tom, as she was always called—liked a wide prospect.
The most frugal, the most industrious of housewives was Mrs. Tom. No
crime in her eyes equaled that of thriftlessness, and all sins could be
pardoned but that of laziness. Unfortunately for her peace of mind, she was
afflicted with an orphan nephew, the laziest of mortals, whose shortcomings
kept the bustling old lady in a fever from morning till night. A wild young
sister of Mrs. Tom's had run away with a Dutch fiddler, and dying a few
years after, was soon followed to the grave by her husband, who drank more
than was good for him one night, and was found dead in the morning.
Master Carl Henley was accordingly adopted by his living relative and, as
that good lady declared, had been "the death of her" ever since.
A young girl of sixteen, known only as "Christie," was the only other
member of Mrs. Tom's family. Who this girl was, where she had come from,
and what was her family name, was a mystery: and Mrs. Tom, when
questioned on the subject, only shut her lips and shook her head
mysteriously, and spoke never a word. Although she called the old lady
aunt, it was generally believed that she was no relation; but as Christie was
a favorite with all who visited the island, the mystery concerning her,
though it piqued the curiosity of the curious, made them like her none the
less. A big Newfoundland dog and a disagreeable chattering parrot
completed the widow's household.
Mrs. Tom's business was flourishing. She made a regular visit each
week to the mainland, where she disposed of fish, nuts, and berries, in
which the island abounded, and brought back groceries and such things as
she needed. Besides that, she kept a sort of tavern and place of refreshment
for the sailors and fishermen, who sometimes stopped for a day or two on
the island; and for many a mile, both by land and sea, was known the fame
of Mrs. Tom.
Such was Campbell's Isle, and such were its owners and occupants. For
many years now it had been quiet and stagnant enough, until the
development of sundry startling events that for long afterward were
remembered in the country around and electrified for a time the whole
community.
CHAPTER II
THE MAGIC MIRROR.

"I turned my eyes, and as I turned surveyed
An awful vision."
The sun was sinking in the far west as the little schooner Evening Star
went dancing over the bright waves towards Campbell's Isle. Captain Guy
Campbell stood leaning negligently over the taffrail, solacing himself with a
cigar, and conversing at intervals with a slight, somewhat haughty-looking
young man, who stood beside him, watching the waves flashing, as they
sped along. No two could be more opposite, as far as looks went, than those
two, yet both were handsome and about the same age.
Like all his race, young Campbell was very tall, and dark as a Spaniard.
His short, black, curling hair shadowed a forehead high, bold, and
commanding. Dark, keen, proud eyes flashed from beneath jetty eye-brows,
and the firm, resolute mouth gave to his dark face a look almost fierce. His
figure was exquisitely proportioned and there was a certain bold frankness,
mingled with a reckless, devil-may-care expression in his fine face, that
atoned for his swarthy complexion and stern brows.
His companion was a tall, elegant young man, with an air of proud
superiority about him, as though he were "somebody," and knew it. His
complexion was fair as a lady's, and would have been effeminate but for the
dark, bold eyes and his dashing air generally. There was something
particularly winning in his handsome face, especially when he smiled, that
lit up his whole countenance with new beauty. Yet, with all, there was a
certain faithless expression about the finely formed mouth that would have
led a close observer to hesitate before trusting him too far. This, reader, was
Mr. Willard Drummond, a young half-American, half-Parisian, and heir to
one of the finest estates in the Old Dominion. The last five years he had
passed in Paris, and when he was thinking of returning home he had
encountered Campbell and his sister. Fond of luxury and ease as the young
patrician was, he gave up all, after that, for the attraction he discovered on
board the schooner Evening Star. And Captain Campbell, pleased with his
new friend, invited him to cross the ocean with him, and spend a few weeks
with him in his ancestral home, whither he was obliged to stop while some
repairs were being made in his vessel, which invitation Willard Drummond,
nothing loth, accepted.
"Well, Campbell, how is that patient of yours this evening?" inquired

Drummond, after a pause.
"Don't know," replied Captain Campbell, carelessly; "I haven't seen him
since morning. Sibyl is with him now."
"By the way, where did you pick him up? He was not one of your crew,
I understand."
"No; I met him in Liverpool. He came to me one day, and asked me to

take him home. I replied that I had no accommodations, and would much
rather not be troubled with passengers. However, he pleaded so hard for me
to accommodate him, and looked so like something from the other world all
the time, that I had not the heart to refuse the poor fellow. Before we had
been three days out at sea he was taken ill, and has been raving and
shrieking ever since, as you know."
"What do you suppose is the matter with him?"
"Well, I haven't much experience as nurse myself, but I think it's brain
fever, or something of that kind; Sibyl, however, thinks that bitter remorse
for something he has done is preying on his mind, and girls always know
best in these cases."
"He is, if I may judge by his looks, of humble station," said Mr.
Drummond, in an indifferent tone.
"Yes; there can be no doubt of that, though he appears to have plenty of

money."
"Has he given his name?"
"Yes; Richard Grove."
"Hum! Well, it would be unpleasant to have him die on board, of

course," said Drummond.
"Oh, I think he'll live to reach our destination; he does not appear to be
sinking very fast."
"We must now be quite near this island home of yours, Captain
Campbell; I grow impatient to see it."
"We shall reach it about moonrise to-night, if the wind holds as it is

now."
"And what, may I ask, do you intend doing with this—Richard Grove,
when you get there? Will you take him into your Robinson Crusoe castle
and nurse him until he gets well, as that enterprising canoe-builder did
Friday's father?
"No, I think not. There is an old lady on the island, who is never so
happy as when she has some one to nurse. I think we'll consign him to her."
"Then there is another habitation on the island beside yours?" said

Drummond, looking up with more interest than he had yet manifested.
"Yes; old Mrs. Tom, a distant connection of our family, I believe. And,
by the way, Drummond, there is a pretty little girl in the case. I suppose that
will interest you more than the old woman."
"Pretty girls are an old story by this time," said Drummond, with a
yawn.
"Yes, with such a renowned lady-killer as you, no doubt."
"I never saw but one girl in the world worth the trouble of loving," said
Drummond, looking thoughtfully into the water.
"Ah, what a paragon she must have been. May I ask what quarter of the
globe has the honor of containing so peerless a beauty?"
"I never said she was a beauty, mon ami. But never mind that. When do
you expect to be ready for sea again?"
"As soon as possible—in a few weeks, perhaps—for I fear that we'll all
soon get tired of the loneliness of the place."
"You ought to be pretty well accustomed to its loneliness by this time."
"Not I, faith! It's now three years since I have been there."
"Is it possible? I thought you Campbells were too much attached to your
ancestral home to desert it so long as that."
"Well, it's a dreary place, and I have such an attachment for a wild,
exciting life that positively I could not endure it. I should die of stagnation.
As for Sibyl, my wild, impulsive sister, she would now as soon think of
entering a convent as passing her life there."
"Yet you said it was partly by her request you were going there now?"
"Yes, she expressed a wish to show you the place." A slight flush of
pleasure colored the clear face of Drummond. "I don't know what's got into
Sibyl lately," continued her brother. "I never saw a girl so changed. She
used to be the craziest leap-over-the-moon madcap that ever existed; now
she is growing as tame as—as little Christie."
Drummond's fine eyes were fixed keenly on the frank, open face of
Captain Campbell; but nothing was to be read there more than his words
contained. With a peculiar smile he turned away, and said, carelessly:
"And who is this little Christie to whom you refer?"
"She's the protege of the old lady on the island—fair as the dream of an
opium-eater, enchanting as a houri, and with the voice of an angel."
"Whew! the bold Campbell, the daring descendant of old Guy the
Fearless, has lost his heart at last!" laughed Willard Drummond.
"Not I," answered Guy, carelessly. "I never yet saw the woman who
could touch my heart, and, please Heaven, never will."
"Well, here's a wonder—a young man of three-and-twenty, and never in
love! Do you expect me to believe such a fable, my good friend?"
"Believe or not, as you will, it is nevertheless true."
"What—do you mean to say you have never felt a touch of the grande
passion—the slightest symptom of that infectious disorder?"
"Pooh! boyish fancies go for nothing. I have now and then felt a queer
sensation about the region of my heart at the sight of sundry faces at
different times, but as for being fatally and incorrigibly in love, never, on
my honor!"
"Well, before you reach the age of thirty, you'll have a different story to
tell, or I'm mistaken."
"No; there is no danger, I fancy, unless indeed," he added, fixing his

eyes quizzically on Drummond's handsome face, "I should happen to meet
this little enchantress you spoke of awhile ago."
A cloud passed over the brow of his companion; but it cleared away in a
moment as a quick, light footstep was heard approaching, and the next
instant Sibyl Campbell, the haughty daughter of a haughty race, stood
bright, dazzling, and smiling before them.
No one ever looked once in the face of Sibyl Campbell without turning
to gaze again. Peerlessly beautiful as she was, it was not her beauty that
would startle you, but the look of wild power, of intense daring, of fierce
passions, of unyielding energy, of a will powerful for love or hate, of a
nature loving, passionate, fiery, impulsive, and daring, yet gentle and
winning.
She might have been seventeen years of age—certainly not more. In

stature she was tall, and with a form regally beautiful, splendidly
developed, with a haughty grace peculiarly her own. Her face was perfectly
oval: her complexion, naturally olive, had been tanned by sun and wind to a
rich, clear, gipsyish darkness. Her hair, that hung in a profusion of long
curls, was of jetty blackness, save where the sun fell on it, bringing out red
rings of fire. Her large Syrian eyes, full of passion and power, were of the
most intense blackness, now flashing with sparks of light, and anon
swimming in liquid tenderness. Her high, bold brow might have become a
crown—certainly it was regal in its pride and scorn. Her mouth, which was
the only voluptuous feature in her face, was small, with full, ripe, red lips,
rivaling in bloom the deep crimson of her dark cheeks.
Her dress was like herself—odd and picturesque, consisting of a short

skirt of black silk, a bodice of crimson velvet, with gilt buttons. She held in
one hand a black velvet hat, with a long, sweeping plume, swinging it gayly
by the strings as she came toward them.
She was a strange, wild-looking creature, altogether; yet what would

first strike an observer was her queenly air of pride, her lofty hauteur, her
almost unendurable arrogance. For her unbending pride, as well as her
surprising beauty, the haughty little lady had obtained, even in childhood,
the title of "Queen of the Isle." And queenly she looked, with her noble
brow, her flashing, glorious eyes, her dainty, curving lips, her graceful,
statuesque form—in every sense of the word "a queen of noble Nature's
crowning."
And Willard Drummond, passionate admirer of beauty as he was, what

thought he of this dazzling creature? He leaned negligently still against the
taffrail, with his eyes fixed on her sparkling, sunbright face, noting every
look and gesture as one might gaze on some strange, beautiful creation, half
in fear, half in love, but wholly in admiration. Yes, he loved her, or thought
he did; and gazing with him on the moonlit waves, when the solemn stars
shone serenely above him, he had told her so, and she had believed him.
And she, wild, untutored child of nature, who can tell the deep devotion, the
intense passion, the fiery, all-absorbing love for him that filled her
impulsive young heart?
"Love was to her impassioned soul

Not, as to others, a mere part
Of her existence; but the whole—
The very life-breath of her heart."
As she advanced, Willard Drummond started up, saying, gayly:
"Welcome back, Miss Sibyl. I thought the sunlight had deserted us

altogether; but you have brought it back in your eyes."
"How's your patient, Sibyl?" said Captain Campbell, who, not being in
love, found Mr. Drummond's high-flown compliments very tiresome
sometimes.
"Much worse, I am afraid," she answered in a peculiarly musical voice.

"I do not think he will live to see the morrow's sun. His ravings are frightful
to hear—some terrible crime seems to be weighing him down as much as
disease."
"After all, the human soul is an awful possession for a guilty man," said
Captain Campbell, thoughtfully. "Things can be smoothed over during life,
but when one comes to die—"
"They feel what retributive justice is, I suppose," said Drummond, in his
customary careless tone; "and apropos of that, somebody will suffer terrible
remorse after I die. I am to be murdered, if there is any truth in fortune-
telling."
He spoke lightly, with a half smile; but Sibyl's face paled involuntarily
as she exclaimed:
"Murdered, did you say? Who could have predicted anything so

dreadful?"
"An old astrologer, or enchanter, or wizard of some kind, in Germany,

when I was there. The affair seems so improbable, so utterly absurd, in
short, that I never like to allude to it."
"You are not fool enough to believe such nonsense, I hope," said
Captain Campbell.
"I don't know as it is nonsense. 'There are more things in heaven and
earth than are dreamed of in philosophy,' you know."
"Yes—I was sure you would quote that; everyone does that when he
advances some absurd doctrine; but it's all the greatest stuff, nevertheless."
"But did he tell you who you were to be—"
Sibyl stopped short; even in jest she could not pronounce the word.
"Murdered by?" said Willard, quietly finishing the sentence for her.
"No, he told me nothing. I saw it all."
"Saw it! How? I do not understand."
"Oh, the story is hardly worth relating, and ought not to be told in the
presence of such a skeptic as Captain Guy Campbell," said Drummond,
running his fingers lightly through his dark, glossy locks.
"Heaven forbid I should wait to be inflicted by it!" said Captain

Campbell, starting up. "I will relieve you of my presence, and allow you to
entertain my superstitious sister here with your awful destiny, of which she
will doubtless believe every word."
"I should be sorry to believe anything so dreadful," said Sibyl, gravely;

"but I do think there are some gifted ones to whom the future has been
revealed. I wish I could meet them, and find out what it has in store for
me."
"Let me be your prophet," said Drummond, softly. "Beautiful Sibyl,

there can be nothing but bliss for an angel like you."
Her radiant face flushed with pride, love, and triumph at his words.
"Do you believe in omens?" she said, laughingly. "See how brightly and
beautifully yonder moon is rising! Now, if it reaches the arch of heaven
unclouded, I shall believe your prediction."
Even as she spoke, a dense cloud passed athwart the sky, and the moon
was obscured in darkness.
The dark, bright face of Sibyl paled at the dread omen. Involuntarily her
eyes sought Drummond's who also had been gazing at the sky.
"Heaven avert the omen!" she cried, with a shudder. "Oh, Willard, the
unclouded moon grew dark even while I spoke."
"And now the cloud is past, and it sails on brighter than ever," he said,
with a smile. "See, fairest Sibyl, all is calm and peaceful once more. My
prediction will be verified, after all."
She drew a deep breath, and looked so intensely relieved that he

laughed. Sibyl blushed vividly, as she said:
"I know you must think me weak and childish; but I am superstitious by
nature. Dreams, inspirations, and presentiments, that no one else thinks of,
are all vivid realities to me. But you promised to tell me the German
wizard's prediction concerning your future, so, pray, go on."
"Well, let me see," said Willard Drummond, leaning his head on his
hand. "It is now three years ago that a celebrated Egyptian fortune-teller
visited the town in Germany where I resided. His fame soon spread far and
wide, and crowds of the incredulous came from every part to visit him. He
could not speak a word of any language but his own; but he had an
interpreter who did all the talking necessary, which was very little.
"I was then at a celebrated university; and, with two or three of my

fellow-students, resolved, one day, to visit the wizard. Arrived at his house,
we were shown into a large room, and called up one by one in the presence
of the Egyptian.
"Our object in going was more for sport than anything else; but when
we saw the first who was called—a wild, reckless young fellow, who feared
nothing earthly—return pale and serious, our mirth was at an end. One by
one the others were called, and all came back grave and thoughtful. By
some chance, I was the last.
"I am not, like you, bright Sibyl, naturally superstitious; but I confess,
when the interpreter ushered me into the presence of this wizard, I felt a sort
of chilly awe creeping over me. He was the most singular-looking being I
ever beheld. His face was exactly like that of one who has been for some
days dead—a sort of dark-greenish white, with pale-blue lips, and sharp,
Asiatic features. His eyes, black and piercingly sharp, looked forth from
two deep caverns of sockets, and seemed the only living feature in his
ghastly face. There were caldrons, and lizards, and cross-bones, and tame
serpents, and curious devices carved on the walls, ceiling and floor, and the
white, grinning skulls that were scattered about formed a hideously
revolting sight in that darkened room.
"The Egyptian stood before a smoking caldron, and, drawn up to his full
height, his size appeared almost colossal. His dress was a long, black robe,
all woven over with scorpions, and snakes, and other equally pleasing
objects, that seemed starting out dazzlingly white from this dark
background. Altogether, the room looked so like a charnel-house, and the
wizard so like a supernatural being, that I am not ashamed to own I felt
myself growing nervous as I looked around.
"The interpreter, who stood behind, opened the scene by asking me my

name, age, birthplace, and divers other questions of a like nature, which he
wrote down in some sort of hieroglyphics and handed to the Egyptian. Then
bidding me advance and keep my eyes fixed on the caldron and not speak a
word, the interpreter left the room.
"My heart beat faster than was its wont as I approached this strange
being, and found myself completely alone with him in this ghostly, weird
place. He took a handful of what I imagined to be incense of some kind, and
threw it on the red, living coals, muttering some strange sounds in an
unknown tongue as he did so. Presently a cloud of smoke arose, dense,
black, and suffocating, filling the whole room with the gloom of Tartarus.
Slowly, as if endowed with instinct, it lifted itself up and spread out before
me. And, looking up, I beheld—"
Willard Drummond paused, as if irresolute whether to reveal the rest or

not; but Sibyl grasped his arm, and in a voice that was fairly hoarse with
intense excitement, said:
"Go on."
"I saw," he continued, looking beyond her, as if describing something
then passing before him, "the interior of a church thronged with people.
Flowers were strewn along the aisles, and I seemed to hear faintly the grand
cadences of a triumphal hymn. A clergyman, book in hand, stood before a
bridal pair, performing the marriage ceremony. The features of the man of
God are indelibly impressed on my memory, but the two who stood before
him had their backs toward me. For about five seconds they remained thus
stationary, then it began to grow more indistinct; the forms grew shadowy
and undefined, and began to disappear. Just before they vanished altogether,
the faces of the wedded pair turned for an instant toward me, and in the
bridegroom, Sibyl, I beheld myself. The vapor lifted and lifted, until all was
gone, and nothing was to be seen but the black walls of the room and the
glowing, fiery coals in the caldron.
"Again the Egyptian threw the incense on the fire, and again mumbled
his unintelligible jargon. Again the thick, black smoke arose, filling the
room; and again became stationary, forming a shadowy panorama before
me. This time I saw a prison-cell—dark, dismal, and noisome. A rough
straw pallet stood on one side, and on the other a pitcher of water and a loaf
—orthodox prison fare from time immemorial. On the ground, chained to
the wall, groveled a woman, in shining bridal robes, her long midnight
tresses trailing on the foul floor. No words can describe to you the utter
despair and mortal anguish depicted in her crouching attitude. I stood spell-
bound to the spot, unable to move, in breathless interest. Then the scene
began to fade away; the prostrate figure lifted its head, and I beheld the face
of her whom a moment before seemed to stand beside me at the altar. But
no words of mine can describe to you the mortal woe, the unutterable
despair, in that haggard but beautiful face. Sibyl! Sibyl! it will haunt me to
my dying day. I put out my hand, as if to retain her, but in that instant all
disappeared."
Once more Willard Drummond paused; this time he was deadly pale,
and his eyes were wild and excited. Sibyl stood near him, her great black,
mystic eyes dilated, every trace of color fading from her face, leaving even
her lips as pale as death.
"The third time this strange enchanter went through the same ceremony
as before," continued he; "and, as in the previous cases, a new scene
appeared before me. Now, the time appeared to be night; and the place, a
dark, lonesome wood. A furious storm of lightning, and thunder, and rain,
was raging, and the trees creaked and bent in the fierce wind. On the ground
lay the dead body of a man weltering in blood. A dark, crimson stream
flowed from a great, frightful gash in his head, from which the life seemed
just to have gone. As the white face of the murdered man was upturned to
the light—cut, bloody, and disfigured as it was—Sibyl, I recognized myself
once more, As Heaven hears me, I saw it as plainly as I see yonder pale, fair
moon now. A white, ghostly form, whether of woman or spirit I know not,
seemed hovering near, darting, as it were, in and out amid the trees. Even as
I gazed, it grew thin and shadowy, until all was gone again.
"For the fourth and last time, the Egyptian threw a strange incense on
the fire, and 'spoke the words of power," and a new vision met my horrified
gaze. I seemed to behold an immense concourse of people, a vast mob,
swaying to and fro in the wildest excitement. A low, hoarse growl, as of
distant thunder, passed at intervals through the vast crowd, and every eye
was raised to an object above them. I looked up, too, and beheld a sight that
seemed freezing the very blood in my veins. It was a scaffold; and standing
on it, with the ignominious halter round her white, beautiful neck, was she
who had stood beside me at the altar, whom I had seen chained in her
prison-cell, doomed to die by the hand of the public hangman now. Her
beautiful hands were stretched out wildly, imploringly, to the crowd below,
who only hooted her in her agony and despair. The executioner led her to
the fatal drop, a great shout arose from the crowd, then all faded away; and
looking up, as if from an appalling dream, I saw the interpreter beckoning
me from the door. How I reeled from the room, with throbbing brow and
feverish pulse, I know not. Everything seemed swimming around me; and,
in a state of the wildest excitement, I was hurried home by my companions.
"The next day the Egyptian left the city, and where he went after, I
never heard.
"Such was the glimpse of the future I beheld. It was many months after
before I completely recovered from the shock I received. How to account
for it I do not know. Certain I am that I beheld it, truly, as I have told it in
every particular, for the impression it made upon me at the time was so
powerful that everything connected with it is indelibly engraven on my
memory. It may seem strange, absurd, impossible; but that I have nothing to
do with; I only know I saw it, incredible as it seems. But, good heaven!
Sibyl, dearest, are you ill—fainting!"
Pale, trembling, and excited, the once fearless Sibyl Campbell clung to
his arm, white with vague, sickening horror. Superstitious to an unusual
degree, an awful presentiment had clutched her heart; and, for a moment
she seemed dying in his arms.
"Sibyl! Sibyl! my dearest love!" he said, in alarm, "what is it?"
"Nothing—nothing," she answered, in a tremulous voice; "but, oh,

Willard! do you believe the prediction?"
"Strange, wild girl that you are! has this idle talk frightened you so?" he
said, smiling at her wild, dilated eyes.
"If it should prove true," she said, covering her face with a shudder.
"Willard, tell me—do you believe it?"
"My dark-eyed darling, how can I tell whether to believe it or not? It

has not come true, and there seems no likelihood of its ever doing so. Do
not think of it any more; if I had thought it would have unnerved you so, I
would never have told you."
"But, Willard, did any of his other predictions prove true?"
"I would rather not answer that question, Sibyl," he said, while a cloud
darkened for a moment his fine face.
"You must tell me," she cried, starting up, and looking at him with her
large, lustrous eyes.
"Well, then—yes," said Drummond, reluctantly. "Young Vaughn, one of

those who accompanied me, saw a funeral procession, and himself robed
for the grave lying in the coffin. Five weeks after, he was accidentally shot."
She put up her arm in a vague, wild sort of way, as if to ward off some
approaching danger.
"Oh, Willard! this is dreadful—dreadful! What if all he predicted should

come to pass!"
"Well, I should be obliged to do the best I could. What will be, will be—
you know. But I have no such fear. Nonsense, Sibyl! a Campbell of the Isle
trembling thus at imaginary danger!—the ghost of Guy the Fearless will
start from his grave, if he discovers it!"
The color came proudly back to her cheek at his bantering words, as she
said, more coldly and calmly:
"For myself, I could never tremble; but for——"
She paused, and her beautiful lip quivered.
"For me, then, dear love, those fears are," he said tenderly. "A thousand
thanks for this proof of your love: but, believe me, the cause is only
imaginary. Why, Sibyl, I had nearly forgotten all about the matter, until your
brother's remark to-night recalled it to my memory. Promise me, now, you
will never think of it more—much less speak of it."
"Tell me one thing more, Willard, and I promise—only one," said Sibyl,
laying her hand on his shoulder, and looking up in his face earnestly, while
her voice trembled in spite of all her efforts.
"Well," he said, anxiously.
"Did you recognize the face of the person whom you saw beside you at
the altar, and who afterward died on I the scaffold?"
He was silent, and looked with a troubled eye out over the shining
waters.
"Willard, dearest Willard! tell me, have you, ever yet seen her?"
"Why will you question me thus, dearest Sibyl?"
"Answer me truly, Willard, on your honor."
"Well, then, dearest, I have."
Sibyl drew her breath quick and short, and held his arm with a
convulsive grasp.
"Who is she?" she asked.
Willard turned, and looking steadily into her wild, searching eyes,
replied, in a thrilling whisper:
CHAPTER III.
THE MANIAC'S CURSE.

"Her wretched brain gave way,
And she became a wreck at random driven,
Without one glimpse of reason or of heaven."—LALLA ROOKH.
The schooner Evening Star lay at anchor in a little rock-bound inlet, on

the northern side of the island previously referred to. A boat had just put off
from her, containing Captain Guy Campbell, Mr. Willard Drummond, Sibyl
Campbell, and the sick passenger, Richard Grove. He lay on a sort of
mattress, half supported by Captain Campbell; and in the pale, cold
moonlight, looked wan and emaciated to a fearful degree. The features,
sharply defined, were like those of a skeleton, and, in their ghastly rigidity,
seemed like those of a corpse. But life, intensely burning life, shone in the
wild, troubled eyes. Willard Drummond and Sibyl sat talking together, in
low tones, at the other end of the boat, fearful of disturbing the dying man.
As the boat touched the shore, Drummond leaped out, and extended his
hand to Sibyl; but the wild sea-nymph, declining the needless aid, sprang
lightly out, and stood beside him.
The figure of a woman, who had been standing on a rock, watching

their approach, now came forward, exclaiming delightedly:
"Laws-a-massy, Miss Sibyl! Who ever s'posed we'd see you here again?
Where hev you been to this long time?"
"My dear Mrs. Tom!" said Sibyl, smilingly, holding out her hand; "I am
delighted to see you. Where I have been is a troublesome question to
answer, seeing I have been almost everywhere you could mention."
"Laws, now! hev you? 'Spect you had nice times sailin' round, though it
does seem odd how you could stand all the sea-sickness you must have
come through. 'Tain' every young critter would do it. But then you allus was
different from most young folks. Jemimi! how you've growed, an' how
handsome you've got! Jest as pooty as a picter! An' that, I s'pose, is young
Master Guy!" continued the loquacious new-comer, eagerly, as the young
captain leaped lightly ashore.
Sibyl nodded, and blushed slightly, as she encountered the gaze of

Drummond, who stood watching Mrs. Tom, with a half-smile of amusement
on his fine face.
"Master Guy!" said the officious Mrs. Tom, bustling forward; "you
hain't forgotten your old aunty, I hope? My gracious! you've got as tall as a
hop-pole! Growed out of my knowledge altogether!"
"Why, Mrs. Tom, is it possible?" exclaimed Captain Guy, catching her

hand in his hearty grasp. "Looking as young and smart as ever, too, and as
fresh and breezy as a May morning! 'Pon my word, I'm delighted to see you
looking so well! How is pretty Christie and Master Carl?"
"Oh, Christie is well enough, and pootier than ever; and, what's more,
she's as good as she's handsome. But Carl—oh, Master Guy! that there
young limb'll break my heart yet! I hain't the slightest doubt of it. Of all the
thrif'less, good-for-nothing lazy-bones—"
"Oh, well, Mrs. Tom, he'll outgrow that. The best thing you can do is to
let me take him to sea with me the next time I go, and that will cure him of
his laziness, if anything will. In the meantime, I have a patient for you to
take care of, if you have no objection. He can't last much longer, poor
fellow, and you are a better nurse than Sibyl. What do you say, Mrs. Tom?
Shall I send him up to your house?"
Mrs. Tom was a brown faced, black-eyed, keen-looking, wide-awake,

gossiping little woman, of four feet high, with a tongue that could, and did,
say sharp things sometimes; but with a heart so warm and large that it is a
wonder how it ever found room in so small a body. However, I have been
told, as a general thing, little people are, by far, cleverer and warmer-
hearted than their tall neighbors—as if nature were anxious to atone for
their shortened stature by giving them a double allowance of heart and
brains.
Nursing was Mrs. Tom's peculiar element. Nothing delighted her more
than to get possession of a patient, whom she could doctor back to health.
But unfortunately this desire of her heart was seldom gratified; for both
Carl and Christie were so distressingly healthy that "yarb tea" and "chicken
broth" were only thrown away upon them. Her frequent visits to the
mainland, however, afforded her an opportunity of physicking
indiscriminately certain unfortunate little wretches, who were always
having influenza, and measles, and hooping-cough, and other little
complaints too numerous to mention, and which fled before Mrs. Tom's
approach and the power of her "yarb tea." Of late there had been a "plentiful
scarcity" even of these escape-valves, so her eyes twinkled now with their
delight at the prospect of this godsend.
"Send him up? Sartinly you will, Master Guy. I'll take care of him. This
here's the best road up to the side of the rocks; 'tain't so rough as it is here."
"Lift him up," said Captain Campbell to the sailors who had rowed them
ashore, "Gently, boys," he said, as the sick man groaned. "Don't hurt him.
Follow Mrs. Tom to her cottage—that's the way. I'll be down early to-
morrow to see him, Mrs. Tom. This way, Drummond; follow me. I'll bid
you good-night, Mrs. Tom. Remember me to Christie."
And Captain Campbell sprang up the rocks, followed by Sibyl and

Drummond, in the direction of Campbell's Castle.
Mrs. Tom, with a rapidity which the two sturdy seamen found it difficult
to follow, burdened as they were, walked toward her cottage.
The home of Mrs. Tom was a low, one-story house, consisting of one
large room and bed-room, with a loft above, where all sorts of lumber and
garden implements were thrown, and where Master Carl sought his repose.
A garden in front, and a well-graveled path, led up to the front door, and
into the apartment which served as kitchen, parlor, dining-room, and
sleeping-room for Christie and Mrs. Tom. The furniture was of the plainest
description, and scanty at that, for Mrs. Tom was poor, in spite of all her
industry; but, as might be expected from so thrifty a housewife, everything
was like waxwork. The small, diamond-shaped panes in the windows
flashed like jewels in the moonlight; and the floors and chairs were
scrubbed as white as human hands could make them. Behind the house was
a large vegetable garden, nominally cultivated by Carl, but really by Mrs.
Tom, who preferred doing the work herself to watching her lazy nephew.
As the men entered with their burden, Mrs. Tom threw open the bed-
room door, and the sick man was deposited on the bed. Lights were brought
by Carl, a round-faced, yellow-haired, sleepy-looking youth, of fifteen, with
dull, unmeaning blue eyes, and a slow, indolent gait; the very opposite in
every way of his brisk, bustling little aunt.
"Be off with you to bed!" said Mrs. Tom. "It's the best place for any one
so lazy as you are. Clear out, now, for I'm going to sit up with this here sick
man, and want quiet."
With evident willingness Carl shuffled off, leaving Mrs. Tom alone with
her patient.
The little woman approached the bed, and looked at his pinched, sallow
features with an experienced eye. It was evident to her he could not survive
the night.
"I wonder if he knows his end's so near at hand?" said Mrs. Tom to
herself. "He ought to know, anyhow. I'll tell him when he awakes, 'cause it's
no use for me trying to do anything with him."
The man was not asleep. As she spoke he opened his large, wild-looking
black eyes, and gazed around vacantly.
"Mister," began Mrs. Tom, "I don't know your name, but 'taint no odds.
Do you know how long you have to live?"
"How long?" said the man, looking at her with a gaze so wild that, had
Mrs. Tom been the least bit nervous, would have terrified her beyond
measure.
"Not three hours," said Mrs. Tom gravely.
A sort of wild horror overspread the face of the dying man.
"So soon! oh, Heaven, so soon!" he murmured, "and with all

unconfessed still. I cannot die with this crime on my soul. I must reveal the
miserable secret that has eaten away my very life."
Mrs. Tom listened to this unexpected outburst in wonder and

amazement.
"Listen," said the man, turning to Mrs. Tom, and speaking rapidly in his
excitement. "One night, about thirteen years ago, as I was returning home
from my day's labor, I was overtaken by a violent storm. I was a
considerable distance from home, and there was no house near where I
could remain for the night. It was intensely dark, and I staggered blindly
along in the drenching rain until, by a sudden flash of lightning, I chanced
to espy the ruins of an old house, that had long been deserted. Thankful
even for this refuge from the storm, I entered it, and, retreating into a
corner, I sat on an empty box waiting for the tempest to abate.

Full Download Sleisenger and Fordtran S Gastrointestinal and Liver Disease Review and Assessment Expert Consult Online and Print 9e 9th Edition Anthony J. Dimarino MD PDF

Uploaded by

Copyright:

Available Formats

Full Download Sleisenger and Fordtran S Gastrointestinal and Liver Disease Review and Assessment Expert Consult Online and Print 9e 9th Edition Anthony J. Dimarino MD PDF

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Full Download Sleisenger and Fordtran S Gastrointestinal and Liver Disease Review and Assessment Expert Consult Online and Print 9e 9th Edition Anthony J. Dimarino MD PDF

Uploaded by

Copyright:

Available Formats

Get ebook downloads in full at ebookname.

Sleisenger and Fordtran s Gastrointestinal and

Explore and download more ebook at https://ebookname.com

Sleisenger and Fordtran s Gastrointestinal and Liver

Review of Orthopaedics Expert Consult Online and Print

Assisted Ventilation of the Neonate Expert Consult

Java Precisely third edition Peter Sestoft

Disgust and its disorders theory assessment and

Polymer Morphology Principles Characterization and

Everyday Surveillance Vigilance And Visibility In

Handbook of Neurocritical Care 1st Edition Wendy C.

Sleisenger and Fordtran’s GASTROINTESTINAL AND ISBN: 978-1-437-70730-4

Copyright © 2010 by Saunders, an affiliate of Elsevier Inc. All rights reserved.

Previous editions copyrighted 2007, 1999, 1996

Library of Congress Cataloging-in-Publication Data

Acquisitions Editor: Druanne Martin

Anthony J. DiMarino, Jr., MD

Howard S. Kroop, MD Susie Rivera, MD

Nicholas T. Orfanidis, MD Bridget Jennings Seymour, MD

Questions 5 The Wnt pathway is important in which of the fol-

C. IL-5 C. Large potentially antigenic macromolecules are

A. Stool DNA for TP53 B. Activation of nuclear factor-κB by IL-18

A. True A. Ulcerative colitis

hormone to have arexigenic effects. Lipase is an

the neighboring cells and also be released as neu- 13 D (S&F, ch1)

12 A (S&F, ch3) 16 C (S&F, ch2)

20 B (S&F, ch1) 26 B (S&F, ch3)

29 A (S&F, ch2) increase in the bax-to-bcl-2 ratio. Both pathways

42 A (S&F, ch3) 43 D (S&F, ch3)

51 Which of the following statements regarding calÂ� C. Dietary protein-induced enteropathy

A. It has no side effects. Which of the following statements is the most

Answers 45 A (S&F, ch4)

46 A (S&F, ch9) 52 A (S&F, ch4)

60 D (S&F, ch4) 65 A (S&F, ch4)

67 A (S&F, ch5) complications. All of the other choices, commonly

71 A (S&F, ch7) 76 B (S&F, ch6)

77 A (S&F, ch5) secretion of growth hormone. Leptin is associated

CLINICAL FEATURE OR COMPLICATION

ASSOCIATED WITH WEIGHT LOSS AND ASSOCIATED WITH PURGING OR REFEEDING

CLINICAL FEATURE OR COMPLICATION

ASSOCIATED WITH WEIGHT LOSS AND ASSOCIATED WITH PURGING OR REFEEDING

BODY MASS INDEX (KG/M2) NUTRITIONAL STATUS

Questions 84 A 20-year-old white woman who had hematochezia

88 All of the following statements about esophaÂ�

89 Early mucosa-associated lymphoid tissue (MALT)

Title: The queen of the isle

Author: May Agnes Fleming

Release date: February 2, 2024 [eBook #72860]

Original publication: New York: G. W. Dillingham, Publisher, 1886

*** START OF THE PROJECT GUTENBERG EBOOK THE QUEEN OF

QUEEN OF THE ISLE.

MAY AGNES FLEMING.

THE QUEEN OF THE ISLE;

This island had been, from time immemorial, in the possession of a

In one of his adventures he had taken captive a young Spanish girl,

Besides the lodge, or Campbell's Castle, as it was sometimes called, the

THE MAGIC MIRROR.

"Well, Campbell, how is that patient of yours this evening?" inquired

"No; I met him in Liverpool. He came to me one day, and asked me to