Introduction to Gastrointestinal Diseases

178 Pages·2017·3.128 MB·English

by  Jakub Fichna

Jakub Fichna Editor
Introduction to
Gastrointestinal
Diseases Vol. 2
Introduction to Gastrointestinal Diseases Vol. 2
Jakub Fichna
Editor
Introduction to
Gastrointestinal
Diseases Vol. 2
Editor
Jakub Fichna
Department of Biochemistry
Medical University of Lodz
Mazowiecka, Lodz
Poland
ISBN 978-3-319-59884-0 ISBN 978-3-319-59885-7 (eBook)
DOI 10.1007/978-3-319-59885-7
Library of Congress Control Number: 2016955335
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Preface
Peptic ulcer disease (PUD) and colorectal cancer (CRC)—although distant in patho-
physiology (and, somewhat anecdotally, also spatially)—take an important toll
worldwide. It has been estimated that nearly 90 million new cases are noted every
year for PUD and about 1.4 million for CRC. Early diagnosis and high-end treat-
ment are crucial in both for their successful eradication, yet they are barely acces-
sible in most countries, being a heavy economic burden.
In the modern world, PUD and CRC are practically inevitable: the first one
because of widespread Helicobacter pylori, the major culprit for PUD propagation,
and both because of environmental and societal factors that particularly heavily
influence the development of the diseases. However, raising awareness of PUD and
CRC epidemiology and factors underlying etiopathology and promoting a healthy
lifestyle are believed to decrease—to some extent—the number of new cases.
Our goal when preparing this volume was not only to raise awareness and edu-
cate the patients but also to encourage the doctors to engage in this education. The
best specialists in the field—both basic scientists and clinicians—were invited to
comprehensively, yet in an informative manner, discuss the pathophysiology of
PUD and CRC. We hope that this volume will become a useful guideline for both
the patients and the doctors in PUD and CRC treatment as well as prevention.
Lodz, Poland Jakub Fichna
v
Contents
Part I Peptic Ulcer Disease
1 Physiology of the Stomach and the Duodenum . . . . . . . . . . . . . . . . . . 3
Jakub Fichna
2 Pathophysiology and Risk Factors in Peptic Ulcer Disease . . . . . . . . 7
Hubert Zatorski
3 C linical Features in Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . 21
Hubert Zatorski
4 Diagnostic Criteria in Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . 27
Paula Mosińska and Maciej Sałaga
5 Pharmacological Treatment of Peptic Ulcer Disease . . . . . . . . . . . . . . 39
Maciej Sałaga and Paula Mosińska
6 Surgical Treatment of Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . 53
Marcin Włodarczyk, Paweł Siwiński,
and Aleksandra Sobolewska-Włodarczyk
7 Patient’s Guide: Diet and Lifestyle in Peptic Ulcer Disease . . . . . . . . 65
Paula Mosińska and Andrzej Wasilewski
8 Patient’s Guide: Helicobacter pylori in Peptic Ulcer Disease . . . . . . . 83
Andrzej Wasilewski and Paula Mosińska
9 Patient’s Guide: Cooperation Between the Doctor
and the Patient in Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . . . 93
Adam Fabisiak and Natalia Fabisiak
Part II Colorectal Cancer
10 Epidemiology of Colorectal Cancer. . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Julia Krajewska
11 Pathogenesis of Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Adam I. Cygankiewicz, Damian Jacenik, and Wanda M. Krajewska
vii
viii Contents
12 Risk Factors in Colorectal Cancer. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Damian Jacenik, Adam I. Cygankiewicz, and Wanda M. Krajewska
13 Clinical Features of Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . 129
Marcin Włodarczyk and Aleksandra Sobolewska-Włodarczyk
14 Diagnosis and Screening in Colorectal Cancer . . . . . . . . . . . . . . . . . . 135
Łukasz Dziki and Radzisław Trzciński
15 S urgical Treatment in Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . 141
Michał Mik and Adam Dziki
16 C linical Treatment in Colorectal Cancer: Other Aspects . . . . . . . . . . 145
Agata Jarmuż and Marta Zielińska
17 Patient’s Guide in Colorectal Cancer: Prophylaxis,
Diet, and Lifestyle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
Marta Zielińska and Jakub Włodarczyk
18 Patient’s Guide in Colorectal Cancer: Observation After
Treatment and Treatment of Relapse . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Marek Waluga and Michał Żorniak
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177
Part I
Peptic Ulcer Disease
Physiology of the Stomach 1
and the Duodenum
Jakub Fichna
1.1 Anatomy and Physiology of the Stomach
Stomach is a muscular, J-shaped (when empty) organ located in the upper abdomen,
which lies on a variable visceral bed that includes the diaphragm, pancreas, and
transverse mesocolon. The relationship of the stomach to the surrounding viscera is
altered by the amount of its contents, the stage that the digestive process has reached,
the degree of development of the gastric musculature, and the condition of the adja-
cent intestines.
The empty stomach is only about the size of the fist but can stretch to hold as
much as 4 L of food and fluid, or more than 75 times its empty volume, and then
return to its resting size when empty.
The stomach is connected to the esophagus, at the gastroesophageal junction,
and the proximal part of the small intestine, duodenum. Based on histological dif-
ferences, it can be divided into five regions, i.e.:
– The cardia—below the esophagus; contains cardiac sphincter, which prevents
stomach contents from reentering the esophagus.
– The fundus—left of the cardia and below the diaphragm; usually contains air and
is thus visible radiographically.
– The body—main part of the stomach, in which mixing and digestion of the food
occurs.
– The pyloric antrum—where partly digested food awaits release to the small intestine.
– The pyloric canal—connecting the stomach to the small intestine; the pyloric sphinc-
ter, located in this part, controls the movement of digested food from the stomach to
the duodenum and prevents the contents of the latter reenter the stomach.
J. Fichna
Department of Biochemistry, Medical University of Lodz,
Mazowiecka 6/8, Lodz 92-215, Poland
e-mail: [email protected]
© Springer International Publishing AG 2017 3
J. Fichna (ed.), Introduction to Gastrointestinal Diseases Vol. 2,
DOI 10.1007/978-3-319-59885-7_1
4 J. Fichna
In the absence of food, the stomach deflates inward, and its mucosa and submu-
cosa fall into a large fold called a ruga.
The stomach wall consists of several layers, namely:
– The mucosa (mucous membrane)—the inner lining of the stomach that consists
of three components: the epithelial lining, the lamina propria, and the muscularis
mucosae. It contains specialized cells that produce hydrochloric acid (parietal
cells) and proteolytic enzyme pepsin (chief cells, in the inactive proenzyme form
of pepsinogen), mucus (mucous cells—the goblet cells which make up the sur-
face layer of the simple columnar epithelium, to protect the lining of the stom-
ach), and hormones (e.g., gastrin). Additionally, parietal cells secrete intrinsic
factor, which is necessary for the absorption of vitamin B12 in the small
intestine.
– The submucosa—a layer of loose areolar tissue with some elastic fibers, which
contains blood and lymph vessels, and nerve cells.
– The muscularis propria (muscularis externa)—the main muscular layer of the
wall, with three layers of smooth muscles: an inner oblique, middle circular, and
an external longitudinal layer.
– The serosa (visceral peritoneum)—a thin layer of loose connective tissue cover-
ing the stomach from the outside.
Gastric motility and secretion is controlled by both neural and hormonal signals.
The stomach receives innervation from several sources: (1) sympathetic fibers via
the splanchnic nerves and celiac ganglion (synapse) supply blood vessels and mus-
culature, (2) parasympathetic fibers from the medulla travel in the gastric branches
of the vagi, and (3) sensory vagal fibers include those concerned with gastric secre-
tion. A number of hormones have been shown to influence gastric motility—for
example, both gastrin and cholecystokinin act to relax the proximal stomach and
enhance contractions in the distal stomach.
Gastric secretion occurs in three phases: cephalic, gastric, and intestinal.
– The cephalic phase (reflex phase) of gastric secretion, which is relatively brief,
takes place before food enters the stomach. The smell, taste, sight, or thought of
food trigger this phase, and gastric secretion is, here, a conditioned reflex.
– The gastric phase of secretion lasts 3–4 h and is triggered by local neural and
hormonal mechanisms stimulated by the entry of food into the stomach.
– The intestinal phase of gastric secretion has both excitatory and inhibitory ele-
ments. The duodenum has a major role in regulating the stomach and its empty-
ing in this phase.
Physiological function of the stomach is mixing and digesting food, which is
also temporarily stored in this organ. The food in the stomach is transformed into a
liquid termed chyme, which, by rhythmic muscular contractions (peristalsis) of the
pyloric part, is emptied into the duodenum for absorption. In this process, called
gastric emptying, rhythmic mixing waves force about 3 mL of chyme at a time