GASTROINTESTINAL PATHOLOGY PART1امراض الجهاز الهظمي الجزء الاول

محاضرات للاقسام الطبية لطلبة كلية الرافدين الجامعة
PATHOLOGY OF GASTRO INTESTINAl, DIGESTIVE SYSTEM part1 امراض المعدة والامعاء ,الجهاز الهظمي

The gastrointestinal (GI) system is specialized to process ingested particulate or liquid nutrients by reducing them to an “absorbable” size (digestion). This means that large, polymeric macromolecules (starches, lipids, proteins, and nucleic acids) must be reduced to their monomeric molecular subunits (e.g. – proteins to amino acids) for ease of transport across cell membranes of the GI mucosal lining. Four basic processes are necessary to complete this nutrient degradation:

(1) mechanical degradation (i.e.- chewing and churning);

(2) liquefaction via secretion of GI accessory glands (i.e.- salivary, hepatic, pancreatic secretions, etc.);

(3) enzymatic hydrolysis (i.e.- amylases break starch molecules into monosaccharide sugar subunits);

(4) absorption via extensive mucosal membrane surface of lower GI tract.

The entire GI tract is described as a “regionally specialized tube” with each region being specialized to carry out one or more of the above processes of digestion.

The esophagus is a muscular tube connecting the laryngopharynx and the stomach
cardia. The muscular component of the esophagus consists of two smooth muscle layers
within the wall, one with longitudinally oriented fibers and another with circular fibers.
Coordinated contractions of these two muscle layers produce peristaltic waves that move
food material toward the stomach. However, when a peristaltic wave begins at the
pharyngeal end of the esophagus, the cardia end must stretch to accommodate the
shortening. A congenitally short esophagus or one damaged by alcohol abuse can not
contract appropriately and peristaltic waves can pull a portion of the stomach cardia
through the hiatus of the diaphragm, a hiatal hernia. With hiatal hernias, stomach
digestive fluids are trapped in the herniated portion and are continually exposed to the
esophageal lining. The esophagus does not have the extensive mucus secretion that
protects the stomach lining and is subject to enzymatic erosion with resultant
inflammation (esophagitis).

stomach is well protected by copius mucus secretions, the stomach
lining is subject to inflammation (gastritis) from a variety of sources ranging from
microbial infection to alcohol abuse. A common cause of gastritis relates to excessive
acid ingestion, particularly salicylic acid (asprin).
Chronic inflammation of the stomach lining can lead to ulceration, but ulcers are
more common in either the duodenum or esophagus. Previously, these ulcerations of the
esophagus, stomach and duodenum were thought to be the result of excessive stomach
acid secretion, which exceeded the protective capacity of the mucus. Now, many of these
ulcers are known to have a bacterial cause. Without intervention, ulcerations can erode
completely through the GI tract wall (perforation) allowing septic contents into the body
cavity (coelom)