Page 578 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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564 C H A P T E R 14 Oral Cavity and Gastrointestinal Tract • Achalasia, characterized by incomplete LES relaxation,
timing is critical, because 5-year survival rates are 75% for increased LES tone, and esophageal aperistalsis, is a
patients with superficial esophageal carcinoma but much common form of functional esophageal obstruction.
lower for patients with more advanced tumors. Lymph
node metastases, which are common, are associated with • Esophagitis can result from chemical or infectious mucosal
poor prognosis. The overall 5-year survival rate remains a injury. Infections are most frequent in immunocompro-
dismal 9%. mised persons.
S U M M A RY • The most common cause of esophagitis is gastroesopha-
Diseases of the Esophagus geal reflux disease (GERD), which must be differentiated
from eosinophilic esophagitis.
• Esophageal obstruction may occur as a result of mechanical
or functional anomalies. Mechanical causes include devel- • Barrett esophagus, which may develop in patients with
opmental defects, fibrotic strictures, and tumors. chronic GERD, is associated with increased risk of esopha-
geal adenocarcinoma.
• Esophageal squamous cell carcinoma is associated with
alcohol and tobacco use, poverty, caustic esophageal
injury, achalasia, tylosis, and Plummer-Vinson syndrome.
STOMACH of an “unstirred” layer of fluid over the epithelium that pro-
tects the mucosa and has a neutral pH as a result of bicarbo
Disorders of the stomach are a frequent cause of clinical nate ion secretion by surface epithelial cells. Finally, the rich
disease, with inflammatory and neoplastic lesions being vascular supply to the gastric mucosa delivers oxygen,
particularly common. In the United States, symptoms bicarbonate, and nutrients while washing away acid that has
related to gastric acid account for nearly one third of all back-diffused into the lamina propria. Acute or chronic gas-
health care spending on gastrointestinal disease. In addi- tritis can occur after disruption of any of these protective
tion, despite a decreasing incidence in certain locales, mechanisms. For example, reduced mucin synthesis in
including the United States, gastric cancer remains a elderly persons is suggested to be one factor that explains
leading cause of death worldwide. their increased susceptibility to gastritis. Nonsteroidal
anti-inflammatory drugs (NSAIDs) may interfere with cyto-
The stomach is divided into four major anatomic regions: protection normally provided by prostaglandins or reduce
the cardia, fundus, body, and antrum. The cardia is lined bicarbonate secretion, both of which increase the susceptibil-
mainly by mucin-secreting foveolar cells that form shallow ity of the gastric mucosa to injury. Ingestion of harsh chemi-
glands. The antral glands are similar but also contain endo- cals, particularly acids or bases, either accidentally or as a
crine cells, such as G cells, that release gastrin to stimulate suicide attempt, also results in severe gastric injury, predomi-
luminal acid secretion by parietal cells within the gastric nantly as a consequence of direct damage to mucosal epithe-
fundus and body. The well-developed glands of the body lial and stromal cells. Direct cellular injury also is implicated
and fundus also contain chief cells that produce and secrete in gastritis due to excessive alcohol consumption, NSAIDs,
digestive enzymes such as pepsin. radiation therapy, and chemotherapy.
INFLAMMATORY DISEASE MORPHOLOGY
OF THE STOMACH
On histologic examination, mild acute gastritis may be difficult
Acute Gastritis to recognize, since the lamina propria shows only moderate
edema and slight vascular congestion. The surface epithe-
Acute gastritis is a transient mucosal inflammatory process lium is intact, although scattered neutrophils may be
that may be asymptomatic or cause variable degrees of present. Lamina propria lymphocytes and plasma cells are not
epigastric pain, nausea, and vomiting. In more severe cases prominent. The presence of neutrophils above the basement
there may be mucosal erosion, ulceration, hemorrhage, membrane—specifically, in direct contact with epithelial
hematemesis, melena, or, rarely, massive blood loss. cells—is abnormal in all parts of the gastrointestinal tract and
signifies active inflammation. With more severe mucosal
PAT H O G E N E S I S damage, erosion, or loss of the superficial epithelium, may
occur, leading to formation of mucosal neutrophilic infiltrates
The gastric lumen is strongly acidic, with a pH close to one— and purulent exudates. Hemorrhage also may occur, mani-
more than a million times more acidic than the blood. This festing as dark puncta in an otherwise hyperemic mucosa.
harsh environment contributes to digestion but also has the Concurrent presence of erosion and hemorrhage is termed
potential to damage the mucosa. Multiple mechanisms have acute erosive hemorrhagic gastritis.
evolved to protect the gastric mucosa (Fig. 14–13). Mucin
secreted by surface foveolar cells forms a thin layer of
mucus that prevents large food particles from directly touch-
ing the epithelium. The mucus layer also promotes formation
