Page 579 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

NORMAL INJURY Inflammatory Disease of the Stomach 565
Damaging Forces: H. pylori infection
Gastric acidity NSAID ULCER
Peptic enzymes Aspirin
Cigarettes
Mucus Alcohol
Gastric hyperacidity
Duodenal-gastric

reflux

Mucosa Defensive INJURIOUS EXPOSURES Necrotic (N)
Muscularis Forces: OR debris

mucosae Surface mucus IMPAIRED DEFENSES Acute
Submucosa secretion Ischemia inflammatory (I)
Shock cells
Bicarbonate Delayed gastric
secretion into mucus emptying Granulation (G)
Host factors tissue
Mucosal blood flow
Apical surface Fibrosis (S)

membrane transport
Epithelial regenerative

capacity
Elaboration of

prostaglandins

Figure 14–13 Mechanisms of gastric injury and protection. This diagram illustrates the progression from more mild forms of injury to ulceration that
may occur with acute or chronic gastritis. Ulcers include layers of necrotic debris (N), inflammation (I), and granulation tissue (G); a fibrotic scar (S),
which develops over time, is present only in chronic lesions.

Acute Peptic Ulceration MORPHOLOGY

Focal, acute peptic injury is a well-known complication of Lesions described as acute gastric ulcers range in depth from
therapy with NSAIDs as well as severe physiologic stress. shallow erosions caused by superficial epithelial damage to
Such lesions include deeper lesions that penetrate the mucosa. Acute ulcers are
• Stress ulcers, most commonly affecting critically ill rounded and typically are less than 1 cm in diameter. The
ulcer base frequently is stained brown to black by acid-
patients with shock, sepsis, or severe trauma digested extravasated red cells, in some cases associated with
• Curling ulcers, occurring in the proximal duodenum and transmural inflammation and local serositis. While these
lesions may occur singly, more often multiple ulcers are
associated with severe burns or trauma present within the stomach and duodenum. Acute stress
• Cushing ulcers, arising in the stomach, duodenum, or ulcers are sharply demarcated, with essentially normal adja-
cent mucosa, although there may be suffusion of blood into
esophagus of persons with intracranial disease, have a the mucosa and submucosa and some inflammatory reaction.
high incidence of perforation The scarring and thickening of blood vessels that characterize
chronic peptic ulcers are absent. Healing with complete
PATHOGE NESIS reepithelialization occurs days or weeks after the injurious
factors are removed.
The pathogenesis of acute ulceration is complex and incom-
pletely understood. NSAID-induced ulcers are caused by Clinical Features
direct chemical irritation as well as cyclooxygenase inhibition, Symptoms of gastric ulcers include nausea, vomiting, and
which prevents prostaglandin synthesis. This eliminates the coffee-ground hematemesis. Bleeding from superficial
protective effects of prostaglandins, which include enhanced gastric erosions or ulcers that may require transfusion
bicarbonate secretion and increased vascular perfusion. develops in 1% to 4% of these patients. Other complica-
Lesions associated with intracranial injury are thought to be tions, including perforation, can also occur. Proton pump
caused by direct stimulation of vagal nuclei, which causes inhibitors, or the less frequently used histamine H2 recep-
gastric acid hypersecretion. Systemic acidosis, a frequent tor antagonists, may blunt the impact of stress ulceration,
finding in critically ill patients, also may contribute to mucosal but the most important determinant of outcome is the
injury by lowering the intracellular pH of mucosal cells. severity of the underlying condition.
Hypoxia and reduced blood flow caused by stress-induced
splanchnic vasoconstriction also contribute to acute ulcer
pathogenesis.