Porth's Essentials of Pathophysiology, 4e

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Disorders of Gastrointestinal Function

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HCO 3 – production is equal to H + secretion, mucosal injury does not occur. Changes in gastric blood flow, as in shock, tend to decrease HCO 3 – production. This is particularly true in situations in which decreased blood flow is accompanied by acidosis. 16 Prostaglandins, chemical mediators derived from cell membrane lipids, play an important role in protecting the gastric mucosa from injury. 6 The prosta- glandins exert their effects through several mechanisms, including improved mucosal blood flow, decreased acid secretion, increased bicarbonate secretion, and enhanced mucus production. The fact that drugs such as aspirin and the nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis contributes to their abil- ity to produce gastric mucosal irritation and injury. Gastritis Gastritis refers to inflammation of the gastric mucosa. There are many causes of gastritis, most of which can be associated with either acute or chronic gastritis. Acute Gastritis Acute gastritis is characterized by an acute mucosal inflammatory process, usually transient in nature. The inflammation may be accompanied by hemorrhage into the mucosa of the stomach and, in severe cases, by sloughing of the superficial mucosa and acute gastric bleeding. The condition is most commonly associated with local irritants such as aspirin or other NSAIDs, alcohol, or bacterial toxins. 6,17 Oral administration of corticosteroid drugs, which inhibit prostaglandin syn- thesis, may also cause acute hemorrhagic gastritis. Any serious illness or trauma that is accompanied by pro- found physiologic stress renders the gastric mucosa more vulnerable to acute hemorrhagic gastritis (dis- cussed under stress ulcers). 7 Uremia, treatment with can- cer chemotherapy drugs, and gastric radiation are other causes of acute gastritis. The complaints of persons with acute gastritis vary. Persons with aspirin-related gastritis can be totally unaware of the condition or may complain only of heart- burn or sour stomach. Gastritis associated with exces- sive alcohol consumption is often a different situation; it often causes transient gastric distress, which may lead to vomiting and, in more severe situations, to bleeding and hematemesis. Gastritis caused by the toxins of infec- tious organisms, such as the staphylococcal enterotox- ins, usually has an abrupt and violent onset, with gastric distress and vomiting ensuing approximately 5 hours after the ingestion of a contaminated food source. Acute gastritis usually is a self-limiting disorder, with complete regeneration and healing of the gastric mucosa occur- ring within several days of removal of the inciting agent. Chronic Gastritis Chronic gastritis is characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes, eventually leading to atrophy of – is produced, and as long as HCO 3

Disorders of the Stomach The stomach is a reservoir for contents entering the digestive tract. It lies in the upper abdomen, anterior to the pancreas, splenic vessels, and left kidney. Anteriorly, the stomach is bounded by the anterior abdominal wall and the left inferior lobe of the liver. While in the stom- ach, food is churned and mixed with hydrochloric acid (HCl) and pepsin before being released into the small intestine. Normally, the mucosal surface of the stom- ach provides a barrier that protects it from the hydro- chloric acid and pepsin contained in gastric secretions. Disorders of the stomach include gastritis, peptic ulcer, and gastric carcinoma. Gastric Mucosal Barrier The stomach lining usually is impermeable to the acid it secretes, a property that allows the stomach to con- tain acid and pepsin without having its walls digested. Several factors contribute to the protection of the gastric mucosa, including an impermeable epithelial cell surface covering, coupled secretion of hydrogen (H + ) and bicar- bonate (HCO 3 – ) ions, and the characteristics of gastric mucus. 16 These mechanisms are collectively referred to as the gastric mucosal barrier. The cells of the epithelial layer of the stomach are connected by tight junctions that prevent acid pen- etration, and they are covered with an impermeable hydrophobic lipid layer that prevents diffusion of ion- ized water-soluble molecules. Aspirin, which is nonion- ized and lipid soluble in acid solutions, rapidly diffuses across this lipid layer, increasing mucosal permeability and damaging epithelial cells. 16,17 Gastric irritation and occult bleeding occur in a significant number of persons who take aspirin on a regular basis. Alcohol, which is lipid soluble, can also disrupt the mucosal barrier. When there is reflux of duodenal contents in the stom- ach, bile acids also can attack the lipid components of the mucosal barrier and produce gastric irritation. Normally, the secretion of HCl by the parietal cells of the stomach is accompanied by secretion of HCO 3 – (see Chapter 28, Fig. 28-9). For every H + that is secreted, a ■■ Gastroesophageal reflux is a common problem in infants and children. Symptoms are typically mild and abate in most children by 2 years of age. However, some infants and small children have significant reflux that interferes with feeding, causes esophagitis, and results in respiratory symptoms and other complications. ■■ Cancer of the esophagus is a relatively uncommon form of cancer that is commonly linked to gastroesophageal reflux and Barrett esophagus (adenocarcinoma) or alcohol and tobacco use (squamous cell carcinoma).