Pathophysiology

Hydrochloric acid and pepsin destroy gastric and duodenal mucosa. Mucous and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucous and bicarbonate production and by enhancing mucosal blood flow, thereby supporting metabolism. Ihe balance between these protective and destructive forces determines whether peptic ulcer disease will occur. Helicobacter pylon infection or NSAIDs are thought to be the causal agents of peptic ulcer disease in almost all cases.12 Helicobacter pylori infection is present in 95 percent of duodenal ulcers and 80 percent of gastric ulcers. 9 Although traditional treatment of peptic ulcers by various modalities heals most ulcers, eradication of H. pylori reduces recurrence rates from 80 to 15 percent for duodenal and from 50 to 10 percent for gastric ulcers.9 Helicobacter pylori is a spiral, urease-producing, flagellated bacterium that is found living between the mucous gel and the mucosa primarily in the gastric antrum.68 Ihe production of urease, cytotoxins, proteases, and other compounds is thought to disturb the mucous gel and cause tissue injury. 28 In the presence of acid and pepsin, ulceration may occur. Chronic active (usually asymptomatic) gastritis is an almost universal finding with H. pylori infection, but only 10 to 20 percent of infected people develop peptic ulcer disease. 8,10 It is unclear why most infected persons do not develop symptomatic peptic ulcer disease, but it most likely reflects an interaction of factors, including both host and pathogen (different virulence of strains of bacteria). 10

Helicobacter pylori has been linked to mucosa-associated lymphoid tissue (MALI) lymphoma, and regression has been documented with eradication of infection. In addition, H. pylori infection is considered a definite risk factor for adenocarcinoma of the stomach. However, since the prevalence of gastric cancer in the United States is very low and the H. pylori infection rate very high, other factors undoubtedly are involved.89

NSAIDs inhibit prostaglandin synthesis, thereby decreasing mucous and bicarbonate production and mucosal blood flow, allowing ulcer formation. 2 Gastrin-secreting tumors produce ulceration due to high levels of acid and pepsin production, but acid alone rarely causes ulceration. 1 1! However, inhibition of acid secretion may allow ulcers to heal and is the basis for traditional ulcer treatments.

Hereditary factors cause a predisposition to peptic ulcer disease. Ihere is an association between chronic renal failure, renal transplantation, cirrhosis, and chronic obstructive pulmonary disease and peptic ulceration, but the precise mechanism is unclear. Cigarette smoking is a predisposing factor for peptic ulcer disease, perhaps due to an inhibition of bicarbonate ion production or to increased gastric emptying (but not to increased acid production). Emotional stress may predispose to peptic ulcer disease, but diet and alcohol use do not.

Acute gastritis may be related to ischemia from severe illness (shock, trauma, severe burns, organ failure, etc.) or the direct toxic effects of agents (NSAIDs, alcohol, bile acids, etc.). Helicobacter pylori infection causes both acute and chronic gastritis (both usually asymptomatic). Chronic gastritis may also be caused by autoimmune factors that destroy gastric parietal cells, resulting in the loss of acid production and the loss of intrinsic factor production, which in turn cause malabsorption of vitamin B12 and therefore pernicious anemia.

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