-IBIS-1.5.0-
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digestive system
peptic ulcer disease
diagnoses

definition and etiology

definition: a type of ulcer in the upper gastrointestinal tract that occurs in mucosa that has contact with acid and pepsin

etiology: Ulcers occur when the effects of acid and pepsin overwhelm the body's natural ability to defend itself with mucus production. There are two main types: duodenal ulcer and gastric ulcer.

• duodenal ulcer: Most ulcers of this type occur in the first part of the duodenum. They are typically round/oval, less than 1 cm in diameter, and are chronic and recurrent (60% of healed ulcers will recur within 1 year; and 80-90% will recur within 2 years). Predisposing factors for ulcer development include family history, cigarette smoking, and mental/emotional stress/anger/anxiety. Recent estimates suggest that up to 10% of the population will experience a duodenal ulcer at some time during their life. The condition is more common in males, (especially in their forties), and is more common than gastric ulcers. Duodenal ulcers appear to follow increased secretion of acid and pepsin, and are more common in patients with chronic obstructive lung disease, Zollinger-Ellison syndrome, cirrhosis and hyperparathyroidism, all of which are associated with increased serum gastrin.

• gastric ulcer: This type of ulcer is typically seen in patients in their 50s or older, and occur about equally in the sexes. Almost all are located in the antrum. Benign ulcers almost always occur with gastritis. Unlike duodenal ulcers, which appear to follow high acid-pepsin secretion, gastric ulcers are more often due to the lack of protection from the mucosal cells, as patients with gastric ulcers tend to have normal or even reduced amounts of HCl secretion. There is a strong association with consumption of aspirin, steroids and NSAIDs.

Some physicians have noted a strong correlation between gastric ulcers and gall bladder dysfunction (Easley).

Causal and/or Aggravating factors:
Decreased production of protective substances lining the stomach
Allergies
Abnormal bacterial flora produces urease. This converts urea present in the stomach, producing localized ammonia and bicarbonate. It migrates into the mucosa where it inhibits mucus secreting cells. It also produces protease and lipase which digest the mucus layer.
Poor nutritional status especially of Zinc, Vitamin A, Glutamine, EFA, Vitamin E
Smoking decreases bicarbonate and decreases gastric emptying time (Person, Ahlbom and Hellers. Gut 31:1377-81, 1990)
Aspirin increases membrane permeability and is irritating.
Caffeine and Alcohol both stimulate acid secretion.
NSAID
Xanthine oxidase
Chlorine


signs and symptoms

duodenal
: many patients with active disease will be asymptomatic

signs and symptoms:
epigastric pain: often burning, gnawing, or vague; pain is worse 2-3 hours after eating and frequently wakes the patient at night; pain is better with food or antacids
epigastric tenderness to palpation, worse on midline

lab findings:
(+) barium x-ray of upper GI
(+) endoscopy and/or duodenoscopy
CCK for gallbladder function
secretory tests and serum gastrin

gastric:

signs and symptoms:
epigastric pain: can often be made worse from food, and antacids help less than with duodenal ulcers
hemorrhage occurs in approximately 25% of patients; melena, hematemesis
anorexia, nausea and vomiting may occur

lab findings:
(+) Heliobacter pylori
(+) barium x-ray
(+) endoscopy
lab findings consistent with underlying conditions
lab findings due to complications: dehydration, hypokalemic acidosis with gastric retention; hemorrhage; increased WBC with left shift, dehydration, increased serum amylase with perforation

course and prognosis

• Duodenal
: Without treatment the ulcer can become chronic with persistent pain, and may perforate or cause hemorrhaging. Conventional treatment consists of antacids, H-2-receptor antagonists, anticholinergic agents, coating agents, and prostaglandins. Some conventional sources suggest that dietary recommendations are not necessary, although they do suggest that patients avoid caffeine and alcohol. Full healing typically occurs within 2-6 weeks, though recurrences are common where dietary and lifestyle factors remain unchanged.

• Gastric: Gastric ulcer may also progress to hemorrhage or perforation. A gastric ulcer perforation is 3 times more likely to be fatal than a duodenal, probably because the patients are usually older. Gastric ulcer patients should be watched closely: if an ulcer fails to heal to half its size within 3 weeks, gastric cancer must be ruled out. Healing typically occurs within 4-12 weeks. Conventional treatment consists of bedrest, antacids, and H-2-receptor antagonists. Antibiotics may be prescribed if Heliobacter pylori is suspected. Patients are recommended to avoid ASA, alcohol, and caffeine drinks.

differential diagnosis

pancreatitis
gastroenteritis
gall bladder disease
appendicitis
dyspepsia
coronary artery disease
stomach cancer


footnotes

Aiba Y, Suzuki N, Kabir A, Takagi A, Koga Y. Lactic acid-mediated suppression of Helicobacter pylori by the oral administration of Lactobacillus salivarius as a probiotic in a gnotobiotic murine model. Am J Gastroentol 1998;93(11):2097-2101.

Fendrick AM, Chernew ME, Hirth RA, Bloom BS, Bandekar RR, Scheiman JM. Clinical and Economic Effects of Population-Based Helicobacter pylori screening to prevent gastric cancer. Arch Intern Med 1999;159:142-148.

Kameshima H, Yagihashi A, Yajima T, Watanabe N. Helicobacter pylori infection induces telomerase activity in pre-malignant lesions. Am J Gastro 1999;4(2):547-548.

Laurila A, Bloigu A, Nayha S, Hassi J, Leinonen M, Saikku P. Association of Helicobacter pylori infection with elevated serum lipids. Atherosclerosis 1999;142(1):207-10.

Person, Ahlbom & Hellers. Inflammatory bowel disease and tobacco smoke a case control study. Gut 31:1377-81, 1990.
Abstract: A case control study was carried out in Stockholm, Sweden between 1984-87 to evaluate the association of childhood cigarette smoking and exposure to environmental tobacco smoke and the subsequent development of irritable bowel disease. Over 500 patients were evaluated and it was found that there was a significant increase risk of developing Crohns disease later in life if the child was exposed to secondary cigarette smoke.

Sawaoka H, Kawano S, Tsuji S, Tsuji M, Sun W, Gunawan ES, Hori M. Helicobacter pylori infection induces cyclooxygenase-2 expression in human gastric mucosa. Prostaglandins Leuko Essent Fatty Acids 1998;59(5):313-6.

Taha AS, Dahill S, Morran C, Hudson N, Hawkey CJ, Lee FD, et al. Neutrophils, Helicobacter pylori and nonsteroidal anti-inflammatory drug uses. Gastroentrol 1999;116:254-258.

Tien-Chien Tu, Chia-Long Lee, Chi-Hwa Wu, Tzen-Kwan Chen, Chung-Chuan Chan, Shih-Hung Huang, Shui-Cheng Lee. Comparison of invasive and noninvasive tests for detecting Helicobacter pylori infection in bleeding ulcers. Gastrointestinal Endoscop 1999;49(3 Pt 1):302-306.

Ozasa K, Kurata JH, Higashi A, Hayashi K, Inokuchi H, Miki K, et al. Helicobacter pylori infection and atrophic gastritis: A nested case-control study. Digestive Diseases and Sciences 1999;44(2):253-56.

Feldman M, Cryer B, Lee E, Peterson WL. Role of seroconversion in confirming cure of Helicobacter pylori infection. JAMA 1998;280(4): 363-365.