PART THIRTEEN PEPTIC ULCER

Clinical Presentation

Castritis represents a nonspecific inflammation of the stomach. Clinically, the three most common and important causes of gastritis are infection with the bacteria Helicobacter pylori, ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs), and stress-related mucosal changes.

Helicobacter pylori H. pylori is a gram-negative, curved, flagellated rod found only in gastric epithelium or in gastric metaplastic epithelium. H. pylori clearly causes histo-logic gastritis and is found in 80% to 95% of patients with duodenal ulcers and 70 % to 90 % of patients with gastric ul-cers. However, only a minority of patients with H. pylori gas-tritis develop peptic ulcer disease or gastric cancer. There is a clear age-related prevalence of H. pylori infection in healthy subjects, increasing from 10 % in those younger than age 30 to 60% in subjects older than age 60 in the Western world. The majority are infected early in life, although the mode of trans. mission remains unknown. H. pylori colonization is more com-mon in blacks, individuals in lower socioeconomic classes, and inhabitants of custodial institutions. In the developing world, infection is far more common, with over 80% of the popula-tion infected by age 20. Infection with H. pylori typically is lifelong unless treated.

H. pylori is a noninvasive organism that colonizes the mu-cus layer overlying gastric epithelium. Factors important in the organism's ability to colonize the stomach include its flagellae, which facilitate locomotion, ability to adhere to the mucus lay-er, and production of urease. Urease increases juxtamucosal pH, creating a more hospitable microclimate than that of the acidic stomach. Colonization causes acute and chronic inflam-mation consisting of neutrophils, plasma cells, T cells, and macrophages accompanied by varying degrees of epithelial cell injury, all of which resolve after treatment.

The ultimate clinical outcome of infection depends on a complex interplay between virulence factors of the organism, the host response, environmental factors, and age at the time of infection. It is now clear that there are many different strains of H. pylori with different virulence factors. Two such virulence factors are the vacA and cagA genes. The vacA gene encodes a vacuolating cytotoxin that directly damages epithelial cells and is more common in patients with peptic ulcer disease. There is a strong association between production of the vacuo-lating cytotoxin and presence of the cagA gene, both of which are more common in patients with peptic ulcer disease. The most common endpoint of H. pylori infection is chronic super-ficial gastritis, which may persist for years. Duodenal and gas-tric ulcers develop in the minority of infected patients. Atroph-ic gastritis is another end result of infection that may increase the risk of gastric cancer. Finally, the mucosal lymphocytic response to H. pylori infection may lead to a monoclonal B cell proliferation in mucosa-associated lymphoid tissue (MALT) lymphoma.

Nonsteroidal Anti-inflammatory Drugs The NSAIDs are among the most widely used classes of drugs. There is a clear relationship between ingestion of NSAIDs and injury to the gastrointestinal tract. Two types of mucosal injury are caused by NSAIDs. The first form develops after acute inges-tion and is related to direct topical injury to mucosal cells. A-cute ingestion of aspirin enhances mucosal permeability by low-ering the mucosal potential difference and enhancing back-dif-fusion of hydrogen ions. Hyperemia, subepithelial hemor-rhage, and superficial erosions are seen endoscopically, al-though these lesions are typically asymptomatic. Microscopi-cally, there is a "reactive" pattern of injury characterized by little or no increase in inflammatory cells, With longer term NSAID use, these lesions disappear and frank ulceration may develop. Chronic NSAID ingestion results in inhibition of gas-troduodenal mucosal prostaglandin synthesis caused by inhibi-tion of the enzyme eyclooxygenase, and hence a decrease in mucus and bicarbonate production and mucosal blood flow.

Stress-Related Gastric Mucosal Damage Whereas mu-cosal damage develops in the majority of critically ill patients, there is a low incidence of clinically significant upper gastroin-testinal bleeding. The etiology of stress-related mucosal injury is multifactorial. Mucosal ischemia caused by decreased blood flow (from shock, hypotension, or catecholamine release) im-pairs mucosal resistance to acid back-diffusion, Hyperemia of the mucosa evolves into erosions and then frank ulceration in the stomach and duodenum, which may go on to bleed.

A variety of prophylactic treatment strategies are effective in preventing upper gastrointestinal bleeding in critically ill pa-tients although there is no proof that prophylaxis decreases mortality. Antacids administered every 2 hours neutralize gas-tric acid but are inconvenient to use because of increased nurs-ing time and diarrhea. Sucralfate at a dose of 1 g every 6 hours is also effective but requires placement of a nasogastric tube. H2 receptor antagonists given as either a continuous infusion or by bolus injection every 12 hours in the case of more potent a-gents such as famotidine or ranitidine are safe, convenient, and should be titrated to an intragastric pH of greater than 4 to minimize the activity of pepsin. Studies now show that admin-istration of Ha receptor antagonists does not increase the risk of of pneumonia in these patients.

Studies suggest that routine prophylaxis is no longer indi-cated in all critically ill patients. Coagulopathy and respiratory failure requiring mechanical ventilation for 48 hours are clear risk factors for clinically significant bleeding in the intensive care unit. Other patients who need prophylaxis include those with central nervous system trauma, burns, organ transplanta-tion a history of peptic ulcer disease with or without bleeding, multiorgan failure, trauma, and major surgery.

There are a wide variety of other causes of gastritis. Atrophic gastritis is characterized by a variable loss of g&stric glands accompa-nied by varying degrees d intestinal metaplasia. Multifocal gastric atrophy is associated with chrome H. pylori infection and is espe-cially common in populations at increased risk for adenocarcinoma of the stomach. Atrophy of the oxyntic mucosa may also be encoun-tered in the elderly and is accompanied by achlorhydria or hypochlorhydria. Gastric atrophy may also be encountered in pa-tients with pernicious anemia, which is characterized by malabsorp-tion d vitamin B12, absolute achlorhydria, and megaloblastic ane-mia. Atrophy in these patients is autoimmune in etiology, with an-tib0dies to intrinsic factor. A variety of uncommon digorders may cause gastritis. Lymphocytic gastritis is characterized by a mononu-clear infiltration of T cells. Often in association with celiac disuse, collagenous/lymphocytic colitis, and Mfinfitrier' s disease. Eosinophilic gastritis is characterized by an eosinophilic infiltration d any of the layers of the stomach. Especially in the antrum. M¡§¦n¡§¦trier's disease is characterized by glant gastric folds in the fun-dus and the body of the stomach, with a histologic appearance of increased mucosal thickness, glandular atrophy, and an increase in the size of the gastric pits. A variety of infections may involve the stomach in addition to H. pylori. These are typically seen in irn-munocompmmised patients in the setting of human immunoddi-ciency virus infection, chemotherapy, or organ transplantation. Some of the more important infections include tuberculosis, syphilis, and cytomegalovirus infection, although many other fungi and parasitic infections are possible. Systemic diseases such as sar-coid and Crohn' s disease may also involve the stomach. Both will have characteristic granulomas histologically.

Gastritis in traditional Chinese medicine pertains to the categories of "pi" (feeling of fullness in the upper abdomen ), "wei wan tong" (stomachache), etc.

1. The chief symptoms are chronic upper abdominal pain, fullness and discomfort, belching and acid regurgitation which often occur after meals. Mild hemorrhage of upper digestive tract may be induced by some precipitating factors in a few cases. Severe atrophic gastritis may be accompanied with ane-mia and pathologic leanness.

2. Physical examination reveals mild but diffuse tender-ness in the upper abdominal region.

3. Laboratory examination:

(1) Gastric juice analysis: Gastric acid is normal in super-ficial gastritis, but mostly reduced or gone in atrophic gastri-tis.

(2) X-ray barium examination: Positive rate is not high. Atrophic gastritis presents gastric hypotension, triviality or disappearance of gastric mucosal folds. The main purpose of radiological examination is to exclude peptic ulcer and cancer.

(3) Gastrofiberscope : This method is most contributive in confirming diagnosis. Through it superficial mucosal erosion with hyperemia, swelling or red spots and increased ropy liq-uid could be discovered in chronic superficial gastritis; in chronic atrophic gastritis, such findings can be caught as thinned and greyish-pale mucosa, slenderized mucosal folds with exposure of submucosal vessels, and granular or nodular proliferation. The combined application of gastrofiberscope and biopsy proves to be an accurate method for the diagnosis of chronic gastritis.

1. Stagnation of the Stomach-q/:

Clinical manifestations: Epigastric distension and fullness or pain, loss of appetite, indigestion, or diarrhea, white coat-ing of the tongue, and slippery pulse.

Therapeutic method: Regulating the stomach-q/ to re-lieve distension and fullness.

Recipe: Pinellia Decoction for Purging Stomach-fire.

Ingredients:

Rhizoma Pinelliae 9g

Rhizoma Zingiberis 9g

Radix Scutellariae 9g

Rhizoma Coptididis 6g

Radix Codonopsis Pilosulae 12g

Rhizoma Glycyrrhizae 9g

Fructus Ziziphi Jujubae 12 pieces

Administration: The decoction of a dose is 200-300ml. Take equal shares in the morning and in the evening.

Modification: For the case of a more severe stomachache, Rhizoma Paeoniae Albe 15g and Rhizoma Corydalis 9g may be employed.

2. Hyperactive Liver-qi Attacking the Stomach:

Clinical manifestations: Epigastric distension, pain, full-ness, oppression and discomfort which is aggravated after meals, frequent belching which may be aggravated by emo-tional upset, thin and white coating of the tongue, and deep taut pulse.

Therapeutic method: Relieving hyperactive liver-q/ and regulating the stomach.

Recipe: Modified Bupleurum Powder for Relieving Liver-q/.

Ingredients:

Radix Bupleuri 10g

Rhizoma Cyperi 10g

Radix Paeoniae Alba lOg

Fructus Aurantii l0g

Fructus Meliae Toosendan log

Rhizoma Corydalis 10g

Pericarpium Cirri Reticulatae 10g

Caulis Perillae 10g

Radix Glycyrrhizae 6g

Administration: Decoct the above drugs in water to get 200-300ml of decoction. Take equal portions in the morning and in the evening.

Modification: In case of acid regurgitation, burning sen-sation and distress in the stomach, add

Herba Taraxaci 15g

Rhizoma Coptidis 9g

Fructus Evodiae 6g

3. Insufficiency-cold of the Spleen and Stomach:

Clinical manifestations: Vague pain in the stomach, vom-iting of watery fluid, preference for warmth and press, aggra-vation from cold, mental fatigue and weakness, loose stools, pale tongue, deep thready and weak pulse.

Therapeutic method: Warming middle-jiao and dispelling pathogenic cold.

Recipe: Modified Decoction of Astragalus for Tonifying Middle-jiao .

Ingredients:

Radix Astragali seu Hedysari 30g

Ramulus Cinnamomi 9g

Radix Paeoniae Alba 18g

Radix Aucklandiae 9g

Rhizoma Zingiberis 6g

Fructus Amomi 10g

Fructus Ziziphi Jujubae 5 pieces

Radix Glycyrrhizae Praeparate 6g

Administration: Decoct the above drugs in water to get 200--300ml of decoction. Take one half of it in the morning and the other half in the evening.

Modification: If the case is complicated with anorexia and belching with fetid odour, add

Massa Fermentata Medicinalis 10g

Fructus Hordei Germinatus 10g

If the cas with acid regurgitation, add

Concha Arcae 30g

If the case with dominant cold of insufficiency type, add

Radix Codonopsis Pilosulae 10g

Rhizoma Atractylodis Macrocephalae 10g

Poria 10g

4. Deficiency of the Stomach-yin due to Stomach-heat:

Clinical manifestations: Irregular stomachache with burn-ing sensation which is aggravated in the afternoon or on empty stomach and is relieved after meals, dry mouth and throat, or thirst, loss of appetite, dry stool, red tongue with yellowish and dry fur, and taut and thready or rapid pulse.

Therapeutic method: Clearing away heat from the stom-ach and nourishing the stomach-yin.

Recipe: Modified Decoction for Nourishing the Stomach.

Ingredients:

Radix Glehniae 10g

Radix Ophiopogonis 10g

Rhizoma Potygonati Odorati

Radix Paeoniae Alba 10g

Radix Scutellariae 10g

Rhizoma Coptidis 10g

Rhizoma Anemarrhenae 10g

Pericarpium Citri Reticulatae 10g

Herba Taraxaci 20g

Radix Glycyrrhizae 6g

Administration: All the above drugs are to be decocted in water to get 200-300ml of decoction. Take equal portions in the morning and in the evening.