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Acid Peptic Ulcer Diease

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Page 1: Acid Peptic Ulcer Diease
Page 2: Acid Peptic Ulcer Diease

An eroded lesion in either the esophageal, gastric, or duodenalmucosa resulting from the action of gastric secretions and typicallyH.pulori bacterial inflammation.

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• Normal gastric and duodenal mucosa is protected from the digestiveactions of acid and pepsin by the secretion of mucus, the production ofbicarbonate, the removal of excess acid by normal blood flow, and therapid renewal and repair of epithelial cell injury.• Peptic ulcer refers to an ulcer that occurs as a result of the breakdownof these normal defense and repair mechanisms.• Typically more than one of the mechanisms must be malfunctioningfor symptomatic peptic ulcer to develop.• Peptic ulcer typically show evidence of chronic inflammation andrepair processes surrounding the lesion.

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Acid peptic ulcer may develop due to any of the following reasons.• H.pylori infection.• Increased number of parietal cell or acid secretion.• Increased gastric emptying rates.• Reduced ability of the duodenum to handle an acid load.• Stress• Excessive use of non steroidal anti inflammatory drugs (NSAID) andcorticosteroids.

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• Increased gastric tone and painful hunger contraction when stomachis empty.•Piercing, burning and gnawing pain which usually relieved by takingfood.• Frequent vomiting sometimes with blood too.• Anorexia

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• Gastrointestinal bleeding• Intestinal perforation•Peritonitis (inflammation of the lining of abdominal cavity)• Anemia• Intestinal narrowing and obstruction• Shock

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• Restoration of good nutritional status with dietary modificationsand counseling.• Alleviate the symptoms.• Neutralize acids.• Reduce acid secretion.• Preservation of epithelial resistance to the destructive action ofgastric juices.

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• Milk neutralizes gastric acidity only for 20 to 60 minutes after itsingestion and the PH reverts back to the basal levels. Current studiesindicate that a diet with high milk content has an adverse effect on thehealing rate of ulcer because of high calcium. So protein from cottagecheese, egg, chicken and fish in adequate amounts is beneficial forregeneration of cell. Additional protein 10-15g/day above the RDA can begiven.• The products of fat digestion in the small intestine stimulateentrogastrone, which inhibits gastric juice secretion. PUFA such as linoleicand eicosapentanoic acid have been found to effective against duodenalulcer by inhibiting in vitro growth of H.Pylori. Around 25-30 g visible fat inemulsified form can be given. Avoid fried foods as they cause digestiveproblems.

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• 55 to 65% of CHO can be given in simple and complex form but insoft well cooked form. Soluble fiber is more beneficial than insolubleas insoluble fiber delays gastric emptying time hence prevents themucosal damage by acidic gastric juice.• Fruits in general are related to an alkaline ash diet. If they are notwell tolerated by some individuals, avoid them.• Avoid taking alcohol, caffeine, black pepper ad meat extracts asthey significantly change gastric pH.• Clinical observations have shown that tolerance for a variety ofstandard foods is highly individual. Pulse, soyabean, cabbage,cauliflower, onions, peas, apple, watermelon are some of the foodsidentified.

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• Cigarette smoking cause an adverse effect because of the presence ofnicotine which cause pyloric incompetence, increased reflux ofduodenal juice into the stomach, increased gastric acid secretion byfavoring gastric secretion, decrease pancreatic bicarbonate synthesis.

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Stage 1• Initially, for bleeding ulcer, if the patient is extremely nauseated or vomiting he must be kept NBM• This is followed by an hourly feeding to begin with milk and cream 100g/hr followed by small feeding of easily digestible food like soft cooked eggs, custards, refined flour products, cottage cheese, low fiber vegetables like gourds, clear soup with no seasoning and herbs, soft over ripe fruit whips and light desserts.• The diet must be feed orally and of liquid/semi liquid/ soft consistency which is easy to digest

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Stage 2• Marked recovery from pain.• 6 meal pattern followed.• Light, blend, low fiber diet.• Mechanical/ thermal, chemical irritation of gastric mucosa to be avoided.•Late night feeding avoided as the end products of digestion may cause the epigastric pain.

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Stage 3• Number of feeds reduced to 3-4.• Discharged from hospital – discharged diet• Increased amount/ feed

Stage 4• Liberalizing the diet depending on the patient’s individualtolerance and schedule.• Ensuring optimum intake of calorie, protein, fats, vitamins andminerals.•Relaxed atmosphere on eating.• Lifestyle change.