1.Inroduction. 2.Objectives. After going through this module, you will be able to

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1 Paper14 -Medical Nutrition Therapy for Peptic Ulcer Patients F14 TN10- -what is peptic ulcer, causes of peptic ulcer, symptoms, diagnosis of peptic ulcer, dietary management 1.Inroduction The mucosa of the stomach and duodenum is protected from the digestive action of acid and pepsin by the secretion of mucous, production of bicarbonates, removal of excess acid by normal blood flow and rapid renewal and repair of epithelial cell injury. When there is a breakdown in these normal defenses and repair mechanisms ulcer is formed in gastrointestinal tract. Peptic ulcer is developed if any one of the above mechanisms is at default. 2.Objectives After going through this module, you will be able to Explain the gastrointestinal problems of peptic ulcer Learn the symptoms and risk factors and outline the medical management therapy in peptic ulcer 3. What is Peptic Ulcer? When there is an imbalance between the gastro duodenal mucosal defense mechanism and damages due to gastric acid and pepsin and superimposed injury from environmental or immunologic agents peptic ulcers are formed. The mucous membrane lining the digestive tract erodes and causes a gradual breakdown of tissues. This breakdown causes epigastric pain, gnawing, or burning pain in the abdomen. When the protective layer of intestine or stomach is broken down ulcer is formed. Because of these the hydrochloric acid and enzyme pepsin in the digestive juices damage the intestine and stomach tissue.this lead to sore formation in the inner lining of the stomach or upper small intestine which is termed as Peptic Ulcer. So peptic ulcers are open sores that develop on the mucosal lining of the esophagus, stomach and upper small intestine. More peptic ulcer is observed in the duodenum than in the stomach. Now it has been noted that Helicobacter pylori (H.pylori) infection spread through food, water or close contact with the infected person. If untreated in childhood it can cause gastritis, peptic ulcer and stomach cancer later in life. 3.1.Changes taking place in the development of peptic ulcer The damage in the mucous membrane lining causes breakdown of tissues and thereby increases number of parietal and chief cells, increases sensitivity to food and other stimuli such as caffeine.

2 Excess vagal stimulation decreases inhibition of gastric secretion, inadequate mucosal blood supply, impairs mucus production. Bile or pancreatic enzyme reflexes from duodenum and colonization by H.pylori and aspirin and non steroidal anti inflammatory drugs or alcohol ingestion can cause or worsen ulcers. These above factors lead to increased gastric acid production and impaired mucosal barrier production and resulting in peptic ulcer formation. 3.2.Types and Sites of Ulcer Ulcer may be formed in stomach, duodenum or in esophagus. In stomach, it is called gastric ulcer, in duodenum, it is called duodenal ulcer, and in esophagus it is called esophageal ulcer Gastric ulcer is common in antrum, mostly occur in lesser curvature of the stomach but less common in anterior and posterior wall the greater curvature. These are benign sometimes and develop as tumour. Duodenal ulcers occur mainly in duodenal cap -first portion, anterior wall How gastric ulcer is formed? It is formed by the breakdown of gastric mucosa. Local epithelial tissue damage occurs because of cytokines released by H.pylori, and because of abnormal mucus production associated with gastritis affecting the body and antrum Gastrin stimulates the parietal cell proliferation and increases parietal cells as a result decrease in somatostatin leads to acid hyper secretion How duodenal ulcer is formed?

3 It is formed as a result of increased acid secretion in the duodenum because of decreased bicarbonate secretion by H.pylori infection, increased parietal cell mass due to alcohol and spicy foods and Zollinger- Ellison syndrome( Increased production of gastrin),decreased inhibition of acid secretion,possibly by H.pylori damaging somatostatin producing cells in the antrum by H.pylori.Smoking impairs the healing of gastric mucosa. The persons with Blood group O and genetic susceptibility factors also influences the occurrences duodenal ulcers 4. Causes of peptic ulcer of The old hypothesis stated that ulcerations caused by hyper acidity are not tenable. About 70 per cent of gastric ulcers and 50 per cent of duodenal ulcers are not associated with abnormally high acid production One of the most common causes of peptic ulcers is Helicobacter pylori (H.Pylori) infection 4.1. The details of helicobacter pylori H.pylori is a helix shaped organism gram-negative and slow growing organism. Length of the organism is 3 micrometers and the diameter is 0.5 micro meters. It has 4-6 flagella.it is a microaerophilic, which requires lower concentration of oxygen found in the atmosphere. So it lives comfortably in the acid medium. It is noted that 80 to 95 per cent of persons with H.Pylori infection are affected by peptic ulcer disease. Helicobacter pylori infection impairs

4 the protective mechanisms of the GI tract against low ph and digestive enzymes and causes ulceration of the mucosa. 4.2.Excessive alcoholism, can irritate the stomach and erode the mucous membrane lining and increases the stomach acid. Use of tobacco products reduces bi-carbonate secretion, mucosal blood flow and develops inflammation, which in turn damages gastric mucosa. In Hypercalcaemia there is increase in gastric acid secretion which leads to ulcer. Those who do not secrete blood group antibodies into gastric secretions tend to get ulcer. Genetic factor The lifetime prevalence of developing ulcer disease in first degree relatives of ulcer patients is about three times greater than the general population Other causes of Peptic ulcer Persons affected by malnutrition or with any nutrient deficiencies are affected by ulcer. Stress due to emotional, trauma,and surgery cause ulcer. Smoking Effects of smoking on peptic ulcer Increased the rate of gastric emptying Diminished pancreatic bicarbonate secretion Decreased duodenal ph Reduced mucosal blood flow Inhibition of mucosal prostaglandins According to Maity et al., (2003) nicotine present in tobacco not only induces ulceration and also potentiates ulceration caused by H.pylori, alcohol and NSAID. Excessive alcohol consumption- increases the acid that produced in the stomach besides the irritation and erosion of mucous lining of the stomach. It is uncertain whether alcohol alone is responsible for ulcer or it just aggravates the symptom of ulcer Caffeine in beverages and food stimulate acid secretion in the stomach. This aggravates ulcer but caffeine solely cannot be attributed to stimulation of acids Irregular meals poor food habits also contributes to ulcer Injury or death of mucous producing cells Hyperacidity excess acid production in the stomach. The hormone gastrin stimulates the production of acid in the stomach. The factor which increases gastrin production will in turn increase the production of stomach acid.

5 4.4.Duodenal Ulcer Duodenal ulcer is the most common in middle age with peak years. Duodenal sites are as common as gastric sites. As far as the genetic factor is concerned first degree relative s are more affected by duodenal ulcer. Male population is affected more than female. The ratio is 4:1.Duodenal ulcer is more common among persons with blood group O. It is associated with increased serum pepsinogen. H.Pylori infection is common up to 95 percent. Smoking affects ulcer patients. 4.5.Gastric ulcer Duodenal ulcer is common in late middle age and incidence increases with age. Similar to duodenal ulcer male are more affected, the ratio being 2:1 More common among person with blood group A. Less related to H.Pylori than duodenal ulcer. Patients with a gastric ulcer have a concomitant duodenal ulcer. Use of NSAIDs associated with a threefold increase in risk of gastric ulcer. NSAIDs inhibits the production of cyclooxygenase that produces prostaglandins. This hormone protects the stomach lining from chemical and physical injury per cent of patients with a gastric ulcer has a concomitant duodenal ulcer Stress ulcers Chronic stress was strongly associated with an increased risk of peptic ulcer and a combination of chronic stress and irregular mealtime was a significant risk factor. Stress ulcers consist of a group of lesions and usually in the esophagus, the stomach or the duodenum. Persons with critically ill or other illness develop stress ulcer. Stress Ulcer is usually reduced once the stress level goes down. Stress also aggravates H.pylori infection. Ulcers are not purely infectious disease but the psychological factors also play a significant role Stress promotes pylori infection-how? Stress causes excess production of stomach acid and H.pylori thrives in acidic environment Stress is more when severe trauma and burns, surgical conditions, renal failure, radiation therapy in cancer and shock affect the person. 5.Symptoms of Peptic ulcer The peptic ulcer patients may have several symptoms, sometimes asymptomatic also but vary with each individual. The symptoms commonly observed are:

6 Heart burn,aching, gnawing pain in upper abdomen / epigastric pain (between ribs and navel)/ between the belly button and the breast bone. Sometime back pain or radiating pain in the back Pain last for few minutes to a few hours and continue or come and go for weeks and the use of antacid or acid reducer may control the pain Flatulence, Bloating, distension Loss of appetite and weight loss Nausea, vomiting, anorexia Intolerance to fatty foods When peptic ulcer prolongs for long period the patient may affected by bleeding ulcer and proliferations and emergency situations Warning signs of bleeding ulcer Vomit food eaten hours or days before Ongoing nausea or repeated vomiting Feel unusually weak or dizzy Sudden severe pain Loss of weight No pain reduction with medication Feel cold Melena-stools with dark red blood look like tar Blood in stools Vomit blood 6.Diagnosis of peptic ulcer 6.1.Radiological diagnosis:

7 Barium X-ray or Upper GI series (UGI)- the patient need to drink chalky liquid that increases the contrast on the X ray, to show the presence of ulcer. Since the liquid contains barium this test is called barium swallow 6.2.Laboratory tests: Urea breath test- H.pylori contains enzyme urease which breaks down urea in the stomach to ammonia and cabon dioxide. When urea solution is swallowed the carbon dioxide released through breath by H.pylori is traced. Blood is tested to identify the presence of invaded H.pylori Tissue test: if endoscopy biopsy has been done a sample of tissue will be taken to detect the bacteria ELISA test is conducted to detect the levels if Immunoglobulin G, Immunoglobulin A 6.3.Endoscopy (EGD): A thin flexible tube with a tiny camera at the end is passed throught he stomach. it helps to diagnose the presence of ulcer in the lining of the stomach 7. Dietary management Mechanically irritating foods- fiber rich foods like green leafy vegetables, cauliflower and cabbage Chemically irritating foods- coffee, tea, gravies, spiced foods, fried foods and highly seasoned foods. Thermally irritating foods- Very cold and very hot foods 7.1. Dietary modifications: Energy: Patients suffering from peptic ulcers are undernourished and therefore, need an increased energy intake. Carbohydrate: carbohydrates are used to meet the energy needs. Foods containing harsh and irritating fibre should be avoided. Protein: A high protein diet is advised, it provides necessary amino acids for synthesis of tissue protein which promotes healing. Proteins also have a buffering action. Though milk protein has a good buffering action, the high calcium content of milk stimulates acid production. Eggs and other high protein foods can be included in the diet. Fat: Fat should be used in moderate amounts. Emulsified fats like butter, cream etc. are tolerated.

8 Role of Foods in peptic ulcer Earlier milk or cream is considered as acid neutralizer and important in coating of stomach. But now milk or cream is not considered as medicinal value Avoid drinks like alcohol, Coffee and caffeine, which stimulate acid secretion Avoid foods high in fat and chocolate - irritates stomach, harder to digest, produce more stomach acids and aggravate the condition- Eat lean meat cuts that facilitate easy digestion and remove visible fat in the meat. Fish and chicken proteins are preferable than red meat and remove fatty skin. Include omega -3 fatty acids rich fish mainly salmon, mackerel, sardines and herring; it helps in producing prostaglandins, which in turn protects the mucosa lining of the stomach and intestines. Since most of the foods are less acidic the ph of food before ingestion has little therapeutic importance Spices like cayenne and black pepper may increase stomach acid and cause superficial erosions Prostaglandins from omega 3and 6 involved in immune and cyloprotective physiology of the gastro intestinal mucosa and they are useful in the treatment of H.pylori infection and peptic damage Diet high in Vitamin A lower the risk of Ulcer (Harvard cohort study) Catechins present in green tea may suppress H.pylori induced gastritis through antioxidant and antibacterial actions (yet to be proved). Probiotics inhibit the growth of H pylori and reducing the side effects of eradication treatment. Avoid nutrient deficiency in ulcer management Antioxidants rich fruits and vegetables heal ulcer The study by Kuriki et al., 2007, revealed that high intake of salt by the person who affected by H.pylori are prone to develop stomach cancer. So include seaweed which is better than salt to enhance flavor of the foods Foods that protects the mucosal lining of the stomach and intestines Fish, rich in Omega 3 fatty acid Fruits and vegetables like carrot, kale, broccoli, red/green pepper, cabbage juice, kiwi fruits, grapes-containing beta carotene and vitamin C

9 Berries with antioxidants Cold-pressed sunflower oil, soybean oil with Vitamin E Seaweed, cheddar cheese, almonds, sunflower seeds, sesame seeds-with the sources of amino acids Slippery elm foods- Mixed low fat and soy milk powders with other herbs or antioxidants that benefit and protect the stomach lining. E.g. milk shake, smoothies Medical Nutrition Therapy Individual tolerance is the basis for diet planning and dietary restrictions. Diet is considered supplemental to the primary therapy of antacids and histamine hydrogen blockers Guidelines Have meals in a relaxed atmosphere Frequent small meals with less spicy may increase comfort Avoid specific food, which causes discomfort Avoid alcohol and caffeine containing beverages Avoid bed time snacks that stimulates acid production at night Stop eating at least two hours before bedtime Protein food has buffering effect Include variety of healthy foods from all food groups Wise selection of foods by omitting foods causing irritation, distress and gnawing pain 7.4. Foods to be liberally included and avoided

10 Liberally Included Milk Bread, puffed rice, refined cereals, double sieved flour Soft boiled eggs, lean meat, fish, Pulses well cooked and mashed Vegetables- all gourds, brinjal, ladies finger, potatoes Avoided Spicy foods and gravies- black pepper, chili powder, green chili, garlic powder, Red meat- high in fat, Carbonated beverages, citrus fruits. Sodium rich foods- all chips, salted nuts, cheese, corn flakes, pickles, canned vegetable and fish, ready to eat foods, sauces, salted fish, preserved salted sun dried foods like vathal and vadams and other preserved foods. Alcohol, Coffee, Decaf coffee, Tea, Whole milk, Chocolate milk, Hot cocoa, Whole grain foods Red meat- high in fat, Legumes with skin Strongly flavoured vegetables- cabbage cauliflower, broccoli and peas Summary provide adequate nutrition provide rest to the digestive tract maintain continuous neutralization of gastric acid minimize acid secretion and reduce mechanical, chemical and thermal irritation to the lining of the stomach Text book references

11 1. Robinson C.H. (2007) Normal and Therapeutic nutrition, 12 th edition, Mac millan Publishing Co. Inc, Newyork. 2. Krause M.V and Mahan L.K (2010) Food, Nutrition and Diet therapy, 9 th edition, W.B. Saunder Co, Philadeephia 3. Srilakshmi. B (2012), Dietetics, New Age International Pvt Ltd, New Delhi. 4. Shubhangini Joshi2009 NUTRITION & DIETETICS Journal references 1.Maity P, Biswas K, Roy S, Banerjee RK, Bandyopadhyay U.( 2003 )Mol Cell Biochem. Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. Nov;253(1-2): Kuriki K, Wakai K, Matsuo K, Hiraki A, Suzuki T, Yamamura Y, Yamao K, Nakamura T, Tatematsu M, Tajima K. (2007) Gastric cancer risk and erythrocyte composition of docosahexaenoic acid with anti-inflammatory effects. Cancer Epidemiol Biomarkers Prev. 16(11): PMID: Krag, M; Perner, A; Wetterslev, J; Wise, MP; Hylander Møller, M (Jan 2014). "Stress ulcer prophylaxis versus placebo or no prophylaxis in critically ill patients. A systematic review of randomised clinical trials with meta-analysis and trial sequential analysis.". Intensive care medicine 40 (1): Krag, M; Perner, A; Wetterslev, J; Møller, MH (Aug 2013). "Stress ulcer prophylaxis in the intensive care unit: is it indicated? A topical systematic review.". Acta anaesthesiologica Scandinavica 57 (7): PMID