Code and Title of the Paper: F14TN Therapeutic Nutrition 
       Code and Title of the Module: F14TN10 Medical Nutrition Therapy for Peptic Ulcer Patients  
       Name of the Content Writer: Dr. V. Saradha Ramadas 
                         Quadrant – I 
       1. Introduction 
       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. 
       Excess vagal stimulation decreases inhibition of gastric secretion, inadequate mucosal blood 
        
       Code and Title of the Paper: F14TN Therapeutic Nutrition 
       Code and Title of the Module: F14TN10 Medical Nutrition Therapy for Peptic Ulcer Patients  
       Name of the Content Writer: Dr. V. Saradha Ramadas 
       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 
       3.2.1.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. 
       3.2.2.How duodenal ulcer  is formed? 
        
                 Code and Title of the Paper: F14TN Therapeutic Nutrition 
                 Code and Title of the Module: F14TN10 Medical Nutrition Therapy for Peptic Ulcer Patients  
                 Name of the Content Writer: Dr. V. Saradha Ramadas 
                 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      of     
                 duodenal ulcers 
                 4. Causes of peptic ulcer 
                          
                        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 
                  
                 Code and Title of the Paper: F14TN Therapeutic Nutrition 
                 Code and Title of the Module: F14TN10 Medical Nutrition Therapy for Peptic Ulcer Patients  
                 Name of the Content Writer: Dr. V. Saradha Ramadas 
                 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. 
                  
                 4.3. 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 
                         4.3.1. 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.