MUCOSAL BARRIER PEPTIC ULCER 1 GASTRIC MUOSAL BARRIER

MUCOSAL BARRIER & PEPTIC ULCER 1

GASTRIC MUOSAL BARRIER v The gastric mucosal barrier is the property of the stomach that allows it to contain acid v If the barrier is broken, then the acid diffuses back into the mucosa and damage the stomach wall v The gastric mucosal barrier is made up of 3 components: 2

GASTRIC MUCOSAL BARRIER a) Compact epithelial cell lining with tight junctions b) Gastric mucus covering (gel like coating) c) Bicarbonate ions, secreted by the surface epithelial cells. The bicarbonate ions act to neutralize harsh acids 3

GASTRIC MUCOSAL BARRIER • The gastric mucosal barrier is the property of the stomach that allows it to contain acid. • The barrier consists of three protective components. These provide the additional resistance for the mucosal surface of the stomach. to neutralize harsh acids. 4

THREE COMPONENTS v The three components include: • a) A compact epithelial cell lining. Cells in the epithelium of the stomach are bound by tight junctions that repel harsh fluids that may injure the stomach lining. • b) A special mucus covering, derived from mucus secreted by surface epithelial cells and Foveolar cells. This insoluble mucus forms a protective gel-like coating over the entire surface of the gastric mucosa. The mucus protects the gastric mucosa from auto digestion by e. g. pepsin and from erosion by acids and other caustic materials that are ingested. • c) Bicarbonate ions, secreted by the surface epithelial cells. The bicarbonate ions act as buffers 5

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MUCUS v Mucus is secreted by mucus cells v Present allover the GIT v Acts as a protectant and lubricant of wall of gut v Mucus is a viscous gel which contains mucin, phospholipids, electrolytes (mainly HCO 3) and water v Separates the epithelial cells from acid of stomach 7

CONT’D v This maintains the Ph of epithelial cells alkaline despite gastric acid v Mucus is strongly resistant to digestion by gastric enzymes v Has buffering properties (neutralize acid) v Helps in propulsive movement by lubrication v Easy slippage of food 8

PEPTIC ULCER v. Ulcer : - An Ulcer is a discontinuity or break in a bodily membrane, or breach in the epithelium v. Ulcer may occur anywhere in the body v. When it occurs in stomach its gastric ulcer v. In duodenum its duodenal ulcer 9

CONT’D v. Ulcer occurring in either of these two sites is called peptic ulcer v. Its also known as acid peptic disease (APD) 10

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PATHO PHYSIOLOGY OF PEPTIC ULCER v. Defect in the mucosal barrier v. Hyper secretion of acid v. Helicobacterial infection 13

DEFECT IN THE MUCOSAL BARRIER v. If the secretion of mucus is impaired v. Or bicarbonate production is impaired v. Such damage is caused by drugs like asprin, NSAID v. Chronic stress conditions (stress ulcer) 14

HYPER SECRETION OF ACID v Chronic anxiety v Common in people with busy life style (Type A personality) v Hurry, worry, curry v Intake of spicy food – leads to hyper chlorhydria v Conditions with hyper chlorhydria (Zollinger Ellison syndrome ) gastrin secreting tumor 15

H. PYLORI INFECTION v. Major cause of peptic ulcer v. This bacterial infection causes Damage to the mucosal barrier v. Increase in gastrin secretion from G cells v. Reduce somatostatin from D cells v. Initially causes gastritis which later on leads to peptic ulcer 16

CONTD …. . v Helicobacter pylori, previously Campylobacter pylori, is a Gram-negative, micro aerophilic bacterium found in the stomach, and may be present in other parts of the body, such as the eye. v It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause. v It is also linked to the development of duodenal ulcers and stomach cancer. However, over 80% of individuals 17

CONTD…. . v More than 50% of the world's population harbor H. pylori in their upper gastrointestinal tract. v Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. v H. pylori's helical shape (from which the genus name is derived)(Screw like, spiral) is thought to have evolved to penetrate the mucoid lining of the stomach. 18

SIGNS & SYMPTOMS OF H. PYLORI INFECTION v Up to 85% of people infected with H. pylori never experience symptoms or complications. v Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea. v Where this develops into chronic gastritis, the symptoms, if present, are often those of non-ulcer dyspepsia: • • • stomach pains Nausea Bloating Belching sometimes vomiting or black stool. 19

v Individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer. v Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma. v H. pylori possibly plays a role only in the first stage that leads to common chronic inflammation, but not in further stages leading to carcinogenesis. v A meta-analysis conducted in 2009 concluded the eradication of H. pylori reduces gastric cancer risk in previously infected individuals, suggesting the continued presence of H. pylori constitutes a relative risk factor of 65% for gastric cancers; in terms of absolute risk, the increase was from 1. 1% to 1. 7%. v H. pylori has also been associated with colorectal polyps and colorectal cancer. 20

ADAPTATION TO THE STOMACH’S ACIDIC ENVIRONMENT v To avoid the acidic environment of the interior of the stomach (lumen), H. pylori uses its flagella to burrow into the mucus lining of the stomach to reach the epithelial cells underneath, where the p. H is more neutral. v H. pylori is able to sense the p. H gradient in the mucus and move towards the less acidic region (chemotaxis). v This also keeps the bacteria from being swept away into the lumen with the bacteria’s mucus environment, which is constantly moving from its site of creation at the epithelium to its dissolution at the lumen interface. 21

CONTD…. . v H. pylori is found in the mucus, on the inner surface of the epithelium, and occasionally inside the epithelial cells themselves. v It adheres to the epithelial cells by producing adhesions, which bind to lipids and carbohydrates in the epithelial cell membrane. v One such adhesion, Bab. A, binds to the Lewis b antigen displayed on the surface of stomach epithelial cells. v Another such adhesion, Sab. A, binds to increased levels of sialyl-Lewis x antigen expressed on gastric mucosa. 22

CONTD…. . v In addition to using chemotaxis to avoid areas of low p. H, H. pylori also neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. v The ammonia, which is basic, then neutralizes stomach acid. 23

SYMPTOMS OF PEPTIC ULCER v. Upper abdominal pain v. Pain usually by empty stomach relieved by food or antacid v. Vomiting v. Blood vomiting and perforation in severe cases 24

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FACTORS THAT STIMULATE ACID SECRETION v. Acetylcholine v. Gastrin v. Histamine 26

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TREATMENT v Anti histamines v Anticholinergic drugs v Proton pump blockers v Sucralfate v Gastrin blockers v Antacids 28

NON SPECIFIC TREATMENT v. Avoid stress v. Adequate sleep v. Regulation of diet v. Avoid spicy foods, alcohol v. Withdrawal of drugs like aspirin, NSAIDS 29

SURGICAL TREATMENT v. Vagotomy v. Gastrectomy 30

FACTORS THAT CAN DAMAGE THE BARRIER v. Bacterial Infection by Helicobacter pylori v-Alcohol v-Aspirin v-NSAID 31

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