PEPTIC ULSER

Introduction :
A peptic ulcer is defined as an erosion in the lining of the stomach or first part of the small intestine, an area called the duodenum. There are two main sites of peptic ulcer Gastric and Duodenal.

Rare peptic ulcer may be seen in : Cardiac end of oesophagus Meckels diverticulum In any segment of bowel which has been surgically anastomosed to the gastric fundus

Peptic ulcer may be classified as: Acute ulcer (shallow and multiple) Chronic ulcer (single, deep, scirrhous)

AETIOLOGY And PATHOGENESIS

1) Acute Peptic Ulcer These acute ulcer may occur following stress, so they are often called stress ulcer. This may occur following hupotension from haemorrhage, endotoxin shock or cardiac infraction. About half the patients give history of ingestion of aspirin or butazolidin. Sepsis is animportant aetologic factor. Undrained pus may be responsible for acute stress ulcers. Upper G.I. bleeding from these ulcer may be seen in critically ill patients and should be a reason to search for pus. These acute ulcer may be seen after cerebral trauma or neurosurgical operations knwon as cushings ulcer. In this type of ulcer higher rate of acid secretion and higher gastrin level are seen. After major burns acute ulcer may be seen known as curlings ulcer. Within first 48 hours, multiple acute erosions may develop anywhere in body and fundus of stomach. Also patients on steroids may develop acute ulcer known as steroid ulcer.

2) Chronic Peptic Ulcer Gastric ulcer patients secrete either low normal or below normal amount of acid. Various conditions which cause these ulcer are given below : Diminished Mucosal Resistance : This is due to lowering of the ability to resist the effect of acid pepsin digestion. Pyloroduodenal Reflux : Reurgitated bile and other duodenal juices have been taken to be the prime cause of preulcerative superficial gastric. Though such biliary reflux may account for a large number of gastric ulcer case. Deficient Mucous Barrier : A surface layer of mucus protects normally from the digestive effect of hyfrochloric acid and pepsin. When this mucus barrier becomes deficient gastric ulcer may develop. Mucousal Trauma : 85% of gastric ulcer occur along the lesser curve. This fact together with the observation that fluids tend to pass through lesser curve of stomach suggests that a mechanical factor might be involved. Local Ischaemia : Arteriovenous shunts which are present in the submucosa of stomach are under control of sympathetic nervous system and excessive stress and strain may cause diminution of blood suppy to the mucous membrane of stomach leading to ulcer formation. Antral Stasis : This usually produces increased acid secretion and it is an accepted fact that the majority of patients with gastric ulcer have low acid content in the stomach. But its seen that nearer the ulcer to pylorus more is the acid secretion of the stomach. Factors like reflux of bile and pancreatic juice and pyloric dysfunction are important in the pathogenesis of gastric ulcer. Non-steroidal anti- inflammatory drugs (NSAIDS) : These drugs seem to disrupt the prostaglandin driven support of mucousal barrier. These prostaglandins are related to production of mucosal gel layer in the stomach, which provides a protective barrier to the gastric and duodenal lining. Helicobacter Pylori : It is a spirochaetal bacterium(gram negative), which exists in the deep mucosal layer of the antrum. The main characteristic feature of H. Pylori is its ability to hydrolise urea resulting in strong alkali. This urase activity protects the bacteria from hydrogen ions in gastric acid juice and provides a source of nitrogen for H. Pylori. The effect of ammonia on the antral G-cell is to cause the release of gastrin and it is responsible for hypergastrinaemia in patients with peptic ulcer disease. H. Pylori is associated with development of chronic gastritis affecting antrum. Irradication of H. Pyroli speeds up gastric ulcer healing and diminishes the recurrence rate.

PATHOLOGY
Ulcer whether gastric or duodenal tends to occur in alkaline mucosa. Gastric ulcer may be acute or chronic. Approximately 80% of chronic ulcer are found on or near the lesser curvature, majority being closer to incisura angularis. 10% - are found in antrum 2% - are found in pyloric canal 3% - are found in the cardia 5% - are found in fundus and body of stomach Gastric ulcer are larger, tend to penetrate deeply and associate with greater degree of fibrosis. A chronic peptic ulcer may present as a white scar under the serosa. Vascular adhesions, salmon pink appearance may observed in the neighbourhood of the peritoneal aspect. When felt, ulcerated area will be hard, fibrotic and button like. An ulcer bed can be palpated by the tip of the finger which imaginates the gut. Few simple ulcer may undergo malignant degeneration. Acute gastric ulcer are multiple, oval or circular in shape, vary in size from 1 to 2 mm in diameter(called erosions) to about 1 cm in diameter(called acute ulcers). They are shallow, punched out and usually dont invade muscular coat. They do not leave scars behind when they heal.

CLINICAL FEATURES
Symptoms : 1) Acute Peptic ulcer Symptoms of short duration, slight attack of dyspepsia may go unnoticed. These ulcer are more recognised when they cause haematemesis. It may perforate occasionally, when it occurs in wall of duodenum may progress to chronic ulceration. 2) Chronic Peptic ulcer Pain in upper abdomen is the main symptom of chronic peptic ulcer. It has a definite relation with food, in case of gastric ulcer pain is aggravated following intake of food.

INVESTIGATIONS
1) Examination of Blood : Hb level will be low in patients with chronic blood loss (melaena and haematemesis). A raised ESR in gastric ulcer suggests malignancy. 2) Examination of Stool : Occult blood in stool may be detected in all cases of acute ulcer due to oozing of blood from ulcer. 3) Gastric function tests : These tests are performed as first things in morning and are comprised of basal secretion and maximum secretion by stimulants such as insulin histamine and pentagastrin. Patients should have had no eatables or drinks from previous night and should not have taken antacid or anticholinergic drugs for past 24 hours. 4) Radiological Investigations : Barium meal X-ray is used for radiological investigations of ulcers. It is diagnostic in case of peptic ulcer. In case of gastric ulcer an ulcer crater will be visible projecting from smooth outline of stomach. It also gives clue about benign gastric and carcinomatons ulcer. 5) Endoscopy : It gives valuable results and helps in diagnosis of shallow gastric ulcer, which is not easily visible by barium meal X-ray. It also demonstrates acute mucosal erosion.

TREATMENT
Conservative (medical) Treatment

This form of treatment suggests complete rest as far as practicable. Anxiety and elements of stress and strain should be kept at bay. Diet should be regulated and spicy foods should be avoided. Blend diet is advised for better recovery. Intake of alcohol is strictly prohibited.

1) For Chronic Gastric ulcer : Careful history must be taken whether the patient is taking any ulcerogenic drug, for example NSAIDS and Corticosteroids. Specimen should be sent for CHO test for Helicobacter Pylore. Initial therapy is an H2 receptor blockers for example cimetidine or ranitidine. H2 receptor antagonist and proton pump inhibitors few patients may be relatively refractory to conventional doses of H2 receptor antagonists. In these cases proton pump inhibitors can be used and majority of ulcer heal within two weeks. Most accepted ideal treatment regimen for irradication of H. Pylori is the triple therapy with bismuth compounds for example colloidal bismuth subcitrate 120 mg/qds, in combination with tetracycline 500 mg/tds. The duration of medical treatment : in case of gastric ulcer the case should be reviewed after 6 weeks by barium meal X-ray and endoscopy. If there is no improvement by proper medical treatment given for six weeks, medical treatment should be stopped and surgical treatment should be opted.

Surgical Treatment : 1) Billroth I partial gastrectomy is still operation of choice in gastric ulcer. This operation involves excision of distal two thirds of stomach followed by anastomosis between remnant of stomach and duodenum.

2) Vagotomy and pyloroplasty , associated with frozen section biopsy of the gastric ulcer (if benign), is generally gaining popularity.

3) Highly selective Vagotomy or proximal gastric vagotomy ,i.e., excision of ulcer is being performed. It is designed to denervate the acid secretory part of the stomach, keeping the vagal supply to alkali secreting gastric antrum and other abdominal viscera, thus motility of stomach is mot hampered.