| ID | 37 |
|---|---|
| Name | PEPTIC ULCER DISEASE |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. Endoscopy of upper GI tract - This is the best diagnostic method if available. Reddish and velvety- normal mucosa. Pale and whitish mucosa- ulcer present. 2. Ba-meal X-ray of stomach and duodenum with cap series -Cap deformity and ulcer crater can be seen if ulcer is present. 3. Detection of H. pylori - H. pylori can be determined by- i. Histopathology- the biopsy material obtained at endoscopy. Or, ii. Presence of urease in a fresh biopsy specimen (Rapid ClO-test). Or, iii. By a serologic test (an ELISA test). |
| Management | Management: Aim of management- I. General measures (including reduction of risk factors): The first step in the treatment of peptic ulcer involves the reduction of risk factors (NSAIDs, cigarettes etc) & general measures. II. Short-term treatment to relieve symptoms & induce ulcer healing. III. Long-term or maintenance treafment to prevent relapse. I. General measures (including reduction of risk factors): 1. Bed rest- during acute exacerbation. 2. Diet- a. Regular timing of meals. b. Nutritious diet. c. Irritant and highly spicy food should be avoided. e. In acute phase it is often useful to give full liquid or soft diet 3. Smoking strictly prohibited 4. Steroid, Aspirin & NSAID groups of drugs should be avoided. II. Short-term treatment: The pharmacologic agents that are used in the short-term treatment of peptic ulcers to relieve acute symptoms & enhance the healing are divided into four categories- 1. Acid neutralization: Antacids neutralize existing acid in the stomach, but the neutralizing action of these agents is short-lived, and frequent doseages are required. Ulcers frequently return when antacids are discontinued. Magnesium containing antacids, can cause diarrhea, while aluminum containing antacids cause constipation. 2. Acid antisecretory agents: Histamine (a protein chemical mediator) in the stomach stimulates gastric acid secretion. Histamine antagonists (H2 receptor antagonists) are drugs to block the action of histamine on gastric cells & thus reducing acid secretion. H2 receptor antagonists are- Cimetidine, Ranitidine, Famotidine & Nizatidine. Proton pump inhibitors are more potent than H2 blockers in suppressing acid secretion. Different proton-pump inhibitors are- Omearazole, Lansoprazole, Pantoprazole & Rabeprazole. 3. Mucosal protective agents: Sucralfate, Bismuth, & Misoprostol (a prostaglandin analogue). 4. Agents that promote healing through eradication ofH. pylori: Proton-pump inhibitors (viz. omeprazole, lansoprazole), Some antibiotics (e.g amoxycillin clarithromycin, tetracycline), & metronidazole. |
| Introduction | Peptic ulcer is a very common & publicly known gastrointestinal hazard in our locality. Patients usually present with nonspecific epigastric pain with variable relationship to meals, characterized by rhythmicity and periodicity. This is usually defind as an ‘ulcer or a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid & pepsin’. The other parts of the gastrointestinal tract that are exposed to hydrochloric acid & pepsin digestion, viz. lower end of the oesophagus, small intestine after surgical anastomosis to the stomach or rarely Meckel’s diverticulum are occasionally involved. Both acute and chronic ulcers penetrate the muscularis mucosa but fibrosis doesn’t occur in acute ulcer. Erosions don’t penetrate the muscularis mucosae.2 Ulcers occur five times more commonly in the duodenum of which 95% occur in the bulb or pyloric channel.1 Site & distribution: Chronic gastric ulcer is usually single; around 90% are situated along the lesser curvature within the antrum or at the junction between body & antral mucosa. Chronic duodenal ulcer usually occurs in the first part of the duodenum just distal to the junction of pyloric and duodenal mucosa and 50% are on the anterior wall of the duodenum. In about 10-15% patients both the gastric and duodenal ulcers coexist |
| History | |
| Etiology | Etiology:1233 Three major causes of peptic ulcer disease are now recognized- 1. Chronic H. pylori infection 2. NSAIDs& 3. Acid hypersecretory states. Evidence of H pylori infection or NSAID ingestion should be sought in allpatients with peptic ulcer. A. H. pylori-associated ulcers: H. pylori, a gram-negative rod, appears to be necessary cofactor for the overwhelming majority of duodenal and gastric ulcers. About 90% of duodenal ulcer patients and 70% of gastric ulcer patients are infected with H. pylori and remaining 30% gastric ulcers are related with NSAIDs. Pathogenesis & pathophysiology of infection: These motile organisms localize and live deep beneath the mucous layer adjacent to epithelial surface. Any acidity alters the neutral pH of this surface by the enzyme urease. This produces ammonia from urea and raises the pH. The bacterium causes local inflammatory responses by releasing cytotoxins in the underlying epithelium leading to chronic gastritis. H. pylori exclusively colonizes gastric-type epithelium and is found only associated with patches of gastric metaplasia.2 The role of H. pylori in the pathogenesis of gastric ulcer is not yet clearly understood. Probably it acts by reducing gastric mucosal resistance to attack from acid and pepsin. In about 1% cases it causes a pangastritis leading to gastric atrophy and hypochlorhydria which allows bacteria to proliferate within the stomach and may produce mutagenic nitrites from dietary nitrates predisposing to the development of gastric cancer.2 B. NSAID-induced ulcers: There is a 10-20% prevalence of gastric ulcers and a 2-5% prevalence of duodenal ulcers in chronic NSAID users. They are at least three times more likely than NSAID nonusers to suffer serious gastroin-testinal complications from these ulcers such as bleeding, perforation, or death. Aspirin is the most ulcerogenic NSAID. Peptic ulcer disease may be initiated by NSAID medications- which inhibit prostaglandin production and may induce contact injuries as well. C. Acid hypersecretory states: Ulcers occur only in the presence of acid and pepsin. No acid no ulcer. So it is never found in pernicious anemia (achlorhydric patients). Hypersecretion of acid causes about 35% of cases of duodenal ulcers. Presence of more parietal cells in the stomach is supposed to be important cause of hyperacidity. Zollinger-Ellison Syndrome is caused by gastrin-secreting tumors (gastrinomas), which result in hypergastrincmia and acid hypersecretion. Less than 1% of peptic ulcer disease is caused by gastrinomas. Gastrinomas may arise in the pancreas (40%), duodenal wall (40%), orlytmph nodes (5-15%). Other co-existing factors: A. Genetic factors- 1. Blood group- patient having duodenal ulcer have an increased frequency of blood group “O”. 2. Antigen HLA B5- patient having duodenal ulcer have an increased incidence of HLA B5 antigen. 3. PGI- duodenal ulcer patients usually contain an increased serum pepsinogen lebel (PGI) B. Reduced mucosal resistance- 1. Cigarette smoking - Smoking provokes risk of peptic ulcer. A peptic ulcer patient with smoking, likely to develop complications & rather interfairs with healing of ulcer when treated with standard drugs.2 - Smoking also inhibits the secretion of pancreatic bicarbonate (an endogenous neutralizer of secreted gastric acid) by nicotine. |
| Clinical Features | Clinical features : 1. Recurrent abdominal pain - about 80-90% patients present with recurrent abdominal pain, which has three remarkable characteristics- i. Pain is mostly localized in the epigastrium (and sometimes the patient can indicate by using two or three fingers- ‘pointing sign1), ii. Relationship of pain to food- pain occurs intermittently during day & night usually when the stomach is empty and relieves by food; so, the pain is identified as ‘hunger pain’. But sometimes it is variable and not helpful in diagnosis. Night pain- in case of classical duodenal ulcer, pain wakes the patient from sleep at late night & gets relief by food, drink or antacid, iii. Periodicity- ulcer pain is usually episodic and lasts for a few days to weeks in each episode and in between the patient is quite well. 2. Other symptoms- may include heart burn, water brash, belching and vomiting. Vomiting in more common & typical in gastric ulcer than duodenal ulcer. Persistent vomiting suggests gastric outlet obstruction. Appetite is not affected rather good in duodenal ulcer, but patient is afraid of eating in gastric ulcer. 3. Haematemesis & melaena- in peptic ulcer disease, there may be chronic undetected blood loss, or haematemesis and/or melaena, or even acute perforation. Haemorrhage may also occur in case of NSAID-induced ulcers. |
| Preventions | |
| Treatment | Treatment options for peptic ulcer disease: A. Treatment of active ulcer associated with H. pylori.1 <2 1. First-line therapy: Administer one proton pump inhibitor twice daily (i.e Omeprazole 20mg or Lansoprazole 30mg or Pantoprazole 40mg or Rabeprazole 20mg twice daily) with one of the following antibiotic regimen for 7 days2 (or 10-14 days1): a. Clarithromycin 500mg twice daily + Amoxycillin Igm twice daily. Or b. Clarithromycin 500mg twice daily + Metronidazole 400mg (or 500mg) twice daily. 2. Second-line therapy:2 In case of failure with first-line therapy, a second-line is recommended for 7 days2 (or 10-14 days1): A proton pump inhibitor twice daily (dosages as above) + Bismuth subsalicylate 120mg 4 times daily + Tetracycline 500mg 4 times daily + Metronidazole 400mg (or 500mg) twice daily. N.B i.Some authors advised duration 10-14 days instead of 7 days1. ii. Omeprazole & other proton pump inhibitors must be administered before meal; all antibiotics & Bismuth preparation should administer with meal. iii. Without the eradication of H. pylori, 80% of ulcers will recur within 1 year. 3. Continuation therapy: After completion of eradication therapy, continue treatment with proton pump inhibitor (e.g Omeprazole, Lansoprazole, Pantoprazole or Rabeprazole) once daily, or with H2 receptor blocker (e.g Famotidine, Nizatidine, Ranitidine- for dosage, see below) for 4-8 weeks to promote ulcer healing. B. Treatment of active ulcer not attributable to H. pylori:1 Consider other causes of peptic ulcer (e.g NSAIDs, Zollinger-Ellison syndrome & other acid hypersecretory states). 1. Acid-antisecretory agents a. Proton pump inhibitors: i. Uncomplicated duodenal ulcer: Omeprazole 20mg, or Lansoprazole 30mg, or Pantoprazole 40mg, or Rabeprazole 20mg once daily for 4 weeks, ii. Uncomplicated gastric ulcer or complicated ulcer: Omeprazole 20mg, or Lansoprazole 30mg, or Pantoprazole 40mg, or Rabeprazole 20mg once daily for 8 weeks. Or, b. H2 receptor antagonists: i. Uncomplicated duodenal ulcer: Cimetidine 500mg, or Ranitidine 300mg, or Nizatidine 300mg, or Famotidine 40mg orally once daily at bedtime for 6 weeks, ii. Uncomplicated gastric ulcer: Cimetidine 400mg, or Ranitidine 150mg, or Nizatidine 150mg, or Famotidine 20mg orally twice daily for 8 weeks, iii. Complicated ulcers: Proton pump inhibitors are the drgus of choice. (H2 receptor antagonists are not recommended). 2. Drugs enhancing mucosal defense:2 a Bismuth subsalicylate- 125mg 6 hourly for short duration (4-6 weeks). Bismuth promotes ulcer healing by stimulating mucosal bicarbonate & prostaglandin production. It also acts directly against H. pylori and helps in its eradication. b. Misoprostol- 200mcg 6 hourly for short duration (4-6 weeks). Misoprostol is a synthetic prostaglandin analogue. It promotes ulcer healing by stimulating mucus & bicarbonate secretion & mildly inhibiting acid secretion. It is used solely as a prophylactic agent to prevent NSAID-induced ulcers. c. Sucralfate- Igm 4 times daily for uncomplicated duodenal ulcers. 4. Antacids- low-dose aluminium and magnesium containing antacid regimens (120-240mmol/d) promote ulcer healing through stimulation of gastric mucosal defenses, not by neutralization of gastric acidity. Although, these are now prescribed mainly for symptomatic relief & are widely used for self medication. Dose: 15-30ml liquid antacid 2-4 hourly untill pain subsided, then 2 tsf (10ml) 1 hour after each meal and at bed time for 4-6 weeks. 3. Supporting treatment- Diazepam- especially during acute exacerbation when patient become restless (5mg at bed time). Anticholinergic agents- these agents decrease gastric acid secretion but usually not used. III. Maintenance treatment to prevent ulcer relapse:1 1. NSAID-induced ulcer: Prophylactic therapy reserved for high-risk patients (prior ulcer diseases or ulcer complications, use of corticosteroids or anticoagulants, age >60 years, serious medical illnesses): Proton pump inhibitor once daily before meal (omeprazole 20mg, or rabeprazole 20mg, or lansoprazole 30mg, or pantoprazole 40mg, or esomeprazole 40mg). Misoprostol 200mcg 4 times daily orally. 2. Long-term maintenance therapy indicated in recurrent ulcer patients with H. pylori-negative, or who have failed attempts at eradication therapy: Proton pump inhibitor once daily oraly (omeprazole 20mg, or rabeprazole 20mg, or lansoprazole 30mg, or pantoprazole 40mg, or esomeprazole 40mg). Or, H2 receptor antagonist at bedtime (cimetidine 400-800mg, ranitidine or nizatidine 150-300mg, or famotidine 20-40mg). Indications for maintenance therapy: i. Recurrent ulcers who are with H. pylori-negative. ii. Those patients whose H. pylori can not be eradicated. iii Patient with history of ulcer complication. iv Frequent symptomatic relapse. v. When surgery is not possible due to other causes. Indications for surgery: 1. When adequate medical measures fail. 2. Normal life procedure is hampered. 3. Evidence of outlet obstruction. 4. Repeated haematemesis and malaena not controlled by medical measures. 5. Perforation. 6. Possibility of malignancy. 7. When ulcer developed in young adult or adolescence. |
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