Peptic Ulcer

G.I.
PEPTIC ULCER DISEASE
The term 'peptic ulcer' refers to an ulcer in the lower oesophagus, stomach or duodenum, in the jejunum after surgical anastomosis to the stomach, or, rarely, in the ileum adjacent to a Meckel's diverticulum. Ulcers in the stomach or duodenum may be acute or chronic; both penetrate the muscularis mucosae but the acute ulcer shows no evidence of fibrosis. Erosions do not penetrate the muscularis mucosae.
GASTRIC AND DUODENAL ULCER

Although the prevalence of peptic ulcer is decreasing in many Western communities, it still affects approximately 10% of all adults at some time in their lives. The male to female ratio for DU varies from 5:1 to 2:1, whilst that for GU is 2:1 or less.
Aetiology: Helicobacter pylori

In the industrialised world the prevalence of H. pylori infection in the general population rises steadily with age, and in the UK approximately 50% of those over the age of 50 years are infected. In many parts of the underdeveloped world infection is much more common and is often acquired in childhood. Up to 90% of the population are infected by adult life in some countries. The vast majority of colonised people remain healthy and asymptomatic and only a minority develop clinical disease. Around 90% of duodenal ulcer patients and 70% of gastric ulcer patients are infected with H. pylori; the remaining 30% of gastric ulcers are due to NSAIDs.
Pathogenesis and pathophysiology of infection.

The organism's motility allows it to localise and live deep beneath the mucus layer closely adherent to the epithelial surface. Here the surface pH is close to neutral and any acidity is buffered by the organism's production of the enzyme urease. This produces ammonia from urea and raises the pH around the bacterium. Although it is non-invasive, the bacterium stimulates chronic gastritis by provoking a local inflammatory response in the underlying epithelium due to release of a range of cytotoxins. H. pylori exclusively colonises gastrictype epithelium and is only found in the duodenum in association with patches of gastric metaplasia.
In most people H. pylori causes antral gastritis associated with depletion of somatostatin (from D cells) and gastrin release from G cells. The subsequent hypergastrinaemia stimulates acid production by parietal cells, but in the majority of cases this has no clinical consequences. In a minority of patients (perhaps those who inherit a large parietal cell mass) this effect is exaggerated, leading to duodenal ulceration. The role of H. pylori in the pathogenesis of GU is less clear but H. pylori probably acts by reducing gastric mucosal resistance to attack from acid and pepsin. In approximately 1% of infected people, H. pylori causes a pangastritis leading to gastric atrophy and hypochlorhydria. This allows bacteria to proliferate within the stomach; these may produce mutagenic nitrites from dietary nitrates, predisposing to the development of gastric cancer. The reasons for different outcomes are unclear but bacterial strain differences and host genetic factors are both likely.
Acid-pepsin versus mucosal resistance

An ulcer forms when there is an imbalance between aggressive factors, i.e. the digestive power of acid and pepsin, and defensive factors, i.e. the ability of the gastric and duodenal mucosa to resist this digestive power. This mucosal resistance constitutes the gastric mucosal barrier. Ulcers occur only in the presence of acid and pepsin; they are never found in achlorhydric patients such as those with pernicious anaemia. On the other hand, severe intractable peptic ulceration nearly always occurs in patients with the Zollinger-Ellison syndrome , which is characterised by very high acid secretion. Most DU patients have markedly exaggerated acid secretion in response to stimulation by gastrin, and H. pylori leads to hypergastrinaemia. In GU patients the effects of H. pylori are more complex, and impaired mucosal defence resulting from a combination of H. pylori infection, NSAIDs and smoking may have a more important role.
Control of acid secretion
Seguence of events in the pathophysiology of duodenal ulceration
Conseguences of H.pylori infection
Gastroduodenal mucosal protection
Pathology
Chronic GU is usually single; 90% are situated on the lesser curve within the antrum or at the junction between body and antral mucosa. Chronic DU usually occurs in the first part of the duodenum just distal to the junction of pyloric and duodenal mucosa; 50% are on the anterior wall. GU and DU coexist in 10% of patients and more than one peptic ulcer is found in 10-15% of patients. A chronic ulcer extends to below the muscularis mucosa and the histology shows four layers: surface debris, an infiltrate of neutrophils, granulation tissue and collagen.
Clinical features
PU disease is a chronic condition with a natural history of spontaneous relapse and remission lasting for decades, if not for life. Although they are different diseases, DU and GU share common symptoms which will be considered together. The most common presentation is that of recurrent abdominal pain which has 3 notable characteristics: localisation to the epigastrium, relationship to food and episodic occurrence. Occasional vomiting occurs in about 40% of ulcer subjects; persistent vomiting occurring daily suggests gastric outlet obstruction. In one-third of patients the history is less characteristic. This is especially true in elderly subjects under treatment with NSAIDs. In these patients pain may be absent or so slight that it is experienced only as a vague sense of epigastric unease. Occasionally, the only symptoms are anorexia and nausea, or a sense of undue repletion after meals. In some patients the ulcer is completely 'silent', presenting for the first time with anaemia from chronic undetected blood loss, as an abrupt haematemesis or as acute perforation; in others there is recurrent acute bleeding without ulcer pain between the attacks. It should be noted that the diagnostic value of individual symptoms for PU disease is poor, and the history is often a poor predictor of the presence of an ulcer.
Investigations
The diagnosis can be made by double-contrast barium meal examination or by endoscopy. - Endoscopy is the preferred investigation because it is more accurate and has the enormous advantage that suspicious lesions and H. pylori status can be evaluated by biopsy. For those with a DU seen at barium meal, urea breath testing will accurately define H. pylori status. Very occasionally, a GU may be malignant; therefore endoscopy and biopsy are mandatory when a GU is detected on barium examination. In GU endoscopy must be repeated after suitable treatment to confirm that the ulcer has healed and to obtain further biopsies if it has not. In contrast, it is not necessary to repeat endoscopy after treating DU.
Management
The aims of management are: to relieve symptoms, induce ulcer healing in the short term, cure the ulcer in the long term. H. pylori eradication is the cornerstone of therapy for peptic ulcers, as this will successfully prevent relapse and eliminate the need for longterm therapy in the majority of patients.
H. pylori eradication
First-line (triple) therapy: - IPP at standart dose (12-hourly) for eg. rabeprasol - Amoxicillin -1000 mg (12-hourly) - Claritromycin 500 mg (12-hourly) for 7 days Good result is > 85% eradication!
H. pylori eradication
Second-line (quadruple) therapy: IPP at standart dose (12-hourly) bismuth 120 mg 6-hourly tetracicline 500mg 12-hourly metronidazol-400 mg 12-hourly for 7-10 days
General measures
Cigarette smoking, aspirin and NSAIDs should be avoided. Alcohol in moderation is not harmful and no special dietary advice is required.
Short-term management
Many different drugs are available for the short-term management of acid peptic symptoms
- Antacids. These are widely available for self-medication and are used for relief of minor dyspeptic symptoms. The majority are based on combinations of calcium, aluminium and magnesium salts, all of which have individual sideeffects. Calcium compounds cause constipation, while magnesium-containing agents cause diarrhoea. Aluminium compounds block absorption of digoxin, tetracycline and dietary phosphates. Most have a high sodium content and can exacerbate congestive heart failure.
Histamine H2-receptor antagonist drugs.
These are competitive inhibitors of histamine at the H2-receptor on the parietal cell. Dyspeptic symptoms remit promptly, usually within days of starting treatment, and 80% of duodenal ulcerswill heal after 4 weeks. These drugs do not inhibit acid secretion to the same degree as the proton pump inhibitors but are useful for the short-term management of acid dyspeptic symptoms prior to investigation. They are moderately effective for the management of reflux disease.
H+/K+ ATPase ('proton pump') inhibitors(IPP).

These are substituted benzimidazole compounds that specifically and irreversibly inhibit the proton pump hydrogen/potassium ATPase in the parietal cell membrane. They are the most powerful inhibitors of gastric secretion yet discovered, with maximal inhibition occurring 3-6 hours after an oral dose. They have an excellent safety profile. After a few days of treatment virtual achlorhydria is achieved and rapid healing of both GU and DU follows. Omeprazole, lansoprazole and rabeprazole are important components of H. pylori eradication regimens. IPP are also much more effective than H2-antagonists for healing and maintenance of reflux oesophagitis.
Dosis of IPP
Drags Omeprazole Short term 20-40 mg once daily 30 mg once daily 40 mg once daily 20 mg once daily Maintenance 20 mg at night
Lansoprazole
Pantoprazole Rabeprazole
15 mg at night
20 mg once daily 10-20 mg once daily
SIDE-EFFECTS of IPP
Hipergastrinemia Diarrhoea Headache Rashes Interection with warfarin, phenytoin, fewer drugs
Colloidal bismuth compounds.

Colloidal bismuth subcitrate (CBS) is an ammoniacal suspension of a complex colloidal bismuth salt. It has little, if any, effect on gastric acid secretion and its ulcerhealing effect is probably due to a combination of activity against H. pylori and enhancement of mucosal defence mechanisms.
Synthetic prostaglandin analogues (misoprostol).

Prostaglandins exert complex In low doses protect against injury induced by aspirin and NSAIDs by enhancing mucosal blood flow, and by stimulating mucus and bicarbonate secretion and epithelial cell proliferation. At high doses acid secretion is inhibited. Misoprostol is effective for the prevention and treatment of NSAID-induced ulcers, but in clinical practice IPP are preferred, since they are at least as effective and have fewer side-effects.
Maintenance treatment
Continuous maintenance treatment should not be necessary after successful H. pylori eradication. For the minority who require maintenance treatment the lowest effective dose should be used.
INDICATIONS FOR SURGERY IN PEPTIC ULCER

EMERGENCY - Perforation - Haemorrhage
ELECTIVE - Gastric outflow obstruction - Recurrent ulcer following gastric surgery
COMPLICATION of peptic ulcer disease

perforation, gastric outlet obstruction bleeding.

Peptic Ulcer

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G.I.

PEPTIC ULCER DISEASE

GASTRIC AND DUODENAL ULCER

Aetiology: Helicobacter pylori

Pathogenesis and pathophysiology of infection.

Acid-pepsin versus mucosal resistance

Control of acid secretion

Seguence of events in the pathophysiology of duodenal ulceration

Conseguences of H.pylori infection

Gastroduodenal mucosal protection

Histamine H2-receptor antagonist drugs.

H+/K+ ATPase ('proton pump') inhibitors(IPP).

Colloidal bismuth compounds.

Synthetic prostaglandin analogues (misoprostol).

INDICATIONS FOR SURGERY IN PEPTIC ULCER

COMPLICATION of peptic ulcer disease

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