Peptic ulcer disease

Related Subjects: | Upper Gastrointestinal Bleed | Oesophageal Variceal Bleeding | Dieulafoy Lesion | Mallory-Weiss Tear | Gastric Cancer | Peptic Ulcer Disease | Oesophagogastroduodenoscopy (OGD/EGD) | Hereditary Haemorrhagic Telangiectasia |Hypovolaemic or Haemorrhagic Shock

Most patients with peptic ulcer disease have normal gastric acid secretion. GU with punched out heaped up margins suggests cancer indeed 10% of gastric ulcers are malignant

About

• A peptic ulcer is defined as a break in the mucous membrane lining the stomach or duodenum

Physiology

• Acid (Parietal cells) are found in the Fundus/Body
• Gastrin (G cells) - in the Antrum. Increases gastric acid : Release due to gastric distension, protein, calcium. Two forms G-34 and G-17 which is more abundant

Aetiology

• GU : Mucosal breakdown
• DU : Excess acid
• Actually not entirely clear

Location

• Duodenum 80%
• Stomach 19%
• Both duodenum and stomach 5%
• Meckel's diverticulum <1%
• Oesophagus <1%
• Multiple sites consider ZES

Risks for peptic ulcer disease

• Older age
• Males > Females GU 3:1 DU 4:1
• HP infection
• Aspirin and NSAIDs and steroids(mainly GU)
• Zollinger-Ellison syndrome
• Stress, Burns, Major surgery/trauma
• Hyperparathyroidism
• Genetics e.g. DU and Blood group O
• Gastric cell hyperplasia

Peptic ulcer disease

• Gastric Ulcer: Aspirin and NSAIDs may be important risks. Increase with hyperparathyroidism and Zollinger Ellison syndrome. Gastric ulcers are commonest along the lesser curvature of the stomach. 80% HP +ve. Mean age 50-60.
• Duodenal Ulcer : x4 commoner than GU. Men > women. 95% HP +ve. Mean age 30-40

Clinical

• Epigastric discomfort, pointing signs
• DU may have pain into the back
• GU pain may be worse immediately with food
• DU pain worse when hungry and at night
• Dyspepsia, Nausea, Haematemesis, Melaena

Complications

• Haemorrhage: see management of Upper GI haemorrhage
• Perforation: commoner with DU and presents with a sudden localised pain which may become generalised and a rigid abdomen with free air under the diaphragm. Urgent laparotomy with the closure of perforation and drainage of the abdomen. Conservative management in those unlikely to survive the surgery.
• Gastric outlet obstruction: produces copious projectile vomiting and a succussion splash and a Hypochloraemic hypokalaemic metabolic alkalosis - treat with fluid resuscitation, acid suppression and stabilisation and then consider for Stenting or surgery
• Recurrence: further ulcers

Investigations

• Testing for HP. Can use Urea breath tests detecting radioactive carbon from orally taken radiolabelled urea spit by HP urease, IgG serology shows the previous infection and remains positive after eradication, stool antigen test, CLO testing at endoscopy detects urea breakdown to ammonia altering pH and changing indicator from yellow to red. Best red at 24 hours.
• OGD and usually multiple biopsies especially where suspicions of tumour exist with gastric ulcers. Also, test for HP
• Repeat OGD in 6 weeks for Gastric ulcers to exclude malignancy
• Repeat testing for HP at 6 weeks to ensure eradication

Management

• Stop smoking, reduce alcohol
• HP +ve : Eradication has healing rates of over 90%. Ongoing PPI not usually needed
• HP - ve: Stop Aspirin and NSAIDs if implicated. Use proton pump inhibitors to suppress acid production.
• Surgical management has more or less disappeared over the past 20 years except for emergency management of uncontrolled haemorrhage or perforation. See Upper Gastrointestinal haemorrhage. The presence of a spurting vessel at endoscopy that does not respond to adrenaline/epinephrine is ominous.
• Surgical management is simply underrunning the bleeding vessel with a suture. Duodenal perforation managed by approximating ulcer edges or use of an omental patch.