PEPTIC ULCER DISEASE

ACID PEPTIC DISEASE

• Gastric ulcer• Duodenal ulcer• Gastritis• GERD• Stress ulcers• Zollinger Ellison Syndrome

Peptic ulcer

Definition

A mucosal defect equal to or greater than 0.5 cm that

extent to or beyond muscularis mucosa. These ulcers are caused by increased acid/ pepsin secretion or diminished mucosal defense.

Types• Chronic• Acute

Location• Duodenum• Stomach ? (4%)• Gastric and duodenal ulcer together. 10%• Lower oesophagus• Jejunum after anastomosis to stomach• Meckels diverticulm

Gastric / duoedenal ulcer

Prevalance

H2 receptor inhibitors

Proton pump inhibitors

Effective treatment against H Pylori

• Overall risk , 10% • More common in males• Duodenal ulcer 4 times more common than gastric

ulcer• Slight increase in GU due to wide spread use of

NSAIDs

D cells

ECL cells

Cholecystokinin

Secretin

Aetiology

1. Helicobacter pylori• urease– urea- ammonia- hypergastrinaemia-

increased acid secretion• H. pylori- reduces the gastric mucosal resistance

against acid and pepsin. Enzymes, cytotoxins• Local inflammatory response due to cytotoxins• 90% in DU

• 70% in GU

2. Non steroidal anti inflammatory drugs( NSAIDs)

• 30% in GU and smaller percentage in DU

• More commonly associated with complications

• Inhibit cyclooxygenase (COX,1,2) & reduce mucosal protective prostaglandins

Risk factors for NSAIDs induced ulcers

• Age > 60 years• Past history of peptic ulcer• Additional steroids• Multiple NSAIDs,• High dose• Individual NSAIDs. Piroxicam, ibuprufen

3. Heriditary

• Positive family history in DU

• Blood group O

• Increased level of serum pepsinogen 1

4. Smoking

• More prone to develop gastric ulcer than DU

• Ulcer less likely to heal and prone to haemorrhage and perforation

5. Stress

Burns,

Head injury

on ventilators

6. Gastric emptying

– Increased---DU

– Decreased----GU. (stasis), DG refkux

7. low socioeconomic group/ developing world

8. Steroids- atrophy of mucosa

9. Spicy foods

10. Gastrinoma

Summary (aetiology)

(Acid pepsin versus mucosal barrier)

• Increased acid and pepsin secretion.– Gastrin, Histamine, acetylcholine, cholecystokinine

• Reduced mucosal barrier– H. Pyelori

– NSAIDs

– Smoking

– Decreased bicarbonate production

– Decreased protective prostaglandins

Pathology Duodenal ulcer

– First part of duodenum

– 50% on anterior duodenal wall, 50% on posterior wall

– Anterior ulcers tend to perforate while posterior tend to bleed

– Usually single but can be more than one

– Fibrosis – pyloric stenosis

– All benign

Pathology

Gastric ulcer– Usually single, 2-4 cm, smooth base perpendicular

walls

– Located on lesser curve but can occur anywhere

– Larger than duodenal ulcer

– Fibrosis can lead to Hour glass deformity.

– Can penetrate into transverse colon, pancreas.

– All stomach ulcers are not benign. (4% malignant)

Malignancy in gastric ulcer

• Benign ulcers becoming malignant.?

• Malignant to start with

• All stomach ulcers are considered malignant until proved benign on biopsy & follow up

• Always, always take a biopsy of stomach ulcer• 10 well targeted biopsies

Clinical features

• Pain abdomen– Epigastrium, may radiate to back

– Relation with meals- hunger pain

• Periodicity– Episodic- lasting for several weeks (periodicity)

• Vomiting

• Alteration in weight

• Bleeding– Chronic– Acute

• Other symptoms– Dyspepsia, heartburn, epigastric fullness, loss of appetite

• Silent– Anaemia– Haemetemesis– Perforation

D/D pain epigastrium• Duodenal ulcer• Gastric ulcer• Gastritis• Carcinoma• GERD• Pancreatitis• Cholecystitis• Biliary colic• Myocardial infarction• Pleuricy• percarditis

Investigations

• Blood CP

• Stool for occult blood

• Serum amylase

• Ultrasound abdomen

• ECG

• CXR

• Esophagogastrduodenoscopy (EGD)

• Urea breath test• • Direct detection of urease activity/ H pylori in biopsy

specimen

• Biopsy of any stomach ulcer

Treatment• Medical• Surgical

Goals– pain relief

– Eradicate of H. pylori infection

– Healing of ulcer

– Prevent recurrence

Medical treatment

General measures• Cessation of smoking• Avoidance of spicy foods• Avoid NSAIDs if possible

• Antacids. Aluminum hydroxide, Magnesium hydroxide

Ulcer reducing drugs• H2 receptors inhibitors

– cimetidin

– Famotidine

– Ranitidin

• Pproton pump inhibitors– Omeprazole .40 mg OD– Lansoprazole. 30 mg 12hourly– Pantoprazole 40 mg OD

Eradication of H. pylori

• One of the proton pump inhibitors x 02 weeks. Duration may vary

• Combination of two antibiotics x 02 weeks– Amoxycillin– Clithromycin– Metronidazole– Tetracycline

• Bismuth added

Mucosal protective

• Bismuth

• Sucralfate

• Misoprostol

• Cisapride

• Maintenance of treatment

– Usually not required in majority after eradication therapy for H. Pylori

– Lowest effective dose of proton pump inhibitors for prolonged period

• Surgical treatment

• Indications

• Perforation• Haemorrhage• Gastric outlet obstruction• Interactable disease

– Delayed healing. Ulcer persists despite 3 months of active treatment

– Ulcer recurrence with in one year of initial healing despite maintenance therapy

Surgical treatment for uncomplicated duodenal ulcer

Aim

• Diversion of acid from the duodenum• Reducing the acid/ pepsin secretion• Both of the above

Options

• Truncal vagotomy and drainage• Truncal vagatomy and antrectomy• Highly selective vagotomy. First choice• Lparoscopic

• Billroth 1 gastrectomy• Billroth 11 gastrectomy• Gastrojejunostomy

Operation for gastric ulcer

Goal• To excise the ulcer• To reduce the acid/ pepsin output• To minimize the bile reflux and gastric stasis

• Options

• Billroth 1 gastrectomy. (Ulcerated part included)• Billroth II gastrectomy (Ulcerated part included)• T.Vagotomy, Drinage and ulcer excision• Proximal gastrectomy

Complications of ulcer surgery• Recurrent ulcerations• Small stomach syndrome• Bile vomiting• Early and late dumping• Post vagotomy diarrhoea• Malignant transformation• Nutritional cosequences• Gall stones

• Complications of peptic ulcer

– Haemorrhage– Perforation– Gastric outlet obstruction