Peptic Ulcer Disease & Gastritis

When it’s one of those days where you don’t feel like working… and it’s sunny. In London. Actually sunny. And not the deceptively cold type.

Peptic Ulcer Disease (PUD) & Gastritis

Definition: ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin, most commonly gastric and duodenal.

Image result for anatomy of stomach

Aetiology/ risk factors:

-Overall cause is an imbalance between damaging action of acid and pepsin and mucosal protective mechanisms.

-H.pylori (∼85%)

H.pylori is the commonest bacterial pathogen found worldwide. Over 50% of over 40s have it. It causes gastritis, peptic ulcers, gastric cancer and gastric lymphoma.

-Drugs: NSAIDs, steroids, SSRIs

Duodenal: increased gastric acid secretion and increased gastric emptying (decreases duodenal pH)

-Gastric: reflux of duodenal contents, delayed gastric emptying


-Zollinger-Ellison syndrome (peptic ulcers due to gastrin secreting adenoma- rare)

Gastritisassociated with PUD with similar risk factors. Additionally:

-alcohol, reflux/ hiatus hernia, atrophic gastritis

-Granulomas (Crohn’s, Sarcoidosis)


-Zollinger-Ellison & Menetrier’s disease

Epidemiology: common. Annual incidence about 1-4/1000

-More common in males

-Duodenal ulcers 4x more common than gastric ulcers. Mean age = 30s.

-Gastric ulcers occur mainly in the elderly (lesser curve of stomach). Mean age = 50s.


-Epigastric abdominal pain, relieved by antacids

Duodenal ulcer- 50% asymptomatic

epigastric pain, typically before meals/several hours after a meal, or at night, relieved by eating (as gastric sphincter closes) or drinking milk

Gastric ulcer- may be asymptomatic

epigastric pain, worse soon after eating

-weight loss (avoid food because they get pain when they eat)

Bleeding peptic ulcer-

+ haematemesis (typically ‘coffee ground’ appearance)

+malaena (black tarry stool)

Gastritis- epigastric pain, vomiting, haematemesis


-examination may be normal

-tender epigastrium

Bleeding peptic ulcer-

-anaemia: conjunctival pallor, koilonychia etc.

-signs of shock if massive bleeding: tachycardia, hypotension, cold peripheries

Pyloric stenosis (complication)- succession splash

Gently shake the abdomen by holding either side of the pelvis. A positive test occurs when a splashing noise is heard, either with the naked ear, or with the aid of a stethoscope. The test is not valid if the patient has eaten or drunk fluid within the last three hours.


Bloods: FBC (anaemia?), amylase (exclude pancreatitis), U&Es, clotting screens (if GI bleeding), LFT, cross match blood (if actively bleeding, in case of transfusion)

Upper GI endoscopy- stop proton-pump inhibitor (PPI) 2 weeks before. Localises ulcer and important in excluding malignancy in gastric ulcer. May repeat endoscopy to check for healing if there is bleeding or perforation of the ulcer.

Image result for peptic ulcer endoscopy

Biopsy of ulcer/brushings- Test for H.pylori (difficult to visualise on histology), histology/cytology to check for malignancy in gastric ulcers. Duodenal ulcers do not need biopsy as rarely malignant.

Image result for h.pylori biopsy



H.pylori testing- 13C-Urea breath test: radio-labelled urea given by mouth and detection of 13C in the expired air. (Other options = stool antigen, serology, histology, culture, CLO test)

Gastrin concentrations– measure when off PPIs if Zollinger-Ellison syndrome is suspected. Secretin test for Zollinger-Ellison syndrome = IV SECRETIN causes a rise in serum GASTRIN


Lifestyle: reduce alcohol, smoking, aggravating foods

Stop drugs: if possible, stop causative drugs such as NSAIDs or antiplatelets. If not possible, PPI can be given alongside, to prevent and treat PUD. Misoprostol is an alternative (prostaglandin analogue) for prevention of NSAID induced ulcers.

H.pylori eradication: triple therapy is 80-85% effective at eradication

PPI, Amoxicillin 1g, Clarithromycin 500mg- 2x/7d OR

=  PPI, Metronidazole 400mg, Clarithromycin 250mg- 2x/7d

-PPI = Omeprazole (20mg/12h), Lansoprazole (30mg/12h)

Resistant infection = PPI + 2 Antibiotics + Tripotassium dicitratobismuthate (cytoprotective agent) – 14d

Reduce acid:

PPIs e.g. Lansoprazole (30mg/24h PO, 4wks for duodenal, 8wks for gastric ulcers) or H2 blockers e.g. Ranitidine (300mg, PO, each night/8wk)

Surgery- indicated for complications such as haemorrhage, perforation and  pyloric stenosis and may be considered for patients not responsive to medication.

Options include:


Highly selective vagotomy– vagus supply to lower oesophagus and stomach is denervated, leaving the nerve of Latarget to the pylorus intact so gastric emptying is unaffected.

Gastrectomy– rarely required, e.g. in Zollinger-Ellison syndrome (multiple ulcers)

Vagotomy & pyloroplasty– vagotomy + cut and widen the pylorus of the stomach


-Acute management of upper GI haemorrhage

-protect airway and give high flow oxygen

-IV access

-FBC, U&E (raised urea = massive blood meal), LFT, clotting

-cross match 4-6 units of blood (given 1 unit for each 10g/L that Hb is less than 140g/L)

IV fluids, whilst waiting for blood to be cross matched. If haemodynamically deteriorating, give group O Rh-ve blood

-urinary catheter, monitor output

-CXR, ECG, ABG, consider CVP (central venous pressure) line

transfuse with cross-matched blood if needed, until haemodynamically stable

-correct any clotting abnormalities (e.g. vitamin K, fresh frozen plasma, platelets)

-monitor pulse, BP, CVP (keep > 5cmH2O) at least hourly until stable

omeprazole e.g. 80mg IV bolus, then continuous IV infusion at 8mg/h for 3 days. Change to oral PPI after 3 days

-arrange urgent endoscopy

⇒Endoscopic adrenaline injection, diathermy, laser coagulation or heat probe if active bleeding or non-bleeding visible vessel.

⇒Surgery may be needed if endoscopic control fails.

-Follow with eradication therapy if H.pylori is present.

Surgery for severe haemorrhage or rebleeding, especially in elderly, and if uncontrollably bleeding at endoscopy or despite blood transfusions (6 units >60ys, 8 units < 60 years). The bleeding ulcer base is underrun or oversewn.


Most patients undergo surgery, either laparoscopic or open repair. H.pylori eradication commenced post-op.

Some advocate an initial conservative approach in patients without generalised peritonitis.


-NG tube

-IV antibiotics

-Pyloric stenosis

Late complication of duodenal ulcers due to scarring

Patients complain of vomiting large amounts of food some hours after meals.

First = endoscopic balloon dilatation, followed by maximal acid suppression.

If unsuccessful = drainage procedure e.g. gastro-enterostomy or pyloroplasty +/- highly selective vagotomy


-bleeding, perforation, pyloric stenosis

-malignancy- gastric ulcers are more likely to be malignant (especially if anywhere other than the lesser curve of the stomach)

-reduced gastric outflow

Prognosis: Generally good prognosis as peptic ulcers associated with H.pylori can be cured by eradication.

Rockall Score is used to predict rebleeding and mortality of upper GI bleeds.

References: Cheese & Onion, Rapid Medicine

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