Peptic ulcer disease Flashcards
Peptic ulcers
involve ulceration of the mucosa lining the stomach (gastric ulcer) or the duodenum (duodenal ulcers)
Which type of ulcer is more common?
Duodenal ulcers - 4x more common than gastric ulcers
Pathophysiology of PUD
Stomach mucosa is prone to ulceration from:
Breakdown of the protective layer of the stomach and duodenum
Increase in stomach acid
What is the protective layer of the stomach mucosa comprised of?
Mucus and bicarbonate
What breaks down the protective layer?
Medications e.g. steroids & NSAIDs
Helicobacter pylori
Increased acid can result from:
Stress Alcohol Caffeine Smoking Spicy foods
What is the usual presentation of PUD
Non-specific
Epigastric pain/ discomfort
Dyspepsia
Nausea & vomiting
Bleeding causing haematemesis - “coffee ground” vomit or haematemesis
Iron deficiency anaemia due to constant bleeding
Classification of PUD:
Acute: usually due to drugs (NSAIDs or steroids) or “stress”
Chronic: drugs, H.pylori, hypercalcaemia, Zollinger-Ellison
Duodenal ulcers are more common in:
M >F
occur in the 1st part of the duodenum
Gastric ulcers occur:
in the lesser curve of the gastric antrum
Risk factors for duodenal ulcers:
H.pylori (90%) Drugs - NSAIDs, steroids Smoking Alcohol Increased gastric emptying Blood Group O
Risk factors for gastric ulcers:
H.pylori (80%) Smoking Drugs Delayed gastric emptying Stress: - Cushing's: intracranial disease - Curling's: burns, sepsis, trauma
Presentation of duodenal ulcers:
Epigastric pain
Worse before meals and at night
Improved by eating or drinking milk
Presentation of gastric ulcers
Epigastric pain
Worse after eating
Relieved by antacids
Weight loss
Complications of peptic ulcers
Haemorrhage - haematemesis/ melaena - can be life threatening
Perforation - causing peritonitis
Gastric outflow obstruction - scarring and strictures –> pyloric stenosis –> difficulty emptying stomach contents –> distension, colic, nausea and vomiting
Malignancy - increased risk associated with H.pylori
Investigations for PUD
Bloods: FBC, urea (increased in haemorrhage)
C13 breath test/ rapid urease test (CLO test)
OGD - stop PPI/H2RA 2 weeks before
- always take biopsies of the ulcers to rule out malignancy
Gastrin levels if Zollinger-Ellison suspected
Conservative management of PUD
Lose weight Stop smoking and reduce alcohol intake Avoid hot drinks and spicy foods Stop drugs: NSAIDs and steroids OTC antacids
Medical management of PUD
Same as GORD OTC antacids: Gaviscon, Mg trisilicate H.pylori eradication PAC500 or PMC250 Full dose PPI for 1-2mo - PPI lansaprazole 30mg OD - H2RAs: ranitidine 300mg nocte Low dose acid suppression PRN
Surgery for PUD: what are the key concepts?
No acid –> no ulcer
Secretion of the acid is stimulated by gastrin and vagus nerve
What are the types of surgery used for PUD?
- Vagotomy:
- Truncal - reduced acid secretion but prevents pyloric sphincter relaxation therefore must be combined with pyloroplasty
- Selective: vagus nerve only denervated where it supplies lower oesophagus and stomach - Nerves of laterjet, supply pylorus, left intact - Anterectomy with vagotomy
- distal half of the stomach removed and anastomosed with duodenum = Biliroth 1
- to small bowel loop with duodenal stump oversewn = Biliroth 2 or polya - Sub-total gastrectomy with Roux en Y
- occasionally performed for Zollinger-Ellison
What are the physical complications of PUD surgery?
Stump leakage
Abdominal fullness
Reflux or bilious vomiting (improves with time)
Stricture
What are the metabolic complications of PUD surgery?
Dumping syndrome - abdo distension, flushing, n/v
- Early: osmotic hypovolaemia
- Late: reactive hypoglycaemia
Blind loop syndrome - malabsorption, diarrhoea
- overgrowth of bacteria in the duodenal stump
- anaemia: Fe + B12
- osteoporosis
Weight loss: malabsorption of reduced calorie intake
