Peptic ulcers Flashcards
What is a peptic ulcer?
- break in the lining of the mucosa (down to submucosa)
- of stomach or proximal duodenum
- more than 5mm in diameter
- can also occur in distal oesophagus
What are symptoms of peptic ulcers?
- recurrent burning epigastric pain
- duodenal ulcer - pain gets better on eating
- gastric ulcer - pain gets worse on eating
- heartburn/chest (retrosternal) pain
- bleeding -> anaemia, melaena, haematemesis
- belching, bloating, intolerance to fatty foods
- can present w complications of perforation or obstruction
patient can sometimes show site of pain with one finger
Are duodenal or gastric ulcers more common?
duodenal ulcers are 4x more common than gastric ulcers
What signs may be elicited on examination for peptic ulcers?
- epigastric tenderness
- peritonitic if perforated
- generalised abdo pain
- guarding
- rebound tenderness
- patient prostrated lying still
- positive cough test
What are the differential diagnoses for epigastric pain?
- Peptic ulcer disease
- Pancreatitis
- Appendicitis
- AAA
- Small bowel obstruction
- Mesenteric ischaemia
- Inferior wall MI
- Pericarditis
- Cholecystitis
- Cholangitis
- Oesophagitis
- Gastritis
What are the major risk factors for the formation of peptic ulcers?
- H. Pylori infection
- NSAIDs + Aspirin
- Smoking
- Inc age
- FHx/Hx of PUD
- Intensive care patient
- Rarer causes: hyperparathyroidism, Zollinger-Ellison syndrome, gastric ischaemia, infections + Crohn’s
DUs are almost always associated w/ H. Pylori inifection, and GUs with NSAID use
Generally speaking, why/how do peptic ulcers form?
- result from imbalance between defence mechanisms and attack mechanisms
- defence factors = mucin, cellular mucus, bicarb, mucosal blood flow, cell turnover/formation
- attack factors = acid, pepsin, H.pylori, bile salts, NSAIDs
Helicobacter pylori is a spiral shaped bacterium that has been identified as being carcinogenic. It can cause acute gastritis and is thought to be spread via contaminated food + water.
What is the pathogenesis of H. Pylori infection causing peptic ulcers?
- increases gastric acid secretion (by inc gastrin and reduced somatostatin) -> increasing acidity of gastric contents that flow into duodenum
- disrupts the protective mucosal layer
- reduces duodenal bicarbonate production
- produces virulent factors eg. VacA, CagA, urease
- longstanding H.Pylori infection + severe inflammation -> results in disruption of epithelial tight junctions + cell death -> leading to gastric ulcers
What is the pathophysiology of NSAIDs causing peptic ulcers?
By primarily weakening the mucosa’s protective mechanisms
- inhibit COX-1 so PG synthesis is reduced so blood flow + alkaline secretions are reduced
- involve trapping hydrogen ions
- irritates mucosa
- impairs mucosal repair mechanisms
- increase risk of bleeding through anti-platelet actions
Which duodenal ulcers bleed and which perforate?
- posterior duodenal ulcers bleed
- anterior duodenal ulcers perforate
- due to the gastroduodenal artery which comes down behind duodenum
How do you investigate peptic ulcer disease?
- non-invasive H. Pylori testing in pts <55yrs w/out ALARMS
- OGD - pts with ALARMS or >55yrs
- FBC - looking for microcytic anaemia
- Stool heme test
Describe the non-invasive methods to diagnose H. Pylori infection
- Serological tests - detect IgG antibodies against H. Pylori, useful in diagnosis and epidemiological studies. IgA can also be found in saliva - but not as specific + sensitive as serology.
- 13C-Urea breath test - quick, screening tool, pts swallow urea containing isotope + it can be detected in next 30 mins from exhaled breath - indicates presence of urease which H. Pylori secreted in order to survive. Pt must be off PPIs + Abx for accuracy. (THIS IS FIRST LINE NOW)
- Stool antigen test - if positive, faeces will contain H. Pylori antigens, detected by immunoassay. Pt must be off PPIs + Abx for accuracy.
Describe the invasive methods done at endoscopy to diagnose H. Pylori infection
- Rapid urease test (CLO) - biopsy of mucosa taken from antrum of stomach, placed into medium containing urea + an indicator of phenol red. If H. Pylori present, it hydrolyses the urea -> ammonia, increasing pH of medium causing a colour change.
- Histology - blood taken from OGD, put under microscope + visualised by giemsa staining, if infected H. Pylori will be seen. Again, best to be off PPIs.
What is the epidemiology of H. Pylori infection?
- high prevalence in developing countries (80-90%)
- lower in developed countries (20-50%)
- infection rates highest in lower-income groups
- infection usually acquired in childhood
- faecal-oral or oral-oral
What is the association of H. Pylori with gastric cancer?
- The incidence of distal (but not proximal) gastric cancer parallels H. Pylori infection in countries w/ a high incidence of gastric cancer
- Serological studies show ppl infected w/ H. Pylori have a higher incidence of distal gastric carcinoma
- Over 70% of gastric B-cell lymphoma pts have H. Pylori
- H. Pylori gastritis has been shown to contain the clonal B cell that eventually gives rise to MALT lymphoma
