Peptic ulcer disease Flashcards
Protection
Alkaline mucus
Tight junctions between epithelial cells
Peptic ulcers
Higher rate in men than women
15% patients die from ulcer perforation
Peritonitis
Bacteria living in stomach and infection rapidly spread into blood
Risk of multiple organ failures
Stomach
Alkaline mucus secrete alkaline mucus that Forms thin layer over luminal surface
Mucus content neutralises H+ in epithelium
Peptic ulcer disease factors affecting Acid/Pepsin
Helicobacter pylori
Smoking
Genetic factors
Stress
Peptic ulcer disease factors affecting mucosal defence
Smoking
Genetic factors
NSAIDs
Gastric ulceration
More common in women
Avoid food, hence lose weight
Duodenal ulceration
More common in men
No weight loss
Protective factors
Bicarbonate layer
Mucus
Blood flow
Cell renewal
Prostaglandins
Phospholipids
Damaging factors
Acid
Pepsin
Bile salts
Drugs NSAID
H. pylori
Warning signs
Iron-deficient
Anaemic
Chronic blood loss
Weight loss
Progressive dysphagia
Persistant vomiting
H. Pylori stats
40% infected
95% gastric ulcer
80% duodenal ulcer
H. Pylori
Survives in microaerophil
Infects lower part of stomach
Inflammation of gastric mucosa (asymptomatic)
Colonises antrum of stomach
H. Pylori in stomach
Uses Flagella to burrow into mucus lining of stomach where pH is more neutral
Moves towards less acidic environment (chemotaxis)
Adheres to epithelial cells by producing adhesins, bind lipids and carbohydrates
BabA binds to Lewis b antigen displayed
SabA binds to increased levels of sialyl-Lewis x antigen
Produces urease to neutralise acid in stomach
Diagnostic testing for H. pylori
Serologic evaluation of antibodies
Urea breath test (UBT)
Stool antigen test (SAT)
UBT
Patients swallow a capsule containing urea made from isotope of carbon. Urea broken down and turned into CO2 and excreted through breath