CPT2: GI 3 (Peptic Ulcer Disease) Flashcards
Which areas can peptic ulcers develop?
Stomach and duodenum
What is the pH of the stomach and its functions?
- Acidic environment pH 1-2
- Chemical breakdown of food
- Physical breakdown of food
- Churns and pepsin release
- temporary storage
- protection from pathogens
- Secretes intrinsic factor for B12 absorption
Where HCl produced?
Why is the stomach not damaged by low pH?
What stimulates this priduction?
- Hydrochloric acid produced by Parietal cells
- Food breakdown
- Defence from pathogens
- Mucosal cells secrete a mucus barrier/layer to protect the lining of the stomach from attack from stomach acid.
- Mucous layer production is stimulated by prostaglandin E2 and I2
How is HCl produced?
What are stimulators and inhibitors of acid secretion
- The gastric parietal cell produces HCl to maintain pH 1-2
- •The H+/K+/ATPase pump (proton pump) secretes H+ into the stomach
Stimulating factors:
- Histamine
- Acetylcholine (Vagus nerve)
- Gastrin
These act on proton pump inhibitor to stimulate secretion of H+
Inhibiting factors:
- Prostaglandin E2 and I2
- Somatostatin
What is the pathophysiology of gastric ulcers?
A break in the protective mucosal layer leads to inflammation and erosion down through the gastric epithelium down to the muscularis mucosa.
An imbalance between factors promoting mucosal damage and those promoting mucosal defence
What are the layers of the stomach?
What are the disease characteristics of Gastric and duodenal ulcers?
What are complications of Ulceration?
- Severe upper GI bleeding – erosion of ulcer into blood vessel – Haematemesis (blood in vommit)/shock
- Anaemia – small but persistent ulcer bleeding
- Pyloric stenosis – scarring of pylorus leading to obstruction
- Ulcer perforation – erosion through stomach/duodenal wall into peritoneum. Gastric contents leak into abdominal cavity – infection, blood loss
Epidemiology
Aetiology
- 70% Helicobater pylori
- 30% NSAIDS
How does helicobater pylori cause ulcers?
What type of bacteria is it?
How is it transferred?
- Motile Gram negative bacilli.
- Strong association with gastric and duodenal ulcers.
- Host-host transmission (faecal-oral route, contaminated food/water).
- H.pylori uses urease to produce ammonia (NH3) and CO2 from urea breakdown. Ammonia is basic so neutralising gastric acid and helps raise pH.
- This creates a safe zone for more bacteria to accumulate so more ammonia builds up and it is an irritant so starts to damage gastric mucosa and down regulate mucus secretion
- Bacteria also produes exotoxins whivh damage mucosa
- Overall effect from Helicobater and gastric acid and pepsin lead to gastritits (inflammation of stomach)/ dueodetisi
- Causes localised gastritis (inflammation of stomach).
- •Can be asymptomatic – until ulcer forms.
How do NSAIDs cause ulcers?
COX -1 (constitutive) inhibition
- Decrease in PGE2 and PGI2 synthesis
- Decrease in mucus production
- Reduced inhibition of parietal cell HCl production
Direct irritant effect on gastric mucosa
- NSAIDs are weak acids
What are risk factors?
Medicine which cause it?
Bleeding risk with…
Risk factors – smoking, alcohol, stress
Medicines – bisphosphonates, nicorandil, corticosteroids
Bleeding risk – SSRIs, anticoagulants, antiplatelets, corticosteroids
Diagnosis
•Helicobacter pylori testing:
- C13 Urea breath test
- Faecal antigen test
*Patient must not have PPIs in the previous 2 weeks or antibiotics in the previous 4 weeks*
- Patient history – NSAIDs, smoking, stress, alcohol, diet
- Persistent/recurrent symptoms à Endoscopy
How does C12 Urea test work?
- C13 urea is administered to the patient in a capsule or solution
- If H.pylori is present, it will break C13 urea into ammonia and C13 CO2
- C13 CO2 can then be detected using a breath test, confirming presence of H.pylori
Treatment
