Treatment of peptic ulcers Flashcards
Recall the 2 main presenting features of a peptic ulcer
- Epigastric pain 2. Burning sensation
Recall the 3 investigations done for peptic ulcers, and which of these is the gold standard
Gold standard = endoscopy
Both Carbon urea breath test and Stool-antigen test for H pylori will be positive for H pylori, but negative for NSAID induced peptic ulcer
Describe the basis of a carbon urea breath test and the implication of a positive result
Give patient loads of unique carbon isotope-urea and if you get increased levels of specific-isotope CO2 being exhaled = positive for H pylori
How can the history differentiate between a complicated and uncomplicated H.pylori positive peptic ulcer?
Pain after meal times = •H Pylori positive uncomplicated peptic ulcer whereas if meal pain is constant and not just after mal = h.pylori postive complicated peptic ulcer.
`What is the most common cause of peptic ulcer?
Bacterial infection with H Pylori
In around what % of the population is H pylori commensal?
50%
How does H pylori infection cause development of a peptic ulcer?
- It produces urease which can break down the protective mucous layer 2. It releases exotoxins at the epithelium, leading to IL8 release and local inflammation.
Increased gastrin production leads to increased acid production
How do NSAIDS cause development of peptic ulcers?
Directly cytotoxic, reducing mucous production and causing IL8 release at epithelium,
- Increases likelihood of bleeding
- Increased acidity à peptic ulcer
What is the first line treatment for uncomplicated H pylori + peptic ulcers?
Amoxycillin combined with Clarithromycin/ metronidazole, and a PPI for 7-14 days
Describe the treatmentfor a complicated h.pylori postive peptic ulcer?
- Amoxycillin, clarithromycin/metronidazole given together with quinolone 2. Bismuth 3. Omeprazole (PPI) for 4-12 weeks
How do PPIs reduce gastric acid secretion?
Inhibit proton pump on apical side of parietal cells
If NSAID cannot be removed, how is an NSAID-induced peptic ulcer treated?
PPI or H2 antagonist
Why would an H2 receptor antagonist be useful in peptic ulcer treatment?
H2 receptors on parietal cells stimulate proton pump to increase acid secretion
Recall the function of prostaglandins in the stomach
PROTECTIVE 1. Increase blood supply to stimulate mucous production 2. Increase HCO3- production 3. Decrease acid production
Recall the risk factors for peptic ulcers
- Stress 2. genetic 3. Lifestyle (diet/ alcohol/ smoking)
Recall 3 molecules that inhibit gastric acid production
- Secretin 2. GIP 3. Somatostatin
Give an example of a histamine antagonist used in peptic ulcer therapy
Ranitidine
How do H+-K+-ATPase (proton pumps) work, and how these lead to ulcer formation
- Expressed on secretory vesicles within parietal cells
- increased [Ca2+] ® increased cAMP ® translocation of secretory vesicles to parietal cell apical surface ® H+ secretion
Ulcer formation
•Increased activity of proton pump – increased H+ secretion ® reduction gastric pH
Explain how gastric acid is regulated
Gastric acid regulation
- Acetylcholine (ACh) released from neurones (vagus / enteric) acts on muscarinic (M3) receptors -tf increasing [Ca2+]i
- Prostaglandins (PGs) released from local cells act on EP3 receptors - tf increasing cAMP
- Histamine released from enterochromaffin-like cells (ECL) act on H2 receptors - tf increasing cAMP
- Gastrin released from blood stream acts on cholecystokinin B receptors - tf increasing [Ca2+]
Gastric acid secretion
•Raised [Ca2+] & cAMP ® translocation of secretory vesicles to parietal cell apical surface ® H+ secretion
how to treat NSAID-induced peptic ulcers
- Removal of NSAID
- Proton Pump Inhibitor or histamine H2 receptor antagonist (Ranitidine) – 4-8 weeks
- H2 receptor increases acid secretion
