Week 4- Upper GI conditions - gastric cytoprotection, h.pylori, signs and symptoms PUD and dyspepsia Flashcards
what is gastro cytoprotections?
• Auto-digestion of the stomach is prevented by a
thin layer above the mucosa surface that secretes bicarbonate that forms an conc gradient to become neurtal
• Complex matrix of bicarbonate and mucus pH 7.0 -
unstirred layer
• H+ taken away by sub-mucosal blood flow
• decrease blood flow leading to necrosis of mucosa by increasing H+ conc & decreasing O2
• Stress ulcer in shocked or critically ill patients
how do prostglandins help with gastric cytoprotection?
somatastatin increases mucus secretion, increase bicarbonate, increase blood flow, decrases acid
• NSAIDS interfere with prostaglandin synthesis can cause ulcers
how is the oeophageal protection occuring?
- by lower oesophageal sphincter (LOS)
- its in permanent contraction but opened to allow food to pass through
what is gastritis?
-inflammation of gastric mucosa
-80% of people of asymptomatic
-Gastritis - inflammatory response of GI mucosa to
H.Pylori leads chronic gastritis leads to PUD leads to Gastric cancer
what is helicobactor pylori is indicated by gastritis, how does it work?
-• Protect themselves by hydrolysing urea to produce ammonia,
effectively buffer H+ ions
-• Colonisation beneath the mucus layer in the antrum leads to chronic
inflammation, decrease somatostatin leading to increase gastrin production leading to increase acid
• increased stomach acid production leading to chronic inflammation in duodenum,
H.Pylori moves into duodenum and reduces local protection leading to
Duodenal Ulcer
• H.Pylori causes gastritis throughout stomach leading to damaged cells
and decrreasing acid production leading to decreased mucosa, which long term
leading to Gastric
Ulcer leading to Gastric cancer
what kind of ppl are more likely to have duodenal ulcers?
-if they have more parital cells producing more acid that spills over into duodenal damaging it
how to identify H.pylori?
- through stool antigen test
- breath test= radio labelled urea CO2 will be labelled
what is peptic ulcer disease?
• Gastric ulcers (GU) rare under 40
• Duodenal ulcers (DU) predominantly males between 20 - 50
-
what are some factors of peptic ulcer disease?
Gastric hypersecretion
• Reduced mucosal resistance - smoking
what do people with DU have a problem with?
higher than average acid output
what do people with GU have a problem with?
lower mucosal resistance
what is the prognosis for these patients?
- Bleeding occurs in 10-15% of all patients with PUD
- 5-10% of patients with duodenal ulcer will perforate
- 1 in 7 of these will die
- 5-10% of gastric ulcers eventually found to be malignant
- 60% of patients with DU relapse after 1 year
- 50% of patients with GU relapse after 2 years
what are the risk factors for PUD?
• H.pylori major cause of PUD
• NSAIDS common cause of PUD
more common in smokers increased risk with increase no. of cigarettes smoked l
-genetic link 3x more likely is parents have it
-stress related
what are some drugs that can induce dyspepsia?
• NSAIDS, risk increased further if Elderly - History of peptic ulcer - Smoker • Sulfasalazine • Iron preparations • Corticosteroids • Potassium (particularly modified release forms) • Bisphosphonates • Theophylline • Calcium antagonists • Nitrates
why does drug induced dyspepsia occur ?
- 1/3 of patients with rheumatoid arthritis suffer PUD
- Ibuprofen safest NSAID,
- Even patients on 162.5mg aspirin a day icnreased risk 1.5 times
- NSAIDS inhibit prostaglandin synthesis via COX pathway
- COX-1 pathway leading protective prostaglandins (e.g. GI mucosa)
- COX-2 leading to inflammatory prostaglandins
- Safer NSAIDs less inhibitory effect on COX-1
- Celecoxib very little COX-1 activity
