L2-L7 Flashcards
Peptic Ulcer Disease
- lesion on wall of stomach or intestine
stomach ulcer = gastric, intestinal = duodenal
causes breach of lining and gastric acid will damage cells/tissue
breach needs surgically fixed or patient could get sepsis
Stomach Protection Barriers
- alkaline mucous
- tight junctions
alkaline mucus - epithelial cells secrete bicarbonate, neutralising some acid
Tight Junctions - between epithelial cells making it hard for molecules (like acid) to seep out
Causes of Peptic Ulcer Disease
Helicobacter Pylori
- stimulates stomach acid production causing impaired mucosal defence. leads to ulcers
NSAIDS
- prevent AA from producing prostaglandins (which stimulate bicarbonate to neutralise acid)
- this causes there to be more acid in stomach
Smoking/Genetic Factors
Symptoms of Peptic Ulcer Disease
abdominal pain, discomfort
- pain doesnt radiate, stays local
burning pains in upper abdomen
Helicobacter Pylori and Peptic Ulceration
- 40% individuals Peptic Ulcers
in gastric ulcer patients, 95% have H. Pylori
H. Pylori damages protective layer of stomach increasing chance of ulceration
1.Infects lower part of stomach and allows acid & pepsin to attack the stomach(leading to ulcers)
2.produces enzyme urease, degrades urea to make ammonia + CO2 which helps bacteria survive
3.Uses adhesion molecules to stay on stomach wall
Diagnostic Testing for H. Pylori
serological
UBT
SAT
Serologic - blood test, but will be positive if you have have H. Pylori any time in the past
UBT (Urea Breath Test) - takes urea capsule and if they have H. Pylori, higher amount of CO2 will be exhaled
SAT (stool antigen test) - detects antigens from stool and shows i there is current infection
ECL Cells
- in gastric mucosa
secrete histamine as paracrine stimulant
leads to increased acid secretion from parietal cells
Acid Secretion in Stomach
- in parietal cell
1.Muscarinic , h2 , and gastrin receptors promote acid production on parietal cell.
2.Carbonic Anhydrase combines CO2 with carbonic acid to make bicarbonate and H+
3.Bicarbonate exchanged for Cl- which enters lumen
4.Proton HCl pumped into lumen by H+/K+ ATPase allowing K+ inside and stomach acid to be secreted
H2 Antagonists
(Cimetidine, Ranitidine, Nizatidine, Famotidine)
act competitively on H2 muscarinic receptor of parietal cells
reduce basal acid secretion by 60%
treats both duodenal and gastric ulcers
Side Effects: Diarrhoea, headache, Confusion in elderly
cimetidine - interacts with warfarin & cause gynaecomastia
PPI’s
- omeprazole, esomeprazole, lansoprazole
Inhibition of proton pump blocks acid secretion irreversibly
- return of acid secretion by synthesis of new pump protein H+/K+ ATPase
- acid secretion reduced by 90% after dose
Side Effects - GI upset, diarrhoea, skin rashes
increase risk of fracture
Eradication of H. Pylori Infection
- PUD H. Pylori gets triple therapy
PPI + Amoxicillin + Clarithromycin/Metronidazole
- if penicillin allergic give both Clarithromycin & Metronidazole
triple therapy because H. Pylori is known to become resistant so it has to be completely destroyed
Cytoprotective Agents
- Misoprostol (prostaglandin analogue)
misoprostol mimic action of prostaglandins to protect stomach.
take with NSAID to protect stomach
enhances duodenal bicarbonate production & weakly inhibits gastric acid secretion
cant be used during pregnancy
Zollinger Ellison Syndrome
- gastronome in pancreas OR duodenum
Large gastrin secreting tumour (Gastronome) in pancreas or duodenum
- causes gastric acid hypersecretion
removal of tumour is effective treatment
GORD reflux disease
- treatment
dysfunctional lower oesophageal sphincter allows reflux of stomach acid and pepsin
Treatment: antacids, PPI, H2 antagonist
Detection: probe with pH reader to determine acid in oesophagus
Barrets Oesophagus
- pink colour at bottom of oesophagus
irreversible, common in long-term GORD patients
- Will lead to oesophageal cancer – adenocarcinoma
treatment: replace stratified squamous epithelium with columbar epithelium that has goblet cells