Disorders of gastric acid secretion Flashcards
What is the function of the GI tract?
What can the malformation of the GI tract cause?
storage, secretory, digestion, absorption of nutrients, salts, water, metabolism and elimination of (undigested) wastes
↓ nutrient status of the individual
What sites are affected by peptic ulcers?
What are the 3 effects of peptic ulcers?
Sites affected: Oesophagus, stomach and duodenum
Breakage of mucosal barrier
…imbalance between protective and damaging factors of GIT
…exposure of tissues to the erosive effects of gastric acids (HCl, bile acids) and pepsin
What factors are responsible for gastric acid secretion: damaging factors
Histamine Acetylcholine Gastrin Food/protein, alcohol, smoking, caffeine, NSAIDs Zollinger-Ellison syndrome Hyperparathyroidism
Stress? - Can it aggravate it once ulcer is present?
Bile acids are irritants
Genetic?
Helicobacter pylori
Where can peptic ulcers form?
Duodenal cap/ampulla: first part of the duodenum; smooth walled; dilated; mesenteric
The stomach – junction of antrum and body
Distal oesophagus, especially in Barrett’s oesophagus
Meckel’s diverticulum – outpouching or bulge in the small intestine (congenital)
Weight loss surgery (gastroenterostomy) weight loss
What causes the formation of a peptic ulcer?
What is the outcome?
Hyperacidity; reflux of duodenal contents (oesophagus, stomach and duodenum)
Presence of H. pylori is a risk factor for gastric cancer – eradication → ↓ risk
NSAIDs; Genetic factors; Sex – being male?
Complete healing and replacement of tissue and some scarring
When are chronic peptic ulcers common?
Occurs in upper GIT (pepsin and HCl)
Asymptomatic in >80% of people
Low incidence in young; common in over 50s
90% incidence in developing countries
Inflammation plays a key role in the disease process
Where does an acute peptic ulcer form?
Develops from areas of corrosive gastritis (oesophagus, stomach, proximal duodenum), severe stress or shock (burns, trauma)
Acute hypoxia of surface epithelium (i.e., ischaemia of gastric mucosa)
What are the outcomes of an acute peptic ulcer? (3)
Severe bleeding
Heal with no scarring
Chronic peptic ulcer
H. pylori, Smoking, genetic factors, stress, NSAIDs
How do these cause a peptic ulcer
Acid pepsin
impaired mucosal defence
leads to peptic ulcer
What factors protect the stomach from digestion?
Gastric juices: 150mM HCl & pepsin in the stomach
Mucus layer protects the gastric mucosa from the low pH
Secretion of alkaline mucus and HCO3-
Somatostatin inhibits gastrin release (negative feedback control)
Protein content of food
Epithelial cells remove excess H+ via membrane transport systems; tight junctions of epithelial cells prevent back diffusion of H+ ions
Prostaglandins (E and I): inhibit acid secretion and enhance blood flow
- Mucosal blood flow removes excess acid that has diffused across the epithelial layer
- Maintenance of mucosal integrity and repair: growth factors (e.g., epidermal growth factor, insulin-like growth factor I) and PGs
Replacement of damaged cells within the gastric pits
Describe the H.Pylori bacteria
Gram negative; spiral shaped (can be coccoid too) aerobic bacterium
Penetrates gastric mucosa (able to survive under the harsh condition of the stomach)
Highly pathogenic, with many virulence factors
Peptic ulcer = ulcer in the digestive tract (in the stomach or duodenum)
What are the Virulence factors of H. pylori?
Motility: flagella; moves close to the epithelium (pH 7) Produces urease (converts urea to ammonia, which buffers gastric acid and produces CO2)
Cytotoxin-associated antigen (CagA) – inserts pathogenicity islands and confers ulcer-forming potential
Vacuolating toxin A (VacA) – alters the trafficking of intracellular protein in gastric cells
A large number of outer membrane proteins: Adhesins (BabA), phospholipases, porins, iron transporters, and flagellum-associated proteins
H. Pylori is the commonest cause of peptic ulcer – ↑peptic ulcer risk by 10-20%
What tests can be used to identify ulcers?
How do we test for H. pylori?
Diagnostic tests
Endoscopy (oesophagogastroduodenoscopy, EGD)
Histological examination and staining of an EGD biopsy
Test for the presence of H. pylori
Stool antigen test
Evaluate urease activity
Urea breath test
What are the complications of peptic ulcer?
Haemorrhage (GI bleeding)
Perforation (peritonitis) and penetration (liver and pancreas may be affected); leakage of luminal contents
Narrowing of pyloric canal (stricture causing acquired pyloric stenosis in the stomach) or oesophageal stricture
Malignant change becomes 3-6 times likely with H. pylori infection
