Regulation And Disorders Of Gastric Secretion Flashcards
What are the contents of gastric juice in the fasting state?
Cations, anions, pepsinogen, lipase, mucus, intrinsic factors
What does the body of the stomach secrete?
Mucus, pepsinogen and HCL
What does the antrum of the stomach secrete?
Mucus, pepsinogen and gastrin
What is trefoil peptide important for?
Protection of stomach wall
How is gastric acid made in the stomach lumen?
- HCO3 exchanged for Cl- in the blood
- excess Cl- diffuses out into stomach
- potassium hydrogen ATPase pumps hydrogen ions out into the stomach lumen
What are the 5 types of cells in gastric glands?
Surface mucous cells Mucus neck cells Parietal cells ECL cells Chief cells
What do surface mucus cells do?
Secrete mucus, trefoil peptide and bicarbonate
What do mucus neck cells do?
Stem cell compartment
What do parietal cells secrete?
Acid and intrinsic factor secretion
What do ECL cells secrete?
Histamine
What do chief cells secrete?
Pepsinogen
What is resting juice?
Alkaline plasma (basically)
What is the mucus’ function?
Thick and sticky- forms water insoluble gel on epithelial surface
What does mucus do (in stomach)?
Increased HCO3 - protects against hydrogen ion secretion
What is renin replaced by?
Pepsinogen
What does intrinsic factor do?
Helps with absorption of vit B12
What is the function of gastric acid?
Kills bacteria, acidic denature of digested food, creates the optimum pH for activation of pepsinogen, promotes the activation of gastric lipase and secretion of pancreatic HCO3
What do G cells secrete?
Gastrin
What happens in the cephalic phase?
ACh stimulates histamine release from ECL cells and can also act on parietal cells -> HCL secretion
Gastrin stimulates histamine release and can act directly on parietal cells -> HCL secretions
What happens when too much acid is produced?
D cells are stimulated and release somatostatin
What is somatostatin?
Paracrine factor
What happens in the gastric phase?
Stomach distends, peptic concentration and acidity increases
Peptides in food buffer acid and increase pH so somatostatin inhibitition
What happens in the intestinal phase?
Balances the secretory activity of the stomach and the digestive and absorbitive capacities of small intestine
High duodenal acidity reflexively inhibits acid secretion
What inhibits acid secretion?
Duodenal distension, hypertonic solution, amino acids, fatty acids and monosaccharides
What does inhibition of acid secretion in the small intestine depend on?
Composition of chyme, volume of chyme and distension of the duodenum
What is HCL secretion regulated by?
Neuronal pathways and duodenal hormones
What is the direct pathway of acid secretion?
Acts on parietal cells-> increased Acid secretion
What is the indirect pathway of HCL secretion?
Influencing the secretion of gastrin and histamine,which increase acid secretion
What stimulates HCL secretion?
Histamines, ACh, gastrin, caffeine, alcohol, NSAIDs, nicotine, helicobacter pylori,
Why is pepsinogen secreted?
Inputs of chief cells from the nerve plexus when the [H+] is high
What does PGE2 do?
Inhibits parietal cells and stimulate mucus secreting cells
What do NSAIDs inhibit?
PGE2
How does the mucus layer prevent the auto digestion of the stomach?
Protects from low pH
How do the epithelial cells prevent autodigestion of the stomach?
Remove excess H+ via membrane transport systems
How are H+ ions prevented from back diffusing?
Tight junctions of epithelial cells
How do prostaglandins prevent the autodigestion of the stomach?
Inhibit acid secretion and enhance blood flow
What does mucosal blood flow remove?
Excess acid that has diffused across the epithelial layer
What do NSAIDs do?
Cause tropical irritation of the gut
What does the presence of acid in stomach promote?
NSAID-mediated gastric disorders
What are the functions of the GIT?
Storage, secretions, digestion, absorption of nutrients, salts, water, metabolism and elimination of undigested wastes
Where can peptic ulcers form?
Oesophagus, stomach and duodenum
When do peptic ulcers form?
Where there’s a breakage in the mucosal barrier
Where are peptic ulcers particularly common?
Duodenal cap, stomach- junction of antrum and body, distal oesophagus, meckels diverticulum and weight loss surgery
What are the causes of peptic ulcers?
Hyperacidity, presence of H pylori, NSAIDs, genetic factors
What are the outcomes of acute peptic ulcers?
Severe bleeding, healing with no scarring and chronic peptic ulcers
What do acute peptic ulcers develop from?
Areas of corrosive gastritis or acute hypoxia of surface epithelium
How does H pylori cause peptic ulcers?
They can permeate the gastric mucosa and cause ulcers
What are the virulence factors of H pylori?
- flagella move it closer to the epithelium
- produces urease
- cytotoxin-associated antigen (CagA)
- vacuolating toxin A (VacA)
How does urease make H pylori more virulent?
Converts urea to ammonia- buffers gastric acid and produces CO2
How does Cytotoxin-associated antigen make H pylori more virulent?
Inserts pathogenicity islands and confers ulcer-forming potential
How does vacuolating toxin A make H pylori more virulent?
Alters the trafficking of intracellular proteins in gastric cells
What is the most common cause of peptic ulcers?
H pylori
What does H pylori do once its in the cells?
Disregulates gastrin secretion
What happens when gastrin secretion is disregulated?
Gastrin secretion increases
What are the three ways you can diagnose peptic ulcers?
Endoscopy
Histological examination and staining of an EGD biopsy
Test for H pylori presence
What are the tests you can do for the presence of H pylori?
- stool antigen test
- evaluate urease activity
- urea breath test
How do you carry out the urea breath test?
Work out how much CO2 is in urine and how much is in breath by tagging some C-14. There shouldn’t be any C-14 in breath
When do you measure CO2 levels when carrying out the urea breath test?
Before and 10-30 mins after
What are the complications of a peptic ulcer?
Haemorrhage Perforation and penetration Leakage of luminal contents Narrowing of pyloric canal or oesophageal stricture Malignant change
