Lesson 19: Gastric Secretions

Study Notes

Gastric secretions are the stomach's first major digestive component
The stomach is a muscular reservoir for food
The stomach's digestive functions are not essential for the absorption of a mixed meal
A degree of gastric secretion is needed for vitamin B12 absorption
Gastric acid also aids in the absorption of iron
Gastric secretions aid in food sterilization

Gastric secretions: The study of secretions in the stomach
Regulation of acid secretion by parietal cells: The control mechanisms behind acid production in parietal cells
Main mediators: Substances that regulate the process, including histamine (paracrine), gastrin (endocrine), acetylcholine, PGE2, PGI2, and somatostatin
Drugs used to inhibit or neutralize acid gastric secretion: Medications like histamine receptor antagonists, proton pump inhibitors, and antacids
Drugs that protect the mucosa: Substances that safeguard the stomach lining.

The stomach has layers- mucosa, submucosa, muscularis externa, and serosa
- The mucosa has surface epithelium, lamina propria, and muscularis mucosae
Parietal cells reside in gastric pits, within gastric glands.
Chief cells are also in gastric glands
Enteroendocrine cells also reside in gastric glands

Hydrochloric Acid (HCl): Produced by parietal cells, creates an acidic environment for initial food breakdown and has antimicrobial properties.
Pepsinogen: Secreted by chief cells, it becomes pepsin in the acidic environment, a crucial enzyme for protein digestion.
Intrinsic Factor: Also produced by parietal cells, assists in vitamin B12 absorption in the intestines.
Mucus: Secreted by mucous cells, creates a protective layer in the stomach.
Lipase: Produced by chief cells, aids in the initial digestion of triglycerides.

Histamine: Secreted by ECL cells and maintains a basal release of histamine; found near parietal cells, important for initiating and sustaining histamine production,
Gastrin: A polypeptide synthesized by G cells; stimulates HCL production, Located in the pyloric antrum, stomach, duodenum, and pancreas, triggers HCL release.
Acetylcholine: Stimulates muscarinic M3 receptors, elevates intracellular Ca2+ and triggers proton (H+) release into the stomach.
Prostaglandins (PGE2 and PGI2): Important for protecting the stomach lining via bicarbonate secretion and increasing mucus production, inhibiting HCL secretion.
Somatostatin: An inhibitory peptide hormone, regulates and controls other mediators.

Histamine H2 receptor antagonists (e.g., cimetidine, ranitidine, famotidine): Inhibit basal and food-stimulated acid secretion, promote healing of gastric/duodenal ulcers
Proton pump inhibitors (e.g., omeprazole, lansoprazole, pantoprazole): Irreversibly inhibit H+-K+-ATPase, reduce acid secretion both basal and stimulated
Antacids (e.g., hydrotalcite, magnesium and aluminum salts): Neutralize stomach acid, inhibit peptic enzyme activity

Helicobacter pylori infection is a key factor in ulcer development
It colonizes the gastric mucosa, causing chronic inflammation and disrupting mucosal defenses.
It increases acid production and produces toxins

A combined treatment targeting Helicobacter pylori is commonly utilized for ulcer healing: Antibiotics, proton pump inhibitors, and bismuth chelate.

Bismuth chelate: Toxic effects on Helicobacter pylori, OTC for mild cases of gastrointestinal issues (e.g., blackening of the tongue, nausea, vomiting, and encephalopathy with impaired renal excretion.
Sucralfate: Forms complex gels with mucus, stimulates mucus and bicarbonate secretion, and protects the stomach lining.

Stable analogue of PGE2, promotes ulcer healing and aids in preventing chronic gastric issues associated with the use of NSAIDs.
It also increases mucosal blood flow and increases mucus and bicarbonate secretion. Side effects include diarrhea and abdominal cramps. (Not used during pregnancy)