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PostPosted: 11 Oct 2019 10:33 
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OVERVIEW
The gastrointestinal (GI) system, or alimentary tract, begins in the oral cavity or mouth, and includes pharynx, esophagus or food pipe, stomach, small intestine (duodenum, jejunum and ileum), cecum, large intestine or colon, rectum, and associated secretory organs and accessory glands (salivary
glands, exocrine pancreas, liver and gall bladder).

From the lumen outward, the layers of tissue found in most of the GI tract are the mucosa,
submucosa, muscularis propria, and serosa.
The stomach or gastric mucosa consists of lining epithelium and secretory glands

The GI system has a rich nerve supply consisting of both extrinsic and intrinsic nerves. Extrinsic nerves are those from the autonomic nervous system (ANS). In general, the parasympathetic division of the ANS in general stimulates GI function and the sympathetic division inhibits GI function

Intrinsic nerves consist of the enteric nervous system, a subdivision of the peripheral nervous system. The enteric nervous system relays information from the ANS and can also independently regulate several GI functions

GASTRIC ANATOMY IN BRIEF
The gastric mucosa or epithelium consists of numerous glands, many of which open into a common outlet (gastric pits) on the surface of the mucosa. The glands have various types of cells each performing a different function. The parietal cells secrete hydrochloric acid and intrinsic factor (IF), the chief cells secrete pepsinogen, and the neuro-endocrine cells secrete gastrin (G cells) and somatostatin (D cells), and enterochromaffin cells secrete histamine.

ACID SECRETION IN STOMACH
Hydrochloric acid (HCl) is produced by the parietal cells in the stomach.
Basal acid output (BAO) is the minimum amount of HCl secreted during a given period of time in the absence of any stimulatory factors eg food. It is usually < 10 mmol/h.
Maximal acid output (MAO) is the quantity of HCl produced over a certain period when acid stimulants(e.g., histamine) are given. It is usually < 50 mmol/h.
The function of HCl is to denature proteins for easier digestion, break up cells, kill ingested bacteria, and to convert pepsinogen to pepsin.

MECHANISM OF ACID SECRETION IN STOMACH
The H+−K+ ATPase pump present in the parietal cells drives H+ into the lumen in exchange for K+.
The K+ circulates back into the lumen via luminal K+ channels. For every H+ secreted, one HCO3
leaves the parietal cell in exchange for Cl−.
The HCO3 ions are derived from the CO2 and OH produced by normal cell metabolism. Its formation is catalyzed by carbonic anhydrase (CA).
Chloride ion thus accumulates within the cell and then diffuses into the lumen of the gastric glands. Thus, one chloride ion reaches the lumen for each H+ ion secreted by the parietal cell. The H+ and Cl− combine to produce HCl.

REGULATION OF GASTRIC ACID SECRETION
Gastric acid secretion is stimulated in by local, neural, gastric, and intestinal factors. Food intake causes reflex secretion of gastric juices
The vagus nerve releases acetylcholine (ACh), which directly stimulates parietal cells in the fundus of the stomach Additionally, gastrin-releasing peptide (GRP) released by the vagus nerve stimulates secretion
of gastrin from G cells in the antrum of the stomach.
Gastrin released into the blood also activates parietal cells to secrete HCl.
The gastric fundic glands contain H cells (enterochromaffin cells), which are also stimulated by gastrin, ACh, and β2-adrenergic substances. These cells release histamine, which has a local paracrine effect on the neighboring parietal cells to release acid.

Gastric acid secretion is blocked by a pH < 3.0. This inhibits G cells and activates antral D cells, which secrete somatostatin (SIH). SIH inhibits enterochromaffin cells in the fundus(minor effect) and G cells in the antrum (major effect).
Secretin and gastrointestinal polypeptide (GIP) secreted in the small intestine have an inhibitory
effect on gastric acid secretion

DISORDERS OF EXCESS ACID SECRETION
1. PEPTIC ULCER DISEASE
An ulcer is a breach in the mucosa extending into the submucosa and deeper structures of the wall of
the GI tract.
Peptic ulcers can occur in the stomach (gastric ulcer) or duodenum (duodenal ulcers)
Gastric ulcers are caused by the breakdown of the mucosal barrier (mucus and HCO3) that
normally protects the lining of the stomach or increased secretion of acid by various factors (excess alcohol, caffeine, NSAIDs, Helicobacter pylori infection)
Duodenal ulcers are more common than gastric ulcers and are often associated with increased gastric acid secretion
Duodenal ulcers are usually caused by H. pylori infection. H. pylori inhibits somatostatin secretion, resulting in increased gastric acid secretion, as well as reduced HCO3 secretion in the duodenum,
which in turn affects neutralization of the excess H+ coming in from the stomach.
Symptoms of peptic ulcer include burning abdominal discomfort, nausea and vomiting, heartburn, and
weight loss.


2. ZOLLINGER ELLISON SYNDROME
Zollinger–Ellison syndrome is a condition caused by pancreatic adenomas secreting gastrin resulting in multiple ulcers in the stomach and duodenum. These ulcers are frequently resistant to treatment and are accompanied by diarrhea and steatorrhea (increased fat content of stools), as well as symptoms of peptic ulcers. Tests will reveal raised serum gastrin and gastric acid levels.

TREATMENT OF PEPTIC ULCER DISEASE
Peptic ulcer disease is treated with drugs that inhibit gastric acid secretion
H2-receptor antagonists (e.g., cimetidine and ranitidine) competitively inhibit gastric acid secretion from parietal cells by blocking histamine-mediated secretion.
Proton pump inhibitors (e.g., omeprazole, pantoprazole) inhibit the proton (H+/K+ ATPase) pump of the parietal cells in the stomach, thus inhibiting gastric acid secretion
Atropine is a cholinergic muscarinic receptor antagonist that inhibits gastric acid secretion by blocking acetylcholine-mediated acid secretion, but not used routinely.
Proton pump inhibitors are the first-line agents for treating peptic ulcer disease
H pylori infection associated peptic ulcer disease is treated with proton pump inhibitor for 6 to 8 weeks to reduce the secretion of HCl, along with antimicrobials (metronidazole, tetracycline, clarithromycin, or amoxicillin) for 2 weeks to eradicate H. pylori infection.


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PostPosted: 19 Oct 2019 23:47 
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Joined: 26 Feb 2013 10:59
Posts: 663
This is an excellent write up about gastric acid secretion. It is a complex subject and medical students should learn the physiology of acid production clearly to understand how different drugs can be used to treat the various conditions when hyperacidity in the stomach becomes a problem.

I have added a "Youtube" video on the topic by Armando Hasudungan in our web page in the "Physiology Section" of Links. He explains the topic clearly by way of simple diagrams. I am sure anyone interested in the topic will enjoy this 13 minute video.

The following link should take you to the video.
http://www.tnmgc.com/links.php?menu=4&subject=1

(Dr. Armando Hasudungan started making educational videos when he was still a student. He is now doing a Residency Program in Australia and wants to become an oncologist)


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