Question

5.The control of gastric acid secretion in response to a meal involves several events that take place over a 4- or 5-hr period following the meal. These events include (1) a decrease in the pH of the gastric contents, (2) an increase in the rate of acid secretion, (3) an increase in the pH of the gastric contents. Which of the following best describes the correct order of events following a meal ingestion?

Answer 1

Gastric acid is secreted by parietal cells in the proximal two thirds of the stomach. Gastric acid aids digestion by creating the optimal pH for pepsin and gastric lipase and by stimulating pancreatic bicarbonate secretion.

Composition of gastric secretion

Gastric acid secretion is an important non-immunological first line of defence against ingested bacteria. Gastric juice is a variable mixture of:

• Water
• Hydrochloric acid
• Electrolytes( sodium, potassium, calcium, phosphate, sulfate and bicarbonate)
• Organic substances(mucus, pepsins,protein)
• Enzymes
• Intrinsic factor
• Ghrelin

[Note: This juice is highly acidic because of its hydrochloric acid content]

Physiology of Gastric acid secretion

A) STOMACH

• Storage
• Preparing the chyme for digestion in the small intestine
• Initiation for digestion
• Absorption of water and lipid soluble substances.

B) GASTRIC JUICES

C) GASTRIC GLAND

• Surface epithelial cells or mucus cells(alkaline mucus)
• Mucus neck cells or neck chief cells(soluble mucus, pepsinogen)
• Parietal cells or oxyntic cells( hydrochloric acid, intrinsic factor)
• Chief cells or zymogen cells( pepsinogen)
• Enterochromaffin cells(serotonin, histamine)
• Specialized cells( vasoactive intestinal peptide, substance P, glucagon)

D) PHASES OF ACID SECRETION

• Cephalic Phase(30%)
• Gastric Phase(60%)
• Intestinal Phase(10%)

E) PHYSIOLOGY

• Gastric acid production is maintained at a low basal rate in the fasting state by the tonic inhibition of acid secretion by somatostatin from gastric D cells.
• Somatostatin acts in a paracrine manner on G cells in the antrum, along with ECL and parietal cells in the fundus and body of the stomach to suppress gastrin, histamine, and acid secretion.
• Gastric acid secretion as it relates to a meal occurs in three phases:

1. cephalic
2. gastric
3. intestinal phase.

(Note: Most gastric acid secretion occurs in the gastric phase)

• Prior to the ingestion of food, olfactory, gustatory, cephalic, and visual stimuli begin to increase gastric acid production and stimulate gastric motility.
• Higher brain centers send information to the dorsal vagal complex in response to the premeal stimuli.
• Subsequently, vagal output activates enteric nerves to release GRP and Ach.
• GRP stimulates the antral G cells to release gastrin, which activates parietal and chief cells in an endocrine fashion.
• Ach inhibits somatostatin release from D cells resulting in disinhibition of gastrin, histamine, and acid release, as well as the direct stimulation of antral G cells and parietal cells.
• Once feeding begins and the meal enters the gastric lumen, chemical and mechanical factors add to the continued vagal stimulation from the cephalic phase to promote continued gastric secretion.
• Luminal amino acids and short peptides, released from dietary protein by the action of pepsin from chief cells, activate receptors on G cells to release gastrin.(Alcoholic beverages, coffee, and dietary calcium also activate gastrin release).
• The stomach distends as it receives a meal (receptive relaxation) and stretch receptors active long and short reflex arcs that stimulate vagal nerves to release Ach to activate parietal cells directly, or release Ach to activate ECL cells to secrete histamine and GRP to activate G cells to secrete gastrin for indirect gastric acid secretion.
• Distention and the presence of luminal peptides produce continued gastric acid secretion and increased motility.
• Finally, in the intestinal phase, gastric acid secretion is returned to its basal level by several mechanisms.
• Decreased sensory stimuli and gastric distention following a meal lead to a tapering of the cephalic and gastric phase responses.
• The gastrin released during the cephalic and gastric phases exerts negative feedback through D cells in the antrum, which releases somatostatin leading to inhibition of gastrin release.
• Food entering the duodenum leaves the gastric mucosa exposed to the full acidifying effect of parietal cell proton production leading to chemoreceptor activation and neural reflex release of calcitonin gene-related peptide (CGRP) near D cells to release somatostatin.
• This results in restoration of the tonic inhibition of somatostatin upon acid secretion and a return to basal acid production.
• The marked increase in gastric blood flow during this phase boosts gastric cell secretory function.