Regulation of the GI Tract

Question 1

What controls the rate of gastric emptying?

Answer 1

• Pepsin and HCL are the starting point of stomach digestion which continues carbohydrate breakdown via amylase.
• The rate of emptying is proportional to the volume of chyme in the stomach.
• The duodenum must be ready to receive chyme at any moment thus delays emptying either through the enterogastic reflex (Neuronal) which decreases antral activity by signals from the intrinsic nerve plexuses and the ANS, or the release of CCK (hormonal) from the duodenum which inhibits stomach contraction.

Question 2

What stimuli drive the neuronal/hormonal responses.

Answer 2

• Fat which is particularly potent delays gastric emptying.
• Acids as time is needed for bicarbonates (pancreas) to neutralise gastric acid.
• Hypertonicity as carbohydrates and proteins digestive products are osmotically active and draw water into the small intestine.

Question 3

List the components that make up the gastric mucosa.

Answer 3

• Oxyntic gland (proximal stomach)
• Pyloric gland (distal stomach)
• Surface lining the stomach and pits (invaginations on its surface)

Question 4

What are the functions of the oxyntic mucosa (secretions)?

Answer 4

• HCL: Activates pepsinogen (also gland activity) to pepsin while denaturing proteins and killing any microbes.
• Intrinsic factor and gastroferrin which bind B12 and Fe2+ respectively to facilitate absorption.
• Histamine which stimulates HCL secretion.
• Mucus (protective).

Question 5

What is secreted by the pyloric gland?

Answer 5

• Gastrin: Stimulates HCL secretion and motility.
• Somatostatin: Inhibits HCL secretion
• Mucus

Question 6

Describe the action of histamine.

Answer 6

• Secreted by the enterochromaffin like cells in the gastric glands due to stimulation by acetylcholine (Ach).
• Binds to H2 receptors which activates adenylyl cyclase. The increase in c.AMP increases the number of proton pumps thus increasing gastric acid secretion from parietal cells.
• Cl- enters parietal cell via the chloride-bicarbonate exchanger and then into the gastric lumen via the chloride-potassium symporter.
• The bicarbonates are are converted into H+ via carbonic anhydrase which enters gastric lumen via H+/K+ ATPase (proton pump).

Question 7

What is the importance of Ach?

Answer 7

• Ach is released from the parasympathetic cholinergic neurons and bind to M3 ACh receptors on parietal cells causing PLC activation.
• PLC increases intracellular Ca2+ cell signalling to increase the number of proton pumps.

Question 8

Explain the activity of gastrin and somatostatin.

Answer 8

• Gastrin is released from G cells and binds to CCK2 receptors on parietal cells activating PLC.
• Somatostatin is secreted from D cells in the gastric glands and bind to SST2R receptors inhibiting adenylyl cyclase.
• SS binding to SST2R on enterochromaffin cells results in reduced histamine release.
• Prostaglandins also inhibits adenylyl cyclase.

Question 9

What is the cephalic and gastric phase of gastric acid secretion?

Answer 9

1. Cephalic: Preparing the stomach for when food arrives. Its the first phase of gastric acid secretion.
   - Vagus nerves stimulate enteric neurons causing the release of ACh (NT action), released GRP to release gastrin from G cells (endocrine action) and release histamine from ECL cells (paracrine). Also inhibits D cells.
2. Gastric: second phase, the distension of stomach activates reflex causing acid secretion.
   - D cell inhibition is reduced and AA such as tryptophan stimulate G cells.