Functions And Regulation Of The GI tract

Question 1

Give a microscopic overview of the gastrointestinal tract

Answer 1

• Epithelial cells - are specialized for various secretions and absorption of nutrients
• Muscularis mucosa – contractions change the surface areas for secretion or absorption
• Circular muscle – contractions decrease diameter of the lumen
• Longitudinal muscle – contraction shortens the segment of the GIT
• Submucosal plexus (Meissner) and Myenteric plexus – integrate the motility, secretory and endocrine functions of the GIT.

Question 2

Describe the extrinsic innervation of the GIT

Answer 2

Parasympathetic
• Excitatory
• Vagus (Upper GIT) and pelvic nerves (Lower GIT)
• Preganglionics synapse on plexi
• Postganglionics synapse on smooth muscle, secretory and endocrine cells

Sympathetic
• Inhibitory
• Thoracolumbar fibers (T8-L2)
• Preganglionics (cholinergic) synapse
in the prevertebral ganglia
• Post ganglionic (adrenergic) synapse on plexi
• Plexi relay info to target cells

Question 3

Describe the intrinsic innervation of the GIT

Answer 3

• Extrinsic input (from ANS), but ENS can function in the absence of extrinsic input
• uses local reflexes
• Myenteric plexus
• control of enteric motility
• Submucosal
• regulates secretions and blood flow

• receives sensory information from chemo- and mechanoreceptor

Question 4

Summarize neural control of motility and secretions

Answer 4

Parasympathetic: excitatory

Sympathetic: inhibitory

Chemoreceptors/ mechanoreceptors: receive stimuli stretch/distension, composition of fluid

Endocrine cells: regulatory peptides

Question 5

Summarize GIT comtrol summary

Answer 5

Regulation of GIT function is integrated via several coordinated responses:

1. Neural pathways
2. Peptides and other regulatory mediators

Summary of neural pathways:
• Short reflexes integrated in ENS (Enteric Nervous System)
• Long reflexes integrated in CNS (Central nervous system)
• Connections between CNS\ENS via ANS (Autonomic Nervous System

Question 6

What are the types of GIT regulators?

Answer 6

1. Endocrine /hormonal
2. Neurocrine
3. Paracrine

Question 7

What are the stimuli for gastrin?

Answer 7

secreted from gastric antrum after a meal

• Stimuli for release:
• Small peptides and amino acids (especially phenylalanine and tryptophan) in stomach
• Stomach distension
• Vagal stimulation, mediated by gastrin-releasing peptide (GrP)
• Inhibition of gastrin secretion is driven by increasing H+ (acidity) in the lumen of the stomach, which limits stomach acidification. Somatostatin also inhibits gastrin release.

Question 8

What are the effects of gastrin?

Answer 8

Effects:
• Increases H+ secretion by the gastric parietal cells
• Stimulates growth of gastric mucosa

Question 9

Describe neurocrine regulation

Answer 9

Neurocrine:
• Peptides released by the nerves within the gut
• Short-range effects after release
• ACh, Substance P (smooth muscle contraction),
• Norepinephrine, Vasoactive Intestinal Peptide (relaxation)

Question 10

Describe endocrine/hormonal control of the GIT

Answer 10

Endocrine/Hormonal:
• Hormones synthesized by cells in the gastric and intestinal epithelium and released into the blood stream
• Systemic long-range action
• Gastrin, secretin, CCK, the incretins (GIP & GLP)

Question 11

Describe paracrine regulation of the GIT

Answer 11

Paracrine:
• Substances that act locally within the same tissue
• Short-range effects
• Histamine, somatostatin

Question 12

What are the effects of cholecystokinin (CKK)?

Answer 12

Structurally homologous to gastrin

• Effects of CCK:
• Gallbladder contraction and relaxation of the sphincter of oddi for bile secretion
• Stimulates pancreatic enzyme secretion
• Potentiates secretin-induced stimulation of pancreatic HCO3−
secretion
• Inhibits gastric emptying. Meals containing fat stimulate the secretion of CCK, which slows gastric emptying to allow more time for intestinal digestion and absorption.

Question 13

How is CKK stimulated to be released?

Answer 13

• Stimuli for release (from I cells of the duodenal and jejunal mucosa):

• Small peptides and amino acids
• Fatty acids and monoglyceride

Question 14

Describe the structure of secretin

Answer 14

27 amino acids; homologs to glucagon

Question 15

What are the effects of secretin?

Answer 15

Effects
• Reducing acidity (H+) in small intestine
• Stimulates pancreatic HCO3- secretion (neutralizes H+ in the intestinal lumen)
• Stimulates HCO3− and H2O secretion by the liver and increases bile production
• Inhibits H+ secretion by gastric parietal cells

Question 16

What is the stimulus for secretin release?

Answer 16

Stimuli for release (by duodenum S cells)
• H+ in the lumen of the duodenum
• Fatty acids in the lumen of the duodenum

Question 17

What is the impact(endocrine) of incretins like GIP & GLP (endocrine)?

Answer 17

• GIP - Gastric Inhibitory peptide
• GLP - Glucagon like peptide (often more specifically GLP-1)
• both enhance insulin secretion in response to oral carbohydrates
• the total amount of insulin secreted is greater when glucose is administered orally than when administered intravenously, hence digestion is at least partly driven by anticipatory response
• GIP also inhibits H+ secretion by gastric parietal cells, limiting acidification of the stomac

Question 18

What are the paracrine rehulatory mediators?

Answer 18

• released from endocrine cells in the GI mucosa
• diffuse short distances to target cells in GIT

Include sonatostatin & histamine

Question 19

What is the impact of sonatostatin in the GIT?

Answer 19

Somatostatin
• secreted throughout GIT in response to luminal H+

• secretion is inhibited by vagal stimulation
• inhibits the release of all GI hormones
• inhibits gastric H+ secretion

Question 20

What is the impact of histamine on the GIT?

Answer 20

Histamine

• secreted by mast cells of the gastric mucosa
• increases gastric H+ secretion directly, and by potentiating the effects of gastrin and vagal stimulation