119 - Neuronal and Hormonal Control of the GIT 2

Question 1

Effects of acid in the duodenum
1
2
3
4

Answer 1

1) D cells release somatostatin
2) Excites terminals of vagal afferent neurons to trigger vago-vagal reflex –> Brunner’s glands release mucus and bicarbonate.
3) Vago-vagal reflex inhibits gastric emptying
4) Duodenal-pyloro-antral reflex closes pylorus, also inhibits gastric emptying

Question 2

Effect of somatostatin in the stomach

Answer 2

Acts on parietal cells via GPCR, reduces acid secretion

Question 3

Example of a disease state where duodenal-pyloro-antral reflex is subverted

Answer 3

Gastroparesis

Question 4

What release CCK in the duodenum?

Answer 4

I cells (subset of enteroendocrine cells)

Question 5

Effect of CCK on neurons in the duodenum
1
2

Answer 5

1) CCK excites terminals of vagal afferent pathways to brain (EG: one goes to part of brain responsible for appetite, suppresses hunger)
2) CCK excites terminals of enteric sensory neurons (EG: initiation of segmentation process, part of fed-state motor pattern)

Question 6

Secretin

Answer 6

Triggers secretion of bicarbonate-rich solution from pancreas

Question 7

Effect of bicarbonate-rich solution from pancreas
1
2
3

Answer 7

1) Neutralise stomach acid in duodenum
2) Neutralising acid inactivates pepsin, stops somatostatin secretion from duodenal D cells.
3) Terminates acid-stimulated duodenal-antral reflexes and vago-vago reflexes (stops inhibition of gastric emptying)

Question 8

Hormonal effects of CCK
1
2
3

Answer 8

1) Causes gall bladder to contract, forcing bile into duodenum
2) Releases enzymes from pancreas
3) Satiety factor that acts on hypothalamus to partly suppress appetite

Question 9

Hormones that ensure proper environment for digestion in duodenum and jejunum

Answer 9

Secretin and CCK

Question 10

How does CCK suppress appetite?

Answer 10

Excites vagal afferents via a paracrine effect.

May also act directly in hypothalamic regions without blood-brain barrier

Question 11

Name for peristaltic wave from distal duodenum towards stomach

Answer 11

Retropulsion

Question 12

Role of retropulsion at the same time as peristalsis

Answer 12

Mix chyme with bicarbonate-rich solution, pancreatic enzymes. Important in digestion.

Question 13

Effect of failure of retropulsion

Answer 13

Can lead to peptic ulcers, as acid from stomach isn’t completely neutralised by bicarbonate

Question 14

How is the status of the gut normally detected?

Answer 14

Mechanically, as the mucosa is a barrier to the diffusion of chemicals from lumen into the body

Question 15

Example of a chemical signal that can diffuse directly across mucosa

Answer 15

Acid

Question 16

Examples of cells in the gut that can detect chemical signals

Answer 16

Enterochromaffin cells, enteroendocrine cells

Question 17

How do mucosal cells ‘taste’ the lumen?

Answer 17

Have the same pathways for bitter and umami

Question 18

Result of stimulation of mucosal taste pathways

Answer 18

Tastants cause release of serotonin from enterochromaffin cells

Question 19

Cells in mucosa that detect sweet tastes

Answer 19

L cells

Question 20

Effect of L cells detecting ‘sweet’ tastes
1
2
3

Answer 20

1) Contain, release glucacon-like peptides 1 and 2, and pancreatic polypeptide Y
2) These hormones regulate insulin secretion (PYY) and insulin secretion
3) PYY also acts on enteric neurons

Question 21

Emphasis of neural control between stomach and duodenum

Answer 21

In stomach, more emphasis is on vagus nerve.

In duodenum, more emphasis on enteric neural circuits

Question 22

Distinct motor patterns when food is in the duodenum
1
2
3

Answer 22

1) Retropulsion – constrictions running towards pylorus – mixes pancreatic juices and bile with food activating and facilitating digestion
2) Segmentation – local constrictions alternating with relaxation – mix food with digestive enzymes and bile, also bring nutrients to absorptive epithelium
3) Peristalsis propels content into new regions of intestine

Question 23

Transfer of food from duodenum to jejunum
1
2
3

Answer 23

1) Digestion releases nutrient molecules that activate EE and EC cells to modulate ratio of segmenting to peristaltic contractions
2) Rate of transit determines efficacy of digestion and absorption
3) Gastric emptying continues retriggering the basic processes (fat empties last, giving surge of CCK release, slowing transit, increasing food absorption)

Question 24

Speed of bolus through duodenum to jejunum

Answer 24

Slow movement through segmentation.

Can move more quickly by peristalsis

Question 25

Movement of food from jejunum to colon
1
2
3 a, b

Answer 25

• Basic mechanism the same, but stimuli change as digestion is completed
• Absorption of water makes content more viscous, altering feedback from muscle and increasing resistance to flow
• In proximal colon fermentation by the microbiome produces short chain fatty acids
– Acetate, butyrate, propionate
– All stimulate enteric reflexes

Question 26

What stimulates urge to defecate?

Answer 26

Distension of of rectum triggers urge to defecate via sacral primary afferent neurons

Question 27

What does defecation require to take place?

Answer 27

Conscious (cortical) neural activity to relax anal sphincter and contract abdominal muscles for normal defecation

Question 28

Effect of irritable bowel syndrome on defecation

Answer 28

Threshold for stimulation of sacral afferents is decreased, leading to ability to sense content in rectum that isn’t normally detectable

Question 29

Fasted state
1 a, b, c, d
2 a
3

Answer 29

• Neurally regulated interdigestive motor complex
– Also known as migrating motor complex (MMC)
– Wave of constriction initiated in antrum or upper duodenum propagates slowly to ileo-colonic junction
– Only one MMC constriction in small intestine at a time
– Possibly triggered by release of motilin, but many other hormones also released
• Clears bacteria and cellular debris from otherwise empty lumen
– Failure causes bacterial overgrowth
• Common issue post surgery, ileus

Question 30

Other hormones in GIT
1
2

Answer 30

• Ghrelin – growth hormone release inhibitor
– Released from stomach in fasted state and stimulates appetite
–May initiate MMC
• Gastrin releasing peptide
– Found in nerve terminals near G cells
– Acts in parallel to vagally released acetylcholine