Enteric Nervous System and Gut Hormones Flashcards

1
Q

Describe the myelination pattern of the enteric nervous system fibres.

A

Unmyelinated

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2
Q

What do interneurons do?

A

Integrates lots of sensory inputs to generated a coordinated response.

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3
Q

State the two plexuses of the enteric nervous system and what they regulate.

A

Myenteric (Auerbach’s) Plexus - located between circular and longtudinal muscle - controls activity of muscularis externa- controls gut motor function
Submucosal (Meissner’s) Plexus - senses the environment of the lumen and controls blood flow, endothelial and endocrine function

*There are also minor plexuses including the deep muscular plexus inside circular muscle, and the ganglia supplying the biliary system and pancreas.

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4
Q

Where are the cell bodies of the sympathetic preganglionic fibres found?

A

In the thoracic and lumbar spinal cord

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5
Q

Describe where the sympathetic innervation of the gut comes from.

A

Midgut and foregut are innervated by thoracic splanchnic nerves
Rest of the gut is innervated by lumbar splanchnic nerves

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6
Q

Where are the cell bodies of the parasympathetic preganglionic fibres found?

A

In the brainstem and sacral spinal cord

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7
Q

Describe where the parasympathetic innervation of the gut comes from.

A

Most of the gut is innervated by branches of the vagus nerve (down to the level of the transverse colon)
The rest of the gut receives parasympathetic fibres from the pelvic nerves

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8
Q

In general, the ANS controls gut function via the enteric nervous system (through the two plexuses). What is an exception to this?

A

Sympathetic nervous system has direct control over blood flow to the GI tract. It does not have to go through the ENS to regulate blood flow.

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9
Q

Which afferents take information from the chemo and mechanoreceptors in the GI tract to the CNS?

A

Vagal and splanchnic afferents

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10
Q

Describe the structure of enteroendocrine cells.

A

They have a finger like protrusion that detects the environment of the lumen. They are located near blood vessels so they can release hormones into the blood. They can also talk directly to neurons via projections called neuropods.

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11
Q

Which cells release GIP-1, GLP-1, GLP-2, PYY and CCK?

A

GIP-1 = K cells
GLP-1 + GLP-2 + PYY = L cells
CCK = I cells

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12
Q

State some functions of the gastrointestinal endocrine system.

A

Regulation of mechanical processes of digestion
Regulation of chemical and enzymatic processes
Control of post-absorptive processes involved in the assimilation of digested food
Effects on growth and development of the GI tract (e.g. GLP-2 promotes small intestine growth)

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13
Q

What is the incretin effect?

A

Release of insulin following oral glucose is much greater than the release with IV glucose because of the incretins (e.g. GIP-1). The incretins potentiate the insulin response.

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14
Q

Describe paracrine actions of the GI hormones.

A

Somatostatin from the stomach can inhibit acid secretion by paracrine mechanisms.
Histamine release from stomach wall cells is a key physiological stimulus for the release of HCl from gastric parietal cells

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15
Q

Where is gastrin synthesised?

A

Pyloric Antrum and upper small intestine

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16
Q

What stimulates gastrin release and what is its main action? When is gastrin inhibited?

A

Stimulus: Amino acids and fatty acids
Gastric distension
Vagus nerve
Action - stimulates gastric acid secretion
Inhibited - when pH of stomach falls below 3 (don’t want it to be too acidic and ulcerate)

17
Q

Where is somatostatin synthesised?

A

D cells - found throughout the GI tract

18
Q

What does somatostatin do?

A

It is a universal inhibitor - it reduces gastric motility and secretion, intestinal and pancreatic secretions, release of gut hormones, intestinal nutrient and electrolyte transport, growth and proliferation.

19
Q

Name a somatostatin analogue. Why isn’t somatostatin itself used instead of the analogue?

A

Octreotide - because somatostatin is a peptide hormone which has a very short half-life meaning that it would have to be readministered regularly
Analogues are used to treat neuroendocrine tumours

20
Q

Where is secretin produced?

A

S cells found mainly in the upper duodenum and jejunum.

21
Q

What stimulates secretin production and what does it do?

A

When the pH drops below 4.5 in the duodenum.

It stimulates pancreatic bicarbonate secretion (this effect is potentiated by CCK)

22
Q

What is the effect of high concentrations of secretin?

A

Inhibition of gastric acid and gastric emptying

23
Q

Where is CCK mainly produced?

A

Densely located in the small intestine

24
Q

What stimulates CCK release and what does it do?

A

Release is stimulated by the presence of fat and peptides in the upper small intestine
Actions: gallbladder contraction, delay gastric emptying, stimulates pancreatic enzyme release
At high concentrations: decreases food intake and meal size

25
Q

Where is GIP (gastric inhibitory peptide) produced?

A

Stimulated by K cells mainly in the duodenum and jejunum

26
Q

What stimulates GIP release and what does it do?

A

GIP release follows ingestion of a mixed meal

GIP stimulates insulin secretion - causes the incretin effect

27
Q

Where is PYY produced?

A

Released from L cells found throughout the terminal ileum, colon and rectum.

28
Q

What stimulates PYY release and what does it do?

A

Released postprandially

Fullness hormone - reduces intestinal motility, gallbladder contraction and pancreatic exocrine secretion

29
Q

What is PYY3-36?

A

This is a truncated form of PYY that is produced when fasting
This fools your body into thinking that you’ve had a meal and inhibits food intake