113 - Neural and Hormonal Control of GIT Function 1 Flashcards

1
Q
Basic function of GIT
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5
A

1) Digestion of food
2) Absorption of nutrients
3) Excretion of waste
4) Prevention of invasion by pathogens
5) Contains microbiome

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2
Q
Key requirements of GIT regulation 
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A

1) Control intestinal smooth muscle contractions.
2) Regulate secretion of digestive enzymes, solvents for enzymatic function
3) Control reabsorption of water from lumen to prevent dehydration
4) Coordinate widely separated regions (EG: regulation of gastric emptying by gat in duodenum)

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3
Q

Pacemaker cells of the enteric nervous system, regulating contractile activity of intestinal smooth muscle

A

Interstitial cells of Cajal. Modified smooth muscle cells.

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4
Q

Interstitial cells of Cajal function

A

Regulate contractile activity and secretion of water and salt over mm to cm distances
Contain elements needed for complex motor programs

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5
Q

Two systems that interact for GIT function

A

Enteric nervous system, endocrine system.

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6
Q

Segmentation

A

Mixing function of enteric nervous system

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7
Q

Peristalsis

A

Propulsive motor pattern, mediated by enteric nervous system

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8
Q

Function of GIT endocrine system

A

Signal from intestinal mucosa to ancillary organs like brain, pancreas, gall bladder.

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9
Q

Arrangement of the enteric nervous system in the GIT?
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A

1) Ganglia between the longitudinal (outer) and circular (internal) smooth muscle layers in the GIT (myenteric plexus).
2) Submucosal plexus. Innervate mucosa.
3) Interstitial cells of Cajal, all joined with gap junctions (to coordinate). Sit within circular smooth muscle layer.

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10
Q

Number of neuron types in murine enteric nervous system

A

~22

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11
Q

Mucosal enteroendocrine cells
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A

1) Often span epithelium
2) Many defined by mediators they release (EG: serotonin-releasing enterochromaffin cells)
3) Also enterochromaffin-like cells that release histamine

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12
Q

Number of enteroendocrine cells in GIT

A

Over 20

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13
Q

Where is majority of body’s serotonin produced?

A

In gut wall (over 90%) (serotonin-containing enterochromaffin cell)

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14
Q

Examples of hormonal factors released by enteroendocrine cells

A

Serotonin, CCK, secretin, somatostatin, glucagon-like peptides 1 and 2

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15
Q

Roles of vagus in GIT function
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A

1) Vagus pathway for control of swallowing
2) Vagus regulates acid secretion in stomach.
3) Co-ordination of contraction of stomach, duodenum

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16
Q

Part of GIT that vagus controls

A

First part. Vagal control wanes as you go towards colon.

17
Q

Neural aspects responsible for intestino-intestinal reflexes
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2

A

1) Vagus (often excitatory)

2) Dorsal root ganglia (often inhibitory)

18
Q

Function of sympathetic neurons in the GIT

A

Often inhibitory

19
Q

Viscerofugal neurons
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3

A

1) Cell bodies are within GIT wall
2) Project to pre-vertebral sympathetic ganglia (coelial, superior, inferior mesenteric ganglia).
3) Produce reflex inhibition of proximal regions when distal regions are distended.

20
Q

Hormone released when fat is detected

A

Cholecystikinin.

Released from GIT wall, effects local GIT wall, gets into portal system, goes to liver.

21
Q

Basic function of vagal and sympathetic activity on enteric nervous system

A

Usually modulate enteric neural circuits (increase or decrease activity)

22
Q

Effect of neural activity on intestinal smooth muscle

A

Interstitial cells of Cajal act as pacemakers.
Neural activity can change level of excitation or inhibition that can alter whether smooth muscle will contract on stimulation

23
Q

Which nerve mediates cephalic phase?

A

Vagus

24
Q

Amount of gastric acid secretion attributable to cephalic phase

A

~30%

25
Q
Effects of cephalic phase 
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A

1) Causes salivation
2) Gastric acid secretion
3) Pepsin secretion
4) Relaxation of gastric corpus and fundus

26
Q
General control of gastric acid, pepsin secretion in stomach
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A

1) Brain directly innervates parietal cells
2) Brain innervates, via enteric nervous system, enterochromaffin-like cells, D cells.
3) ECL cells release histamine, which stimulates gastric acid release.
4) D cells release somatostatin, which counteracts release of acid.
5) This results in a balance between gastric acid secretion and inhibition thereof.

27
Q
General control of gastric acid, pepsin secretion 
1)
2)
3) a, b
4) a
A

–Acetylcholine from enteric neurons excited by vagal efferent neurons
–Gastrin from G cells in antrum and duodenum
–Histamine from ECL cells
•Excited by ACh from enteric neurons
•Inhibited by somatostatin from local D cells and duodenal D cells
–Somatostatin inhibits parietal cells and G cells
• D cells stimulated by acid in duodenum and by gastrin

28
Q

Control of oesophageal peristalsis

A

Entirely neural, via vagus

29
Q

GORD

A

Gastro-oesophageal reflux disease

30
Q
What happens when food enters stomach?
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A

1) Food enters corpus
2) Distension of corpus activates enteric and vaso-vagal reflexes.
3) This results in more acid and pepsin secretion.
4) Pacemaker activity propagates from corpus to antrum, causing ripples of constriction to propagate to pylorus (grinds food even more)

31
Q

Effect of food and acid entering antrum

A

Triggers reflex inhibition of acid secretion in the corpus.
To maintain an even pH

32
Q

What does fat do in the stomach?

A

Floats to the top of chyme, where it forms a separate layer

33
Q

Consequence of fat floating to top of stomach

A

Fat empties from stomach after everything else

34
Q

What stimulates opening of pylorus?

A

Enteric neuronal activity

35
Q

Components of chyme from stomach

A

Food, acid, pepsin (initially low in fat, later high in fat)

36
Q

Aspect of stomach filling that suppresses hunger

A

Stomach distension