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Alimentary System > 8. Control of Function > Flashcards

8. Control of Function Flashcards

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1
Q

Describe the enteric nervous system?

A

• Plexuses of ganglia
- dense local network of nerves/supporting cells
- nerve and glial cells
• Can produce a coordinated response to specific stimuli independent of CNS

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2
Q

What can cause a dysfunction in the enteric nervous system?

A
  • Inflammation
  • Irritable bowel syndrome
  • Ageing
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3
Q

What is the myenteric plexus?

A
  • aka Auerbach’s plexus
  • Between circular & longitudinal smooth muscle
  • Contains efferent innervations
  • Allows for motility
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4
Q

What is the submucosal plexus?

A 
• aka Meissner's plexus
• Afferent functions
- senses environment within lumen
- mechnoreceptors, chemoreceptors, osmoreceptors
• Efferent functions
- controls local blood flow
- controls epithelial transport
- controls secretory/paracrine/endocrine cell functions
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5
Q

What are the 4 main functions of the enteric nervous system?

A

S - secretion
• Controls the secretion of enzymes, paracrine signals and endocrine hormones
• To regulate local/non-local gut function
P - perfusion
• Careful control of blood flow
• Ensure high perfusion in regions of gut that are working (VSMCs, submucosal glands, enterocytes)
A - absorption
• controlling absorption by adjusting expression of luminal transport proteins
M - motility
• contraction/relaxing of smooth muscle cells in the circular and longitudinal muscle layers
• effective gut transit (accelerate after a meal, stop during exercise)

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6
Q

What are multipolar neurones?

A
  • One axon
  • One body
  • Multiple dendrites
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7
Q

What do sensory enteric neurones do?

A

Respond to mechanical, thermal, osmotic and chemical stimuli

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8
Q

What do motor enteric neurones?

A

• Axons terminate on:

  • smooth muscle cells (circular/longitudinal layers)
  • secretory cells
  • GI blood vessels
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9
Q

What do interneurons do?

A

Neurones between neurones that integrate sensory input and effector output

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10
Q

How would a disruption of autonomic innervation affect the gut?

A
  • Small decrease in functionality

* Very independent

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11
Q

Summarise the sympathetic innervation of the gut

A
  • Preganglionic neurones in splanchnic nerves from thoracic and lumbar regions
  • Thoracic branches => foregut
  • Lumbar branches => hindgut

(pre/postganglionic = short/long - close to spine)

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12
Q

Summarise the parasympathetic innervation of the gut

A
  • Mostly from vagus nerve (X)
  • Descending colon onwards - pelvic splanchnic nerves

(pre/postganglionic = long/short - close to target organ)

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13
Q

How do the sympathetic and parasympathetic pathways influence the GIT?

A
  • Sympathetic - reduce activity (fight or flight)

* Parasympathetic - increase activity (rest and digest)

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14
Q

Describe the general structure of an enteroendocrine cell

A

• Small apical membrane
- Lot of sensory apparatus
• Broad basolateral surface
- Vesicles with secretory products ready for exocytosis

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15
Q

Where is gastrin produced?

A
  • G-cells
  • Distal end of stomach (gastric antrum)
  • Proximal duodenum
  • Pancreas (less)
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16
Q

What stimulates the release of gastrin?

A

• Peptides/amino acids in stomach
• Mechanoreceptors in stomach
• Parasympathetic system
(• inhibited under pH 3)

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17
Q

What does gastrin do?

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A
  • Increase acid secretion
  • Increase gastric emptying
  • Increase pepsinogen secretion
18
Q

Where is secretin produced?

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A
  • S-cells

* Duodenum and jejunum

19
Q

What stimulates the release of secretin?

20
Q

What does secretin do?

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A
  • Increase pancreatic HCO3- secretions
  • Reduce acid secretion
  • Reduce gastric emptying
21
Q

Where is somatostatin produced?

Study These Flashcards
A
  • D-cells

* Stomach, pancreas and small intestine

22
Q

What stimulates the release of somatostatin?

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A

Presence of a meal

23
Q

What does somatostatin do?

Study These Flashcards
A

• Inhibits G-cells from secreting gastrin
• Inhibits enterochromaffin-like cells from secreting histamine
• Decreases gut motility
• Decreases absorption
(• inhibited by vagus nerve)

24
Q

Where is cholecystokinin produced?

Study These Flashcards
A
  • I-cells

* Small intestine

25
What stimulates the release of cholecystokinin?
Fats and peptides
26
What does cholecystokinin do?
* Increases pancreatic enzyme secretion * Reduces gastric emptying * Increases gall bladder contraction * Reduces appetite
27
Where is Glucose-dependent insulinotropic peptide (gastric-inhibitory peptide) produced?
* K-cells | * Duodenum and jejunum
28
What stimulates the release of Glucose-dependent insulinotropic peptide?
Glucose in small intestine
29
What does Glucose-dependent insulinotropic peptide do?
* Upregulation of insulin | * Reduces acid secretion/gastric emptying at high concentrations
30
Which part of the body is responsible for triggering appetite?
• Hypothalamus- combines peripheral signals - Arcuate nucleus - Paraventricular nucleus
31
Outline the role of the Arcuate nucleus in appetite
• Located at base of brain • Incomplete brain barrier - allows peripheral signals to activate the circuitry • Has 2 neuronal populations: - NPY/Agrp: located medially, stimulates food intake - POMC (proopiomelanocortin): located more laterally, inhibits food intake, peptide that can be cleaved in many ways for different purposes • Neurones project into brain and paraventricular nucleus
32
Outline the role of the Paraventricular nucleus in appetite
* Axons from Arcuate nucleus secrete neuropeptides * POMC - alpha melanocyte stimulating hormone * Binds to Melanocortin 4 receptor (regulation of food uptake) * Agoutin-related protein (Agrp) = competitive inhibitor => increases food uptake
33
What can a POMC deficiency or MC4R mutation lead to?
Morbid obesity
34
Outline the role of Leptin in obesity
• 167 amino acid hormone coded for by ob/ob gene • Produced by fat, proportionate to adipose tissue • Concentration sensed by hypothalamus - causes alteration of neuropeptides - regulates appetite - regulates thermogenesis • Leptin resistance - hormone cannot signal => obesity • Ineffective as weight control drug • Congenital leptin deficiency - very rare
35
What is Peptide YY?
* 36 amino acid chain * Secreted from ileum and colon * Released in proportion to calories released * Inhibits paraventricular nucleus => inhibits neuropeptide Y release * Stimulates POMC neurones * Decreases appetite
36
What is Ghrelin?
* Peptide hormone released from the stomach * Fatty acid chain on serine 3 enables binding to receptor * Drives hunger before meals * Stimultes Agrp neurones and paraventricular neurones (neuropeptide Y) * Inhibits POMC neurones * Increases appetite
37
How is water concentration regulated?
* Very tightly regulated (285-295mOsm/kg) * Osmoreceptors in the hypothalamus (OVLT and SFO regions) * Adjacent to structures with an incomplete blood brain barrier * Cell bodies outside the blood brain barrier - bathed in ECF * Threshold - 2-3% increase in osmolality, 10-15% decrease in volume/pressure * Cells shrink and grow in concordance * Changes firing rate of cells - adjusts to basal level of ADH secreted
38
What is vasopressin and what does it do?
* Hormone produced in the hypothalamus when there is low water * Released from posterior pituitary gland * Inserts aquaporin-2 channels into collecting ducts * Increases water reabsorption * Stimulates vasoconstriction * Increases BP * Stimulates thirst
39
How can thirst be satiated?
* Presence of water in GIT - short term feedback | * Correction of original stimulus (osmolality or BP) - long term feedback
40
Summarise the hormonal control of thirst
Low water => low BP => Angiotensin II: • vasoconstriction • upregulates sympathetic nervous system (vasoconstriction) • stimulates aldosterone secretion => increased sodium reabsorption => (gradient) water reabsorption • direct sodium reabsorption => water reabsorption • stimulates ADH release and thirst

Alimentary System (15 decks)

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