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Alimentary System > 8. Control of Function > Flashcards

8. Control of Function Flashcards

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?

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

Where is secretin produced?

A
  • S-cells

* Duodenum and jejunum

19
Q

What stimulates the release of secretin?

A

Low pH

20
Q

What does secretin do?

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

Where is somatostatin produced?

A
  • D-cells

* Stomach, pancreas and small intestine

22
Q

What stimulates the release of somatostatin?

A

Presence of a meal

23
Q

What does somatostatin do?

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?

A
  • I-cells

* Small intestine

25
Q

What stimulates the release of cholecystokinin?

A

Fats and peptides

26
Q

What does cholecystokinin do?

A
  • Increases pancreatic enzyme secretion
  • Reduces gastric emptying
  • Increases gall bladder contraction
  • Reduces appetite
27
Q

Where is Glucose-dependent insulinotropic peptide (gastric-inhibitory peptide) produced?

A
  • K-cells

* Duodenum and jejunum

28
Q

What stimulates the release of Glucose-dependent insulinotropic peptide?

A

Glucose in small intestine

29
Q

What does Glucose-dependent insulinotropic peptide do?

A
  • Upregulation of insulin

* Reduces acid secretion/gastric emptying at high concentrations

30
Q

Which part of the body is responsible for triggering appetite?

A

• Hypothalamus- combines peripheral signals

  • Arcuate nucleus
  • Paraventricular nucleus
31
Q

Outline the role of the Arcuate nucleus in appetite

A

• 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
Q

Outline the role of the Paraventricular nucleus in appetite

A
  • 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
Q

What can a POMC deficiency or MC4R mutation lead to?

A

Morbid obesity

34
Q

Outline the role of Leptin in obesity

A

• 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
Q

What is Peptide YY?

A
  • 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
Q

What is Ghrelin?

A
  • 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
Q

How is water concentration regulated?

A
  • 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
Q

What is vasopressin and what does it do?

A
  • 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
Q

How can thirst be satiated?

A
  • Presence of water in GIT - short term feedback

* Correction of original stimulus (osmolality or BP) - long term feedback

40
Q

Summarise the hormonal control of thirst

A

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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