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GI > GI Hormones & Neurotransmitters > Flashcards

GI Hormones & Neurotransmitters Flashcards

1
Q

What type of cells release gastrin?

A

G cells from the antrum of the stomach (a little bit from the duodenum)

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2
Q

What is the stimuli for secretion of gastrin?

A
  • Peptides/amino acids
  • Distention of the stomach
  • Vagal stimulation via GRP (gastric-releasing peptide)
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3
Q

What does gastrin do?

A
  • Increases gastric H+ secretion
  • Encourages growth of the gastric mucosa
  • Increases gastric motility

At supraphysiological doses, gastrin will have the effects of CCK (and vice versa)

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4
Q

What type of cells release CCK?

A

I cells in the duodenum and jejunum

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5
Q

What is the stimuli for secretion of CCK?

A

Peptides/amino acids

Free fatty acids

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6
Q

What does CCK do?

A
  • SLOWS gastric emptying (more time for digestion)
  • Contracts gallbladder
  • Relaxes Sphincter of Oddi
  • Increases pancreatic enzyme secretion
  • Also increases HCO3- secretion (weaker effect than secretin)
  • Trophic effects on pancreas and gallbladder to replace cells that were used to make enzymes.

At supraphysiologic doses, CCK will have the effects of gastrin, and vice versa

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7
Q

What types of cells release secretin?

A

S cells of the duodenum and jejunum

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8
Q

What is the stimuli for secretin release?

A
  • Acidic pH in early SI (<4.5)

- Free fatty acids

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9
Q

What does secretin do?

A
  • Increases pancreatic and biliary HCO3- release
  • Decreases stomach acid secretion
  • Decreases gastric mucosal growth
  • Trophic effects on pancreas

(Opposite effects of gastrin)

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10
Q

What types of cells release GIP/GLIP and GLP?

A

Incretins are released from K and L cells of the duodenum and jejunum.

K = GIP/GLIP
L = GLP
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11
Q

What is the stimuli for secretion of GIP/GLIP and GLP?

A
  • Oral glucose
  • Peptides/amino acids
  • Free fatty acids

(Food, basically)

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12
Q

What do GIP/GLIP and GLP do?

A
  • Increase pancreatic insulin secretion

- Decrease gastric acid secretion

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13
Q

What types of cells secrete motilin?

A

M cells from the duodenum and jejunum

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14
Q

What is the stimuli for motilin release?

A

Decreased vagal stimulation

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15
Q

What does motilin do?

A
  • Responsible for the fasted migrating motor pattern (prevents SIBO)
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16
Q

What types of cells release somatostatin?

A

D cells of the pancreatic islets and GI mucosa

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17
Q

What is the stimulus for secretion of somatostatin?

A

H+

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18
Q

What does somatostatin do?

A

Helps secretin:

  • Decreases stomach acid secretion
  • Decreases pancreatic enzyme secretion
  • Decreases gallbladder contraction

(this is actually a peptide, not a hormone)

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19
Q

Where are the preganglionic cell bodies for the nerve that provides parasympathetic innervation to MOST the GI located?

A

The preganglionic cell bodies for the vagal nerves are in the medulla.

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20
Q

Where are the preganglionic cell bodies for the nerve that provides parasympathetic innervation to the distal colon and rectum located?

A

The preganglionic cell bodies for the pelvic nerves are in the sacral spinal cord.

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21
Q

Where do postganglionic parasympathetic nerves synapse with preganglionic parasympathetic nerves?

A

In the gut wall.

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22
Q

What neurotransmitter does the vagal nerve release onto enteric neurons in the gut wall?

A

ACh (binds nicotinic receptors on enteric neurons)

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23
Q

What neurotransmitter do postganglionic parasympathetic/enteric neurons release onto effector cells?

A

ACh (binds muscarinic receptors)

24
Q

Where are the sympathetic preganglionic cell bodies located?

A

In the thoracic spinal cord.

25
Q

Where do pre- and postganglionic sympathetic neurons synapse?

A

The prevertebral ganglia:

  • Celiac
  • Superior mesenteric
  • Inferior mesenteric
26
Q

What neurotransmitter do preganglionic sympathetic neurons release onto postganglionic neurons?

A

ACh (binds nicotinic receptors on postganglionic splanchnic nerves)

27
Q

What neurotransmitter do postganglionic sympathetic neurons release onto effector cells?

A

NE (binds enteric neurons, smooth muscle, or secretory cells)

28
Q

What are the net effects of NE release by a postganglionic neuron in the GI system?

A

Slowed digestion and absorption:

  • Decreased motility
  • Decreased secretions
  • Increased sphincter constriction
  • Increased vasoconstriction
29
Q

All neuronal messaging to/from the GI pass through the ENS EXCEPT:

A

Sympathetic NS (inhibitory, NE) can connect directly to secretory cells and smooth muscles of the GI.

These neurons also synapse with ENS neurons, providing some redundancy.

30
Q

Anticholinergic drugs would have what effect on GI motility and secretions?

A

The PNS uses ACh to stimulate motility and secretions. Blocking ACh would result in decreased motility and secretions.

31
Q

Acute stress has what effect on GI motility and secretions?

A

Stress stimulates the SNS. Increased NE will decrease motility and secretions.

32
Q

Opioids have what effect on GI motility and secretions?

A

Opioids inhibit neurotransmitter release. This diminishes PNS activation of the GI, therefore decreased motility and secretions will occur.

33
Q

How does ACh cause contraction of smooth muscles?

A

ACh raises the BER of ICC cells to a spike potential, causing contraction.

ACh causes IP3 channels to open, allowing influx of Ca++ (even greater than a CICR/spontaneous transient depolarization). This results in a greater amplitude spike potential, stimulating a strong contraction.

34
Q

What effect does Epi/NE have on ICCs?

A

Epi/NE inhibits IP3 and stimulation of Ca++/ATPases. Thus more Ca++ is brought back into the SR of the ICC cell/less Ca++ is released, and the cell is brought back to BER. Smooth muscle contraction decreases.

35
Q

How does the autonomic nervous system control gut motility?

A

By changing spike potential frequency, which controls the force of motility.
Remember that the slow wave frequency is set!

36
Q

How is GI arteriole vasodilation controlled?

A
  • NO/VIP
  • ACh
  • Substance P
  • Adenosine

(Ga

37
Q

What effect does leptin have, and where does it come from?

A

Leptin is released from adipocytes. It plays a role in chronic regulation of the hypothalamus, reducing our perception of hunger.

38
Q

What effect does insulin have on our perception of hunger?

A

Insulin is released from the pancreas after meals, and works with the hypothalamus to decrease our perception of hunger on a short-term basis.

39
Q

What role does CCK have in our perception of hunger?

A

CCK provides very short-term regulation, providing stimulus to the hypothalamus to help reduce our perception of hunger.

40
Q

What role does ghrelin have in our perception of hunger?

A

Ghrelin is released by X/A cells in the small intestine during fasting. Travels to the hypothalamus to increase our perception of hunger.

41
Q

How does the upper esophageal sphincter remain constricted at rest?

A

ACh is constantly released onto nicotinic ACh receptors on the UES to allow tonic constriction

42
Q

What two components help the lower esophageal sphincter remain tonically constricted?

A
  • Myogenic component: normal tone and the pressure from diaphragm
  • Neurogenic component: enteric neuron release of NE can cause further constriction
43
Q

What regulates the opening of the lower esophageal sphincter?

A

ACh release from autonomic neurons onto enteric neurons causes a release of NO/VIP, resulting in relaxation of the sphincter.

44
Q

What effect would a vagotomy have on esophageal peristalsis?

A

Primary (long-reflex) peristalsis would be significantly impaired.

Secondary (short reflex) peristalsis would not be impaired.

45
Q

What provides regulation for the migrating motor complex?

A

Motilin, produced by M cells, delivered to ICC cells during phase III.

Increases amplitude of spike potentials –> contractions.

46
Q

What effect would a vagotomy have on perception of fullness after a meal?

A

A vago-vagal reflex is responsible for triggering receptive relaxation (during which stretch stimulates release of NO/VIP in the fundus of the stomach).

Without the vago-vagal reflex, receptive relaxation would be impaired, and the stomach would not relax. This means that a smaller volume of food would create and increased feeling of fullness or discomfort.

47
Q

What effect would a vagotomy have on the migrating motor complex?

A

The vagus nerve is not responsible for stimulating the release of motilin. There would be little effect.

(Could argue that there would be no inhibition of the release of motilin – normally provided by the vagus – after eating, so the MMC might be overactive).

48
Q

Describe the system that has most control over saliva regulation

A

The PNS is the most dominant controlling system.

Innervation is via the facial nerve (CN VII) and glossopharyngeal nerve (CN IX). ACh is released to muscarinic receptors, which causes IP3/Ca++ second messaging system to induce increased rate of salivary production.

49
Q

The SNS has what effect on saliva production?

A

T1 - T3 nerves release NE to B-receptors, resulting in cAMP increasing production of saliva. This saliva is more protein-rich and thus thicker than typical saliva.

50
Q

What type of cells secrete intrinsic factor?

A

Parietal cells

51
Q

What type of cells secrete HCl-?

A

Parietal cells

52
Q

What type of cells secrete pepsinogen?

A

Chief cells

53
Q

Gastrin increases H+ secretion from parietal cells via what pathway?

A

Binds CCKb receptors on parietal cells; IP3/Ca++ second messenger system promotes vesicular translocation of H+/K+ pumps to the cell membrane

54
Q

ACh increases H+ secretion from parietal cells via what pathway?

A

Binds M3 receptors on parietal cells; IP3/Ca++ second messenger system promotes vesicular translocation of H+/K+ pumps to the cell membrane

55
Q

Histamine increases H+ secretion from parietal cells via what pathway?

A

Histamine binds H2 receptors on parietal cells; cAMP second messenger pathway helps maintain a gradient favoring activity of the H+/K+ pump.

56
Q

H+ has what effect on parietal cells?

A

H+ triggers release of somatostatin from D-cells.

Somatostatin inhibits G, ECL, and parietal cells, inhibiting HCl secretion.

GI (6 decks)

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