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GI > gastrointestinal regulatory substances and secretory productsp. 380-381 > Flashcards

gastrointestinal regulatory substances and secretory productsp. 380-381 Flashcards

1
Q

Gastrin: source?

A

G cells

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2
Q

G-cells: produce what?

A

gastrin

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3
Q

G-cells: where?

A

antrum of stomach (most lower part before pylorus), duodenom

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4
Q

gastrin producing cells: where?

A

antrum of stomach (most lower part before pylorus), duodenom

(G-cells)

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5
Q

gastrin: actions? (3)

A

gastric H+ secretion
growth of gastric mucosa
gastric motility

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6
Q

gastric H+ secretion
growth of gastric mucosa
gastric motility

functions of which substance?

A

gastrin

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7
Q

what increases gastrin secretion by g-cells? (3 things)

A
  • stomach distention/alkalinization
  • amino acids and peptides
  • vagal stimulation via GRP (gastrin releasing peptide)
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8
Q

what decreases gastrin secretion by g-cells?

A

pH < 1.5

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9
Q

chronic use of which medication increase gastrin?

A

PPI

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10
Q

chronic use of PPI increases what?

A

gastrin secretion

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11
Q

which pathologies increase gastrin secretion? (2)

A
  • chronic atrophic gastritis (H pylori)
  • Zollinger-Ellison syndrome (gastrinoma)

gastrinoma is a gastrin-secreting tumor

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12
Q

Zollinger-Ellison syndrome: increased secretion of what?

A

gastrin

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13
Q

what is Zollinger-Ellison syndrome?

A

gastrinomas in pancreas or upper part small intestine -> produce gastrin -> too much acid -> peptic ulcers

rare

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14
Q

chronic atrophic gastritis can lead to what?

A

overproduction of Gastrin

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15
Q

Somatostatin: source?

A

D cells

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16
Q

Where are D cells?

A

pancreatic islets, GI mucosa

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17
Q

what do D cells produce?

A

somatostatin

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18
Q

Effects of somatostatin? (4)

A
  • less gastric acid and pepsinogen secretion
  • less pancreatic and intestine fluid secretion
  • less gallbladder contraction
  • less insulin and glucagon release
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19
Q

what leads to increased secretion of somatostatin?

A

more acid

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20
Q

what leads to decreased secretion of somatostatin?

A

vagal stimulation

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21
Q

what is octeotride?

A

a mimic of somatostatin

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22
Q

which medication is the analog of somatostatin?

A

octeotride

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23
Q

what can you treat with octeotride (mimic of somatostatin)? (4)

A
  • agromegaly
  • carcinoid syndrome
  • VIPoma
  • variceal bleeding

carcinoid tumor: neuroendocrine tumors

VIPoma: neuroendocrine tumor secreting vasoactive intestinal peptide (VIP) -> severe diarrhea

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24
Q

cholecystokinin: which cells secrete this?

A

I cells

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25
Q

where are I cells?

A

duodenum, jejunum

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26
Q

I cells: secrete what?

A

cholecystokinin

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27
Q

cholecystokinin: functions? (4)

A
  • more pancreatic secretion
  • more gallbladder contraction
  • slows down gastric emptying
  • relaxes the sphincter of Oddi
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28
Q

what increases cholecystokinin secretion?

A

fatty acids, amino acids

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29
Q

fatty acids and amino acids increase secretion of what?

A

cholecystokinin

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30
Q

via what pathways does cholecystokinin cause pancreatic secretion?

A

neural muscarinic pathways

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31
Q

secretin: secreted via which cells?

A

S cells

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32
Q

where are S cells?

A

duodenum

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33
Q

what are the actions of S cells? (3)

A
  • pancreatic HCO3 secretion
  • less gastric acid secretion
  • bile secretion
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34
Q

what increases secretion of secretin

A

acid and fatty acids in lumen of duodenum

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35
Q

acid and fatty acids in lumen of duodenum: increased secretion of what?

A

secretin

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36
Q

what does HCO3 do in duodenum?

A

neutralizes gastric acid, allowing pancreatic enzymes to function

37
Q

glucose-dependent insulinotropic peptide: secreted by which cells?

38
Q

where are K cells?

A

duodenum, jejunum

39
Q

what do K cells secrete?

A

glucose-dependent insulinotropic peptide

40
Q

glucose-dependent insulinotropic peptide: exocrine functions?

A

less gastric acids secretion

41
Q

glucose-dependent insulinotropic peptide: endocrine functions?

A

insulin release

42
Q

what stimulates release of glucose-dependent insulinotropic peptide?

A

fatty acids, amino acids
oral glucose

43
Q

glucose-dependent insulinotropic peptide: other name?

A

Gastric Inhibitory Peptide (GIP)

44
Q

what is the endocrine effect of oral glucose?

A

increases insulin, compared to IV equivalent

due to glucose-dependent insulinotropic peptide/GIP secretion

45
Q

motilin: where is it secreted?

A

small intestine

46
Q

what is the effect of motilin?

A

it produces migrating motor complexes (MMCs)

47
Q

in which state is motilin more secreted?

A

in fasting state

48
Q

which hormone leads to migration motor complexes (MMCs)?

49
Q

which receptor agonist of which hormone are used to stimulate intestinal peristalsis?

A

motilin

eg erythromicin

50
Q

Vasoactive intestinal peptide (VIP): source?

A

Parasympathetic ganglia in sphincters, gallbladder, small intestine

51
Q

Vasoactive intestinal peptide (VIP): what does it do?

A
  • increases secretion of intestinal water and electrolytes
  • relaxes intestinal smooth muscles and sphincters
52
Q

what leads to more secretion of vasoactive intestinal peptide?

A

intestinal distension, vagal stimulation

53
Q

what leads to less secretion of vasoactive intestinal peptide?

A

adrenergic input

54
Q

what is a VIPoma?

A

pancreatic tumor that secretes VIP

non-alpha, non-beta islet cells

55
Q

what is VIP?

A

vasoactive intestinal peptide

56
Q

what is a pancreatic tumor that secretes vasoactive intestinal peptide called?

57
Q

what do the parasympathetic ganglia in sphincters, gallbladder and small intestine secrete?

A

VIP (vasoactive intestinal peptide)

58
Q

which symptoms is VIPoma associated with?

A

Water Diarrhea, Hypokalemia, Achlorhydria

(WDHA syndrome)

59
Q

Water Diarrhea, Hypokalemia, Achlorhydria

what is this suggestive of?

60
Q

which part of the GI system does nitric oxide affect? what does it do?

A

LES, smooth muscle relaxation

61
Q

Loss of NO secretion. where is this implicated in the GI system?

A

higher LES tone in achalasia

62
Q

which substance is implicated in higher LES tone in achalasia?

63
Q

what is achalasia?

A

failure of smooth muscle to relax, LES to remains closed

64
Q

Ghrelin: where is the source?

65
Q

Ghrelin: what does it do?

A

increase the appetite (‘ghrowlin’ stomach)

66
Q

what does increase Ghrelin secretion?

67
Q

what lowers Ghrelin secretion?

A

eating food

68
Q

Prader-Willi: which hormone is increased?

69
Q

Ghrelin: implicated in which syndrome?

A

Prader-Willi

70
Q

after what type of surgery is Ghrelin decreased?

A

gastric bypass

71
Q

gastric bypass surgery affects which hormone that causes appetite?

72
Q

gastric acid: source?

A

parietal cells in the stomach

73
Q

gastric acid: what does it do?

A

decrease the pH of the stomach (make it more acid)

74
Q

how is gastric acid and intrinsic factor increased?

A

histamine, vagal stimulation, gastrin

75
Q

intrinsic factor: source?

A

Parietal cells in the stomach

76
Q

intrinsic factor: what does it do?

A

binds to Vitamin B12, this is required for uptake in the terminal ileum

77
Q

how is gastric acid and intrinsic factor decreased?

A

somatostatin, GIP, prostaglandin, secretin

78
Q

what does autoimmune destruction of parietal cells lead to?

A

chronic gastritis, pernicious anemia

79
Q

what is pernicious anemia?

A

B12 deficiency and megaloblastic anemia

80
Q

pepsin: source?

A

chief cells in the stomach

81
Q

what does pepsin do?

A

protein digestion

82
Q

what leads to increased secretion of pepsin?

A

vagal stimulation (ACh), local acid

83
Q

what is pepsinogen?

A

the inactive form of pepsin

84
Q

when does pepsinogen converted into pepsin?

A

in the presence of H+

85
Q

bicarbonate: source?

A

mucosal cells (stomach, duodenum, salivery glands, pancreas)
Brunner glands (duodenum)

86
Q

what does bicarbonate do?

A

neutralizes acid

87
Q

what leads to increased secretation of bicarbonate?

A

pancreatic and biliary secretion with secretin

88
Q

where is bicarbonate trapped?

A

in mucus that covers the gastric epithelium

GI (14 decks)

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