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Endocrinology -- Freedman > Exam 2: Hormones of GI Tract > Flashcards

Exam 2: Hormones of GI Tract Flashcards

1
Q

What is the largest and most complex endocrine organ in the body?

A

GI tract

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2
Q

What percentage of the cells that line the GI tract secrete hormones? What are there cells called?

A

1%; enteroendocrine cells

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3
Q

T/F. The GI tract is a sensory organ.

A

True

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4
Q

Through what mechanisms is the GI tract a sensory organ?

A

through both hormonal and neural mechanisms

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5
Q

What are the three ways the GI tract is a sensory organ through both hormonal and neural mechanisms?

A
  1. adjusts its own activity (increase or decrease peristalsis)
  2. alerts body to impending influx of nutrients
  3. informs brain of need to initiate/terminate feeding
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6
Q

How is the GI tract innervated?

A
  • with afferent and efferent SNS and PSNS neurons

- ENS (enteric nervous system) = networks of intrinsic nerves

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7
Q

About how many neurons does the Enteric Nervous system (ENS) in the GI tract contain? What is this comparable to?

A

~ 100 x 10^6 neurons = number in spinal cord

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8
Q

What does the Enteric Nervous system do?

A

transmits info up and down length of GI tract

- sensory, motor, interneurons coordinate secretory, absorptive, and contractile activities

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9
Q

What other parts of the nervous system does the Enteric Nervous system communicate with?

A

ENS SNS PSNS ENS

bidirectional communication

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10
Q

What do the gut NTs include?

A
  • catacholamines (NE, Epi)
  • Ach
  • peptides
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11
Q

What can the peptides from neurons and gut (enteroendocrine cells) act as?

A
  • NT
  • neurohormones or
  • neuromodulates (NM)
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12
Q

What nerve provides PSNS innervation to esophagus, stomach, SI, and proximal colon?

A

Vagus nerve

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13
Q

What supplies PSNS innervation to the remainder of the colon and rectum?

A

pelvic nerves from sacral cord levels

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14
Q

How much of the vagus nerve is sensory? How much is motor?

A

3/4 sensory

1/4 motor

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15
Q

What are scattered throughout the stomach and SI that are associated with various vaso-vagal reflexes?

A

Mechano and chemoreceptors

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16
Q

Once the Vaso-vagal reflexes in the gut are stimulated, what is in response?

A

integrating centers in brainstem signal secreting or contractile responses

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17
Q

T/F. Many responses governed by the vaso-vagal reflexes also are produced by GI hormones.

A

True

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18
Q

What occurs with hormonal stimulation of vagal afferent fibers that express receptors for some of the GI hormones?

A

they communicate w/ brainstem w/o having to cross the BBB

GI hormones—-> Target
or GI hormones —> NS –> target

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19
Q

Describe the pathway of the GI peptides, hormones.

A

Enteroendocrine cells–> secretion into portal circulation –> liver –> systemic circulation –> target cell

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20
Q

Describe the pathway for the GI peptides, Paracrines.

A

Enteroendocrine cell –> diffusion –> target cell

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21
Q

Describe the pathway of the GI peptides, Neurocrines.

A

GI tract neuron–> action potential —> target cell

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22
Q

What are the 8 GI hormones?

A
  1. Gastrin
  2. CCK (cholecystokinin)
  3. Secretin
  4. GIP (glucose dependent insulinotropic peptide)
  5. Motilin
  6. Ghrelin
  7. Panreatic polypeptide
  8. GLP-1 (glucagon like peptides–Enteroglucagon)
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23
Q

What are the two incretins of the GI tract?

A

GIP and GLP-1

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24
Q

What cells secrete gastrin and where?

A

G (gastrin) cells in antrum of stomach

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25
Q

What hormones of the GI tract promotes hydrogen ion secretion? What cells secrete H+ ions?

A

Gastrin

promotes hydrogen ion secretion by gastric parietal cells

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26
Q

What will Gastrin’s fxn of stimulating H+ ion secretion do?

A

lower stomach pH–> and activates pepsinogen (secreted by chief cells)–> which begins process of protein digestion

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27
Q

What type of cells secrete pepsinogen?

A

chief cells

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28
Q

When is Gastrin secreted?

A

in response to eating a meal

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29
Q

What are the stimuli for Gastrin release?

A
  • products of protein digestion (phenylalanine and tryptophan)
  • Distention of stomach
  • stimulation of the Vagus* (via GRP-Gastrin releasing peptide- from vagal nerves)
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30
Q

What inhibits Gastrin?

A

somatostatin and low stomach pH

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31
Q

What are the three physiologic effects of Gastrin?

A
  1. stimulate parietal cells to secrete H+ ions
  2. stimulate growth of gastric mucosa
  3. stimulate gastric emptying
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32
Q

What will excess Gastrin do?

A
  • increase H+ ion secretion

- hypertrophy of gastric mucosa

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33
Q

What will deficiency of Gastrin do?

A
  • decrease H+ ion secretion

- atrophy of gastric mucosa

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34
Q

What disease has a Gastrin secreting tumor, “gastrinoma”?

A

Zollinger-Ellison syndrome

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35
Q

Where is the “gastrinoma” in Zollinger-Ellison syndrome typically?

A

in pancreas (non beta-cell)

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36
Q

What will Zollinger-Ellison Syndrome cause?

A

Gastrin Secretion tumor:

  • increase H+ secretion
  • hypertrophy of gastric mucosa
  • duodenal ulcers due to increase H+ secretion
  • acidification of intestinal lumen –> inactiavte pancreatic lipase –> inhibits digestion of fats –> cause steatorrhea (fat in stool)
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37
Q

What will the acidificaiton of the intestinal lumen due to Zollinger-Ellison syndrome cause?

A

inactivation of pancreatic lipase–> inhibits digestion of fats–> leads to steatorrhea (fats in the stool)

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38
Q

What is the treatment for Zollinger-Ellison Syndrome?

A
  • H2 receptor blockers (cimetidine)
  • Inhibitors of H+ pumps (omeprazole)
  • removal of the tumor
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39
Q

What GI hormone coordinates and promotes fat digestion and absorption?

A

CCK (cholecystokinin)

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40
Q

What are the two receptors that bind CCK? Which one can also bind gastrin?

A
  1. CCKa–> only bind CCK

2. CCKb –> equal affinity for BOTH CCK and gastrin

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41
Q

T/F. CCK peptide is structurally related to gastrin and has some gastrin activity.

A

True

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42
Q

What cells secrete CCK and where?

A

I cells of the duodenal and jejunal mucosa

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43
Q

What is CCK secreted in response to?

A
  • monoglycerides and FAs (NOT TGs)

- small peptides and AAs

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44
Q

What type of meal will stimulate release of CCK?

A

a meal containing fat and protein

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45
Q

What will the release of CCK cause coordinated effect of?

A

to ensure appropriate pancreatic enzymes and bile salts are secreted to aid in digestion and absorption of proteins and fats

46
Q

What are the 5 major actions of CCK?

A
  1. contraction of gallbladder
  2. secretion of pancreatic enzymes
  3. secretion of bicarbonate from pancreas
  4. trophic effect on exocrine pancreas and gallbladder
  5. inhibition of gastric emptying
47
Q

With what simultaneous action does contraction of the gallbladder by CCK cause?

A

with simultaneous relaxation of the sphincter of Oddi (hepatopancreatic sphincter) –> ejects bile from gallbaldder –> into lumen of SI

bile emulsifies and solubilizes dietary lipids

48
Q

What are the pancreatic enzymes that CCK stimulates the pancreas to release? What do they do? (3)

A
  1. Lipases –> digest lipids to FA, monoglycerids, choldesterol
  2. Proteases–> digest protein
  3. Amylase digest CHO
49
Q

What does the secretion of bicarbonate from the pancreas by CCK effect?

A

not a major effect, but potentiatiates the effects of secretin on bicarbonate secretion

50
Q

What will the inhibition of gastric emptying of CCK do?

A

slows gastric emptying which enhances fat digestion and absorption
– decrease chyme delivery to the SI

51
Q

What is unique about Secretin about its peptide stucutre that is different than CCK and Gastrin?

A

all 27 AAs are required for biologic activity (NO active fragments like CCK and gastrin)

52
Q

What secretes secretin and where?

A

secreted by S cells of duodenum

53
Q

What causes secretion of secretin?

A

in response to H+ (pH<4.5) and FAs in SI

54
Q

What promotes secretion of pancreatic and biliary bicarbonate? What effect does this have?*

A

Secretin; neutralizes H+ in lumen of SI

–essential for fat digestion

55
Q

What pH does pancreatic lipases function best at? What pH are the inactivated at?

A

pH 6-8

inactivated when pH < 3

56
Q

What does Secretin inhibit the effects of?

A

of gastrin and parietal cells (by neutralizing H+ ions in lumen of SI with bicarbonate)

57
Q

What does GIP stand for?

A

glucose- dependent insulinotropic peptide

58
Q

What is GIP secreted by and where?

A

K cells in the duodenal/jejunal mucosa

59
Q

What is GIP secreted in response to?

A

all three types of nutrients (glucose, AAs, FAs)

60
Q

What is GIP’s major effect?

A

(is it an incretin)
is stimulation of insulin

(hence why oral glucose has greater effect)

61
Q

What has a greater effect, oral glucose or IV glucose and why?

A

oral glucose greater effect than IV glucose due to oral stimulates both insulin directly and via GIP

62
Q

What does GIP inhibit in animals, but not in humans?

A

inhibits gastric H+ secretion (hence why used to be called “gastric inhibitory peptide)

63
Q

What hormone is responsible for the migrating motility complex?

A

Motilin

64
Q

Where is motilin released and what family is it a member of?

A

secreted from upper duodenum during fasting

member of gastrin-CCK family

65
Q

What does the migrating motility complex that motilin is responsible for do?

A

brief episodes of contractions about 90mins apart

clears stomach and intestine in preparation for next meal

66
Q

What does motilin stimulate?

A
  • stimulation of enzyme secretion by stomach and pancreas

- stimulates contraction of gallbladder (like CCK)

67
Q

T/F. The regulation of motilin secretion is unknown.

A

true

68
Q

What is the only GI hormone that promotes food intake?*

A

Ghrelin

69
Q

What is Ghrelin mainly secreted by and when?

A

mainly by stomach mucosa in b/w eating

other tissues can too; pancreas, brain, ovary, adrenal cortex

70
Q

How does Ghrelin carry out its effect?

A

released into blood and can cross BBB –> affecting the hypothalamus where it stimulates appetite

71
Q

What are the effects of Ghrelin?

A
  • tells hypothalamus to stimulate appetite
  • increase feelings of hunger
  • increase gastric acid secretion, gastric motility, gastric emptying
72
Q

What will stimulation of Ghrelin receptors on afferent neurons initiate?

A

intiates vago-vagal reflexes and local enteric reflexes

73
Q

What is Pancreatic Polypeptide secreted by and in response to what?

A

PP (F) cells; in response to ingestion of all three types of nutrients (like GIP)

74
Q

What does pancreatic polypeptide inhibit secretion of?*

A

inhibits pancreatic secretion of bicarbonate and pancreatic enzymes

75
Q

When is Pancreatic polypeptide secretion increased? Decreased?

A

Increased after:

  • a protein rich meal,
  • fasting,
  • exercise, and
  • acute hypoglycemia

Decreased:

  • by somatostatin and
  • intravenous glucose
76
Q

What does GLP stand for?

A

Glucagon-like peptides or Enteroglucagon

77
Q

What is GLP secreted by and where?

A

L cells in the intestinal mucosa

78
Q

What are the most abundant peptide producing cells in the GI tract and what do they produce?*

A

L cells in intestinal mucosa, producing GLP

79
Q

What are L cells that secrete GLP stimulated by?

A

enteric neurons and luminal nutrients

80
Q

What are L cells that secrete GLP unresponsive to?

A

plasma levels of glucose, FA, and insulin

81
Q

What effect on the liver does GLP have?

A

to increase glycogenolysis and gluconeogenesis (similar to glucagon)

82
Q

What are the two types of GLP (glucagon like peptides) that we have?

A

GLP-1 and GLP-2

83
Q

Which type of GLP inhibits glucagon secretion?*

A

GLP-1

84
Q

Which type of GLP stimulates insulin secretion?*

A

GLP-1

85
Q

Which GLP slows gastric emptying?*

A

GLP-1

86
Q

Which GLP has trophic effect on intestinal mucosa, therefore proliferation, therefore increases surface area for absorption?*

A

GLP-2

87
Q

Which GLP produces mucosal repair and decreases inflammatory responses to bowl injury?*

A

GLP-2

88
Q

What are the functions of GLP-1?

A
  • *inhibits glucagon secretion
  • *stimulates insulin secretion
  • *slows gastric emptying (feel full)
  • inhibits food intake
  • inhibits parietal cells and therefore decreases H+ ions
  • stimulates D cells to secrete somatostatin and therefore decrease H+ ions
89
Q

What are the functions of GLP-2?

A
  • *trophic effect on intestinal mucosa, increasing proliferation, therefore increasing surface area for absorption
  • *produces mucosal repair
  • *decreases inflammatory responses to bowel injury
  • no effect on insulin secretion
  • stimulates AA and glucose transport
  • maintains mucosal barrier to bacteria and enterotoxins
  • may have use to treat IBD
90
Q

What may GLP-2 may have use to treat?

A

inflammatory bowl disease (IBD)

  • Chrons
  • Ulcerative colitis
91
Q

What refers to slowing of gastric and pancreatic exocrine secretion, stomach emptying, and intestinal motility in response to the presence of unabsorbed nutrients in the distal ileum?

A

Ileal Brake Mechanism

92
Q

What is an important isgnal for the ilieal brake mechanism?

A

FA b/c no CHO left in chyme at this point

93
Q

The abundance of what cells does a good job of gauging the efficiency of nutrient absorption?

A

abundance of L cells in distal ileum and colon

94
Q

What feeds back on the stomach to decrease acid secretions, decrease motility, and decrease emptying? What does this result in?*

A

GLP-1 and peptide YY

will prolong transit time and therefore increase nutrient absorption

95
Q

What is the ileal brake mechanism?

A

slowing of gastric and pancreatic exocrine secretion, stomach emptying, and intestinal motility in response to presence of unabsorbed nutrients in the distal ileum

96
Q

What are produced in GI endocrine cells and act locally?

A

paracrines

97
Q

What are two paracrines of the GI tract? What do they do?

A

Somatostatin–> inhibits stomach acid
and
Histamine–> promotes stomach acid

98
Q

What type of cells secrete Somatostatin and from where? In response to what?

A

D cells of antral cells (stomach mucosa) in response to decreased luminal pH

also by deta cells of pancreas and hypothalamus

99
Q

When we see somatostatin what should we think?

A

inhibitory

100
Q

What does somatostatin inhibit?

A

secretion of gastrin and other GI hormones

–inhibits gastrin and blocks H+ secretion)

101
Q

What will histamine (a paracrine of the GI tract) cause?

A

works synergistacally with gastrin and ACh, and will stimulate H+ secretion

102
Q

What cells produce histamine and where?

A

enteroendocrine cells in Gi mucosa especially in stomach near parietal cells

103
Q

What are the 7 neurocrines of the GI tract?

A
  1. ACh (cholinergic neurons)
  2. NE (adrenergic neurons)
  3. VIP (neurons of mucosa and smooth muscle)
  4. Gastrin releasing peptide (neurons of gastric mucosa)
  5. Enkephalins (neurons of mucosa and smooth muscle)
  6. Neuropeptide Y (neurson of mucosa and smooth muscle)
  7. Substance P (cosecreted with ACh
104
Q

What are the actions of ACh on GI tract?

A
  • contraction of smooth ms in wall
  • relaxation of sphincters
  • increase: salivary, gastric, and pancreatic secretions
105
Q

What are the actions of NE on GI tract?

A
  • relaxation of smooth ms in wall
  • contraction of sphincters
  • increase salivary secretion (slightly)
106
Q

What are the actions of VIP on GI tract?

A
  • relaxation of smooth ms
  • increase intestinal secretion
  • increase pancreatic secretion
107
Q

What are the actions of Gastrin releasing peptide (bombesin) on the GI tract?

A
  • increase gastrin secretion
108
Q

What are the actions of Enkephalins (SNS) on the GI tract?

A
  • contraction of smooth muscle

- decrease intestinal secretion

109
Q

What are the actions of Neuropeptide Y on the GI tract?

A
  • relaxation of smooth ms

- decrease intestinal secretion

110
Q

What are the actions of Substance P on the GI tract?

A
  • contraction of smooth ms

- increase salivary secretion

Endocrinology -- Freedman (14 decks)

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