Secretory functions of GI tract peptides ( choudhury) Flashcards

(54 cards)

1
Q

are all GI hormones peptides?

A

yes

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2
Q

how are GI peptides classified ? and what are the three classifications

A

based on method by which peptide is delivered to target site

endocrine
paracrine
neurocrine

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3
Q

what are the 5 GI endocrine hormones

A
Secretin 
Gastrin
CCK (Cholecystokinin) 
Gastric inhibitory peptide (GIP)
Motilin
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4
Q

where are endocrine peptides released and what do they reach

A

released into circulation and reach all tissues

specific receptors are found on target tissues

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5
Q

what are paracrine peptides released from and where do they diffuse and have effects

A

released from endocrine cells and diffuse through extracellular space to target

have effects in areas where cells are contained which release them

can release or inhibit release of endocrine substances

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6
Q

what is an example of a paracrine substance

A

histamine

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7
Q

what effect does ACH have on the GI tract

A

its not a peptide BUT is a neuroregulator of the GI tract which stimulates acid secretion from gastric parietal cells

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8
Q

what are the three candidate endocrine peptides

A

PP
peptide YY
enteroglucagon

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9
Q

where are endocrine factors released in the GI tract and what are the three stimuli for release

A

released from stomach and small intestine mucosa into portal circulation

after stimulation from nerves, distention, chemical stimulation of food intake

pass through liver and heart back to digestive system to regulate movement, secretions, growth, release of other hormones and absorption

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10
Q

where is the site of release of gastrin

A

G cells in gastric mucosa
duodenum
pancreas

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11
Q

what molecules stimulate the release of gastrin

A

protein
distention due to food
nerves

also:
Ca
Decaffeinated coffee
wine

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12
Q

what inhibits the release gastrin release

A

acid (feedback)

secretin

glucagon

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13
Q

what are the sites of release of CCK

A

duodenum
jejunum
ileum (minor)

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14
Q

what stimulates the release of CCK

A

protein
fat

Acid (of secondary importance)

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15
Q

what part of the GI tract release secretin

A

duodenum

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16
Q

what stimulates the release of secretin

A

acid

fatty acids(of secondary importance)

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17
Q

what part of GI tract releases GIP

A

duodenum

jejunum

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18
Q

what part of GI tract releases Motilin

A

Duodenum

jejunum

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19
Q

what stimulates the release of GIP

A

glucose (primarily)

protein
fat

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20
Q

what stimulates the release of motilin

A

nerves (Main)

of secondary importance:
fat
acid

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21
Q

what is the function of microvilli on the surface of endocrine cells

A

contain receptors that sample luminal contents

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22
Q

what is the major regulatory action of secretin

A

Natures antacid

released when pH falls below 4.5

stimulates pancreatic and liver bicarb and fluid secretion

inhibits gastric emptying (acid secretion)

stimulates pancreatic growth

inhibits gastrin release

23
Q

what is the major regulatory action of gastrin

A

stimulates release of HCl by parietal cells of the stomach via release of histamine from ECL cells and direct action

aids in gastric motility

stimulates GI mucosal growth (can lead to carcinoid tumors)

24
Q

conditions leading to decreased acid release lead to what….

A

high serum gastrin levels

25
what are the major regulatory actions of CCK on the GI tract
stimulates gallbladder contractions to release bile for fat digestion and pancreatic bicarb release stimulates pancreatic growth inhibits gastric emptying
26
what is the function of GIP
inhibits gastric secretions and stimulates insulin release
27
what does motilin do
stimulates gastric motility and upper GI motility via the interdigestive migrating myoelectric complex (MMC)
28
what is similar about gastrin and CCK
they have 5 identical amino acids on their C terminal
29
what are the two forms of gastrin
``` G17 (little gastrin) G 34 (big gastrin) ``` gastrin is synthesized as a larger precursor molecule called progastrin
30
what form does most gastrin exist in
G 34 in the basal or interdigestive state
31
after a meal what is the predominant form of gastrin and what does this cause
G17 | stimulates gastric secretion
32
because of the similar structure of CCK and gastrin, what can happen.
desulfated CCK can activate gastrin receptors responsible for acid secretion (CCK-B receptors) gastrin can activate CCK receptors responsible for gall bladder contraction (CCK-A receptors)
33
what molecules are similar in structure to secretin
Glucagon has 14 AA's identical to secretin GIP and VIP have 9 amino acids identical to secretin
34
what is the function of enteroglucagon
this is a lesser known candidate endocrine hormone similar to secretin formed by same gene in pancreatic alpha cells which forms glucagon releases insulin inhibits gastric secretion delays gastric emptying
35
what stimulates the release of enteroglucagon
fat
36
what is the function of pancreatic polypeptide
"PP" inhibits pancreatic bicarb and enzyme secretion
37
what stimulates PP release
protein, fat, glucose
38
what is the function of peptide YY and what stimulates its release
inhibits gastric secretion and emptying as well as intestinal motility
39
what is the function of substance P
stimulates intestinal motility stimulates gallbladder contraction (neurocrine peptide)
40
what is the function of neurotensin
increases blood glucose by stimulation of glycogenolysis and release of glucagon inhibits release of insulin
41
what is the function of VIP
relaxation of smooth muscle (intestine) vasodilator via promotion of production of NO stimulates pancreatic secretion inhibits gastric secretion stimulates intestinal secretion (this is a neurocrine peptide)
42
what is the function of Bombesin (aka GRP)
released by vagal stimulation with resulting release of gastrin this is a neurocrine peptide
43
what is the function of enkephalins what are these used to treat
activation of opiate receptors on circular smooth muscle cells to mediate their contraction and also contraction of lower esophageal, pyloric, and ileocelcal sphincters opiates slow intestinal motility used to treat diarrhea
44
what is the function of somatostatin (paracrine peptide) and where is it found
found in gastric and duodenal mucosa AND pancreas inhibits gastrin release and gastric acid secretion
45
what is the function of histamine what cell is histamine produced in what causes the release of histamine
produced in ECL cells released by gastrin and stimulates acid secretion from parietal cells potentiates action of gastrin and ACh on acid secretion
46
how do we treat hypersecretion of acid
histamine (H2) blockers
47
what is Gastrinoma or Zollinger-Ellison syndrome
non-beta cell tumor of the pancreas or duodenal tumors continually produce and release gastrin into the blood
48
what does gastrinoma result in
hypersecretion of gastric acid by parietal cells and increased acid secretory capacity by hyperplastic mucosa peptic ulcers diarrhea steatorrhea (excess fat in feces) hypokalemia
49
what contributes to the diarrhea that is seen in gastrinoma
high gastrin levels inhibit absorption of fluid and electrolytes by the intestine
50
what contributes to the steatorrhea in gastrinoma (fat in the stool)
inactivation of pancreatic lipase by gastrin along with precipitation of bile salts at a low luminal pH
51
how is gatrinoma (zollinger-ellison) treated
treated with drugs which inhibit acid secretion along with gastrectomy if needed
52
what are the blood tests that indicate gastrinoma
elevated serum gastrin
53
what are three tests that can definitively diagnose gastrinoma (considering gastrin is also elevated in duodenal ulcer disease)
stimulation by protein meal (no measurable change in serum gastrin levels) ``` IV Calcium (increased acid and serum gastrin level) (ca causes increases gatrin release) ``` ``` secretin infusion (increased serum gastrin level) (secretin typically decreases gastrin levels... but in gastrinoma for unknown reason secretin causes gatrin release) ```
54
what is the cause of pancreatic cholera (watery diarrhea syndrome) what does it result in
overproduction of VIP due to pancreatic islet cell tumor results in significant intestinal secretion of fluid and electrolytes with production of lots of diarrhea frequently lethal due to large volume of fluid and electrolyte loss