GI Hormones Flashcards

1
Q

enteroendocrine cells (EECs)

A

specialized cells in the GI tract that secrete GI hormones in response to specific luminal, endocrine, and neural signals

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2
Q

source (cell type) for gastrin

A

G cells

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3
Q

location of G cells

A

*gastric antrum (stomach)
*duodenum

note - G cells secrete gastrin

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4
Q

stimulus for secretion of gastrin

A

*amino acids & peptides
*gastric distension

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5
Q

inhibitors of gastrin production

A

*H+ (acid; via somatostatin)
*secretin

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6
Q

target of gastrin

A

parietal cells (promotes release of stomach acid)

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7
Q

actions of gastrin

A
  1. increases gastric acid secretion (stimulates enterochromaffin-like cells, which release histamine and cause parietal cells to release gastric acid)
  2. increases growth of gastric mucosa
  3. increases gastric motility
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8
Q

gastrinoma

A

*aka Zollinger-Ellison (ZE) Syndrome
*uncontrolled gastrin secretion → excess gastric acid hypersecretion
*presents with abdominal pain, heartburn, steatorrhea, weight loss
*positive secretin stimulation test (increased gastrin levels after secretin administration, which normally inhibits gastrin release)

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9
Q

Zollinger-Ellison (ZE) Syndrome

A

*neoplastic G-cells
*uncontrolled gastrin secretion, leading to very high plasma levels
*drives very high gastric acid output
*causes severe peptic ulceration of stomach, duodenum, and small intestine
*causes watery diarrhea and steatorrhea (fatty diarrhea)
*tx: surgical resection; octreotide

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10
Q

source (cell type) for secretin

A

S cells

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11
Q

location of S cells

A

*duodenum

note - S cells make secretin

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12
Q

stimulus for secretion of secretin

A

*H+ (pH < 4.5)
*fatty acids

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13
Q

inhibitors of secretin production

A

*pH > 4.5 (PPIs, H2-blockers)

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14
Q

targets of secretin

A

*pancreas
*bile ducts
*stomach

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15
Q

secretin in the clinic

A

*used diagnostically to test for ZE syndrome
*secretin inhibits gastrin secretion from NORMAL G cells
*BUT, paradoxically, secretin STIMULATES gastrin secretion from gastrin-producing EEC tumors in ZE syndrome

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16
Q

actions of secretin

A

*INCREASED pancreatic & biliary bicarbonate (HCO3-) secretion
*DECREASED gastric acid secretion
*DECREASED gastric motility
*(+) pancreatic cell growth

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17
Q

source (cell type) for CCK

A

I-cells

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18
Q

location of I-cells

A

*duodenum

note - I cells make CCK

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19
Q

stimulus for secretion of CCK

A

*fatty acids
*amino acids

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20
Q

inhibitors of CCK production

A

*bile acids

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21
Q

targets of CCK

A

*CCK-1 receptors in:
-gallbladder
-pancreas
-stomach
-smooth muscle
-nerves

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22
Q

actions of CCK

A

*INCREASED GALLBLADDER CONTRACTION
*INCREASED BILE SECRETION
*INCREASED PANCREATIC ENZYMES
*decreased gastric emptying & acid
* (+) induces satiety via vagus

23
Q

CCK in the clinic

A

*CCK can be used for evaluating gallbladder function:
-synthetic CCK is used in radiology to evaluate gallbladder function (contractility)

24
Q

source (cell type) for motilin

25
location of M-cells
*duodenum note - M cells make motilin
26
stimulus for secretion of motilin
*neural control
27
inhibitors for production of motilin
food ingestion
28
target of motilin
motilin receptors on GI tract smooth muscle cells
29
actions of motilin
*plasma levels oscillate during inter-digestive period ***activates the migrating myoelectric complex (MMC)**
30
migrating myoelectric complex (MMC)
***cycles of electrical and motor activity** which migrate from the gastric antrum to the ileum every ~90 min ***clears lumen to prepare for next meal** *maintains SB zone of relative sterility ***ACTIVATED by MOTILIN**
31
motilin in the clinic
***used to treat gastroparesis** *erythromycin is an "accidental" ligand for the motilin receptor & causes abdominal side effects ***erythromycin used as a PRO-MOTILITY agent for treatment of gastroparesis** *highly specific motilin receptor agonists are being developed to treat dysmotility syndromes
32
"Incretin Effect"
***ORAL glucose stimulates MORE insulin secretion than IV glucose** -mediated by hormones secreted from proximal gut (**GIP**) and distal gut (**GLP-1)** in response to nutrients *incretins are rapidly deactivated by the plasma enzyme DPP-4
33
acronym for GLP-1
glucagon-like peptide-1 note - GLP-1 is an incretin hormone
34
source (cell type) for GLP-1
L cells
35
location of L cells
*ileum *colon note - L cells make GLP-1
36
stimulus for secretion of GLP-1
*carbs *amino acids *fatty acids
37
inactivation of GLP-1 (and other incretins)
DPP-4 (half life < 2 min)
38
targets of GLP-1
*beta cells *liver *gastric smooth muscle *CNS *heart
39
actions of GLP-1
***INCREASED INSULIN SECRETION** & decreased glucagon secretion ***decreased gastric emptying** * (+) satiety via CNS *other effects on heart, liver, skeletal muscle
40
use of GLP-1 to treat diabetes
1) GLP-1 agonists that are RESISTANT to DPP-4 (such that the GLP-1 is not rapidly inactivated by DPP-4) [ex. Ozempic] 2) DPP-4 inhibitors that prolong effects of ENDOGENOUS GLP-1
41
use of GLP-1 agonists to treat obesity
*ex. Tirzepatide *synthesis of a composite molecule that combines GIP and GLP-1 compounds to inhibit appetite
42
source (cell type) for somatostatin
D cells
43
location of D cells
*stomach *small bowel (SB) *pancreas note - D cells make somatostatin
44
somatostatin in the stomach
stomach: vagal stimulation: DECREASED secretion of somatostatin, leading to increased acid secretion
45
somatostatin in the pancreas
pancreas: vagal stimulation: INCREASED secretion of somatostatin, leading to decreased insulin secretion
46
targets of somatostatin
*EEC (enteroendocrine cells) *smooth muscle *pancreas *pituitary
47
actions of somatostatin
***(-) ALL neuroendocrine cell secretion** *decreased insulin & glucagon secretion *decreased gut and bile fluid secretion *decreased GI motility *decreased mesenteric blood flow
48
somatostatin in the clinic
*a synthetic somatostatin analog (octreotide) can be used for many reasons, including: -ZE syndrome -acromegaly -severe uncontrolled diarrhea -insulinoma *most commonly used for: DIVERTICULAR HEMORRHAGE and variceal hemorrhage
49
source (cell type) for ghrelin
P/D1 cells
50
location of P/D1 cells
stomach note - P/D1 cells make ghrelin
51
stimulus for secretion of ghrelin
fasting
52
inhibitors for production of ghrelin
food intake
53
target of ghrelin
receptors on gastric smooth muscle and CNS
54
actions of ghrelin
***STRONGLY OREXIGENIC (makes you hungry)** *plasma levels oscillate and peak before meals *increased gastric motility