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GI Exam > GI Hormones > Flashcards

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

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7
Q

actions of gastrin

A

*releases mast cell histamine, leading to INCREASED GASTRIC ACID SECRETION
*increased cell proliferation

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8
Q

gastrin in the clinic

A

Zollinger-Ellison (ZE) Syndrome (uncontrolled gastrin secretion)

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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

A

M-cells

25
Q

location of M-cells

A

*duodenum

note - M cells make motilin

26
Q

stimulus for secretion of motilin

A

*neural control

27
Q

inhibitors for production of motilin

A

food ingestion

28
Q

target of motilin

A

motilin receptors on GI tract smooth muscle cells

29
Q

actions of motilin

A

*plasma levels oscillate during inter-digestive period
*activates the migrating myoelectric complex (MMC)

30
Q

migrating myoelectric complex (MMC)

A

*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
Q

motilin in the clinic

A

*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
Q

“Incretin Effect”

A

*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
Q

acronym for GLP-1

A

glucagon-like peptide-1

note - GLP-1 is an incretin hormone

34
Q

source (cell type) for GLP-1

A

L cells

35
Q

location of L cells

A

*ileum
*colon

note - L cells make GLP-1

36
Q

stimulus for secretion of GLP-1

A

*carbs
*amino acids
*fatty acids

37
Q

inactivation of GLP-1 (and other incretins)

A

DPP-4 (half life < 2 min)

38
Q

targets of GLP-1

A

*beta cells
*liver
*gastric smooth muscle
*CNS
*heart

39
Q

actions of GLP-1

A

*INCREASED INSULIN SECRETION & decreased glucagon secretion
*decreased gastric emptying
* (+) satiety via CNS
*other effects on heart, liver, skeletal muscle

40
Q

use of GLP-1 to treat diabetes

A

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
Q

use of GLP-1 agonists to treat obesity

A

*ex. Tirzepatide
*synthesis of a composite molecule that combines GIP and GLP-1 compounds to inhibit appetite

42
Q

source (cell type) for somatostatin

A

D cells

43
Q

location of D cells

A

*stomach
*small bowel (SB)
*pancreas

note - D cells make somatostatin

44
Q

somatostatin in the stomach

A

stomach: vagal stimulation: DECREASED secretion of somatostatin, leading to increased acid secretion

45
Q

somatostatin in the pancreas

A

pancreas: vagal stimulation: INCREASED secretion of somatostatin, leading to decreased insulin secretion

46
Q

targets of somatostatin

A

*EEC (enteroendocrine cells)
*smooth muscle
*pancreas
*pituitary

47
Q

actions of somatostatin

A
  • (-) ALL neuroendocrine cell secretion
    *decreased insulin & glucagon secretion
    *decreased gut and bile fluid secretion
    *decreased GI motility
    *decreased mesenteric blood flow
48
Q

somatostatin in the clinic

A

*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
Q

source (cell type) for ghrelin

A

P/D1 cells

50
Q

location of P/D1 cells

A

stomach

note - P/D1 cells make ghrelin

51
Q

stimulus for secretion of ghrelin

A

fasting

52
Q

inhibitors for production of ghrelin

A

food intake

53
Q

target of ghrelin

A

receptors on gastric smooth muscle and CNS

54
Q

actions of ghrelin

A

*STRONGLY OREXIGENIC (makes you hungry)
*plasma levels oscillate and peak before meals
*increased gastric motility

GI Exam (54 decks)

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