L22: Neuroendocrine Control Flashcards

1
Q

how do ENS neurons connect to other neurons inside and outside of the ENS

A

interneurons and afferent neurons

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2
Q

ENS sample gut content through ________

A

receptors

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3
Q

____ ENS neurons innervate target cells: smooth muscle, secretory and absorptive cells

A

efferent

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4
Q

T/F: In monogastric animals, the ENS can still coordinate digestion even after being severed from the brain

A

T

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5
Q

macronutrients are sensed by receptors expressed in ________ cells of the gut via their microvilli that extend into the gut lumen

A

enteroendocrine

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6
Q

afferent neurons of the ENS are ______ neurons and innervate muscle receptors in the ….

A

cholinergic
mucosa - chemoreceptors, mechanoreceptors
muscle layer - mechanoreceptors

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7
Q

what are the target organs of the efferent neurons of the ENS (inhibitory and excitatory)

A

smooth muscles
secretory cells
endocrine clles

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8
Q

what are the excitatory neurons of the ENS and what do they stimulate

A

ACh and Substance P
stimulate contraction of smooth muscles, secretion and enteroendocrine cell degranulation

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9
Q

what are the inhibitory neurons of the ENS and what do they inhibit

A

VIP, NO, ATP
- inhibit smooth muscle cells
- cause vasodilation

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10
Q

what does the myenteric (Auerbach’s) plexus innervate

A

longitudinal and circular smooth muscle layers; concerned with control of gut movements

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11
Q

what does the submucosal (Meissner’s) plexus innervate

A

glandular epithelium, intestinal endocrine cells and submucosal blood vessels; primarily concerned with control of intestinal secretion

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12
Q

_____ integrate extrinsic and intrinsic input and communicate bw myenteric and submucosal plexus

A

interneurons

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13
Q

what is post-operative ileus and what are the 3 categories of mechanism that can cause it

A

hypomotility or amotility of the GI tract in the absence of an obstruction

  • neurogenic, inflammatory and pharmacologic
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14
Q

what are the pharmacological causes of post-operative ileus

A
  • opioid peptides modulate GI motility through receptors on myenteric and submucosal ganlia that inhibit enteric neuron function
  • exogenous administered opioids decrease transit in GI tract through mu 2 (opioid) receptors in myenteric plexus causing hypomotility
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15
Q

what is the main function of parasympathetic innervation within the ENS

A

promote digestion
- motility patterns
- net fluid secretion
- vasodilation
- entertoendocrine cell degranulation

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16
Q
A
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17
Q

what is the dominant extrinsic neural tone of the alimentary tract controlled by

A

parasympathetic innervation

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18
Q

what is the main function of the sympathetic innervation of the ENS

A

inhibit digestion & recover fluid volume
- stops motility
- increases net fluid abs
- vasoconstriction

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19
Q

ENS can operate w/out CNS input in ______ animals

A

monogastric

20
Q

what is the release stimulus for gastrin

A
  • anticipation of food, stomach distension, presence of proteins/peptides in stomach
21
Q

what inhibits gastrin release

A
  • HCl
  • somatostatin
  • secretin
  • GIP
22
Q

what are the functions of gastrin

A
  • stimulates K+/H+ ATPase pump activity of parietal cells
  • stimulates release of histamine from enterochromaffin like cells
  • histamine stimulates cAMP mediated insertion of K+/H+ ATPase pumps into the apical membrane of parietal cells
  • effects gastric motility
  • minor effect on pancreas acinar cells
23
Q

somatostatin is a peptide hormone synthesized by enteroendocrine ____ cells of the _____, ____ cells in the endocrine pancreas and in the hypothalamus

A

D cells of stomach
endocrine

24
Q

function of somatostatin

A

directly and indirectly inhibits gastric acid secretion

25
Q

how does somatostatin directly vs indirectly inhibit gastric acid secretion

A

Directly: inhibits adenylyl cyclase of parietal cells which antagonizes the stimulatory effects of histamine

Indirectly: inhibits G cells, ECL cells and parietal cells

26
Q

what is the release stimuli for somatostatin

A

very low pH in antrum and CCK

27
Q

somatostatin does the opposite of ?

A

gastrin

28
Q

when is somatostatin release blocked and how

A
  • during cephalic and gastric phase, the release is blocked by vagal stimulation
29
Q

what are the two main functions of secretin

A
  • pH regulation by promoting pancreatic and biliary bicarbonate secretion and bicarbonate secretion in duodenum epithelial cells
  • reduces gastric secretions by blocking G cells
30
Q

secretin release stimuli

A

entry of fat and acid (protons) into duodenum, stimulates S cells

31
Q

what inhibits Cholecystokinin (CCK)

A

somatostatin

32
Q

what cells produce CCK and where

A

enteroendocrine I cells of dudodenal and jejunal mucosa and neurons in the ileum and colon

33
Q

what are the functions of CCK

A
  • enzyme secretion from pancreas
  • contraction of gall bladder to release bile
  • activation of D cells (somatostatin)
34
Q

what causes the release of Cholecystokinin (CCK)

A

presence of FAs/AAs/peptides in chyme entering the duodenum

35
Q

what cells produce Gastric inhibitory peptide (GIP) and where

A

neuroendocrine K cells of duodenal and jejunal mucosa

36
Q

what stimulates the release of GIP

A

glucose and FAs in chyme entering duodenum

37
Q

what are the functions of GIP

A
  • inhibit parietal acid secretion
  • increase insulin release from endocrine pancreas
38
Q

what are the functions of motilin

A

increase gastric emptying and somatostatin release from pancreas

39
Q

what cells produce motilin and where

A

neuroendocrine Mcells of duodenal and jejunal mucosa

40
Q

what is the release stimuli for Motilin

A

increased pH in duodenum
also spontaneously released during interdigestive phase

41
Q

what is Erythromycin

A

a motilin receptor agonist; marolide antibiotic

42
Q

what are the side effects of the antibiotic Erythromycin

A

enhances gastric emptying
side effects: D+, nausea, abdominal pain, V+

43
Q

what happens to salivary gland activity during the intestinal phase

A

cease activity

44
Q

what happens to gastric secretion activity during the inestinal phase

A

secretions decrease, caused by neural and humoral control
* neural: removal of stimuli from stomach
* humoral: somatostatin is synthesized and released from D cell, gastrin and CCK activate D cells, further increasing somatostatin
somatostain inhibits activity of parietal and ECL cells

45
Q

how do endocrine control systems affect secretions into the GI tract during the interdigestive phase (when stomach & SI are empty)

A
  • gastrin release reduced
  • somatostatin inhibits gastric and pancreatic secretions and CCK release
  • motilin stimulates contraction of gut smooth muscle
46
Q

what is Gastrinoma/Zollinger-Ellison Syndrome

A

rare neuroendocrine tumor that arises from malignant transformation of somatostatin secreting delta cells of the endocrine pancrease to gastrin producing cells

gastrin stimulates secretion of gastric acid –> gastrinoma –> peptic ulcers, D+/steatorrhea/hypokalemia

steatorhhea = abnormal amount of lipids in feces