Intro to GI physiology Flashcards
sympathetic innervation of GI that is different from parasympathetic
sympathetic can synapse on myenteric plexus or directly on motor neurons that innervate muscle or on secretory neurons that secrete
vago-vagal reflex tract
vagus sensory afferents in digestive track (nodose ganglion) send info to nucleus of tractus solitaries (NTS) synapses here then sends efferents through vagus nerve back to digestive tract
paracrine signaling includes what molecules and what cells release them
somatostatin and histamine
enteroendocrine cells
somatostatin: secreted by what cells Stimuli actions where else secreted
- D cells of GI mucosa
- stimuli: decreased pH in the lumen
- actions: decrease gastric H+ secretion and inhibits secretion of other GI hormones
- Secreted in hypothalamus and delta cells of exocrine pancreas
Histamine is secreted by what cells
enterochromaffin-like cells in gastric glands (ECL)
target and action of histamine
parietal cells to secrete acid production
how do hormones get to specific receptor
- enteroendocrine cells have secretary granules filled with hormone peptides that are released upon stimulation
- secreted into portal circulation, pass through liver, and go to systemic circulation
- bind to specific receptors on target cell
criteria to be a hormone
1) substance must be secreted in response to physiologic stimulus and carried in bloodstream to distant site
2) function must be independent of neural activity
3) must have been isolated, purified, chemically identified, and synthesized
Gastrin:
site of secretion
Stimuli of secretion
- G cells of the antrum of stomach
- small peptides and aa, distension of the stomach, vagal stimulation via GRP
CCK
site of secretion
stimuli of secretion
site is I cells of duodenum and jejunum
small peptides and aa, fatty acids
secretin:
site of secretion
stimuli of secretion
S cells of duodenum
fatty acids in duodenum, and H+ in duodenum
Glucose-dependent insulinotropic peptide
duodenum and jejunum
oral glucose, aa, fatty acids
Gastrin actions
parietal cells secretion of gastric acid
stimulates growth of gastric mucosa
Zollinger-Ellison syndrome
increase gastrin and H+ from parietal cells
- hypertrophy of gastric mucosa
- duodenal ulcers
- steatorrhea
steatorrhea
from gastrin-secreting tumors: increased H+ secretion results in acidification of intestinal lumen, so pancreatic lipase inactive so fat not absorbed so its excreted in stool
CCK actions
HCO3- pancreatic bicarb secretion potentiation (w/secretin)
Exocrine pancreas and gallbladder growth
Pancreatic enzyme secretion
Inhibits gastric emptying
contraction of gallbladder and relaxation of sphincter of oddi
Secretin actions
pancreatic and biliary HCO3- secretion
decrease gastric H+ secretion
inhibits trophic effect of gastrin on gastric mucosa
GIP is secreted by what cells?
K cells of duodenal and jejunal mucosa in response to FA,aa,glucose
GIP actions
- increase insulin secretion from pancreatic B cells
- decrease gastric H+ secretion
vasoactive intestinal peptide source
neurons of mucosa and SM
gastrin releasing peptide source
neurons from gastric mucosa
enkephalins source
neurons of mucosa and SM
NPY source
neurons of mucosa and SM
substance P source
Co-release with ACh
Ach action
- contraction of SM
- relaxation of sphincters
- increased salivary secretion
- increased gastric secretion
- increased pancreatic secretion
Norepinephrine actions
relaxation of SM
contraction of sphincters
increased salivary secretion
VIP action
relaxation of SM
increased intestinal secretion
increased pancreatic secretion
Gastrin-releasing peptide (GRP) action
increased gastrin secretion
enkephalins actions
- contraction of SM
- increased intestinal secretion
NPY actions
relaxation of SM
increased intestinal secretion
substance P action
conctraction of SM
increased salivary secretion
satiety center is located in which nucleus?
ventromedial nucleus
feeding center is located where?
lateral nucleus
integrative center btwn feeding and satiety
arcuate nucleus
a-melanocortin (a-MSH) pathway
- a-MSH released by POMC neurons
- a-MSH binds to MCR-4 present in second order neurons
- inhibits food intake and increases metabolism (anorexigenic)
neuropeptide y pathway
hunger stimulates release NPY
NPY binds Y1R
neurons that release NPY also release AGRP which antagonizes MCR-4
=
increase feeding behavior and storage of calories (orexigenic)
cases of obesity have been related to mutations in the ___ and ___ genes
POMC and MCR-4
ghrelin
secreted by endocrine cells in stomach
binds to growth hormone secretagogue receptors
in hyoothalamus it stimulates neurons that release NPY
other actions of ghrelin
increases appetite, gastric motility, gastric acid secretion, adipogenesis
insulin binds
to receptors in satiety and hunger centers within hypothalamus
insulin inhibits and stimulates
inhibits NPY
stimulates POMC
insulin actions
decrease appetite and increase metabolism
CCK elicits ___
decreases what and increases what
satiety acts on vagal-->NTS-->hypothalamus circuit -decreases ghrelin decreases gastric emptying increases gastric distension
PYY binds
Y2 receptors of hypothalamus and inhibits NPY, releases inhib of POMC
potential as appetite suppressor
Leptin is secreted by what cells
adipose tissue and by endocrine cells in stomach
leptin binds to what
POMC and NPY, stimulates POMC inhibits NPY
leptin increase and decrease
increase metab
decrease ghrelin and appetite
