Oxyntic and pyloric glands, their cells, their secretions Flashcards
Oxyntic glands
D cells (somatostatin) Chief cells (pepsinogen) Parietal cells (HCL, intrinsic factor) mucous neck cells enterochromaffin cells (histamine secreting)
Pyloric glands
D cells (somatostatin) G cells (gastrin) enterochromaffin cells (histamine secreting)
mechanism of HCL secretion by parietal cells
apical domain transporters
internal activity
basal membrane transporters
apical: H-K exchanger ATPase, bringing K in, and pushing H into the lumen
internally, carbonic anhydrase combines CO2+H2O to form H and HCO3
H is then taken BACK out into the lumen by the H-K exchange ATPase
basal side:
Na/K ATPase
HCO3/CL exchanger, brings Cl into the cell from blood
omeprazole targets
the H-K ATPase exchanger on the apical membrane of the parietal cell
it secretes H in exchange for K; K is brought from the blood via Na/K ATPase
Cl is brought into the cell by pumping HCO3 into the blood
Cl diffuses out of the apical part of the cell, following H
H and Cl form HCL
omprazole targets the H secretor so HCL cant form in the lumen
what kind of “tide” do we find near parietal cells?
the “alkaline tide” across the basal membrane as HCO3 is reabsorbed into the blood
Histamine
a paracrine
released by enterochromaffin cells in response to ACh and gastrin hormone
histamine stimulates parietal cell HCL secretion
binds to H2 receptors on parietal cells
what receptors does histamine bind to on the parietal cells?
H2 receptors
what blocks the receptors that histamine acts on?
cimetidine blocks H2 receptors
histamine — H2 receptor —>
cAMP —> H secretion through H/K ATPase
ACh
stimulates HCL secretion
released from Vagus
ACH from the vagus binds to the ____ receptor
M3 mAChR on parietal cells
what blocks the the M3 mAChR receptor?
atropine
binding of ACh to M3 leads to IP3/Ca cascade that results in secretion of H/K ATPase activation
ACh indirectly activates ECL cells which release histamine
Gastrin
what secretes it, what happens to it
released by G cells in the antrum into the blood, returned to stomach by circulation
binds to CCKb receptors and causes IP3/Ca cascade —> H/K ATPase activation
indirectly stimulates ECL cells to release histamine
CCKb
affinity for gastrin and CCK
CCKa
affinity for CCK only
gastrin is stimulated by
stomach distention
presence of small peptides and amino acids, and vagus nerve
Atropin blocks
vagal stimulation of M3 mAChR receptors, but does not block vagal stimulation of G cells secreting gastrin
somatostatin
a paracrine
inhibits HCL
released from D cells, mostly located in antrum
binds to somatostatin receptors (receptor type 2, SSTR2) on parietal cell
binding of somatostatin to its receptor inhibits adenylate cyclase that results in inhibition of H (direct pathway)
indirect pathway: inhibits both histamine released from ECL cells and gastrin release from G cells
what inhibitor is used to treat gastric ulcers?
omeprazole
blocks H-K ATPase
what inhibitor is used to treat doudenal ulcers?
cimetidine, treats both duodenal, gastric ulcers, gastroesophageal reflux disorders by blocking H2 histamine receptors
atropine blocks what and why, but does not block what and why
blocks the M3 mAChR on parietal cells; a DIRECT pw block
does not Gastrin cells because they use GRP receptors
Gastric HCL secretion 3 phases
- cephalic
- gastric
- intestinal phase
Gastric ulcer
low H high gastrin levels because H is low forms primarily because of mucosal barrier is defective h pylori usually associated with this diagnostic instrument: urease enzyme
Duodenal ulcer
high H
high gastrin levels in response food ingestion
h pylori infection less here, but can spread from stomach and inhibit somatostatin, causing increase
Zollinger Ellison Syndrome
usually the result of a tumor in the head of the pancreas secreting gastrin
high H, high Gastrin
Exocrine pancreas
makes up around 90% of the pancreas
glands are like salivary glands: acinus with centroacinar and ductal cells
acinus releases enzymes, centroacinar and ductal cells release HCO3
Exocrine pancreas innervation: sympathetics AND parasympathetics
sym comes from celiac and superior mesenteric plexuses
parasym: comes from vagus n
vagal pregang synapse at ENS
postgang synapse on the exocrine pancreas
sym: decrease in activity
parasym: increase in activity
contrast to salivary glands where sym and parasym do the same thing
High yield question
pancreas secretes which enzymes in their active and inactive form
secretes amylases and lipases in their active form, but proteases in their inactive form
centeroacinar and ductal cells release
Na, K, Cl, HCO3
when pancreatic flow rate is low, the two highest ions secreted include
chlorine and sodium
when pancreatic flow rate is high, the two highest ions secreted include
HCO3 and Na
HCO3/CL relationship in pancreatic seretions
reciprocal
Cephalic phase of pancreas
same as for salivary glands but results mainly in enzymatic secretion
gastric phase of pancreas
like salivary glands but mostly enzymatic secretion
intestinal phase of pancreas
like salivary glands but enzymatic AND aqueous secretions