120-121b Secretion Flashcards
CN parasympathetic innervation for submandibular, sublingual, paotid glands?
VII - facial
VII
IX - glassopharyngeal
salivary secretion function?
1) Protective - HCO3 neutralizes bacterial acid; Antibodies
2) Digestion - amylase for starch digestion (most from pancreas though); mucin lubricate food
salivary secretion control?
- Autonomic
- due to stimuli in cephalic phase (smell, sight, etc)
is the ANS antagonistic (sym vs parasym) for salivary secretion?
NO - synergistic with each other
sympathetic innervation pathway to salivary glands?
spinal cord (t1-4) –>
superior cervical ganglion –>
blood vessels –>
glands
sympathetic input to salivary glands uses what nt? does what?
NE
1) salivary secretion at low volume w/ high protein from innervation of glands
2) vasoconstriction from innervation of blood supply
* *different neurons do these 2 things**
parasympathetic innervation to salivary uses what nt? does what?
ACh + cotransmitters
Not vagus - preganglionic in brain stem, post gang are in otic and submandibular ganglion
1) large volume of saliva that is watery
2) vasodilation due to increased metabolism of gland + release of VIP (vasoactive polypeptide)
Salivary glands layout
acinar cells lead to striated duct cells
function of myoepithelial cells? innervation?
contractile - squeeze fluid from acinus into duct
parasympathetic and sympathetic
what determines composition of salivary?
secretory rate
low flow = hypotonic w/ K>Na (unusual)
high flow = more isotonic - approaches concentration of plasma for cations, bicarb stays constant; duct cell modification is overwhelmed
what happens to saliva in acinus? straited ducts?
acinus = isotonic ions (including HCO3) + amylase and other proteins
striated ducts = modification of ionic content remove Na and Cl
add HCO3 and K
pancreas/salivary acinar secretion - what drives process? what order do things happen? overall?
1) basolateral 3Na/2K ATPase drives process - increases K inside cell, decrease Na inside cell –> makes inside negative
2) Negative gradient drives Cl thru apical side into lumen -> makes lumen negative
3) negative lumen attracts Na to lumen between cells
overall - active transport of Na and Cl (indirectly)
salivary and pancreatic Ductile cell secretion/modification - what drives? what is the process? Can water leave lumen? overall?
1) basolateral 3Na/2K ATPase sets up a gradient for Na to enter the cell in exchange for H+ ion which causes basic cell interior
2) Bicarb (basic) thus forced out of cell on apical side in exchange for Cl
3) Cl then leaks out on apical side via CFTR channel back into lumen
tight jxns between ductile cells prevent movement of water in/out of lumen –> drives osmolarity down and leads to hypotonic secretion
Overall: Na replaced with K in lumen in a 3/2 ratio
saliva -tonicity, content?
hypotonic - low in Na, high in K, high in Bicarb
why is saliva hypotonic?
tight junctions in ducts prevent water movement - intial acinus secretion is nearly isotonic but modified by ducts
stomach - where are gastric acid secretions occurring? by what cell?
gastric glands
parietal cell
gastric acid content at low flow? high flow? tonicity?
low = Na Cl - can actually be basic (surface cell)
high = H Cl - with lots of K and very low Na (parietal cell)
isotonic at all flow rates
Parietal cell secretion process? overal?
1) hydrolysis of water - creates H+ (requires a lot of E)
2) H+ pumped into lumen by H/K ATPase (proton pump) which leaves OH- in cell so combines with CO2 via CA to make bicarb which leaves cell in exchange of Cl-
overall - equal and opposite - secretes acid into lumen and base into interstital/blood stream
what signals control parietal secretion (intracellular signal)? where type of input are these? where do they come from?
1) ACh on M3 receptor (Ca)
neuronal
Vagas + intrinsic from ENS
2) Histamine on H2 receptor (cAMP)
paracrine
ECL cell
3) Gastrin on CCK3 receptors (Ca)
hormonal
G cells in antrum (also acts on ECL cell to increase histamine release)
**act synergistically due to convergance of intracellular pathways
what makes pepsin? role? how is stored? how is activated?
chief cells (stomach)
protein digestion
pepsinogen to prevent eating self
acid cleaves part of protein to activate AND pepsin can cleave pepsinogen
primary stimulus for gastric motility and secretion?
stomach distention (gastric phase) activates vagovagal and local ENS reflexes
what intestinal hormones reduce gastric motility and secretion (cell type, location)?
Secretin (S cells, duodenum) and CCK (I cells, duodenum, jejunum)
why does the stomach not digest itself?
gastric acid secretion low b/w meals
stomach cells have tight junctions
interstitial is high in bicarb
mucosal protective batter from bicarb from surface cell (insoluble mucus secretion)
what do damaged cells release? what does this do?
histamine - activates parietal cells
exocrine pancreas - cell types and what do they secrete?
acinus - proteins/enzymes via CCK(I cells in duod) and secretin (s cells in duodenum)
duct cell - HCO3 from secretin(S cells in duodenum)
pancreatic sectretion and flow rate
varies with flow but cation constant at all flow rates
low = Na/Cl
high=Na/HCO3
HCO3 neutralizes acid coming into intestine to raise pH to make enzymes function
pancreas secretion - overview
active Na and Cl secretion
what drives pancreas secretion?
ACh and CCK
pancreatic duct cell function? method? what controls
secrete HCO3
similar to duct cell in salivary gland - H+ driven out of cell via Na/K ATPase gradient AND direct H+ ATPase –> creates pH imbalance which drives bicarb out w/ water and Na following between cells (isotonic)
CCK and secretin control
