Barrier Function Flashcards
what parts of the GI tract are stratified squamous epithelium?
upper digestive tract (through esophagus), then continues in the anal canal
everything in between is simple columnar
luminal layer of the stratified squamous epithelium of the esophagus
6-7 layers
functional layer - serving as a barrier…since these layers have tight junctions
middle (prickle layer) of the esophageal epithelium
no tight junctions
ion transport
lower layer of esophageal epithelium
replication
no tight junctions
surface cells of the simple columnar epithelium
mostly comprised of cells that secrete mucus and HCO3-
secretion of HCL - general uses, risks
needed for both digestion and absorption of nutrients and for protection against bacterial colonization
risk –> damage to epithelial lining with which it comes in contact
could lead to gastroesophageal reflux disease (GERD) or peptic ulcer disease (PUD)
stomach and duodenum pre-epithelial defense system against acid damage
buffer zone at the surface, due to the presence of an adherent mucus coat that is rich in HCO3-
mucus and HCO3- secreted by surface cells
esophagus pre-epithelial defense to acid damage
minimal because the squamous epithelium does NOT secrete mucus or HCO3-
epithelial defense against acid damage (esophagus –> duodenum)
- hydrophobic cell membranes
- apical membrane channels that inhibit cation entry at acidic luminal pH
- tight junctions
- intracellular and intercellular bufferes
- basolateral membrane transporters (cell alkanizers for removal of excess H+ from cell)
Na+ entry into epithelial cells (regarding acid defense system)
Na+ entry into cells aids H+ extrusion
occurs along a concentration gradient with extracellular Na+ being high (equilubrated with blood)…
Na+/K+ pumps keep intracellular Na+ low
buffers for acid defense in cell
HCO3- (also outside cell)
PO4(2-)
anionic proteins
basolateral cell alkanizer transporters
Na+/H+ exchanger (H+ out)
Na+ and HCO3-)/Cl- exchanger (Cl- out
basolateral cell acidifier transporters
Cl-/HCO3- exchanger (HCO3- out)
post-epithelial acid defense (blood side)
esophagus –> duodenum
interstitial fluid within the wall and epithelium is in equilibrium with the fluid compartment of the blood
therefore…
the post epithelial defense is due to the circulation of blood through the organ’s capillary network
a network that continuously replenishes the tissues O2, nutrients, and HCO3- for acid buffering…while serving to remove waste
stomach additional defense system against acid (unlike the duodenum and esophagus)
‘alkaline tide’
refers to the fact that the byproduct of HCL production by gastric parietal cells is prodction of HCO3-
therefore…HCL production by parietal is matched by transportation of HCO3- into capillary circulation
capillary circulation then delivers the HCO3- to the surface cells for buffering of H+
how does HCO3- get from the blood –> luminal side of surface cells to buffer the H+ (alkaline tide defense system in stomach)
parietal cell:
H2CO3 –> H + HCO3-
HCO3- leaves via Cl/HCO3- exchanger into blood
surface cell:
HCO3- enters basolateral side via reverse HCO3-/Cl- exchanger
diffuses through cytoplasm to another exchanger into luminal membrane where… H+ + HCO3- –> H2CO3
then…H2CO3 –> CO2 + H20 (CO2 diffuses back into lumen)
2 repair mechanisms following injury
stomach and duodenum and esophagus
- restitution
2. replication
‘mucus cap’
only stomach and duodenum
created via the restitution and replication repair mechanisms
results from release of mucus from surface mucus cells to cover the injury site…further entrapping HCO3- at the site
therefore cap also provides a buffer zone to protect the would from acid access and inhibition of repair
epithelial restitution
small defects with intact basolateral membrane
no DNA or protein synthesis
rapid 30-60 minutes
migration of adjacent viable cells over defect
epithelial replication
large defects
collagen deposition is needed
needs DNA and protein synthesis…thus slow; days to weeks to complete
prostaglandin E2
needed for stomach and duodenum repair (not esophagus)
stimulation of the following:
- mucus secretion
- HCO3- secretion
- blood flow
- promotes epithelial restitution
NSAIDS and peptic ulcer disease
NSAIDS inhibit COX1
therefore inhibit prostaglandin E2 in repair mechanisms for acidic damage…
Celebrex
COX2 inhibitor
retains anti-inflammatory properties while preserving the ability of prostaglandins to protect epithelium
exuberant collagen deposition
can lead to stricture that can obstruct the downstream movement of food through the organ
