Digestion and Absorption Flashcards
Saliva Secretion
When released from acinar cells, saliva is isotonic. However, in ducts, Na and Cl are pumped out, some HCO3 pumped in, and saliva become hypotonic. Rich in salivary amylase and lingual lipase.
How does bicarbonate concentration change as salivary flow increases?
It increases!
What happens when food arrives in the stomach
Vagal activity, Gastric distension, gastrin release, histamine release. Causes parietal cell release of HCl, Chief cell secretion of pepsinogen.
Activation of parietal cell and second messengers.
Parietal cells are in fundus Gastrin binds to CCK B increases Ca, Histamine increases cAMP, binds to H2. ACh binds to M3, releases Ca. When second messengers increase, H-K ATPases sitting in tubulovesicles are inserted into the canalicular membrane.
How is HCl secreted from parietal cells?
As K is moved in from the lumen, H is moved out. Cl passes through a chloride channel. These things are brought into the cell from the Na K ATPase, and the Cl/HCO3 exchanger at the basolateral membrane.
What cells are in gastric fundus? Where are G cells located?
Chief cells, parietal cells,ECL cells. G cells in antrum, secrete gastrin to circulation.
How does distension cause gastric secretion
Stretch receptors send info to Dorsal Vagal Complex in brain, which activates the release of GRP onto G cells, which secrete gastrin into circulation, causing release of gastric secretions.
Pancreatic duct cell secretion machinery
At apical membrane, CFTR for release of Cl, also Cl HCO3 exchanger for release of HCO3.
How does secretin increase HCO3 release?
Increases CFTR, which increases CL HCO3 exchange. Increase HCO3 brought into the cell at the basolateral membrane with HCO3 Na cotransporter.
How does pancreatic bicarbonate concentration change as pancreatic flow increases?
It increases!
How is release from pancreatic acinar cells mediated?
VIP and secretin increase cAMP. GRP, ACh, CCK increase Ca, all promote vesicle fusion and release.
Formation of Bile Acids (primary vs secondary)
From cholesterol. Primary bile acids from the liver are conjugated with glycine and taurine and secreted into bile. Reabsorbed in the terminal ileum. Secondary bile acids are formed in the colon from primary bile acids, when bacteria conjugate them). They are absorbed, changed by liver and stored in gallbladder.
Why conjugate bile acids?
Lowers pKa, which enhances hydrophilicity to reduce passive diffusion during transport in biliary tree.
What are micelles?
Pockets of hydrophobic and hydrophilic interactions that are formed by bile acids. Take up FA’s and stuff.
What happens to micelles transporting FAs.
They are taken up into enterocytes and changed into chylomicrons, which then enter lymph. Micelles are recycled.
Where are epithelial cells born and where do they migrate?
They’re born at the bottom of the intestinal crype and migrate up villus. This process takes 5-6 days.
How much volume is presented to the SI?
8000mL, 6000 Absorbed. 1500 absorbed in colon, 100-200 excreted in fecal matter.
Mechanism of H2O absorption
During fasting, no spaces exist between mucosal cells. During absorption, spaces form. Absorbate transferred to nearest capillary.
Solute transport produces an osmotic gradient. H20 moves passively down osmotic gradient, absorbate is isotonic. H2O moves into capillary down hydrostatic gradient.
Differences in passive permeability between jejunum, ileum, colon.
Jenunum has widest holes, then ileum, then colon.
Transport of sodium in intestine.
The major ion that drives absorption. Taken into a cell actively by 3 mechanisms: 1) solute coupled sodium transport, where Na is coupled with glucose or amino acids SGLT1. 2) Sodium-hydrogen exchanger that’s coupled with Cl (in) - HCO3 pump. HCO3 and H produce H2O and CO2 in intestine. 3) Electrogenic Na channel diffusion promoted by aldosterone.
