Lecture 7 and 8: The Small Intestine Flashcards
(46 cards)
What is the basis for the digestion/absorption of nutrients in the small intestine?
intense motility and secretions in the lumen
large surface area of mucosal cells
Gastric emptying occurs after an ________ (increase/decrease) in intraluminal pressure in the proximal portion of the stomach
increase
What happens to duodenal segmental contractions during gastric emptying?
They are inhibited
What characteristics of the chyme do vagal afferents respond to?
1) acidity
2) hyperosmotic content
Which 2 factors contribute to the inhibition of slowing of gastric emptying?
1) fat in duodenum
2) H+ in duodenum
Which is mediated by CCK
When is CCK released?
when fatty acids are present in the duodenum
What effect does CCK have on gastric emptying?
SLOWS it - contracts pylorus to ensure there is sufficient time for fat to be digested/absorbed
What are the 2 main functions of CCK?
1) slow gastric emptying (contract pylorus)
2) relax sphincter of Oddi and contract gallbladder (promote bile and pancreatic secretion)
How does the duodenum detect low pH of chyme?
H+ receptors in mucosa –> relay message to gastric smooth muscle via interneurons of myenteric plexus
What are the 2 components of the exocrine pancreatic secretions?
1) Aqueous (HCO3)
2) enzymatic component
What is the function of HCOs in the aqueous secretion from the pancreas?
neutralize the H+ from the stomach
True or false: pancreatic enzymes are active at acidic pH
FALSE
Endocrine is __% of pancreas, exocrine is __%
2; 90
How does Secretin drive pancreatic ductal secretion?
increases cAMP in duct cells
the increase of cAMP in duct cells opens the CFTR ____ channels which allow an outflow of __ into the duct lumen
Cl-
The efflux of Cl- into the lumen drives the __________
Cl-/HCO3 antiporter
Cl comes back into cell, HCO3 goes out
Where does the ductal intracellular bicarb come from?
1) across basolateral membrane via NBC-1 symporter
2) generated intracellularly by carbonic anhydrase
What moves the H+ into the blood from the ductal cell?
Na/H exchanger
Since the CFTR transporter is so important in secreting HCO3 to neutralize the acid, what happens in patients with cystic fibrosis?
mutated CFTR so HCO3 secretion is defective (decrease in pancreatic ductal secretion so acinar enzymes are not washed out ultimately destroying the gland)
Which cells release CCK?
I cells
What 3 things trigger CCK release?
1) direct interaction of fatty acids or amino acids with I cells
2) binding of fatty acids or amino acids or both to sensor paracrine cells that release CCK-RP
3) release of monitor peptide by pancreatic acinar cells
What are the 2 ways CCK stimulates acinar secretion in the pancreas?
ENDOCRINE: binds to CCK1 receptor
NEURAL reflexes: activate vagovagal reflex leading to release of Ach, GRP, and VIP by enteric neurons
How do CCK, Ach, and GRP effect the release of acinar enzymes?
mobilize intracellular Ca++ which phosphorylates various structures and moves enzyme-filled granules to the apical membrane where they fuse and release their contents
Where are pancreatic enzymes activated from their zymogen form to their active form?
lumen of duodenum