GIT physiology 3 Flashcards
carbohydrates are digested by
name-ases
proteins are digested by
proteases/peptidases
fats are digested by
lipases
epithelial cells lining the pancreatic ducts
duct cells
duct cells secrete
HCO3-, Na+, K+ and water
enzymes are secreted by
acinar cells
pancreatic secretions pH
alkaline
about pH 8
functions of the pancreatic secretions
digestion of lipids, proteins and carbohydrates
neutralising pH of acid chyme entering the duodenum
create suitable pH for pancreatic digestive enzymes
major pancreatic enzymes
trypsin chymotrypsin carboxypeptidases elastases nucleases pancreatic amylase pancreatic lipase cholesterol esterase phospholipase
why is the pancreas not digested
proteases are synthesised in an inactive form
trypsinogen
inactive form of trypsin
trypsinogen is activated by
enterokinase
tryspin
activates others eg. chymotrypsinogen, procarboxypeptidase
acute pancreatitis
pancreas may digest itself within hours
synthesis and exocytosis of enzymes are controlled by
CCK and ACh
inactive proteases are synthesised and stores as
zymogen granules
regulation of pancreatic secretion
- acetyl choline
- secretin
- cholecystokinin
- somatostatin
cephalic phase
acetyl choline from vagus nerve
does not result in any secretion into the duodenum, just starts production
secretin and cholecystokinin
produced by chemically sensitive cells in the duodenum
not initiated until gastric emptying
cholecystokinin produced by
gut mucosal “I” cells
secretin released in response to
acid in the duodenum
secretin acts on
duct cells - produce bicarbonate
secretin is produced by
duodenal “S” cells
somatostatin produced by
intestinal “D” cells
cholecystokinin secreted in response to
duodenal fat and protein
cholecystokinin acts on
enzyme production/secretion by acinar cells
opens duodenal papilla - CCK receptors on the smooth muscle on the sphincter of oddi
sphincter of oddi
allows pancreatic juices and bile to enter
somatostatin acts on
is inhibitory
3 phases of pancreatic secretiion
- cephalic phase
- gastric phase
- intestinal phase
cephalic phase controlled by
vagus nerve
gastric phase
gastrin binds CCK-receptos
intestinal phase
CCK, secretin and ACh released
S cells produce
secretin
stimulus to secrete secretin
H+ ion contact with mucosal S calls
also protein catabolites
half life of secretin
short - 5 mins
main action of secretin
stimulates HCO3- secretion by pancreas duct cells
neuropeptide
decreases gastric H+ secretion
causes pyloric sphincter contraction
I cells secrete
CCK
stimulus for CCK secretion
long chain fatty acids, peptides, AAs, (generally protein digestion products
CCK is inhibited by
trypsin in lumen and somatostatin from D cells in the small intestine
main action of CCK
stimulates pancreatic acinar cell enzyme production and secretin
relaxation of the sphincter of odd
neuropeptide
inhibits gastric emptying, stimulates enetrokinase synthesis, enhances intestinal motility, glucagon release
bile stored in
gall bladder
bile discharged into
duodenum
role of bile
emulsifies fats to increase access to lipases
bile acids synthesised from
cholesterol
bile acids synthesised by
hepatocytes
bile acids conjugated with
glycine or taurine
ionises the bile acids
prevents immediate reabsorption
2 degree bile acids converted by
converted by bacteria
removes glycine/taurine
enables reabsorption
why are bile acids conjugated
to prevent immidiate reabsorption
conversion to 2 degree bile acids enables
reabsorption
bile acids cycle between
the liver and the small intestine
total bile acid pool
about 3g
percentage bile acids lost daily
5-10%
the biliary system
produces bile
remove excess cholesterol
remove bilirubin by modifying it
things lost by diffusion in the biliary system
- water
- glucose
- calcium
- glutathione
- amino acids
- urea
causes of gallstone
too much absorption of water from bile
too much absorption of bile acids from bile
too much cholesterol in bile
immflamuation of epithelium
bile is release in response to
CCK
pancreatic secretion is regulated by
ACh, secretin, and CCK