PHYS Gut Secretions II - Week 4 Flashcards
How is bile secreted?
From liver via bile ducts.
Role of cystic duct
Transports bile btw meals to store in gall bladder.
Composition of bile:
Bile salts, cholesterol, lecithin, electrolytes & H2O, bile pigments.
Critical electrolyte in bile
Bicarbonate - neutralises acidic chyme in duodenum.
Bile pigment source
Breakdown of haem.
Describe process of fatty droplet breakdown in duodenum.
Fatty droplets float on top of acidic chyme and enter duodenum from stomach -> mixing contractions of small intestine -> breakdown of fat globules -> smaller droplets -> bile salts & phospholipid lecithin embed themselves around fat droplets -> emulsion droplets -> pancreas secretes co-lipase -> pushes aside bile salts & lecithin to enable pancreatic lipase to enter emulsion droplets -> breakdown of triglycerides -> monoglycerides & fatty acids -> diffusion across intestinal epithelial cells -> bloodstream.
When is secretin release triggered and what is the affect?
Release of secretin is triggered – acidic chyme @ duodenal wall ->
stimulate liver -> increased bile production
& stimulates ductal cells of the pancreas -> alkaline secretion.
When is CCK release triggered and what is the affect?
Release of CCK is triggered – fat droplets floating above chyme @ duodenal wall ->
stimulate gallbladder -> gallbladder contracts (aided also by vagal stimulation) -> hepatopancreatic sphincter relaxes -> bile enters duodenum.
& stimulates ductal cells of the pancreas -> enzyme-rich pancreatic juices.
What cells synthesis & secrete pancreatic enzymes and from what granules?
Acinar cells (exocrine) via zymogen granules.
Pancreatic enzymes list. State what enzymes are responsible for protein, TAGs, polysaccharides, nucleic acid digestion. State whether secrete in inactive or active form.
Trypsin, chymotrypsin, elastase (I-A) - break peptide bonds in proteins -> peptide fragments. Carboxypeptidease (I-A) - split terminal aa from carboxyl end of protein. Pancreatic lipase (A) - triacylglycerols -> free FAs & monoglycerides. Cholesterol esterase, phospholipase (A). a-amylase (A) - polysaccharides -> glucose & maltose. Ribonuclease & deoxyribonucleic acids (A) - nucleic acids -> mononucleotides.
Causes of pancreatitis.
- Defective ductal secretion of HCO3- & H2O
- Decreased release of pancreatic enzymes
- Inappropriate activation of pancreatic enzymes (i.e., within the pancreas -> auto-digestion of pancreas) .
Symptoms of pancreatitis.
- Continuous abdominal pain
- Weight loss
- Steatorrhoea (fat malabsorption)
Treatment of pancreatitis.
- Improve nutrition with pancreatic supplements
- Complete abstention from alcohol
- Pain relief.
What can auto-digestion of the pancreas be triggered by?
Excessive alcohol intake.
Vagal/parasymp nerve regulation of pancreatic secretion entry.
Vagal stimulation causes weak contractions of gallbladder post acidic, fatty chyme entry into duodenum.
During cephalic & gastric phases, vagal nerve fibre stimulation -> pancreatic juice release.