PHYS Gut Secretions II - Week 4 Flashcards

1
Q

How is bile secreted?

A

From liver via bile ducts.

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2
Q

Role of cystic duct

A

Transports bile btw meals to store in gall bladder.

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3
Q

Composition of bile:

A

Bile salts, cholesterol, lecithin, electrolytes & H2O, bile pigments.

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4
Q

Critical electrolyte in bile

A

Bicarbonate - neutralises acidic chyme in duodenum.

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5
Q

Bile pigment source

A

Breakdown of haem.

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6
Q

Describe process of fatty droplet breakdown in duodenum.

A

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.

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7
Q

When is secretin release triggered and what is the affect?

A

Release of secretin is triggered – acidic chyme @ duodenal wall ->
stimulate liver -> increased bile production
& stimulates ductal cells of the pancreas -> alkaline secretion.

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8
Q

When is CCK release triggered and what is the affect?

A

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.

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9
Q

What cells synthesis & secrete pancreatic enzymes and from what granules?

A

Acinar cells (exocrine) via zymogen granules.

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10
Q

Pancreatic enzymes list. State what enzymes are responsible for protein, TAGs, polysaccharides, nucleic acid digestion. State whether secrete in inactive or active form.

A

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.

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11
Q

Causes of pancreatitis.

A
  • 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) .
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12
Q

Symptoms of pancreatitis.

A
  • Continuous abdominal pain
  • Weight loss
  • Steatorrhoea (fat malabsorption)
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13
Q

Treatment of pancreatitis.

A
  • Improve nutrition with pancreatic supplements
  • Complete abstention from alcohol
  • Pain relief.
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14
Q

What can auto-digestion of the pancreas be triggered by?

A

Excessive alcohol intake.

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15
Q

Vagal/parasymp nerve regulation of pancreatic secretion entry.

A

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.

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16
Q

What activates trypsinogen, chymotrypsinogen, procarboxypolypeptidase enzymes?

A
  • Trypsinogen -> trypsin via enterokinase (secreted by intestinal mucosa post contact w chyme) OR trypsin that has already been formed from previously secreted trypsinogen.
  • Chymotrypsinogen -> chymotrypsin via trypsin
  • Procaboxypolypeptidase -> carboxypeptidase via trypsin.
17
Q

What does the pancreas secrete to protect itself from auto-digestion?

A

Pancreas also secretes trypsin inhibitor which protects pancreas in case of blockage or damage as any trypsin can lead to the activation of enzymes mentioned above and consequent pancreatic auto-digestion, which can be fatal.

18
Q

What secretes enterokinase and when is it secreted?

A

Secreted by intestinal mucosa (duodenum) post contact w chyme.