GIT Digestion (GIT) Flashcards

1
Q

What are the three groups of enzymes in digestion?

A

Soluble enzymes - released by the pancreas

Brush-border enzymes - tethered to enteric cells

Cytosolic enzymes - inside enteric cells

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2
Q

What are the proportions of exocrine and endocrine work done by the pancreas?

A

Exocrine - 99%
Endocrine - 1%

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3
Q

What are pancreatic secretions, what are its functions?

A

Pancreatic secretions are an alkaline, enzyme rich solution.

Function to digest lipids/proteins/CHO, neutralise pH of acidic chyme entering the duodenum and create suitable pH for pancreatic enzymes.

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4
Q

What is the composition of pancreatic secretions?

A

HCO3-, Na+, K+ and water (secreted by duct cells)
as well as
Pancreatic enzymes (secreted by acinar cells)

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5
Q

Describe the innervation of the pancreatic acinus.

A

VAGUS innervation.
Has duct cell that secrete alkaline fluid, and acinar cells that produce and secrete enzymes.

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6
Q

Name the three types of proteases and their functions.

A

Trypsin (and chemotrypsin) digest protein into peptides.

Carboxypeptidases digest peptides into AAs.

Elastases digest elastin into peptides.

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7
Q

What do nucleases do?

A

Digest DNA/RNA into dNTPs.

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8
Q

What are the three types of lipases, and what do they digest?

A

Pancreatic lipase - digest fats into FAs

Cholesterol esterase - digest cholesterol esters into cholesterol and FAs

Phosphlipase - digest phospholipids into FAs

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9
Q

Why doesn’t the pancreas digest itself?

A

Proteases are made in an inactive form in the pancreas.

Enterokinase activates trypsinogen into trypsin. Trypsin then activates the other proteases.

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10
Q

What does the pancreas produce to inhibit enzyme action within the organ?

A

Pancreatic acinar cells produce trypsin inhibitors.

In acute pancreatitis, deficiency in trypsin inhibitor production can cause the pancreas to digest itself.

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11
Q

Describe the production, storage and release of proteases by the pancreas.

A

Inactive proteases are synthesised and stored as zymogen granules (inactive, vesicles).

There are two pathways of release:

  1. Constitutive pathway (very low levels of secretion)
  2. Regulated secretory pathway: Receptors for CCK (cholecystokinin) and ACh activate phospholipase-C to exocytose the proteases.
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12
Q

What are the two sources from which the pancreas gets HCO3- to put in its alkaline secretions?

A
  1. CO2 combines with water to form carbonic anhydrase. HCO3- is pumped into duct lumen while Cl- is brought in.
  2. Scavenger HCO3- from blood that has passed the stomach. HCO3- is pumped into duct lumen while Cl- is brought in.

Na+/K+ PUMP drives the movement of Cl-

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13
Q

Describe the 4 molecules which regulate pancreatic secretions. When are they secreted, what do they stimulate secretion of?

A

Acetylcholine (from vagus nerve) stimulates BOTH HCO3- and enzyme release.

Secretin (from duodenal S cells) secreted in response to pH <4.5 (acidic environment from acidic chyme entering duodenum). Stimulate HCO3- secretion.

Cholecystokinin (from gut mucosal I cells) secreted in response to duodenal fat and protein. Stimulates enzyme secretion.

Somatostatin (from intestinal D cells). Inhibitory.

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14
Q

Describe the relative amounts of secretion in the cephalic, gastric and intestinal phase of digesiton.

A

Cephalic = 10% - 20% of total secretion (ACh)

Gastric = 5% - 10% of total secretion (gastrin binds CCK receptors)

Intestinal = 80% of secretion (lots of CCK, secretin and ACh)

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15
Q

What type of cells secrete secretin, when, and what does it do?

A

Secreted by duodenal S cells.

Secretion stimulated by pH <4.5 (acidic chyme enters duodenum).

Triggers HCO3- secretion by pancreatic duct cells and decreases gastric H+ secretion.

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16
Q

What type of cells secrete cholecystokinin, when and what does it do>?

A

Cholecystokinin is secreted by gut mucosa “I” cells.

Secretion stimulated by fats and proteins in digestion products.

Triggers release of pancreatic enzymes, inhibits gastric emptying and relaxes the sphincter of Oddi

17
Q

What inhibits the action of cholecystokinin?

A

Trypsin in lumen

Somatostatin from D cells.

18
Q

Describe the lifecycle of bile

A

Bile acids + bile is produced by the liver and stored in the gall bladder.

Primary bile acids are made by hepatocytes and are conjugated with glycine or taurine. This ionises them and prevents immediate reabsorption.

Bacteria in the intestinal lumen remove the glycine/taurine, enabling reabsorption.

90%-95% of bile acids are reabsorbed in ileum

5%-10% are lost to colon, so liver makes 5%-10% per day.

19
Q

What can cause gall stone formation?

A
  • Too much absorption of water from bile
  • Too much absorption of bile acids from bile
  • Too much cholesterol in bile
  • Inflammation of epithelium
20
Q

After stone are formed in the gall bladder, the gall bladder can contract, pushing them into other places. Where can they go?

A

Contraction can push stones into the bile duct (bad) or hepatic duct (REALLY bad)

21
Q

Describe the role of the sphincter of Oddi in gall bladder filling and emptying

A

When the gall bladder is filling, sphincter of Oddi is closed.

Fatty acids and proteins in duodenum trigger release of CCK. CCK relaxes sphincter of Oddi and stimulates gall bladder contraction. Bile enters intestine.

22
Q
A