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GI Week 3 > Lecture 29: Pancreatic Physiology and Bile Salts > Flashcards

Lecture 29: Pancreatic Physiology and Bile Salts Flashcards

1
Q

What is the Santorini duct?

A

The minor duct of the pancreas (from the dorsal end)

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2
Q

What is the Wirsung duct?

A

The major duct of the pancreas from the ventral end

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3
Q

What is pancreatic divisum?

A

Failure of fusion of pancreatic ducts (minor and major ducts separate)
Therefore minor ducts drain most of the exocrine shit

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4
Q

What is the insuloacinar portal system?

A

When islet hormones have a local influence on exocrine secretion
Venous blood from islets perfuse neighboring acini before entering portal ein
Insulin stimulates enzyme synthesis/secretion
Somatostatin and glucagon inhibit enzyme secretion

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5
Q

What receptors are on the ductile cells of the pancreas?

A

Secretin receptor that leads to bicarb secretion
Ach receptor
Everything else is in the acinus

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6
Q

What is the MoA of secretin?

A

Major stimulus for water and bicarb
Activates adenylate cyclase in duct cells
Opens apical chloride channel (CFTR)
Bicarbonate then exchanged for luminal chloride

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7
Q

How can CF lead to pancreatitis?

A

CFTR doesn’t work so bicarb cant be released by secretin

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8
Q

What is the function of secretin?

A

Major stimulus for water and bicarb
Retards gastric emptying and secretion
Promotes mesenteric blood flow

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9
Q

What two enzymes are synthesized and stored in the active form?

A
  1. amylase
  2. lipase
    All enzymes are synthesized and secreted as proenzymes
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10
Q

How do you prevent autodigestion?

A
  1. proteolytic enzymes stored in zymogen granules and secreted as inactive precursors
  2. Peptide inhibitor in cytosol (pancreatic secretory trypsin inhibitor, PSTI or SPINK1)
    • sufficient to inactivate 10% of trypsin in zymogen granules and secretion
  3. Cytosolic proteases can lyse limited trypsin
  4. Protease inhibitors (alpha-1-antitrysin, alpha macroglobulin) in pancreatic intersitium and blood
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11
Q

What is SPINK1 or PSTI? Significance?

A

Pancreatic secretory trypsin inhibitor
Patients with SPINK1 mutation have no Pancreatic secretory tryspin inhibitor
This leads to greater prevalence of pancreatitis

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12
Q

What are the types of digestive enzymes secreted by the pancreas?

A
  1. proteolytic
    • trypsinogen
    • chymotrypsinogen
    • proelastase
    • procarboxypeptidase
  2. Amylolytic
    • amylase
  3. Lipolytic
    • lipase
    • procolipase
    • prophospholipase A2
    • carboxylesterase lipase
  4. Nucleases
    • DNAse
    • RNAse
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13
Q

What are the characteristics of amylase?

A

Functions at neutral pH
Have the following products of digestion = maltose, maltotriose and dextrins
Brush border enzymes further digest amylolytic products forming glucose
Mostly produced in the pancreas

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14
Q

What is the MoA of amylase?

A

Splits 1,4 glycoside linkages but not 1,6 glycoside linkages of starch

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15
Q

What are the characteristics of lipases?

A

Functions at neutralpH
Aided by bile salts
Lipase breaks the triglyceride into monoglyceride and the 3 fatty acids

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16
Q

What does lipase do?

A

Takes TG to Monoglyceride and 2 fatty acids

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17
Q

What is steatorrhea?

A 
Fat in the stool
Caused by
	i. excess gastric acid 
	ii. inadequate enzyme or bicarb excretion
	iii. poor bile flow
	iv. intestinal dysmotility scleroderma
MALDIGESTION
Malabsorption can result from mucosal disease even if digestion is adequate
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18
Q

What is the difference between malabsorption and maldigestion?

A

For the former, pancreas is fine and fat is broken down but still cant be absorbed

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19
Q

What initiates protein digestion?

A

Gastric pepsin

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20
Q

What does digestion trigger?

A 
AA, peptides and FA in intestine, CCK is released
CCK stimulates pancreatic secretion
	-inhibit gastric emptying
	-alter intestinal motility
	-induce satiety
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21
Q

Can diet influence the enzymes produced in the pancreas?

A

Yes, if you consume more carbs, you get more amylase production

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22
Q

What is the MoA of VIP and secretin?

A

Increase cyclic AMP

Activates protein Kinase A

23
Q

What is the MoA of CCK, acetylcholine, GRP, and substance P

A

Increases cytoplasmic calcium

24
Q

What is GRP?

A

Gastrin releasing peptide

25
Q

What are the two types of agonists in the acini of the pancreas?

A
  1. one increases cyclic AMP
  2. increases Ca concentration
    Both act synergistically
26
Q

What are the characteristics of CCK?

A
  1. major stimulus of pancreatic secretion
  2. releaxes sphincter of Oddi
  3. delays gastric emptying
  4. contracts gallbladder
27
Q

Where is CCK released?

A

Released by peptides, AAs and fatty acids after a meal

28
Q

What are the phases of pancreatic secretion?

A
  1. Stimulatory
    • cephalic
    • gastric
    • intestinal
  2. Inhibitory
    • postprandial
29
Q

What is the cephalic phase mediated by?

A

Mediated by vagus nerve

Sham feeding = 50% of maximal enzyme secretion

30
Q

How do you inhibit the cephalic phase of pancreatic secretion?

A

Atropine

31
Q

What mediates gastric phase of pancreatic secretion?

A

Just gastric distention

Vagovagal reflex

32
Q

What mediates the intestinal phase of pancreatic secretion?

A

Acid and chyme in intestine

pH below 4.5 releases secretin from mucosa

33
Q

What are the characteristics of post-prandial inhibition of pancreatic secretion?

A

Intraluminal trypsin not complexed to meal protein INHIBITS CCK release
Oleic acid in distal ileum/colon inhibits gastric emptying
Intravenous AA and glucose inhibit CCK release due to glucagon and somatostatin

34
Q

What 2 luminal peptides stimulate mucosal release of CCK (MoA of trypsin)?

A
  1. monitor peptide
  2. CK releasing peptide
    Both digested by trypsin and by digestion
    When digested, this is how trypsin inhibits CCK
35
Q

How do you test for pancreatic function?

A

Test for fat in the stool as well as pancreatic enzyme secretion amount
72 hour fecal fat (needs to eat 100 gram fat diet)
Needs 90% of amylase to disappear in order for this test to work
The point is that if you see steatorrhea, it is hard to get to that point so the guy really burnt out their pancreas

36
Q

What are the functional tests of pancreatic function?

A

Collection of duodenal secretion after meal, CCK or secretin stimulation

37
Q

What are the structural tests of pancreas?

A
  1. ultrasound
  2. MRI
  3. CT
38
Q

What are the functions of bile?

A
  1. excrete polar metabolits of lipid waste (bilirubin)
  2. bile salts for fat and fat soluble vitamin absorption
  3. excrete cholesterol
  4. Secretory IgA
  5. Bilirubin and cholesterol in solution
39
Q

What are the different types of bile salts?

A
  1. Ursodeoxycholic acid = increases flow

2. Lithocholic acid = reduces flow

40
Q

What is the rate-limiting step in secretion?

A

Bile is secreted AGAINST its gradient into the canaliculi

That is rate-limiting

41
Q

What is significant about canaliculus?

A

Is surrounded by canalicular pumps

Example: MDR3, MRP2 and SPGP

42
Q

What does MDR3 do?

A

ATP dependent canalicular pump

Transports phospholipids into canaliculose

43
Q

What does MRP2 do?

A

Transports glucuronide into canaliculi

44
Q

How do you control intracellular bile salts?

A

Farnesoid X factor (FXR), a nuclear receptor, senses bile salt
FXR stimulation suppresses bile salt synthesis and increases canalicular secretion
Causes feedback suppression of possibly toxic cellular bile salt level

45
Q

What is FXR?

A

Farnesoid X factor
A nuclear receptor
Upregulation of FXR = suppression of bile salt synthesis

46
Q

What are the two types of bile salts?

A
  1. primary bile salts (synthesized in liver)

2. Secondary bile saltes (formed by bacteria in the colon)

47
Q

What is the point of bile salt conjugation?

A

Before secretion of bile salt into bile, carboxyl side chains are conjugated with taurine or glycine
Conjugation produces stronger acids which ionizes the upper small intestine…important because IONIZATION prevents back diffusion in bile ducts and intestine
Ileal receptors bind ONLY conjugated bile salts

48
Q

What is important about lecithin?

A

Added to increase ability to solubilize cholesterol

Mixed micelle

49
Q

What is the critical micellar concentration?

A

Above this point, ionized bile salts form clusters (micelles) with the hydrophilic portions OUTWARD

50
Q

Where are conjugated bile salts absorbed?

A

In the ileum and returned to liver by portal vein

Hepatocytes effectively remove bile salts from sinusoids for re-secretion

51
Q

What is significant about lithocholic bile salts?

A

Toxic to liver so body makes it water soluble, permitting it to be excreted fast

52
Q

What happens when there is bacterial overgrowth?

A

Allows for precipitation of bile salts
Inadequate formation of micelles
You will see steatorrhea

53
Q

Why is bile salt important for cholesterol?

A

This is the main way that cholesterol is secreted!!

Protects body from toxic effects of bile salts

GI Week 3 (11 decks)

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