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Digestive > 25 - Control of pancreatic and biliary solutions > Flashcards

25 - Control of pancreatic and biliary solutions Flashcards

1
Q

The second part of the duodenum is where

A

The pancreatic and biliary systems join (via the major duodenal papilla)

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2
Q

3 central roles of the duodenum

A
  1. inhibit gastric emptying
  2. inhibit gastric acid secretion
  3. stimulate pancreatic and biliary secretion
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3
Q

2 mechanisms that allow the duodenum to carry out its functions?

A
  1. Endocrine cells respond to nutrients (AA/FA)

2. Neural - vagal afferents respond to luminal contents

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4
Q

I cells, S cells and enterochromaffin in the doudenum are…

A

Enteroendocrine cells

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5
Q

The cells sense the stimulus at … surface and secrete hormones through the … surface into the blood

A

The enteroendocrine cells sense the stimulus at the apical surface facing the gut lumen and release through the basolateral surface into the circulation

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6
Q

I cells

A

respond to AA/FA to release CCK to inhibit gastric empyting and secretion

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7
Q

S Cells

A

Respond to drop in pH in duodenum to release secretin to inhibit gastric emptying and secretion

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8
Q

Enterochromaffin Cells

A

Responds to irritant/food in lumen to release SEROTONIN to stimulate gut motility and vomiting

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9
Q

Exocrine pancreas consists of

A

Ducts and acinar cells/glands

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10
Q

Acinar cells release….

Ductal cells release….

A

Digestive enzymes to digest fats and proteins

HCO3- (alkaline solution) to neutralise the acidic chyme entering the duodenum

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11
Q

Acinar cells are filled with

A

Secretory granules with zymogens/precurosr enzymes to prevent autodigestion of pancreas. Some enzymes are activated in the duodenum to STOP auto-degradation of the pancreas

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12
Q

Acinar cells have a lot of …. for protein production

A

ER

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13
Q

Enteropeptidases cleave … at the brush border of the SI which then activates …. and is autocatalytic on …. via … …

A

Enteropeptidases cleave trypsionegen at the brush border of the duodenum which forms active trypsin which activates chymotryspinogen to chymotrypsin and is autocatalytic/-ve FB on trypsinogen via proteolytic cleavage

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14
Q

Site of zymogen activation is the

A

Duodenal lumen via enteropeptidases via proteolytic cleavage

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15
Q

Pancreatic lipase converts

A

Triglycerides > monoglycerides and free FAs

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16
Q

Amylase converts

A

Starch > sugars

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17
Q

…. stimulates and controls pancreatic enzyme release

A

CCK

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18
Q

CCK stimulates pancreatic enzyme release by 2 pathways these are

A
  1. CCK release into blood to acinar cells to directly release enz
  2. CCK release from I cells stimulates vagus afferents next to I cells which send a message to the vagus nerve in the brain stem which send vagus efferent fibres to stimulate acinar cells to release pancreatic enz
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19
Q

What else stimulates acinar cells to release gastric enzymes?

A

Gastrin for G cells

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20
Q

The 2 types of ductal cells are…

A

Centro-acinar cells and intercalated ductal cells

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21
Q

Centro-acinar and intercalated ductal cells release

A

HCO3- and water to neutralise gastric acid in duodenum

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22
Q

Ductal cell secretion of HCO3- is needed for 4 reasons including …

A
  1. Prevent mucosal damage
  2. Optimal pH for enterkinases/brush border enzymes and pancreatic enzymes (neutral pH)
  3. Inactivates gastric PEPSIN (digests proteins so stops degradation of other enzymes and SI)
  4. Neural pH increases the solubility of fatty acids and bile acid
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23
Q

Describe the transport of HCO3- across the enterocyte?

A

HCO3- is taken up from the circulation and secreted INTO the lumen so…

  1. HCO3- taken up from the basolateral surface
  2. CO2 and H2O is also taken up into the cell where it is converted to HCO3- by carbonic anhydrase
  3. HCO3- is secreted into the lumen via the Cl-/HCO3- exchanger which is powered by the Cl- transporter CFTR
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24
Q

CFTR

A

Cystic Fibrosis Conductance Transmembrane Receptor

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25
Q

Pancreatic ductal HCO3- secretion is controlled by

A

Secretin

26
Q

How does secretin cause alkaline HCO3- secretion from pancreatic ductal cells?

A
  • HCl > S cells > secretin > blood > ductal cells
  • increase cAMP
  • cAMP stimulates CFTR so more CL- secreted
  • powers Cl/HCO3- exchanger
  • increase in HCO3-/alkaline secretion
27
Q

How does vagal innervation affect pancreas cells?

A

Releases ACh which stimulates the release of both HCO3- and digestive enzymes

28
Q

What does CCK do?

A 
GB contraction
Bile production 
Digestive enz release from pancreas
Inhibit gastric secretion and emptying
RELAX sphincter of Oddi (to allow more bile to be secreted)
29
Q

Cystic Fibrosis

A
  • autosomal recessive
  • many mutations
  • CFTR has little to no function so pancreatic ductal cell secretions are thick viscous mucus that clogs passages
30
Q

CFTR is involved in

A
  • CF transmembrane conductance regulator
  • chlorode channel
  • involved in production of sweat, mucus, digestive fluids
  • big role in HCO3- secretions
31
Q

CF can lead to … as …

A
  • pancreatic insufficiency (exo and endo)
  • Cl- accumulates in cells
  • cells negatively charged
  • H2O and Na dragged out of lumen into cells
  • pancreatic secretions hyper-viscous
  • pancreatic ducts become blocked
  • insufficient pancreatic enzymes released and build up in pancreas
  • inappropriate activation of enzymes > autodigestion > pancreatitis > damaged and replaced by fibrosis (chronic pancreatitis)
  • maldigestion and malabsorption
32
Q

Main 2 causes of pancreatitis?

A

Alcohol and gallstones

33
Q

Other causes of pancreatitis?

A 
autoimmune
drugs
trauma 
structural anomalies (PANCREAS DIVISUM)
metabolic
viral (mumps)
cystic fibrosis 
genetic
34
Q

Pancreas divisum?

A
  • ventral and dorsal ducts fail to fuse during development
  • means pancreatic and bile duct don’t fuse to enter the duo together and enter separately
  • common congenital anomality and cause of pancreatitis
35
Q

Pancreatic insufficiency (exocrine)

A
  • need 90% loss of exocrine function
  • loss of lipase most important leading to fat malabsorption
  • weight loss and steatorrhoea
  • treat with pancreatic enzyme supplements
36
Q

Pancreatic insufficiency (endocrine)

A
  • hormones to regulate BG
  • insulin deficiency
  • treat per diabetes
37
Q

3 features of chronic pancreatitis?

A
  1. calcification and fibrosis
  2. dilation of pancreatic duct
  3. irregular side branches
38
Q

How much bile is made a day?

A

400-800mL

39
Q

Bile contains

A 
water
electrolytes
bile acids
cholesterol 
phospholipids 
bilirubin
40
Q

… of bile salts are re-absorbed via the … … the other … are lost in the … and are made from …

A

95% are reabsorbed via enterohepatic circulation (portal v > SINUSOIDS > liver) the other 5% are lost in faeces and are made from cholesterol

41
Q

Bile salts taken back up into circulation via

A

Bile salt/na exchangers and Na/K atpases

42
Q

2 functions of bile?

A
  1. Bile acids for fat and fat sol vitamins

2. Elimination of waste products (bilirubin, cholesterol, medicines) secreted into bile and into faeces

43
Q

2 sources of bile acids?

A
  1. 95% recycled at terminal ileum

2. 5% synthesised by cholesterol

44
Q

Flow of bile?

A

hepatocytes > canaliculi > larger bile ducts > watery secretion of HCO3- added by the ductal epithelial cells > common hepatic > cystic duct > GB

45
Q

What else is added to the bile as it flows down the bile ducts?

A

HCO3- by ductal cells

46
Q

How is bile flow through cannuliculi driven?

A
  1. Bile acid dependent (osmotic)
  2. Bile acid independent (via transport of other solutes and electrolytes

> as well as reabsorption and secretion of water and electrolytes by ducts (secretion in response to secretin)

47
Q

Why does bile from the liver enter the GB?

A

Closure of the Sphincter of Oddi

48
Q

What does GB do

A

conc and store bile

49
Q

Cholestasis

A

Obstruction of bile flow

50
Q

Cholestasis leads to

A
  • increased pressure in biliary tract and liver
  • rupture of tight junctions between hepatocytes and leakage of bile
  • bile contents spill back into circulation causing jaundice/hyperbilirubinaemia
51
Q

Cholesterol stones

A

Due to cholesterol precipitating in GB

Most common

52
Q

Pigment stones

A

Bilirubin and calcium salts in bile. Can cause cholestasis if goes into duct

53
Q

How to determine gallstones

A

US

54
Q

Gallstones will often cause bile duct to …

A

dilate

55
Q

how are gallstones removed

A

basket via ERCP

56
Q

Besides gallstones what else (benign) can cause obstruction and so jaundice and cholestasis?

A

Biliary strictures

57
Q

Malignant causes of biliary obstruction are called

A

cancer of the biliary tract - cholangiocarcinoma

58
Q

What else can cause biliary obstruction?

A

Cancer at the head of the pancreas

59
Q

What are 5 effects of prolonged bile duct obstruction due to malignancy?

A
  1. Jaundice
  2. itching
  3. nausea
  4. fat and fat soluble vitamin malabsorption
  5. renal perfusion leading to renal failure
60
Q

Observable features of someone with cholangiocarcinoma?

A
  • yellow sclera
  • scratch marks
  • bruising
  • palpable gallbladder (Courvoiser’s sign- enlarged gall bladder with jaundice means it is UNLIKELY to be gall stones and more like to be cancer)
  • pancreatic mass
  • palpable lymph node in left supraclavicular fossa (sign of any intra-abdominal malignancy)
  • pale stool
61
Q

What does a palpable GB signify?

A

Not likely to be stones more likely to be cancer of the GB

62
Q

How to give symptomatic relief to those with GB cancer?

A

Stent for bile to flow through into duodenum and bypass blockage. Now curing just symptoms

Digestive (24 decks)

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