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PPP > Bile and biliary system > Flashcards

Bile and biliary system Flashcards

1
Q

What happens to bile salts once they’ve aided in fat absorption?

A
  • return to lumen of enterocyte + absorbed through small intestine passively + via active transport in distal ileum
  • reabsorbed into blood circ - taken up by liver + goes back into bile salt pool
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2
Q

How can a deficit in bile salts be caused and how is this fixed?

A
  • loss of bile slats in feaces
  • resyn in liver but majority re-circ and reabsorbed in small intestine
    – balance between loss and re-syn
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3
Q

What does the gall bladder contain?

A
  • Stored bile salts

- bile conc up to 15x

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4
Q

What is the Sphincter of Oddi?

A

where pancreatic duct joins common bile duct into duodenum

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5
Q

What is the effect of CCK?

A
  • gallbladder constriction - release bile into common bile duct which enters duodenum through sphincter
  • Relaxation of sphincter of Oddi
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6
Q

What is effect of secretin?

A
  • stim secretion of bile rich in HCO3- from liver

- stim HCO3- secretion from pancreas

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7
Q

What also causes weak contraction of gall bladder?

A

Vagal stim

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8
Q

How is bile prod stim in liver?

A

Para impulses along vagus nerve stim bile prod

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9
Q

How are bile salts conc in gall bladder?

A
  • HCO3-/Cl- exchanger allowing Cl- gradient
  • allows removal of water from lumen of gallbladder – conc bile salts
  • Na/K pump maintains Na gradient
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10
Q

What is bilirubin?

A

Major component of bile

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11
Q

Where does bilirubin comes from?

A

85% from breakdown of RBCs

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12
Q

What are properties of bilirubin?

A
  • fat sol
  • toxic
  • bound to albumin in blood
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13
Q

Where is bilirubin taken up?

A

By liver

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14
Q

How much and where is bilirubin absorbed per day?

A

15% reabsorbed from intestine by enterohepatic circ (between liver and intestine)

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15
Q

What is biliary disease caused by?

A
  • abnormalities in bile composition, biliary anatomy, and function.
  • liver determines chem comp of bile, + this may be mod later by gallbladder + biliary epi.
  • Cholesterol, ordinarily insol in water, comes into solution by forming vesicles with phospholipids (principally lecithin)/mixed micelles with bile salts + phospholipids.
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16
Q

What is dev of jaundice in absence of abdominal pain suggestive of?

A

a malignant obstruction of the bile duct e.g. gall stone.

17
Q

Describe onset and symptoms of painless jaundice

A
  • normal plasma bilirubin: 3-10mg/ml, jaundice: 18mg/ml
  • gradual
  • may be associated with anorexia; weight loss; and soft/loose stools.
18
Q

What Nonbiliary causes of painless jaundice should be considered?

A
  • increased bilirubin production (e.g., from hemolysis, blood transfusions, or ineffective erythropoiesis)
  • decreased bilirubin clearance due to hereditary defects
19
Q

What happens to long chain FAs and other products of lipid digestion?

A
  • converted back to TAGs, phospholip, + esters of chol in SER
20
Q

What happens to lipids in SER?

A
  • fat droplets form in cisternae

- apoproteins syn in RER transferred to SER + ass with newly syn TAGs

21
Q

How are short chain FAs absorbed?

A
  • pass directly through enterocyte and enter capillary
  • efficient diffusion into enterocyte through unstirred layers as they’re H2O sol
  • then transported directly to hepatic portal vein in liver
22
Q

What happens to the apoproteins in GA?

A
  • Chlymicrons + VLDL arrive

- apoproteins glycosylated

23
Q

What is the function of bile salt micelles?

A
  • form ring around long chain FAs in unstirred H2O layer
  • transform multilamellar vesicles into unilamellar vesicles + then into mixed micelles which are composed of bile salts, mixed lipids, i.e. fatty acids, monoglycerides, lysophospholipids and cholesterol.
  • mixed micelles create high [lipid] in unstirred H2O layer - diffusion into enterocytes
24
Q

Why can Glycerol, short-chain and medium-chain fatty acids pass through enterocyte and enter
blood capillaries?

A
  • have small size

- pass across fenestrations = high perm to small mol e.g. aa, glucose, water capillaries

25
Q

How do micelles enter enterocyte?

A
  • When fatty acid/bile salt mixed micelles reach surface of enterocyte, they encounter a low pH environment at the brush-border,
  • fatty acids leave micelle to enter the enterocyte by nonionic diffusion or by collision and incorporation into lipid bilayer.
26
Q

What happens to emulsion droplets arriving from stomach?

A

Pancreatic lipases and biliary bile salts, lecithin and cholesterol adsorb to the surface

27
Q

Describe large chain FA absorption in enterocyte

A

enterocyte re-esterifies mixed lipids to TAGs, phospholipids + esters of chol in SER

  • apoproteins syn in RER transferred to SER - ass with newly syn TAGs - become chylomicrons
  • chylo in vesicles fuse with fuse with BL mem of enterocyte - as too large to enter fenestrated cap - enter the lymph through larger interendo channels of the lymphatic cap.
  • Lymph flows to thoracic duct to enter blood circ via L subclavian
    vein.
  • protein + lipid comp of both chylomicrons + VLDLs mod during passage through lymph + entry into blood.
28
Q

What can be said about unstirred H2O layer?

A
  • unstirred water layer at mucosal surface of intestine is ~40 um thick and does not constitute a major absorptive barrier.
29
Q

What are chylomicrons?

A
  • largest of 5 lipoprotein particles in blood (others are VLDL, IDL, LDL and HDL)
  • emulsion-like particles
30
Q

What happens to components of chylomicrons after leave gut?

A

Delivered to target organs

31
Q

Describe transport of bile in liver

A
  • Bilirubin + bile acids exocytosed into bile ductile

- Secretin + vagal stim activate HCO3-, secretion, H2O - help bile acids + bili flow thorugh bile canliculi

32
Q

How is bilirubin removed from body?

A
  • bili-rubin albumin complex in sys circ
  • bili Enters hepatocytes + conjugated to bilirubin - mono + diglucuronides
  • exocytosed as bilirubin - glucuronide + urobilinogen - gets conc in gall bladder by H2O removal
  • enters small intestine - further breakdown
  • excreted in faeces - brown colour
33
Q

Describe digestion and absorption of fats

A
  • enters stomach and broken down my lipase of tongue glands and pancreatic lipase
  • emulsification by gastric contractions
  • breakdown in stomach (10-30%)
    pancreatic lipase and bile salts enter duodenum
  • breakdown + micelle formation in duodenum + jejunem (70-90%)
  • absorption in small intestine
  • excretion (5%)
34
Q

What are causes of gallstones?

A
  • too much absorption of H2O from bile,
  • ” of bile acids from bile
  • too much chol in bile
  • inflammation of epi
35
Q

What can gallstones cause?

A
  • Could build up pressure in pancreatic duct
  • obstruct release of micelles for fat absorption + cause back pressure in pancreatic duct – proenz enter parenchyma (tissue space) + ass with lysosomes + become activated + dissolve tissue
36
Q

Describe Relationship between bile flow and liver blood flow and the role of oxygen delivery on bile flow and what this means

A
  • when O2 limiting – linear relationship where as blood flow inc, bile flow inc
  • but as get O2 delivery + super sat of O2 - bile flow indep of blood flow
  • shows Hydrostatic/liver sinusoidal blood pressure not mech that drives bile secretion
  • Secretion of bile is active process requiring energy expenditure - occurs against a pressure gradient from bile ductules to vasculature e.g. if pressure in bile duct above that in liver circ
  • secreting bile not consequence of raising hydrostatic from blood to bile duct
37
Q

What stim secretin secretion?

A

Acidic chyme entering duodenum stim secretin stim into blood

38
Q

How is bile conc in the gall bladder?

A
  • HCO3-/Cl- exchanger on lum mem of epi cell - gens Cl- gradient into cell + out into ISF - H2O follows
  • removal of H2O from lumen of gallbladder into ISF - conc bile salts inside
  • Na+/K+ pump on BL mem maintains Na+ gradient out of cell so H2O follows
39
Q

Why is bili removal by liver important?

A
  • don’t get jaundice

PPP (6 decks)

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