Bile and biliary system Flashcards
What happens to bile salts once they’ve aided in fat absorption?
- 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
How can a deficit in bile salts be caused and how is this fixed?
- loss of bile slats in feaces
- resyn in liver but majority re-circ and reabsorbed in small intestine
– balance between loss and re-syn
What does the gall bladder contain?
- Stored bile salts
- bile conc up to 15x
What is the Sphincter of Oddi?
where pancreatic duct joins common bile duct into duodenum
What is the effect of CCK?
- gallbladder constriction - release bile into common bile duct which enters duodenum through sphincter
- Relaxation of sphincter of Oddi
What is effect of secretin?
- stim secretion of bile rich in HCO3- from liver
- stim HCO3- secretion from pancreas
What also causes weak contraction of gall bladder?
Vagal stim
How is bile prod stim in liver?
Para impulses along vagus nerve stim bile prod
How are bile salts conc in gall bladder?
- HCO3-/Cl- exchanger allowing Cl- gradient
- allows removal of water from lumen of gallbladder – conc bile salts
- Na/K pump maintains Na gradient
What is bilirubin?
Major component of bile
Where does bilirubin comes from?
85% from breakdown of RBCs
What are properties of bilirubin?
- fat sol
- toxic
- bound to albumin in blood
Where is bilirubin taken up?
By liver
How much and where is bilirubin absorbed per day?
15% reabsorbed from intestine by enterohepatic circ (between liver and intestine)
What is biliary disease caused by?
- 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.
What is dev of jaundice in absence of abdominal pain suggestive of?
a malignant obstruction of the bile duct e.g. gall stone.
Describe onset and symptoms of painless jaundice
- normal plasma bilirubin: 3-10mg/ml, jaundice: 18mg/ml
- gradual
- may be associated with anorexia; weight loss; and soft/loose stools.
What Nonbiliary causes of painless jaundice should be considered?
- increased bilirubin production (e.g., from hemolysis, blood transfusions, or ineffective erythropoiesis)
- decreased bilirubin clearance due to hereditary defects
What happens to long chain FAs and other products of lipid digestion?
- converted back to TAGs, phospholip, + esters of chol in SER
What happens to lipids in SER?
- fat droplets form in cisternae
- apoproteins syn in RER transferred to SER + ass with newly syn TAGs
How are short chain FAs absorbed?
- 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
What happens to the apoproteins in GA?
- Chlymicrons + VLDL arrive
- apoproteins glycosylated
What is the function of bile salt micelles?
- 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
Why can Glycerol, short-chain and medium-chain fatty acids pass through enterocyte and enter
blood capillaries?
- have small size
- pass across fenestrations = high perm to small mol e.g. aa, glucose, water capillaries
