Biliary Secretions: Liver and Gallbladder Function Flashcards
functions of the liver
bile production and secretion
metabolism of carbohydrates, proteins, and lipids
bilirubin production and excretion
detoxification of substances
what makes up bile
bile salts 50% bile pigments 2% cholesterol 4% phospholipids 40% ions h20
cirrhosis
chronic liver disease in which normal liver cells are damaged and replaced by scar tissue
excessive alcohol intake is most common cause of cirrhosis
alcohol abuse leads to accumulation of fat within hepatocytes
fatty liver leads to steatohepatis
steatohepatitis is fatty liver accompanied by inflammation which leads to scarring of liver and cirrhosis
formation of bile acids
primary bile acids - hepatocytes
secondary bile acids - lumen of small intestine
bile salts - conjugation occurs in liver
relative amount of the four bile acids
cholic acid, chenodeoxycholic acid, deoxycholic acid, lithocholic acid
bile salts
amphipathic molecules
roles: emulsify lipids and form micelles
primary bile salts are more effective at solubilizing lipids than secondary bile salts
phospholipids
amphipathic molecules but are not soluble in water
bile salts soulubilize phospholipids forming micelles
cholesterol
it is solubilized as part of the micelle
weakly polar molecule it is in the interior of the micelle
bile pigments
bilirubin is the most important
do not take part in micellar formation
ions and water
predominant cation is Na
predominant anions are Cl and HCO3
the secretion of bile acids carriers water and ions into the bile by osmotic filtration
additional ions and water are supplied by the cells lining the ducts
this secretion is stimulated by secretin
behavior of bile acids depending on concentration
decreased - no aggregation
increased - micelle formation takes place
critical micellar concentration
the point of micelle formation
in the liver ducts and gallbladder is in micellar solution
mechanism of bile secretion and absorption of bile salts
synthesis and secretion of bile salts
bile salts are stored and concentrated in the gallbladder
CCK induced gallbladder contraction and sphincter of Oddi relaxation
absorption of bile into the portal circulation
delivery of bile salts to the liver
canalicular membrane
newly synthesized bile acids the returning bile acids are secreted into he bile canaliculi
canalicular bile is secreted by ductule cells in response to the osmotic effects of anion transport
enterohepatic circulation
bile salts are transported from the ileum to the portal blood
bile salts back to liver
synthesis of bile salts to replace the amount that was lost
uptake of bile salts across the basolateral membrane of the enterocyte is mediated by
Na dependent transport protein sodium taurocholate cotransporting polypeptide
Na independent transport protein, organic anion transport proteins
rates of bile acid synthesis and secretion
increased secretion increases the rate of return of bile acids which exerts a negative feedback
two mechanisms of bile secretion
secretin stimulates the secretion of HCO3 and water from the ductile cells resulting in a significant increase in bile volume HCO3 concentration and pH and a decrease in the concentration of bile salts
interdigestive period of digestion bile flow
gallbladder fills with bile
gallbladder is relaxed
sphincter of oddi is closed
on eating bile flow
CCK mediated
contraction of the bladder
relaxation of the sphincter of oddi
bilirubin production and excretion
UDP glycyronyl transferase is synthesized slowly after birth
conjugated bilirubin = biliribin glucuronide
urobilin and sterocobilin give stool dark color
physiological neonatal jaundice
infant has increased level of unconjugated bilirubin in the blood during the first week of life
bilirubin production is elevated because of increased breakdown of fetal erythrocytes
low activity of UDP glucuronyl transferase which is the enzyme responsible for binding bilirubin to glucuronic acid thus making bilirubin water soluble
hemolytic anemia
form of anemia due to hemolysis
breakdown the RBC leads to jaundice
any cause of hemolytic anemia would lead to increased production of bilirubin
increased bilirubin level overwhelmed livers capacity to produce conjugated bilirubin resulting in increased unconjugated bilirubin
gilbert’s syndrome
increased levels of unconjugated bilirubin in the blood
due to mutation in gene that codes for uridine diphosphate glucuronosyltransferase
crigler-najjar syndrome type 1
increased levels of unconjugated bilirubin in the blood
starts early in life
no function of UDP glucuronyltransferase
kernicterus: form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and n tissue
crigler-najjar syndrome type 2
increased levels of unconjugated bilirubin in the blood
starts later in life
less than 20% function of UDP glucuronyltransferase
less likely to develop kernicterus
treatment for crigler-najjar
light treatment is needed throughout life
blood transfusions may help control the amount of bilirubin in blood
oral calcium phosphate and carbonate to form complexes with bilirubin in the gut
liver transplant for type 1
phenobarbitol for type 2
dubin-johnson
increase conjugated bilirubin in the serum without elevation of liver enzymes
defect in the ability of hepatocytes to secrete conjugated bilirubin into the bile
mild jaundice throughout life
liver has black pigmentation
rotor syndrome
buildup of both unconjugated and conjugated bilirubin in the blood, but majority is conjugated
liver cells are not pigmented
gallstones
concentrations that form in the biliary system
occur when there is excess in either pigments of bilirubin breakdown or cholesterol
