Disorders of Gallbladder and Biliary Tract Flashcards
where is bile formed?
hepatocytes/canaliculus
describe the course of bile after formation
- formed in hepatocytes/bile ducts
- modified in ductules and ducts
- concentrated, stored, in gallbladder
- delivery of bile to duodenum is regulated by Sphincter of Oddi
describe the zones of the liver
zone I: portal area, effected first by toxic inj, viral hepatitis
zone II: in-between
zone III: central vein area; affected first by ischemia, alc hep.
what are sinusoids?
irregular capillaries w/ fenestrated endothelium, no BM –> macromlecules have full access to basal surface of hepatocytes through Disse
how does secretion into bile canaliculus work?
an active process “bile salt pump”
what is bile made of?
bile acids, phospholipids, chol*, bilirubin, ions/water
*bile is the only relevant mechanism for cholesterol excretion
how is bilirubin formed, how does it get to the hepatocyte?
breakdown of erythrocytes –> bilirubin. bilirubin bound by albumin in blood, delivered to hepatocytes –> conjugated by glucoronyl transferase –> conjugated bili –> secreted into bile canaliculus
main function of the gallbladder
concentrates bile
Contractile function of the gallbladder is impt b/c….
decreased emptying is a major risk factor for gallstone formation
2 functions of bile
- fat digestion and absorption (of fat soluble vitamins)
- elimination of waste products (chol)
what controls bile secretion?
mainly CCK: released from duodenum in response to fat, AA, peptides –>
- Gb contraction
- sphincter relaxation
- release of pancreatic enzymes
- inhibition of gastric emptying
also secretin
micelles
in bile acid
emulsify lipids –> soluble
important for digestion, transport, absorption of lipid soluble substances (like ADEK)
enterohepatic circulation of bile acids
bile acids are almost all recycled (little excreted)
99% taken up in terminal ileum
what happens w/ loss of ileal function?
no longer retaining sufficient bile acids –>risk of….
- steatorrhea
- diarrhea
- nephrolithiasis
- cholelithiasis
cholelithiasis sx
- epigastric/RUQ pain
- crescendo-plateau-decrescendo
- nausea/vomiting
- preceding pain attacks
causes of jaundice
increased unconj bili
- overproduction of bilirubin (ex. hemolysis)
- defective uptake
- defective conjugation
increased conj bili
- defective excretion (intra/extra-hepatic)
name and describe 3 hereditary hyperbilirubinemias
Gilbert’s: decreased GT
Crigler-Najar:
- type I: no GT
- type II: very low GT
Dubin-Johnson and Rotor syndrome: probelm w/ excretion of bili
causes of cholestasis
intrahepatic or extrahepatic
cholestasis sx
jaundice, gray stool, dark urine
pruritis
cholestasis labs
increased bili, ALP, GGT
increased chol, xanthomas
malabsorption of fat and fat soluble vitamins
causes of extrahepatic cholestasis
high direct/conj bili
- gallstones
- strictures
- neoplasia
- parasites
risk factors for gallstones
- increasing age
- female gender (cholesterol stones): pregnancy, estrogens
- genetics, fam hx
- lifestyle: obesity, abstinence of ETOH, low physical activity, diet, rapid weight loss
- disease: DM, Crohn’s
what % of the pop has gallstones?
10% of adults
mostly asymptomatic
gallstones and pregnancy
pathophys: increased Gb volume, decreased Gb contractility
Sx: absent Murphy’s sign, AP normally elevated in pregnancy
management: safest time for cholecystectomy is 2nd trimester
acute cholecystitis
acute inflammation of gallbladder wall, usually caused by obstruction from gallstone
sx, exam, labs, imaging of acute cholecystitis
ongoing RUQ/epigastric pain
Murphy’s sign
Labs: elevated bili, AST, ALT
Imaging: US
pathological finding in chronic cholecystitis
Rokitansky-Aschoff sinus
acute acalculous cholecystitis
in pts w/ severe and acute systemic illnesses
due to ischemia, gb stasis, biliary sludge, secondary bacterial contamination
gangrenous (necrotizing) cholecystitis
rare, 10% mortality, perforation common
coagulative necrosis of gb wall
what is the most sensitive diagnostic procedure for gallstones and dilated bile ducts?
abdominal US
why would you do an ERCP for gallstones?
only do it for tx b/c risk of pancreatitis (5%)
choledocholithiasis sx, exam
sx: recurrent RUQ/epigastric pain, may resolve, preceding episodes
exam nonspecific
labs in choledocholithiasis
classic cholestatic picture: increased Bili, ALP, GGT, AST, ALT
may be transient
complications of choledocholithiasis
cholangitis, pancreatitis, cirrhosis
pathogenesis of cholangitis
obstruction –> stasis –> bacterial overgrowth –> infection
cholangitis clinical picture
Charcot’s triad: RUQ pain, jaundice, fever
Reynold’s pentad: Charcot + MS changes + shock
on exam: very ill appearing, jaundice, tenderness
labs: elevated bili, ALP, GGT, AST, ALT
imaging: US - dilated CBD
possible complications of gallstones
- cholecystitis: acute/chronic, empyema, perforation
- choledocholtihiasis: obstructive jaundice, ascending cholangitis
- pancreatitis
- more rare: biliary enteric fistula, gallstone ileus, porcelain gallbladder
gallbladder carcinoma
very rare
late dx, poor prognosis
risk factors: gallstones, other chole probs
sclerosing cholangitis
primary: chronic, fibrosing, inflammatory process of bile ducts –> obliteration of biliary tree and cirrhosis
secondary: chronic biliary obstruction w/ secondary fibrosis –> biliary cirrhosis
sclerosing cholangitis is associated with….
UC (and more rarely, Crohn’s)
cholangiocarcinoma
tumor of cholangiocytes
rare but increasing incidence (10-15% hepatic malignancies)
poor survival
Klatskin tumor
cholangiocarcinoma of bifurcation
