Disorders of Gallbladder and Biliary Tract Flashcards

1
Q

where is bile formed?

A

hepatocytes/canaliculus

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2
Q

describe the course of bile after formation

A
  1. formed in hepatocytes/bile ducts
  2. modified in ductules and ducts
  3. concentrated, stored, in gallbladder
  4. delivery of bile to duodenum is regulated by Sphincter of Oddi
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3
Q

describe the zones of the liver

A

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.

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4
Q

what are sinusoids?

A

irregular capillaries w/ fenestrated endothelium, no BM –> macromlecules have full access to basal surface of hepatocytes through Disse

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5
Q

how does secretion into bile canaliculus work?

A

an active process “bile salt pump”

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6
Q

what is bile made of?

A

bile acids, phospholipids, chol*, bilirubin, ions/water

*bile is the only relevant mechanism for cholesterol excretion

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7
Q

how is bilirubin formed, how does it get to the hepatocyte?

A

breakdown of erythrocytes –> bilirubin. bilirubin bound by albumin in blood, delivered to hepatocytes –> conjugated by glucoronyl transferase –> conjugated bili –> secreted into bile canaliculus

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8
Q

main function of the gallbladder

A

concentrates bile

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9
Q

Contractile function of the gallbladder is impt b/c….

A

decreased emptying is a major risk factor for gallstone formation

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10
Q

2 functions of bile

A
  1. fat digestion and absorption (of fat soluble vitamins)
  2. elimination of waste products (chol)
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11
Q

what controls bile secretion?

A

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

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12
Q

micelles

A

in bile acid

emulsify lipids –> soluble

important for digestion, transport, absorption of lipid soluble substances (like ADEK)

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13
Q

enterohepatic circulation of bile acids

A

bile acids are almost all recycled (little excreted)

99% taken up in terminal ileum

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14
Q

what happens w/ loss of ileal function?

A

no longer retaining sufficient bile acids –>risk of….

  • steatorrhea
  • diarrhea
  • nephrolithiasis
  • cholelithiasis
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15
Q

cholelithiasis sx

A
  • epigastric/RUQ pain
  • crescendo-plateau-decrescendo
  • nausea/vomiting
  • preceding pain attacks
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16
Q

causes of jaundice

A

increased unconj bili

  • overproduction of bilirubin (ex. hemolysis)
  • defective uptake
  • defective conjugation

increased conj bili

  • defective excretion (intra/extra-hepatic)
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17
Q

name and describe 3 hereditary hyperbilirubinemias

A

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

18
Q

causes of cholestasis

A

intrahepatic or extrahepatic

19
Q

cholestasis sx

A

jaundice, gray stool, dark urine

pruritis

20
Q

cholestasis labs

A

increased bili, ALP, GGT

increased chol, xanthomas

malabsorption of fat and fat soluble vitamins

21
Q

causes of extrahepatic cholestasis

A

high direct/conj bili

  • gallstones
  • strictures
  • neoplasia
  • parasites
22
Q

risk factors for gallstones

A
  • 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
23
Q

what % of the pop has gallstones?

A

10% of adults

mostly asymptomatic

24
Q

gallstones and pregnancy

A

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

25
Q

acute cholecystitis

A

acute inflammation of gallbladder wall, usually caused by obstruction from gallstone

26
Q

sx, exam, labs, imaging of acute cholecystitis

A

ongoing RUQ/epigastric pain

Murphy’s sign

Labs: elevated bili, AST, ALT

Imaging: US

27
Q

pathological finding in chronic cholecystitis

A

Rokitansky-Aschoff sinus

28
Q

acute acalculous cholecystitis

A

in pts w/ severe and acute systemic illnesses

due to ischemia, gb stasis, biliary sludge, secondary bacterial contamination

29
Q

gangrenous (necrotizing) cholecystitis

A

rare, 10% mortality, perforation common

coagulative necrosis of gb wall

30
Q

what is the most sensitive diagnostic procedure for gallstones and dilated bile ducts?

A

abdominal US

31
Q

why would you do an ERCP for gallstones?

A

only do it for tx b/c risk of pancreatitis (5%)

32
Q

choledocholithiasis sx, exam

A

sx: recurrent RUQ/epigastric pain, may resolve, preceding episodes

exam nonspecific

33
Q

labs in choledocholithiasis

A

classic cholestatic picture: increased Bili, ALP, GGT, AST, ALT

may be transient

34
Q

complications of choledocholithiasis

A

cholangitis, pancreatitis, cirrhosis

35
Q

pathogenesis of cholangitis

A

obstruction –> stasis –> bacterial overgrowth –> infection

36
Q

cholangitis clinical picture

A

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

37
Q

possible complications of gallstones

A
  • cholecystitis: acute/chronic, empyema, perforation
  • choledocholtihiasis: obstructive jaundice, ascending cholangitis
  • pancreatitis
  • more rare: biliary enteric fistula, gallstone ileus, porcelain gallbladder
38
Q

gallbladder carcinoma

A

very rare

late dx, poor prognosis

risk factors: gallstones, other chole probs

39
Q

sclerosing cholangitis

A

primary: chronic, fibrosing, inflammatory process of bile ducts –> obliteration of biliary tree and cirrhosis
secondary: chronic biliary obstruction w/ secondary fibrosis –> biliary cirrhosis

40
Q

sclerosing cholangitis is associated with….

A

UC (and more rarely, Crohn’s)

41
Q

cholangiocarcinoma

A

tumor of cholangiocytes

rare but increasing incidence (10-15% hepatic malignancies)

poor survival

42
Q

Klatskin tumor

A

cholangiocarcinoma of bifurcation