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
acute cholecystitis
acute inflammation of gallbladder wall, usually caused by obstruction from gallstone
26
sx, exam, labs, imaging of acute cholecystitis
ongoing RUQ/epigastric pain Murphy's sign Labs: elevated bili, AST, ALT Imaging: US
27
pathological finding in chronic cholecystitis
Rokitansky-Aschoff sinus
28
acute acalculous cholecystitis
in pts w/ severe and acute systemic illnesses due to ischemia, gb stasis, biliary sludge, secondary bacterial contamination
29
gangrenous (necrotizing) cholecystitis
rare, 10% mortality, perforation common coagulative necrosis of gb wall
30
what is the most sensitive diagnostic procedure for gallstones and dilated bile ducts?
abdominal US
31
why would you do an ERCP for gallstones?
only do it for tx b/c risk of pancreatitis (5%)
32
choledocholithiasis sx, exam
sx: recurrent RUQ/epigastric pain, may resolve, preceding episodes exam nonspecific
33
labs in choledocholithiasis
classic cholestatic picture: increased Bili, ALP, GGT, AST, ALT may be transient
34
complications of choledocholithiasis
cholangitis, pancreatitis, cirrhosis
35
pathogenesis of cholangitis
obstruction --\> stasis --\> bacterial overgrowth --\> infection
36
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
37
possible complications of gallstones
* cholecystitis: acute/chronic, empyema, perforation * choledocholtihiasis: obstructive jaundice, ascending cholangitis * pancreatitis * more rare: biliary enteric fistula, gallstone ileus, porcelain gallbladder
38
gallbladder carcinoma
very rare late dx, poor prognosis risk factors: gallstones, other chole probs
39
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
40
sclerosing cholangitis is associated with....
UC (and more rarely, Crohn's)
41
cholangiocarcinoma
tumor of cholangiocytes rare but increasing incidence (10-15% hepatic malignancies) poor survival
42
Klatskin tumor
cholangiocarcinoma of bifurcation