Chapter 32 - Biliary System Flashcards

1
Q

What is the triangle of Calot?

A

Cystic duct, common hepatic duct, cystic artery.

This is now cystic duct, common hepatic duct, and inferior edge of the liver.

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2
Q

What blood vessels supply the hepatic and CBD?

A

Right hepatic and retroduodenal branches of the GDA

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3
Q

What side of the CBD are the lymphatics on?

A

Right

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4
Q

What type of cells makes up the mucosa of the gallbladder? Submucosa?

A

Columnar epithelium

NO submucosa

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5
Q

What will relax the sphincter of Oddi?

A

Glucagon

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6
Q

What is the normal size of the GB wall? Pancreatic duct?

A

GB wall: 2-4mm

Pancreatic duct: <10mm s/p chole

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7
Q

Where is the highest concentration of CCK and secretin cells?

A

Duodenum

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8
Q

What are Rokitansky-Aschoff sinuses?

A

Invagination of the epithelium of the wall of the gallbladder; formed from increased gallbladder pressure

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9
Q

What are the ducts of Luschka?

A

Biliary ducts that can leak after chole

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10
Q

What stimulates increased bile excretion?

A

CCK, secretin, vagal input

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11
Q

What biochem signals cause decreased bile excretion?

A

VIP, somatostatin, sympathetic stimulation

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12
Q

What are the 3 essential functions of bile?

A

Fat-soluble vitamin absorption, bilirubin excretion, cholesterol excretion

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13
Q

How does the gallbladder form concentrated bile?

A

Active resorption of Na and H20

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14
Q

How many times a day does the bile salt pool cycle?

A

4-8 times/day

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15
Q

Where does active resorption of conjugated bile acids occur? Passive resorption of nonconjugated bile acids?

A

Active: terminal ileum (50%), passive: small intestine and colon

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16
Q

Where is bile secreted from?

A

Bile canalicular cells (20%), hepatocytes (80%)

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17
Q

What is the breakdown product of conjugated bilirubin that gives stool brown colon?

A

Stercobilin

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18
Q

What is the breakdown product of conjugated bilirubin that gets reabsorbed and released in urine?

A

Urobilin

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19
Q

Pathway of cholesterol and bile acid synthesis?

A

HMG CoA –> (HMG CoA reductase) –> cholesterol –> (7-alpha-hydroxylase) –> bile acids

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20
Q

What is the rate-limiting step in cholesterol synthesis?

A

HMG CoA reductase

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21
Q

What causes stones in obese people? In thin people?

A

Obese: overactive HMG CoA reductase

Thin: underactive 7-alpha-hydroxylase

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22
Q

What % of the population has gallstones?

A

10%

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23
Q

What % of gallstones are radiopaque?

A

10%

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24
Q

What causes nonpigmented stones?

A

Increase cholesterol insolubilization; caused by stasis, calcium nucleation by mucin glycoproteins, increased water reabsorption from gallbladder; decreased lecithin and bile acids

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25
Q

What is the most common type of stone found in the US?

A

Nonpigmented (75%)

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26
Q

What is the most common type of stone found worldwide?

A

Pigmented

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27
Q

What causes pigmented stones?

A

Solubilization of unconjugated bilirubin with precipitation of calcium bilirubinate and insoluble salts

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28
Q

What causes black stones?

A

Hemolytic disorders or cirrhosis; also in pts with chronic TPN, ileal resection; increased bilirubin load, decreased hepatic function and bile stasis

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29
Q

What causes brown stones? Where are they found?

A

Infection causing deconjugation of bilirubin; found in CBD, formed in ducts

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30
Q

Most common bacteria causing brown stones?

A

E. coli

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31
Q

What pathologies need to be checked for in a patient with brown stones?

A

Ampullary stenosis, duodenal diverticula, abnormal sphincter of Oddi

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32
Q

Cholecystitis is caused by what?

A

Obstruction of the cystic duct by gallstone

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33
Q

What is suppurative cholecystitis?

A

Associated with frank purulence in the GB, can be associated with sepsis and shock

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34
Q

Most common organisms in acute cholecystitis?

A

E. coli, klebsiella, enterococcus

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35
Q

Risk factors for stone formation?

A

Age >40, female, obesity, pregnancy, rapid wt loss, vagotomy, TPN, ileal resection

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36
Q

Sensitivity of US in picking up stones?

A

95%

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37
Q

What is the definition of biliary dyskinesia (percentage of volume excreted over certain time)?

A

<40% of gallbladder volume excreted after CCK over 1 hour

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38
Q

Causes of air in the biliary system?

A

Previous ERCP and sphincterotomy, cholangitis, erosion of the biliary system into duodenum (gallstone ileus)

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39
Q

What are signs of acalculous cholecystitis? Pathology?

A

Thickened wall, RUQ pain, elevated WBCs; bile stasis leading to distention and ischemia

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40
Q

When does acalculous cholecystitis occur?

A

After burns, prolonged TPN, trauma, other major surgery

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41
Q

Diagnosis of acalculous cholecystitis?

A

US shows sludge, GB wall thickening, pericholecystic fluid; HIDA (+)

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42
Q

What is the common organism causing emphysematous gallbladder disease?

A

C. perfringens

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43
Q

What is gallstone ileus?

A

Fistula between GB and duodenum that releases stone, causing SBO; elderly, can see pneumobilia on plain film

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44
Q

Most common site of obstruction in gallstone ileus?

A

Terminal ileum

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45
Q

Treatment for gallstone ileus?

A

Remove stone with enterotomy proximal to obstruction (enterolithotomy), usually through laparotomy incision, may need bowel resection if necrosis/ischemia/perforation, inspect the whole bowel.

Perform chole and fistula resection if pt is low risk (ASA 1 or 2). If high risk, do lap chole later.

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46
Q

What is the benefit of interoperative cholangiography?

A

Allows for intraoperative detection of biliary injury. Studies have not definitively shown benefit in preventing injury.

47
Q

In what % of patients does the right posterior duct enter the CBD separately? What segment is it from?

A

10%, segment 6 or 7

48
Q

What is the treatment if the right posterior duct is injured during lap chole?

A

If >2mm, need to open and perform hepatico-j

49
Q

Treatment for intraop CBD injury?

A
  • If <50% circumference - perform primary repair
  • all other cases - hepaticoj or choledochoj
50
Q

What is the workup for persistent nausea and vomiting or jaundice following lap chole?

A
  • US for fluid collection: if collection, perc drain
  • bilious drainage: ERCP and stent vs repair
  • no fluid collection, dilated hepatic ducts - concern for transected bile duct
51
Q

Treatment for anastamotic leaks following transplant or hepaticoj?

A

ERCP and stents

52
Q

Treatment for sepsis following lap chole?

A

Fluid resuscitation, stabilize; concern for complete transection of CBD and cholangitis

53
Q

Most common situation in which CBD or hepatic duct strictures occur?

A

After lap chole

54
Q

What is the most important cause of late postoperative biliary strictures?

A

Ischemia; can also be caused by chronic pancreatitis, stricture of biliary enteric anastomosis

55
Q

Diagnosis of CBD or hepatic duct stricture?

A

ERCP; US will show dilated ducts

56
Q

Treatment of CBD or hepatic duct strictures?

A

ERCP with sphincterotomy and possible stent placement; PTC tube if that fails

7d post injury, hepaticoj 6-8wks after injury

57
Q

What causes hemobilia?

A

Fistula between bile duct and hepatic arterial system; most commonly occurs with trauma, also infections, primary gallstones, aneurysms, tumors

58
Q

Presentation of hemobilia?

A

UGI bleed, jaundice, RUQP

59
Q

Diagnosis of hemobilia? Treatment?

A

Angiogram; resuscitation, angio and embolization, operation if that fails

60
Q

What is the most common cancer of the biliary tract?

A

Gallbladder adenocarcinoma

61
Q

What is the most common site of mets from gallbladder adenocarcinoma?

A

Liver

62
Q

Risk of cancer with porcelain gallbladder?

A

10-20%, need chole

63
Q

What % of patients w/ GB cancer present with stage IV disease?

A

90%

64
Q

Symptoms of gallbladder CA?

A

Painless jaundice 1st, then RUQ pain (could be cholangitis at this point)

Weight loss, fatigue, loss of appetite

65
Q

Treatment based on stage of GB CA?

A
  • Stage I (mucosa): chole
  • Stage II+ (into muscle): wide resection around liver bed - 2-3cm margins, regional lymphadenectomy, may need Whipple, lobectomy or resection of CBD
66
Q

Contraindication for lap chole?

A

Gallbladder CA - high incidence of tumor implants in trocar sites.

Inability to tolerate pneumoperitoneum.

General contraindications for surgery.

Not recommended in ASA III/IV or septic pts w/ milder disease.

67
Q

5-yr survival of gallbladder CA?

A

5%

68
Q

Risk factors for bile duct cancer (cholangiocarcinoma)?

A

C. sinensis infection, typhoid, UC, choledochal cysts, sclerosing cholangitis, congenital hepatic fibrosis, chronic bile duct infection

69
Q

Symptoms of cholangiocarcinoma?

A

Early: painless jaundice, can also get cholangitis; late: wt loss, anemia, pruritis; persistent increase in alk phos and bilirubin

70
Q

Diagnosis of cholangiocarcinoma?

A
  • CA19-9, CEA, AFP
  • Initial CT/MRI/US: dx if typical findings
  • proximal lesion → MRCP: dx if typical findings
  • distal lesion, or MRCP not typical → ERCP
  • still not typical after ERCP → MRI/CT guided bx
71
Q

What does the discovery of a focal bile duct stenosis in pts without h/o biliary surgery or pancreatitis suggest?

A

Bile duct ca

72
Q

Where are Klatskin tumors?

A

In upper 1/3 of bile duct; most common type, worst prognosis

73
Q

Treatment for Klatskin tumor?

A
  • Lobectomy and stenting of contralateral bile duct if localized to right or left lobe; usually unresectable (MDCT, MRCP, ERCP, bx)
  • Resectability often determined at surgery. Cannot have…
    • retropancreatic, paraceliac nodal metastases, liver mets
    • invasion of the portal vein or main hepatic artery
    • extrahepatic adjacent organ invasion
    • disseminated disease
74
Q

Treatment for cholangiocarcinoma in middle 1/3? Lower 1/3?

A

Middle: hepaticojejunostomy

Lower: Whipple

75
Q

5-yr survival for cholangio?

A

20%

76
Q

What % of choledochal cysts are extrahepatic?

A

90%

77
Q

What is the cancer risk with choledochal cysts?

A

15%

78
Q

Symptoms of choledochal cyst?

A

Episodic pain, fever, jaundice, cholangitis

79
Q

Choledochal cyst presentation in infants?

A

Similar to biliary atresia

80
Q

Possible cause of choledochal cysts?

A

Abnormal reflux of pancreatic enzymes during development secondary to bad angle of insertion

81
Q

Most common type of choledochal cyst?

A

Type I: saccular or fusiform dilation of extrahepatic ducts

82
Q

Treatment for choledochal cyst?

A

Excision with hepaticoj and chole; type IV partially intrahepatic/type V totally intrahepatic will need liver resection

83
Q

What patients have primary sclerosing cholangitis?

A

Men in 4-5th decade; associated with retroperitoneal fibrosis, Riedel’s thyroiditis, pancreatitis, UC, DM

84
Q

Symptoms of PSC?

A

Fatigue, fluctuating jaundice, pruritus, wt loss, RUQ pain

85
Q

Does PSC get better after colon resection for UC?

A

NO

86
Q

Consequences and complications of PSC?

A

Portal HTN and hepatic failure (scarring and patching with progressive fibrosis of intra/extrahepatic ducts); chirrhosis, cholangiocarcinoma

87
Q

Diagnosis of PSC? Treatment?

A

ERCP showing multiple strictures and dilations; transplant needed long term, PTC drainage/choledochoj may be effective, balloon dilation for symptomatic relief

88
Q

Treatment for pruritus symptoms in PSC.

A

Cholestyramine

89
Q

Primary biliary cirrhosis occurs in what size ducts?

A

Medium-sized hepatic ducts

90
Q

Consequences of PBC?

A

Cholestasis –> cirrhosis –> portal HTN

91
Q

Symptoms of PBC?

A

Fatigue, pruritus, jaundice, xanthomas

92
Q

What type of antibodies are associated with PBC?

A

Antimitochondrial antibodies

93
Q

Cancer risk with PBC?

A

No increased risk of cancer

94
Q

Treatment for PBC?

A

Transplant

95
Q

What is Charcot’s triad?

A

RUQ pain, jaundice, fever - indicates cholangitis

96
Q

What is Reynold’s pentad

A

RUQ pain, jaundice, fever, altered mental status, shock - suggests sepsis from cholangitis

97
Q

Most common organisms in cholangitis?

A

E. coli and Klebsiella

98
Q

Late complications of cholangitis?

A

Stricture and hepatic abscess

99
Q

1 serious complication of cholangitis?

A

Renal failure; related to sepsis

100
Q

Most common etiology of cholangitis? Other causes?

A

Gallstones; also biliary strictures, neoplasm, chronic pancreatitis, congenital choledochal cysts, duodenal diverticula

101
Q

What is the cause of systemic bacteremia from cholangitis?

A

At >20mmHg, cholovenous reflux occurs –> systemic bacteremia

102
Q

Treatment for cholangitis?

A

Fluid resus, abx, ERCP with sphincterotomy nd stone extraction, if fails - PTC

103
Q

What is oriental cholangiohepatitis?

A

Recurrent cholangitis from primary CBD stones; in Asia; caused by C. sinensis, A. lumbricoides, T. trichiuria, E. coli

104
Q

Treatment for oriental cholangiohepatitis?

A

Hepaticoj and antiparasitic medications

105
Q

What is the most common cause of shock following lap chole early (1st 24h)? Late (after 1st 24h)?

A

Early: hemorrhagic shock from clip that fell off cystic artery; late: septic shock from accidental clip on CBD with subsequent cholangitis

106
Q

What is adenomyomatosis?

A

Thickened nodule of mucosa and muscle associated with Rokitansky-Aschoff sinus; not premalignant, does not cause stones; tx: chole

107
Q

What is granular cell myoblastoma?

A

Benign neuroectoderm tumor of the GB; can occur in biliary tract with signs of cholecystitis; tx: chole

108
Q

What is cholesterolosis?

A

Speckled cholesterol deposits on GB wall

109
Q

What size GB polyp more likely to be malignant?

A

>1cm

110
Q

What is delta bilirubin?

A

Bound to albumin covalently, half-life 18d, may take a while to clear after long-standing jaundice

111
Q

What is Mirizzi syndrome?

A

Compression of the common hepatic duct by a stone in the infundibulum of the GB or inflammation arising from the GB or cystic duct; causing stricture and hepatic duct obstruction

112
Q

What abx can cause gallbladder sludging and cholestatic jaundice?

A

Ceftriaxone

113
Q

What are indications for asymptomatic cholecystectomy?

A

Pts undergoing liver TXP or gastric bypass