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Fiser's ABSITE Ryan SHORT > Chapter 32 - Biliary System > Flashcards

Chapter 32 - Biliary System Flashcards

1
Q

What is the triangle of Calot?

A

Cystic duct, CBD, 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 is the mucosal of the gallbladder? Submucosa?

A

Columnar epithelium; NO submucosa

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5
Q

What will contract the sphincter of Oddi?

A

Morphine

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6
Q

What will relax the sphincter of Oddi?

A

Glucagon

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7
Q

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

A

GB wall: 2-4mm

Pancreatic duct: <10mm s/p chole

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8
Q

Where is the highest concentration of CCK and secretin cells?

A

Duodenum

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9
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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10
Q

What are the ducts of Luschka?

A

Biliary ducts that can leak after chole

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11
Q

What stimulates increased bile excretion?

A

CCK, secretin, vagal input

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12
Q

What causes decreased bile excretion?

A

VIP, somatostatin, sympathetic stimulation

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13
Q

What are the 3 essential functions of bile?

A

Fat-soluble vitamin absorption, bilirubin excretion, cholesterol excretion

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14
Q

How does the gallbladder form concentrated bile?

A

Active resorption of Na and H20

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15
Q

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

A

4-8 times/day

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16
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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17
Q

Where is bile secreted from?

A

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

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18
Q

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

A

Stercobilin

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19
Q

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

A

Urobilin

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20
Q

Pathway of cholesterol and bile acid synthesis?

A

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

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21
Q

What is the rate-limiting step in cholesterol synthesis?

A

HMG CoA reductase

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22
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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23
Q

What % of the population has gallstones?

A

10%

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24
Q

What % of gallstones are radiopaque?

A

10%

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25
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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26
Q

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

A

Nonpigmented (75%)

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27
Q

What is the most common type of stone found worldwide?

A

Pigmented

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28
Q

What causes pigmented stones?

A

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

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29
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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30
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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31
Q

Most common bacteria causing brown stones?

A

E. coli

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32
Q

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

A

Ampullary stenosis, duodenal diverticula, abnormal sphincter of Oddi

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33
Q

Cholecystitis is caused by what?

A

Obstruction of the cystic duct by gallstone

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34
Q

What is suppurative cholecystitis?

A

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

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35
Q

Most common organisms in acute cholecystitis?

A

E. coli, klebsiella, enterococcus

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36
Q

Risk factors for stone formation?

A

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

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37
Q

Sensitivity of US in picking up stones?

A

95%

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38
Q

What is the definition of biliary dyskinesia?

A

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

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39
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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40
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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41
Q

When does acalculous cholecystitis occur?

A

After burns, prolonged TPN, trauma, other major surgery

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42
Q

Diagnosis of acalculous cholecystitis?

A

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

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43
Q

What is the common organism causing emphysematous gallbladder disease?

A

C. perfringens

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44
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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45
Q

Most common site of obstruction in gallstone ileus?

A

Terminal ileum

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46
Q

Treatment for gallstone ileus?

A

Remove stone with enterotomy proximal to obstruction; perform chole and fistula resection

47
Q

What is the benefit of interoperative cholangiography?

A

Does not prevent injuries; may limit severity, increases early diagnosis of injury to CBD

48
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

49
Q

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

A

If >2mm, need to open and perform hepaticoj

50
Q

Treatment for intraop CBD injury?

A

If <50% of the circumference, can perform primary repair; in all other cases need hepaticoj or choledochoj

51
Q

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

A

US to look for fluid collection: if collection, perc drain - bilious: ERCP and stent vs repair; no fluid collection, dilated hepatic ducts - concern for transected bile duct

52
Q

Treatment for anastamotic leaks following transplant or hepaticoj?

A

ERCP and stents

53
Q

Treatment for sepsis following lap chole?

A

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

54
Q

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

A

After lap chole

55
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

56
Q

Diagnosis of CBD or hepatic duct stricture?

A

ERCP; US will show dilated ducts

57
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

58
Q

What causes hemobilia?

A

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

59
Q

Presentation of hemobilia?

A

UGI bleed, jaundice, RUQP

60
Q

Diagnosis of hemobilia? Treatment?

A

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

61
Q

What is the most common cancer of the biliary tract?

A

Gallbladder adenocarcinoma

62
Q

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

A

Liver

63
Q

Risk of cancer with porcelain gallbladder?

A

10-20%, need chole

64
Q

What % of patients present with stage IV disease?

A

90%

65
Q

Symptoms of gallbladder CA?

A

Jaundice 1st, then RUQ pain

66
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

67
Q

Contraindication for lap chole?

A

Gallbladder CA; high incidence of tumor implants in trocar sites

68
Q

5-yr survival of gallbladder CA?

A

5%

69
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

70
Q

Symptoms of cholangiocarcinoma?

A

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

71
Q

Diagnosis of cholangio?

A

ERCP 1st, MRI may help define the lesion

72
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

73
Q

Where are Klatskin tumors?

A

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

74
Q

Treatment for Klatskin tumor?

A

Lobectomy and stenting of contralateral bile duct if localized to right or left lobe; usually unresectable

75
Q

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

A

Middle: hepaticoj, lower: Whipple

76
Q

5-yr survival for cholangio?

A

20%

77
Q

What % of choledochal cysts are extrahepatic?

A

90%

78
Q

What is the cancer risk with choledochal cysts?

A

15%

79
Q

Symptoms of choledochal cyst?

A

Episodic pain, fever, jaundice, cholangitis

80
Q

Presentation in infants?

A

Similar to biliary atresia

81
Q

Possible cause of choledochal cysts?

A

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

82
Q

Most common type of choledochal cyst?

A

Type I: saccular or fusiform dilation of extrahepatic ducts

83
Q

Treatment for choldochal cyst?

A

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

84
Q

What patients have primary sclerosing cholangitis?

A

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

85
Q

Symptoms of PSC?

A

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

86
Q

Does PSC get better after cholon resection for UC?

A

NO

87
Q

Consequences and complications of PSC?

A

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

88
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

89
Q

Treatment for pruritus symptoms?

A

Cholestyramine

90
Q

Primary biliary cirrhosis occurs in what size ducts?

A

Medium-sized hepatic ducts

91
Q

Consequences of PBC?

A

Cholestasis –> cirrhosis –> portal HTN

92
Q

Symptoms of PBC?

A

Fatigue, pruritus, jaundice, xanthomas

93
Q

What type of antibodies are associated with PBC?

A

Antimitochondrial antibodies

94
Q

Cancer risk with PBC?

A

No increased risk of cancer

95
Q

Treatment for PBC?

A

Transplant

96
Q

What is Charcot’s triad?

A

RUQ pain, jaundice, fever - indicates cholangitis

97
Q

What is Reynold’s pentad

A

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

98
Q

Most common organisms in cholangitis?

A

E. coli and Klebsiella

99
Q

Late complications of cholangitis?

A

Stricture and hepatic abscess

100
Q

1 serious complication of cholangitis?

A

Renal failure; related to sepsis

101
Q

Most common etiology of cholangitis? Other causes?

A

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

102
Q

What is the cause of systemic bacteremia from cholangitis?

A

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

103
Q

Treatment for cholangitis?

A

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

104
Q

What is oriental cholangiohepatitis?

A

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

105
Q

Treatment for oriental cholangiohepatitis?

A

Hepaticoj and antiparasitic medications

106
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

107
Q

What is adenomyomatosis?

A

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

108
Q

What is granular cell myoblastoma?

A

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

109
Q

What is cholesterolosis?

A

Speckled cholesterol deposits on GB wall

110
Q

What size GB polyp more likely to be malignant?

A

> 1cm

111
Q

What is delta bilirubin?

A

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

112
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

113
Q

What abx can cause gallbladder sludging and cholestatic jaundice?

A

Ceftriaxone

114
Q

What are indications for asymptomatic cholecystectomy?

A

Pts undergoing liver TXP or gastric bypass

Fiser's ABSITE Ryan SHORT (50 decks)

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