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Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn > Chapter 32 - Biliary System > Flashcards

Chapter 32 - Biliary System Flashcards

1
Q

What blood vessels supply the hepatic and CBD?

A

Right hepatic and retroduodenal branches of the GDA.

Injuring these can lead to stricture.

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2
Q

What side of the CBD are the lymphatics on?

A

Right.

This is important for hepatoduodenal/portal node dissections done with GB cancer.

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3
Q

What type of cells makes up the mucosa of the gallbladder? Is there submucosa?

A

Columnar epithelium

NO submucosa

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4
Q

What will relax the sphincter of Oddi?

A

Glucagon (can use intraop to try to clear stones in choledocholithiasis)

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5
Q

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

A

GB wall: 2-4 mm

Pancreatic duct: 1.5-3.5 mm

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6
Q

Where is the highest concentration of CCK and secretin cells? Discuss CCK.

A
  • Duodenum
  • response to fatty acids
  • produced by I cells
  • stimulates GB contraction, Oddi relax, panc secrx
  • produces some satiety
  • inhibited by somatostatin
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7
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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8
Q

What are the ducts of Luschka?

A

Biliary ducts that attach to the GB in the fossa that can leak after chole

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9
Q

What stimulates increased bile excretion?

What kind of channel is secretion dependent on?

A
  • secretin (most potent), CCK, vagal input
  • chloride channel, active transport
  • bile has high concentration of bicarb
  • secretes around 1L/day
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10
Q

What biochem signals cause decreased bile excretion?

A

VIP, somatostatin, sympathetic stimulation

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11
Q

What are the 3 essential functions of bile?

A
  • fat-soluble vitamin absorption (emulsifies lipids)
  • bilirubin excretion
  • cholesterol excretion
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12
Q

How does the gallbladder form concentrated bile?

A

Active resorption of Na and H20

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13
Q

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

A

4-8 times/day

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14
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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15
Q

Where is bile secreted from?

A

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

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16
Q

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

A

Stercobilin

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17
Q

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

A

Urobilin

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18
Q

Pathway of cholesterol and bile acid synthesis?

A

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

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19
Q

What is the rate-limiting step in cholesterol synthesis?

A

HMG CoA reductase

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20
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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21
Q

What % of the population has gallstones?

A

10%

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22
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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23
Q

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

A

Nonpigmented (75%)

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24
Q

What is the most common type of stone found worldwide?

A

Pigmented

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25
Q

What causes pigmented stones?

A

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

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26
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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27
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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28
Q

Most common bacteria causing brown stones?

A

E. coli

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29
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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30
Q

Cholecystitis is caused by what?

A

Obstruction of the cystic duct by gallstone

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31
Q

What is suppurative cholecystitis?

A

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

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32
Q

Most common organisms in acute cholecystitis?

A

E. coli, klebsiella, enterococcus

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33
Q

Risk factors for stone formation?

A

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

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34
Q

Sensitivity of US in picking up stones?

A

95%

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35
Q

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

A
  • Twenty minutes after the injection of CCK, an ejection fraction of less than 35% is considered abnormal.
  • Or <40% of gallbladder volume excreted after CCK over 1 hour.
  • Tx w/ cholecystectomy.
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36
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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37
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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38
Q

When does acalculous cholecystitis occur?

A

After burns, prolonged TPN, trauma, other major surgery

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39
Q

Diagnosis of acalculous cholecystitis?

A

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

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40
Q

What is the common organism causing emphysematous gallbladder disease?

A

C. perfringens

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41
Q

What is gallstone ileus?

A

Fistula between GB and duodenum that releases stone, causing SBO

usually elderly patient

can see pneumobilia on plain film with stone in RLQ

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42
Q

Most common site of obstruction in gallstone ileus?

A

Terminal ileum

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43
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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44
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.

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45
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

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46
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

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47
Q

Treatment for intraop CBD injury?

A
  • If <50% circumference - perform primary repair
  • all other cases - hepaticoj or choledochoj
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48
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
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49
Q

Treatment for anastamotic leaks following transplant or hepaticoj?

A

ERCP and stents

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50
Q

Treatment for sepsis following lap chole?

A

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

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51
Q

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

A

After lap chole

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52
Q

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

A

Ischemia (injury to R hepatic artery); can also be caused by chronic pancreatitis, stricture of biliary enteric anastomosis

53
Q

Diagnosis of CBD or hepatic duct stricture?

A

ERCP; US will show dilated ducts

54
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

55
Q

What causes hemobilia?

A

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

56
Q

Presentation of hemobilia?

A

UGI bleed, jaundice, RUQP

57
Q

Diagnosis of hemobilia? Treatment?

A
  • Start with resuscitation and ABCs
  • EGD is first test for UGIB
  • Angiogram is diagnostic and therapeutic w/ embolization
  • Operation if that fails
58
Q

What is the most common cancer of the biliary tract?

A

Gallbladder adenocarcinoma

59
Q

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

A

Liver

60
Q

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

A

90%

61
Q

Symptoms of gallbladder CA?

Where does it spread first? How do you know if it will? What do you do?

A
  • Painless jaundice 1st, then RUQ pain (could be cholangitis at this point). Chronically - weight loss, fatigue, loss of appetite.
  • Spreads lymphatically to cystic duct nodes first.
    • Any GB cancer past mucosa can spread.
    • Do liver bed excision.
    • N1 - portal and perihepatic
    • N2 - para-aortic, celiac
62
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
63
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.

64
Q

5-yr survival of gallbladder CA?

A

5%

65
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

66
Q

Symptoms of cholangiocarcinoma?

A

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

67
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
68
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

69
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
70
Q

Where are Klatskin tumors?

A

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

71
Q

Treatment for cholangiocarcinoma in upper 1/3? Middle 1/3? Lower 1/3? Locally advanced upper?

A
  • Upper: involving the confluence (hilar CCa) require duct resection and partial hepatectomy
  • Middle: bile duct resection w/ regional LADx and hepaticojejunostomy
  • Lower: Whipple (pancreaticoduodenectomy)
72
Q

5-yr survival for cholangio?

A

20%

73
Q

What % of choledochal cysts are extrahepatic?

A

90%

74
Q

What is the cancer risk with choledochal cysts?

A

15% (require resection)

75
Q

Symptoms of choledochal cyst?

A

Episodic pain, fever, jaundice, cholangitis

76
Q

Choledochal cyst presentation in infants?

A

Similar to biliary atresia

77
Q

Possible cause of choledochal cysts?

A

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

78
Q

Most common type of choledochal cyst?

A

Type I: saccular or fusiform dilation of extrahepatic ducts

79
Q

Treatment for choledochal cyst?

A

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

80
Q

What patients have primary sclerosing cholangitis?

A

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

81
Q

Symptoms of PSC?

A

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

82
Q

Does PSC get better after colon resection for UC?

A

NO

83
Q

Consequences and complications of PSC?

A

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

84
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

85
Q

Treatment for pruritus symptoms in PSC. Temporizing management? Definitive management?

A
  • Cholestyramine; though medication often has little effect.
  • Stenting can temporize.
  • Definitive treatment will be with a transplant.
  • Disease will recur in the transplant, but not usually enough to cause severe symptoms.
86
Q

Primary biliary cirrhosis occurs in what size ducts?

A

Medium-sized hepatic ducts

87
Q

Consequences of PBC?

A

Cholestasis –> cirrhosis –> portal HTN

88
Q

Symptoms of PBC?

A

Fatigue, pruritus, jaundice, xanthomas

89
Q

What type of antibodies are associated with PBC?

A

Antimitochondrial antibodies

90
Q

Cancer risk with PBC?

A

No increased risk of cancer

91
Q

Treatment for PBC?

A

Transplant

92
Q

What is Charcot’s triad?

A

RUQ pain, jaundice, fever - indicates cholangitis

93
Q

What is Reynold’s pentad

A

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

94
Q

Most common organisms in cholangitis?

A

E. coli and Klebsiella

95
Q

Late complications of cholangitis?

A

Stricture and hepatic abscess

96
Q

1 serious complication of cholangitis?

A

Renal failure; related to sepsis

97
Q

Most common etiology of cholangitis? Other causes?

A

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

98
Q

What is the cause of systemic bacteremia from cholangitis?

A

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

99
Q

Treatment for cholangitis?

A

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

100
Q

What is oriental cholangiohepatitis?

A

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

101
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

102
Q

What is adenomyomatosis?

A

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

103
Q

What is granular cell myoblastoma?

A

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

104
Q

What is cholesterolosis?

A

Speckled cholesterol deposits on GB wall

105
Q

What size GB polyp more likely to be malignant?

A
  • >1cm
  • most are cholesterol polyps w/o cancer potential
  • most are asymptomatic
  • tx: most get f/u US q6m x2yr; chole if…
    • sx and no other cause
    • 10 mm
    • PSC
    • associated gallstones
106
Q

What is delta bilirubin?

A

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

107
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

108
Q

What abx can cause gallbladder sludging and cholestatic jaundice?

A

Ceftriaxone

109
Q

What are indications for asymptomatic cholecystectomy?

A

Pts undergoing liver TXP, gastric bypass, or PNET resection

110
Q

How do you manage an abdominal abscess caused by a previously spilled gallbladder stone?

A

Laparoscopic drainage and FB removal

111
Q

How does splanchnic nerve stimulation affect bile flow?

A

decreases it (inhibitory to motor activity)

112
Q

Discuss bile leak s/p lap chole.

A
  • Psx: within 1 week, jaundice, elevated bilirubin; RUQ pain, fevers, chills
  • Etiology: inflammation dislodges clips
  • Dx: US or CT
  • Tx: perc drain of fluid, endoscopic biliary stent
    • re-eval in 6 wks: no resolution - MRCP/ERCP
      • find CBD injury, then repair once inflammation has resolved
    • septic shock and peritonitis: ex-lap and wide drainage, temporize
113
Q

What is the primary source of bilirubin in the body?

A

breakdown of RBCs (senescence vs hemolysis)

114
Q

Cholangiocarcinoma most common morphology?

Most favorable histology?

A
  • Nodular
  • Papillary
  • Usually 50-70y M w/ PSC, UC, biliary infection, choledochal cysts
115
Q

Describe enterohepatic circulation.

A
  • Bile salts synthesized from cholesterol in liver, where they are conjugated to either glycine or taurine to form the primary bile salts: cholic acid and chenodeoxycholic acid.
  • Once secreted into the bile, they pass into duodenum, are absorbed in small intestine (mostly terminal ileum).
  • The portal system returns the bile salts to the liver.
  • Extremely conservative: 95% of bile pool recycled.
  • Of ~2-4g into duodenum/day, ~0.6g makes it to the colon.
  • Colon bacteria form secondary bile salts: deoxycholate and lithocholate. A small amount is reabsorbed passively.
116
Q

What is the most common cause of a benign biliary stricture?

A

previous lap chole

117
Q

What is the Bismuth-Corlette classification for perihilar cholangiocarcinomas?

A
  • Type I tumors involve the common hepatic duct.
  • Type II tumors are at the hepatic bifurcation.
  • Type III tumors involve the secondary hepatic ducts on one side.
  • Type IV tumors involve the secondary hepatic ducts on both sides.
118
Q

What is the management of unresectable cholangiocarcinoma? What is the role of chemotherapy?

A

Palliative stent placement or bypass.

Chemotherapy does not help much and therefore has little role.

The only treatment that improves survival is surgical resection with adequate margins.

119
Q

What if gallbladder cancer involves the infundibulum? What happens to the resection?

A

must include CBD and hepaticojejunostomy

120
Q

Endoscopic retrograde cholangiopancreatography is performed and demonstrates a mass in the second portion of the duodenum at the ampulla of Vater.
A double-contrast upper gastrointestinal series reveals “soap bubble” or “paint brush” sign.

What is this?

A

small bowel villous adenoma

Approximately 25% of these villous and tubulovillous adenomas harbor malignancy

121
Q

Treatment of choice for high-risk patients with acute cholecystitis?

A

Percutaneous transhepatic cholecystostomy

122
Q

The diagnostic modality of choice in a patient with a known gallbladder polyp for reassessment of characteristics would be?

A

US

123
Q

How do you manage sphincter of Oddi dysfunction?

A
  • rule out other causes
  • if fulfills clinical criteria, and sx do not include abnormal LFTs and dilation of CBD, get manometry study
  • tx: endoscopic sphincterotomy
124
Q

How do you make the incision in choledochotomy?

A

Longitudinally, below the insertion of the cystic duct.

  • The blood supply to the extrahepatic bile duct runs along the duct at the 3-o’clock and 9-o’clock positions. A transverse incision would risk compromise of the blood supply to the bile duct.
  • The incision should be made in the common bile duct rather than the common hepatic duct to avoid postsurgical proximal bile duct stenosis that would require a more complex repair.
125
Q

Management of gallstone pancreatitis

A
  • resuscitation
  • RUQ US
  • manage choledocholithiasis/cholangitis if found
  • serial assessment until resolution of pain
  • cholecystectomy only once there is resolution of pancreatitis
126
Q

Relative contraindications to laparoscopic transcystic common bile duct exploration

A
  • stones above the cystic duct
  • small cystic duct (<3 mm)
  • gallstones greater than 6-8 mm
  • >8 gallstones in the duct
127
Q

ultrasound findings best describe cholesterolosis of the gallbladder

A

Multiple, hyperechoic, pedunculated, non-shadowing

128
Q

When does a gallbladder adenoma begin to increase risk for cancer?

A

Follows adenoma-carcinoma sequence (like colon cancer). Risk increases at 10 mm.

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