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06 - absite > Chapter 32: Gallbladder > Flashcards

Chapter 32: Gallbladder Flashcards

1
Q

Where does gallbladder lie?

A

Beneath segments 4 and 5

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2
Q

Where does gallbladder lie?

A

Beneath segments 4 and 5

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3
Q

What is the cystic artery a branch of?

A

The right hepatic artery

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4
Q

Where is the cystic artery found?

A

Triangle of Calot

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5
Q

Where is the triangle of calot?

A

Lateral - cystic duct
Medial - Common bile duct
Superior - liver

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6
Q

What is the longitudinal blood supply of the hepatic and common bile duct?

A

Right hepatic (lateral) and retroduodenal branches of the gastroduodenal artery (medial_

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7
Q

Where do the cystic veins drains?

A

Right branch of the portal vein

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8
Q

Where are lymphatics in relation to the common bile duct?

A

Lymphatics are on the right side of the common bile duct

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9
Q

Where do parasympathetic fibers come from to gallbladder?

A

Parasympathetic fibers come from the left (anterior) trunk of the vagus.

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10
Q

Where do sympathetic fibers come from?

A

T7-T10 (splanchnic and celiac ganglions)

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11
Q

Mucosa for gallbladder

A

Gallbladder has no submucosa; mucosa is columnar epithelium

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12
Q

Peristalsis of common bile duct and common hepatic duct

A

Do not have peristalsis

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13
Q

How does the gallbladder fill?

A

Gallbladder normally fills by contraction of sphincter of Oddi at the ampulla of Vater

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14
Q

Medication: contracts the sphincter of Oddi

A

Morphine

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15
Q

Medication: relaxes the sphincter of Oddi

A

Glucagon

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16
Q

Normal size: common bile duct (CBD)

A
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17
Q

Normal size: gallbladder wall

A
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18
Q

What happens to total bile salt pools after cholecystectomy?

A

Total bile salt pools decrease

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19
Q

What happens to total bile salt pools after cholecystectomy?

A

Total bile salt pools decrease

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20
Q

What is the cystic artery a branch of?

A

The right hepatic artery

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21
Q

Biliary ducts that can leak after a cholecystectomy, lie in the gallbladder fossa

A

Ducts of Luschka

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22
Q

Where is the triangle of calot?

A

Lateral - cystic duct
Medial - Common bile duct
Superior - liver

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23
Q

What is the longitudinal blood supply of the hepatic and common bile duct?

A

Right hepatic (lateral) and retroduodenal branches of the gastroduodenal artery (medial_

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24
Q

Where do the cystic veins drains?

A

Right branch of the portal vein

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25
Q

Where are lymphatics in relation to the common bile duct?

A

Lymphatics are on the right side of the common bile duct

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26
Q

Where do parasympathetic fibers come from to gallbladder?

A

Parasympathetic fibers come from the left (anterior) trunk of the vagus.

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27
Q

Where do sympathetic fibers come from?

A

T7-T10 (splanchnic and celiac ganglions)

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28
Q

Mucosa for gallbladder

A

Gallbladder has no submucosa; mucosa is columnar epithelium

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29
Q

Peristalsis of common bile duct and common hepatic duct

A

Do not have peristalsis

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30
Q

How does the gallbladder fill?

A

Gallbladder normally fills by contraction of sphincter of Oddi at the ampulla of Vater

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31
Q

Medication: contracts the sphincter of Oddi

A

Morphine

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32
Q

Medication: relaxes the sphincter of Oddi

A

Glucagon

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33
Q

Normal size: common bile duct (CBD)

A
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34
Q

Normal size: gallbladder wall

A
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35
Q

Rate limiting step in cholesterol synthesis

A

HMG CoA reductase

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36
Q

What happens to total bile salt pools after cholecystectomy?

A

Total bile salt pools decrease

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37
Q

Where are the highest concentration of CCK and secretin cells?

A

Duodenum

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38
Q

Epithelial invaginations in the gallbladder wall; formed from increased gallbladder pressure

A

Rokitansky-Aschoff sinuses

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39
Q

Biliary ducts that can leak after a cholecystectomy, lie in the gallbladder fossa

A

Ducts of Luschka

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40
Q

Increases bile excretion

A

CCK, secretin, and vagal input

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41
Q

Decreases bile excretion

A

Somatostatin, sympathetic stimulation

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42
Q

What causes gallbladder contraction?

A

CCK causes constant, steady, tonic contraction

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43
Q

Essential functions of bile

A

Fat-soluble vitamin absorption, essential fat absorption, bilirubin and cholesterol excretion

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44
Q

How does gallbladder form concentrated bile?

A

Active resorption of NaCl and water

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45
Q

Where does active resorption of conjugated bile salts occur?

A

Terminal ileum (50%)

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46
Q

Where does passive resorption of non conjugated bile salts occur?

A

Small intestine (45%) and colon (5%)

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47
Q

Time: postprandial gallbladder emptying

A

Maximum at 2 hours (80%)

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48
Q

What secretes bile?

A

Hepatocytes (80%) and bile canalicular cells (20%)

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49
Q

What causes color of bile?

A

Mostly due to conjugated bilirubin

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50
Q

Breakdown product of conjugated bilirubin in gut; gives stool brown color

A

Stercobilin

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51
Q

Conjugated bilirubin is broken down in the gut and reabsorbed; gets converted to urobilinogen and eventually urobilin, which is released in the urine (yellow color)

A

Urobilinogen

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52
Q

Pathway of bile salts (acids) formation

A

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

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53
Q

Rate limiting step in cholesterol synthesis

A

HMG CoA reductase

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54
Q

occurs in 10% of the population; vast majority are asymptomatic
- only 10% of gallstones are radiopague

A

gallstones

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55
Q

What causes cholesterol stones?

A

Stasis, calcium nucleation, and increased water reabsorption form gallbladder. Also caused by decreased lecithin and bile salts

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56
Q
  • found almost exclusively in the gallbladder

- most common type of stone found in the united state (75%)

A

Nonpigmented stones - cholesterol stones

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57
Q
  • most common type of stone found in the united states

- most common type of stone found worldwide

A
  • US: nonpigmented (cholesterol)

- World: pigmented (calcium bilirubinate, black, brown)

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58
Q

Caused by solubilization of unconjugated bilirubin with precipitation

A

Calcium bilirubinate stones (pigmented stones)

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59
Q

Do not work on pigmented stones

A

Dissolution agents (monoctanoin)

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60
Q

What causes black stones?

A

Hemolytic disorders, cirrhosis, ileal resection (loss of bile salts), chronic TPN

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61
Q

Factors for development of black stones

A

Increased bilirubin load.
Decreased hepatic function.
Bile stasis -> all get calcium bilirubinate stones.

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62
Q

Can be caused by hemolytic disorders, cirrhosis, ileal resection (loss of bile salts), chronic TPN.

  • Almost always form in gallbladder.
  • Tx: cholecystectomy if symptomatic
A

Black stones (pigmented stones)

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63
Q
  • primary CBD stones, formed in ducts, Asians

- Infection causing deconjugation of bilirbuin

A

Brown stones

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64
Q

Most common organism causing brown stones

A

E coli

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65
Q

How does E coli cause brown stones?

A

Produces beta-glucuronidase, which deconjugates bilirubin with formation of calcium bilirubinate

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66
Q

What do you need to check for with brown stones?

A

Ampullary stenosis, duodenal diverticula, abnormal sphincter of Oddi

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67
Q

Where are brown stones most commonly formed?

A

Most commonly form in the bile ducts (are primary common bile duct stones)

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68
Q

Tx: brown stones

A

Almost all patients with primary stones need a biliary drainage procedure - sphincteroplasty (90% successful)

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69
Q

What are considered secondary common bile duct stones?

A

Cholesterol stones and black stones found in the CBD

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70
Q
  • Primary common bile duct stones

- Secondary common bile duct stones

A
  • Primary: brown stones

- Secondary: cholesterol and black stones

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71
Q
  • Caused by obstruction of the cystic duct by a gallstone
  • Results in gallbladder wall distention and wall inflammation
  • RUQ pain, referred pain to the right shoulder and scapula, n/v, loss of appetite.
  • attacks frequently occur after a fatty meal; pain is persistent (unlike biliary colic)
A

Cholecystitis

72
Q

Patient resists deep inspiration with deep palpation to the RUQ secondary to pain

A

Murphy’s sign

73
Q

Lab tests likely to be elevated in cholecystitits

A

Alkaline phosphatase and WBCs

74
Q

Associated with frank purulence in the gallbladder -> can be associated with sepsis and shock

A

Suppurative cholecystitis

75
Q

Most common organisms in cholecystitis

A

E. coli (#1), Klebsiella, Enterococcus

76
Q

Risk factors for stone development

A

Age > 40, female, obesity, pregnancy, rapid weight loss, vagotomy, TPN (pigmented stones), ileal resection (pigmented stones)

77
Q

Is ultrasound effective in cholecystitis?

A

95% sensitive for picking up stones.

- Hyperechoic focus, posterior shadowing, movement of focus with changes in position.

78
Q

Best initial evaluation test for jaundice of RUQ pain.

A

Ultrasound

79
Q

What are ultrasound findings suggestive of acute cholecystitis?

A

Gallstones, gall bladder wall thickening (>4mm), pericholecystic fluid

80
Q

Size of common bile duct suggesting CBD stone and obstruction

A

> 8 mm

81
Q

Technetium taken up by liver and excreted in the biliary tract

A

HIDA scan

82
Q

Most sensitive test for cholecystitis (also uses HIDA)

A

CCK-CS test (cholecystokinin cholescntigraphy)

83
Q

Indications for cholecystectomy after CCK-CS test

A
  • If gallbladder not seen (the cystic duct likely has a stone in it)
  • Takes > 60 minutes to empty (chronic cholecystitis)
  • Ejection fraction
84
Q

Indications for immediate ERCP

A

Signs that a common bile duct stone is present -> jaundice, cholangitis, US shows stones in CBD

85
Q

Indications for pre-op ERCP

A

Any of the following needs to be persistently high for > 24 hours to justify pre-op ERCP

  • AST or ALT ( > 200)
  • Bilirubin > 4
  • Amylase or lipase (> 1000)
86
Q

How many patients undergoing cholecystectomy will have a retained CBD stone?

A
87
Q

Treatment for cholecystitis

A

Cholecystectomy; cholecystostomy tube can be placed in patients who are very ill and cannot tolerate surgery

88
Q

Best treatment for late common bile duct stone

A

ERCP. Spincterotomy allows for removal of stone.

89
Q

Risks: ERCP

A

bleeding, pancreatitis, perforation

90
Q

Transient cystic duct obstruction caused by passage of a gallstone

A

Biliary colic; resolves within 4-6 hours

91
Q

When does air in the biliary system occur?

A

Most commonly occurs with previous ERCP and sphincterotomy

- Can also occur with cholangitis or erosion of the biliary system into the duodenum (i.e. gallstone ileus)

92
Q

How does bacterial infection of bile occur?

A

Dissemination form portal system is the most common route (not retrograde through sphincter of Oddi)

93
Q

Highest incidence of positive bile cultures

A

Occurs with postoperative strictures (usually E. coli, often polymicrobial)

94
Q

thickened wall, RUQ pain, increased WBCs, no stones

A

Acalculous cholecystitis

95
Q

What causes acalculous cholecystitis?

A

Severe burns, prolonged TPN, trauma, or major surgery

96
Q

Primary pathology: acalculous cholecystitis

A 
Bile stasis (narcotic fasting), leading to distention and ischemia
- Also have increased viscosity secondary to dehydration, ileus, transfusions
97
Q

Ultrasound/HIDA: acalculous cholecystitis

A
  • US: Sludge, gallbladder wall thickening, and pericholecystic fluid
  • HIDA: positive
98
Q

Tx: acalculous cholecystitis

A

Cholecystectomy; percutaneous drainage if patient too unstable

99
Q
  • Gas in the gallbladder wall -> can see on plain film
  • Symptoms: severe, rapid-onset abdominal pina, nausea, vomiting, and sepsis
  • perforation more common in these patients
A

Emphysematous gallbladder disease

100
Q

Patient population associated with emphysematous gallbladder disease

A

Increased in diabetes; usually secondary to Clostridium perfringens

101
Q

Tx: emphysematous gallbladder disease

A

Emergent cholecystectomy; percutaneous drainage if patient is too unstable

102
Q

Fistula between gallbladder and duodenum that releases stone, causing small bowel obstruction; elderly.
- can see pneumobilia (air in the biliary system) on plain film

A

Gallstone ileus

103
Q

Most common site of obstruction in gallstone ileus

A

Terminal ileum

104
Q

Tx: gallstone ileus

A

Remove stone through enterotomy proximal to obstruction

- perform cholecystectomy and fistula resection if patient can tolerate it (if old and frail, just leave the fistula)

105
Q

When do common bile duct injuries most commonly occur?

A

After laparoscopic cholecystectomy

106
Q

Management of intraoperative CBD injury

A

If

107
Q

Persistent nausea and vomiting or jaundice following lap chole..

A

Get ultrasound to look for fluid collection

108
Q

Ultrasound shows fluid collection after lap chole

A

May be bile leak -> percutaneous drain into the collection.

  • bilious fluid: get ERCP -> sphincterotomy & stent if due to cystic duct remnant leak, small injuries to hepatic or CBD, leak of DOL
  • Large lesions: hepaticojejunostomy or choledochojejunostomy
109
Q

N/V/jaundice s/p lap chole:

- US shows fluid collection with dilated hepatic ducts

A

Likely have a completely transected common bile duct (PTC tube initially, then hepaticojejunostomy or choledochojejunostomy)
- Early symptoms (7d): hepaticojejunostomy 6-8wks after injury (tissue too friably for surgery after 7 days)

110
Q

Management: sepsis following lap chole

A

Fluid resuscitation and stabilize. May be due to complete transection of the CBD and cholangitis -> get U/S to look for dilated intrahepatic ducts or fluid collections

111
Q

Management of anastomotic leaks following transplantation or hepaticojejunostomy

A

Usually handled with percutaneous drainage of fluid collection followed by ERCP with temporary stent (leak will heal)

112
Q

Lap chole: most important cause of late postoperative bile duct strictures

A

Ischemia

113
Q

Causes of bile duct strictures

A

Ischemia following lap chole, chronic pancreatitis, gallbladder CA, bile duct CA

114
Q

Symptoms: bile duct strictures

A

Sepsis, cholangitis, jaundice

115
Q

Dx: bile duct strictures without a history of pancreatitis or biliary surgery

A

CA until proven otherwise

116
Q

Dx: Bile duct strictures

A

MRCP defines anatomy, look for mass -> if CA not rule out with MRCP, need ERCP with brush biopsies

117
Q

Tx: bile duct strictures

A

If due to ischemia or chronic pancreatitis -> choledochojejunostomy (best long-term solution).
- If due to cancer, follow appropriate workup

118
Q

Pathophys: hemobilia

A

Fistula between bile duct and hepatic arterial system (most commonly)

119
Q

UGIB, jaundice, RUQ pain

A

Hemobilia

120
Q

What is the insult causing hemobilia?

A

Trauma or percutaneous instrumentation to liver (eg, PTC tube)

121
Q

Dx: hemobilia

A

Angiogram

122
Q

Tx: hemobilia

A

Angioembolization; operation if that fails.

123
Q

Rare, although MC CA of the biliary tract

A

Gallbladder adenocarcinoma

- Four times more common than bile duct CA; most have stones

124
Q

Most common site of metastasis of gallbladder adenocarcinoma

A

liver

125
Q

Risk of gallbladder CA in porcelain gallbladder

A

15%

126
Q

Tx: porcelain gallbladder

A

Cholecystectomy

127
Q

How does gallbladder adenocarcinoma spread?

A

1st spreads to segments 4 and 5; 1st nodes are the cystic duct nodes (right side)

128
Q

Symptoms: jaundice 1st (bile duct invasion with obstruction) then RUQ pain

A

Gallbladder adenocarcinoma

129
Q

Tx: gallbladder adenocarcinoma

A

If muscle not involved -> cholecystectomy sufficient

  • If in muscle but not beyond -> need wedge resection of segments 4b and 5
  • if beyond muscle and still resectable -> need formal resection of segments IVb and V
130
Q

Why is the laparoscopic approach contraindicated for gallbladder cancer?

A

High incidence of tumor implants in trocar sites when discovered after laparoscopic cholecystectomy

131
Q

Overall 5 year survival in bladder adenocarcinoma

A

5%

132
Q
  • Occurs in elderly; males
  • risk factors: C sinensis infection, ulcerative colitis, choledochal cysts, primary sclerosing cholangitis, chronic bile duct infection
A

Bile duct cancer (cholangiocarcinoma)

133
Q

Symptoms:
early - painless jaundice;
late - weight loss, pruritus

A

Bile duct cancer (cholangiocarcioma)

134
Q

Persistent increase in bilirubin and alkaline phosphatase

  • Dx: MRCP (defines anatomy, looks for mass)
  • Invades contiguous structures early
A

Bile duct cancer (cholangiocarcinoma)

135
Q

What is highly suggestive of bile duct cancer?

A

Discovery of a focal bile duct stenosis in patients without a history of biliary surgery or pancreatitis

136
Q

Tx: bile duct cancer (cholangiocarcinoma)

A
  • Upper 1/3 (Klatskin tumors): can try lobectomy and stenting of contralateral bile duct if localized to either the right or left lobes
  • Middle 1/3: hepaticojejunostomy
  • Lower 1/3: Whipple
137
Q

Treatment: unresectable bile duct cancer (cholangiocarcinoma)

A

Palliative stenting for unresectable disease

138
Q

5-year survival rate bile duct cancer (cholangiocarcinoma)

A

20%

139
Q
  • Female gender; Asians; 90% are extrahepatic; 15% CA risk (cholangiocarcinoma)
  • older patients have episodic pain, fever, jaundice, cholangitis
A

Choledochal cysts

140
Q

How do choledochal cysts present in children?

A

Infants can have symptoms similar to biliary atresia

141
Q

Most common types of choledochal cysts

A

Most are type I: fusiform or saccular dilatation of extra hepatic ducts (very dilated)

142
Q

What causes choledochal cysts?

A

Caused by abnormal reflux of pancreatic enzymes during uterine development

143
Q

Tx: choledochal cysts

A

Cyst excision with hepaticojejunostomy and cholecystectomy usual

144
Q

Choledochal cysts: partially intrahepatic

A

Type 4 cysts

145
Q

Choledochal cysts: totally intrahepatic

A

Type 5 (Caroli’s disease)

146
Q

Management: type 4 and type 5 choledochal cysts

A

Will need partial liver resection or liver TXP

147
Q
  • Men in 4th-5th decade
  • Can be associated with ulcerative colitis, pancreatitis, diabetes
  • Symptoms: jaundice, fatigue, pruritus (from bile acids), weight loss, RUQ pain
A

Primary sclerosing cholangitis

148
Q

Pathophysiology: primary sclerosing cholangitis

A
  • Get multiple strictures throughout the hepatic ducts

- Leads to portal HTN and hepatic failure (progressive fibrosis of intrahepatic and extra hepatic ducts)

149
Q

Relationship of primary sclerosing cholangitis to colon resection for ulcerative colitis

A

Does not get better after colon resection for ulcerative colitis

150
Q

Complications: primary sclerosing cholangitis

A

Cirrhosis, cholangiocarcinoma

151
Q

Tx: primary sclerosing cholangitis

A
  • Liver TXP needed long term for most; PTC tube drainage, choledochojejunostomy or balloon dilatation of dominant strictures may provide symptomatic relief
  • Cholestyramine: can decrease pruritus symptoms (decrease bile acids)
  • UDCA (ursodeoxycholic acid) - can decrease symptoms (decrease bile acids) and improve liver enzymes
152
Q
  • women; medium-sized hepatic ducts
  • cholestasis -> cirrhosis -> portal hypertension
  • Symptoms: jaundice, fatigue, pruritus, xanthomas
A

Primary biliary cirrhosis

153
Q

Antibodies for primary biliary cirrhosis

A

Antimitochrondrial antibiodies

154
Q

Risk for cancer in primary sclerosing cholangitis

A

No increased risk for cancer

155
Q

Tx: primary biliary cirrhosis

A

Liver TXP

156
Q
  • usually caused by obstruction of the bile duct (most commonly due to gallstones)
  • can also be caused by indwelling tubes (Eg PTC tube)
A

Cholangitis

157
Q

RUQ pain.
Fever.
Jaundice.

A

Charcot’s triad - cholangitis

158
Q

Charcot’s triad plus mental status changes and shock (suggests sepsis)

A

Reynold’s pentad - cholangitis

159
Q

MC organisms causing cholangitis

A

E. coli (#1) and Klebsiella

160
Q

What causes colovenous reflux?

A

> 200 mmHg pressure -> systemic bacteremia

161
Q

Dx: cholangitis

A

Increased AST/ALT, bilirubin, alkaline phosphatase, and WBCs.
- US: dilated CBD (>8 mm, > 10mm after cholecystectomy) if due to obstruction of the biliary system

162
Q

Late complications of cholangitis

A

Stricture and hepatic abscess

163
Q

1 serious complication cholangitis; related to sepsis

A

Renal failure

164
Q

Causes of cholangitis

A

Infection, biliary strictures, neoplasm, choledochal cysts, duodenal diverticula

165
Q

Tx: cholangitis

A

Fluid resuscitation and antibiotics intially.

  • Emergent ERCP with sphincterotomy and stone extraction; if ERCP fails, place PTC tube to decompress the biliary system.
  • If the patient has cholangitis due to infected PTC tube, change the PTC tube
166
Q

Cause of shock following lap chole: early (1st 24 hours)

A

Hemorrhagic shock from clip that fell off cystic artery

167
Q

Cause of shock following lap chole: late (after 1st 24 hours)

A

Septic shock from accidental clip on CBD with subsequent cholangitis

168
Q

Thickened nodule of mucosa and muscle associated with Rokitansky-Aschoff sinus

  • Not premalignant; does not cause stones, can cause RUQ pain
  • Tx: cholecystectomy
A

Adenomyomatosis

169
Q

Benign neuroectoderm tumor of gallbladder

  • Can occur in biliary tract with signs of cholecystitis
  • Tx: cholecystectomy
A

Granular cell myoblastoma

170
Q

Speckled cholesterol deposits on the gallbladder wall

A

Cholesterolosis

171
Q

if > 1 cm, need to worry about malignancy

  • polyps in patients > 60 years more likely malignant
  • TX: cholecystectomy
A

Gallbladder polyps

172
Q

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

A

Delta bilirubin

173
Q

Compression of the common hepatic duct

- Tx: cholecystectomy; may need hepaticojejunostomy for hepatic duct stricture

A

Mirrizzi syndrome

174
Q

What causes Mirizzi syndrome (compression of the common hepatic duct)?

A

1) stone in the gallbladder infundibulum
2) inflammation arising from the gallbladder or cystic duct extending to the contiguous hepatic duct, causes common hepatic duct stricture

175
Q

Antibiotic: can cause gallbladder slugging and cholestatic jaundice

A

Ceftriaxone

176
Q

Indications for asymptomatic cholecystectomy

A

In patients undergoing liver TXP or gastric bypass procedure (if stones are present)

06 - absite (44 decks)

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