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Appendix > Gallbladder > Flashcards

Gallbladder Flashcards

1
Q

Actions of cholecystokinin?

A

inhibits gastric motility
increases pyloric contraction

relaxes sphincter of Oddi
stimulates GB contraction

stimulates pancreatic secretions

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2
Q

Where is CCK produced?

A

I cells of duodenum and jejunum

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3
Q

I cells of duodenum and jejunum produce what?

A

CCK

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4
Q

This hormone produced by enteroendocrine cells, specifically I cells of duodenum and jejunum;

A

CCK

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5
Q

This hormone relaxes the Sphincter of Oddi, stimulates GB contraction, increases pancreatic secretion release, and inhibits gastric emptying:

A

CCK

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6
Q

How is the GB different from rest of GI tract?

A

lacks muscularis mucosa and submucosa

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7
Q

Cystic artery is a branch off of?

A

right hepatic artery (>90% of time)

** cystic artery usually branches into anterior and posterior divisions when it reaches neck of GB

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8
Q

Triangle of Calot?

A

cystic duct
common hepatic duct
inferior edge of liver

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9
Q

The CBD enters the 2nd portion of the duodenum thru a muscularis structure called the?

A

sphincter of oddi

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10
Q

The right and left hepatic ducts join to form the common hepatic duct, which is usually 1-4 cm long, how wide is?

A

4mm

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11
Q

Spiral valves of Heister?

A

mucosal folds of cystic duct near the GB neck

can make cannulation of cystic duct difficult

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12
Q

How long and wide is the CBD?

A

5-10 mm wide

7-10 cm long

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13
Q

Location of CBD in portal triad?

A

to right of hepatic artery

anterior to portal vein

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14
Q

The union of the CBD and pancreatic duct has three configurations;

A

70% of pts–> they join together outside the duodenum and then pierce the duodenum as a single tube

20% of pts–> they join together within the duodenal wall

10% of pts–> they enter duodenum as separate tubes

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15
Q

Function of sphincter of oddi?

A

circular smooth muscle

controls bile flow

sometimes controls pancreatic juice flow

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16
Q

BLood supply to the bile ducts derived from what arteries?

A

gastroduodenal
right hepatic arteries

**major trunks run at the 3 and 9 oclock positions

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17
Q

Classic description of the extra-hepatic biliary tree is found in what % of pts?

A

1/3

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18
Q

What % of pts have the classic extra-hepatic biliary tree anatomy?

A

33%

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19
Q

Rare congenital GB variants?

A

absent GB–> rare, 0.03% of cases

duplicated GB–> 1/4000 cases

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20
Q

What are Luschka ducts?

A

small ducts that drain directly from liver into GB

if missed can cause biloma leak

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21
Q

Cystic artery comes off right hepatic artery how often?

A

80-90% of time

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22
Q

20% of cases, right hepatic artery comes off of what?

A

SMA

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23
Q

How much bile does the liver produce daily?

A

500-1000 cc

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24
Q

Vagal effect on bile secretion?

A

stimulates bile release

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25
Q

Composition of bile?

A 
water
electrolytes
bile salts
cholesterol
lecithins 
bile pigments
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26
Q

pH of hepatic bile?

A

usually neutral or slightly alkaline

protein diet can make it more acidic

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27
Q

What are the two main bile salts and what do they do?

A

cholate

chenodeoxycholate

**made in liver from cholesterol

**conjugated in liver with taurine and glycine and act within the bile as anions

**bile acids excreted into bile by hepatocytes and aid in fat digestion

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28
Q

In intestines, 80% of bile acids absorbed where?

What happens to remaining 20% of bile acids?

A

terminal ileum

** rest are deconjungated by gut bacteria forming secondary bile acids; deoxycholate, lithocholate

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29
Q

What;s entero-hepatic circulation?

A

reabsorbing about 95% of excreted bile back into liver

** 5% excreted in stool

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30
Q

Principal lipids found in bile?

A

cholesterol

phospholipids

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31
Q

Why is bile green?

A

presence of bilirubin diglucuronide (metabolic product of bilirubin breakdown)

100x more concentrated than in plasma

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32
Q

Main function of GB?

A

store and concentrate hepatic bile and deliver it to duodenum after a meal

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33
Q

What happens to bile once its in GB?

A

in fasting state, 80% of bile is stored in GB

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34
Q

How does the GB handle storing so much bile?

A

it has great absorptive capacity

GB mucosa has greatest absorptive capacity per unit area of any structure in the body

rapidly absorbs Na, Cl, water and concentrates bile 10 fold

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35
Q

What do epithelial cells of the GB secrete into Gb lumen?

A

H ions–> decreased bile pH, which promotes Ca solubility

glycoproteins –> prevent lytic action of bile on GB lumen

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36
Q

Whats white bile?

A

glycoproteins released from GB infundibulum glands

seen in hydrops of GB

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37
Q

What hormone stimulates GB emptying?

A

CCK

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38
Q

Where is CCK made?

A

CCK made endogenously by duodenal mucosa in response to a meal

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39
Q

What happens to Gb when stimulated by a meal?

A

empties 50-70% of its contents within 30-40 mins

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40
Q

Neural pathways that stimulate and inhibit the GB?

A

vagal stimulation—> stimulates GB contraction, emptying

SNS splanchnic stimulation–> inhibits GB contraction

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41
Q

What stimulates CCK release from duodenum?

A

acids, fats, amino acids in duodenum

CCK half life is 2-3 mins

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42
Q

Actions of CCK?

A

stimulates GB contraction

relaxes sphincter of Oddi

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43
Q

What happens to pts GB after vagotomies?

A

GB gets no vagal stimulation, size and volume of Gb increase

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44
Q

What does VIP do to GB?

A

inhibits contraction

relaxes GB

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45
Q

What does somatistatins do to GB ?

A

inhibit contraction

**pts with somatistatinomas tend to form gallstones due to bile stasis

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46
Q

Spontaneous motility of sphincter of oddi is regulated by what cells?

A

interstitial cells of Cajal

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47
Q

Relationship of sphincter of oddi in fasting state and in response to a meal?

A

fasting state; sphincter contracted, GB fills via retrograde movement

meal; sphincter relaxed, GB flows out from GB

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48
Q

Cholestasis, or obstruction of bile flow is characterized by what elevated markers?

A 
elevated bilirubin (conjugated form)
elevated ALK
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49
Q

In pts suspected of having biliary etiology what test ordered first?

A

US

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50
Q

Sensitivity and specificity of US to identify gallstones?

A

> 90%

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51
Q

What is the specificity and sensitivity of US to identify gallstones?

A

> 90%

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52
Q

Why do stones produce an acoustic shadow on US?

A

they are acoustically dense structures

they reflect US waves back to the US transducer

they block passage of sounds waves behind them

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53
Q

How does a HIDA Scan work?

A

technitium labeled dimethyl iminodiacetic acid is injected IV

cleared by Kupffer cells in the liver–> excreted in bile

uptake by liver seen in 10 mins

uptake by GB and bile ducts seen in 60 mins

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54
Q

Sensitivity and specificity of diagnosis acute cholecystitis with HIDA scan?

A

> 95%

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55
Q

False positives with HIDA seen in what pt populations?

A

critically ill pts

pts on TPN

pts with bile stasis

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56
Q

What are two complications of ERCP?

A

cholangitis

pancreatitis

(occur in 5% of pts)

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57
Q

What are some risk factors for gallstone development?

A 
obesity
pregnancy
diet
Crohn's dx
hemoglobinopathies
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58
Q

Who is more prone to developing gallstones? Men v Women?

A

women

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59
Q

What % of pts with gallstones become symptomatic with biliary colic every year?

A

3%

60
Q

What is the only absolute indication for prophylactic cholecystectomy?

A

porcellain gallbladder; wall of GB gets calcified

premalignant entity

61
Q

What are the two types of stone we have?

A

cholesterol vs pigment stones (black or brown)

62
Q

In western countries what types of stones are more common, cholesterol vs pigment stones?

A

cholesterol stones (80%)

***in asian countries pigment stones more common

63
Q

How do cholesterol stones form in the GB?

A

bile is super-saturated with cholesterol

64
Q

What are pigment stones pigmented?

A

presence of calcium bilirubinate

65
Q

Black gallstones are a result of what type of disorders?

A

usually due to hereditary disorders

66
Q

What causes formation of brown gallstones?

A

form in the GB or bile ducts usually secondary to infection and bile stasis

67
Q

In Asian countries, brown stones form as a result of?

A

parasitic infection of ducts

68
Q

What is hydrops of the GB?

A

when you have an impacted stoned without acute cholecystitis

the bile gets absorbed but the GB epithelium still makes mucus, and the GB gets distended with mucinous material

69
Q

Tx for hydrops of GB?

A

early cholecystectomy recommended

70
Q

What is chronic cholecystitis?

A

often called biliary colic

pts develop recurrent attacks of pain when a stone blocks cystic duct; causing increased wall tension in GB wall

71
Q

What are Aschoff-Rokitansky sinuses?

A

in chronic cholecystitis, sometimes the mucosa gets atrophied and we get protrusion of epithelium into muscle layer

72
Q

Whats a strawberry gallbladder?

A

seen in cholesterolosis, where cholesterol builds up in side macrophages in GB mucosa

73
Q

Why do we offer diabetics with symptomatic gallstones prompt surgery?

A

more prone to developing acute cholecystitis

often more severe

74
Q

Pregnant pts with symptomatic gallstones who can’t be managed with diet modifications can undergo cholecystectomy when?

A

2nd trimester

75
Q

What causes acute cholecystitis?

A

90-90% of time due to gallstones

76
Q

What % of cases of acute cholecystitis due to a tumor blocking cystic duct?

A

<1%

77
Q

What is an emphysematous GB?

A

in acute cholecystitis you can get a secondary bacterial infection

gas may be seen in GB lumen and in GB wall on imaging

78
Q

What is an acute gangrenous cholecystitis?

A

GB remains obstructed

a secondary bacterial infection starts

can get an abscess, empyema form within the GB

79
Q

Difference in clinical presentation of acute cholecystitis vs chronic cholecystitis?

A

acute chole–> pain is often un-remitting, lasting for days

80
Q

Mirizzi syndrome?

A

impacted stone in infundibulum of GB that blocks the common bile duct

81
Q

In what two pt populations do we see acute cholecystitis having a subtle presentation resulting in delay in diagnosis?

A

diabetics + elederly

  • *higher risk of complications
  • *morbidity is 10-fold higher
82
Q

What is a + HIDA scan?

A

lack of filling of Gb after 4 hr

83
Q

Antibiotics in acute cholecystitis should cover what bugs?

A

gram negative aerobes and anaerobes

  • *2nd gen cephalosporin
    • 3rd gen cephalosporin + flagyl
84
Q

What % of pts with gallstones also have choledocholithiasis?

A

6-12%

***in western cultures most CBD stones are stones formed in the GB that pass down into the CBD (termed secondary CBD stones)

85
Q

Where do we see primary CBD stones primarily?

A

in Western countries where we have bile stasis and parasitic infections

86
Q

What % of pts with CBD stones have normal liver chemsitries?

A

1/3

87
Q

Gold standard to diagnose CBD stones?

A

ERCP

also therapeutic

88
Q

How long does it take for a T-tube to mature?

A

2 -4 weeks

89
Q

Is bile sterile?

A

hepatic bile is sterile

bile in bile ducts is kept sterile by constant bile flow and Ig in bile

**mechanical hinderance of bile flow facilitates bacterial contamination

90
Q

What is needed to develop ascending cholangitis?

A

biliary obstruction (gallstones most commonly) + bacterial contamination

91
Q

Common bacteria found in bile in pts with cholangitis?

A

E.coli

klebsiella

strept

bactroides

92
Q

Most common presentation of cholangitis is?

A

fever
RUQ
jaundice

93
Q

Charcot’s tried of cholangitis?

A

fever
RUQ
jaundice

94
Q

Raynauds pentad of cholangitis?

A

septic shock
AMS

fever
RUQ
jaundice

95
Q

Tx for cholangitis??

A

IVF + abx

surgical decompression via PCT, ERCP or emergent surgery with t-tube

96
Q

Mortality of acute cholangitis?

A

5%

97
Q

Absolute contraindications for laparoscopic cholecystectomy?

A

uncontrolled coagulopathy and end-stage liver dx

98
Q

What is the conversion rate from laparoscopic to open cholecystectomies in elective settings vs emergent bassi?

A

elective—> 5 % conversion rate

emergent—> 10-30% conversion to open rate

99
Q

Mortality rate of laparoscopic cholecystectomy is?

A

0.1%

100
Q

Compared to open cholecystectomy, lap chole is associated with higher rates of ?

A

damage to bile ducts

101
Q

What % of pts with gallstone pancreatitis who do not have elective cholecystectomy on first admission develop gallstone pancreatitis again?

A

25%

102
Q

Gold standard for diagnosis CBD stones?

A

endoscopic cholnagiography

103
Q

If a choledochotomy is performed, what do we leave in place?

A

T-tubule

104
Q

Before removing a T-tubule what do we do first?

A

perform a T-tube cholangiogram

if retained stones present, can be removed endoscopically or via T-tube tract once it has matured (2-4 weeks)

105
Q

If CBD stones are small, they can sometimes be flushed down the duct into the duodenum with irrigation after the sphincter of oddi is relaxed with?

A

glucagon

106
Q

If irrigation of CBd stones with flushing and glucagon is not successful, what do we do?

A

can pass a balloon catheter via cystic duct down to CBD and inflated to retrieve CBD stones

107
Q

If stones cannot be cleared from CBD or when duct is very dilated, (>1.5 cm), what do we do?

A

choledocho drainage procedure

choledochoduodenostomy –>2nd part of duodenum mobilized and sutured side to side with CBD

choledochojejunostomy–> bringing 45 cm of jejunum and anstomosing is end to side to CBD

108
Q

How does sepsis/hypotension contribute to development of acalculous cholecystitis?

A

can get GB ischemia from shock/trauma

109
Q

What are choledochal cysts?

A

congenital dilations of intra-hepatic/extra-hepatic ducts

110
Q

What are the five types of choledochal cysts?

A

Type 1–> fusiform dilation of the extra-hepatic biliary tree ***most common, makes up >50% of choledochal cysts

Type 2–> saccular diverticulum of an extra-hepatic bile duct

type 3–> bile duct dilatation within the duodenal wall (5%)

type 4a–> dilations found in both intra-hepatic and extra-hepatic bile ducts

type 4b–> cysts found in extra-hepatic bile ducts only

type V–> Carollis dx–> intrahepatic biliary cysts, very rare, 1%

111
Q

Most common type of choledochal cysts?

A

type 1–> fusiform dilation of extra-hepatic biliary tree

112
Q

Whats the risk of cholangiocarcinoma with choledochal cysts?

A

15%

113
Q

Tx for choledochal cysts?

A

1, 2, 4–> excision of extra-hepatic biliary tree, cholecystectomy, roux-en-y hepaticojejunostomy

3–> sphincterotomy

114
Q

GB carcinoma is a rare entity, diagnosed in elderly with over 5 year survival?

A

5%

peak incidence in 7th decade
2x more common females

115
Q

What % of pts undergoing cholecystectomy routinely are found to have GB cancer?

A

1%

116
Q

Most important risk factor for gallbladder cancer is?

A

cholelithiasisis

> 95% of pts with carcinoma of GB have cholelithiasis

117
Q

what are some risk factors for developing GB cancer?

A

cholelithiaiss (usually stones >3 cm have 10-fold increased risk)

GB polyps >10 mm

porcelain GB (20% risk of GB cancer)

pts w/ choledochoal cysts (15% risk)

118
Q

80-90% of Gb tumors are what type?

A

adenocarcinomas ; (3 types; papillary, nodular, tubular)

119
Q

How does GB cancer spread?

A

via lymphatics

120
Q

Where does GB cancer usually mets to liver?

A

segments IV, V

121
Q

GB lacks muscularis mucosa and submucosa, why is this important for GB cancer spread?

A

GB cancer spreads via lymphatics, found only in subserosa layer

122
Q

Tx for GB carcinoma?

A

surgery only curative treatment

**but palliative procedures for pts with unresetcable tumors remain most commonly performed procedures

123
Q

Whats T1 Gb cancer?

A

limited to muscularis layer

Tx—> simple cholecystectomy (5 year survival is 100%)

124
Q

What are T2 Gb tumors?

A

tumor invades peri-muscular connective tissue

does not invade into liver, does not extend beyond serosa

Tx–> cholecystectomy, segment IVB, V, lymphadenectomy

125
Q

T3 and T4 GB tumors?

A

invade beyond the serosa, or liver, or distant organs

126
Q

This is a rare tumor arising from biliary epithelium:

A

cholangiocarcinoma

127
Q

Most cholangiocarcinomas are located where?

A

2/3 located at hepatic duct bifurcation

128
Q

Risk factors assc w/cholangion carcinoma?

A 
PSC
choledochal cysts
UC
hepatolithiasis 
clonorchis infection
129
Q

Most cholangiocarcinomas are adenocarcinomas, with most common type being?

A

nodular

130
Q

Peri-hilar cholangiocarcinomas are reffered to as?

A

klatskin tumors

131
Q

Bismuth classification of cholnagiocarcinomas?

A

type 1–> confined to common hepatic duct

type 2–> involve hepatic duct bifurcation without involvement of right and left hepatic ducts

type 3a–> extend into right hepatic duct from bifurcation

type 3b–> extend into left hepatic duct from bifurcation

type 4–> involve both right and left hepatic ducts and bifurcation

132
Q

Most common presentaiton of cholangiocarcinoma?

A

painless jaundice

133
Q

Tumor marker most commonly used for cholangiocarcinoma is?

A

CA 19-9

134
Q

Rate of bile duct injury with laparoscopic cholecystectomy vs open?

A

lap chole; 0.3- 0.7%

open chole: 0.1–0.2 %

135
Q

How soon after a cholecystostomy tube is place do pts start to feel better?

A

within 24 hrs

(some pts may not experience relief after tube pacement, bc tubes are not beneficial for gangrene of the GB or perforation)

136
Q

If you have a transection of a CBD or a hepatic duct during cholecystectomy, what anastomosis is preferred, hepaticojejunostomy or choledochoduodenostomy?

A

hepaticojejunostomy preferred

less leaks

(choledochoduodenostomies usually preferred for low duct injuries where tension on anastomosis is reduced)

137
Q

For CBD stones, why is choledochotmy not initial thing done?

A

causes stricutres of CBD everytime you manipulate it

start with transcystic exploration

transduodenal sphincteroplasty is last option (very morbid)

138
Q

What is the repair of choice for a proximal bile duct injury or injury involing >1 cm of duct?

A

hepaticojejunostomy

139
Q

When doing a choledochotomy to check for stones, where is the dissection done?

A

anterior surface of CBD to avoid devascularization

hole is about 1.5 cm

repair after is done primarily or over T-tube

140
Q

How do we manage a delayed >72 hr, bile duct injury?

A

control the infection by:

start abx
drain the fluid collection
decompress the biliary tree (percutaneous transhepatic cholangiograms)

141
Q

Todani classification used to classify what?

A

choledochal cysts

142
Q

In terms of wound classifications, how do we classify a simple acute chole with little to no bile spillage?

A

clean-contaminated

(if we get spillage of bile and stones; wound is contaminated) –> higher risk of post-op intra-abdominal absces

gangrenous chole–> considered a dirty wound classification

143
Q

After atempting to flush a CBD stone, unsuccessfully, what can we do next?

A

give glucagon 1 to 2 mg IV followed by repeat flushing

relaxes the sphincter of oddi

144
Q

What anomaly is associated with choledochal cysts?

A

an anomalous pancreaticobiliary junction

  • *fused long common pancreatic and biliary channel
  • **reflux of pancreatic enzymes into biliary channel causing inflammation
145
Q

With GB polyps, what’s the risk of GB cancer?

A

GB polyps >10 mm carry 25 % cancer risk

146
Q

In pts with long standing obstructive jaundice, which lab test would be abnormal?

A

elevated PT

bile needed for fat absorption, including ADEK vitamins

K important for factors 7, 9, 10 absorption

147
Q

What hormone relaxes the sphincter of oddi and what hormone promotes contraction?

A

glucagon–> RELAXES SOD

morphine–> CONTRACTS sod

Appendix (39 decks)

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