Gallbladder Flashcards
Actions of cholecystokinin?
inhibits gastric motility
increases pyloric contraction
relaxes sphincter of Oddi
stimulates GB contraction
stimulates pancreatic secretions
Where is CCK produced?
I cells of duodenum and jejunum
I cells of duodenum and jejunum produce what?
CCK
This hormone produced by enteroendocrine cells, specifically I cells of duodenum and jejunum;
CCK
This hormone relaxes the Sphincter of Oddi, stimulates GB contraction, increases pancreatic secretion release, and inhibits gastric emptying:
CCK
How is the GB different from rest of GI tract?
lacks muscularis mucosa and submucosa
Cystic artery is a branch off of?
right hepatic artery (>90% of time)
** cystic artery usually branches into anterior and posterior divisions when it reaches neck of GB
Triangle of Calot?
cystic duct
common hepatic duct
inferior edge of liver
The CBD enters the 2nd portion of the duodenum thru a muscularis structure called the?
sphincter of oddi
The right and left hepatic ducts join to form the common hepatic duct, which is usually 1-4 cm long, how wide is?
4mm
Spiral valves of Heister?
mucosal folds of cystic duct near the GB neck
can make cannulation of cystic duct difficult
How long and wide is the CBD?
5-10 mm wide
7-10 cm long
Location of CBD in portal triad?
to right of hepatic artery
anterior to portal vein
The union of the CBD and pancreatic duct has three configurations;
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
Function of sphincter of oddi?
circular smooth muscle
controls bile flow
sometimes controls pancreatic juice flow
BLood supply to the bile ducts derived from what arteries?
gastroduodenal
right hepatic arteries
**major trunks run at the 3 and 9 oclock positions
Classic description of the extra-hepatic biliary tree is found in what % of pts?
1/3
What % of pts have the classic extra-hepatic biliary tree anatomy?
33%
Rare congenital GB variants?
absent GB–> rare, 0.03% of cases
duplicated GB–> 1/4000 cases
What are Luschka ducts?
small ducts that drain directly from liver into GB
if missed can cause biloma leak
Cystic artery comes off right hepatic artery how often?
80-90% of time
20% of cases, right hepatic artery comes off of what?
SMA
How much bile does the liver produce daily?
500-1000 cc
Vagal effect on bile secretion?
stimulates bile release
Composition of bile?
water electrolytes bile salts cholesterol lecithins bile pigments
pH of hepatic bile?
usually neutral or slightly alkaline
protein diet can make it more acidic
What are the two main bile salts and what do they do?
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
In intestines, 80% of bile acids absorbed where?
What happens to remaining 20% of bile acids?
terminal ileum
** rest are deconjungated by gut bacteria forming secondary bile acids; deoxycholate, lithocholate
What;s entero-hepatic circulation?
reabsorbing about 95% of excreted bile back into liver
** 5% excreted in stool
Principal lipids found in bile?
cholesterol
phospholipids
Why is bile green?
presence of bilirubin diglucuronide (metabolic product of bilirubin breakdown)
100x more concentrated than in plasma
Main function of GB?
store and concentrate hepatic bile and deliver it to duodenum after a meal
What happens to bile once its in GB?
in fasting state, 80% of bile is stored in GB
How does the GB handle storing so much bile?
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
What do epithelial cells of the GB secrete into Gb lumen?
H ions–> decreased bile pH, which promotes Ca solubility
glycoproteins –> prevent lytic action of bile on GB lumen
Whats white bile?
glycoproteins released from GB infundibulum glands
seen in hydrops of GB
What hormone stimulates GB emptying?
CCK
Where is CCK made?
CCK made endogenously by duodenal mucosa in response to a meal
What happens to Gb when stimulated by a meal?
empties 50-70% of its contents within 30-40 mins
Neural pathways that stimulate and inhibit the GB?
vagal stimulation—> stimulates GB contraction, emptying
SNS splanchnic stimulation–> inhibits GB contraction
What stimulates CCK release from duodenum?
acids, fats, amino acids in duodenum
CCK half life is 2-3 mins
Actions of CCK?
stimulates GB contraction
relaxes sphincter of Oddi
What happens to pts GB after vagotomies?
GB gets no vagal stimulation, size and volume of Gb increase
What does VIP do to GB?
inhibits contraction
relaxes GB
What does somatistatins do to GB ?
inhibit contraction
**pts with somatistatinomas tend to form gallstones due to bile stasis
Spontaneous motility of sphincter of oddi is regulated by what cells?
interstitial cells of Cajal
Relationship of sphincter of oddi in fasting state and in response to a meal?
fasting state; sphincter contracted, GB fills via retrograde movement
meal; sphincter relaxed, GB flows out from GB
Cholestasis, or obstruction of bile flow is characterized by what elevated markers?
elevated bilirubin (conjugated form) elevated ALK
In pts suspected of having biliary etiology what test ordered first?
US
Sensitivity and specificity of US to identify gallstones?
> 90%
What is the specificity and sensitivity of US to identify gallstones?
> 90%
Why do stones produce an acoustic shadow on US?
they are acoustically dense structures
they reflect US waves back to the US transducer
they block passage of sounds waves behind them
How does a HIDA Scan work?
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
Sensitivity and specificity of diagnosis acute cholecystitis with HIDA scan?
> 95%
False positives with HIDA seen in what pt populations?
critically ill pts
pts on TPN
pts with bile stasis
What are two complications of ERCP?
cholangitis
pancreatitis
(occur in 5% of pts)
What are some risk factors for gallstone development?
obesity pregnancy diet Crohn's dx hemoglobinopathies
Who is more prone to developing gallstones? Men v Women?
women
What % of pts with gallstones become symptomatic with biliary colic every year?
3%
What is the only absolute indication for prophylactic cholecystectomy?
porcellain gallbladder; wall of GB gets calcified
premalignant entity
What are the two types of stone we have?
cholesterol vs pigment stones (black or brown)
In western countries what types of stones are more common, cholesterol vs pigment stones?
cholesterol stones (80%)
***in asian countries pigment stones more common
How do cholesterol stones form in the GB?
bile is super-saturated with cholesterol
What are pigment stones pigmented?
presence of calcium bilirubinate
Black gallstones are a result of what type of disorders?
usually due to hereditary disorders
What causes formation of brown gallstones?
form in the GB or bile ducts usually secondary to infection and bile stasis
In Asian countries, brown stones form as a result of?
parasitic infection of ducts
What is hydrops of the GB?
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
Tx for hydrops of GB?
early cholecystectomy recommended
What is chronic cholecystitis?
often called biliary colic
pts develop recurrent attacks of pain when a stone blocks cystic duct; causing increased wall tension in GB wall
What are Aschoff-Rokitansky sinuses?
in chronic cholecystitis, sometimes the mucosa gets atrophied and we get protrusion of epithelium into muscle layer
Whats a strawberry gallbladder?
seen in cholesterolosis, where cholesterol builds up in side macrophages in GB mucosa
Why do we offer diabetics with symptomatic gallstones prompt surgery?
more prone to developing acute cholecystitis
often more severe
Pregnant pts with symptomatic gallstones who can’t be managed with diet modifications can undergo cholecystectomy when?
2nd trimester
What causes acute cholecystitis?
90-90% of time due to gallstones
What % of cases of acute cholecystitis due to a tumor blocking cystic duct?
<1%
What is an emphysematous GB?
in acute cholecystitis you can get a secondary bacterial infection
gas may be seen in GB lumen and in GB wall on imaging
What is an acute gangrenous cholecystitis?
GB remains obstructed
a secondary bacterial infection starts
can get an abscess, empyema form within the GB
Difference in clinical presentation of acute cholecystitis vs chronic cholecystitis?
acute chole–> pain is often un-remitting, lasting for days
Mirizzi syndrome?
impacted stone in infundibulum of GB that blocks the common bile duct
In what two pt populations do we see acute cholecystitis having a subtle presentation resulting in delay in diagnosis?
diabetics + elederly
- *higher risk of complications
- *morbidity is 10-fold higher
What is a + HIDA scan?
lack of filling of Gb after 4 hr
Antibiotics in acute cholecystitis should cover what bugs?
gram negative aerobes and anaerobes
- *2nd gen cephalosporin
- 3rd gen cephalosporin + flagyl
What % of pts with gallstones also have choledocholithiasis?
6-12%
***in western cultures most CBD stones are stones formed in the GB that pass down into the CBD (termed secondary CBD stones)
Where do we see primary CBD stones primarily?
in Western countries where we have bile stasis and parasitic infections
What % of pts with CBD stones have normal liver chemsitries?
1/3
Gold standard to diagnose CBD stones?
ERCP
also therapeutic
How long does it take for a T-tube to mature?
2 -4 weeks
Is bile sterile?
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
What is needed to develop ascending cholangitis?
biliary obstruction (gallstones most commonly) + bacterial contamination
Common bacteria found in bile in pts with cholangitis?
E.coli
klebsiella
strept
bactroides
Most common presentation of cholangitis is?
fever
RUQ
jaundice
Charcot’s tried of cholangitis?
fever
RUQ
jaundice
Raynauds pentad of cholangitis?
septic shock
AMS
fever
RUQ
jaundice
Tx for cholangitis??
IVF + abx
surgical decompression via PCT, ERCP or emergent surgery with t-tube
Mortality of acute cholangitis?
5%
Absolute contraindications for laparoscopic cholecystectomy?
uncontrolled coagulopathy and end-stage liver dx
What is the conversion rate from laparoscopic to open cholecystectomies in elective settings vs emergent bassi?
elective—> 5 % conversion rate
emergent—> 10-30% conversion to open rate
Mortality rate of laparoscopic cholecystectomy is?
0.1%
Compared to open cholecystectomy, lap chole is associated with higher rates of ?
damage to bile ducts
What % of pts with gallstone pancreatitis who do not have elective cholecystectomy on first admission develop gallstone pancreatitis again?
25%
Gold standard for diagnosis CBD stones?
endoscopic cholnagiography
If a choledochotomy is performed, what do we leave in place?
T-tubule
Before removing a T-tubule what do we do first?
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)
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?
glucagon
If irrigation of CBd stones with flushing and glucagon is not successful, what do we do?
can pass a balloon catheter via cystic duct down to CBD and inflated to retrieve CBD stones
If stones cannot be cleared from CBD or when duct is very dilated, (>1.5 cm), what do we do?
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
How does sepsis/hypotension contribute to development of acalculous cholecystitis?
can get GB ischemia from shock/trauma
What are choledochal cysts?
congenital dilations of intra-hepatic/extra-hepatic ducts
What are the five types of choledochal cysts?
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%
Most common type of choledochal cysts?
type 1–> fusiform dilation of extra-hepatic biliary tree
Whats the risk of cholangiocarcinoma with choledochal cysts?
15%
Tx for choledochal cysts?
1, 2, 4–> excision of extra-hepatic biliary tree, cholecystectomy, roux-en-y hepaticojejunostomy
3–> sphincterotomy
GB carcinoma is a rare entity, diagnosed in elderly with over 5 year survival?
5%
peak incidence in 7th decade
2x more common females
What % of pts undergoing cholecystectomy routinely are found to have GB cancer?
1%
Most important risk factor for gallbladder cancer is?
cholelithiasisis
> 95% of pts with carcinoma of GB have cholelithiasis
what are some risk factors for developing GB cancer?
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)
80-90% of Gb tumors are what type?
adenocarcinomas ; (3 types; papillary, nodular, tubular)
How does GB cancer spread?
via lymphatics
Where does GB cancer usually mets to liver?
segments IV, V
GB lacks muscularis mucosa and submucosa, why is this important for GB cancer spread?
GB cancer spreads via lymphatics, found only in subserosa layer
Tx for GB carcinoma?
surgery only curative treatment
**but palliative procedures for pts with unresetcable tumors remain most commonly performed procedures
Whats T1 Gb cancer?
limited to muscularis layer
Tx—> simple cholecystectomy (5 year survival is 100%)
What are T2 Gb tumors?
tumor invades peri-muscular connective tissue
does not invade into liver, does not extend beyond serosa
Tx–> cholecystectomy, segment IVB, V, lymphadenectomy
T3 and T4 GB tumors?
invade beyond the serosa, or liver, or distant organs
This is a rare tumor arising from biliary epithelium:
cholangiocarcinoma
Most cholangiocarcinomas are located where?
2/3 located at hepatic duct bifurcation
Risk factors assc w/cholangion carcinoma?
PSC choledochal cysts UC hepatolithiasis clonorchis infection
Most cholangiocarcinomas are adenocarcinomas, with most common type being?
nodular
Peri-hilar cholangiocarcinomas are reffered to as?
klatskin tumors
Bismuth classification of cholnagiocarcinomas?
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
Most common presentaiton of cholangiocarcinoma?
painless jaundice
Tumor marker most commonly used for cholangiocarcinoma is?
CA 19-9
Rate of bile duct injury with laparoscopic cholecystectomy vs open?
lap chole; 0.3- 0.7%
open chole: 0.1–0.2 %
How soon after a cholecystostomy tube is place do pts start to feel better?
within 24 hrs
(some pts may not experience relief after tube pacement, bc tubes are not beneficial for gangrene of the GB or perforation)
If you have a transection of a CBD or a hepatic duct during cholecystectomy, what anastomosis is preferred, hepaticojejunostomy or choledochoduodenostomy?
hepaticojejunostomy preferred
less leaks
(choledochoduodenostomies usually preferred for low duct injuries where tension on anastomosis is reduced)
For CBD stones, why is choledochotmy not initial thing done?
causes stricutres of CBD everytime you manipulate it
start with transcystic exploration
transduodenal sphincteroplasty is last option (very morbid)
What is the repair of choice for a proximal bile duct injury or injury involing >1 cm of duct?
hepaticojejunostomy
When doing a choledochotomy to check for stones, where is the dissection done?
anterior surface of CBD to avoid devascularization
hole is about 1.5 cm
repair after is done primarily or over T-tube
How do we manage a delayed >72 hr, bile duct injury?
control the infection by:
start abx
drain the fluid collection
decompress the biliary tree (percutaneous transhepatic cholangiograms)
Todani classification used to classify what?
choledochal cysts
In terms of wound classifications, how do we classify a simple acute chole with little to no bile spillage?
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
After atempting to flush a CBD stone, unsuccessfully, what can we do next?
give glucagon 1 to 2 mg IV followed by repeat flushing
relaxes the sphincter of oddi
What anomaly is associated with choledochal cysts?
an anomalous pancreaticobiliary junction
- *fused long common pancreatic and biliary channel
- **reflux of pancreatic enzymes into biliary channel causing inflammation
With GB polyps, what’s the risk of GB cancer?
GB polyps >10 mm carry 25 % cancer risk
In pts with long standing obstructive jaundice, which lab test would be abnormal?
elevated PT
bile needed for fat absorption, including ADEK vitamins
K important for factors 7, 9, 10 absorption
What hormone relaxes the sphincter of oddi and what hormone promotes contraction?
glucagon–> RELAXES SOD
morphine–> CONTRACTS sod
