Gallbladder Flashcards
Impacted stone in the cystic duct, cystic duct remnant or gallbladder neck
Mirizzi syndrome
Inflammation around stone may cause partial mechanical obstruction of the CHD
Mirizzi syndrome
RUQ pain
Jaundice
Recurrent cholangitis
Cholangitic cirrhosis
Clinical presentation of Mirizzi syndrome
Sonographic finding of Mirizzi Syndrome
Dilatation of CHD and intrahepatic ducts above impacted stone w/ normal CBD
GB considered contracted if measures:
Less than 2 cm in diameter after appropriate fasting
Non visualization of GB
In 15-25% of PTs with cholelithiasis
“Double arc” sign
WES sign
WES triad
Wall
Echo
Shadow
Chronic cholecystitis
Gallbladder wall fibrosis due to recurrent episodes of acute cholecystitis
Lab values w/ chronic cholecystitis
May be elevated: AST ALT ALP direct bilirubin
Sonographic findings of Chronic Cholecystitis
Contracted GB w/ shadowing from stones
Hyperechoic wall 4-5mm
May see sludge
Decreased response after CCK injection
Cholecystomegaly AKA
Hydropic GB
Hydropic GB
GB distention w/o wall thickening
Prolonged total obstruction of cystic duct
GB filled with mucous secretions from wall
Difference between Hydropic GB and courvousier’s GB
Courvoisier’s due to obstruction distal to cystic duct
Risk factors for cholecystomegaly
Obstruction of cystic duct/GB neck Kawasakis disease Scarlet fever Recent surgery Prolonged biliary stasis
Sonographic findings of Hydropic GB
TRV/AP > 4cm
Thin walls
Evaluate for Mirizzi syndrome
Courvoisier GB
GB distention w/o wall thickening due to obstruction outside of GB
Causes of Courvoisier GB
Pancreatic head mass
Duodenal papilla mass
Ampulla of Vater mass
CBD mass
Sonographic findings of Courvoisier GB
Same as Hydropic GB
Porcelain GB
Complete/patchy calcification of GB wall
Incidence of porcelain GB
In 0.6-0.8% of PTs
More frequent in females (5:1)
Risk factors for porcelain GB
Cholelithiasis
Sonographic findings of Porcelain GB
May appear as stone filled but lacks WES sign
Adenoma
Benign epithelial tumor
Localized overgrowth of epithelial lining
Adenoma incidence
<5% of all GB polyps
Risk factors for Adenoma
Cholelithiasis
Chronic cholecystitis
Sonographic findings of Adenoma
Solitary <1 cm in diameter Homogeneous, hyperechoic immobile mass DO NOT shadow or move Usually near fundus Thickening of GB wall near polyp increases malignancy suspicion
Adenomyomatosis AKA
Diverticulosis of GB
A form of hyperplastic cholecystosis
Adenomyomatosis
Adenomyomatosis occurs where in most cases?
Almost exclusively in fundus
Sonographic findings of Adenomyomatosis
Thickening of GB wall
Intraluminal diverticula may be seen
Comet tail artifacts in B mode
Twinkle artifact w/ color Doppler
Small cholesterol stones/crystals lodged in Rokitansky-Aschoff sinuses
Adenomyomatosis
Degenerative or proliferation changes due to deposits of cholesterol in GB or mucosal membranes
Cholesterolosis
AKA hyperplastic cholecystosis
Focal form of cholesterolosis
Cholesterol polyps
Strawberry GB
Diffuse form of cholesterolosis
How big do polyps usually measure with cholesterolosis?
2-10 mm
Strawberry GB is diagnosed with sonography.
T/F
False
Primary GB carcinoma
Malignant neoplasm of GB wall
Represents 98% of neoplasms in GB
Adenocarcinoma
Incidence of primary GB carcinoma
Most common biliary malignancy
Most in PTs >50 years
More common in Native Americans and Hispanic Americans w/cholelithiasis
More common in females (3:1)
Risk factors for Primary GB carcinoma
Obesity Smoking Female Chronic salmonella typhi infection Exposure to industrial chemicals Cholelithiasis Chronic cholecystitis Porcelain GB Polyp >2 cm Primary sclerosis cholangitis Congenital biliary anomalies IBD
Most common pattern of disease with Primary GB carcinoma
Mass from GB fossa replacing GB and invading adjacent liver
Patterns of GB carcinoma
Irregular GB wall thickening
Polyploid intraluminal lesions w/ irregular borders
“Trapped stone”
Tumors in infundibular/fundal region
May grow into cystic duct and porta hepatis mimicking cholangiocarcinoma
Direct extension Mets commonly arise from:
Cancers of stomach, pancreas, and bile ducts
Hematogenous and lymphatic Mets
Lung
Kidney
Esophagus
Malignant melanoma
Differential of Mets from primary GB carcinoma
Cholelithiasis usually absent
Non-inflammatory causes of GB: Diffuse
Normal contracted GB Hypoalbuminemia-hypoproteinemia Ascites Acute hepatitis CHF Renal disease AIDS Pancreatitis Cirrhosis Sepsis
Non-inflammatory causes of GB wall thickening:
Focal
Adenomyomatosis Adenomatous polyp Cholesterol polyp Papillary Adenomas Primary GB carcinoma Mets
Pseudo-wall thickening
TGC too high
Beam average artifact
Tumefactive sludge
Thickened GB wall
> 3 mm
