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functions as a reservoir for bile produced at the head of the pancreas, the common
by the liver. It is 7-10 cm long, 3 cm wide bile duct meets the pancreatic duct, and
at its broadest measure, and has a they exit into the second part of the
capacity of 30-50 mL duodenum, forming the hepatopancreatic
ampulla (ampulla of Vater)
Adenomyomatosis
one of the many causes for gallbladder
wall thickening
pathologically, it is identified by
proliferation of the gallbladder mucosa
with diverticular outpuochings known as
Rokitansky-Aschoff sinuses
typically cholesterol deposits are seen
within the gallbladder wall and cause a
the common bile duct passes posterior to comet tail artifact
the first portion of the duodenum. It then
descends via a groove on the Causes of GB wall thickening
superolateral portions of the posterior
biliary causes include:
head of the pancreas sometimes traveling
-acute cholecystitis, gall bladder
through the pancreas head. The four
carcinoma, polyps, as well as adenomyomatosis
nonbiliary causes include:
-CHF, hepatitis, pancreatitis as well as
AIDs cholangiopathy
Complications
empyema
gangrene
perforation
CT findings
Chronic Cholecystitis with GB polyps
chronic inflammation of the gallbladder
results from recurrent attacks of acute
cholecystitis
fibrotic reaction usually causes the
gallbladder to become small and
contracted
Porcelain Gallbladder
has been termed calcifying cholecystitis,
cholecystopathia chronic calcaria, or
calcified gallbladder
are 5 times more common in women than
in men
most often considered a sequel of low-
grade chronic inflammation Complications
some have postulated that it is secondary biliary colic- 56 %
to intramural hemorrhage or an imbalance acute cholecystitis- 36 %
in calcium metabolism acute pancreatitis- 4 %
choledocholithiasis- 3 %
gall bladder cancer- 0.3 %
cholangitis- 0.2 %
Gall Stones
Cholelithiasis
is the pathologic state of stones or calculi
within the gallbladder lumen
associated with chronic gallbladder
inflammation and gall stones in 95 % of
cases
it appears as an echogenic arc with dense
posterior shadowing
Ultrasound findings
GB wall thickening
single or multiple intraluminal mass
extraluminal mass extending to the liver
on T2-weighted sequences where signal- polyps larger than 1 cm in diameter
void stones are contrasted against high-
signal bile Extraluminal mass extending to the liver
on T1 weighted sequences, bile usually this often is accompanied by a large mass
shows a homogenous low signal replacing the GB fossa
the mass often is complex with areas of
necrosis visible
this is the most common manifestation of
GB carcinoma, accounting for 40-65 % of
GB carcinomas
3 Functional Lobes
right
left
caudate
Amebic Abscess
trnasmitted by fecal-oral route
the organism, E. histolytica, first infects
the colon, then gains access to the liver
via portal venous system
patients generally present with right upper
quadrant pain
Causes
alcohol
alpha 1-antitrypsin
postnecrotic (hepatitis)
metabolic disease: Wilson,
hemochromatosis, glycogen storage
disease
congestive heart failure
Pathology
hepatocyte necrosis
fibrosis
nodular regeneration
Radiographic Findings
Hemochromatosis
iron overload leads to deposition in the idiopathic, usually asymptomatic and
liver. The liver can be enlarged variable in size. They cannot be
primary hemochromatosis: an autosomal distinguished from cysts that arise from
recessive disease that has abnormal prior hematomas or abscesses
absorption of iron in the intestine and thus they can be associated with other disease
causes iron to be deposited in processes such as tuberous sclerosis and
hepatocytes, spleen, pancreas, and the polycystic kidney disease
myocardium 40 % of patients with polycystic kidney
secondary hemochromatosis: caused by diseae have liver cysts
multiple transfusions with deposition of 60 % of patients with multiple liver cysts
iron in the reticuloendothelial cells of the have polycystic kidney disease
liver and the spleen. However, the
pancreas is not usually involved. If the Radiographic Findings
pancreas is involved, the
hemochromatosis is usually of the primary
type
US (95-99 % accurate)
anechoic
posterior enhancement (increased
transmitted sound)
well-defined or imperceptible walls
CT: hyperdense liver (>75 HU). There are
similar findings in Wilson’s disease,
amiodarone toxicity, and previous
thorotrast exposure
Simple Cysts
the most common liver masses
may be solitary or multiple
cysts are found in 2-10 % of population,
has increased frequency with age and is
more common in females aged 50-70
true hepatic cysts have bile duct origin
and cuboidal epithelial lining. They are
US: hyperechoic and well-defined
T1 weighted- homogeneously hypointense
(arrowhead)
T2 weighted- homogeneously
hyperintense (arrow) due to water
property (comparable to the intensity of
CSF or gallbladder bile
Differential Diagnosis
cystic liver mass with internal echoes,
thick septations, or a perceptible wall T1 weighted MRI- hypointense to liver
noted on US include (arrows). If gadolinium-diethylenetriamine
-hemorrhagic cyst penta-acetic acid (Gd-DTPA) is used,
-abscess peripheral enhancement is seen initially
-echinococcal cyst with central enhancement within 15-30
-biliary cystadenoma minutes. Enhancement is persistent
-cystic metastasis (e.g. ovarian)
-HCC with necrosis
Hemangioma
is a benign proliferation of vascular tissue
lined with endothelium which has slow
hepatic arterial blood flow
two types are capillary (more common)
and cavernous
occurs in the right lobe
can easily be confused with metastases or T2-weighted MRI- hyperinetense to the
hepatoma liver (just like a cyst; arrows). Looks as
bright as a light bulb! Intensity is as high
the most common cause of a hyperechoic
as that of pure fluid (CSF or bile)
liver mass on US
large hemangioma may appear
heterogenous. There may be thrombosis
Focal Nodular Hyperplasia
or a central stellate scar with a giant most likely seen in young women (3 %)
hemangioma
Pathology
a non-capsulated nodular mass
was thought to be a
vascular/hamartomatous malformation
is composed of normal hepatocytes,
Kupffer cells, and bile ducts but arranged
abnormally
is less than 5 cm in diameter, most
commonly found peripherally in the right
lobe
classic appearance: solitary, well-
circumscibed mass with a central stellate
scar of fibrosis even though the central
scar is seen in only 20 % of the cases
US Findings
0-2 <5%
3-4 15-20%
5-6 40%
Acute Necrotizing Pancreatitis
≥7 >99%
• Pancreatic necrosis is a known
complication of acute pancreatitis.
• Areas of necrosis are usually multifocal
Balthazar et al developed a classification system and rarely involve the entire gland.
for patients with acute pancreatitis based on • Necrosis develops earl in severe
radiologic findings pancreatitis and is usually established
within 96 hours of the onset of clinical
symptoms.
G Radiographic Prognosis
rade Findings
SPLEEN
Accessory Spleens
Splenic Cysts
Case
Splenomegaly
• lymphoma
• leukemia
• cirrhosis
• portal hypertension