Hepatic Tumors and Cysts - University of Louisville

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HEPATIC TUMORSuAND
CYSTS.Lo
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NAEEM
ASLAM.
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UNIVERSITY
OF LOUISVILLE,
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KENTUCKY.
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Contents of discussion.
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Brief Case report.
Classification of liver tumors.
Brief discussion of common tumors.
Hepatocellular Carcinoma.
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Case Report.
Presenting complaints.
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Right upper Abdominal pain- 3-4 months.
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HOPI.
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A 57 yr old white male with h/o hepatitis
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C diagnosed 10 yrs ago complains
of
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vague upper abdominal pain
for last 3-4
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months.
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Pain is dull, aching
in nature and mostly
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constant. (4/10).
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It is not
relieved or aggravated by
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food,
posture
and
is
non
radiating.
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Nausea +, denies vomiting.
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Decreased appetite. of
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Review of othertsystems
– ive.
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Review of systems.
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PMH.
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1. Hepatitis C (Genotype 1) non responder
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to interferon and ribavirin.
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2 Obesity. (BMI 43)
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3 HTN.
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PSH. s/p cholecystectomy
12 yrs ago.
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Medications. Norvasc/lipitor. (not itaking
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them.
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Allergies.
NKDA.
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Personaliv
H/0 IV drugs in past, and ex
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drinker. Quit 2 yrs ago.
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Examination.
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P 88 BP 160/90 Temp 98.4 RR 16
„
CNS. Alert oriented x 3, 5/5 all limbs
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CVS. S1+ S2 RRR noorub or murmur.
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Respiratory
. A.E equal, normal vesicular
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bilateral.
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Abdomen , mild tenderness rightis
upper
u
quadrant + No rebound or guarding
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L dullness
noted. Hepatomegaly. fShifting
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and fluid thrill –ve. BS
+ive.
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Extremities.
Bilateral trace edema.
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Labs.
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WBC 8, HB 9, PLT 80,000
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Na 133, K 4.6,
BUN/Crt 35/1.0is
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INR 1.1 PT 14.9 PTT 36 sec.
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ALT(SGPT) 99 U/L
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AST(SGOT) 108 U/L o
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ALKALINE PHOSPHATASE
177 H U/L ( 50 to
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136)
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TOT. iBILIRUBIN
0.6 mg/dL (.3 to 1.5 )
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LDH
747 H U/L
(300 to 650)
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ALBUMIN 2.7 g/dL (3.0 to 4.8 )
Ultrasound.
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The liver is enlarged measuring 18 s
cm
in its
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maximum length.
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A 4.3 x 3.5 cm echogenic L
mass is located in
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the right hepatic lobeo
near the dome.
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Portal venous flow
is normal.
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Common hepatic duct is upper limits of
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normal
measuring 6 mm in maximum
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Udiameter.
CT scan.
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Hypervascular mass measuring
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measuring 4.2 cm is seen in the
right
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lobe of the liver highly suspicious
for
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HCC.
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Splenomegaly.
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Recannulization
of the umbilical
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vein as well
as some small epigastric
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varices e
consistent with portal
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hypertension.
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AFP.
652 ng/ml (0.0 to 15.0 )
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What to do next?
1 Liver Biopsy.
2 Make him DNR.
3 Supportive care.
4 None of the above.
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Further workup for metastatic disease
was
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negative.
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Patient had CT guided
liver biopsy which
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showed HCC.rs
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What will be the treatment?
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Resection.
Transplantation.
TACE.
Chemotherapy.
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Because of patient BMI patient was
not
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considered for surgical intervention.
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Patient underwent TACE
without any
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improvement.
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Patient now being
considered for
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chemotherapy.
(Sorafenib)
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APPROACH TO SPACE-OCCUPYING
LESIONS OF THE LIVER
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Classification of Hepatic tumors and
cysts.
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Hepatocellular Adenoma.
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Seen more commonly in females. v
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Has strong association with prolonged
use
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of oral contraceptives.
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f contraceptive use
Duration of exposureoto
increases the riskyof adenoma formation.
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5-7 yr exposure
increases
the
risk
to
5
s
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times normal
and it goes up to 25 times
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withn9 yrs of exposure.
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• Estrogens as well as progestrogensvplay
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role in adenoma growth.
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• Growth of adenomas appears
to be
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hormone dependent
(increase
in
size
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during during pregnancy
and regression
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after cessation
of
oral
contraceptive
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use).ve
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Clinical Features.
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Asymptomatic.
Pain in the right hypochondrium or
epigastrium (bleeding or infarction of
adenoma).
Acute hemoperitoneum.
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Diagnosis of Hepatic Adenoma
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Ultrasonography
2-
CT scan.
3-
Hepatic angiography . Approximately 50%
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of hepatocellular adenomas are avascular,. The
tumor has a clearly defined margin and, often,
nearly parallel vessels entering it from the
periphery (“spoke-wheel appearance”)
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4-
MRI may be a useful alternative to hepatic
angiography .
5-
Needle biopsy and fine-needle
aspiration are of limited value as
adenomas mimic normal liver tissue.
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Normal Liver tissue.
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Hepatic Adenoma.
The hepatic adenoma is on the right and is
composed of cells that closely resemble normal
hepatocytes
Treatment.
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Surgical treatment (resection ) isv
recommended because of riskis
of
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rupture.
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Avoid taking oral contraceptive
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Pregnancy should
be
avoided.
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There is a s
risk
of malignant
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transformation.
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Cavernous Hemangioma
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The most common benign tumor ofv
the
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liver and is found in as many as i7%
of
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autopsies.
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Seen in all ages. (30-50f yrs)
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Increase in size with
pregnancy
or
the
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administration
of
estrogens
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Clinical Features.
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Asymptomatic .
Larger or multiple lesions produce
symptoms like upper abdominal pain ,
early satiety, nausea, and vomiting.
If more than 4 cm in diameter are called
Giant cavernous hemangiomas.
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Diagnosis.
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Imaging Studies:
„ Ultrasound.
„ Computed tomography. (Dynamic
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contrast-enhanced CT scanning is preferred to
routine CT scanning)
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Magneticsresonance
imaging
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Nuclear
medicine
studies.
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Arteriography
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Contrast enhanced CT – 4 phases.
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1. Pre contrast.
2.
3.
Hemangioma appear hypodense in this phase.
Arterial phase. (30 seconds after contrast
given. Contrast is entering liver via hepatic artery).
Enhancement of the peripheral portions of the lesion.
(ring enhancement) The center of the lesion remains
hypodense.
Portal phase. (60 seconds later. Contrast
returning to liver by mesentric and portal veins.)
Contrast enhancement progresses centripetally.
Delayed images . (several minutes later) The
center of lesion appear hyperdense.
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4.
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Dynamic CT. (a) The hypodense lesion on the right liver
lobe shows peripheral enhancement at the early phase of
this study with (b) subsequent hyperdensity (retention) in
the late phase
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Has a sensitivity and specificity of greater
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than 90% and is the imaging modality of
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choice.
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T1 - weighted images-f Hypointense.
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T2 - weighted images
- Hyperintense.
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(Light bulb sign)
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MRI.
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Ultrasound
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Well-defined hyperechoic masses (though
few can appear relatively hypoechoic when
imaged within a fatty liver.
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Accuracy of Imaging Studies
Imaging Tools
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Sensitivity
(%)
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US
46
Combined B-mode and color Doppler US
69
Contrast-enhanced CT scan
66
T2-weighted MRI
96
Gadolinium-enhanced MRI combined with dynamic CT
scan
100
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Radiological follow-up for
Hemangioma.?
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• It remains uncertain if follow-up radiologic
studies are warranted to reassess the size of
the hemangioma.
• Some recommend to have US at 6 months and
at 12 months after the initial diagnosis. If there
is no change in hemangioma size long-term
follow-up radiologic studies are probably not
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necessary.
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Treatment of Hemangiomas.
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No treatment if no symptoms.
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The management of a large
(ie,
>10
cm)
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hepatic hemangioma
is
controversial.
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Large symptomatic
hemangiomas should
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undergo treatment
.
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TUMOR-LIKE HEPATIC
LESIONS
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Focal Nodular Hyperplasia .
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Nodular regenerative hyperplasia .
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FOCAL NODULAR HYPERPLASIA
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More common in women than
in men.
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Seen in all ages (30-40f yrs)
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The cause of focal
nodular hyperplasia is
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unknown. ? role
for oral contraceptive .
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.
Clinical Features.
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Asymptomatic
Pain (bleeding into or necrosis of the
lesion)
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Diagnosis.
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Ultrasonography and CT is not specific for
FNH.
Doppler ultrasonography with intraarterial infusion of CO2 microbubbles is
characteristic.
Selective hepatic arteriography. (vascular
lesions).
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Show central scar and radiating fibrous
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septa that divide the lesion o
into lobules.
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Microscopically, focal nodular
hyperplasia
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closely resemblesyinactive cirrhosis.
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Pathology.
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Treatment
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Periodic ultrasonography should be
performed and a lesion seeno
touincrease
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substantially in size should
be resected.
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Large symptomatic
or
complicated
lesions
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should be resected.
(or enucleated).
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Discontinuation
of contraceptive steroids
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No treatment if not symptomatic.
HEPATIC CYSTS
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1- FIBROCYSTIC DISEASES OF THE
v
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LIVER
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a. Polycystic liver disease. o
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b. Caroli's disease (type
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choledochal
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y
cyst)
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2- Hydatid cyst.
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n congenital cysts
3-U
solitary
Polycystic Liver Disease
A. Childhood variety.
„ Autosomal recessive disorder.
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Rapidly fatal as a consequence of the
associated (autosomal recessive)
polycystic kidney disease (ARPKD).
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PKHD1
is the responsible gene and is
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identified
U at chromosomal locus 6p21-cen.
Adulthood variety.
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Multiple cysts of the liver are diagnosed
in
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adulthood. They present either in association
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with autosomal dominant polycystic
kidney
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disease (ADPKD) or as isolated
polycystic
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liver disease.
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Gene affected in ADPKD1
is located on the
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short arm of chromosome
16
at
locus
q13
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q23 and expresses
a protein, polycystin-1
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The genee
responsible for ADPKD2 is located
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on chromosome
4 and expresses polycystini
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Clinical features.
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Asymptomatic.
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Discomfort or pain, postprandial ifullness,
u
upper abdominal mass
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f
Liver biochemical test results
generally are
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not abnormal, a serum
alkaline
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phosphatases
and
GGT levels may be
increaseder
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Treatment of Polycystic Liver
disease.
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Usually no treatment required
„ Fenestration (unroofing)
„ Injection of sclerosing agents (alcohol or
doxycycline).
„ Octreotide trial.
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Octreotide inhibits hepatic cystogenesis in
a rodent model of polycystic liver disease
by reducing cholangiocyte adenosine 3',5'cyclic monophosphate.
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In polycystic liver diseases (PCLDs), increased
cholangiocyte proliferation and fluid secretion
are key features cAMP is an important regulator
of these processes.
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(Gastroenterology. 2007 Mar;132(3):1104-16)
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RESULTS.
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Octreotide lowered cAMP content in
cholangiocytes and serum by 32%-39% and
inhibited hepatic disease progression.
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It lead to 22%-60% reductions in liver weight,
cyst volume, hepatic fibrosis, and mitotic indices.
Similar effects were observed in kidneys of PCK
rats.
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CONCLUSIONS:
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This preclinical study provides a strong rationale
for assessing the potential value of octreotide in
the treatment of PCLDs.
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(Gastroenterology. 2007 Mar;132(3):1104-16)
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Hepatocellular Carcinoma (HCC)
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The commonest primary malignant v
tumor
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of the liver.
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.
Seen more commonly in Men>females
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Fifth most common cancer
in men and the
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eighth most common
in women
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The incidence
increases progressively
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with advancing
age
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Clinical Features.
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Asymptomatic.
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Symptom
Frequency(%)
59-95
„ Abdominal pain
34-71
„ Weight loss
22-53
„ Weakness
28-43
„ Abdominal swelling
„ Nonspecific gastrointestinal symptoms 25-28
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Jaundice si
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25-26
Physical findings
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Sign
Hepatomegaly
Hepatic bruit
Ascites
Splenomegaly
Jaundice
Wasting
Fever
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Frequencyv(%)
s
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-98
54u
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6-25
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f 35-61
27-42
4-35
25-41
11-54
Paraneoplastic Syndromes
Associated with HCC.
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Hypoglycemia
Polycythemia (erythrocytosis)
Hypercalcemia
Osteoporosis
Hypertrophic osteoarthropathy
Thyrotoxicosis
Polymyositis
Neuropathy
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Hypoglycemia with Hepatic tumors
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Mild form of hypoglycemia
because of
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inability of diseased liver
to satisfy the
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demands of glucose o
by both a large rapid
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growing tumoriand the other tissues of
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the body.
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A. Type A hypoglycemia.
Type B hypoglycemia.
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•
•
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Seen less commonly.
More severe hypoglycemia.
Presence of pro- IGF II in serum. Big
IGFII increase glucose uptake and
decrease gluconeogenesis. Also
suppresses growth hormone and
glucagon secretion leading to
hypoglycemia.
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Risk Factors for Hepatocellular
Carcinoma
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Major Risk Factors
„ Chronic hepatitis B virus infection
„ Chronic hepatitis C virus infection
„ Cirrhosis
„ Dietary exposure to aflatoxin B1
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Minor Risk Factors
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Oral contraceptive steroids
Cigarette smoking
Dietary iron overload in persons of black African
ancestry
Hereditary hemochromatosis
Wilson disease
á1-Antitrypsin deficiency
Type 1 hereditary tyrosinemia
Type 1 and type 2 glycogen storage disease
Hypercitrullinemia
Ataxia-telangiectasia
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Diagnosis of HCC
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Radiology (USG/CT/MRI)
Biopsy
AFP serology.
The sequence of tests used to diagnose
HCC depends on the size of the lesion.
n
U
r
e
iv
y
t
i
s
f
o
TUMOR MARKERS.
e
l
l
i
v
is
Marker
Sensitivity (%)
Specificity
(%)
Comments
Alphafetoprotein
50-90%
90
Relatively quick
and easy to
measure; most
extensively
studied
y
t
i
s
Des-ã58-91
carboxyprothro
mbin
n
U
r
e
iv
á-L-Fucosidase 75
f
o
u
o
L
84
Quick and easy
to measure.
Much more
expensive than
a-fetoprotein
70-90
Quick and easy
to measure;
relatively
inexpensive
u
o
Safe, easily available, and
cost
effective.
L
f
o
y
Approximately two
thirds of HCC are
t
i
s
hyperechoic,
whereas the remainder are
r
e
partly hyperechoic
and partly hypoechoic
v
i
n
U
Ultrasonography
¾
¾
e
l
l
i
v
is
u
o
L
e
l
l
i
v
is
Computed Tomography
„ Magnetic Resonance Imaging
„ Hepatic Angiography
„
n
U
r
e
iv
y
t
i
s
f
o
Treatment.
e
l
l
i
v
s
Treatment of hepatocellular carcinoma
i
u
o
depends on
L
f
the extent of the disease
o
presence or absence
of cirrhosis,
y
t
i
s
degree of hepatic
dysfunction.
r
e
v
i
n
U
„
„
„
Different Treatment Options.
e
l
l
i
v
s
1
Surgery. (Resection/Transplantation.)
i
u
o
L
2
Transarterial Embolization
and
f
Chemoembolization
(TACE)
o
y
t
i
s
3
RFA (radiofrequency
ablation)/
r
e
Percutaneous
Ablation
v
i
n
4 UChemotherapy
EARLY STAGE DISEASE
Includes patients with
e
l
l
i
v
is
u
o
1 Child–Pugh A and B (preserved
liver
L
f
function)
o
2 Solitary HCC orty
up to 3 nodules 3 cm in
i
size.
s
r
e
3. No evidence
of metastatic disease.
v
i
n
U
e
l
l
i
v
s
Early stage disease patients can be
i
u
effectively treated by:
o
L
Resection.
f
Liver transplantation.o
y
t
i
Percutaneoussablation.
r
e
v
i
5-year survival figures ranging from 50% to
n
75%.
U
¾
¾
¾
Surgical Resection.
e
l
l
i
v
is
Selection of candidates for resection has
been based on
1. Child -Pugh classification (inconsistent
predictive value)
2. Evidence of Portal Hypertension.
A . Ascites, splenomegaly, varices,
thrombocytopenia (<100,000)
B Hepatic vein catheterization. (not
needed if above present.
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
s
Predictor of excellent outcome
after
i
u
o
surgery.
L
f
o
y
t
i
s
r
e
v
i
n
U
¾
¾
Absence of portal hypertension (hepatic
venous pressure gradient less than 10 mm Hg)
and normal bilirubin.
These patient may achieve a 5-year survival of
more than 70%
Recurrence rate after resection.
„
„
e
l
l
i
v
s
Tumor recurrence rate exceeds 70%
at 5
i
u
years.
o
L
The most powerful predictors
of
f
o
recurrence are the presence
of
y
t
i
microvascular invasion
and/or additional
s
r
tumor sites besides the primary lesion.
e
v
i
n
U
Liver Transplantation.
„
„
„
e
l
l
i
v
s
Liver transplantation is an effective
option
i
u
for patients with HCC corresponding
to the
o
L
Milano criteria:
f
Solitary tumor <5 cmoor up to three
y
t
nodules <3 cm.i
s
r
Living donor
transplantation can be
e
v
i
offered
for HCC if the waiting time is
n
Ulong enough .
¾
¾
e
l
l
i
v
s
Surgical removal of liver tumors ioffers
the
u
best chance for a cure.
o
L
f
o
Surgical removal y
is not possible for more
t
i
than 75% with
primary and 90% with
s
r
secondary
(metastases)
liver cancer
e
v
i
n
U
Other Options for non surgical
candidates.
Percutaneous Ablation
„
„
„
f
o
u
o
L
e
l
l
i
v
is
This is the best treatment option for patients
with early stage HCC who are not suitable for
resection or transplantation.
Percutaneous ablation is usually performed
under ultrasound guidance.
Ethanol injection is the best known
and best studied approach.
n
U
r
e
iv
y
t
i
s
Radiofrequency Ablation (RFA) of
tumors
„
„
e
l
l
i
v
s
Using radiofrequency (RF) energy
to cook
i
u
and kill cancerous tissue. o
L
Alternative to surgical resection.
f
o
y
t
i
s
r
e
v
i
n
U
Radiofrequency ablation.
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
Transarterial Chemoembolization
for liver cancer. (TACE)
e
l
l
i
v
is
u
Delivers a high dose of chemotherapy
o
L
directly to the tumor while
depriving the
f
o
tumor of its blood supply
by blocking
y
t
(embolizing) the
arteries feeding the
i
s
r
tumor.
e
v
i
n
U
e
l
l
i
v
is
Indication.
u
o
L
TACE is recommended as first line noncurative therapy for non-surgical patients
with large/multifocal HCC who do not
have vascular invasion or extrahepatic
spread. (child Pugh A and B)
n
U
r
e
iv
y
t
i
s
f
o
TACE.
„
e
l
l
i
v
s
Includes delivery of a combination
of
i
u
o
embolic agent and chemotherapeutic
L
f
agent.
o
(Ethiodol Poppyseed
Oil accumulates
y
t
i
s
preferentially
in HCC +Adriamycin or
r
e
cisplatin)
v
i
n
U
Complications of TACE.
„
„
„
„
„
„
„
„
e
l
l
i
v
is
Hepatic injury (30.8%) - Abnormal liver function
tests, acute hepatic failure, and hepatic
infarction
Severe postembolization syndrome (15.1%)
right upper quadrant pain, nausea, vomiting,
fevers (> 38°C), leukocytosis, adynamic ileus,
and elevation of liver function test
Gallbladder infarction (14%)
Nontarget embolization (4.6%)
Gastrointestinal bleeding (2.8%)
Septicemia (2.6%)
Pulmonary embolism (1.7%)
Splenic infarction (1.1%)
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
Using
imaging, a
catheter is
fed through
the femoral
artery to the
blood vessels
feeding the
tumor
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
ƒ Small embolic particles are injected to block the blood vessel
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
ƒ The drugs and lack of blood supply cause the tumor to shrink
r
e
iv
y
t
i
s
ƒ ( Information provided by the Society of Interventional Radiology, 2004)
n
U
f
o
u
o
L
e
l
l
i
v
is
Chemotherapy .
¾
¾
e
l
l
i
v
s
Alkylating agents, antitumor antibiotics,
i
u
o
antimetabolites, plant alkaloids,
platinum
L
f
derivatives, and procarbazine.
o
y
t
i
s
Response rates
have been less than 20%.
r
e
v
i
n
U
u
o
L
e
l
l
i
v
is
Surveillance for HCC
f
o
(HEPATOLOGY, Vol. 42, No. 5, 2005)
n
U
r
e
iv
y
t
i
s
Who needs surveillance ?
e
l
l
i
v
is
u
Asian males 40 years o
L
f
Asian females 50 years
o
All cirrhotic hepatitis
B carriers
y
t
i
s
Family history
of HCC
r
e
Africans
over age 20
v
i
n
U
Hepatitis B carriers
„
„
„
„
„
u
o
L
Non-hepatitis B cirrhosis
„
„
„
„
f
o
Hepatitis C
Alcoholic cirrhosis
Genetic hemochromatosis
Primary biliary cirrhosis
n
U
r
e
iv
y
t
i
s
e
l
l
i
v
is
Non Hepatitis B cirrhosis.
„
„
„
e
l
l
i
v
s
Following groups have an increased
risk of
i
u
HCC no recommendations for
or against
o
L
surveillance can be made
because a lack
f
o
of data
y
t
i
deficiency.
Alpha1-antitrypsin
s
r
steatohepatitis.
Non-alcoholic
e
v
i
Autoimmune
hepatitis.
n
U
e
l
l
i
v
is
Surveillance Tests.
AFP
OR
„ Ultrasound.
„
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
AFP (Alfa- feto protein)
e
l
l
i
v
is
¾
Has a role in the diagnosis of HCC.
¾
Cirrhotic patients with a mass in the liver an
AFP greater than 200 ng/mL has a very high
positive predictive value for HCC.
¾
Persistently elevated AFP has been clearly
shown to be a risk factor for HCC.
¾
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
AFP can be used to help define patients at
risk but appears to have limited utility as a
screening test.
e
l
l
i
v
is
Combined use of AFP and ultrasonography
increases detection rates, but also increases
costs and false-positive rates.
y
t
i
s
Test.
r
e
iv
AFP
Ultrasound
n
U
AFP + Ultrasound
f
o
u
o
L
False Positive
rates.
5.0%
2.9%
7.5%
„
„
e
l
l
i
v
s
Ultrasound alone cost about $2000
per
i
u
tumor found.
o
L
where as the combination
cost (AFP +
f
o
ultrasound) about $3000
per tumor found.
y
t
i
s
r
e
v
i
n
U
CT scan
u
o
L
Not recommended for routine
screening
• Risk of radiation exposure.
• High false-positive rate.
n
U
r
e
iv
y
t
i
s
f
o
e
l
l
i
v
is
Surveillance Interval
„
„
e
l
l
i
v
s
, but
Most experts use a 6-month interval
i
u
there are no firm data to suggest
that 6
o
L
months is better than f12 months.
o
y
t
i
s
The surveillance
interval is determined by
r
e
the tumor
growth rates and not by the
v
i
n
degree
of risk.
U
Recommendations
e
l
l
i
v
is
(HEPATOLOGY, Vol. 42, No. 5, 2005)
u
o
L
1. Surveillance for HCC should be performed
using ultrasonography .
2. AFP alone should not be used for screening
unless ultrasound is not available.
3. Patients should be screened at 6 to12 month
intervals .
4 The surveillance interval does not need to be
shortened for patients at higher risk of HCC.
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
Mass on surveillance Ultrasound in cirrhotic liver.
y
t
i
s
r
e
iv
< 1 cm
n
U
f
o
1‐2 cm
e
l
l
i
v
is
>2cm
Lesions less than 1 cm.
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
Lesions 1-2 cm
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
Atypical vascular pattern.
Lesions greater than 2 cm.
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is
Hepatocellular Cancer
n
U
r
e
iv
y
t
i
s
f
o
u
o
L
e
l
l
i
v
is