3. Anatomic Sites of Malignancy
Esophagus
Stomach
Colon/Rectum
Anus
Pancreas
Liver
�
4. Incidence and MortalityIncidence and Mortality
in 2011in 2011
EsophagealEsophageal
CancerCancer
14,520 new cases14,520 new cases
13,570 deaths13,570 deaths
Gastric CancerGastric Cancer
21,860 new cases21,860 new cases
11,550 deaths11,550 deaths
U.S.:
1,372,910 new cancer cases and 570,280 deaths
CA Cancer J Clin 2011; 55:10-30
9. Predisposing FactorsPredisposing Factors
for SCCA Esophagusfor SCCA Esophagus
TobaccoTobacco
AlcoholAlcohol
DietDiet
Chronic esophagitisChronic esophagitis
AgeAge
RaceRace
GenderGender
Role of HPV?Role of HPV?
10. Other Risk FactorsOther Risk Factors
Previous head and neck or lung cancerPrevious head and neck or lung cancer
(annual rate 3-7%).(annual rate 3-7%).
Plummer-Vinson syndrome (IronPlummer-Vinson syndrome (Iron
deficiency).deficiency).
Esophageal diverticulae.Esophageal diverticulae.
Lye strictures: long latent period.Lye strictures: long latent period.
Radiation injury (therapeutic, atomic bomb).Radiation injury (therapeutic, atomic bomb).
..
11. AchalasiaAchalasia
Cancer arises in 1-10% of patientsCancer arises in 1-10% of patients
symptomatic for an average 15-25 years.symptomatic for an average 15-25 years.
Usually squamous cell carcinoma ofUsually squamous cell carcinoma of
middle third of esophagus.middle third of esophagus.
Presents at younger age than usual.Presents at younger age than usual.
12. TylosisTylosis
Autosomal dominant gene.Autosomal dominant gene.
50% incidence of esophageal cancer by50% incidence of esophageal cancer by
age 45.age 45.
95% risk by age 65.95% risk by age 65.
13. AdenocarcinomaAdenocarcinoma
of the Esophagusof the Esophagus
Incidence rates increased >350%Incidence rates increased >350%
since the mid 1970s.since the mid 1970s.
Increasing 20% per year in U.S.Increasing 20% per year in U.S.
Even higher in U.K., Australia,Even higher in U.K., Australia,
Holland.Holland.
Rates for gastric cardiaRates for gastric cardia
adenocarcinoma also increased.adenocarcinoma also increased.
14. AdenocarcinomaAdenocarcinoma
of the Esophagusof the Esophagus
6-8 times higher in men than in women.6-8 times higher in men than in women.
3-4 times higher in whites than in blacks.3-4 times higher in whites than in blacks.
White men represent 82% of cases.White men represent 82% of cases.
Gut 50:368-372, 2002
15. AdenocarcinomaAdenocarcinoma
of the Esophagusof the Esophagus
Obesity eating to much fod at oncesObesity eating to much fod at onces
Reflux disease and Barrett'sReflux disease and Barrett's
esophagus.esophagus.
DietDiet
SmokingSmoking
SclerodermaScleroderma
16. Esophageal AdenocarcinomaEsophageal Adenocarcinoma
and Obesityand Obesity
US study: 4 x risk, highest quartile BMIUS study: 4 x risk, highest quartile BMI
compared to lowest.compared to lowest.
BMI >30 vs BMI <22,BMI >30 vs BMI <22, ↑↑risk 16 fold.risk 16 fold.
Similar trends in gastric cardia adenoca.Similar trends in gastric cardia adenoca.
JNCI 90:150-155, 1998
17. Esophageal AdenocarcinomaEsophageal Adenocarcinoma
and Reflux Diseaseand Reflux Disease
Swedish study: Having reflux symptomsSwedish study: Having reflux symptoms
more than 3 times a week associatedmore than 3 times a week associated
with 17 fold increased risk.with 17 fold increased risk.
U.S. study: daily GERD symptomsU.S. study: daily GERD symptoms
↑↑ risk 5 times.risk 5 times.
NEJM 340:825-831, 1999; Cancer Causes Control 11:231-238, 2000
19. Barrett's EsophagusBarrett's Esophagus
Dysplastic changes in distal esophagusDysplastic changes in distal esophagus
and gastroesophageal junction.and gastroesophageal junction.
30-40 fold increase in adenocarcinoma of30-40 fold increase in adenocarcinoma of
the esophagus.the esophagus.
10-15% of Barrett’s patients will develop10-15% of Barrett’s patients will develop
adenocarcinoma.adenocarcinoma.
Risk of cancer is about 0.5% per year.Risk of cancer is about 0.5% per year.
20. Barrett’s OesophagusBarrett’s Oesophagus
columnar-lined oesophagus (CLO)columnar-lined oesophagus (CLO)
Pre-malignant conditionPre-malignant condition
Normal squamous epithelium ofNormal squamous epithelium of
oesophagus replaced by columnaroesophagus replaced by columnar
epitheliumepithelium
(epithelial metaplasia)(epithelial metaplasia)
Strong association between chronicStrong association between chronic
heartburn, Barrett’s oesophagus &heartburn, Barrett’s oesophagus &
oesophageal canceroesophageal cancer
Adaptive & protective response toAdaptive & protective response to
chronic gastro-oesophageal refluxchronic gastro-oesophageal reflux
Direct precursor to oesophagealDirect precursor to oesophageal
cancercancer
21. Malignant TransformationMalignant Transformation
in Barrett'sin Barrett's
Long-standing gastroesophageal reflux.Long-standing gastroesophageal reflux.
Field cancerization effect.Field cancerization effect.
Medical therapy does not reverseMedical therapy does not reverse
progression to malignancy.progression to malignancy.
With ablation, new epithelium may growWith ablation, new epithelium may grow
over dysplastic clones.over dysplastic clones.
22. Endoscopic SurveillanceEndoscopic Surveillance
of Barrett’s Esophagusof Barrett’s Esophagus
With high-grade dysplasia, 19-26%With high-grade dysplasia, 19-26%
develop invasive cancer within 2 to 7.5develop invasive cancer within 2 to 7.5
years.years.
American College of Gastroenterology:American College of Gastroenterology:
No dysplasia x 2 years: q 2 yearsNo dysplasia x 2 years: q 2 years
Low-grade dysplasia: q 6 mo. x 2, then qLow-grade dysplasia: q 6 mo. x 2, then q
yearyear
High-grade dysplasia: surgery, ablation orHigh-grade dysplasia: surgery, ablation or
EGD q 3 mo.EGD q 3 mo.
Am J Gastroenterol 1998; 93:1028-1032Am J Gastroenterol 1998; 93:1028-1032
24. Esophageal CancerEsophageal Cancer
Two types:Two types:
Squamous Cell Carcinoma (SCC)Squamous Cell Carcinoma (SCC)- previously the- previously the
most dominant esophageal cancer and worldwidemost dominant esophageal cancer and worldwide
accounts for 30-40% of esophageal canceraccounts for 30-40% of esophageal cancer
AdenocarcinomaAdenocarcinoma- over past two decades incidence- over past two decades incidence
is rising. Incidence within Barrett’s is 0.4-0.5%/yris rising. Incidence within Barrett’s is 0.4-0.5%/yr
Now both tumors occur with equal frequencyNow both tumors occur with equal frequency
Differ in tumor location, predisposing factors,Differ in tumor location, predisposing factors,
prognosis and treatmentprognosis and treatment
25. Risk FactorsRisk Factors
Epidemiology of esophageal cancer in the United StatesEpidemiology of esophageal cancer in the United States
Squamous cellSquamous cell AdenocarcinomaAdenocarcinoma
New cases per yearNew cases per year 60006000 60006000
Male-to-female ratioMale-to-female ratio 3:13:1 7:17:1
Black-to-white ratioBlack-to-white ratio 6:16:1 1:41:4
Most common location Middle esophagusMost common location Middle esophagus Distal esophagusDistal esophagus
Major risk factorsMajor risk factors Smoking, alcoholSmoking, alcohol Barrett's esophagusBarrett's esophagus
26. Esophageal Cancer and BEEsophageal Cancer and BE
Incidence of Adenocarcinoma ofIncidence of Adenocarcinoma of
esophagus is increasing- 3.2/100,000esophagus is increasing- 3.2/100,000
people from 0.7/100,000 in the 1970’speople from 0.7/100,000 in the 1970’s
Overall risk of adenoca in BE is 30-52Overall risk of adenoca in BE is 30-52
times higher than general population,times higher than general population,
however most people with BE will neverhowever most people with BE will never
develop dysplasia or cancerdevelop dysplasia or cancer
27. Clinical PresentationClinical Presentation
Dysphagia occurs in 90% of patients,Dysphagia occurs in 90% of patients,
odynophagia 50%odynophagia 50%
Solids more problematic than liquidsSolids more problematic than liquids
Other symptoms may include hoarseness,Other symptoms may include hoarseness,
hematemesis, and nauseahematemesis, and nausea
More advanced disease may causeMore advanced disease may cause
feeling of “food getting stuck” orfeeling of “food getting stuck” or
regurgitationregurgitation
Weight loss commonWeight loss common
28. Diagnosis/StagingDiagnosis/Staging
Barium Esophagram- more accurate withBarium Esophagram- more accurate with
larger lesions- may serve as a primary testlarger lesions- may serve as a primary test
in patients with Dysphagiain patients with Dysphagia
Endoscopy with biopsiesEndoscopy with biopsies
Endoscopic UltrasoundEndoscopic Ultrasound
CT/PETCT/PET
33. Diagnosis/StagingDiagnosis/Staging
EUSEUS- Sensitivity for T staging is 90%, N- Sensitivity for T staging is 90%, N
(lymph node) staging is 80%(lymph node) staging is 80%
Limitations: cannot detect distant diseaseLimitations: cannot detect distant disease
and overstages T3 lesionsand overstages T3 lesions
CTCT- T staging sensitivity 60%. Useful for- T staging sensitivity 60%. Useful for
detecting distant disease and T4 lesionsdetecting distant disease and T4 lesions
34. Diagnosis/StagingDiagnosis/Staging
PETPET- used with CT to create a fusion- used with CT to create a fusion
image that allows the CT image to beimage that allows the CT image to be
correlated with the nuclear scancorrelated with the nuclear scan
Valuable in detecting nodal mets andValuable in detecting nodal mets and
detecting residual cancer after treatmentdetecting residual cancer after treatment
Poor at T staging and for lesions less thanPoor at T staging and for lesions less than
1 cm1 cm
36. TreatmentTreatment
ChemotherapyChemotherapy- cisplatin based results in- cisplatin based results in
42-64% response rate. Combination42-64% response rate. Combination
therapy for advanced diseasetherapy for advanced disease
Other agents include fluorouracil, taxanes,Other agents include fluorouracil, taxanes,
irinotecanirinotecan
RadiotherapyRadiotherapy- used in combination with- used in combination with
chemo- main benefit is relieving dysphagiachemo- main benefit is relieving dysphagia
by reduction of tumorby reduction of tumor
37. TreatmentTreatment
Endoscopic TherapyEndoscopic Therapy- T1 lesions - Photodynamic- T1 lesions - Photodynamic
therapy or EMRtherapy or EMR
SurgerySurgery- esophagectomy (Ivor-Lewis) is primary- esophagectomy (Ivor-Lewis) is primary
treatmenttreatment
Overall mortality rate from procedure is 5-10%,Overall mortality rate from procedure is 5-10%,
morbidity 10% from anastomotic leakage,morbidity 10% from anastomotic leakage,
pulmonary problems, cardiac eventspulmonary problems, cardiac events
Survival rate- 20% at 1 yr, 5% at 5 yearsSurvival rate- 20% at 1 yr, 5% at 5 years
38. TreatmentTreatment
Most beneficial in Stage I, II diseaseMost beneficial in Stage I, II disease
Debate is whether pre-operativeDebate is whether pre-operative
neoadjuvant therapy affects outcomeneoadjuvant therapy affects outcome
Resectable lesions- improves survival 7-Resectable lesions- improves survival 7-
9% at 2 years9% at 2 years
Goal is to make pt node negativeGoal is to make pt node negative
Main Problem- 50-60% present withMain Problem- 50-60% present with
incurable locally advanced or metastaticincurable locally advanced or metastatic
diseasedisease
39. Gastric CancerGastric Cancer
750,000 cases annually. 22,000 new cases in750,000 cases annually. 22,000 new cases in
the US each yearthe US each year
Rise in cancer of the proximal stomach and GEJRise in cancer of the proximal stomach and GEJ
Risk FactorsRisk Factors: Diet, Genetics, H. Pylori infection,: Diet, Genetics, H. Pylori infection,
Pernicious anemia, Pts with partial gastrectomy,Pernicious anemia, Pts with partial gastrectomy,
Atrophic gastritis, Menetrier’s diseaseAtrophic gastritis, Menetrier’s disease
40. Risk FactorsRisk Factors
Dietary Factors- foods rich in nitrates,Dietary Factors- foods rich in nitrates,
preserved meat and vegetablespreserved meat and vegetables
Genetic FactorsGenetic Factors- Lynch syndrome II.- Lynch syndrome II.
Microsatellite instability (MSI) is present inMicrosatellite instability (MSI) is present in
up to 33% of gastric cancersup to 33% of gastric cancers
Pernicious AnemiaPernicious Anemia- auto-immune atrophic- auto-immune atrophic
gastritis increased risk by 2-3xgastritis increased risk by 2-3x
45. Diagnostic StudiesDiagnostic Studies
Contrast radiograpyContrast radiograpy- may be initial test for vague- may be initial test for vague
symptomssymptoms
EndoscopyEndoscopy
CTCT- cannot determine depth of invasion. Good- cannot determine depth of invasion. Good
for detecting distant diseasefor detecting distant disease
EUSEUS- more accurate and T and N staging than- more accurate and T and N staging than
CTCT
46. Staging/PrognosisStaging/Prognosis
Early gastric cancer- 5-yr survival rate ofEarly gastric cancer- 5-yr survival rate of
80-90%80-90%
Survival for Stage III or IV disease is 5-Survival for Stage III or IV disease is 5-
20% at 5 years20% at 5 years
47. TreatmentTreatment
Surgical resection and lymph nodeSurgical resection and lymph node
removal are the only chance for cureremoval are the only chance for cure
66% of patients present with advanced66% of patients present with advanced
disease that is incurable by surgery alonedisease that is incurable by surgery alone
Resistant to radiotherapy- used mostly forResistant to radiotherapy- used mostly for
palliationpalliation
Chemo- decreases tumor burden in 15%Chemo- decreases tumor burden in 15%
of patients at bestof patients at best
48. Gastric CancerGastric Cancer
Gastric LymphomaGastric Lymphoma--
most of B-cell originmost of B-cell origin
Primary gastricPrimary gastric
lymphoma rarelymphoma rare
Non-Hodgkin’s mostNon-Hodgkin’s most
common typecommon type
5 year survival rate is5 year survival rate is
50%50%
49. B-cell lymphomaB-cell lymphoma
Low grade B-cellLow grade B-cell
lymphoma associatedlymphoma associated
with chronic H. Pyloriwith chronic H. Pylori
infectioninfection
EUS is most reliableEUS is most reliable
method for stagingmethod for staging
Treatment of H. PyloriTreatment of H. Pylori
eradicates the tumoreradicates the tumor
50. Other Gastric TumorsOther Gastric Tumors
Carcinoid TumorsCarcinoid Tumors- 0.3% of all gastric- 0.3% of all gastric
tumors. Produce 5-HIAA and can causetumors. Produce 5-HIAA and can cause
carcinoid syndrome. May lead to hyper-carcinoid syndrome. May lead to hyper-
gastrinemiagastrinemia
GISTGIST- originate usually from the- originate usually from the
muscularis propria- need to differentiatemuscularis propria- need to differentiate
from leiomyoma, leiomyosarcoma, lipomafrom leiomyoma, leiomyosarcoma, lipoma
63. IncidenceIncidence
One of the leading causes of cancerOne of the leading causes of cancer
mortalitymortality
28,000 new cases per year28,000 new cases per year
Incidence increases with ageIncidence increases with age
Rarely before 50 y/o – usually 60 to 70 y/oRarely before 50 y/o – usually 60 to 70 y/o
Slightly more in menSlightly more in men
Less than 20% live longer than one yearLess than 20% live longer than one year
64. Etiology of Pancreatic CancerEtiology of Pancreatic Cancer
Exact cause unknownExact cause unknown
Smokers at high riskSmokers at high risk
High fat, high protein, high caffeine, hiHigh fat, high protein, high caffeine, hi
alcohol dietsalcohol diets
May be geneticMay be genetic
65. PathophysiologyPathophysiology
Usually arises from epithelial cells of theUsually arises from epithelial cells of the
pancreatic ductspancreatic ducts
Tumor discovered in late stages so hasTumor discovered in late stages so has
spread throughout pancreasspread throughout pancreas
Can be a result of metastatic disease fromCan be a result of metastatic disease from
lung, breast, thyroid, kidney, or skinlung, breast, thyroid, kidney, or skin
Rapid growing with spread to surroundingRapid growing with spread to surrounding
tissuetissue
66. More PathoMore Patho
Most common site is the head of theMost common site is the head of the
pancreaspancreas
Necrotic pancreatic tumors increaseNecrotic pancreatic tumors increase
thromboplastic factorsthromboplastic factors
Thrombophlebitis seen as a resultThrombophlebitis seen as a result
67.
68. DiagnosticsDiagnostics
No specific blood tests to diagnoseNo specific blood tests to diagnose
Elevated amylase, lipase, alkalineElevated amylase, lipase, alkaline
phosphatase, bilirubin, CEA, C19-9phosphatase, bilirubin, CEA, C19-9
CT, UltrasonographyCT, Ultrasonography
Needle biopsyNeedle biopsy
ParacentesisParacentesis
ERCP – most definitive diagnostic testERCP – most definitive diagnostic test
69. Signs and SymptomsSigns and Symptoms
Vague, dull, abdominal painVague, dull, abdominal pain
Weigh loss, weaknessWeigh loss, weakness
Anorexia, nausea, vomitingAnorexia, nausea, vomiting
Glucose intoleranceGlucose intolerance
FlatulenceFlatulence
GI bleedingGI bleeding
AscitesAscites
Leg/calf painLeg/calf pain
Jaundice (if head of pancreas involved)Jaundice (if head of pancreas involved)
Clay colored stoolsClay colored stools
Dark urineDark urine
70. Clinical ManagementClinical Management
Goal is to prevent spread of tumorGoal is to prevent spread of tumor
Chemotherapy or radiationChemotherapy or radiation
Pain controlPain control
Total resectionTotal resection
Head of pancreas removalHead of pancreas removal
Whipple procedureWhipple procedure
71. Whipple ProcedureWhipple Procedure
Radical pancreaticoduodenectomyRadical pancreaticoduodenectomy
Used for cancer of the pancreas head onlyUsed for cancer of the pancreas head only
Removal of:Removal of:
Pancreas headPancreas head
DuodenumDuodenum
StomachStomach
Portion of jejunumPortion of jejunum
GallbladderGallbladder
SpleenSpleen
Duct anastomoses: pancreatic, common bile toDuct anastomoses: pancreatic, common bile to
jejunumjejunum
72.
73. Clinical Management ContinuedClinical Management Continued
Nutritional support: TPN, tube feedingNutritional support: TPN, tube feeding
Needs critical care nursing postoperativelyNeeds critical care nursing postoperatively
Fluid and electrolyte replacementFluid and electrolyte replacement
Glucose monitoringGlucose monitoring
77. The Application ofThe Application of
Expandable MetalExpandable Metal
Stents within theStents within the
Gastrointestinal TractGastrointestinal Tract
Baron, T. H. N Engl J Med 2001;344:1681-1687
83. ObjectiveObjective
1.1. Identify the most important features ofIdentify the most important features of
common benign liver tumorscommon benign liver tumors
2.2. Know the risk factors, diagnosis, andKnow the risk factors, diagnosis, and
management of hepatocellularmanagement of hepatocellular
carcinomacarcinoma
86. HemangiomaHemangioma
Clinical FeaturesClinical Features
The commonest liver tumorThe commonest liver tumor
5% of autopsies5% of autopsies
Usually single smallUsually single small
Well demarcated capsuleWell demarcated capsule
Usually asymptomaticUsually asymptomatic
87. HemangiomaHemangioma
Diagnosis and ManagementDiagnosis and Management
DiagnosisDiagnosis
US: echogenic spot, well demarcatedUS: echogenic spot, well demarcated
CT: venous enhancement from periphery toCT: venous enhancement from periphery to
centercenter
MRI: high intensity areaMRI: high intensity area
No need for FNANo need for FNA
TreatmentTreatment
No need for treatmentNo need for treatment
89. Focal Nodular Hyperplasia (FNH)Focal Nodular Hyperplasia (FNH)
Clinical FeaturesClinical Features
Benign nodule formation of normal liverBenign nodule formation of normal liver
tissuetissue
Central stellate scarCentral stellate scar
More common in young and middle ageMore common in young and middle age
womenwomen
No relation with sex hormonesNo relation with sex hormones
Usually asymptomaticUsually asymptomatic
May cause minimal painMay cause minimal pain
90. Focal Nodular Hyperplasia (FNH)Focal Nodular Hyperplasia (FNH)
Diagnosis and ManagementDiagnosis and Management
DiagnosisDiagnosis::
US: Nodule with varying echogenicityUS: Nodule with varying echogenicity
CT: Hypervascular mass with central scarCT: Hypervascular mass with central scar
MRI: iso or hypo intenseMRI: iso or hypo intense
FNA: Normal hepatocytes and Kupffer cells withFNA: Normal hepatocytes and Kupffer cells with
central core.central core.
TreatmentTreatment::
No treatment necessaryNo treatment necessary
Pregnancy and hormones OKPregnancy and hormones OK
92. Hepatic AdenomaHepatic Adenoma
Clinical featuresClinical features
Benign neoplasm composed of normalBenign neoplasm composed of normal
hepatocytes no portal tract, central veins,hepatocytes no portal tract, central veins,
or bile ductsor bile ducts
More common in womenMore common in women
Associated with contraceptive hormonesAssociated with contraceptive hormones
Usually asymptomatic but may have RUQUsually asymptomatic but may have RUQ
painpain
Mat presents with rupture, hemorrhage, orMat presents with rupture, hemorrhage, or
malignant transformation (very rare)malignant transformation (very rare)
93. Hepatic AdenomaHepatic Adenoma
Diagnosis and ManagementDiagnosis and Management
DXDX
US: filling defectUS: filling defect
CT: Diffuse arterial enhancementCT: Diffuse arterial enhancement
MRI: hypo or hyper intense lesionMRI: hypo or hyper intense lesion
FNA : may be neededFNA : may be needed
TxTx
Stop hormonesStop hormones
Observe every 6m for 2 yObserve every 6m for 2 y
If no regression then surgical excisionIf no regression then surgical excision
95. Liver CystsLiver Cysts
May be single or multipleMay be single or multiple
May be part of polycystic kidney diseaseMay be part of polycystic kidney disease
Patients often asymptomaticPatients often asymptomatic
No specific management requiredNo specific management required
Hydated cystHydated cyst
96. Malignant Liver TumorsMalignant Liver Tumors
1.1. Hepatocellular carcinoma (HCC)Hepatocellular carcinoma (HCC)
2.2. Fibro-lamellar carcinoma of the liverFibro-lamellar carcinoma of the liver
3.3. HepatoblastomaHepatoblastoma
4.4. Intrahepatic cholangiocarcinomaIntrahepatic cholangiocarcinoma
5.5. OthersOthers
97. HCC: IncidenceHCC: Incidence
The most common primary liver cancerThe most common primary liver cancer
The most common tumor in Saudi menThe most common tumor in Saudi men
Increasing in US and all the worldIncreasing in US and all the world
98. HCC: Risk FactorsHCC: Risk Factors
The most important risk factor isThe most important risk factor is cirrhosiscirrhosis
from any cause:from any cause:
1.1. Hepatitis B (integrates in DNA)Hepatitis B (integrates in DNA)
2.2. Hepatitis CHepatitis C
3.3. AlcoholAlcohol
4.4. AflatoxinAflatoxin
5.5. OtherOther
99. HCC: Clinical FeaturesHCC: Clinical Features
Wt loss and RUQ pain (most common)Wt loss and RUQ pain (most common)
AsymptomaticAsymptomatic
Worsening of pre-existing chronic liver disWorsening of pre-existing chronic liver dis
Acute liver failureAcute liver failure
O/E:O/E:
Signs of cirrhosisSigns of cirrhosis
Hard enlarged RUQ massHard enlarged RUQ mass
Liver bruit (rare)Liver bruit (rare)
100. HCC: MetastasesHCC: Metastases
Rest of the liverRest of the liver
Portal veinPortal vein
Lymph nodesLymph nodes
LungLung
BoneBone
BrainBrain
102. HCC: labsHCC: labs
Labs of liver cirrhosisLabs of liver cirrhosis
AFP (Alfa feto protein)AFP (Alfa feto protein)
Is an HCC tumor markerIs an HCC tumor marker
Values more than 100ng/ml are highlyValues more than 100ng/ml are highly
suggestive of HCCsuggestive of HCC
Elevation seen in more than 70% of ptElevation seen in more than 70% of pt
103. HCC: DiagnosisHCC: Diagnosis
Clinical presentationClinical presentation
Elevated AFPElevated AFP
USUS
Triphasic CT scan: very early arterialTriphasic CT scan: very early arterial
perfusionperfusion
MRIMRI
BiopsyBiopsy
108. HCC: LiverHCC: Liver
TransplantationTransplantation
Best available treatmentBest available treatment
Removes tumor and liverRemoves tumor and liver
Only if single tumor less than 5cm or lessOnly if single tumor less than 5cm or less
than 3 tumors less than 3 cm eachthan 3 tumors less than 3 cm each
Recurrence rate is lowRecurrence rate is low
Not widely availableNot widely available
109. HCC: ResectionHCC: Resection
Feasible for small tumors with preservedFeasible for small tumors with preserved
liver function (no jaundice or portal HTN)liver function (no jaundice or portal HTN)
Recurrence rate is highRecurrence rate is high
110. HCC: Local AblationHCC: Local Ablation
For non resectable ptFor non resectable pt
For pt with advanced liver cirrhosisFor pt with advanced liver cirrhosis
Alcohol injectionAlcohol injection
Radiofrequency ablationRadiofrequency ablation
Temporary measure onlyTemporary measure only
113. HCC: ChemoembolizationHCC: Chemoembolization
Inject chemotherapy selectively in hepaticInject chemotherapy selectively in hepatic
arteryartery
Then inject an embolic agentThen inject an embolic agent
Only in pt with early cirrhosisOnly in pt with early cirrhosis
No role for systemic chemotherapyNo role for systemic chemotherapy
119. Fibro-Lamellar CarcinomaFibro-Lamellar Carcinoma
Presents in young pt (5-35)Presents in young pt (5-35)
Not related to cirrhosisNot related to cirrhosis
AFP is normalAFP is normal
CT shows typical stellate scar with radialCT shows typical stellate scar with radial
septa showing persistant enhancementsepta showing persistant enhancement
120. Secondary LiverSecondary Liver
MetastasesMetastases
The most common site for blood bornThe most common site for blood born
metastasesmetastases
Common primaries : colon, breast, lung,Common primaries : colon, breast, lung,
stomach, pancreases, and melanomastomach, pancreases, and melanoma
Mild cholestatic picture (ALP, LDH) withMild cholestatic picture (ALP, LDH) with
preserved liver functionpreserved liver function
Dx imaging or FNADx imaging or FNA
Treatment depends on the primary cancerTreatment depends on the primary cancer
In some cases resection or chemoembolizationIn some cases resection or chemoembolization
is possibleis possible
Hinweis der Redaktion
Esophageal cancer is top 7th cause of death in men
Gastric cancer is top 10th cause of death in women
Tylosis
Plummer-Vinson syndrome
Oncogenic types of HPV found especially in high endemic areas, 0-60% of specimens
For squamous cell carcinoma, risk goes down after smoking cessation.
For squamous cell carcinoma, risk goes down after smoking cessation.
Effects independent of obesity.
Risk is roughly 1% per year
Medical therapy can suppress inflammation so dysplastic areas can be identified.
Ablation by
- Lasers
- Photodynamic therapy with Photoprin.
Patients with severe esophagitis, nodularity, Barrett&apos;s ulcer or stricture are more likely to go on to high grade dysplasia.
Some recommend immediate esophagectomy for confirmed high grade dysplasia.
Head of pancreas can be treated if found early
Tail tumors are usually not found until mets has occurred
Head of pancreas cancer
ERCP visualization and aspiration
Ascitic fluid from paracentesis may show malignant cells
Limited success with chemo or radiation
Radiation: seeds of radioactive iodine combined with intra-arterial chemo
Morphine in high doses
Body or tail of pancreas tumors are not candidates for surgery as metastasis has already occurred
Complete resection done rarely
Resection of the proximal pancreas, adjoining duodenum, distal portion of the stomach, and distal portion of the common bile duct
Tube feeding usually with J tube placement
Figure 1. Transverse CT scan shows hemorrhage caused by rupture of a superficial 4.5-cm HCC. Scan was obtained because of a decrease in hematocrit level 24 hours following RF ablation. High-attenuation fluid, denoting hemorrhage, is observed surrounding the liver (white arrows). Black arrow points to the ablated hepatoma. The patient was successfully treated with a blood transfusion. Follow-up CT scans showed complete resolution of this complication.