Gastrointestinal Tumors. Sites Of Malignancy

1. GASTROINTESTINALGASTROINTESTINAL
TUMORSTUMORS

2. Gastrointestinal TractGastrointestinal Tract

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

5. SponsoredSponsored
Medical Lecture Notes –Medical Lecture Notes – All SubjectsAll Subjects
USMLE Exam (America) –USMLE Exam (America) – PracticePractice

6. CA Cancer J Clin 2011; 55:10-30

7. CA Cancer J Clin 2011; 55:10-30

8. Non-cardia cancer
Squamous
cell carcinoma
Adenocarcinoma of the
distal esophagus
Cancer of the cardia
Subcardial cancer

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

18. Gastro-Oesophageal RefluxGastro-Oesophageal Reflux
DiseaseDisease
reflux of gastric contents into oesophagus, resulting in mucosal damagereflux of gastric contents into oesophagus, resulting in mucosal damage

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

23. Structure of Esophagus

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

29. Diagnosis/StagingDiagnosis/Staging

30. HistologyHistology
Squamous Cell Cancer Adenocarcinoma

31. EUS-Esophageal CancerEUS-Esophageal Cancer

32. EUS-Esophageal CancerEUS-Esophageal Cancer

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

35. PET Scan –Esophageal CaPET Scan –Esophageal Ca

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

41. Risk FactorsRisk Factors
 Partial gastrectomy- slightly increased riskPartial gastrectomy- slightly increased risk
 Menetrier’s DiseaseMenetrier’s Disease- rugal fold- rugal fold
hypertrophy, hypochlorhydria and protein-hypertrophy, hypochlorhydria and protein-
losing enteropathylosing enteropathy
 Adenomatous Gastric PolypsAdenomatous Gastric Polyps

42. Pathologic FeaturesPathologic Features
 Distal cancer- H. Pylori relatedDistal cancer- H. Pylori related
 Proximal cancer- GERD/Barrett’s dzProximal cancer- GERD/Barrett’s dz
 Chronic gastritisChronic gastritis  Atrophic GastritisAtrophic Gastritis 
Intestinal MetaplasiaIntestinal Metaplasia  Dysplasia/CancerDysplasia/Cancer
 Intestinal type vs diffuse typeIntestinal type vs diffuse type

43. Gastric CancerGastric Cancer

44. Clinical FeaturesClinical Features
 Vague symptoms- early satiety, abdominalVague symptoms- early satiety, abdominal
pain, bloating, dyspepsia, weight loss,pain, bloating, dyspepsia, weight loss,
anorexiaanorexia
 Gastric bleeding, microcytic anemia,Gastric bleeding, microcytic anemia,
vomingvoming
 Associated paraneoplastic syndromes-Associated paraneoplastic syndromes-
 Acanthosis NigricansAcanthosis Nigricans
 Venous Thrombi (Trousseau’s syndrome)Venous Thrombi (Trousseau’s syndrome)
 Sister Mary Joseph’s nodeSister Mary Joseph’s node
 Virchow’s nodeVirchow’s node

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

51. Other Gastric LesionsOther Gastric Lesions

52. EUS-StomachEUS-Stomach

53. Small Bowel CancersSmall Bowel Cancers
 Adenocarcinoma- know about FAP,Adenocarcinoma- know about FAP,
HNPCCHNPCC
 Lymphomas- especially in AIDS ptLymphomas- especially in AIDS pt
 Crohn’s diseaseCrohn’s disease
 Celiac diseaseCeliac disease
 Neuroendocrine tumorsNeuroendocrine tumors
 Gardner’s, Peutz-Jegher’s, JuvenileGardner’s, Peutz-Jegher’s, Juvenile
Polyposis syndrome, Cowden diseasePolyposis syndrome, Cowden disease

54. Colon AnatomyColon Anatomy

55. Colon Carcinogenesis and the EffectsColon Carcinogenesis and the Effects
of Chemopreventive Agentsof Chemopreventive Agents

56. Colon AdenocarcinomaColon Adenocarcinoma

57. Colon Cancer StagingColon Cancer Staging

58. Colon Cancer ResectionColon Cancer Resection

59. Colon CA SurgeryColon CA Surgery

60. Bowel PreparationBowel Preparation

61. Recent Therapy AdvancesRecent Therapy Advances
 Chemotherapy
 Oxaliplatin, Irinotecan
 Combination: FOLFOX, FOLFIRI
 Targeted Small Molecules
 Avastin, Erbitux
 Metastatectomy, RFA, Chemoembolization
 Prevention
 ASA, Celebrex

62. Pancreatic CancerPancreatic Cancer

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

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

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

74. Discharge PlanningDischarge Planning
 Palliative carePalliative care
 Preparation for deathPreparation for death
 Family supportFamily support

75. Pancreatic Cancer StagingPancreatic Cancer Staging

76. Treatment ModalitiesTreatment Modalities
 Surgery
 Radiation
 Chemotherapy
 Multimodality
 Targeted Molecules (Avastin, Erbitux)
 Directed Therapy (RFA, Microspheres)
 Palliative Devices (Stents)

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

78. Pancreatic CAPancreatic CA Biliary StentBiliary Stent

79. GI Malignancy TherapyGI Malignancy Therapy
 Primary – Surgical (except Anal,
Esophageal)
 Neoadjuvant – Anal, Esophageal
 Adjuvant – Gastric, Pancreatic, Colorectal
 Locally Advanced – Multimodality
 Metastatic – Systemic, Rarely Surgery

81. Liver TumorsLiver Tumors

82. Liver TumorLiver Tumor

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

84. ClassificationClassification
 HemangiomaHemangioma
 Focal nodularFocal nodular
hyperplasiahyperplasia
 AdenomaAdenoma
 Liver cystsLiver cysts
1.1. Primary liverPrimary liver
cancerscancers
 HepatocellularHepatocellular
carcinomacarcinoma
 Fibrolamellar carcinomaFibrolamellar carcinoma
 HepatoblastomaHepatoblastoma
2. Metastases2. Metastases
Benign Malignant

85. Benign Liver LesionsBenign Liver Lesions
1.1. HemangiomaHemangioma
2.2. Focal nodular hyperplasiaFocal nodular hyperplasia
3.3. AdenomaAdenoma
4.4. CystsCysts

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

88. CT/HemangiomaCT/Hemangioma

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

91. CT/FNHCT/FNH

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

94. AdenomaAdenoma

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

101. HCC: Systemic FeaturesHCC: Systemic Features
 HypercalcemiaHypercalcemia
 HypoglycemiaHypoglycemia
 HyperlipidemiaHyperlipidemia
 HyperthyroidismHyperthyroidism

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

104. US: HCCUS: HCC

105. CT: Venous PhaseCT: Venous Phase

106. CT: Arterial PhaseCT: Arterial Phase

107. HCC: PrognosisHCC: Prognosis
 Tumor sizeTumor size
 Extrahepatic spreadExtrahepatic spread
 Underlying liver diseaseUnderlying liver disease
 Pt performance statusPt performance status

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

111. Radio Frequency AblationRadio Frequency Ablation

112. Ethanol InjectionEthanol Injection

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

114. ChemoembolizationChemoembolization

115. Resection TypesResection Types
 Anatomical resection  Atypical resection

116. The LiverThe Liver

117. Figure 1
Livraghi T et al. Radiology 2003;226:441-451
©2003 by Radiological Society of North America

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