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3 cancer de vesícula biliar

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3 cancer de vesícula biliar

  1. 1. GENERALIDADES• El carcinoma de vesícula es la 2° malignidad biliar primaria más común y la 5° del TGI.• En la mayoría de los casos es diagnosticada en etapas avanzadas.• Pronóstico malo ▫ supervivencia a 5 años  0-10%, ▫ la mayoría mueren antes de los 6 meses
  2. 2. EPIDEMIOLOGÍA• Distribución heterogénea  los índices más altos están en India, Sudamérica, Asia. ▫ Es raro en Europa occidental, EUA (1.2:100,000).• La incidencia está relacionada con la incidencia de colelitiasis.• La raza blanca > afroamericanos.• La edad 7°-8° década de la vida.• Más predisposición en mujeres.
  3. 3. ETIOLOGÍA MultifactorialFACTORES DE RIESGOAdenomiomatosis Invaginaciones de la mucosa con formación de quistes en la muscularis propia. Esta alteración generalmente es benigna.Unión anómala del Reflujo de secreciones pancreáticas sistema pancreaticobiliar inflamación crónica de la mucosa.ductal (UASPBD) 10% de pacientes con carcinoma de vesícula tienen UASPBD y 15-40% de los pacientes con UASPBD tienen carcinoma de vesícula. Aparece 10 años antes . Tx  Qx profilácticaCarcinógenos metilcolantreno, O-aminoazotoluenO, y nitrosaminasColangiocarcinoma
  4. 4. Colelitiasis (>1cm) Es el factor más importante. Hay litiasis en 65-90% de pacientes con carcinoma de vesícula El carcinoma de vesícula se desarrolla en 1-3% de los pacientes con colelitiasis. Hay una correlación positiva entre el riesgo de carcinoma de vesícula y el número y tamaño de los litos  >1cmPortador cronico de S.typhi o paratyphiPariente de primer aumenta el riesgo 13.9%grado con Cancer devesicular biliar.Enfermedadinflamatoria intestinalIntrahepatic biliary Lesión precursora de carcinomadysplasia
  5. 5. Vesícula de porcelana Es una calcificación excesiva de la pared de la vesícula. Se considera un gran factor de riesgo, en especial con calcificación mucosa selectiva (tipos II y III) que con calcificación difusa.Colangitis esclerosante El adenocarcinoma de vesícula biliar se desarrolla enprimaria hasta un 20% de los pacientes con CEP. El 50% de las tumoraciones de la vesícula biliar en pacientes con CEP son malignos. Colecistectomía profiláctica.
  6. 6. PATOLOGÍA• 90%  Adenocarcinoma ▫ La variante Papilar es menos invasiva y agresiva• 10 %  carcinoma anaplasico, carcinoma de células escamosas y carcinoma adenoescamoso• Distribución dentro de la vesícula: ▫ 60%  fondo ▫ 30% cuerpo ▫ 10%  cuello.• Invasión directa (Hígado), metástasis linfática o hematogena.
  7. 7. PATOGENIA• Depende de la etiología• Inflamación Displasia Carcinoma in situ adenocarcinoma• Tiempo de progresión 10-15 años• Aumento de iNOS, COX-2• Mutación de gen TP-53, (temprano), Mutación de gen K-ras (60%)• Inestabilidad de microsatelites en regiones que albergan genes supresores de tumores
  8. 8. CUADRO CLÍNICO • Inicialmente es clínicamente silencioso • Dolor abdominal, ictericia [secundaria a invasión directa de conductos biliares o metástasis al ligamento hepatoduodenal] • Enfermedad mas avanzada: ▫ Perdida de peso ▫ Distensión abdominal ▫ Síntomas secundarios a compresión o invasión de órganos adyacentes • Marcadores tumorales: CAE y CA 19-9 (no específicos)
  9. 9. DIAGNOSTICO• Eco abdominal ▫ Sensibilidad 85% y especificidad 80% ▫ Engrosamiento focal o difuso de la pared, masa intraluminal que se origina de la pared y una masa subhepática que reemplaza la vesícula biliar e invade órganos adyacentes.• La RM y la TC  si los resultados del ultrasonido son indeterminados.• PET  detección de metástasis a distancia.
  10. 10. ESTADIFICASIÓN TNM and American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC)TNM Staging Systems for Gallbladder Carcinoma CRITERIASTAGETx Primary tumor cannot be assessed Regional lymph nodes cannot be NxT0 No evidence of primary tumor assessedTis Carcinoma in situ N0 No regional lymph node metastasesT1a Tumor invades lamina propria Metastases in cystic duct,T1b Tumor invades muscularis propria N1 pericholedochal, and/or hilar lymph Tumor invades perimuscular connective nodesT2 tissue without extension beyond serosa Metastases into peripancreatic (head or into liver only), periduodenal, periportal, celiac, N2 Tumor invades serosa OR Tumor invades and/or superior mesenteric lymphT3 one adjacent organ OR Both (extension nodes ≤2 cm into liver) Mx Distant metastases cannot be assessed Tumor extends >2 cm into liver AND/OR M0 No distant metastases Tumor extends into ≥2 adjacent organs M1 Distant metastasesT4 (stomach, duodenum, colon, pancreas, omentum, extrahepatic bile ducts, liver)
  11. 11. AJCC/UICC Stage Tumor Node Metastasis0 Tis N0 M0IA T1 N0 M0IB T2 N0 M0II A T3 N0 M0II B T1-3 N1 M0III T4 Any N M0IV Any T Any N M1
  12. 12. TRATAMIENTO Cirugía• Única opción potencialmente curable• Solo 15-47% son candidatos al momento del diagnostico (debido a etapa avanzada)• Contraindicaciones: ▫ Múltiples metástasis hepáticas o peritoneales ▫ Ascitis maligna ▫ Metástasis a distancia ▫ Afección amplia del ligamento hepatoduodenal ▫ Oclusión de los vasos principales
  13. 13. • Hay tasas mayores de recurrencia después de colecistectomía simple. Se prefiere colecistectomía radical en estadio >1b• La quimioterapia y radioterapia no son tratamientos estandar. ▫ Carcinoma de vesicula biliar es radioresistente
  14. 14. BIBLIOGRAFÍA:• Feldman, M, Friedman, L & Brandt, L. (2010) Sleisenger and Fordtrans Gastrointestinal and Liver Disease. 9th edition. Saunders Elsevier editorial

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