PATOLOGIA HEPATICA UIS 2012
Transcript of PATOLOGIA HEPATICA UIS 2012
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PATOLOGIA HEPÁTICA
JORGE ANDRÉS GARCÍA VERA
MD PATÓLOGO
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OBJETIVOS
Conocer la fisiopatología de la ictericia yla hepatitis.
Mencionar agentes etiológicosimportantes en la lesión hepática
Identificar y correlacionar los diferenteshallazgos morfológicos
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RECORDEMOS
Anatomia-Fisiologia
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ANATOMÍA
HIGADO
1400 -1600 gr
Es el órganoparenquimatoso
de mayor tamaño
Doble circulación
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• 25% del gasto cardiaco.
• 60-70 % vena porta y 30-40% por la arteriahepática.
• Drenaje vena hepática
• Hilio Hepático:
– Arteria hepática
– Vena hepática
– Conducto biliar común
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• Bilis-Canalículo biliar-Conductillos-Conductos
hepáticos derecho e izquierdo.
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MICROARQUITECTURA
• Clásica:
– Lóbulos hexagonales
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HIGADO
CONEXIÓNENTRE LA
CIRCULACIÓNSISTEMICA YESPLÁCNICA
HOMEOSTASISY ELIMINACIONDE TOXINAS
METABOLISMODE FARMACOS
SINTESIS YEXCRECCIONDE BILIS
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PATRONES MORFOLÓGICOS DELESIÓN HEPÁTICA
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Degeneración y acumulación intracelular
Necrosis y apoptosis
Inflamación
Regeneración
Fibrosis
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Degeneración y acumulaciónintracelular
Tumefacción celular .
Pigmentos biliares,hierro, cobre, lípidos,
partículas víricas…
Colestasis
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Hialina de Mallory
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Mujer embarazada de 28 años, en su tercer trimestrede embarazo. Hallazgo de autopsia
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HIGADO GRASO AGUDO DELEMBARAZO
• Tercer trimestre
•
ESTEATOSIS MICROVACUOLAR
• Encefalopatía
Zapata R, Higado agudo graso y Sindrome de Hellp Gastr Latinoam 2004; Vol 15, Nº 2: 150 - 157
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Diagnóstico
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Necrosis y Apoptosis
• Necrosis coagulativa-Isquemia.
• Apoptosis-Lesión toxica, vírica o inmunitaria
• Necrosis focal, zonal, submasiva, masiva.
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• Centrolobulillar o zona 3. Isquemia
• Necrosis medio zonal. Fiebre Amarilla
• Necrosis zona 1?
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Inflamación
• Aguda o crónica
• Portal
• Periportal
• HEPATITIS
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Regeneración
Posterior a necrosis
Nódulos de regeneración
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Si la necrosis no alcanza al tejido conectivo sepuede regenerar de forma casi perfecta laestructura del hígado
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Fibrosis
Respuesta ainjuria crónica
DAÑOHEPATICO
IRREVERSIBLE.
CIRROSIS
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LABORATORIOS
Integridad
delhepatocito
• Transaminasas
• LDH
Función de
excreciónbiliar
• BT-BD-BI
• FA
Función
Hepatocitaria• Albúmina sérica
• TP
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ICTERICIA/ COLESTASIS
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ICTERICIA
Producciónde
bilirrubina
Eliminaciónde
bilirrubina
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COLESTASIS
• Obstrucción de la vía biliar intra oextrahepática
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HEPATOPATIAS
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Toxica
Microorganismos-infecciosas
Metabólicas
Inmunitarias
Vasculares
Neoplasias
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1. Hepatopatía Tóxica
Toxicidad directaAlcohol, fármacos
Toxicidad indirectaMetabolitos,Inflamación
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Toxicidad por alcohol
ENFERMEDADHEPÁTICAALCOHÓLICA
Esteatosishepática
HepatitisAlcohólica
Cirrosis
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Esteatosis Hepática
MICROVESICULAR MACROVESICULAR FIBROSIS
Cambios grasos son REVERSIBLES
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Hepatitis Alcohólica
Edema y necrosishepatocitos
H. de Mallory
Reacciónneutrofílica:
Fibrosis
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Cirrosis alcohólica
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2. Hepatopatía por microorganismos
•Citomegalovirus CMV-Mononucleosis-Virus hepatotropos
Virus
TB miliar
•Staphylococo- Salmonella
Bacterias
•Cándida
Hongos
•Malaria- Amebiasis
Parásitos
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Absceso hepático amebiano
Perucca E. ABSCESO HEPÁTICO AMEBIANO EN EL EMBARAZO: REPORTE DE UN CASO. REV CHIL OBSTET GINECOL 2010; 75(1)
E. histolytica.
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Hepatitis Viral
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Formas Clínicas
Estado de portador
Infección aguda
Hepatitis Crónica
HepatitisFulminante
Cirrosis
Hepatocarcinoma
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Virus Hepatotropos
VHA VHB VHC VHD VHE VHF VHG
Todos producen patrones clínicos y morfológicos similares de hepatitisaguda , varían en su potencial de inducir estados de portador yenfermedad crónica o fulminante.
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Portador
Presencia de antígenos en suero durante
6 meses a partir de su detección
Sano o portador con enfermedad
crónica
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Hepatitis Aguda
Periodo deincubaciónvariable
Fase preictéricasintomática
Fase ictéricasintomática
Convalecencia
Cualquier virus hepatotropo
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Necrosis aislada o focalCuerpos de Councilman
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Hepatitis Viral Crónica
• Evidencia sintomática, bioquímica oserológicos de inflamación hepática durantemás de 6 meses, sin mejoría sostenida, con
comprobación histológica de inflamación ynecrosis.
• VHB, VHC
• Predispone al desarrollo de carcinomahepatocelular
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Características VHA VHB VHC VHD VHE
AGENTE ARN ADN ARN ARN ARN
HEPATITIS CRONICA No Si 5-10 % Si > 60% < 5% coinfeccción
80% superinfección
no
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Hepatitis Fulminante
• Encefalopatía hepática en un plazo de 2 a 3semanas después del inicio de los síntomas.
• Vírica 12%
• Toxicad por fármacos o químicos 50%
• Mortalidad 25-90%
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HEPATITIS A
Virus RNA
Trasmisión fecal-oralEstado de portador NOHepatitis Crónica NO
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HEPATITIS B
• Virus DNA
• Transmisión sexual- vertical- parenteral
• Estado portador SI• Hepatitis Crónica SI
• Carcinoma Hepatocelular SI
Todos los fluidos corporales excepto lasheces
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VHB
Hepatitisaguda
seguida deresolución
Hepatitis
fulminante
CoinfecciónVHD
Hepatitis
Crónica
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HEPATITIS C
• Junto con la hepatopatía alcohólica es la causamás común de daño hepático crónico.
• Anticuerpos antiVHC no proporcionaninmunidad efectiva.
Uso de drogas 60%
Transmisión sexual 15%
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HEPATITIS D
Virus RNA replicacióndeficiente
Necesita HBsAg
Coinfección aguda:VHB+VHC
Sobre infección: portadorcrónico VHB
Mayor riesgo de H.crónica y fulminante
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HEPATITIS E
• Mortalidad en las mujeres embarazadas hastaun 20%.
• No se asocia a enfermedad hepática crónica.
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ALTERACIONES METABOLICAS
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HIPERBILIRRUBINEMIA
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• Anemia hemolítica, hemorragias, eritropoyesis ineficaz
Exceso de producción
Reducción dela captación
• Ictericia fisiológica del recién nacido, ictérica por lactancia,Crigler-Najjar, Gilbert
Alteraciones de la conjugación
• Hiperbilirrubinemia conjugada, Síndrome de DubinJohnson, Síndrome de Rotor
Alteración excreción
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HEMOCROMATOSIS
Acumulación excesiva de hierro en el cuerpo.
Hemocromatosis primaria. Mutación en HFE.Alteración en la Hepcidina (inhibe la absorción).
Hemocromatosis secundaria
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• Cirrosis micronodular
•
Diabetes mellitus• Pigmentación cutánea
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40 años con alteraciones neurológicas episodio
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40 años con alteraciones neurológicas, episodiopsicótico. Presenta adicionalmente cirrosis
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ENFERMEDAD DE WILSON
• Autosómica recesiva
• Acumulación de cobre en tejidos y órganos.
• Hígado, cerebro, ojo.
• Mutación gen ATP7B en el cromosoma 13.excreción disminuida.
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Miranda M, Venegas P. El anillo de Kayser-Fleischer como signo diagnóstico en
la Enfermedad de Wilson Rev. chil. neuro-psiquiatr. v.40 n.2 Santiago abr. 2002
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ENFERMEDAD DE WILSON
• Atrofia de ganglios basales
• Hígado graso
• Hepatitis crónica
•
Cirrosis
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Biopsia hepática. Enfisema panacinar
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DEFICIT ALFA 1 ANTITRIPSINA
• Acumulación intracitoplasmática
• Inclusiones citoplasmáticas PAS +
•
Enfisema pulmonar y alteración hepática
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CIRROSIS, HIPERTENSIÓN PORTAL EINSUFICIENCIA HEPATICA
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CIRROSIS
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• Enfermedad crónica ,difusa e irreversible del
hígado, caracterizada por la existencia defibrosis y nódulos de regeneración queconducen a una alteración de la estructuravascular.
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• PUENTES FIBROSOS SEPTALES
• NODULOS PARENQUIMATOSOS
• ALTERACIONES DE ARQUITECTURA VASCULAR
ETIOLOGIA
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ETIOLOGIAEnfermedad hepática alcohólica 60-70%
Hepatitis viral 10%
Enfermedades biliares 5-10%
Hemocromatosis primaria 5%
Enfermedad de Wilson Rara
Deficit de alfa 1 antitripsina Rara
Cirrosis criptogénetica 10-15%
CLASIFICACION MORFOLÓGICA
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CLASIFICACION MORFOLÓGICA
Micronodular
Macronodular
Mixta
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FISIOPATOLOGÍA
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FISIOPATOLOGÍA
Célula de Ito oestrellada
Colagenizacióndel espacio Disse,obliteración de
las fenestracionesdel sinusoide
Resistencia alflujo de sangre,
difusión alteradade moléculas.
Cortocircuito dela circulación
portal
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Agresor
Inflamación
Fibrosis
Cirrosis
CLASIFICACIÓN ETIOLÓGICA
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• Alcohólica
• Postnecrótica
• Biliar
• Pigmentada
•
Otras• Criptogénica
CLASIFICACIÓN ETIOLÓGICA
CIRROSIS ALCOHÓLICA
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CIRROSIS ALCOHÓLICA
• Estado terminal de la hepatopatía alcohólica
• MICRONODULAR
•
CIRROSIS DE LAENNEC
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CIRROSIS POSTNECROTICA
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CIRROSIS POSTNECROTICA
• Hepatitis infecciosa
• Hepatotoxinas
• MACRONODULAR
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CIRROSIS BILIAR
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CIRROSIS BILIAR
• Lesión u obstrucción prolongada del sistemabiliar intrahepático o extrahepático.
• Trastorno de la excreción biliar, destruccióndel parénquima hepático y fibrosis progresiva.
• PRIMARIA
• SECUNDARIA
• Destrucción granulomatosa de
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• Destrucción granulomatosa deconductillos biliares intrahepáticos.
• Mecanismo autoinmune: Acsmitocondriales
Cirrosis
biliarprimaria
• Obstrucción biliar prolongada de losconductos biliares extrahepáticos.
• Estenosis post-operatorias
• Coledocolitiasis• Neoplasias
• Atresia biliar
Cirrosisbiliar
secundaria
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HTP
Aumento de la resistencia al flujo de sangre portal
CAUSAS
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CAUSAS
Prehepáticas
•Trombosis de laVena porta
Intrahepáticas
• CIRROSIS
Posthepáticas
•ICC
• S. Budd-Chiari
Consecuencias Clínicas
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Consecuencias Clínicas
AscitisCortocircuitosvenosos porto-
sistémicos
Esplenomegaliacongestiva
Encefalopatíahepática
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Complicaciones
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Complicaciones
• Síndrome hepato-renal 8%• Mal pronóstico
•
Peritonitis espontanea 10 %• Mortalidad 20 %
Cortocircuitos portosistémicos
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Cortocircuitos portosistémicos
• Venas rectales y perirrectales (hemorroides)
• Unión cardioesofágica (varices esofágicas)
• Retroperitoneo y ligamento falciforme delhígado (venas colaterales periumbilicales)
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Consecuencias
de lainsuficiencia
hepática
Encefalopatía hepática
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Encefalopatía hepática
Rigidez Hiperreflexia
AsterixisAumento de
niveles de
amonio en sangre
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Coagulopatía
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Coagulopatía
• Disminución en la síntesis de los factores de lacoagulación.
• Disminución absorción VIT K
• CID
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ALTERACIONES VASCULARES
diagnóstico
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diagnóstico
Congestión pasiva crónica
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Congestión pasiva crónica
Desordenes vasculares
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Desordenes vasculares
• Trombosis de la vena porta – Síndrome de Banti
• Trombosis séptica de la porta
• Trombosis de las venas suprahepáticas
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Peliosis Hepática
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NEOPLASIAS
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NODULOS HEPATICOS
Hiperplasia nodular focal: nódulo bien delimitado y mal encapsulado.
Mujeres en edad fértil
Hiperplasia nodular regenerativa: afecta el hígado en su totalidad.
Nódulos displasicos > 1mm en cirróticos
Displasia de alto y bajo grado
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Burgos L, Silva J, Losada H, Manterola C, Guzman P. Hiperplasia focal nodular. Rev ChilCir v.62 n.2 Santiago abr. 2010
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Burgos L, Silva J, Losada H, Manterola C, Guzman P. Hiperplasia focal nodular. Rev ChilCir v.62 n.2 Santiago abr. 2010
Neoplasias Benignas
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p g
• Hemangiomas cavernosos
• Tamaño variable
• Importancia clínica
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• Adenomas de células hepáticas
– Mujeres jóvenes que consumen ACO.
• Importancia clínica
– Dx diferencial de Mtt
– Subcapsulares riesgo de ruptura
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• La mayoría son metástasis
• Carcinoma hepatocelular
•
Colangiocarcinoma intrahepático• Mixto
• Hepatoblastoma• Angiosarcoma
Factores de riesgo CHC
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g
CirrosisNódulo
displásico
Aflatoxinas(metabolito del
hongoAspergillus)
HemocromatosisTirosinemia 40%de los afectados
Etiologia CHC
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g
Infección viralVHB-VHC
Alcoholismocrónico
Contaminantesalimentos
(aflatoxinas)
CHC
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• Hepatoma-Hepatocarcinoma
• 85% de los tumores primarios
• Mal pronóstico
PATOGENIA
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Lesión celulary replicación
Carcinogenesis
Daño del DNA
Mutación debeta catenina
MORFOLOGIA
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• Unifocal• Multifocal
• Infiltrativo
• Angioinvasión
• MTT intrahepáticas
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HepPar -1 (80-90%) AFP, CEA
Clínica
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•
Condición de base : CIRROSIS
• Hepatomegalia
• Ascitis (liquido hemorrágico)
• Síntomas constitucionales
• Alfafetoproteina aumentada
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• Muerte por :
– Caquexia
– Varices gatrointestinales o esofágicas
– Falla hepática
– Rotura del tumor con hemorragia fatal. – Metástasis
Variante fibrolamelar
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• Hombres y mujeres adultos jóvenes.• Único, firme, bandas fibroticas que lo
atraviesan
• No factores de riesgo conocidos• Mejor pronóstico
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• Epitelio de los conductos biliares
• Desmoplasia prominente
• MTT hematógenas y linfáticas
Colangiocarcinoma intrahepático
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• Afecciones del árbol biliar
• Estasis biliar
• Colangitis esclerosante
• Thorotrast
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