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CIRROSIS HEPATICA

ANATOMIA PATOLOGICA PRACTICA


GABRIELA MERINO REAL

LIVER CIRRHOSIS
Liver cirrhosis is the 12th cause of death by disease around the world. In South America it is the 5th cause of general mortality and the 2nd one between all those related to gastrointestinal and hepatobiliary diseases. This affects principally males. The principal causes are alcoholism and chronic viral hepatitis. The principal cause of hospitalization is upper gastrointestinal bleeding. Most of the patients have an advanced disease at the moment of diagnosis.

WHAT IS LIVER CIRRHOSIS?


Cirrhosis is a condition in which the liver slowly deteriorates and malfunctions due to chronic injury. Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. It also impairs the liver ability to:
Control infections Remove bacteria and toxins from the blood Process nutrients, hormones and drugs Make proteins that regulate blood clotting Produce bile to help absorb fats

WHAT CAUSES LC?


Cirrhosis has various causes. Heavy alcohol consumption and chronic hepatitis C have been the most common cause of cirrhosis. Obesity is becoming a common cause of cirrhosis, either as the sole cause or in combination with alcohol, hepatitis C or both. Many people with this disease have more than one cause of liver damage. It is not caused by trauma to the liver or short-term causes of damage. Usually years of chronic injury are required to cause cirrhosis.

ALCOHOL-RELATED LIVER DISEASE


Most people who consume alcohol do not suffer damage to the liver. But heavy alcohol use over several years can cause chronic injury to it. The amount of alcohol it takes to damage the liver varies greatly from person to person. For women, consuming two to three drinks per day and for men three to four drinks per day, can lead to liver damage and cirrhosis.

CHRONIC HEPATITIS C
The hepatitis C virus is a liver infection that is spread by contact with an infected persons blood. Chronic hepatitis C causes inflammation and damage to the liver over time that can lead to cirrhosis.

CHRONIC HEPATITIS B AND D


Hepatitis B virus is a liver infection that is spread by contact with and infected persons blood, semen or other body fluid. Hepatitis B, like Hepatitis , causes liver inflammation and injury that can lead to cirrhosis. The Hepatitis D is another virus that infects the liver and can cirrhosis, but it occurs only in people who already have Hepatitis B.

NONALCOHOLIC FATTY LIVER DISEASE


In NAFLD, fat builds up in the liver and eventually causes cirrhosis. This increasingly common liver disease is associated with obesity, diabetes, protein malnutrition, coronary artery disease, and corticosteroid medications.

AUTOIMMUNE HEPATITIS
This form of Hepatitis is caused by the bodys immune system attacking liver cells and causing inflammation, damage, and eventually cirrhosis. Researchers believe genetic factors may make some people more prone to autoimmune diseases. About 70 percent of those with autoimmune hepatitis are female.

DISEASES THAT DAMAGE OR DESTROY BILE DUCTS


Several different diseases can damage or destroy the ducts that carry bile from the liver, causing bile to back up in the liver and leading to cirrhosis. In adults, the most common condition in this category is the primary biliary cirrhosis, a disease in which the bile ducts become inflamed and damaged and, ultimately disappear. In infants, damaged bile ducts are commonly caused by biliary atresia, condition in which the ducts are absent or injured.

INHERITED DISEASES
Cystic fibrosis, alpha-1 antitrypsin deficiency, hemochromatosis, galactosemia and glycogen storage diseases are inherited diseases that interfere whit how the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly. Cirrhosis can result from theses conditions.

DRUGS, TOXINS AND INFECTIONS


Other causes of cirrhosis include drug reactions, prolonged exposure to toxic chemicals, parasitic infections, and repeated bouts of heart failure with liver congestion.

WHAT ARE THE SYMPTOMS?


Many people with cirrhosis have no symptoms in the early stages of the disease. However, as the disease progresses, a person may experience:
Weakness Fatigue Loss of appetite Nausea Vomiting Weight loss Abdominal pain and bloating when fluid accumulates in the abdomen Itching

WHAT ARE THE COMPLICATIONS?


As liver function deteriorates, one or more complications may develop. In some people, complications may be the first sings of the disease. Some complications are :
Edema and ascites Bruising and bleeding Portal hypertension Splenomegaly Jaundice Gallstones Sensitivity to medications Hepatic encephalopathy Liver cancer Insulin resistance and type 2 diabetes Other problems

HOW IS CIRRHOSIS DIAGNOSED?


The diagnosis of cirrhosis is usually based on the presence of a risk factor for cirrhosis, such as alcohol use or obesity; and is confirmed by physical examination, blood tests, and imaging. For example, on abdominal examination, the liver may feel hard or enlarged with signs of ascites. A liver biopsy can confirm the diagnosis of cirrhosis but is not always necessary.

HOW IS CIRRHOSIS TREATED?


Treatment for cirrhosis depends on the cause of the disease and whether complications are present. The goals of the treatment are to slow the progression of scar tissue in the liver and prevent or treat the complications of the disease. Eating a nutritious diet and avoiding alcohol and other substances are in fact included in all treatments.

CARACTERSTICAS PATOLGICAS
MACROSCOPA Y MICROSCOPA

CIRROSIS MICRONODULAR
Macroscopa Hgado de tamao normal o pequeo, aumentado de consistencia. Se observa difusa y homogneamente micronodular (1 a 3 mm) con tabiques conjuntivos rosado- blanquecinos, deprimidos, firmes o elsticos, que rodean completamente los ndulos. Microscopa En los tabiques fibrosos se observa infiltracin linfo-histiocitaria de grado variable. Los tabiques rodean o disecan los ndulos de hepatocitos; stos son de disposicin trabecular o desordenada con signos regenerativos. Rara vez pueden reconocerse venas centrolobulillares. En los tabiques suele encontrarse una proliferacin de conductillos biliares, y, especialmente en la periferia de los ndulos regenerativos, pseudoconductos constituidos por hepatocitos. La cirrosis micronodular es frecuente consecuencia del dao heptico por alcohol. Tambin puede ser consecutiva a una hepatitis crnica activa, dao de la va biliar, primario o secundario, o dficit de alfa-1antitripsina.

CIRROSIS MACRONODULAR
Macroscopa El hgado se observa de tamao conservado, menos frecuentemente pequeo. Los ndulos miden de 3 mm a 3 cm de dimetro; entre ellos, bandas o tabiques fibrosos, grisblanquecinos o gris-rojizos. Microscopa Los tabiques se forman por colapso del retculo de zonas necrticas (tabiques pasivos) a los que se agrega fibrosis activa. Se reconocen espacios portales y venas centrales. Algunas de estas ltimas estn comunicadas con espacios portales por tabiques o estn claramente incluidas en las cicatrices. La cirrosis macronodular se observa como secuela de hepatitis necrotizante viral, enfermedad de Wilson, hepatitis crnica activa con reagudizaciones, dficit de alfa-1- antitripsina y en las fases tardas de dao por alcohol con cirrosis micronodular establecida.

CIRROSIS BILIAR PRIMARIA


Enfermedad de causa desconocida, de patogenia autoinmunitaria, con anticuerpos antimitocondriales circulantes. Afecta principalmente a mujeres de edad mediana. Histologa: la lesin comienza por degeneracin del epitelio de conductillos biliares, seguida de una reaccin inflamatoria crnica portal y periportal con necrosis en sacabocado, granulomas epiteloideos vecinos a los conductillos biliares, desaparicin de conductillos biliares y signos de colestasia. En una fase ulterior hay fibrosis portal con formacin de puentes y ulterior evolucin a cirrosis.

CIRROSIS BILIAR SECUNDARIA


Es producida por una obstruccin de la va biliar extraheptica. La colangitis, que afecta a los conductos tambin en los espacios portales, daa progresivamente a los hepatocitos perilobulillares. La inflamacin portal lleva a una fibrosis perilobulillar, que tiende a disecar los lobulillos y a alterar la arquitectura heptica. Macroscopa El hgado es micronodular, verde-negruzco, duro. La va biliar se observa dilatada y puede haber extensas cicatrices perihiliares. Es caracterstico el aspecto en guirnaldas del parnquima remanente.

IMGENES

Corte histolgico a bajo aumento. Esteatosis heptica. Se observan dos foquitos de hepatocitos parcialmente disgregados, con infiltracin por leucocitos.

Corte histolgico a gran aumento que muestra hepatocitos con degeneracin hialina de Mallory; agunos estn disgregados, con infiltracin por polinucleares.

Corte histolgico a bajo aumento, que muestra a la derecha una vena centrolobulillar con fibrosis circundante, que tiende a formar un puente hacia arriba a la izquierda. Abajo, a la izquierda, un foco triangular de fibrosis que se extiende en puente hacia arriba a la izquierda.

Hgado con el parnquima normal difusamente reemplazado por ndulos pardoamarillentos que miden menos de 5 mm. de dimetro. El tinte amarillento corresponde a la infiltracin grasosa (Cirrosis alcohlica de Laennec)

Detalle de un corte de hgado con nodulillos pardoamarillentos, algunos rojizos, delimitados por bandas deprimidas (fibrosas).

Corte histolgico a bajo aumento que demuestra microndulos, algunos con esteatosis. Los ndulos delimitados por bandas fibrosas de color azul (tincin tricrmica de Masson).

Hgado con ndulos de diversos tamaos: la mayora de ellos miden ms de 1 cm. Se observan reas deprimidas extensas, que corresponden a fibrosis secundaria a colapso de reas de necrosis confluente.

Hgado con el parnquima normal difusamente reemplazado por ndulos que miden ms de 5 mm. de dimetro en un paciente con enfermedad de Wilson.

Ndulos de gran tamao: dentro del ndulo superior se observa un espacio porta. Los ndulos estn delimitados por bandas netas de tejido fibroso (tincin de Van Gieson).

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