CIRRHOSIS.

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Presentation transcript:

CIRRHOSIS

CIRRHOSIS Term was 1st coined by Laennec in 1826 Cirrhosis is the end result of many chronic liver diseases. DEFINITION: It is defined histologically as presence of fibrosis and regenerative nodules in the liver

Causes Alcohol 60-70% Chronic viral hepatitis(B or C) 10% Non alcoholic fatty liver disease Immune primary sclerosing cholangitis autoimmune liver disease Primary Biliary cirrrhosis

Cont… Genetic haemochromatosis alpha-antitrypsin deficiency wilson’s disease. Cryptogenic 10-15% Drug induced

Cirrhosis: Pathophysiology Primary event is injury to hepatocellular elements Destruction of hepatocytes, bile duct cells, vascular endothelial cells Repair through cellular proliferation and regeneration Formation of fibrous scar Prevents normal flow of nutrients to hepatocytes and increases vascular resistance

Cirrhosis: Pathophysiology Initially, fibrosis may be reversible if inciting events are removed With sustained injury, process of fibrosis becomes irreversible and leads to cirrhosis Cirrhotic levels of alcohol in: males >60-80g/day for 10yrs females 20-40g/day for 10yrs.

Normal liver Cirrhotic liver

Classification of Cirrhosis WHO divided cirrhosis into 3 categories based on morphological characteristics of the hepatic nodules Micronodular Macronodular Mixed

Micronodular Cirrhosis Nodules are <3 mm in diameter Relatively uniform in size Distributed throughout the liver Liver is of uniform size or mildly enlarged Reflect relatively early disease

Micro nodular cirrhosis

Macronodular & Mixed Cirrhosis Nodules are >3 mm in diameter and vary considerably in size Usually contain portal tracts and efferent veins Liver is usually normal or reduced in size Mixed pattern if both type of nodules are present in equal proportions

Macronodular cirrhosis

Clinical features Hepatomegaly Jaundice Ascites Circulatory changes 1)spider naevi 2)palmar erythema 3)cyanosis Endocrine changes loss of libido,hair loss men- gynaecomastia , testicular atrophy,impotence female-breast atrophy, irregular menses,amenorrhoea

PALMAR ERYTHEMA SPIDER NAEVI

Haemorrhagic tendency bruises,purpura,epistaxis,menorrhagia Portal hypertension splenomegaly,collateral vessels,variceal bleeding,fetor hepaticus. Hepatic encephalopathy Other features- pigmentation,clubbing.

Investigation Complete blood picture -anemia - leucopenia and thrombocytopenia -acanthocytosis Liver function tests -hyperbilirubinaemia - A:G ratio reversal -transaminases-AST and ALT raised. -alkaline phosphatase may be mildly raised Prothrobin time-prolonged Hepatitis B and C markers Blood ammonia- is raised Respiratory alkalosis

Metabolic abnormalities glucose intolerance hyponatraemia hypokalaemia hypomagnesaemia hypophosphataemia Ultrasonic examination liver size and echotexture alteration splenic size collaterals ascites size of portal vein. Liver biopsy confirms the diagnosis

Treatment Treatment of underlying cause,removal of causitive agents like drugs,alcohol. High protein diet, minimum 1g/kg/day 2000-3000 kcal/day Multivitamin supplementation Specific treatment of complications Liver transplantation

Prognosis-Child-Pugh classification SCORE 1 2 3 Encephalopathy none mild marked Bilirubin <34 34-50 >50 Albumin >35 28-35 <28 Prothrobin time <4 4-6 >6 Ascites <7-child’s A, 7-9-child’s B, >9-child’s C

COMPLICATIONS Portal hypertension Ascites Bacterial peritonitis Hepatic encephalopathy Renal failure Portal vein thrombosis Hepatocellular carcinoma

Thank You