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CIRRHOSIS
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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
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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
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Cont… Genetic haemochromatosis alpha-antitrypsin deficiency
wilson’s disease. Cryptogenic % Drug induced
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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
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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.
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Normal liver Cirrhotic liver
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Classification of Cirrhosis
WHO divided cirrhosis into 3 categories based on morphological characteristics of the hepatic nodules Micronodular Macronodular Mixed
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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
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Micro nodular cirrhosis
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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
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Macronodular cirrhosis
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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
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PALMAR ERYTHEMA SPIDER NAEVI
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Haemorrhagic tendency bruises,purpura,epistaxis,menorrhagia
Portal hypertension splenomegaly,collateral vessels,variceal bleeding,fetor hepaticus. Hepatic encephalopathy Other features- pigmentation,clubbing.
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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
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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
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Treatment Treatment of underlying cause,removal of causitive agents like drugs,alcohol. High protein diet, minimum 1g/kg/day kcal/day Multivitamin supplementation Specific treatment of complications Liver transplantation
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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
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COMPLICATIONS Portal hypertension Ascites Bacterial peritonitis
Hepatic encephalopathy Renal failure Portal vein thrombosis Hepatocellular carcinoma
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