liver cirrhosis
TRANSCRIPT
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Cirrhosis of the liver
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Definition
• Cirrhosis is a common chronic, progressive and
diffusive liver disease, caused by one or several
agents act repeatedly and persistently.
• Histologically, cirrhosis is an irreversible
alteration of the liver architecture, consisting of
hepatic fibrosis and areas of nodular regeneration
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Epidemiology
• Worldwide major heath problem
• Over 500,000 deaths per year
• Over 20% were latent
• 2 ~ 10% in postmortem examination
• Common and death leading disease in China
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Etiology and pathogenesis
• Viral hepatitis
• Parasites (schistosomiasis)
• Alcoholic liver disease
• Cholestasis
• Hepatic-Venous outflow obstruction
• Toxicant and drugs
• Metabolic abnormality
• Malnutrition
• Cryptogenic cirrhosis
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Viral hepatitis
• HBV
• HCV
• HBV + HDV
• HAV
• HEV
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Viral hepatitis (HBV)
• Global prevalence: >300 million carriers 5% world population
• Varies widely High prevalence: 8% ~ 15% Far East (southeast Asia China Philippines Indonesia) Middle East Africa parts of South America
Intermediate prevalence: 2% ~ 7% Japan parts of south America parts of central Asia eastern and southern Europe
Low prevalence: <2% US Canada northern Europe Australia
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Viral hepatitis
• Elimination of viral infected hepatocytes is dependent on recognition of viral determinants in association with HLA proteins on the infected hepatocytes by cytotoxic T cells.
• HLA protein display is modulated by exposure to interferon and cytotoxic T cell, NK lytic processes.
• During chronic HBV infection, infected liver cells failed to induce IFN. Therefore, viral protein synthesis is not decreased, HLA protein display is not enhanced.
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Parasites (Schistosomiasis)
• Ova deposited in the portal zones
• Exciting a fibrous tissue reaction
• Co-existence of malaria and cirrhosis reflects
malnutrition, viral hepatitis and toxic factors
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Alcoholic liver disease
• 1/3 cause of cirrhosis in Western country• Most important factor:
“threshold” dose: 600 Kg (men) 150~300 Kg (women)
average daily consumption of alcohol
> 40 ~ 80 g/D, over 10 ~ 15 years
• Liver: primary site of ethanol metabolism• Ethanol can be oxidized by three enzymes systems
ADH CYP2E1 catalase
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Alcoholic liver disease
Mechanism• Direct effect by ethanol, or its first metabolite
(acetaldehyde redox shift oxidant stress)
• Cell-mediated immune
Three histopathologic lesion:
fatty liver, alcoholic hepatitis, cirrhosis
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Biliary cirrhosis
Primary Biliary Cirrhosis:
• Progressive destruction of small and intrahepatic
bile ducts
• Prevalence: 40~150 cases/million
• Women >90 of cases 50y
• Abnormal immunoregulation
• Associated with HLA phenotyeps
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Biliary cirrhosis
Secondary biliary cirrhosis:
Obstruction of the biliary tree, further divided into
two groups
intra-hepatic and extra-hepatic obstruction
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Hepatic-Venous outflow obstruction
• Veno-occlusive disease
• Budd-chiari syndrome
• Constrictive pericarditis
• Chronic congestive heart failure
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Toxicant and drugs
• Tetrachloride carbon
• - methyldopa
• Tetracycline
• Phosphorus
• Arsenic
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Metabolic abnormality
• Iron storage disease (Hemochromatosis)
• Copper storage disease (Wilson’s disease)
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Malnutrition
• Chronic inflammatory bowel disease
• Prolonged lack of dietary proteins and vitamins
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Cryptogenic cirrhosis
• Etiology is unknown
• Viral infection are suscepted in some cases
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Pathophysiology
• Alcoholic cirrhosis – accumulation of fat and scar formation in the liver cells
• Postnecrotic cirrhosis – broad bands of scar tissue resulted from viral, toxic, or autoimmune hepatitis
• Biliary cirrhosis – diffuse fibrosis with jaundice from chronic biliary obstruction
• Cardiac cirrhosis – from long-standing right sided heart failure
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Pathology and classification
Histopathological diagnosis:
• Excessive fibrous tissue
• Regenerating nodules
• Complete distortion of the normal relationship
of hepatic venous outflow radicles and portal veins.
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Anatomical types of regenerating nodules
• Micronodular
• Macronodular
• Mixed cirrhosis
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Micronodular cirrhosis
• Features: Thick regular septa
Regenerating small nodules (<3mm)
Involvement of every lobule
• Alcoholism
Malnutrition
Biliary obstruction
Hemochromatosis
Venous outflow obstruction
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Macronodular cirrhosis
• Features: Septa
Nodules of variable size
(>3mm, even 1~ 3 cm)
Normal lobules in the large nodules
• Two subtypes: postnecrotic
posthepatitic
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Macronodular cirrhosis
Postnecrotic type:
• Coarsely scarred liver
• Large nodules surrounded by broad fibrous septa
• Clumping togathered numerous portal trials
• Toxic cirrhosis
• Cryptogenic cirrhosis
• Multilobular cirrhosis
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Macronodular cirrhosis
Posthepatitic type:
• Macronodules separated by slender fibrous strands
• Connect individual portal areas to each other
• Viral hepatitis
• Wilson’s disease
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Mixed cirrhosis
Features:
• Presenting both micro- and macronodules
• From micronodules to macronodules
• Alcoholism
• Antitrypsin deficiency
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Some aspects of pathology
• The most useful morphologic classification:
gross appearance of the liver
• The morphologic diagnosis of cirrhosis is more
reliable than the histopathological diagnosis
• Schistosomiasis: incomplete septal cirrhosis
coarse portal fibrosis
• Initially enlarged/subsequcetly shrinks
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Clinical manifestation
• Onset: Cryptical and slowly progressive
Majority: 3~5 years or 10 years
Minority: 3~6 months
• Stages: Compensated
Decompensated
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Compensated stage
• Fatigue
• Loss of appetite
• Anorexia
• Abdominal discomfort
• Abdominal pain
• Hepatomegaly (slightly or moderately)
• Splenomegaly
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Decompensated stage
• Deterioration of liver function
• Feature of portal hypertention
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connection.lww.com/ Products/morton/Ch41.asp
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Deterioration of liver function
• General deterioration Deterioration of heath, anorexia, weight loss, weakness, fatigue, Flatulent dyspepsia, abdominal distress, swelling of legs or abdomen, mild fever, loss of libido and hemorrhage.
• Findings of physical examination
Jaundice
Dermatological and sexual signs
Liver (enlarge or shrunken)
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Jaundice
It always implies liver cell destruction exceeds the capacity for regeneration
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Dermatologic and sexual signs
• Skin pigmentation
• Clubbing fingers
• Spider angioma
• Liver palms (palmar erythema)
• Purpura
• Spontaneous bruising / epistaxes
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Dermatologic and sexual signs
• Feminization and hypogonadism Gynecomastia
testicular atrophy
sparse body hair
changes in hair distribution
menstrual irregularities
Mechanism: serum testosterone estrogens
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Liver
• Early stage
Enlarged and palpable
firm regular edge
a fine to coarsely nodular surface
• Later stage
Shrunk and impalpable
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Features of portal hypertension
• Portal-systemic collaterals
• Ascites
• Splenomegaly
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Anatomy and physiology of portal venous system
• Begins in the capillaries of the intestines• Terminates in the hepatic sinusoids • Formed by the confluence of the superior and inferior
mesenteric veins and splenic vein• Liver receives 1500ml/min, 2/3 from portal vein
Hepatic artery provides 50% oxygen• The pressure within the sinusoids is low • Lack of valves
***: Between the splanchnic venules and the heart
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Portal-systemic collaterals
• Esophageal and gastric varices
• Dilation of the remnant of the umbilical vein
• Dilation of abdominal veins
• Hemorrhoidial venous collaterals
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Splenomegaly
• Slightly or moderatory enlarged
• Hypersplenism
Leukopenia
Thrombocytopenia
Anemia
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Ascites
• Prominent feature of portal-hypertension
• 70% of patients are positive
• An early sign in presinusoidal portal hypertension
relative late in intrahepatic portal hypertension
• Massive ascites: abdominal herniae (腹疝)
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Complications
• Upper gastrointestinal bleeding
• Hepatic encephalopathy
• Infection
• Hepatorenal syndrome
• Primary liver cancer
• Imbalance of electrolytes and acid-alkaline
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Upper gastrointestinal bleeding
• Major complication
• Incredible high mortality
• Source of bleeding:
esophageal varices 60%~80%
gastric varices 7%
congestive gastropathy 5%~20%
(paptic ulcer, acute erosive gastritis etc)
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Hepatic encephalopathy
The most severe and deadly complications
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Infection
Increased risk for bacterial infection
pneumonia
biliary infection
E.coli infection and
spontaneous bacterial peritonitis (SBP)
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SBP
• Pathogen of SBP: gram’s negative bacteria
•Features of SBP: fever, abdominal pain or tenderness
decreased bowel sounds
•Suspected patients: sudden onset of HE or hypotension
•Diagnosis: elevated ascites fluid white blood cells
positive ascitic fluid culture
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Hepatorenal syndrome
• Decreased renal function due to severe liver disease
• Histologically normal kidney
• Involved factors
Sympathetic nervous system
Renin-angiotensin-aldosterone
Prostaglandins
Endotoxemia
Others ( vasopressin , leukotriene etc)
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Primary liver cancer
• Suspected signs
Hepatomegaly within short time
Persistent abdominal pain
Enlarged liver with uneven surface or mass
Bloody ascites
• Serum α-fetoprotein (α-FP) 70%
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Imbalance of electrolytes and acid-alkaline
• Hyponatraemia
• Hypokalaemia
• Metabolic alkalosis
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Laboratory and other tests
• Urine
• Serum
• Hematology
• Ultrasonograply
• Barium esophagogram
• Endoscopy
• Liver biopsy
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Diagnosis
• Patients with a history of viral hepatitis, prolonged
alcohol overconsumption, schistosome infection,
hemochromatosis• Features of deterioration of liver function and
portal hypertension• Enlarged or shrunk liver with nodular surface• Abnormal liver function tests• Liver biopsy shows widespread fibrosis with
nodular regeneration
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Complete diagnosis
Etiology
Morphology
Hepatic function
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Specific clinical clues to etiology of cirrhosis
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Posthepatitic cirrhosis
• Previous acute hepatitis, transfusion, illicit drugs
• Multiorgan involment such as rash, arthritis,
thyroiditis, colitis etc.
• Serum HBV or HCV positive
• Some markers of hepatitis, elevated gamma
globulin or positive anti-nuclear antibodies.
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Schistosomiasis
• Contacting with fresh water contaminated with
cercariae in epidemic area
• Splenomegaly being the earliest and most
prominent sign
• Bleeding from esophageal varices may be the
initial clinical presentation
• Liver function is relatively good
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Alcoholic cirrhosis
• Alcoholic beverage consumption >40~80 g for over
10 years
• Large parotid, myopathy, neuropathy, contraction
of the palmar fascia
• sGOT > sGPT, sGOT/sGPT ratio>2
• Polymorpho-nuclear leukocytosis
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Primary biliary cirrhosis
• Female (90%), middle age (40~60y), Pruritus
before icterus
• Xanthomas Raynaud’s phenomen
sclerodactyly telangiectasis
skin hyperpigmentation
• Elevated AKP, IgM, antimitochondrial antibody
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Wilson’s disease
• Family history of liver or neurologic disease
• Childhood onset
• Kayser-Fleischer corneal rings
• Grossly flapping tremor, spastic gait, other
CNS disorder, osteochondritis
• Low serum ceruloplasmin
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Hemochromatosis
• Positive family history
• Skin pigmentation, diabetes, pseudogout,
cardiomyopathy, loss of body hair, testicular atrophy
• Elevated serum ferritin
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Hepatic function (Child-Pugh score)
Index Range ScoreNeuropathy None 1
I, II 2 III, IV 3
Ascite None 1
Mild 2 Massive 3
Serum bilirubin <2 1
(mg / dl) 2~3 2 >3 3
Serum albumin >3.5 1
(g / dl) 2.8~3.5 2 <2.8 3
Ratio of prothrombin time activity >50 1
30~50 2 <30 3
A: 5~8 scores; B: 9~11 scores; C: 12~15 scores
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Differential diagnosis
• Hepatomegaly
• Ascites
• Complications
Upper GI bleeding
Hepatic encephalopathy
Hepatorenal syndrome
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Hepatomegaly
• Chronic hepatitis
• Primary liver cancer
• Parasitization
• Hemologic diseases (leukemia, lymphoma)
• Metabolic diseases
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Ascites
• Tuberculous peritonitis
• Constrictive pericarditis
• Chronic glumerulonephritis
• Intraperitoneal tumors
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Upper GI bleeding
• Peptic ulcer, acute erosive gastritis, gastric cancer
and esophageal varices are four major sources of
upper GI bleeding
• In cirrhotic patients, bleeding are not entirely due
to varices
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Hepatic encephalopathy
• Hypoglycemia
• Uremia
• Diabetic ketoacidosis
• Nonketonic hyperosmolar syndrome
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Hepatorenal syndrome
• Prerenal azotemia
• Acute tubular necrosis
• Drug nephrotoxicity
• Diagnosis is supported by avid urinary
sodium retention
Urine sodium concentration < 5 mmol / L
unremarkable urinary sediment
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Treatment
• Supportive therapy
• Eliminating the specific causes
• Using antifibrotic drugs
• Management of ascites
• Management of complications
• Liver transplantation
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Supportive therapy
• Appropriate rest 1g protein/kg, 2000 Calories daily
Vitamin(s), thiamine, vitamin K, iron and folic acid
• Removal of exogenous aggravating agents liver tonics, offending drugs
control of infection and electrolyte
• Correction of hypoalbuminemia and coagulation fresh frozen plasma, platelet concentrates or
prothrombin complex
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Etiology and definitive treatment of cirrhosis
Etiology Treatment
Virus hepatitis ? Antivirals
Schistosomiasis Praziquantel 60~80mg/kg for 2 days
Alcohol Abstention
Iron overload Vensection. Deferoxamine 0.5~1g/kg
Copper overload penicillamine 0.8~1.2 g/day
α1 antitrypsin deficiency ? Transplant
Tyrosinaemia Withdraw dietary tyrosine
Galactosaemia Withdraw milk and milk products
Cholestasis Relieve biliary obstruction
Budd-Chiari syndrome Relieve main venous block
Immunological factors Prednison or predisolon 20~60 mg/day
Toxins and drugs Identify and stop
Cryptogenic ---
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Antifibrotic drugs
• Penicillamine
Primary biliary cirrhosis
Wilson’s disease
Inhibiting the formation of cross-links of collagen
• Colchicine
Inhibiting assembly of collagen
Increasing collagenase production
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Management of ascites• Ascites with severe, acute liver disease
Improvement of liver function
• Ascites with stable or steadily worsening liver
function
Maximal reabsorption rate: 700~900 ml/day
Goal of management: weight loss < 1.0kg/day (ascites + peripheral edema)
weight loss < 0.5kg/day (ascites)
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Management of ascites
• Sodium restriction
• Fluid restriction
• Diuresis
• Paracentesis
• Side-to-side portacaval shunt
• Peritoneovenous shunt
• Transjugular intrahepatic portosystemic shunts
(TIPS)
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Sodium restriction
• 1g sodium retaines 200 ml fluid
• > 0.75 g will result in ascites in cirrhotic patients
• < 0.5 g/d (22 mEg), restricted in patients without
ascites
• Strict bed rest
improving renal clearance in the supine position
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Fluid restriction
≈1000 ml/day
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Diuresis• If sodium restriction are failed
• Diuretic for ascites
Urine loss
loop diuretic
Na++ K++ Furosemide
Bumetamide
Distal diuretic
Na+ K Spironolactone
Triamterene
Amiloride
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Diuresis
• Drugs of choice: Spironolactone Inhibiting aldosterone synthesis
Causing natriuresis with sparing potassium
100mg~400mg/d may induce diuresis
• Furosemide and/or thiazides
both natriuresis and potassium wasting• Spironolactone(distal diuretic)+Furosemide(loop diuretic)
sufficient to initial diuresis
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Paracentesis
• Paracentesis of 1~2 L of ascitic fluid
effective, less costly
• Albumin or plasma infusion
expensive
• Ascites reinfusion
inexpensive
for refractory or massive ascites
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Portal-systemic shunts
• Side-to-side portacaval shunts
• Peritoneovenous shunts (Le Veen shunt)
• Transjugular intrahepatic portosystemic shunts
(TIPS)
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Management of complications
Variceal bleeding:
• General managements maintain intravascular volum
close monitoring blood pressure, urine output and
mental status
• Medical managements
use of vasoconstrictors (vasopression or somatostatin)
sclerotherapy
band ligation
beta-adrenergic blockade
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Management of complications
Spontaneous bacterial peritonitis:
• Empirical therapy with cefotoxanine or ampicillin
and an aminoglycoside
• Specific antibiotic therapy are selected
• 10~14 days duration
• Recurrent episodes are high
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Management of complications
Hepatic encephalopathy
Hepatorenal syndrome
Treatment is usually unsuccessful
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Liver transplantation
• Latest advance in management of cirrhosis
• Frequently done in Western country
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Summary• Definition fibrosis + nodular regeneration
• Viral hepatitis (China) alcohol (Western Country)
• Micro- , Macro- and mixed cirrhosis
• Decompensated stage:
Deterioration of liver function
Portal hypertension
• Complications
• Hepatic function: Child-Pugh score
• Sodium, fluid restriction, diuresis (Spirolactone)