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CIRRHOSIS.pdf
1. DR.AFRIN NEEHA , DNB GENERAL MEDICINE
CIRRHOSIS OF LIVER
ALCOHOL ASSOCIATED, CHRONIC HEP B /C ASSOCIATED, AIH AND
NAFLD,CARDIAC CIRRHOSIS, COMPLICATIONS-PORTAL HYPERTENSION
3. Case 1
• 55 yr /M
• C/0 fever,bloating,yellow
discoloration of eyes
• Examination:
• Tender and palpable liver
• H/0 alcohol misuse from
last 20 years
• No other comorbidities
• Skin
fi
nding?
• Diagnosis?
• Further workup?
• Treatment?
4.
5.
6.
7. ALCOHOL ASSOCIATED CIRRHOSIS
• Alcohol ass. Fatty liver ,Alcohol associated hepatitis, alcohol associated cirrhosis
• Ch.alcohol use can produce
fi
brosis in absence of in
fl
ammation/necrosis
• Alcohol ass.cirrhosis: nodules<3 mm D-micronodular cirrhosis.
• Micro nodular and macro nodular cirrhosis.
• Alcohol associated cirrhosis accounts for 48% of deaths due to cirrhosis
• CT appears in both periportal and pericentral zones and eventually connects
portal triads with central veins forming regenerative nodules.
• C/F: non speci
fi
c :vague right upper quadrant abdominal pain , fever , nausea and
vomiting, diarrhea, anorexia and malaise.
• Speci
fi
c: ascites, edema , UGI hge, jaundice /encephalopathy
8. ALCOHOLIC HEPATITS
• Rapid onset of jaundice (serum bilirubin>3mg/dl), fever , malaise ,tender
hepatomegaly and clinical signs of decompensation(ascites, bacterial
infection, vatical bleeding, and hepatic encephalopathy)
• SIRS+AKI (secondary to hepatorenal syndrome)
• Lab
fi
nding:ALH ,AST:ALT>1.5(400), serum bilirubin >3
• To rule out: biliary obstruction and HCC
• ALH have underlying cirrhosis-80%
9.
10. • Zieves syndrome?
• AST:ALT ratio =2:1
• TREATMENT:
• ABSTINENCE
• Drugs that reduce craving of alcohol:
• Acamprosate calcium and baclofen
• glucocorticoids->7 days failure to
improve bilirubin- treatment failure
• Continued for 28 days
• IV NAC + glucocorticoids:survival
bene
fi
t in alcoholic hepatitis.
19. HEP C /B ASSOCIATED
• HCV exposed- 80 % developed ch.hep C
• Non cytopathic virus, immune mediated liver damage.
• micro and macro nodular cirrhosis on liver Bx.(similar
fi
ndings in hep B)
• Dx: HCV RNA, analysis of HCV genotype or hep b serologies to include
HbsAg, anti hbs, HbeAg, anti Hbe aqnd quantitative HBV DNA levels
• Treatment:
• Several clinical trials and case series: decompensated liver disease can
become compensated with the use of antiviral therapy in hep b(entecavir and
tenofovir)- reduced risk of viral resistance
• Hep c: DAA protocol:- >95% cure (8-12 weeks)n well tolerated.
25. NAFL- CIRRHOSIS
• NAFLD cirrhosis associated with 1-25 risk of developing primary liver
cancer(HCC& intrahepatic cholangiocarcinoma)
• NAFLD associated with insulin resistance , overweight/obesity and metabolic
syndrome.
• Advanced hepatic
fi
brosis is primary predictor of liver related morbidity and
mortality
• NAFLD related cirrhosis associated annual incidence of primary liver
cancer:1-2% per year
• Increased heritability of NAFLD: TMS6SF2,MBOAT7,PNPLA3(Intracellukar
tra
ffi
cking of lipids)
• Premalignant?
26.
27.
28. DX and RX
• Serum aminotransferases do not re
fl
ect NASH vs NAFLD
• Non invasive quanti
fi
cation of liver fat: MRI-PDFF:proton density fat fraction
• NAFLD
fi
brosis score and FIB4 (two most commonly employed non invasive tests to assess severity of
hepatic
fi
brosis
• Liver sti
ff
ness: MRE(magnetic resonance elastography ) and Fibroscan
• NASH :2*3 increased risk of metabolic syndrome
• NAFLD, independently associated with endothelial dysfunction, increased carotid intimal thickness and
number of plaques in carotid and coronary arteries.
• Three components:
• Speci
fi
c therapy
• Treatment of associated comorbidities
• Treatment of complications