12. Liver Disease Flashcards
Five forms of viral hepatitis.
What is the leading cause of chronic viral hepatitis?
When if viral hepatitis considered acute?
Five forms: hepatitis A, B, C, D, E
Leading cause of chronic viral hepatitis is chronic hepatitis B and C
Viral hepatitis is considered acute when inflammation lasts 6 months or less.
With chronic viral hepatitis, longstanding repetition of inflammation and healing process leads to liver fibrosis.
What is hepatitis A?
How does clinical illness manifest?
Mode of transmission?
Complications?
Treatment?
HEPATITIS A
RNA virus with average incubation period of 35-70 days. Typically self limiting leading to acute hepatitis.
Malaise, myalgias, arthralgia, anorexia, nausea, vomiting, diarrhea, low-grade fevers, jaundice. (Usually subside over 2-3 weeks). No chronic form.
Fecal-oral, sewage contaminated shellfish.
Prevention: pooled gamma globulin, hepatitis A vaccine.
Complications: can lead to fulminant liver failure (<0.2% mortality rate)
Can be prevented with vaccine. No specific treatment (supportive care). Avoid physical exertion, alcohol, and hepatotoxic agents.
What is Hepatitis B?
Four phases of infection with hepatitis B.
Mode of transmission?
Risk factors?
Prevention?
Clinical features?
Complications?
Treatment?
HEPATITIS B
DNA virus with average incubation of 60-110 days, insidious onset leading to acute hepatitis. Chronic hepatitis in 1-5% of immunocompetent adults, substantial proportion of immunocompromised adults, and as high as 90% of infected children.
Four phases: (1) immune tolerant, (2) immune clearance, (3) inactive HBsAg carrier state, (4) reactivated chronic Hep B
Mode of transmission: vertical transmission (mother to fetus), percutaneous, sexual.
Risk factors: IVDA, unprotected sex, needle sticks, tattoos, piercings, hemodialysis, blood transfusions.
Prevention: hepatitis B immunoglobulin, hepatitis B vaccine.
Clinical features: similar to Hep A, malaise, myalgias, arthralgia, anorexia, nausea, vomiting, diarrhea, low-grade fevers, jaundice.
Complications: asymptomatic to fulminant disease and death. If aminotransferase levels remain elevated for more than 6 months, patient is considered to have chronic hepatitis B. 20% progress to cirrhosis. Hepatocellular carcinoma in cirrhotic patient 2-4% per year.
Treatment: vaccines available. Treatment is supportive care. Chronic hep B patients may be treated with nucleoside or nucleotide analogs with goal of lowering HBV DNA levels and possible seroconversion.
What is Hepatitis C?
Clinical illness?
Mode of transmission?
Risk factors?
Complications?
Treatment?
RNA virus with average incubation period of 35-70 days.
Often mild illness, usually asymptomatic. Majority progress to chronic liver disease.
Mode of transmission is percutaneous (risk factors = IVDA, incarceration, needle stick, tattoos, body piercing, hemodialysis, blood transfusion.)
Prevention after exposure = interferon plus ribavirin.
Complications: cirrhosis in 20% of affected patients after 20 years. Risk of hepatocellular carcinoma. Associated with cryoglobulinemia and membranoproliferative glomerulonephritis. HCV increases risk of non-Hodgkin lymphoma.
Treatment: no vaccine unlike A and B. Antiviral medication and interferon for treatment. Most patients able to clear chronic hep C infections after multidrug regimen (Harvoni, Mavyret). Liver transplantation.
Alcoholic Liver Disease
Excessive alcohol intake leading to fatty liver followed by hepatitis and cirrhosis.
- 50g daily (5 standard drinks) for 10 years or more.
Acute or chronic inflammation – parenchymal necrosis of liver. Alcoholic steatosis is reversible with cessation of alcohol. Can progress to cirrhosis.
Treatment: alcohol cessation, nutritional support. Folic acid, thiamine, zinc. Methylprednisolone or other corticosteroid may reduce short term mortality in patients with alcoholic hepatitis and encephalopathy.
Non-alcoholic Fatty Liver Disease (NAFLD)
Aggregation of hepatic fat not due to alcohol use. Most common liver disease in US and worldwide.
Metabolic syndrome, DM type II, TPN, history of gastric bypass, some medications.
Treat by managing primary medical problem.
Autoimmune hepatitis
Less common cause of chronic liver disease. Destruction of hepatocytes by T-cell and autoantibody-mediated molecules. Primary biliary cirrhosis and primary sclerosing cholangitis are among these autoimmune diseases.
Primary Biliary Cirrhosis
Age group?
Etiology?
Clinical manifestations?
Lab findings?
PBC manifests due to chronic autoimmune destruction of small intrahepatic bile ducts and cholestasis. At risk for hepatocellular carcinoma. Onset insidious. Women 40-60 yrs.
Genetic and environmental risk factors (Sjogren, autoimmune thyroid disease, Raynaud syndrome, scleroderma, hypothyroidism, celiac disease).
Clinical manifestations = xanthomas, pruritis, hyperpigmented skin, jaundice, fatigue.
Lab findings = elevated alkaline phosphatase/aminotransferases. Patients positive for antimitochondrial antibodies serologically.
Treatment: ursodeoxycholic acid slows progression, stabilizes histology, improves long-term survival, reduces esophageal varices. Liver transplant can increase survival but disease can recur in graft.
Cirrhosis
Multiple etiologies: hepatic inflammation and fibrosis leading to liver cirrhosis and liver failure. Patients are unable to synthesize coagulation factors and metabolize toxic chemicals.
Scarring/fibrosis of hepatocyte architecture, increased resistance to intrahepatic blood flow, portal hypertension.
Gastroesophageal varices, hemorrhage, ascites, hypersplenism.
Hepatorenal syndrome, hepatic encephalopathy, hepatopulmonary syndrome, portopulmonary hypertension, malnutrition, coagulopathy.
Thrombocytopenia due to sequestration of platelets as a result of hypersplenism (portal hypertension)
More prone to infection (destruction of hepatic reticuloendothelial system - mononuclear phagocytic system).
Management of cirrhosis
No alcohol
Protein/calorie rich diet
HAV, HBV, pneumococcal, and influenza vaccines.
Manage varices.
Ascites and edema treated with diuretics, paracentesis.
Transjugular intrahepatic portosystemic shunt (TIPS) for severe ascites and variceal bleeding.
Lactulose to treat hepatic encephalopathy, decrease ammonia levels.
Liver transplantation in select cases.
What are two scoring systems to assess severity and survival probability of chronic liver disease?
Child-Pugh score
Model for End-Stage Liver Disease (MELD)
MELD
Model for End-Stage Liver Disease (MELD)
Predicts 90-day mortality without liver transplant. Based on sodium, INR, bilirubin, creatinine. Values 6-40 (score of 40 = 90% mortality in 3 months).
Child-Turcotte-Pugh (CTP)
CTP score predicts survival rate up to 2 years. Based on bilirubin, albumin, PT (or INR), ascites, and hepatic encephalopathy.
Categories A, B, and C.
A= 95% survival 2 years
B= 57% survival 2 years
C= 35% survival 2 years
A and B can proceed with surgery after medical optimization of coagulopathy and encephalopathy.
CTP class C have perioperative mortality rate more than 80% (no elective surgery).
Physical exam findings of liver diesase
Spider nevi
Jaundice
Splenomegaly
Ascites
Hepatomegaly
Caput medusa (engorged paraumbilical veins)
ECG findings in cirrhotic cardiomyopathy
Increased QT interval
