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Flashcards in Hepatitis Deck (40)
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Define acute viral hepatitis

Acute hepatitis caused by virus


Clinical features

1. May be subclinical

2. Flu-like prodrome preceeding icteric phase by 1-2 weeks ƒƒnausea, vomiting, anorexia, taste/smell disturbance, headaches, fatigue, myalgia, low-grade fever ƒƒarthralgia and urticaria (especially HBV)

3. Pale stools, dark urine 1-5 days before jaundice

4. Hepatomegaly, RUQ pain

5. May have splenomegaly, cervical lymphadenopathy



1. AST and ALT (10-20X normal)

2. ALP and bilirubin minimally elevated

3. Viral serology



1. Supportive:




2. Avoid alcohol, drugs


Indications for admission

1. Encephalopathy

2. Coagulopathy

3. Severe vomiting

4. Hypoglycemia



1. Hepatocellular necrosis (+LFTs)

2. Cholestasis (pale stools, jaundice)

3. Encephalopathy

4. Coagulopathy

5. Hypoglycemia


Prognostic indicators poor

1. comorbidities

2. persistently high bilirubin (>340 mmol; 20 mg/dL)

3. increased INR

4. decreased albumin

5. hypoglycemia

6. Cholestasis


In which viral hepatitis is cholestasis more common

Hepatitis A


Hepatitis A: type of virus, transmission, common age group, incubation

1. RNA

2. Fecal-oral

3. Common in children, in adults more common to be fulminant disease

4. Incubation 2-6 weeks


When does AST/ALT rise in hep A and return to normal

Rise within 1 month, returns to normal 5-20 weeks


Clinical features in hepatitis A

Key factors

1. presence of risk factors

2. fever

3. malaise

4. nausea and vomiting

5. jaundice

6. hepatomegaly

7. RUQ pain

8. clay-coloured stools


Investigations in hepatitis A and results

1. 1st tests to order serum transaminases->elevated serum bilirubin->?elevated blood urea->+if renal failure serum creatinine->+if renal failure

2. prothrombin time

3. IgM anti-hepatitis A virus (HAV)->elevated in acute


Management hepatitis A unvaccinated people with recent exposure to hepatitis A 

IM immunoglobulin for prevention

1. Supportive




2. Avoid alcohol


Hepatitis B: virus type, transmission (4), incubation

1. DNA

2. Blood products, sexual, IVDU, vertical, direct

3. 6 months


Risk factors for hepatitis B


1. perinatal exposure in an infant born to an HBV-infected mother

2. multiple sexual partners

3. men who have sex with men (MSM)

4. injection drug use

5. Asian, eastern European, or African ancestry

6. FHx of HBV and/or chronic liver disease

7. FHx of hepatocellular carcinoma (HCC)

8. household contact with HBV


1. male sex history of STDs

2. infected with HIV infected with hepatitis C virus (HCV)

3. blood or blood product transfusion

4. health care worker (HCW)

5. history of incarceration haemodialysis


Interpreting hepatitis B serology for acute, chronic, resolved and immunised->HBsAg, Anti-HBS, HBeAg, Anti-HBe, Anti-HBc

Hepatitis B

Serology HBsAg Anti-HBs HBeAg Anti-HBe Anti-HBc Liver Enzymes

Acute HBV + – + – IgM

Chronic HBV (high HBV DNA) + – + – IgG ALT, AST elevated

Chronic HBV (low HBV DNA) + – – + IgG ALT, AST normal

Resolved infection – ± – ± IgG

Immunization – + – – –


Clinical features of hepatitis B

1. Key factors presence of risk factors

2. May have normal physical examination

3. jaundice

4. hepatomegaly

5. ascites

6. fever/chill malaise

7. maculopapular or urticarial rash

8. RUQ pain

9. fatigue nausea/vomiting

10. arthralgia/arthritis

11. palmar erythema

12. spider angiomata

13. splenomegaly

14. asterixis


Phases of chronic hepatitis B overview

1) immune tolerance

2) immune clearance

3) immune control

4) immune escape


Immune tolerance in hepatitis B

1. extremely high HBV-DNA (>20,000 IU/mL), HBeAg positive, but normal ALT/AST; due to little immune control and minimal immune-mediated liver damage; characteristic of perinatal infection (or ‘incubation period’ in adult with newly acquired HBV


Immune clearance

1. falling but still elevated HBV-DNA levels (>20,000 IU/mL),

2. HBeAg positive; due to immune attack on the virus and immune mediated liver damage; characterized by progressive disease without treatment and increasing liver fibrosis (sometimes progressing to cirrhosis and/or hepatocellular carcinoma); likely to benefit from treatment


Immune control

1. lower HBV-DNA immune response suppresses viral replication to low or undetectable levels. Inflammation reduces and serum alanine aminotransferase normalises. The establishment of immune control is associated with HBeAg seroconversion, and these patients are thought not to have ongoing damage. Once seroconversion occurs, patients may stay in this phase indefinitely


Immune escape

1. (“core or precore mutant”): elevated HBV-DNA (>2,000 IU/mL), HBeAg negative because of pre-core or core promoter gene mutation, anti-HBe positive, ALT/AST high; characterized by progressive disease without treatment and increasing liver fibrosis (sometimes progressing to cirrhosis and/or hepatocellular carcinoma); likely to benefit from treatment



1st tests to order

1. hepatic panel->+ALT/AST, +bilirubin, +ALP

2. FBC->microcytic anemia, thrombocytopenia (portal HTN)

3. basic metabolic panel (BMP)->hyponatremia (fluid overload, diuretics to treat), urea (+in pre-renal azootemia) coagulation profile (PT/INR)

3. serum HBsAg, serum HBsAb, serum HBcAb (IgM) serum HBcAb (IgM + IgG), serum HBeAg HBV DNA


What does HbeAg suggest

high infectivity


What serology defines carrier status in hepatitis B

+HbsAg >6 months after exposure.


In what phase of chronic hepatitis B is antiviral therapy targeted

Antiviral treatment of chronic hepatitis B is directed at patients in the immune clearance phase (phase 2) and the immune escape phase (phase 4).


Antiviral therapy options for hepatitis B chronic

1. entecavir 0.5 mg orally, once daily, continued for 12 months after HBeAg seroconversion or long term if no seroconversion OR

1. tenofovir 300 mg orally, once daily, continued for 12 months after HBeAg seroconversion or long term if no seroconversion OR

1. peginterferon alfa-2a 180 micrograms SC, once weekly for 48 weeks.


Complications in hepatitis B

1. Fulminant liver failure

2. Cirrhosis

3. Hep B glomerulonephritis

4. Cholestasis

5. Hepatocellular carcinoma


Interferon side effects

1. influenza-like illness, fever, chills, headache, malaise, myalgia, fatigue, anorexia, weight loss, and mild hair loss. They may also have a myelosuppressive effect


Patient instructions with hepatitis B

1. Barrier protection

2. Do not share razors, toothbrushes

3. Cover open wounds/scratches

4. Clean blood spills with bleach/detergent

5. Do not donate blood, semen, organ

6. Avoid heavy alcohol use

7. Sexual partners and all household contacts of HBsAg-positive people should be vaccinated for HBV if they test negative for HBV serological markers.


Starting antiviral treatment early in acute hepatitis C- options

1. Starting antiviral treatment within 12 weeks of onset of hepatitis maximises the chance of viral clearance, without reducing the chance of response.

2. peginterferon alfa-2a 180 micrograms SC, once weekly for 24 weeks or peginterferon alfa-2b 1.5 micrograms/kg SC, once weekly for 24 weeks.


Transmission in hep C

Blood transfusion, sexual


Number developing chronic in hepatitis C, cirrhosis

85% chronic, 20-30% cirrhotic


Why is genotyping in hepatitis C important

Peginterferon therapy is less effective in G1, 4, 5, 6


Contraindications for PEG

1. Allergy

2. Autoimmune hepatitis

3. Severe liver dysfunction

4. Decompensated liver cirrhosis


Investigations in hepatitis C

1. LFTs normal until cirrhosis develops

2. anti-HCV antibodies

3. Recombinant immunoblot assay HCV-PCR

4. Liver biopsy

5. HCV genotyping


How is diagnosis established in hep C infection

Presence of HCV-RNA


Is chronic hepatitis B more likely in infants or adults

More in infants


Differential for acute hepatitis

1. Alcohol

2. Drugs

3. Toxins


5. Leptospirosis

6. Malaria

7. Q fever

8. Syphillis

9. Yellow fever

10. Chronic hepatitis


Hepatitis D co-infection vs superinfection

co-infection: acquire HDV and HBV at the same time ƒƒbetter prognosis than superinfection (acute HDV infection on pre-existing HBV infection