Hepatitis Flashcards
Define acute viral hepatitis
Acute hepatitis caused by virus
Clinical features
- May be subclinical
- Flu-like prodrome preceeding icteric phase by 1-2 weeks nausea, vomiting, anorexia, taste/smell disturbance, headaches, fatigue, myalgia, low-grade fever arthralgia and urticaria (especially HBV)
- Pale stools, dark urine 1-5 days before jaundice
- Hepatomegaly, RUQ pain
- May have splenomegaly, cervical lymphadenopathy
Investigations
- AST and ALT (10-20X normal)
- ALP and bilirubin minimally elevated
- Viral serology
Management
- Supportive:
Hydration
Diet
Analgesia
- Avoid alcohol, drugs
Indications for admission
- Encephalopathy
- Coagulopathy
- Severe vomiting
- Hypoglycemia
Complications
- Hepatocellular necrosis (+LFTs)
- Cholestasis (pale stools, jaundice)
- Encephalopathy
- Coagulopathy
- Hypoglycemia
Prognostic indicators poor
- comorbidities
- persistently high bilirubin (>340 mmol; 20 mg/dL)
- increased INR
- decreased albumin
- hypoglycemia
- Cholestasis
In which viral hepatitis is cholestasis more common
Hepatitis A
Hepatitis A: type of virus, transmission, common age group, incubation
- RNA
- Fecal-oral
- Common in children, in adults more common to be fulminant disease
- 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
- presence of risk factors
- fever
- malaise
- nausea and vomiting
- jaundice
- hepatomegaly
- RUQ pain
- clay-coloured stools
Investigations in hepatitis A and results
- 1st tests to order serum transaminases->elevated serum bilirubin->?elevated blood urea->+if renal failure serum creatinine->+if renal failure
- prothrombin time
- IgM anti-hepatitis A virus (HAV)->elevated in acute
Management hepatitis A unvaccinated people with recent exposure to hepatitis A
IM immunoglobulin for prevention
- Supportive
Analgesia
Fluids
Nutrition
- Avoid alcohol
Hepatitis B: virus type, transmission (4), incubation
- DNA
- Blood products, sexual, IVDU, vertical, direct
- 6 months
Risk factors for hepatitis B
Strong
- perinatal exposure in an infant born to an HBV-infected mother
- multiple sexual partners
- men who have sex with men (MSM)
- injection drug use
- Asian, eastern European, or African ancestry
- FHx of HBV and/or chronic liver disease
- FHx of hepatocellular carcinoma (HCC)
- household contact with HBV
Weak
- male sex history of STDs
- infected with HIV infected with hepatitis C virus (HCV)
- blood or blood product transfusion
- health care worker (HCW)
- 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
- Key factors presence of risk factors
- May have normal physical examination
- jaundice
- hepatomegaly
- ascites
- fever/chill malaise
- maculopapular or urticarial rash
- RUQ pain
- fatigue nausea/vomiting
- arthralgia/arthritis
- palmar erythema
- spider angiomata
- splenomegaly
- asterixis
Phases of chronic hepatitis B overview
1) immune tolerance
2) immune clearance
3) immune control
4) immune escape
Immune tolerance in hepatitis B
- 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
- falling but still elevated HBV-DNA levels (>20,000 IU/mL),
- 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
- 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
- (“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
Investigations
1st tests to order
- hepatic panel->+ALT/AST, +bilirubin, +ALP
- FBC->microcytic anemia, thrombocytopenia (portal HTN)
- basic metabolic panel (BMP)->hyponatremia (fluid overload, diuretics to treat), urea (+in pre-renal azootemia) coagulation profile (PT/INR)
- 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
- entecavir 0.5 mg orally, once daily, continued for 12 months after HBeAg seroconversion or long term if no seroconversion OR
- tenofovir 300 mg orally, once daily, continued for 12 months after HBeAg seroconversion or long term if no seroconversion OR
- peginterferon alfa-2a 180 micrograms SC, once weekly for 48 weeks.
Complications in hepatitis B
- Fulminant liver failure
- Cirrhosis
- Hep B glomerulonephritis
- Cholestasis
- Hepatocellular carcinoma
Interferon side effects
- 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
- Barrier protection
- Do not share razors, toothbrushes
- Cover open wounds/scratches
- Clean blood spills with bleach/detergent
- Do not donate blood, semen, organ
- Avoid heavy alcohol use
- 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
- Starting antiviral treatment within 12 weeks of onset of hepatitis maximises the chance of viral clearance, without reducing the chance of response.
- 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
- Allergy
- Autoimmune hepatitis
- Severe liver dysfunction
- Decompensated liver cirrhosis
Investigations in hepatitis C
- LFTs normal until cirrhosis develops
- anti-HCV antibodies
- Recombinant immunoblot assay HCV-PCR
- Liver biopsy
- 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
- Alcohol
- Drugs
- Toxins
- EBV/CMV
- Leptospirosis
- Malaria
- Q fever
- Syphillis
- Yellow fever
- Chronic hepatitis
Hepatitis D co-infection vs superinfection
co-infection: acquire HDV and HBV at the same time better prognosis than superinfection (acute HDV infection on pre-existing HBV infection
