Hepatitis Flashcards

1
Q

HBV - epi

A
  1. Hepatitis B virus (HBV) - DNA virus
  2. Spread by infected blood, blood products or sexual contact
  3. Incubation period 2-6mo
  4. 0.5-0.8% of Australian population chronically affected with HBV
  5. Most pregnant chronic carriers of HBV were born overseas, in high HBV prevalence areas such as the Asia-Pacific. However, Indigenous Australians, partners of HBV carriers and injecting drug users also have an increased HBV prevalence
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2
Q

HBV - symptoms

A
  1. Non-specific prodromal illness (5) = headache, myalgia, arthralgia, nausea, anorexia
  2. Prodrome precedes development of jaundice by a few days to 2 weeks
  3. Vomiting/diarrhoea may follow
  4. Abdominal discomfort common
  5. Dark urine and pale stools may precede jaundice
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3
Q

HBV - signs (3)

A
  1. Liver often tender but only minimally enlarged
  2. Occasionally, mild splenomegaly and cervical lymphadenopathy seen
  3. Jaundice may be mild
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4
Q

HBV - dx

A
  1. Based on clinical picture + serological markers for hepatitis B
  2. HB surface antibody (anti-HBs) = present in immune and immunised individuals (bc immunisation contains viral particles that replicate the virus’ outer capsule)
  3. HB core antibody = only seen following natural infection
  4. HB surface antigen = indicates the presence of the virus/current infection. When it persists in the serum for >6mo, the person is said to be a carrier. This occurs in 5% of those infected as adults but in 90% of those infected as infants
  5. HBe antigen = highly infectious carrier/active viral replication
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5
Q

HBV (acute) - mx

A
  1. Supportive tx with monitoring for acute liver failure (
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6
Q

HBV (chronic) - mx

A

Chronic hepatitis B = persistent detection of hepatitis B surface antigen (HBsAg) for >6mo

  1. All pts who are HBsAg positive should be fully assessed to determine the stage of disease, and regularly reassessed over the course of their infection
  2. Natural hx of chronic HBV determines the optimal timing of tx. Four phases of HBV infection = immune tolerance, immune clearance, immune control, immune escape. In immune clearance and immune escape, there is risk of progression to cirrhosis. Hence, antiviral tx is directed at these pts
  3. HBeAg positive patients = entecavir, tenofovir, or peginterferon alfa-2a, time of stopping treatment controversial. For entecavir or tenofovir, continue tx for 12mo after HBeAg seroconversion or long term. For peginterferon alfa-2a, tx for 48 weeks
  4. HBeAg negative pts = entecavir or tenofovir. Lifelong therapy unless HBsAg seroconversion (uncommon)
  5. Pts with cirrhosis = entecavir or tenofovir, indefinitely
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7
Q

HCV - epi (3)

A
  1. 1.5% of Australian population chronically infected with HCV
  2. Major risk factors = injecting drug use (past or present), hx blood transfusion (pre-1990 Australia, any time overseas), immigration from high-prevalence regions (Asia, Africa, Middle East)
  3. Acute HCV results in chronic infection in >70% of cases. Can result in end-stage liver disease (including cirrhosis, liver cancer and death)
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8
Q

HCV - symptoms

A
  1. Acute symptomatic infection with HCV is rare
  2. Most pts are only identified when they develop chronic liver disease/cirrhosis

Symptoms of cirrhosis

  1. Non-specific = weakness, fatigue, muscle cramps, weight loss, anorexia, NV, upper abdominal discomfort
  2. Jaundice (usually mild)
  3. Occasionally - SOB + large right pleural effusion
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9
Q

Cirrhosis - signs

A
  1. Isolated hepatomegaly, or signs of portal hypertension = splenomegaly, collateral vessels, variceal bleeding
  2. Hepatomegaly - common when cirrhosis is due to ALD or haemochromotosis. Reduction in liver size is common when cirrhosis is due to viral hepatitis or autoimmune liver disease
  3. Jaundice
  4. Ascites
  5. Circulatory changes = spider telangiectasia, palmar erythema, cyanosis
  6. Endocrine changes = loss of libido, hair loss
  7. Gender-specific endocrine changes = gynaecomastia (M), testicular atrophy (M), breast atrophy (F), irregular menses (F)
  8. Haemorrhagic tendency = purpura, epistaxis
  9. Hepatic encephalopathy
  10. Clubbing (?)
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10
Q

HCV - ix

A
  1. Serology for anti-HCV (may take 6-12 weeks for antibodies to appear following acute infection). Active infection confirmed by presence of serum hepatitis C RNA in anyone who is antibody positive. Molecular analysis - viral genotype
  2. Serology for HAV, HBV and HIV
  3. LFTs
  4. Upper abdominal U/S, liver histology (staging the degree of liver damage)
  5. FBE, UEC, INR, BGL
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11
Q

HCV - mx

A
  1. Minimise alcohol and cannabis use, quit smoking, lose weight if overweight (if cirrhosis, should not drink alcohol)
  2. If serologically negative for HAV or HBV, should vaccinate
  3. Peginterferon + ribavirin (standard of care, but new interferon-free regimens now available)
  4. Regimen depends on HCV genotype
  5. Monitoring during tx - measure HCV RNA at baseline, end of tx and 12 weeks after end of tx to check for a sustained virological response
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