hepatitis C Flashcards

1
Q

What is Hep C?

A

blood borne
single stranded
enveloped
RNA virus

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2
Q

declining incidence of Hep C?

A
  • screening of blood and blood products
  • safer needle use practice among IVDUs
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3
Q

transmission

A
  • IVDU
  • Vertical transmission (mother to child)
  • Sexual exposure
  • Transfusion
  • Occupational exposure – needle stick injury
  • Tattooing, acupuncture, piercing and dental work
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4
Q

after exposure to HCV

A
  • Incubation period – 6-8 weeks
  • Acute infection - serology can take up to 6 mths to become +ve
  • If not cleared → Chronic HCV
  • Genotype and viral load do not usually affect disease progression
  • 20% have cirrhosis at 20-30 years after infected
  • Liver Failure – 2-5% of patients with cirrhosis/year
  • HCC – 1-4% of patients with cirrhosis/year
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5
Q

public interventions for HCV

A
  • Prevent new infections
  • Inc awareness of infection
  • Inc diagnosis
  • Treating diagnosed individuals
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6
Q

RF for disease progression

A
  • Alcohol (> 6 units/day = progression)
  • Older age at infection
  • Infection duration
  • Male sex
  • Obesity
  • Diabetes/insulin resistance
  • HIV and/or HBV co infection
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7
Q

Who should be screened for HCV?

A
  • Unexplained LFTs
  • Injected drugs
  • Blood transfusion pre-1991
  • Children of infected mothers
  • Sexual partners of infected people
  • Exposure to blood with risk of transmission
  • Received tattoos, piercings, or acupuncture with poor infection control procedures
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8
Q

signs and symptoms

A
  • Usually asymptomatic
  • Jaundice
  • Malaise
  • Dark urine
  • RUQ pain
  • Loss of appetite, dec weight
  • Nausea
  • Cirrhosis (swollen liver, muscle weakness, swollen ankles, bloated, itchy skin)
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9
Q

diagnosis of HCV

A
  • Differential: CHB, ALD, haemochromatosis
  • Risk Factors
  • Sx
  • Blood Tests
  • Hep C antibodies
  • Serology for Hep C viral RNA (viral load)
  • Liver Biopsy
  • Viral Genotyping
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10
Q

primary aim of Tx

A

to achieve viral eradication
OR
sustained viral response (SVR)

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11
Q

secondary aim of Tx

A

prevent transmission

slow progression of liver disease

inc QoL

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12
Q

When is response rate to Tx lower?

A

cirrhosis or fibrosis

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13
Q

before starting treatment

A
  • HCV genotype & subtype
  • HCV RNA (viral load)
  • Tx naïve or experienced
  • Liver disease – cirrhosis, staging of hepatic fibrosis
  • Bloods – FBC, INR, LFTs, renal fxn
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14
Q

DAAs

A

direct acting antivirals

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15
Q

types of DAAs

A

– NS3/4A protease inhibitors (PIs)
– nucleoside and nucleotide NS5B polymerase iInhibitors
– NS5A inhibitors
– non-nucleoside NS5B polymerase inhibitors

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16
Q

How do NS3/4A protease inhibitors work?

A

block viral enzyme (protease)

17
Q

How do nucleoside and nucleotide NS5B polymerase iInhibitors work?

A

directly block HCV RNA preventing replication

18
Q

How do NS5A Inhibitors work?

A

block NS5A HCV protein needed for replication

19
Q

How do non-nucleoside NS5B polymerase inhibitors work?

A

Insert directly into HCV blocking other parts of HCV from binding and replicating

20
Q

What does Tx depend on?

A

– Genotype
– Naïve or previous Tx
– Cirrhotic or not
– Cirrhosis compensated or decompensated
– HCV in pregnancy
– Renal impairment plus Tx patients
– Coinfection HIV/HCV
– HCV recurrence post liver transplant

21
Q

What is childs Pugh?

A

general measure of severity of cirrhosis

grade & score:
A, 5-6 = well functioning
C, 10-15 = decompensated