What is Hep C?
blood borne
single stranded
enveloped
RNA virus
declining incidence of Hep C?
transmission
after exposure to HCV
public interventions for HCV
RF for disease progression
Who should be screened for HCV?
signs and symptoms
diagnosis of HCV
primary aim of Tx
to achieve viral eradication
OR
sustained viral response (SVR)
secondary aim of Tx
prevent transmission
slow progression of liver disease
inc QoL
When is response rate to Tx lower?
cirrhosis or fibrosis
before starting treatment
DAAs
direct acting antivirals
types of DAAs
– NS3/4A protease inhibitors (PIs)
– nucleoside and nucleotide NS5B polymerase iInhibitors
– NS5A inhibitors
– non-nucleoside NS5B polymerase inhibitors
How do NS3/4A protease inhibitors work?
block viral enzyme (protease)
How do nucleoside and nucleotide NS5B polymerase iInhibitors work?
directly block HCV RNA preventing replication
How do NS5A Inhibitors work?
block NS5A HCV protein needed for replication
How do non-nucleoside NS5B polymerase inhibitors work?
Insert directly into HCV blocking other parts of HCV from binding and replicating
What does Tx depend on?
– 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
What is childs Pugh?
general measure of severity of cirrhosis
grade & score:
A, 5-6 = well functioning
C, 10-15 = decompensated