Pharm- Hepatitis Flashcards by Sydney Featherstone

Agents for HBV

Entacavir
Tenofovir
Peginterferon alfa

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Agents for HCV

Simeprevir 
Daclatasvir
Sofosbuvir
Dasabuvir 
Ribavirin

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Transmission of HAV

fecal-oral

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Transmission of HBV

sexual
parenteral
perinatal

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Transmission of HCV

sexual
parenteral
perinatal

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HBsAg

high levels occur during acute or chronic infection.

If found, the patient is infectious!

Normal immune response produces Ab’s to this Ag

We use this to make the HBV vaccine

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anti-HBs

Recover or immunity from HBV

Also arise after successful vaccination

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Anti-HBc (total HBC core Ab)

Appears at onset of infection

Will persist for life

Indicates previous or ongoing infection

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IgM anti-HBc

Recent (acute) infection <6mths

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HBeAg

High levels of HBV

Found during acute and chronic infection

Indicates viral replication

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HBeAb

Lower levels of HBV

Immune system may produce them after an acute infection or after a burst in viral replication.

Seroconversion (Ag –> Ab) is a good predictor of viral clearance in pt’s receiving treatment

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Goal of HBV therapy

decrease morbidity and mortality

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Goal of HCV therapy

Viral eradication (sustained viral response- SVR)

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Sustained viral response

viral eradication, the absence of HCV RNA by PCR for 12wks after completion of therapy

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Advantages of IFNa compared to NA’s

Finite treatment duration
No resistance issues
Durable response

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Disadvantages of IFNa compared to NA’s

Side effects

Cannot be used for pt’s with decompensated liver dz

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Advantages of NA’s compared to IFNa

PO administration
Better tolerated
High response rate
Can be used for pt’s with decompensated liver dz

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Disadvantages of NA’s compared to IFNa

?sustained response
Resistance
Side effects (peripheral neuropathy, lactic acidosis, hepatic steatosis)

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MOA of IFNa

cytokine! So inhibits everything…

Antiviral, immunomodulatory, and anti-proliferative actions. Inhibits viral penetration, translation, transcription, protein processing, maturation, and release. Enhanced phagocytic activity of macrophages and augmentation of proliferation/survival of cytotoxic T-cells.

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PK of peg-IFNa

“peg” = increased half life, slows clearance

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ADR’s of IFNa

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flu-like symptoms 
transient increase in LFT's 
Neurotoxicity
Myelosuppresion
Fatigue

C/I of IFNa

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decompensated liver dz
Psych pt’s
Pregnancy

DDI’s of IFNa

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Theophylline

Methadone

MOA of Entacavir

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guanosine analog, inhibits DNA polymerase

Use of Entacavir

1st line treatment of HBV

ADR's of Entacavir

``` HA fatigue rash nausea dizziness ```

MOA of Tenofovir

adenosine analog, inhibits DNA polymerase

Use of Tenofovir

1st line treatment of HBV

ADR's of Tenofovir

N/V/D | decreased bone mineral density

NS3/4 Protease Inhibitors

Simeprevir | "-previr"

NS5A Protease Inhibitors

Daclatasvir | "-asvir"

NS5B RNA-Dependent RNA Polymerase Inhibitors

Sofosbuvir - Nucleot(s)ide Polymerase Inhibitors Dasabuvir - Non-Nucleoside Polymerase Inhibitor "-buvir"

MOA of Daclatasvir

binds N-terminus of NS5A, thereby inhibiting viral RNA replication and virion assembly

PK of Daclatasvir

CYP3A metabolism (C/I when on CYP3A inducers)

ADR's of Daclatasvir

Fatigue HA N/D increased lipase

MOA of Ledipasvir(-sofosbuvir)

inhibits NS5A protein necessary for viral replication; also acts as a chain terminator

ADR's of Ledipasvir(-sofosbuvir)

Insomnia!!! | Fatigue, HA, N/D, increased serum lipase

MOA of Ombitasvir-paritaprevir-ritonavir + dasabuvir

Ombitasvir- inhibits NS5A Paritaprevir- inhibits NS3/4A (polyprotein cleavage) Dasabuvir- inhibits RNA-dependent RNA polymerase Ritonavir- CYP3A inhibitor to increase plasma concentrations of the other drugs

PK of Ombitasvir-paritaprevir-ritonavir + dasabuvir

CYP metabolism | All are excreted in feces

ADR's of Ombitasvir-paritaprevir-ritonavir + dasabuvir

Pruritus/skin reactions Asthenia (generalized weakness) Elevated ALT Fatigue, HA, nausea, insomnia

MOA of Sofosbuvir

inhibits NS5B RNA dependent RNA polymerase, acts as a chain terminator

PK of Sofosbuvir

80% excreted in urine, substrate of P-glycoprotein

ADR's of Sofosbuvir

Anemia Neutropenia Myalgia Fatigue, HA, insomnia, pruritus, N/D, flu-like symptoms, weakness

MOA of Simeprevir

inhibits NS3/4A protease

PK of Simeprevir

CYP3A4 oxidative metabolism, excreted in feces

ADR's of Simeprevir

Pruritis/skin rash Nausea Myalgias Increased serum bilirubin

DDI's of Simeprevir

avoid with CYP inducers i.e. rifampin may increase concentration of other CYP3A4 substrates i.e. statins

MOA of Ribavirin

guanosine analog; inhibits initiation/elongation of RNA

Therapeutic uses of Ribavirin

``` Chronic HCV Influenza A and B Parainfluenza RSV Paramyxoviruses HIV-1 ```

ADR's of Ribavirin

hemolytic anemia depression fatigue, nausea, rash, insomnia

C/I's of Ribavirin

anemia ESRD ischemic vascular disease pregnancy (teratogenic)

CYP associations

Metabolized by CYP - Daclatasvir - Ombitasvir-paritaprevir-ritonavir plus dasabuvir - Simepravir CYP3A is inhibited by Ritonavir

Pharm- Hepatitis Flashcards

(52 cards)