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My Decks > Pharm- Hepatitis > Flashcards

Pharm- Hepatitis Flashcards

1
Q

Agents for HBV

A

Entacavir
Tenofovir
Peginterferon alfa

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2
Q

Agents for HCV

A 
Simeprevir 
Daclatasvir
Sofosbuvir
Dasabuvir 
Ribavirin
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3
Q

Transmission of HAV

A

fecal-oral

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4
Q

Transmission of HBV

A

sexual
parenteral
perinatal

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5
Q

Transmission of HCV

A

sexual
parenteral
perinatal

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6
Q

HBsAg

A

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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7
Q

anti-HBs

A

Recover or immunity from HBV

Also arise after successful vaccination

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8
Q

Anti-HBc (total HBC core Ab)

A

Appears at onset of infection

Will persist for life

Indicates previous or ongoing infection

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9
Q

IgM anti-HBc

A

Recent (acute) infection <6mths

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10
Q

HBeAg

A

High levels of HBV

Found during acute and chronic infection

Indicates viral replication

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11
Q

HBeAb

A

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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12
Q

Goal of HBV therapy

A

decrease morbidity and mortality

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13
Q

Goal of HCV therapy

A

Viral eradication (sustained viral response- SVR)

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14
Q

Sustained viral response

A

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

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15
Q

Advantages of IFNa compared to NA’s

A

Finite treatment duration
No resistance issues
Durable response

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16
Q

Disadvantages of IFNa compared to NA’s

A

Side effects

Cannot be used for pt’s with decompensated liver dz

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17
Q

Advantages of NA’s compared to IFNa

A

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

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18
Q

Disadvantages of NA’s compared to IFNa

A

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

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19
Q

MOA of IFNa

A

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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20
Q

PK of peg-IFNa

A

“peg” = increased half life, slows clearance

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21
Q

ADR’s of IFNa

A 
flu-like symptoms 
transient increase in LFT's 
Neurotoxicity
Myelosuppresion
Fatigue
22
Q

C/I of IFNa

A

decompensated liver dz
Psych pt’s
Pregnancy

23
Q

DDI’s of IFNa

A

Theophylline

Methadone

24
Q

MOA of Entacavir

A

guanosine analog, inhibits DNA polymerase

25
Q

Use of Entacavir

A

1st line treatment of HBV

26
Q

ADR’s of Entacavir

A 
HA
fatigue
rash 
nausea
dizziness
27
Q

MOA of Tenofovir

A

adenosine analog, inhibits DNA polymerase

28
Q

Use of Tenofovir

A

1st line treatment of HBV

29
Q

ADR’s of Tenofovir

A

N/V/D

decreased bone mineral density

30
Q

NS3/4 Protease Inhibitors

A

Simeprevir

“-previr”

31
Q

NS5A Protease Inhibitors

A

Daclatasvir

“-asvir”

32
Q

NS5B RNA-Dependent RNA Polymerase Inhibitors

A

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

33
Q

MOA of Daclatasvir

A

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

34
Q

PK of Daclatasvir

A

CYP3A metabolism (C/I when on CYP3A inducers)

35
Q

ADR’s of Daclatasvir

A

Fatigue
HA
N/D
increased lipase

36
Q

MOA of Ledipasvir(-sofosbuvir)

A

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

37
Q

ADR’s of Ledipasvir(-sofosbuvir)

A

Insomnia!!!

Fatigue, HA, N/D, increased serum lipase

38
Q

MOA of Ombitasvir-paritaprevir-ritonavir + dasabuvir

A

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

39
Q

PK of Ombitasvir-paritaprevir-ritonavir + dasabuvir

A

CYP metabolism

All are excreted in feces

40
Q

ADR’s of Ombitasvir-paritaprevir-ritonavir + dasabuvir

A

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

41
Q

MOA of Sofosbuvir

A

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

42
Q

PK of Sofosbuvir

A

80% excreted in urine, substrate of P-glycoprotein

43
Q

ADR’s of Sofosbuvir

A

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

44
Q

MOA of Simeprevir

A

inhibits NS3/4A protease

45
Q

PK of Simeprevir

A

CYP3A4 oxidative metabolism, excreted in feces

46
Q

ADR’s of Simeprevir

A

Pruritis/skin rash
Nausea
Myalgias
Increased serum bilirubin

47
Q

DDI’s of Simeprevir

A

avoid with CYP inducers i.e. rifampin

may increase concentration of other CYP3A4 substrates i.e. statins

48
Q

MOA of Ribavirin

A

guanosine analog; inhibits initiation/elongation of RNA

49
Q

Therapeutic uses of Ribavirin

A 
Chronic HCV
Influenza A and B 
Parainfluenza
RSV
Paramyxoviruses 
HIV-1
50
Q

ADR’s of Ribavirin

A

hemolytic anemia
depression
fatigue, nausea, rash, insomnia

51
Q

C/I’s of Ribavirin

A

anemia
ESRD
ischemic vascular disease
pregnancy (teratogenic)

52
Q

CYP associations

A

Metabolized by CYP

  • Daclatasvir
  • Ombitasvir-paritaprevir-ritonavir plus dasabuvir
  • Simepravir

CYP3A is inhibited by Ritonavir

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