Viral Hepatitis Flashcards

1
Q

What are the acute forms of hepatitis?

A

A and E

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2
Q

What are the acute and chronic forms of hepatitis?

A

B, C, and D

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3
Q

What is the only way that Hep D can occur?

A

In patients that also have hep B

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4
Q

What are the s/sx of hepatitis?

A
Often asymptomatic
N/V
Splenomegaly
Elevated liver enzymes
Weight loss
Fatigue
Fever
Jaundice
RUQ pain
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5
Q

What is the route of transmission of Hep A?

A

Oral-Fecal

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6
Q

What are the RFs of Hep A

A

Area w/poor sanitation
Poor hygenic practices
IV drug use
Homosexual activity in men

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7
Q

Is there a chronic form of Hep A?

A

no

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8
Q

What is the prevention for Hep A in at risk children and adults?

A

Havrix
Vaqta
Twinrix

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9
Q

What is twinrix?

A

Combo HAV and HBV vaccine

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10
Q

Is there IgG available for pre- and post-exposure prophylaxis for Hep A?

A

Yes

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11
Q

What is the diagnostic criteria for Hep A?

A

HAV IgM

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12
Q

What is the outcome of Hep A?

A

Rarely fatal

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13
Q

What is the route of transmission for Hep B?

A

Blood

Bodily secretions

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14
Q

What are the RFs for Hep B?

A

IVDU
Sexual activity
Occupational exposure to infected blood or bodily secretions
Uterine exposure to infected female

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15
Q

Is there a chronic form of HBV?

A

Yes 10%

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16
Q

Who gets screened for HBV?

A

Patients w/RF
Pregnant females
Pts with HCV or HIV

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17
Q

What is the prevention for at risk children and adults for HBV?

A

Energix-B
Recombivax HB
Twinrix

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18
Q

Is IgG available for pre- and post-exposure prophylaxis of HBV?

A

Yes

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19
Q

What are the diagnostic criteria for HBV?

A

HBsAg
HBcAb
HBeAg
HBV DNA

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20
Q

What is the outcome of HBV?

A

Hepatocellular carcinoma or cirrhosis

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21
Q

What is the route of transmission for Hep C?

A

Blood

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22
Q

What are the RFs for Hep C?

A

IVDU
Blood transfusion prior to 1992
Intranasal drug users who share paraphernalia
Tattoos or body piercings if performed without proper infection control practices

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23
Q

Is there a chronic form of Hep C?

A

Yes (80%)

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24
Q

What is the screening for Hep C?

A
Illicit drug use
Blood transfusion prior to 1992
Blood clotting factors prior to 1987
Unexplained elevated liver enzymes
Organ transplant
Children born into HCV infected mothers
Occupational exposure to HCV infected blood or needle stick
In 2012, CDC and USPSTF recommended a 1x screen for all baby boomers
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25
Q

Is there prevention for at risk children and adults with HepC?

A

no

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26
Q

Is IgG available for pre- and post-exposure prophylaxis?

A

No

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27
Q

What are the diagnostic criteria for HepC?

A

HCV RNA

Anti-HCV

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28
Q

What are the outcomes of HCV?

A

Cirrhosis

Cancer (less common)

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29
Q

What is HBsAg?

A

Hepatitis B surface antigen
Surface protein of the HBV that is used as a marker to detect infection. If this blood test is positive, then the HBV is present

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30
Q

What is HBsAb or anti-HBs?

A

Hepatitis B surface antibody
The antibody formed in response to the surface protein of the Hep B virus. It can be produced in response to vaccination or recovery from an actual hep B infection. If this test is positive, then the immune system has successfully developed a protective antibody against the HBV that provides long-ter immunity

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31
Q

What is HBcAb or anti-HBc?

A

Hepatitis B Antibody
The antibody only refers to a part of the virus itself; it does not provide any protection or immunity against HBV. This test is often used by blood banks to screen blood donations. A positive test indicated a person may have been exposed to the HBV, but the result can only be confirmed in relationship to the above two tests

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32
Q

What is HBeAg?

A

Hepatitis B e Antigen
A marker of a high degree of HBV infectivity, it correlates with a high level of HBV replication. It is primarily used to help determine the clinical management of patients with chronic HBV infection

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33
Q

What is HBV DNA?

A

A marker of viral replication. It correlates well with infectivity. It is used to assess and monitor the treatment of patients with chronic HBV infection

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34
Q

What are drugs for HBV?

A

Pegylated interferon
Nucleos(t)ide Reverse Transcriptase Inhibitors
First line agents
Other agents

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35
Q

What are the first line agents for HBV?

A

Entecavir

TNF/TNF-alafenamide

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36
Q

How are TNF and TNF-alafenamide related?

A

TNF-alafenamide is a pro-drug of TNF and has less SE related to the kidneys and bone
TNF-alafenamide is shown to be non-inferior

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37
Q

What are the other agents for HBV?

A

Not first line d/t higher incidence of resistance
Lamuvidine - oldest agent (used to be gold standard)
Adefovir
Telbivudine
Emtricitabine - unlabeled use in HBV with co-existent HIV infection

38
Q

What is the MOA for pegylated interferon?

A

Proteins produced by nucleated cells that when activated have antiviral, antiproliferative, and immune-regulating activity

39
Q

What are the types of pegylated interferon?

A
Interferon alfa-2 (Intron A)
Peg-interferon alfa-2a (pegasys)
Immune modulator (helps suppress virus)
40
Q

What is the MOA of NRTIs

A

Inhibits HBV DNA polymerase resulting in inhibition of HBV viral replication

41
Q

When do you not used pegylated interferon alfa-2a?

A

Pts w/:
Cirrhosis
Post-transplant
Co-infection with HCV/HIV

42
Q

What are the NRTIs?

A
Lamivudine
Adefovir
Telbivudine
Entecavir
TNF
TNF-alaf
43
Q

How should NRTI use be monitored?

A

Monitor renal function prior to and during treatment

44
Q

How are NRTI’s used in an HIV co-infected individual?

A

Use in combo therapy with TNF/emtricitabine (Truvada) as part of HAART
Never use Lamivudine, TNF, or emtricitabine monotherapy unless the pt’s HIV status is determined to be negative first

45
Q

What are the combination NRTI therapies?

A

Not warranted if patient is NRTI naive

Might be beneficial in patients w/cirrhosis or in patients w/pre-existing resistance

46
Q

What combination therapies are not recommended?

A

peg INF and NRTI

Sequential NRTI therapy

47
Q

What does chronic HBV treatment depend on?

A

HBeAg (+) or (-)
HBV DNA level
ALT level
Disease stage/grade

48
Q

What are the goals of chronic HBV therapy?

A

Prevent cirrhosis and hepatocellular carcinoma
Normalization of ALT
Improved histology on biopsy
Undetectable HBV DNA and loss of HBeAg

49
Q

What are the levels in a patient with a partial response to HBV therapy?

A

60-2000 IU/mL

50
Q

What are the levels in a patient with no response to HBV treatment?

A

> 2000 IU/mL

51
Q

Which NRTIs have low resistance?

A

Entecavir
TNF
TNF alaf

52
Q

Which NRTI do you switch to if there is resistance?

A

TNF

TNF alaf

53
Q

Which NRTI do you switch to if there is resistance to TNF or TNF alaf?

A

Switch to or add entecavir

54
Q

What do you do with NRTIs if there is multi-drug resistance?

A

Switch to entecavir plus either TNF or TNF-alaf

55
Q

What is peg-interferon alfa-2a’s duration of therapy in HBV?

A

48 weeks

56
Q

What is NRTIs duration of therapy in HBV?

A

Years to life long
For HBeAg-positive pts: 6 months after HBeAg seroconversion and an undetectable HBV viral load
For HBeAg-negative pts: treatment should be continued until HBsAg clearance

57
Q

What are peg-inf ADRs?

A
Flu-like syndrome
Myalgia
HA
Fatigue
Weight loss
Depression
Hair loss
Injection site rxn
58
Q

What are the NRTI ADRs?

A
Generally well tolerated 
GI (N/V)
HA
Fatigue
Rash
59
Q

What are the NRTI BBWs?

A

Severe, acute exacerbation of hep B may occur upon D/c

Lactic acidosis and severe hepatomegaly

60
Q

What are the monitoring parameters for HBV?

A
HBV DNA
HBsAg
HBsAb
HBeAg
HBeAb
CBC
Chem-23 (includes LFTs)
61
Q

What are the medications for Hep C?

A

Ribavirin

Direct Acting Antivirals (DAAs)

62
Q

What is the MOA for Ribavirin?

A

Inhibits viral protein synthesis and the viral replication of RNA and DNA viruses

63
Q

What are the Brands of Ribavirin?

A
Copegus
Ribaspheres
Rebetol
Moderiba
Virazole
64
Q

What are the types of DAAs?

A

NS3/4A Protease inhibitors
NS5B Polymerase inhibitors
NS5A inhibitor

65
Q

What is the MOA of NS3/4A protease inhibitors?

A

Inhibits replication of the hepC virus by reversibly binding to NS3 serine protease

66
Q

What is the MOA of NS5B polymerase inhibitors

A

Inhibits HCV replication by binding to the NS5B RNA polymerase

67
Q

What is the MOA of NS5A inhibitor?

A

Inhibits the HCV NS5A protein necessary for viral replication

68
Q

What is olysio comprised of?

A

Simeprivir (NS3/4A)

Genotype 1

69
Q

What is technivie comprised of?

A

Ombitasvir (NS5A)
Paritaprevir (NS3/4A)
Ritonavir (Cyp450 inhibitor)
Genotype 4

70
Q

What is the viekira pak comprised of?

A

Paritaprevir (NS3/4A)
Ombitasvir (NS5A)
Dasabuvir (NS5B)
Genotype 1a (or unknown genotype 1)

71
Q

What is zepatier comprised of?

A

Elbasvir (NS5A)
Grazoprevir (NS3/4A)
Genotype 1 or 4 (use with ribavirin)

72
Q

What is sovaldi comprised of?

A

Sofosbuvir (NS5B)

Genotypes 1,2,3,4

73
Q

What is harvoni comprised of?

A

Sofosbuvir (NS5B)
Ledipasvir (NS5A)
Genotype 1,2,3,4

74
Q

What is daklinza comprised of?

A

Daclatasvir (NS5A)

Genotype 1,2,3

75
Q

What is epclusa comprised of?

A

Sofosbuvir (NS5B)
Velpatasvir
Genotype 1,2,3,4,5,6

76
Q

What is mavyret comprised of?

A

Pibrentasvir (NS5A)
Glecaprevir (NS3/4A)
Genotype 1,2,3,4,5,6

77
Q

What os vosevi comprised of?

A

Sofosbuvir (NS5B)
Voxilaprevir (NS3/4A)
Genotype 1,2,3,4,5,6

78
Q

What are the BBWs for ALL DAAs for HCV?

A

HBV reactivation has been reported in HCV/HBV co-infected patients who were receiving or had completed treatment with HCV direct-acting antivirals and were not receiving HBV antiviral therapy

79
Q

When do we treat chronic HCV?

A

All patients should be treated when diagnosed. But where resources are limited, the guidelines provide guidance on how to prioritize who to treat

80
Q

What are the different categories of treatment for HCV

A

Treatment naive/relapse

  • w/o cirrhosis
  • with compensated cirrhosis
81
Q

Special situations for treatment of HCV

A

Decompensated cirrhosis
Patients post-liver transplant
Renal impairment
HIV/HCV

82
Q

Monitoring of chronic HCV

A
HCV RNA
Hepatic function panel
CBC
INR
TSH - only if using peg-interferon
83
Q

When will NS5A inhibitors interact with PPIs?

A

BID (HD) PPIs

84
Q

When do we DC therapy for chronic HCV d/t lack of efficacy?

A

If HCV RNA is detectable at week 4, then check against it at week 6. If the HCV RNA level is > 10-fold at week 6, then DC treatment. Otherwise continue treatment

85
Q

When is baseline resistance testing recommended?

A
HCV genotype 1a infection (with compensated cirrhosis) being considered for treatment with simeprevir or sofosbuvir
Elbasvir treatment (initial treatment/retreatment) (test for NS5A resistant variants)
Resistance testing during and after treatment is not recommended
86
Q

What is the goal of HCV treatment

A

Sustained Virologic Response (SVR) - HCV RNA is not detected 12 weeks after treatment is complete

87
Q

What are the ADRs of ribavirin?

A
Preg Cat X
Fatigue
Rash
Hemolytic anemia
HA
Nausea
88
Q

What are the ADRs for DAAs?

A

HA
N/V/D
Fatigue
Anemia

89
Q

What must men and women do to treat SE of HCV therapy?

A

Use birth control up to 6 months after completion of ribavirin

90
Q

What is the role of statins in chronic HCV/HBV therapy?

A

Have been shown to reduce the risk of hepatocellular carcinoma (HCC) and cirrhosis in patients with chronic HBV/HCV

91
Q

What is the MOA of statins in HBV/HCV?

A

Improve hepatic sinusoidal endothelial dysfunction, increase hepatic NO production, and decrease hepatic vascular resistance