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Thera VIII > 10 Hepatitis B Kim > Flashcards

10 Hepatitis B Kim Flashcards

1
Q

What are the HBV modes of transmission?

A

Sexual. Perinatal. Parenteral drug abuse. Child to child. Accidental needle sticks

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2
Q

For HBV, what is the acute infection with progression to chronic infection like?

A

Most patients remain asymptomatic. About 25-40% of patients will progress to cirrhosis. Fibrosis and subsequent cirrhosis. At risk of developing hepatocellular carcinoma (HCC). Liver failure. Death

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3
Q

What is the risk of developing HCC and cirrhosis associated with?

A

The level of serum HBV DNA

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4
Q

Who is likely to get Chronic HBV after an acute infection?

A

Less than 5% of immunocompetent adults. 90-95% of newborn infants. 25-30% of young children. Immunosuppressed individuals are more likely to develop chronic HBV infection after an acute infection regardless of age

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5
Q

What are the HOST risk factors for progression of HBV to cirrhosis or HCC in HBsAg-Positive individuals?

A

Older age (> 40). Male sex. Asian/African ancestory. HCC family history

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6
Q

What are the Clinical risk factors for progression of HBV to cirrhosis or HCC in HBsAg-Positive individuals?

A

Cirrhosis. HCV coinfection

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7
Q

What are the Viral risk factors for progression of HBV to cirrhosis or HCC in HBsAg-Positive individuals?

A

HBeAg-Positive. Higher HBV DNA. Genotype B, C. Precore mutation (no antigen produced). Basal core promoter mutation

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8
Q

What are the preventable/co-morbidity risk factors for progression of HBV to cirrhosis or HCC in HBsAg-Positive individuals?

A

Smoking, alcohol. Obesity, diabetes

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9
Q

Who should be screened for HBV?

A

People born in geographic area with intermediate or high endemicity. People born in US and not vaccinated as infants whos parents were born in geographic area with high HBsAg prevalence (>8%). House hold and sexual contact of HBsAg-Positive people. Current or past IVDA. All pregnant women. Other individuals with high risk of HBV infection

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10
Q

What is used in the diagnosis of Hepatitis B infection?

A

Liver function tests (LFTs). Serology (level of antibodies directed against HBV antigen) most common method. Viral DNA. Liver biopsy

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11
Q

What is HBsAg?

A

Outer SURFACE membrane of HBV. Marker of INFECTION. Primary component of HBV vaccine

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12
Q

What is HBeAg?

A

Inner core of the virus. Marker of ACTIVE viral replication. Correlates with higher titers of HBV and greater infectivity

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13
Q

What is HBcAg?

A

Expressed on the surface of nucleocapside CORE that encloses the viral DNA

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14
Q

What is Anti-HBs?

A

Protective, neutralizing antibody. Indicates recovery from acute infection and confers immunity. Induced after HBV vaccination

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15
Q

What is Anti-HBe?

A

Represents nonreplicative phase and low infectivity

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16
Q

What is Anti-HBc?

A

Indicator of past exposure. IgM anti-HBc (acute infection). IgG anti-HBc (past chronic infection). Not induced by HBV vaccine

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17
Q

What is the Hepatitis B infection serology in acute infection?

A

HBsAg + IgM anti-HBc

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18
Q

What is the Hepatitis B infection serology in acute infection with recovery?

A

Disappearance of HBsAg after 6 months. Appearance of anti-HBs

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19
Q

What is the Hepatitis B infection serology in Chronic infection?

A

HBsAg + IgG anti-HBc. Persistence of HBsAg beyond 6 months

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20
Q

What is the Hepatitis B infection serology in HBeAg-Positive chronic HBV infection?

A

Active viral replication. Associated with high serum HBV DNA. Increased risk of HCC

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21
Q

What is the Hepatitis B infection serology in HBeAg-Negative chronic HBV infection?

A

Loss of HBeAg may occur spontaneously or during antiviral therapy. Mutations of the HBV may prevent formation of HBeAg in patients with active viral replication (precore mutants). Intermittent periods of exacerbation. 14% in US and >33% worldwide. Requires continued, INDEFINITE viral suppression d/t high relapse rates

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22
Q

What are the phases in natural history of Chronic Hepatitis B?

A

Immune tolerance –> HBeAg positive –> HBeAg negative –> Inactive carrier state –> Recovery (only one to be HBsAg negative)

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23
Q

What are the different characteristics of the HBV Genotypes?

A

Eight genotypes (A-H). Genotypes A and B associated with higher response rate to interferons. Genotype C associated with more severe liver disease and increased risk of HCC

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24
Q

What are the goals of HBV treatment?

A

Sustained normalization of ALT levels. Seroconversion from HBeAg to anti-HBe (for ABeAg-positive patients). Seroconversion from HBsAg to anti-HBs. Sustained suppression of viral replication. Prevent cirrhosis and its complications. Prevent HCC. Decrease the need for liver transplantation

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25
Q

For Chronic Hepatitis B, when do you treat right away (no observing)?

A

HBV DNA > 20,000 & ALT > 2x ULN

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26
Q

What are the predictors for a good Interferon-alfa (IFN) response?

A

High pretreatment ALT, lower baseline HBV DNA, significant inflammation on biopsy, HBV genotype A and B

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27
Q

What is the seroconversion like with IFN?

A

HBeAg seroconversion durable in 80-90% of patients after 4-8 years follow-up

28
Q

What are the characteristics of Pegylated IFN (Pegasys)?

A

Improved efficacy and tolerability. No added benefit when combined with Lamivudine. 180mcg SQ once weekly x48 weeks

29
Q

Which types of patients have a low response rate to IFN?

A

Asians and patients with precore mutant virus

30
Q

What are the ADRs associated with IFN?

A

Rash, Alopecia, Retinopathy. Depression. Bone marrow suppression. Fever, chills, HA, myalgia. N/V/D. Fatigue. Thyroid disorder. Less with pegylated formulation

31
Q

What are the advantages of IFN?

A

Finite duration of therapy. More durable response. Lack of resistant mutant

32
Q

What are the disadvantages of IFN?

A

Costs. ADRs. Injection

33
Q

What are Oral Nucleoside and Nucleotide Analogs for?

A

For treatment of Chronic Hepatitis B if active viral replication and either elevated ALT or histologically active disease. Adjust dosing in renal impairment

34
Q

What are the advantages of Oral Nucleoside and Nucleotide Analogs?

A

Increased convenience and improved safety. Well tolerated

35
Q

What are the disadvantages of Oral Nucleoside and Nucleotide Analogs?

A

Lower durability and longer treatment durations. Increased risk of resistance. Risk of lactic acidosis and severe hepatomegaly. Severe acute hepatitis upon discontinuation

36
Q

What is Lamivudine (Epivir-HBV)?

A

NucleoSIDE analog. Approved for both adults and children

37
Q

What are the advantages of Lamivudine?

A

Lower cost and excellent tolerability

38
Q

What are the disadvantages of Lamivudine?

A

Optimal duration of treatment unclear. Resistance: Prevalence of YMDD mutations ranges from 24% at 1 year to 69% at 5 years. Rebound HBV DNA levels to pretreatment values after stopping therapy. Not recommended as monotherapy for long-term therapy

39
Q

What is Adefovir Dipivoxil (Hepsera)?

A

NucleoTIDE analog. Active against wild type and Lamivudine-resistant HBV

40
Q

What are the ADRs associated with Adefovir Dipivoxil?

A

NEPHROTOXICITY in patients who are at risk or have preexisting kidney dysfunction

41
Q

What is the dosage of Adefovir Dipivoxil?

A

10mg QD

42
Q

What is the resistance of Adefovir Dipivoxil?

A

0%, 3%, and 30% at 48, 96, and 240 weeks of treatment

43
Q

What are the disadvantages of Adefovir Dipivoxil?

A

Optimal duration of treatment unknown (Benefits in HBeAg-negative patients achieved from 40 weeks of therapy lost when drug was discontinued). Use declining d/t superiority of Tenofovir

44
Q

What is Entecavir (Baraclude)?

A

NucleoSIDE analog. Effective against wild-type and Lamivudine-resistant HBV. Greater level of viral suppression and efficacy in HBeAg-Negative patients compared with Lamivudine

45
Q

What is the treatment duration of Entecavir?

A

HBeAg-positive: > 1 year until HBeAg seroconversion and undetectable serum HBV DNA; continue therapy for > 6 months after seroconversion. HBeAg negative: > 1 year until HBsAg clearance. Decompensated liver disease: lifelong treatment recommended

46
Q

What is the dosing of Entecavir like?

A

Nucleoside naive: 0.5mg QD. Lamivudine-Refractory or resistant: 1mg QD. Decompensated liver disease: 1mg QD

47
Q

What is the resistance like for Entecavir?

A

Nucleos(t)ide-naive patients: 0.2%, 0.5%, and 1.2% at 48, 96, and 192 weeks of treatment. Lamivudine-refractory patients: 6%, 15%, and 46% at 48, 96, and 192 weeks of treatment

48
Q

What should be done with < 2 log decrease in serum HBV DNA in 6 months of treatment with Entecavir?

A

Additional therapy or switch to an alternative therapy

49
Q

What is Telbivudine (Tyzeka)?

A

NucleoSIDE analog. Greater anti-viral efficacy than Lamivudine. NOT effective against Lamivudine-resistant HBV. “Good for Nothing”

50
Q

What is the resistance to Telbivudine like?

A

3-4% and 9-22% at 1 and 2 years of treatment. 8.1% (HBeAg-negative), 21% (HBeAg-Positive) at 2 years

51
Q

What are the ADRs with Telbivudine?

A

Myopathy and elevated creatine phosphokinase. Several weeks to months after starting therapy. Patients to report unexplained muscle pain, tenderness, or weakness, especially during upward titration. Peripheral neuropathy if used with PegIFN

52
Q

What is Tenofovir Disoproxil Fumarate (Viread)?

A

NucleoTIDE analog structurally similar to Adefovir. Effective against Lamivudine-resistant HBV and incomplete response to ADV but low response in ADV-resistance. Effective against those with inadequate response to Adefovir. Most effective in HBeAg negative patients

53
Q

How is Tenofovir dosed?

A

300mg QD

54
Q

What is the treatment duration of Tenofovir?

A

HBeAg positive: > 1 year until HBeAg seroconversion and undetectable serum HBV DNA; continue therapy for > 6 months after seroconversion. HBeAg negative: > 1 year until HBsAg clearance. Decompensated liver disease: lifelong treatment recommended

55
Q

What are the ADRs associated with Tenofovir?

A

NEPHROTOXICITY (concurrent use with Adefovir should be avoided). Bone mineral density monitoring recommended for patients with history of bone fracture or at risk of osteopenia

56
Q

What is Emtricitabine?

A

NucleoSIDE analog structurally similar to Lamivudine; not approved for Chronic HBV infection (HIV drug)

57
Q

What needs to be assessed for treatment options for Chronic HBV?

A

Patient age. Severity of liver disease. Likelihood of response. Side effects of drugs. Potential complications of treatment

58
Q

What are the HBV drugs usually used for initial therapy?

A

IFN, Entecavir, or Tenofovir. Lamivudine and Telbivudine not preferred as first line agent d/t high rate of resistance

59
Q

Which drugs have the highest rate of resistance in HBV infection?

A

Lamivudine > Adefovir > Telbivudine. Almost none for Entecavir > Tenofovir

60
Q

What is used in patients with Lamivudine or Telbivudine resistance?

A

Add Adefovir or Tenofovir. Stop Lamivudine or Telbivudine and switch to Truvada

61
Q

What is used in patients with Adefovir resistance?

A

Add Lamivudine, Telbivudine, or Entecavir. Switch to Tenofovir or Truvada

62
Q

What is used in patients with Entecavir resistance?

A

Add Adefovir. Switch to Tenofovir or Truvada

63
Q

What combination therapy should be avoided?

A

Lamivudine + Entecavir (Lamivudine predisoposes patient to Entecavir resistance). Telbivudine + Entecavir (Telbivudine predisposes patient to Entecavir resistance). Adefovir + Tenofovir (added nephrotoxicity)

64
Q

What are the characteristics of Liver Transplantation with HBV?

A

Patients with end-stage liver disease d/t HBV. Patients are placed on an oral antiviral agent and Hepatitis B Immunge Globulin (HBIG) to prevent recurrent HBV infection after transplantation

65
Q

What are the HBV recurrence rates after transplantation?

A

No prophylaxis > 70%. HBIG < 30%. HBIG + Antiviral < 10%

66
Q

What are the characteristics of Hepatitis B Immune Globulin?

A

Post-exposure prophylaxis (within 7 days). Prophylaxis of infants born to HBsAg-Positive mothers (at birth and at 3 months). Individuals at increased risk of infection (may be given with vaccine for pre-exposure prophylaxis)

Thera VIII (24 decks)

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