Hepatitis Viruses Flashcards

1
Q

Early lab changes in acute hepatitis infection? [3]

A
  1. Leukopenia
  2. Lymphocytosis
  3. AST/ALT elevation
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2
Q

Ddx of acute hepatitis? [7]

A
  1. HSV
  2. CMV
  3. EBV
  4. Leptospirosis
  5. Dengue Fever
  6. Yellow Fever
  7. Toxic exposures [tylenol, mushrooms]
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3
Q

Ddx of chronic hepatitis? [4]

A
  1. Wilson’s
  2. Autoimmune hepatitis
  3. NASH
  4. Drugs
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4
Q

How long are those with acute hepatitis A infective?

A

3-4 weeks before and 1 week after symptoms development.

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5
Q

Diagnosis of acute hepatitis A? [2]

A
  1. Hepatitis A IgM

2. Hepatitis A RNA [blood and stool]

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6
Q

Acute hepatitis A treatment?

A

Supportive.

Fulminant in <1%, may need liver transplant

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7
Q

Complications of Hep A?

A

Prolonged cholestatic hepatitis
–> Lasts >12 weeks
–> Occurs in <5%
Resolves spontaneously.

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8
Q

Phases of lab positivity with Hep A? [5]

A
  1. Viremia [0-6 wks]
  2. HAV in stool [1-5 wks]
  3. IgM starts being made wk 1
  4. AST elevation [2-10 wks]
  5. IgG starts around week 2-3
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9
Q

How many hep b genotypes are there?

A

10 [A-J]

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10
Q

How long can Hep B live outside the body?

A

1 week.

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11
Q

Presentation of acute hepatitis B

A

70% subclinical
Rarely fulminant hepatitis
Jaundice in 30%, fulminant in 0.1%

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12
Q

Treatment of acute hepatitis B

A

Supportive unless fulminant or HIV co-infection.

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13
Q

Likelihood acute Hep B will become chronic?

A
  1. > 90% of infected neonates
  2. 25% of 1-5 year olds
  3. <5% of adults
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14
Q

Extrahepatic manifestations of chronic hep B [2]

A
  1. Polyarteritis nodosa

2. Renal disease

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15
Q

What is precore and core promoter mutations?

A

Causes HBeAg production to be reduced or prevented

Infectious virions are still produced

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16
Q

What is the immune tolerant phase of chronic hep B

A
  • High levels of HBV replication
  • NO evidence of active liver damage
  • Lasts 10-30 years
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17
Q

What is the immune clearance [immune active] phase of chronic hep B

A
  • Increased rate of spontaneous HBeAG clearance with HBeAb seroconversion
  • Exacerbations of active hepatitis with raised ALT
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18
Q

What is the inactive carrier state of chronic hep B?

A
  • HBV DNA undetectable
  • No liver disease
  • May reactivate with immune compromise.
  • Consider HBV cAb if immune compromising medications are needed
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19
Q

What is reactiviation HBeAg negative chronic hep B?

A
  • Active HBV replication with active liver disease
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20
Q

What does Anti-HBc IgM represent?

A

Recent infection [<6 months]

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21
Q

Interpretation of +surface antigen, +core IgG, +envelope antigen, +/- envelope antibody, HBV DNA high, ALT low or normal.

A

Chronic infection, immune tolerant

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22
Q

Interpretation of +surface antigen, +core IgG, +/-eAg, +/- eAb, HBV DNA variable, HIGH ALT

A

Chronic infection, immune active [consider treatment]

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23
Q

Interpretation of +surface antigen, +core IgG, +eAg, +eAb, low HBV DNA, HIGH ALT.

A

Chronic infection - seroconverting.

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24
Q

Interpretation of +surface antigen, +core IgG, +eAb, low HBV DNA, LOW ALT.

A

Chronic infection, inactive carrier.

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25
Q

Interpretation of +surface antigen, +core IgG, +eAb, variable HBV DNA, HIGH ALT.

A

Chronic infection reactivating. [consider treatment].

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26
Q

Interpretation of +Core IgG, all else negative. HBV negative, ALT normal.

A

Resolved infection, at risk for reactivation.

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27
Q

When should hepatitis B be treated?

A

If ALT is increased.

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28
Q

What is the most effective therapies?

A

Entecavir, tenofovir

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29
Q

What might result in fulminant HBV reactivation in an HIV patient?

A

Discontinuation of tenofovir.

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30
Q

What HBV treatment has high resistance rates?

A

Lamivudine [30%]

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31
Q

How does HCV treatment effect chronic HBV infection?

A

Treating HCV might cause HBV reactivation and flares of hepatitis. May result in death or transplant.
Reactivation usually occurs at week 8 of HCV treatment.

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32
Q

How long should chronic HBV be treated?

A

Life long. 75% with get control of their disease if HBeAg +, about 90% get control of HBeAg negative

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33
Q

Incidence of cirrhosis in chronic HBV

A

300 per 100,000 person years.

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34
Q

What HBV genotype is most likely to cause cirrhosis?

A

Genotype C

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35
Q

Who with HBV should be screened for HCC?

A
  1. ALL with cirrhosis
  2. Asian males 40 and older
  3. Asian females 50 and older
  4. Sub-Saharan Africans 20 and older
  5. Those with HCC history.
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36
Q

How often should HCC screening be done?

A

Every 6 months with US +/- AFP.

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37
Q

Highest risk for HCV?

A
  • IVDU
  • MSM [receptive]
  • Receipt of blood products before 1990
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38
Q

How many genotypes of HCV?

A

6

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39
Q

Which HCV genotype is most common in US?

A

1

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40
Q

Presentation of acute HCV

A
  • Most are asymptomatic
  • Rarely causes fulminant hepatitis
    Jaundice in 20-30%
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41
Q

Treatment of acute HCV?

A
  • Supportive
  • Monitor for recovery
  • More likely to clear if symptomatic OR acquired at birth.
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42
Q

Rate of development of chronic hepatitis C in an adult?

A

50-80%

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43
Q

Risk of cirrhosis in chronic hepatitis C

A

15-30% within 20 year

44
Q

What are extrahepatic manifestations of chronic hepatitis c? [6]

A
  1. Autoimmune thyroiditis
  2. B-cell non-Hodgkin lymphoma
  3. Lichen planus
  4. Porphyria cutanea tarda
  5. Cryoglobulinemia [vasculitis]
  6. Glomerulonephritis
45
Q

Work up in chronic hep C prior to treatment [3]

A
  1. HCV RNA to confirm active infection.
  2. Genotype
  3. Fibrosis staging.
46
Q

Methods to fibrosis stage [3]

A
  1. Liver biopsy
  2. FibroScan [US based]
  3. FibroSURE [blood test]
47
Q

What are the classes of Hep C drugs? [4]

A
  1. Protease inhibitors
  2. NS5A inhibitors
  3. NS5B polymerase inhibitors - nucleoside polymerase inhibitors
  4. NS5B polymerase inhibitors - non-nucleoside polymerase inhibitors
48
Q

Name the HCV protease inhibitors [5]

A
  1. Telaprevir
  2. Boceprevir
  3. Asunaprevir
  4. Simeprevir
  5. Grazoprevir

–> Ends in previr

49
Q

Name the HCV NS5A inhibitors [3]

A
  1. Daclatasvir
  2. Ledipasvir
  3. Elbasvir

–> Ends in asvir

50
Q

Name the HCV NS5B polymerase inhibitors nucleoside polymerase inhibitors [2]

A
  1. Sofosbuvir

2. Mercitabine

51
Q

Name the HCV NS5B polymerase inhibitors non-nucleoside polymerase inhibitors [3]

A
  1. Deleobuvir
  2. Filibuvir
  3. Tegobuvir

–> Ends in buvir

52
Q

How long should HCV be treated?

A

12 weeks.

Up to 24 weeks for cirrhotics or prior treatment failures.

53
Q

Success rate of HCV treatment?

A

> 95%.

54
Q

What defines cure of HCV?

A

Sustained virologic response [SVR] with no detectable virus after 12 weeks.

55
Q

Does cured HCV still need HCC monitoring?

A

If cirrhosis - yes.

56
Q

How is HDV transmitted

A

IVDU
Transfusion
Prbly not sexually or perinatal.

57
Q

Describe HDV/HBV coinfection

A
  • More severe acute infection syndrome

- Clears with HBV clearance

58
Q

Describe HDV/HBV superinfection.

A
  • Can cause flares of hepatitis in chronically HBV-infected persons
  • Can accelerate disease due to HBV.
59
Q

Treatment of HDV?

A
  • Interferon.

- HBV antivirals have NO EFFECT.

60
Q

Most common cause of acute viral hepatitis worldwide?

A

HEV.

61
Q

Who will get severe fulminant hepatitis E?

A

Pregnant women, those with underlying liver disease.

62
Q

Extrahepatic manifestations of HEV? Who gets them? [3]

A

OCCURS ONLY IN CHRONIC CARRIERS.

  1. Cryoglobulinemia
  2. Glomerulonephritis
  3. Guillain-Barre.
63
Q

Animal reservoir for HEV?

A

Pigs/Swine [only Genotypes 3-4].

–> Eating undercooked boar, deer meat in places like Germany, Spain etc a/w catching HEV.

64
Q

What is Hepatitis G and Transfusion-Transmitted Virus?

A

Causes post-transfusion hepatitis

- Self limited.

65
Q

Diagnosis of HDV?

A

HDV IgM, RNA

66
Q

Diagnosis of HEV?

A

HEV IgM

67
Q

Diagnosis of HCV?

A

HCV Ab

HCV RNA if HIV or acute disease

68
Q

If a patient is exposed to Hep A what is the treatment? [2]

A
  1. Vaccinate if exposure within 2 weeks
  2. IVIG if immunocompromised

–> IVIG preferred if over age 40

69
Q

Who gets chronic HEV?

A
  1. People with transplants [may get chronic hepatitis or cirrhosis, tacrolimus associated]
  2. HIV [only 1 case]
70
Q

High risk conditions for chronic HBV reactivation? [3]

A
  1. Transplant
  2. Steroids
  3. Immunosuppression
71
Q

Management of patient who is HBsAg + who is going to get immunosuppression.

A

Empiric treatment with Entecavir OR tenofovir

72
Q

Management of isolated HBV +Core IgG who is going to get immunosuppression.

A

Watchful waiting; monitor HBV DNA and LFTs

73
Q

How does HDV present?

A

Someone with known HBV who develops fulminant hepatitis with new exposure.

74
Q

Ddx of hepatitis in pregnancy? [4]

A
  1. HSV
  2. HELLP
  3. Acute Fatty Liver of Pregnancy
  4. HEV
75
Q

Evaluation of HSV hepatitis in pregnancy?

A

May not have skin lesions
Check serum PCR
If negative HSV is excluded

76
Q

Presentation and labs of acute fatty liver of pregnancy?

A

Severe, fulminant disease looks like sepsis

Low glucose, low fibrinogen, HIGH INR

77
Q

What is necrolytic acral erythema?

A

Rare HCV rash. pruritic, psoriasis-like skin disease characterized by sharply marginated, erythematous to hyperpigmented plaques with variable scale and erosion on the lower extremities
Treated with zinc

78
Q

In what circumstance should a treatment naive patient have HCV resistance testing? [2]

A
  1. Genotype 1a and insurance is making you use elbasvir/grazoprevir
  2. Genotype 3 with cirrhosis and using sofosbuvir/velpatasvir
79
Q

In what circumstance should a treatment experienced patient have HCV resistance testing? [2]

A
  1. Genotype 1a and ledipasvir/sofosbuvir considered

2. Genotype 3 using sofosbuvir/velpatasvir

80
Q

What is FIB4?

A

[Age x AST] / [Platelet Count x √ALT]
Used in chronic hep c to estimate cirrhosis
Low = less cirrhosis and scaring
High = more cirrhosis and scaring

–> Often combined with transient elastography in cirrhosis staging.

81
Q

What is APRI?

A

AST to Platelet Ratio Index

[(AST measured/AST ULN)/(Platelet Count)]

Another way to predict cirrhosis in hep C

82
Q

Most specific test for predicting cirrhosis for HCV?

A

APRI and elastography [91%]

83
Q

Most sensitive test for predicting cirrhosis for HCV?

A

Elastography [89%]

84
Q

Outpatient mgmt of HCV

A
  1. Rule out cirrhosis [fibro, biopsy, elastography]
  2. If cirrhosis rule out HCC and varicies
  3. Rule out decompensated cirrhosis [MELD or CTP scores]
85
Q

Mgmt of patient with HBV and HCV who is about to undergo treatment for HCV

A

Monitor for HBV reactivation and treat if ALT goes up.

86
Q

Two HCV regimens can be used for any genotype.

A
  1. Sofosbuvir + velpatasvir

2. Glecaprevir + pibrentasvir

87
Q

Two HCV regimens that can be used for CKD and ESRD?

A
  1. Glecaprevir + pibrentasvir

2. Elbasvir + Grazoprevir

88
Q

Describe HIV integrase inhibitor interaction with HCV drugs.

A

None

89
Q

Describe HIV protease inhibitor interaction with HCV drugs.

A

AVOID HIV PI with HCV PI.

–> Basically HIV protease inhibitors cannot be used when treating HCV.

90
Q

What HCV medications have reduced absorption with PPIs?

A

NS5A inhibitors

  1. Daclatasvir
  2. Ledipasvir
  3. Elbasvir
  4. velpatasvir
91
Q

NOTE:

A

Avoid cobicistat boosting with hepatitis C type protease inhibitors.

92
Q

What is the only HCV treatment which can be used with efavirenz at the same time?

A

Ledipasvir + Sofosbuvir

93
Q

Should HCV be treated in pregnancy?

A

No.

94
Q

What is the definition of chronic HBV?

A

Surface antigen + 2x separated by 6 months.

95
Q

When should chronic HBV be treated when HBeAg is positive?

A
  1. ALT 2x ULN + HBV DNA >20,000
96
Q

How often should HBV with +HBeAg and no ALT elevations be monitored and with what? [2]

A
  1. ALT + HBV DNA levels q 3-6 months

2. HBeAg q 6-12 months

97
Q

When should chronic HBV be treated when HBeAg is negative?

A
  1. ALT 2x ULN + HBV DNA >2000
98
Q

How often should HBV with (-)HBeAg and no ALT elevations be monitored and with what?

A
  1. ALT + HBV DNA levels q 3-6 months

2. HBsAg yearly

99
Q

Management of chronic hepatitis B with +HBeAg and a HBV DNA level between 2000-20,000

A
  • -> May be seroconverting to HBeAg negative
  • -> Monitor every 1-3 months
  • -> TREAT IF PERSISTS FOR >6 months.
100
Q

What type of HIV resistance does entecavir select for?

A

M184V in HIV.

101
Q

Who should be screened for HDV?

A

ALL with chronic HBV 1x

102
Q

How is HDV screened?

A
  1. Start with anti-HDV

2. HDV RNA if positive

103
Q

Mgmt of IgG Core positive HBV with ALL OTHER negative

A

Vaccinate
Likely is an old clear infection or false +
Check titers after

104
Q

Treatment of chronic HEV?

A

Ribavirin

105
Q

Who with HCV should be screened for HCC?

A
  1. Cirrhosis patients
  2. Stage F3 fibrosis

–> Screen them even if cured of hepatitis C