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Hepatitis Flashcards

1
Q

All hepatitis viruses are RNA except which?

A

Hepatitis B is a DNA virus

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2
Q

Why do some patients with chronic hepatitis not recall the acute infection?

A

Many acute infections are asymptomatic.

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3
Q

Symptoms of acute hepatitis.

A

Fever, malaise, nausea, vomiting, anorexia

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4
Q

Where do pts with acute hepatitis have pain?

A

RUQ: location of liver

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5
Q

Why does hepatitis cause jaundice?

A

There is excess billirubin in the blood because liver cannot do its job (excrete billirubin).

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6
Q

Jaundice causes itching due to

A

bile salts in skin

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7
Q

Why does jaundice cause dark urine?

A

When billirubin levels in the plasma are too high they spill into urine, making it dark.

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8
Q

Clay-colored stools are due to

A

lack of billirubin excretion

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9
Q

How do stools become dark brown?

A
  1. Liver conjugates billirubin and excretes it into bile
  2. Once it gets to the GI tract, it is converted into urobilinogen by bacteria.
  3. Urobilinogen is converted to stercobilin to make stools dark brown.
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10
Q

What enzymes spill into the blood when there is liver inflammation?

A

AST/ALT

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11
Q

Which enzyme is higher in viral hepatitis?

A

ALT

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12
Q

Which enzyme is higher in alcoholic hepatitis?

A

AST

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13
Q

Why is there increased direct billirubin in acute hepatitis?

A

During acute hepatitis, liver can still conjugate/synthesize billirubin but cannot transport it into bile. Level becomes high in plasma.

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14
Q

Hepatitis can cause a false positive in a screening test for what?

A

Syphillis

VDRL elevation

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15
Q

Which hepatitis viruses are non-enveloped and transported via fecal-oral route?

A

A and E

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16
Q

What is the prognosis for Hep A and E?

A

Death or Life-long immunity

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17
Q

Why is Hep D always associated with Hep B?

A

Hep B must provide certain viral components for replication of Hep D

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18
Q

Which hepatitis viruses are blood-sourced and transmitted via percutaneous/permucsoal routes

A

B, C, D

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19
Q

What does chronic mean for hepatitis?

A

Infection lasting greater than 6 months

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20
Q

Which virus has the highest chance of becoming a chronic infection?

A

Hepatitis C

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21
Q

How do you prevent Hepatitis C?

A

Screen blood

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22
Q

Vaccine for Hep B also protects you from?

A

Hep D

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23
Q

Hepatitis A is a member of which family?

A

Picornaviridae: small RNA virus family

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24
Q

Enterovirus 72 =

A

HAV

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25
Q

HAV replication occurs

A

Exclusively in cytoplasm

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26
Q

What are the members of the Picorna Virus family?

A 
PERCH:
Polio
Echo
Rhino
Coxsackie
Hep A
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27
Q

Picornaviridae

A 
Non-enveloped
(+) ssRNA
linear
icosahedral
Synthesize a large polypeptide that is cleaved into viral proteins
Transmitted fecal-orally
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28
Q

Hep A Diagnosis

A

Acute: Anti-HAV IgM antibodies plus symptoms

Prior disease: Anti-HAV IgG antibodies

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29
Q

Hep A Incubation Period

A

30 days

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30
Q

Hep A Transmission

A

Close personal contact
Contaminated food/water
Blood exposure (rare)

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31
Q

Can Hep A cause chronic disease?

A

No. Acute only.

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32
Q

Hep A vaccine is

A

inactivated virus

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33
Q

Hep E is the single member of family

A

Herpeviridae

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34
Q

Hep E

A

Non-enveloped
(+) ssRNA
linear
Icosahedral

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35
Q

Is Hep E transmitted person-to-person

A

rarely

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36
Q

Can Hep E cause chronic disease?

A

No. Acute only.

37
Q

Diagnosis

A

HEV in serum or feces (PCR)

IgM antibodies to HEV

38
Q

Hep E has a higher mortality rate in

A

pregnant women

39
Q

Is there a Hep E vaccine?

A

Yes. In China.

40
Q

Which Hep C genotypes are most common in the U.S.?

A

1, 2 and 3

41
Q

Hep C

A
  1. Hep C is taken up by receptor-mediated endocytosis
  2. Capsid is released into cytoplasm
  3. (+) RNA is translated on the rough ER to a polyprotein that is cleaved
  4. NS5A and NS5B components are involved in (-) intermediates which can become (+) intermediates to continue cycle
  5. Maturation in Golgi Complex
42
Q

HBsAg

A

Hep B Surface Antigen = Envelope glycoprotein

Antibodies to surface antigen

43
Q

HBcAg

A

Hep B Core Antigen = Nucleocapsid proten

44
Q

HBeAg

A

Hep B Early Antigen = Active infection

45
Q

Which protein has been linked to the pathogenesis of HCC?

A

X protein: Promiscuous transactivator of transcription of cellular and viral genes

46
Q

Hepadnavirus

A

Hep B

47
Q

Which hepatitis is a DNA rather than RNA virus

A

Hep B

48
Q

Hep B structure

A

Enveloped, circular, icosahedral capsid

49
Q

What are the 3 unique properties of Hep B?

A
  1. Genome enters hepatocytes and goes to nucleus
    Once it gets into nucleus, DNA becomes fully double stranded
    At that point, it will synthesize RNA and RNA will go to cytoplasm
  2. Reverse transcriptase synthesized
    Viral mRNA is synthesized to viral DNA
    Packaged in capsid
  3. Envelope comes from ER
50
Q

anti-HBsAg

A

Antibody of surface antigen. Marker of immunity.

51
Q

anti-HBcAg

A

Marker of past or current infection

52
Q

IgM Anti-HBc

A

Recent HBV infection (4-6 months)

53
Q

IgG Anti-HBc

A

Old HBV infection

54
Q

Anti-HBe

A

Present in immune or infected person so not helpful

55
Q

HBsAg (-)
Anti-HBc (-)
Anti-HBs (-)

A

Susceptible to HBV infection

56
Q

HBsAg (-)
Anti-HBc (+)
Anti-HBs (+)

A

Immune due to natural infection

57
Q

HBsAg (-)
Anti-HBc (-)
Anti-HBs (+)

A

Immune due to vaccine

58
Q

HBsAg (+)
Anti-HBc (+)
Anti-HBs (-)
IgM Anti-HBc (+)

A

Acutely infected

59
Q

HBsAg (+)
Anti-HBc (+)
Anti-HBs (-)
IgM Anti-HBc (-)

A

Chronically infected

60
Q

Anti-HBc Positive

A
  1. Resolved HBV infection (most common)
  2. May be susceptible with a false positive anti-HBc
  3. May have low level chronic infection
  4. May be resolving an acute infection
61
Q

Hep B Incubation

A

1-4 months

62
Q

Hep B Icteric Hepatitis

A

30%

63
Q

Chronic Hep B

A 
Risk of progression to:
Cirrhosis
Liver failure
HCC (viral DNA integrates into host)
Reactivation (acute hepatitis)
64
Q

Immune Reconstitution

A

If HIV treated w/o treating Hep B severe liver damage results.
Hep B testing usually done prior to HIV therapy.

65
Q

Polyarteritis Nodosa

A 
Caused by Hep B
Fevers, fatigue, arthralgias
Abdominal pain, melena
Neuropathy
Rash
66
Q

Glomerular Disease

A

Caused by Hep B
Most common is membranous nephropathy
Presents as proteinuria, nephrotic syndrome

67
Q

Rise in acute disease. Fall as infection resolves.

A

Antigens

68
Q

Rise as acute infection resolves

A

Antibodies

69
Q

Hep B Vaccine

A

Contains recombinant HBsAg

70
Q

Can Hep B Core Antigen be detected in serum?

A

No. HBcAg is NOT detectable in serum.

71
Q

Window Period

A

HBsAg undetectable
Anti-HBsAg not yet detectable
Can give false appearance of infection
SOLE marker of infection can is anti-HBc (IgM)

72
Q

HBeAg indicates

A

Viral replication

73
Q

anti-HBeAg indicates

A

Fall in viral replication

74
Q

Acute Hep B Treatment

A

Supportive care

75
Q

Chronic Hep B Treatment

A

Interferon
Lamivudine (NRTI)
Other antiviral drugs

76
Q

Pegylated Interferon alpha-2a

A 
Evaluate pt for liver disease
HBsAg in blood for greater than 6 months
HBeAg in blood (ongoing replication)
Elevated serum aminotransferases
Liver biopsy (examine for decompensated liver disease)
77
Q

3TC Lamivudine

A

Nucleoside analog, inhibitor of reverse transcription

78
Q

Adefovir dipivoxil

A

Nucleoside analog, also inhibitor of reverse transcription

79
Q

Entecavir

A

Guanosine analog, also an inhibitor of reverse transcription

80
Q

Telbivudine

A

Thymidine analog, inhibitor of reverse transcription

81
Q

Tenofovir

A

Analog of adenine, inhibitor of reverse transcription

82
Q

Hep C

A

Flavivirus (mostly mosquito illnesses)
Enveloped, (+) ssRNA, linear, icosahedral
High degree of antigenic variation
Difficult for immune system to eradicate effectively
High rate of chronic disease

83
Q

Hep C envelope proteins

A

Contain a hypervariable region
High mutation rate in genome
Lack of proofreading by viral RNA polymerase
Result: Prone to frequent mutations

84
Q

Hep B can cause HCC through

A
  1. Inflammation
  2. Integration through genome
  3. Viral proteins
85
Q

HCV has proteins that can lead to

A

ROS, genomic instability and HCC

86
Q

What is the average incubation period and the incidence of developing a chronic HBV infections?

A

60-90 days; 9-10%.

87
Q

A patient comes to the Infectious Diseases clinic at KUMC complaining of fever, fatigue, upper abdominal discomfort, and dark colored urine. The patient was a 40-year -old man that had returned from central Mexico approximately 4 weeks ago. He was a large animal veterinarian who was visiting a local veterinary school to present lectures on infectious diseases of swine, which included face time with live animals and inspections of raw pig meat. He had no history of intravenous drug use, unprotected sex, drinking contaminated water or eating raw shellfish. His laboratory results revealed elevated serum liver enzymes with a total bilirubin level of 6 mg/dL, direct bilirubin level was 3.9 mg/dL, serum aspartate aminotransferase (AST) concentration was 1458 U/L, alanine aminotransferase (ALT) was 2232 U/L, and alkaline phosphatase (AP) was 196 U/L. The peak of liver enzymes was observed on the tenth day after the start of the clinical manifestations and returned to normal values on day 25. Which of the following viruses was most likely the cause of this patient’s disease?

A

Answer: Hepatitis E virus

HEV is a zoonotic disease that occurs in swine. Certain genotypes of HEV are prevalent in swine but can be transmitted to humans. Hep A is unlikely, as he claims to have not eating raw shellfish or drank contaminated water. Hep B, C, and D are not correct, as he had no risk factors associated with the transmission of these viruses.

88
Q

The patient was started on a 2-month course of treatment with pegylated interferon-alpha-2α. Two months later no significant decrease of HBV DNA levels was observed and HDV RNA remained detectable. Which of the following drugs could be added to the therapy to enhance the virologic response against HBV/HDV?

A

Tenofovir

ID (13 decks)

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