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Host and Defense > EXAM 3 Hepatitis > Flashcards

EXAM 3 Hepatitis Flashcards

1
Q

describe acute hepatitis

A
  • incubation = several weeks
  • flu-like symptoms, fever, myalgias, pharyngitis
  • jaundice, enlarged and painful liver
  • marked elevations in LFTs (liver function tests)
  • resolves spontaneously
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2
Q

hepatitis ___ can cause acute hepatitis

A

A, E, and B (B causes both)

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3
Q

hepatitis ___ causes chronic hepatitis

A

C and B (causes both)

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4
Q

describe chronic hepatitis

A
  • often asymptomatic
  • physical exam can show signs of portal hypertension or liver inflammation
  • LFTs can be normal or elevated
  • persists for years or decades
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5
Q

what type of virus is hepatatitis A?

A

non-enveloped ssRNA virus

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6
Q

the incidence of hep A among children in developing countries reaches ___%

A

100%, with subsequent life-long immunity (because the hep A results in acute hepatitis which will resolve itself, so the child will develop immunity)

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7
Q

what is the transmission of hep A?

A

fecal-oral route

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8
Q

what is the incubation period of hep A?

A

28 days (15-50 days)

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9
Q

describe outbreaks of hep A

A

foodborne outbreaks are common, and are related to overcrowding, poor sanitation, and polluted water sources

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10
Q

hep ___ is the most common cause of acute hepatitis

A

A

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11
Q

what are the risk factors for contracting hep A?

A

day care, international travel, MSM (men who have sex with men), IV drug use

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12
Q

shedding of hep A occurs ___ weeks prior to acute hepatitis and continues 1 week after onset of ___

A
  • 1-3
  • jaundice
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13
Q

with hep A, most adults will have ___, while ___% of children are ___

A
  • symptoms
  • 70%
  • asymptomatic
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14
Q

describe the diagnosis of hep A

A

exposure + acute hepatitis + anti-HAV IgM

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15
Q

what are the complications with hep A?

A
  • coagulopathy
  • encephalopathy
  • renal failure
  • these complications are rare; hep A usually resolves itself
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16
Q

describe prevention of hep A

A
  • two formalin-inactivated vaccines were FDA-licensed in mid-1990s
  • two-dose vaccine with >94% pts demonstrating neutralizing antibodies one month after first dose
  • two doses recommended: 0 and 6-12 months
  • hep A immunoglobulin is available for immediate passive immunity (post exposure prophy if immune compromised)
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17
Q

describe hep A prevention via vaccination

A
  • everyone should get vaccinated
  • children most importantly
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18
Q

describe the virology of hep E

A

non-enveloped ssRNA virus

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19
Q

hep ___ causes acute hepatitis that is clinically indistinguishable from HAV

A

E

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20
Q

how is hep E spread?

A

fecal contamination of water

person-to-person spread is rare

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21
Q

what are the areas where hep E is endemic?

A

asia, north africa, middle east

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22
Q

the incubation of hep E is ___ days

A

40

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23
Q

which hepatitis virus can be acute or chronic?

A

B

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24
Q

describe the virology of hep B

A
  • enveloped DNA virus: partially dsDNA / ssDNA
  • 3200 nucleotides total: smallest known human DNA virus
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25
Q

the compact, overlapping reading frames of hep B produce what?

A
  • surface protein (HBsAg)
  • core nucleocaspid protein (HBcAg)
  • HBeAg
  • DNA pol (DNA- and RNA-dependent DNA polymerase with RNase H activity)
  • HBxAg (transactivator, clinical relevance unknown, can bind p53)
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26
Q

there are 250 million ___ carriers worldwide

A

hep B chronic

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27
Q

hep B is responsible for ___ deaths annually worldwide

A

1 million

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28
Q

how many people in the US have chronic hep B?

29
Q

transmission of hep B can occur in what 3 ways?

A

perinatal, parenteral, sexual

30
Q

___ transmission of hep B predominates in high prevalence areas

A

perinatal

  • infection rate of infants born to HBeAg+ mothers = 90% (decrease to 30% if HBeAg-)
  • neonatal vaccination efficacy = 95%
31
Q

describe parenteral transmission of hep B

A
  • HBV is the most commonly transmitted blood-borne virus in healthcare settings (HBV > HCV > HIV)
  • common among intravenous drug users
32
Q

___ transmission of HBV is the most common mode of transmission in low-prevalence areas

33
Q

___ is a clinical marker of active HBV infection

A

E antigen (HBeAg+)

34
Q

30% of newly hep B infected adults will have ___ hepatitis

A

acute

perinatal/childhood primary infection is asymptomatic

35
Q

the rate of progression of acute hep B to chronic hep B inversely correlates with ___.

perinatal transmission: ___% progress to chronic disease

infection between ages 1-5: ___%

adult-acquired infection: ___%

A
  • age
  • 90%
  • 20-50%
  • <5%
36
Q

describe the relationship between chronic infection and age at infection, and symptomatic infection and age at infection

A
  • chronic infection: more common in younger children, is reduced with age
  • symptomatic infection: asymptomatic until about 12 months of age, then increases with age
37
Q

chronic hep B has a broad spectrum of illness. describe

A

from asymptomatic to chronic hepatitis to cirrhosis / HCC (hepatocellular carcinoma - liver cancer)

38
Q

what are factors that influence the natural history of chronic hep B infection

A
  • virus replication
  • host immune response
  • gender (men more likely to have acute flares)
  • alcohol consumption
  • viral co-infection
39
Q

what are the lab predictors of poor outcome of chronic hep B infection?

A
  • HBeAg positivity
  • HBV serum DNA level >2000 IU/ml
  • high titer HBsAg
  • necro-inflammation on liver biopsy
40
Q

describe the extra-hepatic manifestations of chronic hep B?

A
  • present in up to 20% of chronic HBV patients
  • related to circulating immune complexes
  • polyarteritis nodosa (autoimmune disease)
  • membranous nephritis and MPGN (nephrotic range proteinuria)
  • aplastic anemia
41
Q

what is hepatocellular carcinoma?

A
  • a possible result of chronic hep B infection
  • associated with cirrhosis of any cause including HBV
  • HCC can develop in chronic HBV in absence of cirrhosis
  • HBV DNA level, HBeAg status, co-infection with HCV and HDV
  • screen for HCC among chronic HBV patients (liver U/S q6 mo)
42
Q

describe hep B diagnosis with HBV surface antigen and antibody

A
  • HBsAg is serologic hallmark of infection (1-10 weeks)
  • persistent HBsAg for >6 mo = chronic infection
  • clearance of HBsAg followed by development of anti-HBs, conferring life-long immunity
  • window period in between decrease in HBsAg and increase in anti-HBs can be several months
  • co-existence of both HBsAg and anti-HBs: regard as chronic carrier state
43
Q

describe diagnosis of hep B based on HBV core antigen and antibody

A
  • HBcAg is intracellular and never detected in serum
  • anti-HBc persists throughout infection
  • IgM anti-HBc may be only positive test in window period of acute infection
  • total/IgG anti-HBc is present in recovery (+anti-HBs) and in chronic disease (+HBsAg)
44
Q

describe diagnosis of hep B via e antigen and antibody

A
  • HbeAg is a marker of replication and infectivity
  • correlates with high viral loads
  • conversion from HBeAg to anti-HBe typically associated with disease remission
45
Q

describe diagnosis of hep B via HBV serum DNA PCR

A
  • used for initiation and monitoring of antiviral therapy
46
Q

in the treatment of hep B, what are the two types of antivirals?

A

IFN and nucleoside analogs

47
Q

in hep B, when should you treat?

A

when there is HBV DNA >20,000 (HBeAg+) or >2,000-20,000 (HBeAg-)

and

disease (increased ALT and/or necroinflammation on liver biopsy)

48
Q

___ and ___ are the first line of defense in the treatment of hep B in the US

A

tenofovir and entecavir

49
Q

for the prevention of hep B, ___ vaccine is safe and highly efficacious against all HBV serotypes, and is useful as ___ prophylaxis (+/- HBIg)

A

recombinant antigen, post-exposure

50
Q

describe the virology of hep D

A

defective ssRNA virus

51
Q

hep D is a passenger virus accompanying hep ___

52
Q

___% of HBV+ patients are co-infected with HDV globally

A

10%

low in US and europe, common in IVDU

endemic in mediterranean and north africa

53
Q

why would it be important to vaccinate against hep B to avoid contracting hep D?

A

because without hep B, you cannot get hep D

54
Q

can hep D be cleared by the host?

A

yes, that is typical

55
Q

describe HDV super-infection in chronic HBV+ pts

A
  • leads to chronic HDV infection (>90%)
  • suppresses HBV replication
  • fulminant hepatitis, cirrhosis and HCC much more common
56
Q

how is hep D diagnosed?

A

PCR or anti-HDAg IgM/IgG

57
Q

___ is the only approved treatment for the management of hep D (low success rate)

58
Q

describe the virology of hep C

A

enveloped RNA virus in flavivirus family

related to yellow fever, dengue, and west nile

59
Q

describe the transmission of hep C

A
  • blood borne transmission
  • blood transfusion, IVDU, needle sticks, sex
60
Q

hep C leads to chronic hepatitis in ___% of cases

61
Q

what are the long term risks associated with hep C

A

cirrhosis and hepatocellular carcinoma

62
Q

what are the tests available for the diagnosis of hep C?

A
  • antibody immunoassay
  • molecular testing for presence of HCV RNA
63
Q

in the diagnosis of hep C, always start with ___

A

HCV antibody

  • negative HCV Ab = no infection present
  • positive HCV Ab = past or present infection, need to check for virus
64
Q

describe how hep C can also be diagnosed via HCV RNA

A
  • positive = active infection
  • negative = cleared infection (or false positive Ab)
65
Q

who should be tested for hep C?

A

everyone born between 1945 and 1965

potential exposures

66
Q

describe the management of hep C

A
  • always test for HIV and hep B
  • determine genotype (for drug selection)
  • evaluate for liver damage and cirrhosis
67
Q

what is the treatment goal for hep C management?

A

reduction of HCV RNA to undetectable levels

68
Q

describe sustained virologic response in the management of hep C

A
  • absence of viral RNA 12 weeks after treatment
  • 97-100% chance of cure

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