Hepatitis Alphabet Flashcards

1
Q

Why is percutaneous transmission of Hep A and Hep E rare?

A

viremia is short and no chronic carrier state (HAV) and rare chronicity (HEV)

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2
Q

Where does replication of HAV and HEV occur?

A

in hepatocytes, excretion into bile and feces before onset of symptoms

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3
Q

What are the relative frequencies of subclinical and symptomatic HAV and HEV?

A

subclinical common in young children w HAV

symptomatic w jaundice commoner in older children and adults w HAV and older men w HEV, increased severity in elderly

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4
Q

When do symptoms and jaundice appear in acute HAV?

A

symptoms first while ALT rising - need more infected cells for jaundice than symptoms

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5
Q

What serologies are present in acute inf with HAV?

A

IgM HAV Ab positive

total HAV Ab positive

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6
Q

What serologies are present in acute inf with HEV?

A

IgM and IgG HEV Ab positive

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7
Q

What serologies are present w previous inf with HAV or HEV?

A

IgM HAV Ab and HEV Ab negative

total HAV Ab and IgG HEV Ab positive

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8
Q

What three functions is the hep B viral polymerase responsible for?

A

RNA dependent DNA synthesis

RNAase and DNA dependent DNA synthesis

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9
Q

What are the Hep B viral proteins?

A

core protein - detected in nucleus w HB core Ab, not detected in blood
surface protein - detected in cytoplasm with HB surface Ab, detected in blood

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10
Q

What are the three Ag-Ab systems for Hep B?

A
HBc = marker of exposure
HBs = marker of vaccination or resolution
HBe = marker of replication
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11
Q

What does it indicate if HBe Ag is detected?

A

all machinery necessary for viral replication is available - viral titers in blood are high, high infectivity
indicates ongoing replication

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12
Q

What are the clinical features of HepB?

A

HBs Ag detected after months and symptoms follow weeks later
majority have subclinical/anicteric
remainder have symptomatic/icteric = Phase II
possible serum sickness with skin rash and arthritis

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13
Q

Wat are the risk factors for chronic inf with Hep B?

A

neonatal, immunocompromised, organ transplant pts, renal dz on dialysis, AIDS and cancer pts

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14
Q

Are the long term outcomes of chronic Hep B inf more common after clinically silent dz or symptomatic acute?

A

clinically silent

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15
Q

What is the rationale for using interferon-alpha to treat hep B?

A

potential to decrease viral replication while boosting immune response at same time

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16
Q

Why might there be two peaks of ATs and jaundice with hp D inf?

A

relapsing hep b

Hep D can inf someone who already got hep B

17
Q

What are the goals of treatment for Hep B and Hep C respectively?

A

hep B - convert active to inactive

hep C - convert RNA positive to RNA negative