Hepatitis Flashcards

1
Q

hepatitis A mode of transmission

A

fecal-oral

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2
Q

hepatitis A virus classification

A

picornavirus - negative sense ssRNA

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3
Q

why is overt disease rare for hep A?

A

it is common where sanitation is poor b/c mothers have immunity to it. this gives their kids passive immunity to it. most kids are exposed early in live, when they have partial immunity that gives rise to active immunity. most people are seroconverted by 5.

in developed countries, the infected individuals are older

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4
Q

how long is the incubation period for hep A

A

30 days

fecal excretion occurs after a few days

viremia takes a week

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5
Q

what cells do hepatitis A viruses infect?

A

liver

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6
Q

what are the symptoms of hep A infection?

A

anorexia, nausea, fever, jaundice, dark urine, and abnormal values from liver function tests

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7
Q

liver function tests

A

used to test for the presence of liver damage.

most common- aspartate amino transferase in the serum. this enzyme is normally in the liver but the virus lysis cells when it replicates to release progeny

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8
Q

describe how heme metabolism is related to hepatitis A

A

normally, heme is converted to bilirubin in the spleen, which is transferred through the blod to the liver, where it is added to the bile and excreted to the GI tract (its why feces are brown)

w/ Hep A, the liver functions poorly, causing an increase in bilirubin systemically. this gets deposited in the skin (causing jaundice), filtered by the kidneys (dark urine), and it doesn’t get to the GI tract (light feces).

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9
Q

compare AST levels in Hep A and Hep B

A

Hep A levels have a sharp peak w/in 2 months of infection, and then drop off sharply

in Heb B, the peak is slower to form and lower. it only becomes evident at 2 months

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10
Q

what are 5 most common ways to produce a Hep A epidemic

A
  1. outdoor summer events w/ inadequate sanitary facilities

2 raw or inadequately cooked shellfish contaminated by sewage

3 w/in one family

4 spread by food handler

5 from fecally contaminated food

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11
Q

T/F- Hep A can be spread via blood transfers

A

T- as long as the virus is viremic

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12
Q

describe the use of passive immunity from IgG in Hep A

A

primarily used after possible exposure, but still useful prophylactically.

it prevents jaundice and malaise, but there is some virus replication and liver damage.

it provides protection for about 4 months

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13
Q

describe Hep A immunization

A

killed virus vaccine. recommended for all children plus travelers, male gay partners, ppl who receive blood products

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14
Q

how do you determine if you are affected w/ hep A

A

serological test for Ab against Hep A

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15
Q

how do you interpret serological data w/ IgM and IgG for Hep A?

A

if both negative- no infection, no vaccine

if IgG pos- previously infected or vaccinated, but not currently

both pos- acute Hep A infection or recent vaccination

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16
Q

what dimensions are important to assess when considering a potential epidemic?

A

1 place- geographical clustering

2 person- do patterns suggest a mode of exposure

3 are new cases around the same time?

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17
Q

Hepatitis E characteristics

A

non-enveloped, + stranded RNA

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18
Q

what is the mode of transmission for Hep E viruses?

A

fecal-oral

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19
Q

what are the symptoms of Hep E?

A

similar to A

fever, nausea, jaundice

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20
Q

what is the Hep E prognosis

A

people generally recover. children often have very mild symptoms.

can become chronic in immunosuppressed pts

bad for pregnant women

21
Q

what kind of virus is Hep B

A

hepadenavirus

enveloped, icosahedral

contains circular DNA mostly double stranded but single stranded some places

it carries a reverse transcriptase

22
Q

what is the incubation period for Hep B

23
Q

how is hep B transmitted?

A

blood transfusions, dirty needles

sexually (especially male to male)

perinatal infections from infected mom to newborn

24
Q

are HB-Ags from the envelope or the capsid?

25
HBeAg
an antigen strongly correlated with infectious Hep B Abs to HBeAg are not seen in chronically infected pts, but are seen in pts who have successfully cleared the disease
26
what is the mechanism of damage in Hep B?
the immune system CTLs see the MHC 1 cells presenting the Hep B and attack, causing damage
27
How many pts move on to chronic Hep B?
5%. This is associated with core antigen HBeAg, which predicts chronic hepatitis and liver carcinoma
28
what are outcomes like for perinatally transmitted Hep B?
90% of these newborns become chronic carriers, and 25% will die because of hepatitis or cancer can be helped w/ combo of vaccine and passive IgG
29
describe current vaccines for Hep B
subunit vaccines: (inactivated) purified viral antigens, or viral antigens attached to yeast
30
describe passive immunization for Hep B
IgG must be prepared from people w/ high immunity against Hep B. cannot be taken from normal IgG stoes b/c it will not provide protection
31
difference between passive immunity to Hep A and Hep B
you can take IgG w/ HA and it is protective. It is not protective against HB, which requires IgG from a pool of highly immune donors
32
chemotherapy for Hep B
reverse transcriptase inhibitors, which reduces viral replication to 0, and lowers risk of cancer
33
what precautions are taken to prevent HB infection via blood transfusions
no former hepatitis patients no people who have lied w/ hepatitis pts in 6 months people who have had a transfusion in 6 months people w/ HB-Ag in their serum
34
describe the HCV
flavivirus enveloped plus stranded ssRNA virus
35
what is the most common subtype of HCV?
genotype 1 is 70% of cases, genotype 2 is 20%
36
how is Hep C tested for?
PCR test
37
what is the transmission method for Hep C?
blood/blood contact STI perinatally
38
mechanism for Hep C damage?
mediated by immune system- CTL/MHC 1
39
describe the timeline of Hep C infection?
1-2 weeks- viral RNA detectable 2-6- elevated ALT 4-8 weeks- HCV Ab elevated after 6 months, 25% clear the virus, 75% develop HCV chronically
40
incubation period for Hep C?
60 days
41
prodromal symptoms
found in Hep B and C- non specific symptoms that appear before a definitive symptom in Hep, often arthritis or a rash
42
how do you treat chronic Hep B w/ chemotherapy?
alpha interferon w/ polyethylene glycol drawbacks- expensive, side effects, bad outcomes Hep B can be treated w/ reverse transcriptase inhibitors
43
hep C chemotherapy
pegylated IFN ribavirin telaprevir/boceprevir/simeprevir- inhibit essential protease in Hep C sofosburvir- analog of U, only taken up by viral RNA polymerase and stops replication Daclatasvir- inhibits a viral protein, and inhibits virion release usually these drugs are used in combo w/ IFN
44
HBV hepatocellular carcinoma causes
rare- only 2% of the 5% that become carriers HBV DNA integrates near a proto-oncogene and causes in apporpriate expression excessive damage causes constant regeneration, may predispose to mutations
45
Hep C hepatocellular carcinoma
virus does not integrate into the genome chronic immune response may promote tumor development
46
describe hepatitis D
defective RNA virus circular minus stranded RNA genome
47
describe Hep Ds relationship w/ Hep B
only people w/ Hep B can get Hep D b/c Hep D does not produce envelope glycoproteins, but instead must take them from Hep Bs glycoproteins immunity to Hep B also provides immunity to Hep D
48
how is Hep D detected?
Hep D makes on viral protein that is serologically detectable. PCR analysis is also used
49
Hep D prognosis
5% of pts go on to have chronic condition the infection is worse than singular Hep B infection mortality rises 10 fold over Hep B infection