hepatitis Flashcards

1
Q

Structure of hepatitis viruses

A

A: picornavirus, capsid, RNA. B: hepadnavirus, envelope, DNA. C: flavivirus, envelope, RNA. D: delta virus, enveloped, circular RNA. E: hepevirus, capsid, RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

transmission of hepatitis viruses

A

A and E: fecal -oral. B, C, D: parenteral, sexual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

heptatitis viruses incubation peroids

A

A: 15-50 days. B: 45-160 days. C: 14-180 days. D: 15-64 days. E: 15-50 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hepatitis viruses severity

A

A: mild. B: ocassionally severe. C: usually subclinical. D: co-infection with HBV occcassionally severe. E: mild in nl pts. Severe in pregnant patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hepatitis mortality

A

High with Hep D, and Hep E in pregnant patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

chronicity/ carier state of hepatitis

A

A and E: no chronicity. B, C, D: chronicity occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hepatitis associations with other dz

A

A and E: none. B and C: primary hepatocellular carcinoma, cirrhosis. D: cirrhosis, fulminant hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lab diagnosis of hepatitis

A

A: anti-HAV IgM. B: HBSAg, HBeAg, anti-Hbe IgM. C: anti-HCV ELISA, RT-PCR. D: anti-HDV ELISA. E: anti-HEV IgM, RT PCR on stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute Hepatitis – Clinical Symptoms

A

For all types: Nausea, vomiting, Abdominal pain, Loss of appetite, Fever, Diarrhea, Light (clay) colored stools, Dark urine, Jaundice (yellowing of eyes, skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which hepatitis strains have a vaccine?

A

Hep A, B and D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe Hep A vaccine

A

killed vaccine, one serotype- neutralizing Abs are protective. Also passive vaccination with Abs can be used pre or post exposure, most efficacious if used during 1st week of infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who should be given the Hep A vaccine

A

HAV vaccine is recommended for travelers visiting developing countries of the world. HAV vaccine is now universally recommended for all children in the US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hep A - who is more likely to have jaundice, rare complications

A

kids and adults > 14 yrs are most likely to have jaundice. Fulminant hepatitis, Cholestatic hepatitis, and relapsing hepatitis are coplications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hep A virus pathogenesis- include IgG, IgM, clinical illness, ALT, infectivity

A

Anti-HAV IgM: Present 5-10 days before onset of sx, and no longer detectable after 6 months. IgG: appears early in infection and remains detectable for life (provides lifelong protection). Infectivity: peaks during 2-weeks before jaundice or elevated ALT when conc of virus in stool is highest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HAV viral shedding

A

HAV replicates in liver, is excreted in bile and shed in stool. The concentration of virus in stool declines after jaundice appears. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hep E virus replication/ shedding

A

replicates in gut before invading liver. shed in stool- occurs 4 weeks after oral ingestion and persists for 2 weeks

17
Q

Hep E- when does IgG and IgM rise/ fall? When do sx occur? When do liver enzymes rise?

A

Liver enzymes: rise around 4-5 weeks, persist for 20-90 days. IgM: rises at 2 weeks, falls by 12th week. IgG: rises by 2nd week, stays elevated. Sx: occur as levels of IgG and IgM are rising

18
Q

Hep B vaccine

A

surface antigen vaccine with one serotype. Neutralizing Abs to surface antigen are protective (anti-HBsAg).

19
Q

Hep B dz progression

A

acute liver dz > chronic liver dz > cirrhosis > hepatocellular carcinoma

20
Q

Hep B unique viral structural features

A

partially dsDNA, partially ssDNA. Contains viral RT enzyme. HBsAg glycoprotein.

21
Q

Hep B life cycle

A
  1. Attachment, fusion, translocation of HBV genome to the nucleus. 2. Host DNA repair machinery “fixes” the partially ssDNA genome into circular copy DNA. 3. host RNA pol transcribes cDNA producing mRNA. 4. translation of HBV mRNA to generate viral proteins 5. RT makes cDNA from RNA. 6. budding and egress
22
Q

How does Hep B outcome change with age

A

younger patients have chronic infections. Older patients have less chronic infection, more symptomatic infections. This corresponds with acquired immune response that clears the infection

23
Q

HBsAg

A

Envelope of virus. Not infectious. Marker of convalescence and subsequent immunity.

24
Q

HBcAg

A

core antigen, capsid.

25
Q

HbeAg

A

Associate with infectivity. Anti-HBeAg is not protective but is an eraly marer of resolution of hep B and favorable prognosis

26
Q

Hep B serology

A

HBsAg: detected from week 1-12 and is no longer detectable after 3 months in people who recover. HBeAg: detectable in acute infection- correlates with high titers of HBV and greater infectivity. Anti-HBc IgM: used to diagnose acute HBV, detectable at time of clinical onset and declines within 6 months. anti-HBc IgG: raises at time of clinical onset, persists indefinitely. anti-HBs: indicates recovery and immunity from infection

27
Q

serology profile of Chronic Hep B infection

A

HBsAg and anti-HBc IgG remain detectable for life. HbeAg is variably present. Anti-HBc IgM is negative

28
Q

Acute Hep B treatment

A

No treatment required for nl adult. For neonate of HBsAg positive mother- vaccinate and give Hep B Ig within hours after birth

29
Q

Chronic Hep B treatment

A
  1. IFN/ pegylated IFN. 2. Lamivudine- NRTI. 3. Adefovir- dATP analogue. 4. Entecavir- guanine analogue.
30
Q

Hep D vaccine

A

Can be prevented with Hep B vaccine

31
Q

Hep D co-infection serology

A

IgM andIgG anti-HDV: both are detectable during infection, but both eventually decrease to subdetectable levels after infection resolves. There is no serologic marker to indicate past infection. HDAg: can only be detected in 25%. ALT is elevated during Sx

32
Q

What is a Hep D superinfection

A

patients with chronic HBV infection who are superinfected with HDV. HDV then becomes chronic and persists with HBV

33
Q

Hep D super infection serology

A

HBsAg titer declines as HDAg rises. HDAg and HDV RNA remain detectabl in serum. IgM and IgG anti-HDV rise and remain detectable indefinitely. ALT peaks, then stays moderately elevated

34
Q

Hepatitis C progression

A

acute illness is typically mild. 50-80% will progress to chronic infections. Cirrhosis, liver failure and HCC possible

35
Q

Hep C treatment

A
  1. all oral DAAs: a. NS3 protease targeted by telaprevir, boceprevir and paritaprevir. B. NS5A targeted by ledipasvir and ombitasvir. C. NS5B targeted by sofosbuvir and dasabuvir. 2. IFN and ribavarin
36
Q

Hep C transmission

A

Blood transfusions (before 1992), IV Drug Abuse / Inappropriate use of injection drugs in healthcare settings (Needles), Birth to an HCV-infected mother, Sex, Casual Contact / Household contacts (razors, toothbrushes, largely unexplained routes?)

37
Q

Which Hep C genotype is most responsive to INF therapy

A

genotype 2 or 3 responds well to pegylated INF and ribavirin

38
Q

For each of the Hep viruses, list the markers for ongoing vs past infection

A

A: anti-HAV IgM (recent), anti-HAV IgG (past or vaccine- lifelong immunity). B: HBsAg (infectious), anti-HBsAg (past or vaccine- lifelong immunity). C: HCV Abs (previous or ongoing), HCV RNA (ongoing). D: HDV Ag (ongoing), HDV RNA (ongoing). E: anti-HEV IgM, RNA from stool