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M2 GI/Nutrition > Viral Hepatitis - Franco > Flashcards

Viral Hepatitis - Franco Flashcards

1
Q

Name 8 common clinical manifestations of viral hepatitis

A
  • Fever
  • Malaise
  • Anorexia
  • Nausea
  • Vomiting
  • Jaundice
  • Abdominal/RUQ pain
  • Hepatomegaly
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2
Q

Does hepatitis feature chronicity?

What is indicated by the presence of HepA IgM?

What is indicated by the presence of HepA IgG?

A

Hepatitis A does not have a chronic phase

IgM = acute infection (<6 months)

IgG = previous exposure or vaccination -> patient now immune

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3
Q

The HepA vaccination is recommended for which populations?

A

Infants

People working in or traveling to areas with high incidence of HepA virus (Africa, China, etc)

People with chronic liver disease

People working with HepA virus (healthcare workers, researchers)

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4
Q

Hepatitis A immune globulin therapy for prevention of hepatitis A is indicated for which patient populations?

A

Pre-exposure: travelers to intermediate and high HAV-endemic regions

Post-exposure (within 14 days): household/intimate contacts, institutions (day care), common source exposures (such as infected food handler)

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5
Q

Why do most cases of hepatitis A go unreported?

A

Most (or many) patients have mild or absent symptoms

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6
Q

Is there a vaccine for hepatitis A?

Hepatitis E?

What is indicated by the presence of HepE IgM in the serum?

What is indicated by the presence of HepE IgG in the serum?

A

Yes

No

Acute HepE infection (<6months)

Previous exposure (and now immune, >6 months)

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7
Q

Exaplain the differences between the serologic courses of acute HepB infection with recovery and progression to chronic HepB infection

A
  • HBsAg: In both cases, the surface antigen rises starting around 4 weeks post-exposure.
    • In acute HepB, HBsAg begins to fall and is absent by ~24 weeks.
    • In chronic HepB, HBsAg persists indefinitely
  • IgM anti-HBc: In both cases, IgM anti HBc rises around week 5, peaks at around weeks 12-16, then disappears around week 24-36 (in both cases, chronic takes longer)
  • Total anti-HBc (includes IgM and IgG: In both cases, this value rises around week 5, plateaus around week 12, and persists at this plateau indefinitely. Given the drop-off in IgM, anti-HBc is almost all IgG after 24-36 weeks
  • Seroconversion
    • Acute HepB will eventually seroconvert with a rise in anti-HBs around week 32
    • Chronic HepB does not seroconvert (no anti-HBs formed)
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8
Q

Appriximately what percentage of adults develop chronic hepB after exposure?

A

10%

Young patient: few symptoms, more likely to progress to chronic

Old patients: more symptomatic, less likely to progress to chronic

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9
Q

What does the presence of Hep B surface antigen in the blood mean?

How can you tell if a patient has had the vaccine?

A

Current HepB infection (acute vs. chronic indeterminate)

Vaccinated patients will be negative for the HepB core antigen, but positive for the HepB surface antigen (i.e. core antibodies indicate recovery from a natural infection)

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10
Q

Who is a candidate for HepB vaccination?

A

Practically everybody…

But to be more specific:

  • All infants and previously unvaccinated children under the age of 11
  • People with increased risk for HBV (illicit drugs, MSM, travelers, chronic renal failure, clotting factor recipients, people occupationally exposed to blood or body fluids a.k.a. healthcare workers)
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11
Q

What is indicated for HepB exposure in unvaccinated patients?

What about HBsAg+ pregnant women?

A

HepB immune globulin (HBIG) within 24 hours (second dose @ 1 month)

or

HepB vaccine within 24 hours (second dose @ 1 month, third dose @ 6 months)

**In both cases, the first dose can be given up to 1 week after exposure, but earlier is better**

Pregnant women HBsAg+: give newborn both HBIG and HepB vaccine (this reduces the risk of transmission from 90% to ~2-3%)

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12
Q

With respect to HCC, what is unique about HepB that does not occur with HepC?

A

Hepatitis B is the only hepatitis virus that can directly cause HCC without first progressing through cirrhosis

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13
Q

What are the main therapy goals of chronic hepatitis B therapy (6)?

A
  1. Eliminate or significantly suppress HBV replication
  2. Prevent progression to cirrhosis or HCC
  3. ALT normalization
  4. Histological improvement
  5. Loss of HBeAg, development of HBeAb (i.e. seroconversion)
  6. Loss of HBsAg
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14
Q

What two broad categories of drug are used in chronic HepB therapy?

What is the general purpose/mechanism of each?

A

Interferons: activate immune system

Nucleotide/nucleoside analogues: block reverse transcriptases (block HBV replication)

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15
Q

What is the main advantage of PEG-interferon alfa-2a vs. Interferon alfa-2b

A

PEG-interferon alfa-2a is PEG glycosylated, allowing it to persist longer in the body (dosing frequency is lower)

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16
Q

Among the nucleotide analog treatment options available for HepB, what are the two most common/effective?

Why?

A

Entecavir and Tenofovir

These have (so far) relatively low resistance rates. Other drugs available are commonly resisted by current HepB strains

17
Q

Give (3) major side effects of PEG-interferon

A
  1. flu-like symptoms
  2. neuropsychiatric symptoms/depression
  3. bone marrow depression
18
Q

Approximately what percentage of patients with chronic HepB will seroconvert after therapy?

What percentage will eliminate HBsAg?

A

30%

5-7%

19
Q

Describe the serology of HepB-HepD co-infection with respect to anti-HDV

A

Co-infection with HepB/HepD results in an early rise in IgM anti-HDV and total anti-HDV (almost all IgM) followed by a rapid tapering off of IgM (conversion to IgG) and a slower tapering off of total anti-HDV (IgG goes away too)

Anti-HBs rises later (recovery)

20
Q

What is the result of HepD infection after progression to HepB to its chronic phase?

Describe the serological course with respec to anti-HDV

A

HBV-HDV superinfection

  • IgM anti-HDV rises quickly during a jaundice/symptomatic stage
  • Total anti-HDV continues to rise as IgM begins to fall towards the end of the acute/jaundiced/symptomatic phase (rise of IgG)
  • Total anti-HDV (and elevated ALT) persist indefinitely
21
Q

A massive decrease in the incidence of HepC in the United States (circa 1992) coincided with what important healthcare practice?

A

widespread screening of blood supplies for HepC

22
Q

What are HepC non-structural proteins? Why are these important (therapeutically)?

A

non-structural proteins are responsible for viral replication

There are important targets for anti-HepC drugs

23
Q

A patient is positive for HepC antibody. Do they have an active HepC infection?

A

Unknown - both chronic HepC and those with prior exposure (but cleared the virus or underwent successful treatment) are all seropositive

**HepC viral RNA is present only in those who are viremic** -> basically this is the only way to be sure someone has an active HepC infeciton

24
Q

Approximately what percentage of those infected with HCV recover? What percentage progress to chronic infection?

A

20%

80%

25
Q

What is the target of direct-acting antivirals (DAAVs) used in the treatment of HepC?

Describe their common side effects

A

Target: HepC non-structural proteins

Side effects: relatively few (or none)!

26
Q

Describe clinical use and mechanism of action of Sofosbuvir

A

Clinical use: chronic HCV infection

Mechanism: anti-structural protein. Specifically, it inhibits HCV NS5B RNA-dependent RNAP (required for viral replication)

27
Q

Describe the clinical use and mechanism of action of Ledipasvir

A

Clinical use: chronic HCV infeciton

Mechanism of action: a non-structural protein inhibitor. Specifically, it targets HCV NS5A protein (an ‘assembly factor’ required for viral replication)

M2 GI/Nutrition (43 decks)

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