Viral Hepatitis Flashcards

1
Q

Most common cause of acute hepatitis?

A

Hepatitis A virus

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2
Q

Why has Hepatitis A decreased in the US?

A

Because of vaccination

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3
Q

When is the Hepatitis A virus considered clincally active?

A

When serum transaminases rise

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4
Q

What are the serious sequelae of Hepatitis B infection?

A

Acute and Chronic Liver Disease

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5
Q

What morphology is observed on EM of Hepatitis B virus?

A

HBsAg is observed as rodlike and spherical particles, and Dane particles (the virus)

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6
Q

What gene is likely responsible for the role in the pathogenesis of hepatocellular carcinoma?

A

X gene

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7
Q

What has contributed to the decreased amount of HBV carriers?

A

HBV vaccine

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8
Q

What fluids are the infectious HBV particles found in?

A

Infectious particles are found in blood, saliva, semen

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9
Q

What do the vaccines for HBV contain?

A

Recombinant HBsAg or immunogenic epitopes of HBsAg

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10
Q

What causes most of the damage that occurs in HBV infections?

A

CD8 response to HBV epitopes on infected hepatocytes

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11
Q

Three general courses of HBV infection?

A
  • Acute hepatitis
  • Fulminant hepatitis
  • Chronic hepatitis
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12
Q

First marker that appears in serum of patients with acute hepatitis B?

A

HBsAg

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13
Q

What is the typical progression of a patient infected with HBV?

A

Increase in HBs and HBe Ag followed by a brief stint of Syx and then Anti-HBc/Anti-HBs w/o incorporation of viral genome into hepatocytes

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14
Q

What are the typical Syx and lab findings that suggest an active HBV infection?

A

Increase and persistence of Syx, HBs and HBe Ag and increase in Anti-HBC. The virus persists in the nucleus but is not integrated into the DNA host

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15
Q

What are the typical findings in an asymptomatic HBV carrier?

A

Few if any Syx, Increase in HBsAg, increase then decrease in HBeAg and Increase and persistence in Anti-HBc; HBV DNA is integrated into the hepatocyte DNA

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16
Q

When in the course of acute hepatitis B does HBcAg circulate?

A

It doesn’t

17
Q

What does serum HBeAg correlate with?

A

Period of intense viral replication and hence, maximal infectivity of the patient

18
Q

What occurs in fulminant hepatitis B?

A

Massive liver necrosis, hepatic failure, and high mortality

19
Q

How is chronic HBV Dx?

A

Continued necrosis and inflammation in the liver for more than 6 months

20
Q

What are the three phases of HBV?

A
  1. Immune tolerant phase
  2. Immune active phase
  3. Inactive phase
21
Q

What are the characteristics of the immune tolerant phase?

A

HBeAg positive and very high HBV DNA levels

22
Q

Characteristics of the immune active phase of HBV?

A

HBV viremia and liver cell necrosis (ALT and AST increase)

23
Q

What are the characteristics of the inactive phase of chronic HBV?

A

Anti-HBe is seen but HBeAg is not; HBV DNA is very low

24
Q

What vasculitis is associated with HBV?

A

Polarteritis nodosa

25
Q

What does HDV require for infection?

A

HBsAg and therefore HBV infection

26
Q

What is the progression of hepatitis if HDV is superimposed on HBV?

A

Typical increase in severity of existing chronic hepatitis

27
Q

What is the cause of cell death in HCV?

A

Liver cell injury has been attributed to cytotoxic T-cell responses to virus-infected hepatocytes

28
Q

What are the levels in a self-resolving and chronic hepatitis C infection of ANTI-HCV?

A

ANTI-HCV remains high for both types of infection

29
Q

Describe the clinical course of chronic HCV?

A

Intial large symptomatic disease followed by cyclic waxing and waning of Syx at a lower level

30
Q

What is an even worse sequela following cirrhosis?

A

Hepatocellular carcinoma

31
Q

Most commonly encountered extrahepatic manifestations of HCV?

A

Mixed cryoglobulinemia

32
Q

Of the hepatitis viruses, which has the highest rate of chronic hepatitis?

A

Hep C

33
Q

Which of the Hep viruses is orally transmitted?

A

Hep A - fecal-oral route

34
Q

Which Hep virus does not evolve into liver cancer?

A

Hep A

35
Q

How is HEV transmitted?

A

Vertical, parenteral, waterborne, zoonotic