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Microbiology > Viral Hepatitis Cards > Flashcards

Viral Hepatitis Cards Flashcards

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Biology 101 flashcards
1
Q

Which hepatitis viruses have chronic carrier states?

A

HBV, HCB, HDV

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2
Q

What is the genome of HBV?

A

+dsDNA

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3
Q

What LFT changes are associated with acute viral hepatis?

A

AST and ALT > 1000 IU/L; GGT/Alkphos and other labs may be normal until later infection where there is damage to biliary tree, decreased synthetic function, obstruction, etc.

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4
Q

What populations/communities are associated with Hepatitis A?

A

Daycare/long-term care populations, travelers, IVDU, MSM; especially South America, Africa and Asia

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5
Q

What is the leading cause of viral hepatitis in the developing world?

A

HEV

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6
Q

What are the outcomes of HAV?

A

85% are self-limited with IgG protection; 10-15% relapse; 0.3-2% progress to fulminant hepatitis (particularly in pts with underlying liver disease)

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7
Q

What is the genetic makeup of HAV?

A

+ssRNA, non-enveloped

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8
Q

What is the genetic makeup of HEV?

A

+ssRNA, non-enveloped

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9
Q

What are the outcomes of HEV?

A

Most are self-limiting; severe in pregnancy, underlying liver disease, immunosuppressed

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10
Q

How are HAV and HEV prevented?

A

Sanitation; vaccination (e.g. HEV vaccination in China)

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11
Q

How is HBV transmitted, and who is at risk?

A

Blood/parenteral transmission; at-risk includes IVDU, healthcare workers, risky sex behavior, infants of infected mothers (perinatal) especially in endemic areas

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12
Q

Why is HBV called a pararetrovirus?

A

HBV has an incomplete dsDNA genome; it forms a complete cccDNA, is reverse transcribed to mRNA, then transcribed back into DNA.

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13
Q

How does HBV cause cell damage?

A

Adaptive immune response (cytocoxic T lymphocytes) cause hepatocyte damage/death; HBV itself is non-cytolytic

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14
Q

Describe the two types of HDV infection

A

HDV may be co-infected with HBV or may be a superinfection after HBV; superinfection causes severe hepatitis with 5-15% mortality

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15
Q

Why does HDV require HBV?

A

HDV requires HBsAg as an envelope for replication

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16
Q

How does age of transmission influence pgoression to chronic HBV?

A

Earlier age of transmission = more likely to develop chronic disease. 90% of perinatal exposures develop chronic disease; 2-10% of older children develop chronic disease.

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17
Q

What antigens/antibodies suggest acute HBV?

A

HBsAg +, HBcAb IgM+, HBeAg +, HBV DNA+, possibly HBeAb +

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18
Q

What antigens/antibodies suggest resolved HBV?

A

HBsAg+, HBcAb IgG+, HBeAb+

19
Q

What antigens/antibodies suggest immunization to HBV?

A

HBsAb+

20
Q

What antigens/antibodies suggest chronic HBV infection > 6mo with HBV?

A

HBsAg+, HBcAb IgG+, HBV DNA+, possibly HBeAb or HBeAb +

21
Q

What antibodies/antigens suggest a HBV ‘window period’?

A

All negative except HBcAb IgM/G

22
Q

How is HBV prevented?

A

3-dose recombinant vaccine, 95% effective, given to newborns, children

23
Q

What are the outcomes of HBV?

A

Most are self-limited; chronic HBV increases risk for HCC and cirrhosis; fulminant hepatitis and cirrhosis require transplant

24
Q

What is the leading cause of liver transplant in the US?

A

Hepatitis C

25
Q

What is the most common blood-borne infection in the US?

A

Hepatitis C

26
Q

How is HCV transmitted, and who is at risk?

A

Blood/parental and body fluids; at-risk is mainly IVDU but also unsafe sex practicers

27
Q

How does HCV cause cell damage?

A

Necrosis caused by cytotoxic T cells; HCV is non-cytolytic. Chronic infection may progress to cirrhosis, HCC

28
Q

Describe the HCV genome and protein structure

A

ssRNA, non-enveloped; 10 viral proteins are encoded (3 structural, 7 nonstructural)

29
Q

What are three complications of HCV?

A

Immune complex disease, cryoblobulinemia, vasculitis

30
Q

What are the outcomes of acute and chronic HCV infection?

A

75-85% progress to chronic infection; of chronic, 20-30% progress to cirrhosis; of cirrhosis, 2-7% progress to ESLD or HCC. Only 9% achieve a sustained cure.

31
Q

How is HCV diagnosed?

A

Serology detects anti-HCV Ab between 4 and 12 weeks after infection; detects 97% of cases by 6 months post-exposure. RNA PCR detects 2 weeks after exposure.

32
Q

What is the LFT pattern in HCV?

A

Elevated in acute HCV; may be normal in chronic HCV.

33
Q

Why is there no HCV vaccine?

A

Genetic diversity of HCV (4+ genotypes, poor proofreading and rapid replication), and neutralizing antibodies are not protective.

34
Q

What group in the US is most likely to have undiagnosed HCV?

A

Adults born between 1946 and 1965

35
Q

What is the second generation HCV treatment?

A

NS5A inhibitor and HS5B inhibitor; 100% cure rate of HCV genotype 1 in 8 weeks

36
Q

What is the first generation treatment for HCV?

A

Protease inhibitors + interferon and ribavirin; 80% cure rate

37
Q

Describe the effectiveness of interferon+ribavirin

A

Used in the 1990s to treat HCV due to broad antibiral properties. Genotype 2 and 3 responded well, while GT1 responded only 50% of the time.

38
Q

Describe the genotype frequencies in HCV

A

70% of strains are GT1 (1a>1b), 30% have GT 2 or 3, and 1% have GT4. Treatment will vary depending on genotype.

39
Q

What antibody titer suggests an acute Hepatitis A infection?

A

Hepatitis A IgM antibody

40
Q

Who is at highest risk of becoming a chronic Hepatitis B carrier?

A

Infants or young children

41
Q

What antibody titer suggests a past Hepatitis A infection?

A

Hepatitis A IgG antibody

42
Q

What is the most common mode of Hepatitis A transmission?

A

Fecal-oral (contamination of food or water)

43
Q

When does shedding of infectious Hepatitis A particles begin?

A

2 weeks before symptom onset, and extends 1 week after sympoms abate

44
Q

What is the best way to detect an early Hepatitis C infection (

A

HCV RNA in serum via PCR

Microbiology (9 decks)

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