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Microbiology > Exam #5: Viral Hepatitis > Flashcards

Exam #5: Viral Hepatitis Flashcards

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1
Q

What is hepatitis?

A

Disease marked by inflammation of the liver.

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2
Q

What are the non-viral causes of hepatits i.e. what is your differential diagnosis when a patient has abnormal LFTs?

A
  • Alcoholism
  • Drug abuse
  • Drug overdose/ toxin (Tylenol especially)
  • Metabolic disorder

Viral Hepatitis

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3
Q

What is acute viral hepatitis? What are the symptoms?

A

Viral hepatitis <6 months of symptoms:

  • Jaundice–increased bilirubin leading to yellowing of the skin & sclera
  • Liver inflammation– RUQ abdominal pain
  • Dark urine
  • Acholic stool–clay-colored stool caused by a reduction in bile production
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4
Q

What is the prodrome prior to the onset of hepatits?

A 
Headache
myalgia
arthralgia 
fatigue 
nausea 
vomiting 
pharyngitis 
mild fever
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5
Q

What is bilirubin? Why is hyperbilirubinemia seen in viral hepatitis?

A

Bilirubin is the end-product in the recycling of heme from dying RBCs. It is normally excreted as bile, which requires conjugation in the liver. Viral hepatitis interferes with liver function & prevents normal conjugation of bilirubin; thus, higher than normal levels are seen in the blood & urine.

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6
Q

What are the bilirubin levels that are seen in hepatitis? How do they correlate with the symptoms?

A

Bilirubin levels of 5-20 mg/dL are common in viral hepatitis.

  • 3 mg/dL= jaundice
  • Higher= bilirubin in urine (diagnostic of liver disease)
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7
Q

What liver enzymes are elevated in hepatitis?

A

AST (aspartate aminotransferase)

ALT (alanine aminotransferase)

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8
Q

What is the definition of chronic viral hepatitis? What are the potential complications of chronic hepatitis?

A

Hepatitis that does not resolve in 6 months

Predisposition to primary hepatocellular carcinoma & cirrhosis*
*Usually it takes 15-40 years to see these symptoms

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9
Q

What causes tissue damage in chronic hepatitis? Why are primary heptacellular carcinoma & cirrhosis associated with chronic hepatitis?

A

Continued replication of hepatitis virus & subsequent immune response leads to an inflammatory response & tissue destruction

Note that the the liver regenerates; long-term/ continued regeneration is what predisposes to the development of primary hepatocellular carcinoma

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10
Q

What is fulminant viral hepatitis? What are the symptoms of fulminant hepatitis? What are some of the complications of fulminant hepatits?

A

This is the most severe form of viral hepatitis that affects BRAIN function. There is a massive hepatic necrosis in fulminant hepatitis, which leads to hyperammonemia.

  • Encephalopathy–>confusion, disorientation, coma.
  • Ascites & edema are indicative of liver failure
  • Life threatening complications

*Liver transplant can be lifesaving

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11
Q

What virus family is Hepatitis A a part of? How is it transmitted? Does it lead to chronic infection?

A

Picornovirus
Fecal-Oral
No

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12
Q

What virus family is Hepatitis B a part of? How is it transmitted? Does it lead to chronic infection?

A

Hepadnavirus
Body fluids
Yes

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13
Q

What virus family is Hepatitis C a part of? How is it transmitted? Does it lead to chronic infection?

A

Flavivirus
Body fluids
Yes

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14
Q

What virus family is Hepatitis D a part of? How is it transmitted? Does it lead to chronic infection?

A

Deltavirus
Body fluids
Yes

  • Helper-dependent
  • Direct damage
  • Remember that HDV is helper-Dependent & causes Direct Damage
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15
Q

What virus family is Hepatitis E a part of? How is it transmitted? Does it lead to chronic infection?

A

Hepevirus
Fecal-Oral
No

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16
Q

List the characteristics of Hepatitis A.

A

Picornovirus family

+ssRNA

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17
Q

What are the clinical manifestations of Hepatitis A infection?

A

Incubation period is 28 days
Presents as acute hepatitis
Does NOT cause chronic
Rarely causes fulminant hepatitis

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18
Q

How is Hepatitis A diagnosed?

A
  • anti-HAV IgM antibodies are indicative of ACUTE infection

- anti-HAV IgG antibodies provide protection against re-infection and are indicative of vaccine or prior infection

19
Q

How is Hepatitis A prevented?

A

Vaccination:

  • inactivated whole HAV vaccine
  • IM (2x doses)
  • Given to children (12-23 months)
  • High risk groups

Post-exposure prophylaxis

  • Vaccine can be used as post-exposure prophylaxis
  • anti-HAV IgG can also be given as post-exposure prophylaxis
20
Q

List the characteristics of Hepatitis B. Describe the proteins associated with HBV.

A
  • Hepadnavirus family
  • Partially dsDNA genome (some ss)
  • Reverse transcription is part of its lifecycle
    (most commonly passed via sexual contact)

Note that there are three relevant viral proteins (clinically)

1) HBsAg= surface antigen
2) HBcAg= core antigen (between viral genome and HBsAg) –NOT soluble i.e. NOT in serum
3) HBeAg= core protein that IS SOLUBLE

21
Q

What are the morphological characteristics of Hepatitis B? Which are infectious? What are the antigens associated with each?

A
  • Tubules & Spheres= noninfectious products of HBsAg (surface antigen)
  • Dane particles= infectious, virion coated in tubules & spheres

Note that the presence of tubules & spheres in the bloodstream is indicative of ACTIVE HBV infection.

22
Q

Serologically, how do you tell the difference between acute & chronic hepatitis?

A

HBsAg= marker of active infection (either acute or chronic)
HBsAb (antibody)= is present in vaccinated or previous infected patients, but NOT active infection
HBcAb- IgM= acute infection
HBcAb- IgG= chronic infection (or prior infection)
HBeAg+HBcAb- IgG= chronic replicative

The presence of ONLY antibodies in serum is indicative or RESOLVED infection.

23
Q

What is HBsAg a serologic marker of?

A

Both acute & chronic Infection

24
Q

How many HBV infections progress to chronic infection in the following populations: a) neonates, b) 5 year-olds, c) general population?

A

a) 90% in neonates
b) 15% in 5 year-old
c) 5-10% in general population

*Note that chronic infection increases the risk for liver cirrhosis & primary heptocellular carcinoma

25
Q

What are the symptoms of Hepatitis B infection?

A

Less severe infection than acute HAV

26
Q

How is HBV infection treated?

A

Acute= none
Chronic=
- Lamivudine= reverse transcriptase inhibitor
- Famcylovir/Adefovir= nucleoside inhibitor, which can be done with or without Interferon-alpha

27
Q

What is the HBV vaccine?

A

Recombinant HBV surface protein (HBsAg)

  • IM injection
  • Recommended for all infants with the first dose given soon after delivery
28
Q

Describe the post-exposure phrophylaxis protocol for HBV.

A

HBV vaccine & Hepatitis B Immune globin (HBIG) are used for post-exposure prophylaxis.

  • Premature infants with unknown maternal HBV status & HBV positive receive BOTH
  • Unvaccinated exposed receive (e.g. healthcare worker) receive just vaccine
29
Q

List the characteristics of HCV.

A

Flavivirus family
Enveloped
+ssRNA

  • Highly associated with IV drug use
  • Note that there are six genotypes (most common in the US is Type 1)
30
Q

How is HCV diagnosed?

A

Screening Test with ELISA
Confirmatory Test with Western Blot

Note that this protocol is similar to what is done with HIV

31
Q

What are the serologic features of HCV?

A
  • ALT & Anti-HCV elevations seen ~2months post-expsoure

- HCV RNA seen early (acute infection)

32
Q

What are the disease outcomes of HCV?

A

HCV has a higher propensity to develop into chronic hepatitis than HAV (none) & HBV

  • 15% of patients develop acute hepatitis that is more mild than HAV or HBV (self-resolving)
  • 15% progress to rapid cirrhosis
  • 70% develop chronic/ persistent HCV infection
33
Q

How is HCV treated?

A
  • Treatment is for CHRONIC infection ONLY
  • Treatment regimen differs depending on the exact genotype, but currently, antiviral protocols contain sofosbuvir for every genoptye
  • Sofosbuvir is an RNA dependent RNA polymease inhibitor

*Note that while this new drug has an improved efficacy, it comes at a heavy cost (~1,000 dollars a pill)

34
Q

How is HCV prevented?

A

No vaccine
Reduce risk behavior
Screen blood supply

35
Q

List the characteristics of HDV.

A

Deltavirus
Circular ssRNA
Encodes delta proteins

“Helper-dependent” (needs “co” or prior infection by HBV)

36
Q

What is unique about the lifecycle of HDV?

A

Replication requires HBV proteins; thus, it only infects cells that have been previously or concurrently infected with Hepatitis B virus.

37
Q

What is most likely to cause fulminant hepatits?

A

Concurrent infection with HBV & HDV

38
Q

What is the only hepatitis virus that damage hepatocytes directly?

A

HDV

39
Q

How is HDV diagnsed?

A

ELISA to detect:

  • anti-HDV antibodies
  • delta proteins
40
Q

How is HDV treated?

A

No specific antiviral treatments; thus, supportive therapy ONLY

41
Q

How is HDV prevented?

A

Because HDV absolutely requires HBV infection, prevention includes HBV prevention (HBV vaccination)

42
Q

List the characteristics of HEV.

A

Hepeviridae family
+ssRNA
non-enveloped

43
Q

How is HEV treated?

A

Supportive therapy

44
Q

How is HEV prevented?

A

HEV is spread through the fecal-oral route; thus, prevention entails preventative sanitation measures

There is NO vaccine for HEV

Microbiology (49 decks)

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