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Clin Med II - GI > Hepatitis Fredenburg > Flashcards

Hepatitis Fredenburg Flashcards

1
Q

What herbal substances increase risk of hepatitis?

A
  • St. John’s wort
  • Comfrey
  • Chaparral
  • Ephedra
  • Kava
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2
Q

What social history aspects increase the risk of hepatitis?

A
  • ETOH, illicit substances
  • Sexual history
  • Transfusions
  • Occupational
  • Travel
  • Surgery
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3
Q

What meds can increase risk of hepatitis?

A
  • Vit A
  • Statins
  • Acetaminophen
  • NSAIDs
  • Penicillin derivatives
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4
Q

Where is the first place to notice jaundice?

A

Sclera (icterus)

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5
Q

What are nonhepatic sources of bilirubin?

A

RBCs

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6
Q

What are nonhepatic sources of AST?

A

Skeletal and cardiac muscle

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7
Q

What are nonhepatic sources of LDH?

A

Heart, RBCs

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8
Q

What are nonhepatic sources of ALP?

A

Bone, 1st trimester placenta, kidneys, intestines

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9
Q

How do statins affect the liver?

A
  • Rare reports of fatal hepatic failure
  • Increases aminotransferase levels
  • Guidelines do not restrict use
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10
Q

How do penicillins affect the liver?

A
  • Rare instances of liver injury
  • High IV and IM doses
  • BUT many case reports were before serologic testing was available for hepatitis
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11
Q

How are AST/ALT levels in chronic liver disease?

A

May or may NOT be elevated

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12
Q

What can cause minimal ALT elevations (less than 1.5x normal)?

A
  • Race/gender
  • Obesity
  • Muscle injury
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13
Q

Mildly elevated AST and ALT is normally caused by:

A
  • Fatty infiltration
  • ETOH
  • HLD
  • Obesity
  • T2DM
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14
Q

What causes elevated AST?

A
  • Common bile duct obstruction
  • Cholangitis
  • Alcoholic hepatitis
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15
Q

AST should make you think of:

A

Alcohol

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16
Q

ALT should make you think of:

A

Virus

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17
Q

What does AST:ALT ratio of 2+ suggest?

A

ETOH liver disease

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18
Q

AST:ALT ratio of less than 2 suggests?

A
  • Acute or chronic viral hepatitis
  • Cholestatic disease
  • NASH (non-alcoholic steatohepatitis)
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19
Q

When should elevated aminotransferases cause concern?

A
  • More than one liver enzyme abnormal
  • Clinical s/s of liver disease
  • Greater than 5 fold elevation of an enzyme
  • Persistence of abnormal levels for 6+ months
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20
Q

How is Hep A transmitted?

A

Fecal to oral

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21
Q

What is the most likely period of someone spreading Hep A virus?

A

2 weeks before onset of jaundice

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22
Q

Can Hep A be spread through blood?

A
  • Occasionally

- There is a short period of viremia once infected

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23
Q

Does Hep A cause a chronic infection?

A

No

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24
Q

Treatment of Hep A virus?

A

Immunoglobulin (IG)

-Must be given within 14 days of exposure

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25
Q

How long does IG pre-exposure prophylaxis protect travelers?

A

3-5 months

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26
Q

How does IG work in treating HAV?

A
  • Passive transfer of neutralizing antibodies

- Prevents infection or clinical expression of disease

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27
Q

Describe the HAV vaccine

A
  • Used for PREP
  • Given as 2 dose series
  • Licensed for use in 12+ months old
  • Protects for at least 20 yrs if not more
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28
Q

What are the unresolved issues surrounding HAV vaccine?

A
  • Should it be used as PEP

- Should it be used in community-wide outbreaks

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29
Q

Who should receive HAV vaccine?

A
  • All children 12-18 months old regardless of residence
  • Travelers to HAV endemic countries
  • Homosexual and bisexual men
  • Drug users
  • Chronic liver disease patients
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30
Q

Which hepatitis virus is MC caused by IV drug use?

A

HCV

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31
Q

Which hepatitis virus is MC caused by sexual exposure?

A

HBV

32
Q

Which hepatitis virus is MC caused by perinatal exposure?

A

HBV

33
Q

Which hepatitis virus is MC caused by occupational exposure?

A

HBV

34
Q

What are the MC transmission methods of HBV?

A
  • Percutaneous and permucosal (e.g. IV drug use, needle sticks)
  • Sexual (both homo and hetero)
  • Perinatal (mother to child during labor and delivery)
35
Q

What do you look at to see if someone is chronically infected with HBV?

A

HBsAg (Hep B surface antigen)

36
Q

What does HBeAg indicate?

A

Active HBV replicating

37
Q

What is given for post-exposure prophylaxis of HBV?

A

HBIG

38
Q

How is the HBV vaccine used?

A

For both pre and post exposure

39
Q

Current strategy of HBV vaccine

A
  • Routine for infants
  • Routine of adolescents who didn’t get it in infancy
  • High risk children, adolescents and adults
40
Q

Describe HBIG

A
  • Used for post exposure
  • Prepared from plasma containing high titers anti-HBs
  • Does NOT protect against future exposures
41
Q

What is the primary component of HBV vaccine?

A

HBsAg

42
Q

Describe the HBV vaccine

A
  • Worldwide plasma-derived and recombinant formulations available
  • Only recombinant available in US
  • 3 dose series
  • Highly immunogenic (seroconversion approx 95%)
  • Long lasting protection (no booster recommendation)
43
Q

Which hepatitis virus has no vaccine available?

A

HCV

44
Q

Which populations are MC affected by HCV?

A

Males, middle aged

45
Q

Risk factors for HCV

A
  • Transfusions (more of a problem in the past due to lack of screening blood products)
  • IV drug use (bigger problem now)
  • Sexual
46
Q

What is the risk for HCV involved with tattooing, body piercing, acupuncture?

A

No or insufficient data showing increased risk

47
Q

When is HCV testing routinely recommended?

A
  • Hx of injected illegal drugs
  • Received clotting factors made before 1987
  • Received blood/organs before July 1992
  • Chronic hemodialysis
  • Evidence of liver disease
  • HC workers
  • Children born to HCV positive women
48
Q

In areas where there is high/moderate endemicity of HCV, what is the MC cause?

A

HC related

49
Q

In areas where there is low endemicity of HCV, what is the MC cause?

A

IV drug use

50
Q

How is HCV diagnosed?

A
  • IgG assays for anti-HCV (false negatives possible in 1st 15 wks)
  • Nucleic acid amplification testing to detect HCV RNA in blood (viremia in 80% with acute infection)
51
Q

What is important to know about IgG assays for anti-HCV?

A

False negative can occur in first 15 weeks after exposure

52
Q

When is HCV treatment recommended?

A

-Elevated ALT levels
-Age over 18 yo
-Positive HCV antibody and serum HCV RNA tests
etc etc

53
Q

What is a sustained viral response?

A

Considered a “cure” of HCV (levels we can’t detect, so it could come back theoretically)

54
Q

HCV med regimens

A
  • Pegylated interferon and ribavirin for 24-48 weeks

- New oral agents added are increasing “cure rates” on initial treatment attempts

55
Q

Describe Hepatitis D

A
  • “Delta hepatitis”
  • RNA virus structurally unrelated to A, B, C viruses
  • Acute or chronic
  • Uncommon in US
  • Only occurs WITH HBV
56
Q

Why does HDV only occur with HBV?

A

Incomplete virus that requires helper function of HBV to replicate

57
Q

What population is affected by HDV?

A

Those infected with HBV

58
Q

Vaccination for HDV?

A
  • None available

- BUT is prevented by HBV vaccine in pts NOT already HBV infected

59
Q

Describe coinfection of HDV

A
  • Simultaneous infection with HBV and HDV
  • Presents similar to HBV alone
  • MC outcome is complete clinical recovery and clearance of HBV and HDV
60
Q

Describe superinfection of HDV

A
  • HDV infection in pt already positive for HBsAg

- Progresses more rapidly to develop cirrhosis and possible hepatocellular carcinoma

61
Q

Does fulminant liver failure occur more often in coinfection or superinfection of HDV?

A

Superinfection!

62
Q

Describe HEV

A
  • RNA virus, Hepeviridae family
  • Fecal oral route
  • Japan and Europe MC areas
  • Mainly zoonotic and foodborne
  • Perinatal transmission is common
63
Q

Which hepatitis virus affects pregnant women most?

A

HEV

64
Q

When are US residents most at risk for HEV?

A
  • Traveling to epidemic areas

- Eating raw or undercooked venison, boar, pig liver

65
Q

How does HEV present?

A

Prodromal phase

Icteric phase

66
Q

How is HEV diagnosed?

A
  • Anti-HEV IgM and IgG
  • HEV RNA in serum or stool
  • No diagnostic test approved by FDA
67
Q

What is the treatment of HEV?

A

Supportive

68
Q

What is the prevention of HEV?

A
  • No vaccine or drugs available
  • Avoid drinking contaminated water
  • Avoid eating undercooked or raw animal products
69
Q

Describe HGV

A
  • Prevalence in general population is high
  • Linked to HCV
  • Tx limited to rest, avoiding ETOH
70
Q

Describe HFV

A

“Hypothetical” virus linked to hepatitis - not a major player

71
Q

Describe TTV

A
  • Detected in many people including those with fulminant hepatic failure or chronic hepatitis of unknown etiology
  • No current evidence that chronic TT viremia is responsible for hepatic inflammation, cirrhosis, or hepatocellular carcinoma
72
Q

Prognosis of HAV?

A
  • Usually mild and self limited
  • Infection confers lifelong immunity
  • 3 rare complications (relapsing hepatitis, cholestatic hepatitis, FHF)
73
Q

Prognosis of HBV?

A

FHF develops in 0.5-1% of HBV infected pts

74
Q

Prognosis of HCV?

A
  • Chronic infection develops in 50-60%

- Leading indication for liver transplant in US

75
Q

What is the leading indication for liver transplant in the US?

A

HCV

76
Q

Prognosis of HDV with coinfection of HBV?

A
  • BETTER than superinfection
  • Tend to develop chronic HDV
  • Often leads to rapidly progressive subacute or chronic hepatitis
77
Q

Prognosis of HEV?

A
  • Usually mild and self limited

- A problem in pregnant women though!

Clin Med II - GI (17 decks)

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