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GI 2 > Clin Med - Hepatitis > Flashcards

Clin Med - Hepatitis Flashcards

1
Q

Hepatitis

- define

A
  • diffuse or patchy cell necrosis
  • pan lobar infiltration with WBCs
  • hyperplasia of Kupffer cells
  • variable degrees of cholestasis and resulting jaundice
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2
Q

How does the hepatitis virus affect hepatocytes?

A
  • not directly cytopathic

- clinical manifestations are due to immunologic response of the host

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3
Q

Hepatitis

- presentation

A
  • low-grade fever
  • v/d anorexia
  • dehydration (tachycardia, dry mucous, loss skin turgor, delayed cap refill)
  • scleral icterus, icterus of mucous membranes and TM
  • jaundice, urticaria
  • RUQ pain
  • hepatomegaly with smooth edge
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4
Q

chronic hepatitis presentation

A

Feel fine

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5
Q

Acute hepatitis

- common causes

A
  • hepatitis virus
  • alcohol
  • drugs (high doses of acetaminophen, isoniazid)
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6
Q

Acute hepatitis

- uncommon causes

A
  • cytomegalovirus
  • Epstein-barr virus
  • autoimmune (sarcoidosis, UC)
  • leptospirosis infection
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7
Q

Hep A

  • nucleic acid
  • major transmission
  • incubation
  • epidemics?
  • chronicity?
A
  • RNA
  • fecal-oral
  • 15-45 days
  • Yes
  • No
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8
Q

Hep B

  • nucleic acid
  • major transmission
  • incubation
  • epidemics?
  • chronicity?
A
  • DNA
  • blood, percutaneous
  • 40-180 days
  • No
  • Yes
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9
Q

Hep C

  • nucleic acid
  • major transmission
  • incubation
  • epidemics?
  • chronicity?
A
  • RNA
  • Blood (IVDU, share needles in IV injection)
  • 20-120 days
  • No
  • Yes
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10
Q

Hep D

  • nucleic acid
  • major transmission
  • incubation
  • epidemics?
  • chronicity?
A
  • incomplete RNA
  • needle (blood)
  • 30-180 days
  • No
  • Yes
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11
Q

Hep E

  • nucleic acid
  • major transmission
  • incubation
  • epidemics?
  • chronicity?
A
  • RNA
  • Water (dirty), fecal-oral
  • 14-60 days
  • Yes
  • No
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12
Q

hepatitis differential

A

long list in slide :)

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13
Q

Acute viral hepatitis

A
  • infection of the liver by one of the hep virus (A-E) OR

- other less common viruses (Epstein-Barr, cytomegalovirus, etc..)

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14
Q

Of Hepatitis A, B, and C, which commonly cause acute hepatitis

A

A and B

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15
Q

Acute viral hepatitis

- presentation

A 
- nonspecific viral prodrome
followed by 
- anorexia
- fever
- RUQ pain
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16
Q

Acute viral hepatitis

- when does jaundice appear

A
  • as other sx begin to resolve
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17
Q

Acute viral hepatitis

- resolution?

A
  • most resolve spontaneously
  • some progress to chronic
  • rarely progress to fulminant hepatitis (acute liver failure) which is very bad
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18
Q

What are the four phases of acute viral hepatitis?

A
  1. Incubation
  2. Prodromal (pre-icteric) phase: majority of sx
  3. Icteric phase: dark urine and jaundice
  4. Recovery
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19
Q

Anicteric hepatitis

A
  • no jaundice/icterus
  • common in HCV or children with HAV
  • manifests as minor flu-like symptoms
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20
Q

Recrudescent hepatitis

A

rare, recurrent relapses during recovery phase

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21
Q

What is the first step in dx hepatitis?

A

obtain liver enzyme levels

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22
Q

Decision tree for hep dx:

  • marked elevation of AST and ALT
  • no elevation of Alk phos
A

check viral serologic tests to determine which virus is the cause
- if negative, look for other causes such as alcohol or drugs

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23
Q

Decision tree for hep dx:

- elevation of AST, ALT, and Alk phos

A

look for biliary tree obstruction

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24
Q

Decision tree for hep dx:

no elevation of liver enzymes

A

NOT hepatitis!

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25
Q

What 4 tests does an acute hepatitis panel include?

A
  1. IgM anti-HAV
  2. HBsAG
  3. IgM anti-HBc
  4. anti-HCV OR HCV-RNA
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26
Q

alcoholic hepatitis

A
  • hx of excessive drinking
  • more gradual sx onset
  • vascular spiders, other sx of chronic alcohol abuse
  • AST/ALT rarely >300 IU/L
  • AST gen higher than ALT
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27
Q

how distinguish alcoholic hepatitis from viral?

A

liver biopsy

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28
Q

Acute hepatitis

- which viruses symptomatic which not

A
  • HAV and HBV symptomatic

- HCV may be asymptomatic

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29
Q

Which two hepatitis viruses never become chronic

A

HAV

HEV (less severe)

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30
Q

Fulminant Hepatic Failure (FHF)

A

acute liver failure complicated by hepatic encephalopathy

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31
Q

Chronic hepatitis

  • length of time
  • which two viruses most common
  • common co-morbidity
A
  • > 6 months
  • clinical illness may take months or years to evolve
  • HBC and HCV
  • 20% develop cirrhosis
  • some may remain asymptomatic for life
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32
Q

Chronic hepatitis

- four common causes

A 
- HBV, HCV
non-viral:
- autoimmune hepatitis, primary biliary cirrhosis
- fatty liver (NASH)
- alcoholic hepatitis
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33
Q

How is chronic hep often found?

A
  • routine labs bc asymptomatic

- can present first as cirrhosis

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34
Q

Liver biopsy as dx

- acute vs. chronic

A
  • not needed in acute

- chronic may need to determine etiology

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35
Q

Hepatitis A

- major points overview

A
  • No carrier state-
  • No chronic state
  • Shed a TON in feces before patient knows have an infection
36
Q

HAV Sx

A

several weeks of:

  • malaise
  • anorexia
  • nausea
  • vomiting
  • elevated aminotransferase levels
  • jaundice in severe cases
37
Q

Acute HAV

  • adults vs. children
  • relapse?
  • lifelong experience?
A
  • higher mortality in adults
  • young children can be asymptomatic
  • can relapse for up to a year
  • infected once = lifelong immunity
38
Q

how likely is it HAV acute infection will lead to FHF?

A

< 1%

39
Q

Acute HAV Chart

A

Review in slides

40
Q

Acute HAV

- serum testing

A
  1. IgM anti-HAV: appears quickly, disappears months after initial infection
  2. IgG anti-HAV: takes longer to develop but lasts for a lifetime, confers immunity to future HAV infections
41
Q

HAV tx

A
  • supportive
  • no antiviral available
  • hosp for those at risk of dehydration due to n/v
  • hosp if suspect hepatic failure
42
Q

How to prevent HAV infection

A
  • sanitation
  • hand washing, personal hygiene
  • bleach or 85C for 1 minute kills virus
  • vaccination: routine age 1 and second dose 6-18 months later
43
Q

Who should receive HAV vaccine

A
  • occupational risk (lab, daycare)
  • chronic liver disease (increased FHF risk)
  • travelers (>1 month prior)
  • immunocompromised
  • MSM
  • illicit drug use
  • receive clotting factor concentrates
  • close contact with international adoptee from endemic country
44
Q

Post exposure prophylaxis for HAV

A
  • single dose HAV vaccination
  • If >75 yo, chronic liver dz, immunocompromised: immune globine dose
  • can give up to 2 weeks after exposure but earlier is better
45
Q

HBV

  • onset of sx
  • endemic where?
  • increased risk of waht
A
  • symptomatic at onset
  • endemic in Asia
  • sig increase of hepatocellular carcinoma
46
Q

HBV

- non-percutaneous routes of transmission

A
  • intimate/sexual contact

- perinatal transmission

47
Q

How contagious is HBV vs. HAV?

A

HAV much more contagious

48
Q

Chronic Hep B

  • How does age affect chances of chronic infection
  • what co-morbidity is more likely
A
  • younger age at acute infection, high risk for chronic infection
  • increased risk of cirrhosis
  • much less likely to become chronic than HCV
49
Q

Hep B carrier state

  • what does it mean for pathophysiology of virus?
  • what type of patient more likely to remain chronically infected?
A
  • the existence of inactive HBV carriers suggests the virus is not directly hepatotoxic, it’s the body’s immune response that is damaging…
  • patients with immune problems at greater risk for chronic infection
50
Q

People at high risk HBV

A

SO MANY, highlighted in class:

  • people born in or who have parents who emigrated from endemic areas of the world
  • IVDU
  • high risk sex
  • inmates
51
Q

What is the first step to diagnosing hepatitis

A

AST, ALT, Alk phos!

ALT will be predominantly high unless alcoholic hepatitis which will have higher AST

52
Q

What three serum markers are positive in acute HBV

A
  • HBsAG
  • IgM anti-HBc
  • HBV-DNA
53
Q

What 5 serum markers are positive in chronic HBV

A
  • HBsAG (same as acute)
  • IgG anti-HBc
  • HBV-DNA
  • +/- HBeAG
  • +/- Anti-HBe
54
Q

What three serum markers are positive if have had prior HBV infection

A
  • Anti- HBs
  • +/- IgG anti-HBc
  • +/- Anti-HBe
55
Q

what one serum marker indicates prior HBV vaccination, prior infection, and immunity

A

Anti-HBs

56
Q

HBsAg

A

surface antigen

  • Appears before sx
  • implies infection (acute or chronic)
  • disappears after recovery
57
Q

what is HBV carrier state

A
  • in 5-10% of people who are infected, HBsAG lasts but no antibody is developed
  • Anti-HBc is also present. Never mount antibody response to the surface antigen…
  • called carrier state, chronic infection
58
Q

Anti-HBs

A

surface antibody

  • appears weeks or months after the HBsAg, after recovery
  • persists for life and confers immunity.
  • indicates either past infection or vaccine
    • Need >10mIU/mL for immunity
59
Q

Where is HBcAg found

A

NOT in serum, in liver cells only

60
Q

IgM anti-HBc vs. IgG anti-HBc

A

IgM - elevates early and then falls off. Indicator of acute infection

IgG - elevates slowly, indicates chronic infection

61
Q

HBeAg and Anti-HBe are useful for what

A

e markers are more helpful for prognosis, not used so much for diagnosis

62
Q

HBeAG

A
  • protein from the viral core
  • present only in HBsAG positive serum
  • suggests more active viral replication = greater infectivity
  • not all pts with HBV need treatment, e markers help decide who needs tx and who does not
63
Q

If have HBeAG, what does the presence of anti-HBe indicate?

A

lower infectivity

64
Q

HBeAG and anti-HBe and the risk for liver disease?

A
  • HBeAG indicates greater chance of liver dz

- Anti-HBe indicates less risk

65
Q

HBV-DNA

A
  • fail-proof if you are confused :)
  • in serum if active infection (acute or chronic)
  • PCR to detect virus
  • qualitative or quantitative
  • can use quantitative count to check for suppression in pts being treated
66
Q

Chronic HBV treatment

A
  • antiviral therapy

- refer to GI or hepatologist

67
Q

Goals for HBV tx

A
  • suppress viral replication (no cure)
  • lower morbidity and mortality related to chronic infection (cirrhosis and hepatocellular carcinoma)
  • NOT to cure
68
Q

What is a major cause of worldwide hepatocellular carcinoma?

A

HBV

- maybe >80% of primary hepatocellular carcinoma causes worldwide!

69
Q

what serum marker in HBV indicates a higher risk of hepatocellular carcinoma?

A

HBeAG

70
Q

How to prevent HBV

A

Vaccinations!!

  • all infants, children <19
  • healthcare and first responders
  • sexual workers
  • high risk sex
  • dialysis, DM, CLD, chronic HCV, HIV
  • IVDU
  • incarcerated ppl
  • travelers to endemic areas
71
Q

how to treat infant born to HBV infected mom

A
  • treat with hepatitis B immune globulin (HBIG)
  • vaccinate immediately after delivery
  • generally transmitted at birth; trans-placental transmission can occur but is rare.
72
Q

Hepatitis C

- pearls from Roark

A
  • almost always becomes chronic
  • lots of genotypes
  • increased cancer risk
73
Q

Hep C

  • # of genotypes
  • what is diff between genotypes
  • one exception
A
  • 6 genotypes
  • each responds differently to tx but same pathogenesis and progress
  • exception is #3, more likely steatosis and progression
74
Q

Hep C immunity

A

no immunity against future reinfection:

  • high mutation rate
  • genotypic diversity
  • no effective humoral immunity
75
Q

when did the US start screening blood for Hep B? Hep C

A

Hep B: 1969

Hep C: 1990

76
Q

who is at risk for hep C

A
  • blood transfusion/organ transplantation before 1992
  • IVDU (current or former)
  • tattoos
  • hemodialysis
  • HIV
  • born to HCV+ mom
77
Q

Who should be screened for HCV?

A
  • current/former IVDU
  • born 1945-1965
  • other high risk
    (list on slide but it’s pretty obvious)
78
Q

HCV serology - what are the two tests, what is the best option

A
  • Anti-HCV antibody
  • HCV RNA PCR
  • best is HCV RNA, antibody test just tells you there is an antibody, RNA positive tells you active infection and RNA negative tells you no infection
79
Q

HCV RNA PCR vs. HCV RNA PCR titer

A
  • PCR: qualitative test to detect presense or absence of virus
  • PCR titer: quantitative test to detect amt of virus or “viral load”, usually in millions
80
Q

If do Anti-HCV test and get negative but know pt has exposure what is next?

A

test HCV RNA (this is why you should go straight to RNA test, this was a dumb waste of time and money)

81
Q

If do Anti-HCV test and get positive, what net?

A

test HCV RNA to determine if have current infection or if antibodies are from past infection
(again, this is why you should go straight to RNA test, this was a dumb waste of time and money)

82
Q

Hep D

  • requires what
  • how common
  • nickname
  • acute or chronic?
A
  • requires co-infection with hep B to replicate
  • uncommon in US
  • “delta hepatitis”
  • acute or chronic
83
Q

How prevent Hep D

A

no vaccine avail, can be prevented via HBV vaccine

84
Q

worldwide, where are two patterns of Hep D?

A
  • mediterranean region: non-percutaneous transmission

- US/Northern Europe: IVDU and hemophiliacs

85
Q

Hep E

  • how common in US
  • vaccine?
A
  • rare in use, more in countries with poor sanitation :(

- no vaccine

GI 2 (11 decks)

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