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Gastrointestinal 1 > Pathology of Hepatitis > Flashcards

Pathology of Hepatitis Flashcards

1
Q

What is viral hepatitis?

A
  • inflammation (lymphocytes destroy antigen-expressing hepatocytes; remember Kupfer cells are the macrophages of the liver, which will engulf injured cells) of the liver parenchyma, usually due to hepatitis virus or EBV or CMV.
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2
Q

What does hepatitis cause?

A
  • acute hepatitis, which may progress to chronic hepatitis.
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3
Q

How do patients with ACUTE hepatitis present?

A
  • with jaundice (mixed CB and UCB) with DARK URINE (due to CB), fever, malaise, nausea, and elevated LFTs (ALT > AST).
  • symptoms usually last less than 6 months.
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4
Q

What specific areas does inflammation occur in ACUTE hepatitis?

A
  • LOBULES of the liver and PORTAL TRACTS, and is characterized by apoptosis (pyknosis= shrunken nucleus; remember caspase involvement also) of hepatocytes (via CD8 cytotoxic T cells).
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5
Q

How is CHRONIC hepatitis characterized?

A
  • by symptoms that last > 6 months.
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6
Q

What specific area does inflammation occur in CHRONIC hepatitis?

A
  • predominantly PORTAL TRACT.

* risk of progression to cirrhosis.

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7
Q

How are hepatitis A (HAV) and hepatitis E (HEV) viruses transmitted?

A
  • fecal-oral transmission
  • HAV= via travelers
  • HEV= contaminated water or undercooked seafood.
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8
Q

What is similar between HAV and HEV?

A
  • both cause ACUTE hepatitis only (no chronic state).
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9
Q

What marks active infection and what marks prior infection (or immunization) in both HAV and HEV, respectively?

A
  • anti-virus IgM= ACTIVE infection
  • anti-virus IgG= PRIOR infection (or immunization).
  • NOTE immunization is only available for HAV.
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10
Q

** With what is HEV infection associated in pregnant women?

A
  • fulminant hepatitis= liver failure with massive liver necrosis.
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11
Q

How is hepatitis B (HBV) transmitted?

A
  • parenterally (childbirth, unprotected intercourse, IVDU, and needle stick).
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12
Q

In what does HBV result?

A
  • ACUTE hepatitis and sometimes CHRONIC hepatitis (20%).
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13
Q

What are the 4 possible stages of HBV?

A
  1. Acute
  2. Window
  3. Resolved
  4. Chronic
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14
Q

** What is the first KEY marker of HBV infection?

A

Hepatitis B surface antigen (HBsAG)= first serological marker to arise (1 week-2 months after exposure) during the ACUTE phase.
*This will disappear during the window and resolved periods (convalescent stage) of the infection, but will reappear if infection lasts longer than 6 months!

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15
Q

** What is the KEY immunoglobulin against the acute marker for HBV infection?

A
  • IgM against the CORE (HBcAB= hepatitis B core antibody).

* It will actually knock out the virus (creating the window phase) and IgM is the only thing present.

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16
Q

What will be the only marker present during the resolved phase of HBV infection?

A

IgG

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17
Q

What is the sign of victory against HBV infection?

A

presence of IgG against the SURFACE antigen (HBsAB)

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18
Q

What specific marker indicates infection of HBV?

A 
ENVELOPE antigen (HBeAG) and the important point here is that whenever it is present, it means it can be transmitted!
*remember if you want to MAIL a letter to a friend, you need an ENVELOPE (thus transmitted).
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19
Q

Will the HBeAG (envelope antigen) be present during the window and resolved phases?

A

NO

20
Q

How is hepatitis C (HCV) transmitted?

A
  • parenterally
21
Q

In what does HCV result?

A
  • ACUTE hepatitis and CHRONIC disease occurs in MOST cases (look for MACROnodular changes and fibrosis).
22
Q

What test confirms infection of HCV?

A
  • HCV-RNA

* thus decreased RNA levels indicate recovery

23
Q

What is important to know about hepatitis D (HDV) infection?

A
  • it cannot infect by itself. Rather it is dependent on HBV (HBsAG) for infection.
  • This can occur by a patient already having prior-HBV infection and then getting HDV infection on top of that (superinfection), or pt gets both HBV and HDV at the same time (co-infection)..
24
Q

*** Is superinfection of HDV upon a pre-existing HBV infection more or less severe than a co-infection of HBV and HDV at the same time?

A

MORE SEVERE

25
Q

What will you see as a result of extracellular insult, due to degeneration and intracellular accumulation of the liver?

A
  • hepatocyte swelling (remember this is a sign of reversible cell damage).
  • ballooning degeneration
  • feathery degeneration: cholestasis, swollen foamy hepatocytes.
  • steatosis: microvesicular, macrovesicular
  • iron and/or copper accumulation
26
Q

What type of necrosis can the liver undergo?

A
  • coagulative necrosis (from ischemia)
  • lytic necrosis= cells swell, rupture, leave debris
  • focal necrosis
  • interface necrosis= between periportal parenchyma and portal tracts.
  • bridging necrosis= portal-portal, portal-central, central-central.
27
Q

Is HBsAg immunogenic but NOT infectious?

A

YES and is the basis for vaccination

28
Q

How is HBV associated with hepatocellular carcinoma?

A

X gene activates viral transcription

29
Q

What is the pathogenesis of HBV?

A

Not directly cytopathic.

- CD8 T cells recognize HLA molecules and viral antigens on the surface of infected hepatocytes.

30
Q

If you get FULMINANT hepatitis (rare; think hepatic encephalopathy) what virus usually causes it?

A

HBV

*mortality can be high :(

31
Q

Do most patients with acute HBV have self limited disease with lifelong immunity?

A

YES, but the virus has a long incubation period (up to 6 months) before pt becomes symptomatic. Meaning they can shed the virus for 6 months.

32
Q

Does the core antigen of hep B (HBcAg) circulate in the serum of pts with acute hepatitis?

A

NO, but anti-HBcAg (IgM) will appear after the surface antigen (HBsAg)

33
Q

What does HBcAg presence mean?

A
  • marker of previous infection
34
Q

When does HBV-DNA and DNA polymerase appear?

A
  • soon after HBsAg (SURFACE antigen).

* signfies active viral replication.

35
Q

What does the cytoplasm of infected hepatocytes with HBsAg look like?

A

ground glass appearance with sanded nuclei

36
Q

Will you see HBsAB (antibody against the SURFACE antigen) in CHRONIC HBV?

A

NO. Most concerning of the hepatitis viruses.

37
Q

** With what is CHRONIC HBV associated? (BOARD QUESTION)

A 
polyarteritis nodosa (vasculitis of medium-sized arteries).
*Or if a pt has polyarteritis nodosa, they are likely a carrier of HBV!
38
Q

Can some pts with HBV develop antibodies over years and clear the virus?

A

YES :)
*some pts however will never produce antibodies and suffer from relentless chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma.

39
Q

Is the entire genome of HBV integrated into the host cells?

A

NO, but fragments of it may be integrated leading to production of antigens.

40
Q

Is there currently a vaccine for HCV?

A

NO (too many strains), but there are good treatments available.

41
Q

Can HCV IgG clear the infection?

A

NO

42
Q

With what is HCV sometimes associated?

A
  • lymphoma
  • MPGN
  • Sicca syndrome
  • porphyria cutanea tarda
43
Q

With what hepatitis virus will you likely see fatty changes in the liver?

A

HBV and HCV (more common)

44
Q

Is the clinical course of viral hepatitis variable?

A

YES

45
Q

What is autoimmune hepatitis?

A
  • autoantibodies against hepatocytes with no serological markers of virus.
  • increased HLA B8 or HLA DRw3
  • resembles viral hepatitis histologically, but inflammation is rich in PLASMA CELLS.
46
Q

What are the 2 types of autoimmune hepatitis?

A
  • type I= most common, females under forty and 25% develop cirrhosis.
  • type II= children, target autoantigen is CYP2D6, and most have T1DM and thyroiditis.

Gastrointestinal 1 (21 decks)

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