Chronic Hepa Flashcards

1
Q

are nonprogressive oronly slowly progressive type of chronic hepatitis.

A

Milder forms

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2
Q

Form of chronic hepatitis may be associated
with scarring and architectural reorganization, which, when
advanced, lead ultimately to cirrhosis.

A

severe forms

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3
Q

Classification of chronic hepatitis is based on

A

(1) its cause
(2) its histologic activity, or grade
(3) its degree of progression based
on level of fibrosis, or stage.

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4
Q

Type of Hepatitis which the Diagnositic Tests include HbsAg, IgG anti HBc, HbeAg, and HBV DNA

A

Chronic Hepatitis B

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5
Q

Type of Hepatitis which the Diagnositic Tests include Anti-HCV and HCV RNA.

A

Chronic Hepatitis C

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6
Q

Diagnostic Test for Autoimmune hepatitis

A

ANA, anti-LKM1 +/- hyperglobulinemia

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7
Q

A histologic assessment of necroinflammatory activity, isbased on examination of the liver biopsy.

A

Grade

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8
Q

An assessment of

important histologic features includes

A
  • the degree of periportal necrosis and the disruption of the limiting plate of periportal
    hepatocytes by inflammatory cells (so-called piecemeal necrosis orinterface hepatitis)
  • the degree of confluent necrosis that links or forms bridges between vascular structures—between portal tract andportal tract or even more important bridges between portal tract andcentral vein—referred to as bridging necrosis
  • the degree of
    hepatocyte degeneration and focal necrosis within the lobule

-the degree of portal inflammation

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9
Q

When
fibrosis is so extensive that fibrous septa surround parenchymal
nodules and alter the normal architecture of the liver lobule, the
histologic lesion is defined as

A

cirrhosis

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10
Q

self-limited and do not cause chronic hepatitis

A

hepatitis A

and E

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11
Q
The likelihood of chronicity after acute hepatitis B varies as a
function of
A

age

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12
Q

is more common than HBeAg-reactive chronic hepatitis B in Mediterranean and European
countries and in Asia

A

HBeAg-negative chronic hepatitis B

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13
Q

is a common symptom in Chronic Hepatitis B

A

Fatigue

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14
Q

is a common feature in severe or advanced cases of Chronic Hep B

A

persistent or intermittent jaundice

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15
Q

reminiscent of acute

hepatitis

A
  • Intermittent deepening of jaundice
  • recurrence of malaise and anorexia
  • worsening fatigue,
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16
Q

are associated with tissue deposition of circulating hepatitis B antigen–antibody immune complexes and similar to those seen during the
prodromal phase of acute hepatitis B

A

Extrahepatic

complications of chronic hepatitis B

17
Q

was the first approved therapy (1992) for chronic hepatitis B.
Although it is no longer used to treat hepatitis B,

A

IFN-α

18
Q

The first of the nucleoside analogues to be approved (in 1998) for hepatitis B that inhibits reverse
transcriptase activity of both HIV and HBV and is an effective agent
for chronic hepatitis B

A

dideoxynucleoside lamivudine

19
Q

it is less potent than lamivudine or any of the newer antiviral agents.

A

ADEFOVIR DIPIVOXIL

20
Q

was shown to be effective in the

treatment of hepatitis C, this more convenient IFN preparation was evaluated in the treatment of chronic hepatitis B.

A

PEGYLATED IFN/ PEG IFN

21
Q

an oral cyclopentyl guanosine analogue polymerase inhibitor, appears to be the most potent of the HBV antivirals and is just as well tolerated as lamivudine.

A

Entecavir

22
Q

a cytosine analogue, is similar in efficacy to entecavir but slightly less potent in suppressing HBV
DNA

A

Telbivudine

23
Q

an acyclic nucleotide analogue
and potent antiretroviral agent used to treat HIV infection, is similar to adefovir but more potent in
suppressing HBV DNA and inducing HBeAg responses; it is highly active against both wild-type and lamivudine-resistant HBV and active in patients whose response to adefovir is slow and/or limited.

A

Tenofovir disoproxil fumarate (TDF)

24
Q

a second-generation tenofovir, is a prodrug of tenofovir that requires activation to tenofovir in hepatocytes. This targeted delivery to hepatocytes
allows a lower dose to suffice and reduces systemic exposure by 90%, thereby minimizing TDF-associated proximal tubular renal injury, its associated phosphate wasting, and the potential
consequent loss of bone mineral density.

A

Tenofovir alafenamide (TAF)

25
Q

a fluorinated cytosine analogue very similar to
lamivudine in structure, efficacy, and resistance profile, offers no
advantage over lamivudine

A

emtricitabine

26
Q

approved for the treatment of HIV infection and is an
appealing combination therapy for hepatitis B, especially for
lamivudine-resistant disease

A

emtricitabine +

tenofovir

27
Q

Recommendation Treatment

  • HBeAg-reactive
  • liver disease is mild and inactive
A

No tx, monitor

28
Q

Recommendation Treatment

  • HBeAg-reactive
  • Chronic Hepatitis
A

Treat

29
Q

Recommendation Treatment

  • HBeAg-reactive
  • Cirrhosis compensated
A

Tx w/ oral agents, not PEG IFN

30
Q

Recommendation Treatment

  • HBeAg-reactive
  • Cirrhosis decompensated
  • detectable
A
  • Tx w/ oral agents, not PEG IFN

- Refer to liver transplant

31
Q

Recommendation Treatment

  • HBeAg-reactive
  • Cirrhosis decompensated
  • undetectable
A
  • observe

- refer for liver transplant

32
Q

Recommendation Treatment

  • HBeAg- negative
  • liver diseases is mild and inactive
A

Tx not necessary

33
Q

Recommendation Treatment

  • HBeAg- negative
  • Chronic hepatitis
A

No tx except for major risk factors

34
Q

Recommendation Treatment

  • HBeAg- negative
  • Chronic hepatitis
  • > 2xULN ALT
A

Tx

35
Q

Recommendation Treatment

  • HBeAg- negative
  • Cirrhosis compensated
A

Tx w/ oral agents, not PEG IFN

36
Q

Recommendation Treatment

  • HBeAg- negative
  • Cirrhosis decompensated
  • detectable
A
    • Tx w/ oral agents, not PEG IFN

- Refer to liver transplant

37
Q

Recommendation Treatment

  • HBeAg- negative
  • Cirrhosis decompensated
  • undetectable
A
  • observe

- refer for liver transplant