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Gastro > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

Recovery is rare

Chronic infection is the rule

A

Hepatitis C

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2
Q

MArked cholestasis

A

Hepa E

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3
Q

Microvesicular steatosis

A

Hepa D

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4
Q

Extra hepatic manifestation:

Serum sickness like syndrome

A

Hepa B

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5
Q

Acidophilus degeneration of hepayocytes

A

Councilman / apoptosis bodies

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6
Q

Lab features that suggest progression to chronicity

A
  • lack of complete resolution of anorexia etc
  • bridging/interface or multilobular hepatic necrosis
  • ALT and glob in levels don’t return to normal
  • HbeAg > 3 mos or HbsAg more than 6 months after acute hepatitis
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7
Q

Causes vanishing bile duct syndrome

A

CoAmox

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8
Q

Most pronounced side effect of ribavirin therapy

A

Hemolysis

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9
Q

Favorable genotypes of Hepa C

A

Genotype 2 and 3

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10
Q

Treatment for chronic Hepa C

A

PEG IFN and ribavirin

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11
Q

Best prognostic indicator in Hepa C

A

Liver histology

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12
Q

Treatment of Hepatitis C

A

24 weeks for 2 and 3

48 weeks for genotype 1

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13
Q

HBV DNA levels to treat Hepa B

A

20,000 IU/mL

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14
Q

Persistence of This antibody beyond the 3 months of acute infection predictive of the development of chronic infection

A

HBeAg

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15
Q

Extrahepatic manifestations of Hepatitis B

A

Serum sickness like syndrome
Glomerulonephritus with. Ephrotic syndrome
Generalized vasculitis
Essential mixed cryohlobulinemia

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16
Q

Hepa C extrahepatic manifestation

A

Immune complex glomerulonephrigis

17
Q

This disorder characterized by athritis, cutaneous vasculitis and glomerulonephrigis
And extrahepatic manifestation of hepatitis

A

Essential mixed cryoglobulinemia (EMC)

18
Q

Formed by acidophilic degeneration of hepatocytes

A

Councilman or apostolic bodies

19
Q

Seen in chronic hepatitis B but not in acute hepatitis. And this can be ID histochemically by orcein or aldehyde fuschin

A

HBsAg in Large hepatocytes with ground glass appearance

20
Q

Severe histologic lesion in acute hepatitis

A

Bridging hepatic necrosis/
Subacute or confluent necrosis or interface hepatitis

(Bridging between lobules with collapse of reticulin framework)

21
Q

Accounts got more than 50% fulminant cases of viral hepatitis

A

Hepa B

22
Q

Why do we treat acute hepatitis C?

A

Recovery is rare, progression to chronic hepatitis is the ruletreat with long acting PEG IFN and ribavirin

23
Q

Hepa A vaccination schedule

A

2 doses 0,6-12

24
Q

Hepa B vaccination

A

3 IM deltoid 0,1,6

25
Q

Drug induced hepatic injury:
Acetaminophen
Carbon tetrachloride

A

Direct toxic effect

CCl4= necrosis, fatty infiltration
Acetaminophen= centrilobular necrosis
26
Q

Drug induced hepatic injury:

Coamoxiclav
Isonizid
Ciprofloxacin

A

Idiosyncratic

27
Q

When do we treat Chronic Hepa B patients?

A

HBV DNA >2 x 10^4 IU/ml whose ALT is 2x above the upper limit of normal (if ALT normal treatment is not recommended)

Compensated cirrhosis treat regardless of HBeAg and ALT (if HBV DNA >2 x 10^3 IU/ml )

Decompensated cirrhosis treat and evaluate for liver transplant

28
Q

First line therapy for Hepatitis B

A

PEG IFN - finite duration and highest rate of HBeAg responses
Entecavir
Tenofovir

29
Q

Hepa B drugs creatinine monitoring

A

Adenovirus

Tenofovir

30
Q

Extrahepatic complications of Hepa C unrelated to immune complex injury

A

Shogrens
Lichen plants
Porphyria cutaneous tarda
Type 2 DM

31
Q

Antibodies in chronic hepa C

A

Anti- LKM1

32
Q

Hepatitis drug that should not be used in cirrhosis, transplantation and immunosuppressive

A

PEG IFN

33
Q

There is no documental antiviral resistance with this drug and it has finite treatment (48 weeks)

However it is not effective in high level HBV DNA. >10^9 IU/ml

A

PEG IFN

34
Q

How does hepatitis D affect Hepa B infection?

A

Increases severity of acute hepatitis

Does not increase likelihood of progression to chronic Hepa.

35
Q

Distinguishing serologic feature of chronic hepatitis D

A

Anti-LKM3 positive

Anti LKM1- autoimmune hepatitis

36
Q

Chronic Hepa develops in cases of acute hepatitis C in ?% of cases

A

50-70%

37
Q

Rate in 20 yrs regardless of clinical severity progression to cirrhosis of px with chronic hepatitis C

A

20-25%

Gastro (9 decks)

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