Zaman 1-10-08 Gi-8 Viral Hepatitis

Front 1

Virus families of Hep A - E

Back 1

A: picornavirus
B: hepadnavirus
C: flavivirus
D: satellite
E: calicivirus

Front 2

Which hepatitis is DNA (DS)

Back 2

Hep B

the rest are RNA (SS)

Front 3

Labs of hepatitis

Back 3

Laboratory: Elevated LFT's: ALT (SGOT), AST (SGPT),
bilirubin, alkaline phosphatase, gamma globulin, AFP
(alpha-Fetoprotein). May have pseudo-obstructive lab
values due to liver swelling.

Front 4

signs/symptoms of acute hepatitis

Back 4

Signs: enlarged liver and spleen, mild fever, rash,
urticaria, jaundice, dark urine, yellow sclera.

1.Symptoms: malaise, nausea, vomiting, anorexia, and
artharlgias

Front 5

Signs/symps and labs of chronic hepatitis

Back 5

Symptoms & Signs: Same as for acute
2. Laboratory: Hypoalburninemia, mild hyper
gammaglobulinemia, positive viral markers. elevated LFT's.

Front 6

agents responsible for chronic hepatitis

Back 6

Agents responsible: HBV, HCV, HDV (note only caused
by these agents i.e. HAV and HEV do not cause chronic
hepatitis). R/O ETOH, Wilson's disease, AIAT deficiency
and drugs.

Front 7

Which hepatitis do you diagnose with biopsy?

Back 7

chronic

Front 8

5.Scheur’s grading system: Describe

Back 8

Grade 0-4: degree of inflammation, peicemeal or bridging ncrosis

Stage 0-4: degree of fibrosis

Front 9

Signs/symps of fulminant hepatits

Back 9

Symptoms and signs: shock, bleeding, jaundice,
encephalopathy, multi-system failure. edema

Front 10

Labs of fulminant hepatits

Back 10

Laboratory: hypoalbuminemia, elevated PT/ PTT,
hypocholesterolemia, ALT/AST at very high levels; may
drop if gets better or as liver is completely destroyed
("burned out" liver).

Front 11

Three types of fulminate hepatitis listed by degree of
severity.

Back 11

i. Confluent hepatic necrosis -lobular and portal
hepatitis with bridging (least severe, some pts
recover).
ii. Submassive hepatic necrosis -only a rim of portal
hepatocyles left -a few patients will recover.
iii. Massive hepatitis necrosis -nothing left, hard to
recognize as liver (most severe, no survivors).

Front 12

Treatment of fulminant hep

Back 12

alpha interferon, steroids and supportive
therapy, liver transplantation.

Front 13

transmission of HAV

Back 13

2.Transmission: fecal/oral route.Not transfusion
associated. Shed in stool, water, food, seafood and
fomites.

Front 14

Carrier state for HAV?

Back 14

Carrier state: None, but 33% US. adults are immune
(90% African American adults).

Front 15

Histology of HAV

Back 15

acute lobular inflammation with ballooning degeneration,
hepatocellular necrosis, apoptosis, Councilman bodies
(eosinophilic necrosis).

Front 16

Treatment for HAV

Back 16

Treatment: rest, no hepatic drugs, i.e. (ETOH, Aspirin,
Tylenol other NSAID's)

Front 17

Symptoms of HBV

Back 17

Symptoms: depends on clinical setting: 1% fulminant,
10% chronic. 30% acute, 60% subclinical. A spectrum of
responses depends on how severe the infection and the
setting in which it occurred.

Front 18

Transmission of HBV

Back 18

Transmission: In contrast to HAV, all body fluids have
HBV except feces. Infection by parenteral and close
personal and sexual contact. Less than 0.1% of new HBV
infections caused by transfusion today-all blood donors
are screened for HBV.

Front 19

Incubation period of HBV

Back 19

Incubation period: 45 to 160 days, present in body
secretions

Front 20

Incubation period of HAV

Back 20

14 -45 days, shed in feces

Front 21

HBV is the leading cause of _______
liver disease worldwide. but second to H_V in US.

Back 21

HBV is the leading cause of chronic
liver disease worldwide. but second to HCV in US.

Front 22

Treatment of HBV

Back 22

Depends on clinical, laboratory, and histological findings;
treatment is recombinant alfa-2a interferon, lamivudine,
steroids, and/or supportive therapy.

Front 23

Chronic lobular inflammation (CLH):

The hepatocytes are primarily involved by
inflammation and Hepatocytoloysis.
Mild enzyme elevations.
A few plasma cells;
Lasts from ___ months to years.
Indeterminate prognosis.
Usually Grade (inflammation) _ or _, and Stage
(fibrotic) _ or _.

Back 23

Chronic lobular inflammation (CLH):

The hepatocytes are primarily involved by
inflammation and Hepatocytoloysis.
Mild enzyme elevations.
A few plasma cells;
Lasts from six months to years.
Indeterminate prognosis.
Usually Grade (inflammation) 1 or 2, and Stage
(fibrotic) 1 or 2.

Front 24

Chronic persistent portal
inflammation (CPH):

A mild lymphohistocytic infiltrate with portal "_____itis"
and ground glass hepatocytes..
Seen in 5 -10% of HBV patients but 20 -50% of HCV
patients.
AST 50-500, Marked enzyme elevations,
Usually find Grade _ or _; Stage _ or _ histologically.

Back 24

Chronic persistent portal
inflammation (CPH):

A mild lymphohistocytic infiltrate with portal "Triaditis"
and ground glass hepatocytes..
Seen in 5 -10% of HBV patients but 20 -50% of HCV
patients.
AST 50-500, Marked enzyme elevations,
Usually find Grade 2 or 3; Stage 1 or 2 histologically.

Front 25

Chronic interface inflammation
or chronic active hepatitis (CAH):

An extension of the infiltrate Into the periportal
tissue i.e. interface hepatitis, piecemeal necrosis,
collapse of lobule with bridging necrosis with or
without fibrosis.
Ground glass hepatocytes, plasma cells, acidophil
bodies, cholestasis, 1% AHBV, 50% AHCV, usually
find Grade _ or _, Stage _ to _.

Back 25

Chronic interface inflammation
or chronic active hepatitis (CAH):

An extension of the infiltrate Into the periportal
tissue i.e. interface hepatitis, piecemeal necrosis,
collapse of lobule with bridging necrosis with or
without fibrosis.
Ground glass hepatocytes, plasma cells, acidophil
bodies, cholestasis, 1% AHBV, 50% AHCV, usually
find Grade 3 or 4, Stage 1 to 4.

Front 26

Cirrhosis:

Fibrosis, bile duct
regeneration, and
hepatic nodule
proliferation,
end stage disease
irreversible, Grade _,
Stage _.
Arrange for the
_______ or get a
transplant ASAP.

Back 26

Cirrhosis:

Fibrosis, bile duct
regeneration, and
hepatic nodule
proliferation,
end stage disease
irreversible, Grade 4,
Stage 4.
Arrange for the
funeral or get a
transplant ASAP.

Front 27

Publisher of Hep C virus for the first time

Back 27

Harvey Alter, MD.

Front 28

Hep C symptoms:

Those of chronic hepatitis as with HBV,
may show an elevated A_T to cirrhosis previously
detected by two surrogate markers used to detect in
donor pool -elevated AST and presence of anti- HBcAg,
but picks up only 50% of the infected donors.
___ testing now done for screening. Due to blood
screening, less than 0.1 % of new HCV infections caused
by transfusion
Genotypes 1, 2a, 2b, 3a, and 3b.

Back 28

Hep C symptoms:

Those of chronic hepatitis as with HBV,
may show an elevated AST to cirrhosis previously
detected by two surrogate markers used to detect in
donor pool -elevated AST and presence of anti- HBcAg,
but picks up only 50% of the infected donors.
NAT testing now done for screening. Due to blood
screening, less than 0.1 % of new HCV infections caused
by transfusion
Genotypes 1, 2a, 2b, 3a, and 3b.

Front 29

Chronic hep C is The most common indication for liver __________.

Back 29

Chronic hep C is The most common indication for liver transplant.

Front 30

Which hepatitis do you use a biopsy to diagnose

Back 30

B and C

Front 31

Bridging necrosis?

Back 31

?

Front 32

H_V is a defective RNA virus that needs the HBV virus
to furnish its coat proteins.

Back 32

HDV is a defective RNA virus that needs the HBV virus
to furnish its coat proteins.

Front 33

Persons successfully vaccinated or completely recovered
from H_V cannot contract HDV.
Must not have had H_V vaccination or have an active
HBV disease to acquire HDV.

Back 33

Persons successfully vaccinated or completely recovered
from HBV cannot contract HDV.
Must not have had HBV vaccination or have an active
HBV disease to acquire HDV.

Front 34

Grade and treatment of HDV

Back 34

Grade 2-4, Stage 2-4.
Treatment: Alfa 2a-interferon

Front 35

Symps and incubation of HEV

Back 35

Symptoms: Similar to HAV. 40-day incubation period.

Front 36

Which heps do not go chronic?

Back 36

A and E

Front 37

Histological Findings of HEV:

Similar to HAV but more aggressive with respect to the
extent of the disease
Stage _, Grade ___.
____ plugs common.
Course: <1% fulminant but during epidemics mortality of
infected pregnant women is 10-20%

Back 37

Histological Findings of HEV:

Similar to HAV but more aggressive with respect to the
extent of the disease
Stage 1, Grade 2-4.
Bile plugs common.
Course: <1% fulminant but during epidemics mortality of
infected pregnant women is 10-20%

Front 38

Hepatitis G. Virus (HGV)

Also called GBV-_ virus
RNA virus that, like HCV, is member of _____viridae
family
10% of TAH not accounted for by HAV to HEV,
4% Community acquired Hepatitis infection not
accounted for, must be additional agents out there we
don't know about.
1-2% blood donors have HGV, not hepatrophic, no
elevation in aminotransferases.
May be “passenger” virus; does not appear to be
significant cause of _________ by itself or to alter
clinical outcome of patients with HBV or HCV.
55

Back 38

Hepatitis G. Virus (HGV)

Also called GBV-C virus
RNA virus that, like HCV, is member of Flaviviridae
family
10% of TAH not accounted for by HAV to HEV,
4% Community acquired Hepatitis infection not
accounted for, must be additional agents out there we
don't know about.
1-2% blood donors have HGV, not hepatrophic, no
elevation in aminotransferases.
May be “passenger” virus; does not appear to be
significant cause of hepatitis by itself or to alter
clinical outcome of patients with HBV or HCV.
55

Front 39

differential diagnosis of chronic hepatitis

Back 39

alcohol
NSAIDs, drugs
autoimmune hepatitis
viral hepatitis, B,C,D
(consonants are chronic)
biliary/nonbiliary disease:
stone, pancreas, PSC
unknown cause
Wilson's disease of the liver
a-a-antitrypsin disease of the liver
primary sclerosing cholangitis
more