hep A to G Flashcards
hepatitis clinical presentation?
Ascites
caput medusae
icterus
palmar erythema
teleangiectasia
biochem results?
Causes of Elevated ALT (sGPT) or AST (sGOT) Values in Asymptomatic Patients*
hep and its causes?
A Autoimmune hepatitis
B Hepatitis (A)-B
C Hepatitis C-(G)
D Drugs or toxins
E Ethanol
F Fatty liver
G Growths (i.e., tumors)
H Hemodynamic disorder (congestive heart failure)
I Iron (hemochromatosis), copper (Wilson’s disease) or alpha
1
-antitrypsin deficiency
M Muscle injury
acute vs chronic?
Acute (viral) hepatitis:
asymptomatic
mild icterus, elevated transaminases
severe, prolonged icterus
fulminant hepatitis with liver failure
Chronic (viral) hepatitis:
chronic persisting hepatitis
(virus detectable, few symptoms)
chronic active hepatitis
(continuous tissue destruction)
liver cirrhosis
primary liver cell carcinoma (hepatocellular)
hep clinical pic
hep A virus?
picornavirus, nonenveloped, ss (+) RNA (~10 kbases)
very stable: pH 3 or 60
oC for 10 h
frequently mild or anicteric, „yellow-flu / liver flu“
acute hepatitis, no persistence or chronic outcome
significantly more severe course in chronic hepatitis C
enteral (fecal/oral) transmission, „travel hepatitis“
transmission through contaminated water or raw foods, eg. Oysters (muckeaters…), and in hygienic facilities/ toilets
HAV epidemic in USA (Pittsburgh) from Chi-Chi® food products in the
‚Beaver Valley Mall‘: 490 cases, 3 deaths from liver failure (15.11.03)
(Dead)- vaccine with inactivated HAV (Havrix®: GlaxoSmithKline
Biologicals). The virus (strain HM175) is propagated in MRC-5 human
diploid (lung) cells which were taken from a male fetus aborted at 14 weeks
gestation.
Vaccination recommended for travellers in endemic areas,
and patients with chronic hepatitis B or C. 3 i.m. immunizations (0, 14 days,
6 months), children from 12 months of age.
for immediate / travel protection: passive immunization with
anti-HAV-positive immunoglobulins and/or a 2 step vaccination schedule (0,
4 to 6 months). Basic immunity conferred after the first vaccination
the best way to control hepatitis A infection in the hospital setting is good hygienic practise (re GI viral infections !!!)
hpe a diagnostic marker?
virus in stool, vriema, transaminase increase/icterus (3-9 months)
ttoal anti-HAV (3-12 months)
anti-HAV IgM (3-12 top at 6 months, low at 12 and 3 months.)
Hep E virus?
spherical, non-enveloped, single stranded RNA virus, approximately
32 to 34 nm in diameter.
HEV belongs to a genus of HEV-like viruses (genus Hepevirus).
? preliminarily placed as ‘calicivirus‚ (re GI virus infections)
transmission and clinical properties like HAV:
fecal / oral transmission
usually mild icterus, elevated transaminases
rarely: severe, prolonged icterus, high case fatality in pregnancy
the major etiological agent of enterically transmitted hepatitis
worldwide: especially prevalent in South East Asia and Africa
In 2005 detected in Welsh patients and traced back to PORCINE
HEV…. (part of a Year 3 SSC with NPHS virology and Andrew Godkin)
hep b?
very small ds DNA virus: ca. 3.200 base pairs, Hepadna-Virus
infects only humans and chimpanzees
replication via RNA intermediates using a reverse transcriptase
Pararetrovirus
Enveloped ‚Dane particle‘, filamentous / oval virus-like particles (VLP‘s),
‚Australia antigen
antigen markers for hep b?
hep b markers through months?
diff between acute and chronic hep b markers?
chronic = no anti-HBs
HBsAg is longer.
all the heps and their antigens?
hep b flashcard?
Virus: Hepadna virus, no serotypes, ds circular 3200 bp DNA/RNA chimera
Reservoir tissue: human liver cells
Incubation time: 45 – 180 days (~6 months)
Clinical picture: mostly assymptomatic, icterus: < 5 years: < 10%, > 5
years: 30% - 50%, mortality during acute infection 0,5% - 1%, in
chronic infections < 5 years: 30 - 90%, > 5 years: 2 - 10%. 20%
leading to chronic hepatitis and 0.5% ending in hepatocellular
carcinoma.
Epidemiology: global
Mechanisms of cancerogenesis: unclear (chronic inflammation?)
Lab diagnostics: serology, qual / quant PCR
Prevention: recombinant protein-vaccine: HBsAg from yeast HBvax
Pro®, Aventis Pasteur MSD, combined with inactivated
HAV: Twinrix®,
GlaxoSmithKline Biologicals; combined active-passive vaccination in
HBsAg-positive mothers with unknown status, vaccinations of all
newborns, vaccination of individuals in high risk groups(dialysis
patients, drug abusers)
Therapy: RT inhibitors, eg Lamivudine® (3TC - 2’deoxy, 3’thiacytidine); new
in 2006 entecavir, clevudine, telbivudine
hep D?
Coinfection of HBV with HDV
severe acute hepatitis
low risik of chronic infection
Superinfection
invariably develops into chronic infection
high risik for severe chronic hepatitis
Hepatitis D
Hepatitis D is caused by the Delta agent (Hepatitis D virus: HDV)
HDV is a defective circular small ss (-) RNA virus (1700 bases; viroid-like) and
can only be packaged in the presence of HBsAG in HBV infected cells
=> hepatitis D can only occur in association with HBV infection (satellite virus)
Discovered in 1977 by Dr. Mario Rizzetto and associates in Italy: in
patients affected by Hepatitis B. They observed a new antigen in
hepatitic liver cells different than surface, core and envelope systems that
they called “delta antigen”.
(Gut 18:997-1003,1977)
route of heps?
