Hepatitis 89-90 Flashcards
Differential Dx Hepatitis
Hep A, B, C EtOH injury Drug induced Gallstone Amebic bacterial abscess Viral Causes
Fecal Oral Hepatitis Viruses
HAV
HEV
Blood Borne Hepatits Viruses
HBV
HCV
HDV
OUtcomes of hepatitis
- anicteric
- icteric w/ resolution
- Fulminant
- Chronic
Hep A virus
Picornaviridae Small + sense naked ss RNA icosahedreal capsid cap proteins bind hepatocytes RESISTANT TO HARSH Structural and non structural genes
HAV Epidemiology
Fecal Oral
Shed 2 weeks before
Continues 2 weeks after jaundice
Restaurant, daycare, shellfish, contaminated H2O
HAV clinical
Acute Hepatitis 2-4 weeks incubation Abrupt onset Virus detectable prior to symptoms IgM first IgG next
Initial symptoms HAV
fever, loss appetite, abdominal pain
Later symptoms HAV
Dark Urine, Pale stool, Jaundice, pruitice 4-5 weeks long
HAV pathogenesis
Fecal Oral Internalized by hepatocytes released in bile and GI Humoral and CMI response Non perm damage ADCC and CTL jaundice, urine, stool bcuz of liver damage
HAV OUTCOME
Mild disease, complete recovery 99%
Fulminant hepatitis rare
NOT CHRONIC
LIFE LONG IMMUNITY
HAV Treatment
Post exposure prophylaxis, immune globulin
HAVE Prevention
Sanitation
Vaccine
HAVRIX Vaqta
Twinrix– HAV+HBV
HEV
Hepeviridae Small + naked ssRNA icosahedral capsid Cytoplasmic Replication 3 ORF
HEV Epidemiology
Fecal Oral
Mimics HAV
Higer fatality than HAV
Inadequate water supply and enviromental sanitation
HEV Clinical Features
Acute Hepatitis
2-8 week incubation
ABRUPT
HEV Pathogenesis
Fecal Oral
Both Humoral and CMI
Jaundice bcuz of damage
HEV Diagnosis
Mimics HAV
HEV Treatment and Prevention
Symptomatic
Prevention: Sanitation, recomb vaccine
HBV
Hepadnaviridae Small enveloped partial dsDNA Stable, icosahedral capsid Glycoproteins in capsid
HBV Genome
Sgene
C gene
P gene
X gene
HBV S gene
HBsAg ( LMS proteins)
HBV C gene
HBcAg
HBeAg—> not part of structure, is secreted
HBV P gene
DNA polymerase
Reverse Transcriptase
HBV X gene
Transcriptional Transactivators, aid replication
HBV Replication
dsDNA by viral DNA polymerase
-transcription into 4 mRNAs by HOST Pol
full mRNA –> - DNA by reverse trancriptase
Short mRNA–> synthesize viral proteins
assembly- budding of virions=Dane particle
Release of HBsAg + HBeAg
Purpose of - DNA template in HBV
partial + Synthesis
HBV Epidemiology
Blood Born
Perinatal
20-49 age group
10 genotype A-D most common
HBV Clinical Features
incubation of 3 months INSIDIOUS if symptomatic 3 outcomes 1. acute hepatitis w/ resolution 2. acute hepatitis w/ progression to fulminant hep 3. Chronic Hepatitis 3. a. persistent 3.b. Active
Acute Hepatitis w/ resoltion HBV
hepatic inflammation fever RUQ pain dark urine pale stool resolves 3-6 months
Acute Hepatitis w/ fulminant hepatitis
rapid progrss liver necrosis
acute severe
rapidly fatal
Chronic Hepatitis
persistent infection initial mild infection cirrhosis liver failure or hepatocellular carcinoma
HBV pathogenesis
Enter blood infects hepatocytes No permanent liver damage DNA can insert in host... LATENT Effective CMI & Inflammation = resolution Ineffective CMI & inflammation= 1. immune complex 2. Cirrhosis 3. PHC/HCC
HBV Diagnosis
Acute Hep B -Elevated LIver -HBsAg and HBeAg appear first before symptoms -Chronic B -prolonged elevation of liver HBsAg HBeAg and HBV DNA persist
HBV Treatment
Acute Hepatitis: Symptomatic
Fulminant Hepatitis- liver transplant
Chronic Hepatiis-
HBV Prevention
Vaccination -Recombivax -Twinrix -C-Comvax HBIG - HepaGam HyperHep B Navi-HB
HDV
Small RNA virioid Circular - sense ssRNA surronded by delta Envelope contain HBsAg ** MUST HAVE HBV INFECTION**
HDV Epidemiology, Genotype
Genotype 1 most prevalent
4% HBV infections in U.S. = HDV +
HDV Clinical Features
HBV but increased severity
Coinfection- More acute symptoms
Superinfection- increased severity of existing chronic hepatitis, increased fulminant hepatitis and cirrhosis
HDV Pathogenesis
Enters hepatocytes, Requires HBV infections
CAUSES CPE, also immune response culprable
HDV DIAGNOSIS Co INfection
Abs against HDV and HBcAg
HBsAg clears and appearance of anti-HBs
HDV DIAGNOSIS Superinfection
Persistence of HDV RNA and HBsAg for cronic
Lack of ANTI HBs
Total anti HDV mainly IgG, remain elevated.
HDV Treatment
Treat with HBV treatment
HDV Prevention
Vaccine for HBV protective against HDV
Hep C Virus
Flaviviridae \+ sense enveloped ssRNA Glycoprotein E1 E2 -enveloped Structural and non sturctural proteinsIFN resistance
HCV Replication
associates w/ LDL
LDL + Cellular GAGs
SRb1 and CD81
HCV Epidemiology
Six main genotypes
Genotype 1 most prevalent in US
Infected blood transmission
*HIGH RISK: transplant, IVDU
HCV Clinical
Acute and Chronic Hepatitis
INSIDIOUS ONSET-ACUTE
Chronic- doulbe fatality compared to HBV
HCV Pathogenesis
Production of antiviral and proinflammartory cytokines
Activate other antiviral genes
HCV Persistence
Block type I and type II IFN
Block production of antiviral cytokines
Block production of ISG proteins
IMMUNITY NOT LIFE LASTING
HCV Diagnosis
Detection of anti HCV antibodies
ELISA and RIBA
Recover= ALT levels; persistence of HCV RNA
Treatment HCV
Ribvirin
NS3/4a blockers
HCV Prevention
Education to prevent the spread of the virus
