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45 Cards in this Set
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Causes of hepatic inflammation |
viral hep
alcohol
fat
medications
toxins
autoimmune |
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causes of VIRAL hepatitis |
A-G
Etc, EBV and CMV |
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Exposure to viral hep |
is variable, can have no symptoms and spontaneously resolve from infection
OR
lead to fulminant liver failure; or chronic infection cirrhosis symptoms and death |
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acute vs chronic hep |
acute; follows infection by relatively short incubation period, symptoms and signs are more common, usually resolves without sequele
chronic; definition is 6 mo. of infection, can lead to advanced liver injury/scar, SHOW FEW symptoms until CIRRHOSIS |
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Hep A |
Picornaviridae RNA virus
acute catarrhal jaundice, campaign jaundice, epidemic jaundice
prevalence 20-40% of viral hepatitis in the US, currently uncommon in WNY, NHANES # seroprevalence, overall 34% and 10% age 5 75% greater then 50 |
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Hep A transmission |
enteric transmission (fecal-oral)
risk factors; poor hygiene, crowded conditions, sewage
people at risk, Low SES, MSM, military recruits children in day care |
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Hep A clinical |
incubation period about 30 days
clinical course is usually mild - especially in children
resolves spontaneously
no chronic phase |
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Hep A Dx |
viral particles in stool - impractical
serum antibodies against viral proteins; ANTI-HAV IgM shows recent infection, IgG shows remote infection
liver biopsy not needed
spike in bilirubin and ALT starting around 30 days post |
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Hep A prognosis |
1-2 weeks of symptoms
99% resolve spon.
occasional death from fulminant failure = the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver disease |
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Treatment of Acute Viral Hepatitis |
no specific treatments
no special diet
rest
observe for clincial deterioration, consider measures to prevent spread; hygiene, IgG and vaccincation |
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Prevention of Hep A |
plumbing, hygiene, pre and post exposure propylaxis
Vaccine; 2 doses, long lasting protection |
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Hep B |
hepadnaviridae
DNA virus
CAN insert into the human genome |
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Hep B Epid |
prevalance worldwide 300 million infected, 1 millions deaths per year
USA, 1.2 million infected, dramatic recent decline in acute hep B
incidence in the US is declining |
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Distribution of Hep B |
majority Asian/Pacific islander, then white then black |
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Hep B transmission |
blood and body fluids, peri-natal number 1 in the world, but sex is number 1 in US
groups at risk are immigrants from endemic areas, IVDA, MSM, sexually promiscuous, transfusion, developmentally delayed
HEALTH CARE WORKERS! |
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Hep B presentation |
incubation period about 90 days
symptoms are more common in adults then children, majority are asymptomatic
patients improve in 1-3 weeks 95% will recover 1% will die 5% will develop chronic |
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Hep B Dx |
viral proteins, HBV core antigen is only in the liver tissue, HBV surface antigen is in serum, indicative of the ongoing infection |
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Hep B Dx |
antibodies against viral proteins with IgM/IgG distribution showing the recency
anti-Hbc
anti-HBs past infection of VACCINATION
BUT, Mutants are present E ANTIGEN
HBeAg suggests aggresive infection, and develop anti HBe |
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Hep B Dx contd |
HBV DNA is the gold standard test
correlation with outcomes, can determine mutant viruses, monitor for treatment |
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Hep B genotypes |
Eight different genotypes
A-H
genotype C might be more aggresive, the true significance is not known |
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Dx Summary |
Infection = HBsAG +, Anti HBs - , Anti-HBc IgM recent and IgG longstanding
Resolved infectio; HBsAg- , Anti-HBs +, Anti-HBc IgG +
Vaccinated; Anti-HBs + |
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Hep B time course |
Infection with Recovery; surface takes longer to develop antibodies against, peak in HBsAg in 12 weeks post, anti-Hbc IgM peaks at 16 weeks with IgG coming after 2 weeks later, Anti-Hbs peaks at 34 week
Infection to Chronic; no generation of anti Hbs antibodies and HbeAg persists with anti-HBe abs not developed for years [HBe is produced and secerted into the bloodstream and is an indicator of an agressive actively replicating virus] |
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Hep B immune tolerant |
typically seen in Asians infected at birth
have high levels of DNA, HbSAg, ABeAg positive, little liver injury, liver tests normal, no symptoms |
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Hep B immune clearance phase |
Westerner's infected as adults, immune system attacks infected cells and liver tests are elevated, inflammation may lead to cirhossis |
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Hep B quiescent phase |
nearly normal liver enzymes, HBsAg positive, but HBeAg negative with anti HBe Abs, HBV DNA negative or very low
chronic healthy carriers |
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HBV cccDNA |
closed, covalent, circular
in hepatocyte nucleus
very stable and persistant, cells need to die can't treat |
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Hep B Rx |
acute = no treatment
chronic = interferon, lamivudine, adefovir, entecavir, tenofovir, telbivudine |
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Hep B prevention |
avoid exposure to blood and body fluids
pre-exposure prophylaxis; recombinant vaccine HBsAg
post-exposure prophylaxis (develop an immune response quickly) Hep B hyper Ig or vaccinate |
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Hepatocellular carcinoma |
primary tumor of liver cells
may complicate any longstanding liver disease, HBV or cirrhosis
screening serum alpha fetoprotein |
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Hep B oncogenesis |
integration of the viral genome into the host; random insertion into the human may result in the genomic instability that leads to tumorgenesis
Hep B virus X gene product, acts as a transcriptional transacvtivator of host MYC genes that control cell growth |
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Hepatitis D |
smallest known virus that infects man
resembles plant viruses
degenerate needs Hep B surface antigen to enter hepatocytes |
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Hep B with Hep D |
acute co infection
super infection on top of chronic hep B
diagnosis; HBsAg, anti HDV, HDV rna
treatment; interferon but doesnt work well, poor prognosis |
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Immune pathogenesis |
under most conditions doesnt lead to cell death, but the immune response to viral antigens is either kill liver cells or kill the virus
CD8 recognize the complexed MHC I after processing
however cytotoxic defect where an antibody can block the binding of the T cell with the Ag can allow supressor T cells to prevent cell death |
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Hep C |
0.6-2.4% of the US population
3.8 million americans infected
15-20 thousand in WNY, 18% of Nam era vets
more than 500 million worldwilde |
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Hep C transmission |
Needle sharing
blood transfusion
nasal cocaine, tattoos, health care workers |
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Hep C presentation |
60 days, acute is mild, chronic is very common, symptoms and signs are few until advanced disease, screen at risk at birth |
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Hep C Dx |
elevated aminotransferases, antibodies to HCV proteins, antibodies to HCV proteins
confirm infection with molecular tests |
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Dx testing |
ELISA 90% in high risk 50% predicitve power in low risk
PCR or bDNA tests, expensive but can indicate a current infection
HCV genotype, non-one genotypes do best of the 6 diff, but non-one are uncommon in US |
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Hep Epidem |
Hep B and C are the most deadly, C the most common, mortality increases with age
predictors of poor prognosis; alcohol use, acquistion via transfusion, male gender
Hep C patients very few die of liver disease or will develop symptoms because of the slowness of the chronic phase |
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Hep C mgmt |
reassure/educate
avoid alcohol
consider specific treatment, long acting interferon. ribavirin, telaprevir |
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Direct acting antivirals |
several drugs have just been approved
used in combo
nearly 100% cure of infection
minimal side effects |
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Sofosbuvir |
1000 dollars a pill
can cost 84-160 thousand per course of treatment |
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Hep E |
enteric transmitted Non A non A hep
very uncommon in US common in third world clinically very similar to hep A excellent prognosis except in women |
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Hep F |
no such animal
fulminant
pretty uncommon
poor prognosis
transplant often neede |
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Hep B |
isolated from the blood of a surgeon
common
a cause of hepatic inflammation or an innocent bystander?
suppressed HIV replication |
