Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

70 Cards in this Set

  • Front
  • Back
inflammation of the liver often clinically presents as ?
RUQ pain, jaundice, dark urine, pale stools
bilirubin pathway?
hemoglobin to heme to bilverdin to bilirubin (in plasma and is lipid soluble NOT water soluble, binds albumin and goes to the liver) to conjugated bilirubin via glucuronyl transferase in liver to the bile duct and then intestine. Intestinal bacteria make it into urobilinogens which make your poo brown!
in a patient with hepatitis what kind o bilirubin is increased and where is it increased? What will you see?
unconjugated bilirubin in plasma due to lack of glucuronyl transferase in inflammed liver as well as conjugated bilirubin due to a bile obstruction that usually happens with hepatitis. Thus dark urine from the extra bili and jaundice and yellow eyes
what aminotransferases are raised in hepatitis and which is more specefic to hepatocellular damage?
apartate and alanine (more liver specefic)
what in the labs will go up when the bile duct is obstructed?
alkaline phosphatase
T/F decreased PT time in hepatitis? Lab workup does not include blood smear.
false, it is increased
what are the enterically transmitted hepatitis viruses? Parenterally?
A and E. B, C, D.
what hepatitis viruses are associated with chronic diseaase?
all the ones that infect through the parenteral route (B,C,D)
in viral hepatitis, what is responsible for the hepatocyte death?
immune response
hosts for the hepatitis viruses? Culturability? Ability for study?
humans and SOME non human primates, very hard to grow except in tissue culture (usually human hepatocytes), thus VERY DIFFICULT to study
why are the hepatitis viruses so prone to mutation? What is the clinical significance of thiis?
most of them are RNA viruses which have a very high error rate and hep B (hepadna) uses a RT (RNA intermediate) which causes just as much error. This makes treatment with antiviral drugs very difficult.
describe the structure and biochemistry of hepatitis A virus.
picornavirus in hepatovirus genus. Non enveloped, icosahedral. Receptor is the TIM (t cell immunoglobulin mucin protein), + ssRNA with Vpg 5' and 3' poly A tail. One polyprotein made that is cleaved. Mature virions are released without killing the cell (little CPE)
in terms of epidemics from contaminated body fluids of Hep A, how do you get rid of it in the environment?
it is heat stable, resistant to low pH, resistant to solvents and detergents, BUT is inactivated by chlorinated drinking water.
how many serotypes of Hep A are there and what does infection confer upon the infected?
1 serotype and life long immunity
pathogenesis of Hep A?
enters via GI tract, to the blood, to the liver, replicates in hepatocytes and kupffer's cells (macs of liver), released into bile to the SI and to the poopoo. No CPE, damage to liver is immune mediated
stages of hep A infection?
ingestion, incubation from 15 to 50 days (mean of 4 wks) with virus out in the stool, preicteric (prodromal) stage is symptomatic with fever, loss of appetite, nausea, fatigue, ab pain, and lotsa virus out in the stool; icteric is less symptoms, liver damage and jaundice; convalescent is the recovery phase (99%) that takes about 8 weeks
in Hep A infections, what age groups get jaundice?
mainly those over 14, most others are asymptomatic
complications of Hep A infection?
fulminant hep (extensive necrosis - 80% mortality, 1-3/1000), relapsing hepatits (4-15 wks after initial symptoms but never becomes chronic), cholestatic hepatitis (total blockage of bile, high bilirubin levels)
diagnosis of HepA?
Sx, jaundice, elevated aminotransferases, serology: IgM present 5 to 10 days before onset of Sx and gone by about 6 months, IgG persist for life… EISA (best way to dx is by IgM)
treatment for Hep A?
immune serum globulin given before or early in incubation phase, supportive
hep A epidemiology?
contaminates whater, food (shellfish and other filterfeeders), hands via personal hygeine, (remember it is a fecal oraller)
how often is Hep A spread via blood and other IV drug use?
rare but does happen
describe hep A incidence.
on the downward trend mainly due to vaccinating kids
what is the Hep A vaccine?
adapted virus grown in human fibroblasts, inactivated, adsorbed to AlOH, kids over 1, there is a combined HAV/HBV vaccine (over 18)
how many serotypes exist for Hep B?
3 hep B antigens?
HBsAG (surface), HBcAg (core - capsid), HBeAg (pre-core, same transcript as core protein, secreted protein)
what is the infectious hep B virion called?
dane particle
describe what parts of the DNA genome of Hep B are ds and ss.
neg strand is more full length, pos is shorter, it is circular in the virion, have repeat regions that keep it circular
what particles are seen in pts with chronic hep B?
HBsAg and host cell lipid aggregated in either a spherical or fillamentous form
describe Hep B replication.
HBsAg binds membrane, endo or direct fusion, capsid to the nucleus, releases genome, DNA is repaired to ds COVALENTLY (not covalently linked before) closed circle. Txn to make 3 glycoprotein forms - L,M,S, all are put in the membrane, only S and M are secreted to form the aggregates - core protein, HBeAg (unknown function), RT, and X protein (unknown function but may be essential for replication). one mRNA genomic copy is packaged in cytoplasm with capsid and a RT, then RNA is copied to neg DNA, RNase H degrades RNA, DNA is copied to make the partially ds DNA genome, buds in the ER to get envelope and released by excocytosis. (note it may not release, it may go back to the nuc of same cell!!)
how is Hep B transmitted?
exposure to contaminated blood, blood components, semen, saliva, vaginal secretions; low levels in urine, feces, tears, breast milk
describe the vertical transmission of Hep B.
happens at birth or via breast milk
describe the acute infection of hep B. Include symptoms, pathogenesis, recovery, diagnosis.
45-80 day incubation, prodromal phase is insidious (slow and gradual onset vs abrupt of Hep A) with flu like symptoms, icteric phase is liver damage with jaundice, dark urine, pale stools, and RUQ pain; then recovery phase is renewed appetite. pathogenesis is from the immune system, virus is cleared by the immune response (interferons in mouse models...), fulminant hepatitis only occurs in 1% of the cases. initial serum levels that rise are HBsAg and HBeAg (amount of e depends upon amount of replication), symptoms are a few weeks latent to this and appear when IgM to the core antigen rises, reason no anti-HBsAg is bc there is so much HBsAg in the serum that all the antibodies to it get "mopped up" and no free Ab is seen, thus lots of anti-HBsAg complexes causing not a fun immune response. after Sx's wane, you will see antibody to surface antigen and IgG to the core antigen during the recovery phase. In the lab you would test for elevated liver enzymes, and HBsAg, HBeAg (amount tells how severe/amount of replication is going on), and anti-HBc IgM (tells you acute active infection that lasts for about 6 weeks).
describe chronic hep B pathogenesis and serology.
immune response is limited, but the virus is still in the liver persisting, Sx's are very mild to non-existant due to low immune response. Serologically there is HBsAg and anti HBc, HBeAg exists depending on how much division is going on, anti Hbe will only exist if there is a resolution immune response.
describe the long term effects of chronic Hep B.
can have asymptomatic carriage, immune complex disease from HBsAg/Ab complexes and complement activation with inflammation causing arthralgias and arthritis, glomerulonephritis, polyarteritis nodosa; chronic persistant hepatits (increased ALT), chronic active hepatitis leading to cirrhosis, and heptocellular carcinoma (30 to 30 yrs later, note the oddity that liver cancer cells usually have hep B genes integrated into them... )
what ages of initial infection are more likely to develop chronic infection? Clinical/acute infection?
infections from birth and the young. Adults
treatment for Hep B?
mainly supportive for acute bc only 1 to 2% become chronic, chronic ppl get intereferon or pegylated interferon, can add the analogs lamivudine, adeforvir, or entecavir.
persons at risk for Hep B?
immigrants from endemic regions (China, parts of Africa, Alaska, pacific islands), babies born to chronically infected mothers, IV drug users, promiscuous sex, patients requiring blood products, health-care workers
what is the Hep B vaccine made of?
surface antigens from yeasts
how was Hep C ID-ed?
entirely by molecular cloning.
who are Hep C hosts?
humans are natural host but can infect chimps
describe the classification and structure of hep C.
flavivirus, enveloped with a capsid, 2 glycoproteins, + ssRNA,
where does Hep C replicate?
hepatocytes and B lymphos, possibly T lymphos, binds to CD81 on lymphocytes
describe Hep C life cycle.
pos ssRNA, endocytosis, internal fusion, tsln, one protein, protein cleavage, RNA replication, packaging, intracellular B195envelopment, replication does not damage the cell.
how does Hep C have antigenic variation?
6 genotypes, 90 serotypes, lotsa mutations, one person can be infected with multiple quasispecies
populations at risk for Hep C?
parenteral transmission: individuals who received blood, blood products, or organ donations before testing began in 1991 , IV drug users are most at risk, babies born to infected moms (~6%), sex partners (not very common)
pathogenesis of Hep C?
incubation period is 2 to 26 wks (avg is 6 to 7 wks), liver damage from immune pathology, mild jaundice in 20%, 75-80% become chronic and in 70% can detect increased ALT, primary infections are mild symptomatically thus many are not noticed, cirrhosis in 20% of those that are chronic over 20 to 30 yrs, 25% of cirrhosis pts will have complete liver failure, 1 to 5 % of chronic infections will develop hepatocellular carcinoma
which hep virus is most common cause of liver transplant? What is the complication?
hep C, has reservoir of infection in the B cells thus liver may become diseased again after transplant
describe the stats of Hep C in US
200,000+ new infections/yr before 1991, now 20,000/yr; death from acute liver failure is rare, 40 to 60% of chronic liver disease is hep C related; chronic disease deaths are 8K to 10K/yr
Dx of Hep C?
clinical acute is similar to Hep A and B but milder; lab is ELISA for anti-capsid antigen (if + do it again) is main test, can do RT-PCR too
Hep C treatment?
INF alpha monotherapy (efficacy depends on virus genotype), pegylated interferon/ribavirin combo (again efficacy depends upon virus genome); eliminate alcohol consumption
factors that promote progression or severity of Hep C?
increased alcohol intake, over 40 at time of infection (faster progression to chronic), male, chronic Hep B or HIV infection bc of similar transmission routes
routine testing for Hep C is recommended for what populations?
ever injected illegal drugs, received clotting factors made before 1987, received blood/organs before July 1992, ever on chronic hemodialysis, evidence of liver disease, children born to Hep C pos women
what virus fam is Hep D in? serotypes? Properties of this virus?
deltavirus, one serotype, looks like a viroid, neg sense closed circular ssRNA, with extensive pairing to form a rod like structure, can only replicate in the presence of Hep B virus, one protein which is HDAg that binds the RNA and virus needs HBsAg to form the fully enveloped virion, HDAg and genome go to nucleus where it use host RNA pol II for replication
describe Hep D pathogenesis.
infects or superinfects concurrent Hep B ppl. Concurrent infection can lead to severe acute disease with a low risk of chronic infection (will die or recover), super infection carries a high risk for fulminant hepatits or chronic infection that progresses rapidly to cirrhosis
Dx for Hep D?
anti to HDAg, PCR for Hep D RNA
Hep D treatment?
not very successful - IFN alpha - relapse upon cessation of treatment.
Hep D epidemiology?
man is host, WW, rarer than Hep B but in some places 60% of Hep B's have Hep D, not common in US
vaccine for Hep D?
transmission of HepE?
serotypes of Hep E?
hosts of Hep E?
humans only
virus fam and structure of Hep E?
used to be in calici now on its own, icos capsid, no envelope, + ssRNA, replicates like calici
where does Hep E replicate?
hepatocytes in vivo
what is the assumed lifecycle of Hep E (assumed bc it has not been grown yet)?
primary txn yields one protein, cleavage for the non structurals, txn to neg strand, secondary txn makes 2 subgenomic mRNAs that encode structural proteins, replication from neg template, nothing known about assembly
pathogenesis of Hep E?
oral ingestion, infects liver, incubates 2 to 8 weeks, virus in poopoo (5 wks post exposure), sheds for 2 wks
descrieb Hep E disease and diagnosis.
clinical it has a similar presentation as Hep A, acute only, no chronic, Lab Dx is anti HepE IgM or IgG
Hep E complications?
expect full recovery, higher mortality then Hep A, 1 to 2% mortality, pregnant females have 20% mortality rate for some reason
treatment of Hep E?
supportive, control by checking contaminated water
Hep E epi?
outbreaks in fecally contaminated water, minimal person to person transmission, US cases are usually from travel to endemic areas, closely related virus in swine in the US that may infect humans and probly accounts for some individuals in US having anti Hep E antibodies, mainly in Africa and Asia