18.2 Flashcards
what are morphological features of acute hepatits
necrosis - empty cytoplasm w/ few remnants & rupture of cell membrane → dropout hepatocytes → collapsed sinusoidal collagen
- If severe acute hep- confluent necrosis around central V (cellular debris, collapsed reticulin, congestion/hemorrhage, variable inflam → could lead to parenchymal collapse
apoptosis - hepatocytes shrink, pyknotic and fragmented.
what is the morphology of chronic hepatitis
mononuclear portal infiltration
portal lymphocytes (lymphoplasmacytic) inflam w/ fibrosis
Interface hepatitis - aka piecemeal necrosis is associated w/ lymphocytic infiltrate into adjacent parenchyma and w/ destruction of individual hepatocytes along the edges of the portal tract (can also be seen in AI hep and steatohepatitis)
Progressive hallmark = scarring
HAV
type:
viral fam
incubation
defining characterisitics
nonenveloped (+) ssRNA,
picornavirus/Hepatovirus.
incubation period of 2-6 weeks
benign and self-limiting/ does NOT cause chronic hepatitis or have a carrier state/ rarely causes acute hepatic failure (AHF)/ fatality is very low
what is the transmission and prevalance of HAV
endemic in areas of poor sanitation and hygiene.
ingestion of contaminated water/food (fecal-oral), shed in stool for 2-3 weeks.
Outbreaks can be seen in schools, nurseries, water-borne epidemic areas, places of overcrowding and poor sanitation.
developed countries- consumption of raw/steamed shellfish, which concentrate from seawater contaminated w/ human sewage
May occur via sexual transmission and blood borne (rare, do not need to screen donated blood for this).
DOES NOT occur w/ vertical transmission.
In the USA, the chance of getting HAV increases w/ age, reaching to 50% by age of 50 y/o.
what is the presentation of HAV
sxs & extrahepatic sxs
sporadic febrile illness and present w/ nonspecific symptoms (loss of appetite, fatigue, jaundice)
Extrahepatic manifestations = rash, arthralgia, immune complex mediated complications like leukocytoclastic vasculitis, glomerulonephritis and cryoglobulinemia
Acute liver failure in 0.1-0.3% pt, esp if other causes of CLD. uncommon complication = prolonged cholestasis and relapse of dz w/i 6 months
how do you test and treat HAV
Test for IgM Ab against HAV, which presents w/ onset of symptoms and reduces in a few months. IgG anti-HAV present when resolved.
Most pt resolve w/i 3 months and resolution in nearly all pt by 6 months.
Vaccine = effective in preventing HAV
HBV
type
family
incubation
partially dsDNA virus
hepadnaviridae
Incubation period includes 2-26 weeks
what are the possible outcomes of HBV
- Acute hep w/ recovery/clearance
- Non-progressive chronic hep → HCC
- Progressive chronic hep → HCC
- AHF w/ massive necrosis
- Asymptomatic carrier.
what is the transmission and prevalence of HBV
most prevalent in Asia and W. pacificmost transmission occurs vertically during childbirth
intermediately prevalent in S & E Europe -ansmission occurs horizontally, esp in early childhood.
lowest in W. Europe, USA and Australia- the transmission is due to IV drugs/unprotected sex. In USA 10% of HIV pt are coinfected w/ HBV
what determines the outcome of HBV
Host immune response to virus is the main determinant of the outcome of the infxn.
High-level replication and production of viral protein → cytopathic changes in infected cells. But most hepatocyte injury is caused by CD8+ cytotoxic T cells attacking infected cells. A strong response by CD4+ and CD8+ IFN-g-producing cells = resolution of acute infxn
what are the serum markers for HBV
explain the significance of each
HBsAg, refer to 3 related viral envelope glycoproteins, large, middle and small HBsAG. Large is associated w/ complete virions, while small is released by infected hepatocytes free of viral core element
HBV Pol (DNA pol & reverse transcriptase activity)
Anti-HB Abs rise after acute dz is over and HBsAg disappears. In some cases anti-HBs Ab doesn’t present until months after HBsAg is gone- at these times the Dx can be made by IgM antiHBc AB. In chronic HBV, anti-HBsAB are not made, these can be associated with persistent elevations of serum transaminases.
HBcAG is a nucelocapsid protein, which plays a role in assembly of complete virions and a longer polypeptide transcript w/ a precore and core region (HBeAg)
Anti-HBe Ab represents acute infxn has peaked and is now waning
what is the histological feature of HBV
Ground-glass hepatocytes w/ ER swollen by HBsAg
= hallmark for Dx of chronic hep B
what determines the potential to become chronic for HBV
Age at the time of infxn is the best predictor of chronicity; younger = higher change of chronicity( therefore babies that acquire the virus from mothers at birth and get chronic HBV, have the greatest risk of HCC)
how do you treat HBV
Most HBV cases are self-limited and resolve w/o Tx.
Goal of Tx of chronic HBV w/ IFN and antiviral agents → slow progression, reduce liver damage, prevent cirrhosis or CA, but cannot completely cure.
Vaccine available to PREVENT. The basis of the vaccination is using noninfectious HBsAg to induce anti-HBs Ab, since these persist for life and confer protection.
HCV
type
family
incubation
defining feature
ssRNA, enveloped,
flaviviridae
Incubation ranges from 4-26 weeks
MCC of chronic viral hep
