Flashcards in Acute and Chronic Hepatitis Deck (58):
How is Hep A transmitted?
When do viruses stop being shed in Hep A?
When jaundice resolves.
Does HAV cause chronic infection?
How do you diagnose HAV infection?
Is fulminant HAV infection common?
What are some risk factors for it?
No, fulminant infection is rare.
Chronic liver disease.
What percentage of adults infected with HBV develop chronic infection?
How about children infected with HBV?
Only about 5%.
About 90% of children infected with HBV develop chronic infection.
(this is important)
What does a positive Hep B surface Ag tell you?
The patient is infected with HBV, because this shows that the actual virus is there.
It could be acute or chronic.
What does a positive anti-Hep B surface antibody tell you?
The patient is immune to HBV.
This could be due to vaccination or prior infection.
What does a positive anti-Heb B core IgM tell you?
The patient has an acute HBV infection.
What does a positive anti-Heb B core IgG tell you?
The patient has been exposed to HBV.
(Could be acute, chronic, or cleared infection, depending on other test values.)
What are the 2 prefered antivirals for HBV treatment?
(these have the lowest rates of resistance)
What drug for HBV makes people really feel like crap?
What do you do to kids born to moms with HBV infection?
Right at birth:
Give HBIG (Hep B immunoglobulin)
What's the deal with Hep D?
Hep D depends on the person already having HBV infection.
Increases risk of severe liver diseas from 4% with HBV alone to 34%.
Are a lot of Americans born between 1945-1965 infected with HCV?
Yeah - maybe 1 in 33.
How do most people with HCV get infected?
Is sexual transmission common?
IV drug use.
Sexual transmission seems actually to be very rare (despite what the chart says?).
Does the genotype for HCV matter?
What's the most common genotype in the US (and the world)?
Yes - treatment can vary with genotype.
Type 1 is the most common.
What percentage of people infected with HCV clear it right away?
Do Abs for HCV confer immunity?
No. But they're useful for testing for HCV.
New cases of HCV are on the decline, but peaks in what diseases haven't hit us yet?
Hepatocellular carcinoma and decompensated cirrhosis is expected to peak in 2020.
4 current HCV treatments?
Antivirals: Telaprevir and Boceprevir
(but more are on the way)
How is Hep E transmitted?
Who is particularly at risk for fulminant hepatitis when infected with Hep E?
Do people shed Hep E virus in their stool before they're symptomatic?
Does Hep E cause chronic infection?
3 autoimmune liver diseases?
Primary Biliary Cirrhosis (PBC)
Primary Sclerosing Cholangitis (PSC)
Who gets autoimmune hepatitits?
Women (F:M = 4:1)
Bimodal age: 10-20 and 45-75
Mortality rate of autoimmune hepatitis in symptomatic patients?
What are the 2 auto-Ab classifications of autoimmune hepatitis? Which is most common?
Type 1: ANA and/or SMA + others. (most common)
Type 2: LKM1 + SLA/LP.
What does liver biopsy histology of autoimmune hepatitis look like?
Lymphocytosis and interface hepatitis- periportal necrosis.
+/- plasma cells
Treatment for autoimmune hepatitis?
Prednisone +/- azathioprine.
Do most people with Primary Biliary Cirrhosis have cirrhosis?
Nope, it's a bullshit name.
What is PBC actually?
Inflammation and destruction of interlobular and septal bile ducts -> chronic cholestasis, and sometime cirrhosis.
What antibody do patients with PBC have almost all the time?
AMA (anti-mitochondrial antibody)
What liver enzyme is elevated in PBC?
Alkaline phosphatase - often elevated before patients are symptomatic.
(GGT will be elevated, too)
Who gets PBC?
Women (F:M = 9:1)
Median age of diagosis = 50.
Common presenting signs and symptoms of PBC?
Xanthelasmas - only in 10% of PBC cases.
(other things, like jaundice, hyperpigmentation, splenomegaly)
Do Sicca syndrome, arthritis, and other autoimmune things commonly co-occur with PBC?
How is definitive diagnosis of PBC made?
Liver biopsy showing damage to bile ducts, ductopenia, and noncaseating granulomas.
What does PBC look like on imaging? (eg. MRCP)
Livers with PBC look normal - unless it has progressed to cirrhosis.
Treatment for PBC?
Treat with Ursodiol.
Check Vits ADEK.
Assess for osteoporosis.
(Immunomodulators don't seem to work for PBC.)
What's a xanthelasma?
Cholesterol deposits in the skin around the eyes.
(a subset of xanthomas - cholesterol deposits in skin)
What is primary sclerosing cholangitis (PSC)?
Cholestatic liver disease with inflammation and fibrosis of the biliary tree.
How is PSC different from PBC?
PSC is more aggressive, affects men more (M:F = 2:1), and can be diagnosed with imaging.
What antibody do over 80% of people with PSC have?
What does PSC look like on cholangiogram? (ERCP or MRCP)
"beads on a string" - alternating areas of stricture and dilation.
What do the ducts look like in PSC histology?
Onion skin fibrosis.
What GI condition to 80% of patients with PSC have?
(note that the converse is not true - but 5-7% of UC and 3% of CD patients have PSC)
- and an increased risk of colon cancer
What's the really bad thing about PSC?
There's up to a 30% chance of developing cholangiocarcinoma.
What can you measure to screen for cholangiocarcinoma in PSC patients?
CA19-9... but apparently that doesn't work that well.
What is the mean survival with PSC if symptomatic at diagnosis?
2 examples of "intrinsic" drug-induced liver injury (DILI)?
Pattern of injury?
Pattern of injury = hepatitic
What are some drugs that classically cause idiosyncratic DILI?
Augmentin and statins.
Pattern of injury = more cholestatic
What's the toxic metabolite from acetominophen breakdown?
What do you need to break down NAPQI?
What can you give someone who overdosed on acetominophen to replenish their glutathione?
- this reduces mortality, even when given late.
What's Hy's law?
Hepatocellular DILI with jaundice has higher mortality - about 10%.