Acute and Chronic Hepatitis

Question 1

How is Hep A transmitted?

Answer 1

Fecal-oral route.

Question 2

When do viruses stop being shed in Hep A?

Answer 2

When jaundice resolves.

Question 3

Does HAV cause chronic infection?

Answer 3

No.

Question 4

How do you diagnose HAV infection?

Answer 4

anti-HAV IgM

Question 5

Is fulminant HAV infection common?

What are some risk factors for it?

Answer 5

No, fulminant infection is rare.
Age >40.
Chronic liver disease.

Question 6

What percentage of adults infected with HBV develop chronic infection?
How about children infected with HBV?

Answer 6

Only about 5%.
About 90% of children infected with HBV develop chronic infection.
(this is important)

Question 7

What does a positive Hep B surface Ag tell you?

Answer 7

The patient is infected with HBV, because this shows that the actual virus is there.
It could be acute or chronic.

Question 8

What does a positive anti-Hep B surface antibody tell you?

Answer 8

The patient is immune to HBV.

This could be due to vaccination or prior infection.

Question 9

What does a positive anti-Heb B core IgM tell you?

Answer 9

The patient has an acute HBV infection.

Question 10

What does a positive anti-Heb B core IgG tell you?

Answer 10

The patient has been exposed to HBV.

Could be acute, chronic, or cleared infection, depending on other test values.

Question 11

What are the 2 prefered antivirals for HBV treatment?

Answer 11

Tenofovir
Entecavir
(these have the lowest rates of resistance)

Question 12

What drug for HBV makes people really feel like crap?

Answer 12

Interferon

Question 13

What do you do to kids born to moms with HBV infection?

Answer 13

Right at birth:
Give HBIG (Hep B immunoglobulin)
Vaccinate

Question 14

What’s the deal with Hep D?

Answer 14

Hep D depends on the person already having HBV infection.

Increases risk of severe liver diseas from 4% with HBV alone to 34%.

Question 15

Are a lot of Americans born between 1945-1965 infected with HCV?

Answer 15

Yeah - maybe 1 in 33.

Question 16

How do most people with HCV get infected?

Is sexual transmission common?

Answer 16

IV drug use.

Sexual transmission seems actually to be very rare (despite what the chart says?).

Question 17

Does the genotype for HCV matter?

What’s the most common genotype in the US (and the world)?

Answer 17

Yes - treatment can vary with genotype.

Type 1 is the most common.

Question 18

What percentage of people infected with HCV clear it right away?

Answer 18

20%

Question 19

Do Abs for HCV confer immunity?

Answer 19

No. But they’re useful for testing for HCV.

Question 20

New cases of HCV are on the decline, but peaks in what diseases haven’t hit us yet?

Answer 20

Hepatocellular carcinoma and decompensated cirrhosis is expected to peak in 2020.

Question 21

4 current HCV treatments?

Answer 21

Interferon
Ribavirin
Antivirals: Telaprevir and Boceprevir
(but more are on the way)

Question 22

How is Hep E transmitted?

Answer 22

Fecal-oral route

Question 23

Who is particularly at risk for fulminant hepatitis when infected with Hep E?

Answer 23

Pregnant women.

Question 24

Do people shed Hep E virus in their stool before they’re symptomatic?

Answer 24

Yeah.

Question 25

Does Hep E cause chronic infection?

Answer 25

"????"

Question 26

3 autoimmune liver diseases?

Answer 26

Autoimmune hepatitis Primary Biliary Cirrhosis (PBC) Primary Sclerosing Cholangitis (PSC)

Question 27

Who gets autoimmune hepatitits?

Answer 27

Women (F:M = 4:1) | Bimodal age: 10-20 and 45-75

Question 28

Mortality rate of autoimmune hepatitis in symptomatic patients?

Answer 28

40%

Question 29

What are the 2 auto-Ab classifications of autoimmune hepatitis? Which is most common?

Answer 29

Type 1: ANA and/or SMA + others. (most common) | Type 2: LKM1 + SLA/LP.

Question 30

What does liver biopsy histology of autoimmune hepatitis look like?

Answer 30

Lymphocytosis and interface hepatitis- periportal necrosis. | +/- plasma cells

Question 31

Treatment for autoimmune hepatitis?

Answer 31

Prednisone +/- azathioprine.

Question 32

Do most people with Primary Biliary Cirrhosis have cirrhosis?

Answer 32

Nope, it's a bullshit name.

Question 33

What is PBC actually?

Answer 33

Inflammation and destruction of interlobular and septal bile ducts -> chronic cholestasis, and sometime cirrhosis.

Question 34

What antibody do patients with PBC have almost all the time?

Answer 34

AMA (anti-mitochondrial antibody)

Question 35

What liver enzyme is elevated in PBC?

Answer 35

Alkaline phosphatase - often elevated before patients are symptomatic. (GGT will be elevated, too)

Question 36

Who gets PBC?

Answer 36

Women (F:M = 9:1) | Median age of diagosis = 50.

Question 37

Common presenting signs and symptoms of PBC?

Answer 37

``` Fatigue Pruritis Hepatomegaly Xanthelasmas - only in 10% of PBC cases. (other things, like jaundice, hyperpigmentation, splenomegaly) ```

Question 38

Do Sicca syndrome, arthritis, and other autoimmune things commonly co-occur with PBC?

Answer 38

Yup.

Question 39

How is definitive diagnosis of PBC made?

Answer 39

Liver biopsy showing damage to bile ducts, ductopenia, and noncaseating granulomas.

Question 40

What does PBC look like on imaging? (eg. MRCP)

Answer 40

Livers with PBC look normal - unless it has progressed to cirrhosis.

Question 41

Treatment for PBC?

Answer 41

``` Treat with Ursodiol. Check Vits ADEK. Assess for osteoporosis. Treat hypercholesterolemia. (Immunomodulators don't seem to work for PBC.) ```

Question 42

What's a xanthelasma?

Answer 42

Cholesterol deposits in the skin around the eyes. | a subset of xanthomas - cholesterol deposits in skin

Question 43

What is primary sclerosing cholangitis (PSC)?

Answer 43

Cholestatic liver disease with inflammation and fibrosis of the biliary tree.

Question 44

How is PSC different from PBC?

Answer 44

PSC is more aggressive, affects men more (M:F = 2:1), and can be diagnosed with imaging.

Question 45

What antibody do over 80% of people with PSC have?

Answer 45

p-ANCA

Question 46

What does PSC look like on cholangiogram? (ERCP or MRCP)

Answer 46

"beads on a string" - alternating areas of stricture and dilation.

Question 47

What do the ducts look like in PSC histology?

Answer 47

Onion skin fibrosis.

Question 48

What GI condition to 80% of patients with PSC have?

Answer 48

IBD (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

Question 49

What's the really bad thing about PSC?

Answer 49

There's up to a 30% chance of developing cholangiocarcinoma.

Question 50

What can you measure to screen for cholangiocarcinoma in PSC patients?

Answer 50

CA19-9... but apparently that doesn't work that well.

Question 51

What is the mean survival with PSC if symptomatic at diagnosis?

Answer 51

12 years.

Question 52

2 examples of "intrinsic" drug-induced liver injury (DILI)? | Pattern of injury?

Answer 52

Acetominophen Methotrexate Pattern of injury = hepatitic

Question 53

What are some drugs that classically cause idiosyncratic DILI?

Answer 53

Augmentin and statins. | Pattern of injury = more cholestatic

Question 54

What's the toxic metabolite from acetominophen breakdown?

Answer 54

NAPQI

Question 55

What do you need to break down NAPQI?

Answer 55

Glutathione

Question 56

What can you give someone who overdosed on acetominophen to replenish their glutathione?

Answer 56

N-acetylcysteine. | - this reduces mortality, even when given late.

Question 57

What's Hy's law?

Answer 57

Hepatocellular DILI with jaundice has higher mortality - about 10%.

Question 58

What class of drugs is most commonly implicated in DILI?

Answer 58

Antimicrobials (another reason not to overuse ABx)