Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Acute and Chronic Hepatitis > Flashcards

Acute and Chronic Hepatitis Flashcards

1
Q

How is Hep A transmitted?

A

Fecal-oral route.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When do viruses stop being shed in Hep A?

A

When jaundice resolves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Does HAV cause chronic infection?

A

No.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you diagnose HAV infection?

A

anti-HAV IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Is fulminant HAV infection common?

What are some risk factors for it?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does a positive Hep B surface Ag tell you?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

The patient is immune to HBV.

This could be due to vaccination or prior infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

The patient has an acute HBV infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

The patient has been exposed to HBV.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 prefered antivirals for HBV treatment?

A

Tenofovir
Entecavir
(these have the lowest rates of resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drug for HBV makes people really feel like crap?

A

Interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What’s the deal with Hep D?

A

Hep D depends on the person already having HBV infection.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Yeah - maybe 1 in 33.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do most people with HCV get infected?

Is sexual transmission common?

A

IV drug use.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Does the genotype for HCV matter?

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

A

Yes - treatment can vary with genotype.

Type 1 is the most common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Do Abs for HCV confer immunity?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

4 current HCV treatments?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is Hep E transmitted?

A

Fecal-oral route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Pregnant women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

Yeah.

25
Q

Does Hep E cause chronic infection?

A

”????”

26
Q

3 autoimmune liver diseases?

A

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

27
Q

Who gets autoimmune hepatitits?

A

Women (F:M = 4:1)

Bimodal age: 10-20 and 45-75

28
Q

Mortality rate of autoimmune hepatitis in symptomatic patients?

A

40%

29
Q

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

A

Type 1: ANA and/or SMA + others. (most common)

Type 2: LKM1 + SLA/LP.

30
Q

What does liver biopsy histology of autoimmune hepatitis look like?

A

Lymphocytosis and interface hepatitis- periportal necrosis.

+/- plasma cells

31
Q

Treatment for autoimmune hepatitis?

A

Prednisone +/- azathioprine.

32
Q

Do most people with Primary Biliary Cirrhosis have cirrhosis?

A

Nope, it’s a bullshit name.

33
Q

What is PBC actually?

A

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

34
Q

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

A

AMA (anti-mitochondrial antibody)

35
Q

What liver enzyme is elevated in PBC?

A

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

36
Q

Who gets PBC?

A

Women (F:M = 9:1)

Median age of diagosis = 50.

37
Q

Common presenting signs and symptoms of PBC?

A 
Fatigue
Pruritis
Hepatomegaly
Xanthelasmas - only in 10% of PBC cases.
(other things, like jaundice, hyperpigmentation, splenomegaly)
38
Q

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

A

Yup.

39
Q

How is definitive diagnosis of PBC made?

A

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

40
Q

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

A

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

41
Q

Treatment for PBC?

A 
Treat with Ursodiol.
Check Vits ADEK.
Assess for osteoporosis.
Treat hypercholesterolemia.
(Immunomodulators don't seem to work for PBC.)
42
Q

What’s a xanthelasma?

A

Cholesterol deposits in the skin around the eyes.

a subset of xanthomas - cholesterol deposits in skin

43
Q

What is primary sclerosing cholangitis (PSC)?

A

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

44
Q

How is PSC different from PBC?

A

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

45
Q

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

A

p-ANCA

46
Q

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

A

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

47
Q

What do the ducts look like in PSC histology?

A

Onion skin fibrosis.

48
Q

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

A

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

49
Q

What’s the really bad thing about PSC?

A

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

50
Q

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

A

CA19-9… but apparently that doesn’t work that well.

51
Q

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

A

12 years.

52
Q

2 examples of “intrinsic” drug-induced liver injury (DILI)?

Pattern of injury?

A

Acetominophen
Methotrexate
Pattern of injury = hepatitic

53
Q

What are some drugs that classically cause idiosyncratic DILI?

A

Augmentin and statins.

Pattern of injury = more cholestatic

54
Q

What’s the toxic metabolite from acetominophen breakdown?

A

NAPQI

55
Q

What do you need to break down NAPQI?

A

Glutathione

56
Q

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

A

N-acetylcysteine.

- this reduces mortality, even when given late.

57
Q

What’s Hy’s law?

A

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

58
Q

What class of drugs is most commonly implicated in DILI?

A

Antimicrobials (another reason not to overuse ABx)

GI (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions