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GI Week 4 > Lecture 36: Acute and Chronic Hepatitis > Flashcards

Lecture 36: Acute and Chronic Hepatitis Flashcards

1
Q

What are the characteristics of hepatitis A?

A

Most common cause of viral hepatitis world wide
Acute infection ONLY
Absorbed in the intestine and replicates n hepatocyte
Transmitted fecal-oral

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2
Q

How many people in world have hepatitis B?

A

5% in the world, over 300 million

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3
Q

If you get infected by hepatitis B as an ADULT, how many go to chronic cases?

A

Only 5%

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4
Q

If you get infected by hepatitis B as a CHILD, how many go on to chronic cases?

A

Over 90%!!

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5
Q

What percentage of infants/children who are NEWLY infected with HBV go on to chronic cases?

A

90%!!

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6
Q

What percentage of adults who are NEWLY infected with HBV go on to chronic cases?

A

5%!!

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7
Q

If someone has chronic HBV, they most likely contracted HBV when they were?

A 
A child (90% chance)
Rather than an adult (5%)
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8
Q

What is the serology for Acute HBV?

A

HbsAg +
HbsAb -
HbcoreAb + (IgM)

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9
Q

What is the serology for VACCINATED against HBV?

A

Everything negative EXCEPT for HepBsurfaceAb or HbsAb +

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10
Q

What does the presence of Hep B surface antibody mean?

A

It means that you are VACCINATED or CLEARED the infection

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11
Q

What is the serology for chronic HBV?

A

HBV DNA elevated

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12
Q

What is the treatment for hepatitis B?

A
  1. Tenofovir
  2. Entecavir
  3. Interferon
  4. Adefovir
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13
Q

What are the characteristics of Hepatitis D?

A

Aka the DELTA agent
It will NOT replicate UNLESS there is hepatitis B present
Coinfection with hepatitis B = 34% vs. 5% of fulminant liver failure

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14
Q

What is the relationship between hepatitis B and D?

A

You cant have hepatitis D without hepatitis B

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15
Q

How is HepD spread?

A

Percutaneous exposure

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16
Q

How many people have hepatitis C?

A

3-5 million Americans
1:33 americans between 1945-1965
Gotten through injecting drug use

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17
Q

How many people can CLEAR the hepatitis C infection acutely

A

Only 20%

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18
Q

What is decompensated liver disease?

A

When you have SIGNS AND SYMPTOMS of liver failure
The worse sequelae to cirrhosis
Liver disease in which the liver is damaged and not functioning normally
Compensated liver = you see no signs and symptoms of end stage liver disease

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19
Q

What is the treatment for HCV?

A

Interferon
Ribavirin
Telaprevir and Boceprevir

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20
Q

What is important to remember about hepatitis E?

A

Think about hepatitis E in pregnant women
21% chance of fulminant hepatits the further you are into pregnancy
Most patients clear HEV

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21
Q

What are the characteristics of Hepatitis E?

A

RNA virus
Most common cause of epidemic enterically transmitted hepatitis
Fecal-oral transmission

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22
Q

What is the treatment of HEV?

A

Ribavirin

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23
Q

What are the three types of autoimmune liver disease?

A
  1. Autoimmune hepatitis
  2. Primary Biliary Cirrhosis
  3. Primary Sclerosing Cholangitis
24
Q

What is autoimmune hepatitis?

A

Syndrome of progressive hepatitis characterized by loss of tolerance to hepatic autoantigens that results in

- hepatocellular necroinflammation
- Autoantibodies
- hypergammaglobulinemia and/or increased IgG
- non-pathognomic hstopathology
- responsiveness to immunosuppressive medications
25
Q

What is the epidemiology of autoimmune hepatitis?

A

Uncommon cause
F:M ratio = 4:1
Bimodal distribution = 10 years and 45 years of age
40% mortality in symptomatic patients

26
Q

What is the clinical spectrum of autoimmune hepatitis?

A
  1. acute hepatitis
    • 25-30%, younger, ICTERIC actue viral hepatitis
  2. Asymptomatic
    • extraheaptic manifestaitons can present
  3. Fulminant hepatic FAILURE
    • around 5%
27
Q

What are the two types of autoimmune hepatitis (AIH)?

A

Type 1
Type 2
Type 3 (no autoantibodies associated with it, may be a null category)

28
Q

What are types of antibodies associated with type1/2 AIH? Significance?

A

Type 1 = ANA and SLA
Type 2 = LKM1 and SLA/LP
Type 2 antibodies (LKMI and LA/LP) are MUCH MORE LIKELY to present with other autoimmune diseases

29
Q

What is the treatment for autoimmune hepatitis?

A
  1. Prednisone

2. Azathioprine (immunomodulator, decreases DNA synthesis)

30
Q

What are the characteristics of primary biliary cirrhosis?

A
  1. Ongoing inflammatory destruction of the interlobular and septal bile ducts which leads to chronic cholestasis and biliary cirrhosis
  2. triggered by autoantigens and can produce antibodies such as AMA
  3. Misnomer because most patients don’t actually have cirrhosis
  4. Antimitochondrial antibody (AMA), 90-95% of patients have a positive AMA
  5. usually the CT or MRI is normal!
31
Q

Why is Primary Biliary Cirrhosis a misnomer?

A

Because PATIENTS DON’T ACTUALLY HAVE CIRRHOSIS MOTHERFUCKER!!!

32
Q

What is the antibody that is associated with PBC?

A

AntiMitochondrial Antibody
AMA is present in 90-95% of all patients
If you have AMA, it is A HIGH FUCKING RISK FACTOR for PBC
So if you have AMA then you will eventually get PBC

33
Q

What is the epidemiology of PBC?

A

F:M = 9:1
50 years agoe of onset
Has elevated ALKALINE PHOSPHATASE

34
Q

What are the signs and symptoms of PBC?

A
  1. Fatigue
  2. Pruritus
  3. jaundice
  4. HYPERpigmentation
  5. hepato/splenomegaly
  6. Xanthelasma
  7. Sicca syndrome
  8. Arthritis
  9. Scleroderma
    AUTOIMMUNE SHIT
  10. Lichen planus, discoid lupus, pemphigoid
35
Q

What is Xanthelasma?

A

Sharply demarcated yellowish deposit of fat underneath the skin of the EYELIDS

36
Q

What is the treatment of PBC?

A
  1. Ursodiol

Assess for fat soluble vitamins and osteoporosis

37
Q

What are the fat soluble vitamins? Significance?

A

A, D, E and K

Need to check for these deficiencies in folks with PBC

38
Q

What are the characteristics primary sclerosing cholangitis?

A
  1. Chronic Cholestatic liver disease of unknown etiology characterized by inflammation and fibrosis of the biliary tree
  2. Mean age of onset = 40
  3. M:F = 2:1
  4. Associated with IBD, specifically UC
  5. SCARY as fuck because it could lead to cholangiocarcinoma
39
Q

How many people with primary sclerosing cholangitis have IBD?

A 
80%!!!!
But people with IBD don’t have primary sclerosing cholangitis
5-7% of patients with UC have PSC
3% of patients with CD have PSC
So not otherway around
40
Q

What is the radiologic findngs for PSC?

A

Beads on a string

the lumen looks like it is squeezed at certain points

41
Q

What is the risk of cholangiocarcionoma in PSC?

A

8-30% risk of cholangiocarcionma

CA19-9 is genetic marker

42
Q

What is CA19-9?

A

A genetic marker for tumor

Specifically in cholangiocarcionoma from PSC

43
Q

What are the histological features of PSC?

A

Onion skinning

44
Q

What is the difference between AMA and p-ANCA? Difference between ANA?

A

Former is a genetic marker for PBC
Latter is a genetic marker for PSC (don’t need to check to make definitive diagnosis)
ANA = marker for LUPUS or SLE

45
Q

What is DILI?

A

Drug-induced liver injury

46
Q

What causes DILI?

A
  1. acetaminophen

2. Methotrexate (used for CD, if you remember…so if you are treating Crohns watch out for DILI)

47
Q

What are the two types of agents that lead to DILI?

A
  1. intrinsic
    -acetaminophen
    -methotrexate
    DOSE DEPENDENT
  2. idiosyncratic
    -we didn’t expect it
    DOSE INDPENDENT
48
Q

When you have pruritis, what kind of injury?

A

Cholestatic VS hepatocellular

More likely cholestatic

49
Q

What is pruritus?

A

ITCHINESS MOTHERFUCKER

50
Q

What is the most common cause of acute liver failure in the US?

A

Acetaminophen
Causes hepatotoxicity in 10 grams (10,000 mg)
And usually you are given 500 mg of acetaminophen in a pill
Lower doses result in hepatotoxicity in patients who consume alcohol regularly

51
Q

How does acetaminophen get metabolized?

A
  1. Gets broken down by CYP2E1 to
    i. NAPQI
    ii. glucuronide
    iii. Sulfate
  2. Once NAPQI is formed, it igets broken down by glutathione to Cyteine and Mercapturic Acid
52
Q

How does alcohol combined with acetaminophen lead to toxicity?

A

Alcohol uses up glutathione, which is needed to breakdown NAPQI
Lack of glutathione = increased NAPQI = increased acidity

53
Q

What is NAPQI?

A

A breakdown product of acetaminophen that causes acetaminopjhen toxicity
Stands for N-acetyl-p-benzoQuinone imine

54
Q

What is the treatment for acetaminophen?

A

N-acetylcysteine

This is the precursor to glutathione (so you can produce glutathione to get rid of NAPQI)

55
Q

What drugs are implicated in a drug induced liver injury?

A
  1. augmentin
  2. macrobid
  3. anti-TB
  4. Bactrim
  5. anti-retroviral
  6. Levaquin

GI Week 4 (12 decks)

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