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GI II Exam II > Chapter 18 Key Concepts > Flashcards

Chapter 18 Key Concepts Flashcards

1
Q

Which viral hepatitis NEVER cause chronic Hepatitis, only ACUTE?

A
  1. A
  2. E
    1. Except in immunocompromised and pregnant ppl
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2
Q

Only _________ viral heps can progress to chronic disease?

A
  • B
  • C
  • D
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3
Q

Hep ____ is a single virus that is more often chronic and almost NEVER detected acutely.

A

Hep C

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4
Q

Hep ___ is endemic in equatorial regions and often epidemic.

A

HepE

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5
Q

What is most assessment for grading and staging for chronic viral hepatitis, which is important to help decide whether the patient undergoes difficult antiviral treatment?

A

Biopsy

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6
Q

Patients with ____ & _____ are at increased risk for developing hepatocellular carcinoma.

A
  • Hep B
  • Hep C
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7
Q

What is one clue that patient has viral hepatitis?

A
  • All cause a very ↑ AST/ALT (often >1000); >25x NL
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8
Q

Blood enters the liver through the [portal vein & hepatic A] => Zone 1 (periportal) => Zone 2 (midzone) => Zone 3 (centrolobular) => centra/hepatic vein.

  • What is the 1st zone affected in most liver pathologies and alcohol damage?
  • What is the important exception to this?
A
  • Zone 3 (centrolobular)
  • Exception: Viral hepatitis usually affects zone 1 (periportal) first.
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9
Q

What is Reyes Syndrome?

A
  • Liver damage + encephalopthy that occurs in children who have a viral illness (chicken pox/varicella zoster or Influenza B) who take aspirin.
  • => rapid severe liver failure bc aspirin inhibits B-oxidation => microvascular steatosis (small fat droplets in hepatocytes), causing hepatomegaly.
  • => vomitting/coma/death.
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10
Q

What are hallmark changes of chronic heptitis?

A
    1. Increased portal chronic inflammation => dense mononuclear infiltrates around the portal triad
    1. Interface necrosis
    1. Chronic Hep B => Ground glass infiltrates due to accum of HBsAg in ER; Chronic Hep C => lymphoid follicles and fatty change
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11
Q

What is interface hepatitis (piecemeal necrosis)?

A
  • Lymphocytes infiltrate into the adjacent parenchyma (beyond the limiting plate) and destruction of individual hepatocytes along the edge of the portal tract.
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12
Q

Interface hepatitis is occurs due to:

A
  1. Viral hepatitis (especially chronic)
  2. AI Hepatitis
  3. Steatosis
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13
Q

Large pale, finely granular pink cytoplasmic exclusions on H& E staining =

A

Chronic Hep B infection

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14
Q

What confirms the presecence of ground glass infiltrates/ surface antigen in hep B

A

Immunostaining => looks brown

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15
Q

Which Hep virus must we worry about in the US

A

Hep C

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16
Q

If you are born between _______, ALWAYS test for HepC

A

1945- 1967

17
Q

Health care workers are at risk for Hep____

A

C

18
Q

What is the hallmark for HepC?

A

1. Persistant infection

2. Chronic hepatitis, despite it generally being asymptomatic for 40-50% of pts

19
Q

How to test for Hep C

A

HCV RNA

20
Q

What are mononuclear infiltrates?

A
  1. Lymphocytes
  2. plasma cells
21
Q

Hep C is more likely to cause

  • ______ in acute hepatitis
  • ______ in chronic hepatitis
A
  • Cholestasis = acute
  • Fatty change = chronic
22
Q

Histo Characteristics of Hep C

A
  1. Portal tract expands due to lymphoid follicle
  2. Fatty change
23
Q

How can drugs/toxins damage the liver?

A
    1. Direct toxicity
    1. Xenobiotic => active toxin
    1. Produced by immune mechanisms: drugs or metabolites act as haptens => convert protein => immunogen.
24
Q

What should ALWAYS be included in a DDx of any form of liver disease

A

1. Exposure to a toxin (herbal, dietary, topical, environmental) OR a therapeutic agent

25
Q

Thorotrast can cause?

A
  • 1. Cholangiocarcinoma
  • 2. Angiosarcoma
  • 3. Hepatocellular carcinoma
26
Q

What drugs can cause massive hepatocellular necrosis?

A
  1. Acetominophin
  2. Halothane
27
Q

What drugs can cause microvascular steatosis (diffuse small fat droplets)?

A
    1. Valproate
    1. Tetracycline
    1. Asprine (REYES)
    1. HAART
28
Q

What drugs can cause Budd-Chiari Syndrome

A

OCPs

29
Q

What drugs can cause Steatohepatitis with Mallor Denk bodies

A
  1. Ethanol
  2. Amiodarone
30
Q

Clinical features of

  1. Steatosis:
  2. Steatohepatitis
  3. Steatofibrosis/cirrhosis
A
  1. Hepatomegaly; little sx, midly high BR & Alk phos
  2. Tender hepatomegaly, AST/ALT 2:1 (<300/400 UL), hyperbillirubinemia + high alk phos
  3. Hepatic dysfunction (all enzymes increase), hypoproteinemia and coag abnormalities + anemia
31
Q

________ almost completely has the same histologic features seen in alcoholic steatohepatitis (alcoholic hepatitis)

A

NASH

32
Q

____ has none-very little cirrhosis; no increased risk of death

A

NAFLD

33
Q

______ can progress to cirrhosis and HCC

A

NASH

  • based on + SHH signaling pathway => + stellate cells

GI II Exam II (10 decks)

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