Liver Pathology II Flashcards Preview

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Flashcards in Liver Pathology II Deck (49)
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1
Q

What is the mode of transmission of Hepatitis A?

A

Fecal-oral due to poor hygiene

2
Q

What are the clinical manifestations of Hep A?

A

Mild or asymptomatic with few developing acute liver failure – Severity of illness increases with age and those with underlying chronic liver disease

NO CHRONIC STATE

3
Q

What is the mode of transmission of Hep B?

A

Perinatal - SE Asia

Sexual - primary in US

4
Q

What are the clinical manifestations of Hep B?

A

Can present as Acute or Chronic Hepatitis - rarely is fulminant but there can be acute stage reactivation

5
Q

What is Hep B associated with?

A

Increased risk of Hepatocellular Cancer

6
Q

How does Hep B cause cell injury?

A

It is NOT directly cytotoxic, rather, liver injury is caused by the immune response and cytotoxic T cells.

7
Q

What are ground glass hepatocytes indicative of?

A

Hepatitis B

8
Q

What type of virus is Hep B?

A

DNA Virus

9
Q

What type of virus is Hep C?

A

Single stranded RNA Virus - does NOT incorporate into the human genome

10
Q

What are the clinical manifestations of Hep C?

A

Most cases are asymptomatic

11
Q

What is Hep C associated with?

A

Increased risk of Hepatocellular Cancer

12
Q

What is the main risk for transmission of Hep C?

A

IV drug use

13
Q

What is Hep D associated with?

A

Increased risk of Hepatocellular Cancer

14
Q

What population is Hep D found in with coinfection?

A

Around 5% of HBV patients are coinfected with Hep D

15
Q

What will be seen on serology of a recently coinfected individual with HBV and HDV who was previously healthy?

A
  • IgM anti HDAg

- IgM anti HBcAg

16
Q

What will be seen on serology of a superinfected individual with HBV and HDV?

A
  • IgM and IgG anti-HDV

- HBsAG

17
Q

What are most cases of HDV infection known as?

A

Superinfection. An HBV carrier gets infected with HDV

18
Q

What is the route of transmission of Hep E?

A

Fecal-oral route of transmission – Contaminated water supply

19
Q

What is a major risk for fulminant hepatitis in Hep E?

A

Pregnancy

20
Q

Is there a carrier state for Hep E?

A

No

21
Q

Is there an increased risk of hepatocellular carcinoma with Hep E?

A

No

22
Q

What is the most common viral cause of fulminant hepatitis?

A

HBV

23
Q

What are the common viral causes of chronic hepatitis?

A

HBV and HCV

24
Q

What are some of the clinical findings of acute viral hepatitis?

A
  • Hepatocyte injury / necrosis
  • Fatty change (HCV)
  • Bile duct reaction
  • Kupffer cell hypertrophy
  • Inflammatory cells
25
Q

What does grade of hepatitis refer to?

A

Degree of inflammation

26
Q

What does the stage of hepatitis refer to?

A

Degree of fibrosis

27
Q

What are the most likely causes of fulminant hepatitis?

A

HBV or HAV - the rest are far less likely

28
Q

What population will be more likely to have autoimmune hepatitis?

A

Females more than males

29
Q

What are the Ab seen in autoimmune hepatitis?

A

– ANA (antinuclear antibodies)
– Anti SMA (anti-smooth muscle antibodies)
– Anti LKM-1 (anti-liver kidney microsome-1 antibodies)

30
Q

What are the main inflammatory cells in autoimmune hepatitis?

A

Plasma cells

31
Q

What is a classical sign of autoimmune hepatitis?

A

Interface hepatitis

32
Q

Hepatic Steatosis

A

Alcohol fatty liver disease that is reversible and due to short term consumption of large amounts of alcohol from impaired assembly and secretion of lipoproteins

33
Q

What is Mallory hyaline?

A

It is an acute reaction to alcohol

34
Q

What type of fibrosis is seen with alcoholic hepatitis?

A

Pericellular fibrosis

35
Q

What is the pathogenesis of alcoholic hepatitis?

A

Acetaldehyde is a metabolite of EtOH that induces generation of reactive O2 species and damages cells and reduces glutathione

36
Q

A 42 yo gentleman presents with a 2 week history of progressive jaundice and abdominal distension.
• He has a long-standing history of alcohol use, but over the past 6 months he has significantly increased his alcohol intake due to a divorce. He is drinking a 12 pack of beer and a 1⁄2 pint of liquor daily.
• His AST is 356 and his ALT 157, T.bili 12.6, WBC 17.4, INR 2.3. A liver biopsy in this gentleman would most likely demonstrate which of the following:

1. Cirrhosis with nodule formation but no inflammation
2. Hepatic steatosis
3. Steatohepatitis with inflammation, mallory hyaline bodies, and pericellular fibrosis
4. Interface hepatitis with plasma cell infiltration
5. Groundglass hepatocytes

A
  1. Steatohepatitis with inflammation, mallory hyaline bodies, and pericellular fibrosis
37
Q

Non-alcholoic Fatty Liver Disease

A

Identical to EtOH induced disease and is found most often in obese individuals with dyslipidemia, hyperinsulinemia and insulin resistance

38
Q

What is the difference between non-alcoholic steatohepatitis and steatosis?

A

NASH is:
– Elevated transaminase
– Asymptomatic or fatigue, RUQ discomfort
– Associated with cardivascular disease and metabolic syndrome

Simple steatosis is:
– Elevated transaminases
– Asymptomatic
– Benign

39
Q

A 52-year old woman is referred abnormal LFT’s. She is overweight and has non- insulin requiring diabetes. Physical exam is unremarkable. She may have one or two glasses of wine on the weekends, but denies other alcohol use. Lab results are as follows:
• Bilirubin 1.1, ALT 83, AST 77, Alk Phos 127 Hepatitis A IgG (+); Hepatitis A IgM (-)
• Hepatitis BsAg, BsAb, BcAb all (-)
Hepatitis C Antibody (+); Hepatitis C RNA (-)
• ANA 1:20 (Normal ≤ 1:20)
Anti-Smooth muscle Antibody (-)
Ceruloplasmin, Iron studies, alpha-1-antitrypsin are all normal

The most likely diagnosis is:

A. Non-alcoholic steatohepatitis
B. Hepatitis A
C. Hepatitis C
D. Autoimmune Hepatitis

A

A. Non-alcoholic steatohepatitis

40
Q

Hemochromatosis

A

Disease of iron overload and can be genetic or due to transfusions - Iron deposition in parenchymal tissues

41
Q

What are patients with cirrhosis and hemochromatosis simultaneously at increased risk for?

A

Hepatocellular Carcinoma

42
Q

What is the gene mutation in hereditary hemochromatosis?

A
  • HFE on Ch6 -> C282Y Homozygous (one of most common gene disorders)

They cause excessive absorption of dietary iron

43
Q

What will be seen on liver biopsy of patient with hemochromatosis?

A

Liver biopsy with brown pigmented hepatocytes - iron stain will show BLUE

44
Q

Wilson’s Disease

A

Copper accumulation in the liver and the brain

45
Q

What is the gene mutation in Wilson’s disease?

A

Autosomal Recessive Disorder (ATP7B gene)

- Responsible for linking copper to ceruloplasmin for release into bloodstream

46
Q

What are the signs of Wilson’s disease?

A

– Neuropsychiatric (copper deposition in brain)
– Kayser Fleischer rings (copper ring in eye)
– Liver Failure
– Hemolytic Anemia

47
Q

How is the diagnosis of Wilson’s disease made?

A
  • Low ceruloplasmin
  • Liver biopsy
  • Increased urine copper
48
Q

Alpha 1 Antitrypsin Deficiency

A

Defective production of A1AT in the liver
• Errors in coding sequence prevent its export from the hepatocyte – Abnormal accumulation of the protein results in cell death, inflammation, fibrosis, and cirrhosis

49
Q

What is the gene mutation in A1AT deficiency?

A

Autosomal Recessive - PiZZ on Ch14

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