Councilman Bodies Flashcards

1
Q

What are Councilman bodies?

A

Councilman bodies are apoptotic hepatocytes seen in liver conditions, such as viral hepatitis and yellow fever.

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2
Q

In what type of hepatitis are Councilman bodies commonly observed?

A

Viral hepatitis, particularly yellow fever.

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3
Q

What is the significance of Councilman bodies in liver pathology?

A

They indicate apoptotic death of hepatocytes due to liver injury.

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4
Q

What staining characteristics do Councilman bodies exhibit?

A

They are acidophilic (stain pink) due to the eosinophilic nature of their cytoplasm.

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5
Q

Which type of viral fever can result in the formation of Councilman bodies in the liver?

A

Yellow fever.

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6
Q

What is the typical appearance of Councilman bodies under microscopy?

A

Small, round, acidophilic structures within hepatocytes.

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7
Q

What is another name for Councilman bodies?

A

Apoptotic bodies.

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8
Q

What cellular process leads to the formation of Councilman bodies?

A

Apoptosis (programmed cell death).

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9
Q

Councilman bodies are typically seen in what zone of the liver lobule?

A

The midzonal region of the liver lobule.

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10
Q

How does the immune response contribute to the formation of Councilman bodies?

A

Immune-mediated cytotoxicity can trigger hepatocyte apoptosis, leading to the formation of Councilman bodies.

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11
Q

Can Councilman bodies be observed in non-viral liver diseases?

A

Yes, they can be seen in various forms of liver injury, though more common in viral infections.

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12
Q

What role do Kupffer cells play in the clearance of Councilman bodies?

A

Kupffer cells (liver macrophages) phagocytose and clear the apoptotic hepatocytes.

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13
Q

Describe the mechanism of hepatocyte apoptosis in viral hepatitis.

A

Viral infection triggers immune-mediated damage, leading to activation of apoptotic pathways.

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14
Q

Which protein markers are associated with the apoptosis seen in Councilman bodies?

A

Caspases and other apoptotic markers such as cleaved PARP.

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15
Q

How does mitochondrial dysfunction contribute to the formation of Councilman bodies?

A

Mitochondrial damage leads to the release of cytochrome c, triggering the apoptotic cascade.

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16
Q

In the context of yellow fever, what viral protein is implicated in hepatocyte apoptosis?

A

The NS2B-NS3 protease complex of the yellow fever virus.

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17
Q

What is the typical clinical outcome for a patient with numerous Councilman bodies in the liver?

A

It indicates significant liver damage and may be associated with liver failure.

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18
Q

Are Councilman bodies seen in acute or chronic liver disease?

A

They are typically seen in acute liver injury.

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19
Q

How does oxidative stress in hepatocytes lead to the formation of Councilman bodies?

A

Oxidative stress causes DNA damage, leading to apoptosis.

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20
Q

What immune cells are primarily responsible for inducing apoptosis in hepatocytes during viral hepatitis?

A

Cytotoxic T lymphocytes (CTLs).

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21
Q

What histological feature distinguishes Councilman bodies from necrotic cells?

A

Apoptotic cells (Councilman bodies) show cell shrinkage, while necrotic cells swell and burst.

22
Q

What is the role of the Fas-FasL pathway in the formation of Councilman bodies?

A

The Fas-FasL interaction activates caspases, leading to apoptosis of hepatocytes.

23
Q

How does liver inflammation contribute to the development of Councilman bodies?

A

Inflammatory cytokines, such as TNF-α, promote apoptosis.

24
Q

What is the difference between coagulative necrosis and the apoptosis seen in Councilman bodies?

A

Coagulative necrosis involves cell lysis and inflammation, whereas apoptosis is a controlled, non-inflammatory process.

25
Q

In what other liver conditions might Councilman bodies be seen besides yellow fever?

A

They can also be seen in hepatitis B, hepatitis C, and other forms of viral hepatitis.

26
Q

How does the liver regenerate after the loss of hepatocytes via apoptosis?

A

The liver regenerates through the proliferation of surviving hepatocytes.

27
Q

What is the clinical significance of observing many Councilman bodies in a liver biopsy?

A

It suggests active liver injury and can correlate with disease severity.

28
Q

How does chronic inflammation differ from acute inflammation in terms of Councilman body formation?

A

Councilman bodies are more common in acute inflammation, where apoptosis is a prominent feature.

29
Q

Can liver cells recover after forming Councilman bodies?

A

No, once a cell undergoes apoptosis and becomes a Councilman body, it cannot recover.

30
Q

What antiviral therapies can reduce the formation of Councilman bodies in viral hepatitis?

A

Antiviral treatments targeting the underlying virus, such as interferons and direct-acting antivirals.

31
Q

How does hepatocellular steatosis relate to the formation of Councilman bodies in yellow fever?

A

Hepatocellular steatosis is often seen alongside apoptotic bodies due to metabolic disturbances in the liver.

32
Q

How does the immune system distinguish apoptotic cells like Councilman bodies from viable cells?

A

Apoptotic cells express phosphatidylserine on their outer membrane, signaling for phagocytosis.

33
Q

Can liver function tests detect the presence of Councilman bodies?

A

Indirectly, liver function tests can show elevated transaminases, indicating hepatocyte injury and apoptosis.

34
Q

What role do hepatocyte growth factors play in liver repair following the formation of Councilman bodies?

A

Hepatocyte growth factors stimulate the proliferation of hepatocytes for liver regeneration.

35
Q

In addition to Councilman bodies, what other histological changes are seen in yellow fever?

A

Midzonal necrosis, steatosis, and coagulative necrosis.

36
Q

How do viral hemorrhagic fevers like dengue or Ebola compare with yellow fever in terms of liver pathology?

A

They also cause hepatocyte damage, but may involve more extensive necrosis and hemorrhage.

37
Q

How do researchers use Councilman bodies to track the progression of viral liver diseases?

A

The number and distribution of Councilman bodies can help assess the extent of liver damage.

38
Q

What are the systemic effects of liver failure caused by extensive apoptosis in diseases like yellow fever?

A

Jaundice, coagulopathy, encephalopathy, and multi-organ failure.

39
Q

What pharmacological agents can prevent the formation of Councilman bodies in viral liver diseases?

A

Antivirals, antioxidants, and anti-inflammatory agents.

40
Q

What role do mitochondria play in the apoptosis that leads to Councilman bodies?

A

Mitochondria release cytochrome c, which activates the apoptotic cascade.

41
Q

Can Councilman bodies be seen in liver transplant rejection?

A

Yes, apoptosis of hepatocytes can occur during transplant rejection.

42
Q

What are the key apoptotic markers detectable in liver tissue with Councilman bodies?

A

Caspases, Bcl-2 family proteins, and cleaved PARP.

43
Q

How does viral load correlate with the formation of Councilman bodies in hepatitis?

A

Higher viral loads are often associated with more extensive apoptosis and more Councilman bodies.

44
Q

What is the role of interleukin-1 in hepatocyte apoptosis?

A

IL-1 can promote inflammation and apoptosis in the liver.

45
Q

How do autophagy and apoptosis differ in the context of liver cell death?

A

Autophagy is a cell survival process, while apoptosis leads to programmed cell death.

46
Q

What is the clinical outcome if the liver’s regenerative capacity is overwhelmed by apoptosis?

A

Liver failure, potentially leading to death.

47
Q

How do Councilman bodies contribute to the diagnosis of yellow fever?

A

Their presence in liver biopsies is a histological hallmark of yellow fever.

48
Q

What genetic factors can influence the susceptibility of hepatocytes to apoptosis?

A

Mutations in apoptotic pathway regulators such as p53 or Bcl-2.

49
Q

Can the presence of Councilman bodies be reversed in the liver?

A

No, once apoptosis occurs, the affected hepatocytes cannot be revived.

50
Q

What environmental factors can exacerbate liver apoptosis leading to more Councilman bodies?

A

Alcohol consumption, drug toxicity, and co-infections.