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Karan - MBBS Year 1: Gastrointestinal Week 3 > Pathology of the Liver > Flashcards

Pathology of the Liver Flashcards

1
Q

What are the causes of acute hepatitis?

A
  • Viral (hepatitis A, B, E)
  • Drug-induced liver injury
  • Autoimmune hepatitis
  • No cause can be identified = seronegative
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2
Q

What are some infectious agents that cause hepatitis?

A
  • HAV, HBV and HCV
  • Cytomegalovirus
  • Epstein-Barr virus
  • Herpes simplex virus
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3
Q

What can acute hepatitis progress to?

A
  • Recovery in most cases
  • Fulminant hepatitis in rare cases
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4
Q

What can chronic hepatitis progress to?

A
  • Recovery
  • Cirrhosis and/or hepatocellular carcinoma
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5
Q

What are the microscopic findings for acute hepatitis?

A
  • Lobular inflammation: Liver lobules are infiltrated by inflammatory cells.
  • Hepatocyte injury: swelling (‘ballooning’) or shrinkage and pyknosis (acidophil bodies).
  • Severe cases show confluent areas of hepatocyte necrosis.
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6
Q

Describe fulminant hepatitis.

A
  • Rapid progression of acute liver failure.
  • > 50% of cases are caused by viral hepatitis.
  • Other causes include drugs and toxins
  • Characterised by massive liver necrosis, causing jaundice and mental status changes.
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7
Q

List some causes of fulminant hepatitis.

A
  • Acute viral hepatitis
  • Drug induced hepatitis
  • Circulatory collapse - heart failure, shock (circulatory/septic) with or without DIC
  • Rare diseases e.g autoimmune hepatitis
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8
Q

Give some examples of bridging necrosis in hepatitis.

A

BRIDGING NECROSIS FROM
- Central vein to central vein
- Portal tract to portal traact
- Central vein to portal tract

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9
Q

What are some common causes of chronic hepatitis?

A
  • Chronic Hepatitis B, C and D
  • Autoimmune and drug-induced hepatitis
  • Cryptogenic hepatitis
  • Wilson’s disease
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10
Q

Describe macroscopic and microscopic findings of chronic hepatitis.

A
  • MACROSCOPIC - Liver feels firm due to fibrosis
  • Portal inflammation mostly lymphocytes.
  • Interface hepatitis (‘piecemeal necrosis’) extension of portal inflammation into hepatocytes at the limiting plate.
  • Mild lobular inflammation.
  • Fibrosis is a marker of how advanced the disease is.
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11
Q

Describe disease progression of hepatitis.

A
  • ACUTE INFECTION
  • ACUTE HEPATITIS
  • Most recover - but some develop chronic hepatitis
  • Less than 2% recover and 30% return to a healthy carrier state.
  • 12-20% have cirrhosis of which some progress to hepatocellular carcinoma
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12
Q

Describe steatosis.

A
  • Fatty change reversible with abstinence.
  • Gross appearance: enlarged, yellow, greasy liver.
  • Microscopically, the liver initially shows steatosis (reversible) that can progress to fibrosis around the central vein (irreversible)
  • Continued exposure leads to cirrhosis and severe exposure leads to hepatitis.
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13
Q

Name the 3 steps of alcoholic liver disease.

A
  • Hepatic steatosis
  • Alcoholic hepatitis
  • Alcoholic cirrhosis
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14
Q

Describe pathogenesis of alcoholic liver disease.

A
  • Alcohol metabolism in the liver generates high levels of NADH which stimulates fatty acid synthesis and production of triglycerides, leading to steatosis.
  • In some individuals, oxidative stress from metabolism of alcohol leads to hepatocyte injury and necro-inflammatory activity (ASH).
  • Ongoing necro-inflammatory activity causes liver fibrosis which may progress to cirrhosis.
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15
Q

Describe macroscopic findings of alcoholic liver disease.

A
  • Steatosis causes an enlarged soft greasy liver.
  • Alcoholic steatohepatitis may cause a firm texture due to fibrosis in the liver.
  • Cirrhosis causes diffuse nodularity of the liver.
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16
Q

Describe microscopic appearances of alcoholic liver disease. PART 1

A
  • Steatosis shows large droplets of fat in hepatocytes, which displace the nucleus to one side (macrovesicular steatosis).
  • ASH shows ballooned hepatocytes which may contain Mallory’s hyaline (clumps of dense pink material) and an inflammatory infiltrate rich in neutrophils.
17
Q

Describe microscopic appearances of alcoholic liver disease. PART 2

A
  • Fibrosis in ASH is typically perivenular.
  • Cirrhosis shows diffuse replacement of the liver by nodules of regenerating hepatocytes surrounded by fibrous bands.
18
Q

Describe pathogenesis of cirrhosis.

A
  • Activation of stellate cells into myofibroblast-like cells induced by alcohol
18
Q

Define cirrhosis.

A
  • End-stage liver disease
  • Characterized by disruption of the liver architecture by bands of fibrosis
  • Bands divide the liver into nodules of regenerating liver parenchyma.
19
Q

List some causes of cirrhosis.

A
  • Alcohol
  • Chronic hepatitis - autoimmune, viral or drug-induced
  • Biliary diseases e.g extrahepatic biliary obstruction
  • Metabolic diseases e.g glycogen storage or Wilson disease
  • Cryptogenic causes
20
Q

Describe cirrhosis pathogenesis.

A
  • Liver cell necrosis
  • Inflammation and hepatocyte regulation
  • FIBROSIS occurs
  • Destruction of normal liver architecture - leading to nodule formation
21
Q

What are the types of cirrhosis?

A

MACRONODULAR
MICRONODULAR
MIXED

22
Q

Describe microscopic appearance of cirrhosis.

A
  • Entire liver replaced by nodules of regenerating hepatocytes surrounded by fibrous bands.
  • Bands contain a variable inflammatory infiltrate and reactive bile ductular proliferation.
23
Q

What can cirrhosis progress to?

A
  • Portal hypertension - leading to ascites, congestive splenomegaly and portosystemic shunts
  • Reduced detoxification - leading to reduced osterogen metabolism leading to hyperestrogenima leading to gynecomastia, spider angioma and palmar erythema
24
Q

What factors can lead to ascites?

A
  • Portal hypertension induced by cirrhosis
  • Reduced protein synthesis induced by cirrhosis - hypoalbuminemia and reduced plasma osmotic pressure leading to transudation
  • Splanchnic vasodilation - reduced RBF and RAAS activates leading to H2O and Na+ retention

Karan - MBBS Year 1: Gastrointestinal Week 3 (9 decks)

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