Lecture 17: Liver Pathology Flashcards

1
Q

What is the normal weight of the liver?

A

1400-1600 grams

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2
Q

What is the porta hepatis?

A
  • Portal vein
  • Hepatic artery
  • BIle duct
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3
Q

What are the anatomical divisions of the liver?

A

Lobules

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4
Q

What are the functional divisions of the liver?

A

Acini

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5
Q

Describe the normal liver architecture?

A

Portal tract;

  • Hepatic art.
  • Bile duct
  • Portal vein

Parenchyma

  • Zone 1 (periportal)
  • Zone 2 (Mid-zonal)
  • Zone 3 (Centrilobular)

Terminal hepatic vein

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6
Q

What are two common patterns of liver disease?

A
  • Cirrhosis
  • Portal hypertension

Both potential consequences of liver pathology.

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7
Q

Describe how liver cirrhosis results;

A

End stage liver damage

  • Death and atrophy
  • Inflammation leads to fibrosis = cirrhosis, loss of synthetic function (Hep. damage) (No normal flow from liver to portal vein)

Different sized nodules depending on eitiology.

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8
Q

Describe the change of liver architecture in liver cirrhosis;

A
  • Bridging fibrous septae (Link portal tracts)
  • Parenchymal nodules (Proliferating hepatocytes encircled by fibrosis, Micro and macro nodules)

Disruption of entire architecture

  • Vascular architecture reorganised with shunts; PV and HA blood bypasses functional liver cells
  • Progressive fibrosis
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9
Q

What is portal hypertension and what causes it?

A
  • Increased resistance to portal blood flow
  • Prehapatic (obstructive thrombosis)
  • Posthepatic (Severe R. sided heart failure)
  • Intra hepatic (Cirrhosis)
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10
Q

What is the consequences of portal hypertension?

A
  • Ascites
  • Portosystemic shunts; Bypasses develop where systemic and portal circulation share capillary bed.
  • Congestive splenomegaly
  • Hepatic encephalopathy (Diffuse confusion)
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11
Q

What can cause viral hepatitis?

A
  • Hepatitis A, B, C, D and E virus
  • Cytomegalovirus
  • Epstein-barr virus
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12
Q

What are some notes on Hepatitis A virus;

A
  • Benign self-limited disease
  • Incubation, 2-6 weeks
  • Does not cause chronic hepatitis
  • Substandard hygiene and sanitation
  • Person to person, feacal oral transmission
  • Asymptomatic or mild febrile illness +/- jaundice
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13
Q

What are some notes on hepatitis B virus;

A
  • Acute (resolves) or chronic which may lead to cirrhosis
  • Fulminant hepatitis leads to massive necrosis
  • Associated with hepatitis D infection
  • 4-26 weeks infection
  • Blood and body fluid born
  • Immune response to viral antigens expressed on infected hepatocytes leads to liver cell damage
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14
Q

What are some notes on hepatitis C virus;

A
  • Major cause of liver disease
  • Inoculations and blood transfusions
  • Acute infection usually undetected
  • Chronic disease usually occurs in majority
  • 20+% develop cirrhosis 5-20 years post infection
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15
Q

How are drug and toxin induced liver injury classified?

A
  • Predictable hepatotoxins (acting in dose dependant manner and occurring in most individuals) i.e paracetamol
  • Unpredictable/idiosyncratic hepatotoxins
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16
Q

How can hepatotoxins act?

A
  • Directly through cell toxicity, act through hepatic conversion to an active toxin or active immune mechanisms.
17
Q

What is the pattern of injury for hepatotoxins?

A

Pattern of injury includes;

  • Cholestasis
  • Hepatotcellular necrosis
  • Fatty liver disease
  • Fibrosis
  • Granulomas
  • Vascular lesions and neoplasms.
18
Q

What is the most common thing to cause acute liver failure?

A

Paracetamol

19
Q

What is the most common thing to cause chronic liver failure?

20
Q

What is found in alcoholic fatty liver disease?

A
  • Hepatic steatosis (Fatty change)
  • Alcoholic hepatitis
  • Cirrhosis
21
Q

What are the pathological effects of alcohol?

A
  • Changed lipid metabolism
  • Decreased export of lipoproteins
  • ROS induced cell injury and cytokines
22
Q

What is non alcoholic fatty liver disease associated with?

A
  • Metabolic syndrome
  • Obesity
  • T2D
  • Dyslipidemia (hypercholestremia)
  • Hypertension
23
Q

What is the spectrum of disease activity for NAFLD?

A
  • Initially hepatic steatosis
  • May progress to steatosis and inflammation (NASH: non-alcoholic steatohepatisis)
  • Over 15 years, 11% patient with NASH progress to cirrhosis.
24
Q

What is heamochromatosis?

A
  • Excessive accumulation of body iron in the liver and pancreas.
25
What causes heamochromatosis?
Genetic defect causing excessive iron absorption or parenteral iron administration (transfusion)
26
What is the mutation for heamochromatosis and what is it associated with?
Mutation in HFE gene | - Macronodular cirrhosis, diabetes millitus, skin pigmentation