Liver Pathology Flashcards

1
Q

What is the basic structure of the liver?

A

The hepatic lobule; a hexagonal structure with the hepatic vein in the centre, and the portal tracts at the periphery.

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2
Q

What are the functions of the liver?

A

Metabolism

  • Involved in glycolysis, glycogen storage, synthesis of essential molecule
  • Involved in drug metabolism

Protein synthesis

  • Involved in amino acid synthesis
  • Makes all circulating proteins (except gamma globulins)

Storage

  • Glycogen, vitamin A, D, B12
  • Vitamin K, folate, iron, copper

Hormone metabolism
- Activates vitamin D

Bile synthesis
- 600-1000ml a day

Immune function
- Kupffer cells (macrophages)

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3
Q

Name and describe some benign tumours of the liver

A

Haemangioma

  • Most common benign lesion
  • No symptoms or treatment

Hepatic adenoma

  • Associated with the OCP
  • Present with abdominal pain/intraperitoneal bleeding
  • Treat with resection if symptomatic, large or unresponsive to stopping the OCP
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4
Q

Name and describe some malignant tumours of the liver

A

Metastases

  • Most common malignant lesion of the liver
  • Usually from GI/breast/lung
  • Usually multiple

Hepatocellular carcinoma

  • Caused by cirrhosis, HepB or C, NAFLD
  • Secrete alpha-fetoprotein

Haemangiosarcoma

Hepatoblastoma

  • Liver malignancy of childhood
  • Primitive cells

Cholangiocarcinoma

  • Carcinoma arising from the bile ducts
  • 10% of all liver malignancies
  • Can be intra or extra hepatic
  • Carry a poor prognosis
  • Caused by PSC, parasitic liver disease
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5
Q

What is cirrhosis?

A

A diffuse abnormality of the liver architecture which interferes with function and blood flow. It is characterised with the following:

  • Fibrosis
  • Hepatocyte necrosis
  • Nodules of regenerating hepatocytes
  • Disruption of liver architecture
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6
Q

What are the main causes of cirrhosis?

A
  • Alcoholic liver disease
  • Non-alcoholic fatty liver disease
  • Chronic viral hepatitis
  • Autoimmune hepatitis
  • Biliary causes
  • Genetic causes
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7
Q

What is the modified Child’s Pugh score?

A

A score to indicate prognosis in cirrhosis. It scores based on ascites, encephalopathy, bilirubin levels, albumin levels and prothrombin time. The higher the score, the lower the expected survival.

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8
Q

What is portal hypertension? At what point does the circulation begin to change?

A

It is increased pressure in the portal system, which is usually secondary to :

  • Increased resistance vascular resistance
  • Hyperdynamic circulation
  • Sodium retention and plasma volume expansion

When portal pressure is raised above 10-12mmHg, collateral vessels begin to form to create varices at:

  • Gastro-oesophageal junction
  • Rectum
  • Left renal vein
  • Diaphragm
  • Retroperitoneum
  • Anterior abdominal wall
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9
Q

What can cause portal hypertension?

A

Pre-hepatic:
- Portal vein thrombosis

Hepatic:

  • Pre-sinusoidal: PBC, schistosomiasis
  • Sinusoidal: cirrhosis
  • Post-sinusoidal: veno-occlusive disease

Post-hepatic:
- Budd-Chiari syndrome (blockage of the hepatic vein)

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10
Q

What is the progression of alcoholic liver disease?

A

Hepatic steatosis

  • Large, pale, yellow, greasy liver
  • Accumulation of fat droplets
  • Fully reversible if alcohol stopped

Alcoholic hepatitis

  • Large, fibrotic liver
  • Hepatocyte ballooning and necrosis
  • Mallory Denk bodies
  • Can be seen acutely

Alcoholic cirrhosis

  • Yellow-tan, fatty liver
  • Micronodular cirrhosis
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11
Q

Describe non-alcoholic fatty liver disease

A

It is hepatic steatosis in non-alcoholics, and is increasingly common. Risk factors include obesity and insulin resistance.

  • Simple steatosis: relatively benign
  • NASH: can progress to cirrhosis
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12
Q

Describe autoimmune hepatitis

A

It commonly comes with other autoimmune disease (SLE, coeliac, thyroiditis) and predominately affects females and is associated with HLA-DR3. There are two types:

  • Type 1: anti-SMA, ANA
  • Type 2: anti-LKM

It is treated with immune suppression

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13
Q

Describe the biliary causes of cirrhosis

A

Primary biliary cholangitis (PBC)

  • Autoimmune inflammation of intrahepatic ducts
  • Females 10x at risk, peak at 40-50 years
  • Raised ALP, cholesterol, anti-mitochondrial antibodies in 90%
  • US: no dilatation
  • Histology: granulomas
  • Presents with pruritus and abdominal discomfort
  • Treat with ursodeoxycholic acid

Primary sclerosing cholangitis (PSC)

  • Inflammation of extrahepatic and intrahepatic ducts
  • Multiple stricture formation
  • Males at higher risk, 40-50 years peak
  • Associated with IBD (especially ulcerative colitis)
  • Raised ALP, and p-ANCA
  • US: duct dilatation
  • ERCP: beading of bile ducts
  • Risk of cholangiocarcinoma
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14
Q

What genetic diseases can cause cirrhosis?

A
  • Haemochromatosis
  • Wilson’s disease
  • Alpha-1-antitrypsin deficiency
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15
Q

What is haemochromatosis? What is the associated epidemiology? What is the pathophysiology and histology? What are the associated clinical features? What are the investigations and treatment principles?

A

Increased iron deposition in tissues, and it peaks at 40-50 years

It is an autosomally recessive disease, involving a mutated HFE gene causing increased iron absorption in the gut. A Prussian blue stain can visualise the iron deposits.

Clinically, there is a classic bronzing of the skin, diabetes, hepatomegaly, cardiomyopathy, hypogonadism, pseudogout.

Bloods will show a high iron, and ferritin, and a reduced total iron binding capacity. Treatment is with venesection and Desferrioxamine.

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16
Q

What is Wilson’s disease? What is the associated epidemiology? What is the pathophysiology and histology? What are the associated clinical features? What are the investigations and treatment principles?

A

Increased copper deposition, peaking at 11-14 years

It is an autosomally recessive disease, involving mutations on chromosome 13, reducing copper excretion. A rhodamine stain shows the copper.

Clinically, there is liver disease, neuro disease (basal ganglia deposition) and Kayser-Fleischer rings on the cornea.

Blood will show a low caeruloplasmin, low total (high free) serum copper and high urinary copper. Treatment is with lifelong penicillamine.

17
Q

What is alpha-1-antitrypsin deficiency? What is the pathophysiology and histology? What are the associated clinical features? What are the investigation results?

A

This is an autosomally dominant disease, involving an A1AT accumulation in the liver, and a deficiency elsewhere in the body, causing a hepatitis and emphysema in the lungs.

Histologically, there is intracytoplasmic inclusions of A1AT which stain with Periodic acid Schiff.

Clinically, the patients may show jaundice, and emphysema.

Investigations will show a low A1AT.