Liver and Biliary Disease Flashcards

1
Q

What is the blood supply for the liver?

A

Dual Blood Supply i.e., Hepatic Artery and Portal Vein.

-> Drains into Central Vein, Hepatic Vein and onwards.

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2
Q

What types of cells are present i the liver?

A
  • > Hepatocytes
  • > Bile Ducts
  • > Blood Vessels
  • > Endothelial ells
  • > Kupffer Cells
  • > Stellate Cells
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3
Q

What is the portal triad?

A

Portal Triad consists of Portal Vein, Hepatic Artery and Bile Duct

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4
Q

Which direction does blood and bile flow in the liver lobule?

A

Opposite directions:

  • Blood = From portal triad to central vein
  • Bile = From central vein to bile duct
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5
Q

Which zone in the liver lobule is most metabolically active?

A

Zone 3

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6
Q

What is the normal liver pathology

A

Hepatocytes with microvilli, endothelial cells with spaces between them, Stellate cells sit between the endothelial and hepatocytes
-> Space of Disse.

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7
Q

What are the changes to a normal liver pathology during acute liver injury?

A

During Liver injury

  • > Kuppfer cells activate
  • > endothelial cells stick together reducing blood flow
  • > Basement membrane like collagens secreted by activated stellate cells
  • > Hepatocytes lose their microvilli
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8
Q

What is cirrhosis?

A
  • > Describes the whole liver involvement. The global fibrosis is coupled with the regeneration of hepatocytes leading to nodule formation
  • > The distortion of liver vasculature predisposes to intra and extra hepatic shunting of blood.
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9
Q

How is Cirrhosis classified?

A

i) according to nodule size i.e., Micro/macro nodular, 2mm.

ii) according to aetiology

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10
Q

What are complications of cirrhosis?

A
  • > Portal Hypertension
  • > Hepatic Encephalopathy
  • > Liver Cell Cancer
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11
Q

What are acute and chronic causes of hepatitis?

A

Acute Hepatitis: Viruses, Drugs
[R] – Spotty Necrosis

Chronic Hepatitis: Viruses, Drugs, Auto-Immune

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12
Q

How do you stage and grade hepatitis?

A

Severity of Inflammation – Grade

Severity of Fibrosis - Stage

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13
Q

Describe the progression of hepatitis?

A
  1. “Portal Inflammation” Clear limiting plate, i.e. distinction between the portal tract and hepatocytes
  2. “Interface Hepatitis” No true limiting plate, T-Cell mediated destruction of hepatocytes
  3. “Lobular Inflammation” No obvious delineation, global inflammation
  4. “Fibrosis” Blue collagenous tissue present, in this slice we can see a fibrous pathway between the vascular supply and the central vein - bridging fibrosis. This allows a shortcut for the blood otherwise known as an intra-hepatic shunt
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14
Q

What are the stages of Alcoholic Liver Disease?

A

Step 1. Fatty liver
This is reversible and can occur even after a single episode of heavy drinking

Pale yellow colour as opposed to a beefy red

Step 2. Alcoholic Hepatitis
Features of which include the following, mainly seen in zone 3.

-> Balooning (+/- MALLORY DENK BODIES)
Swellling of the cells containing the pink Hyaline.
-> Apoptosis
-> Pericellular Fibrosis

Step 3. Cirrhosis
Pale, fatty change and small nodules forming.
Alcoholic Cirrhosis is typically micronodular

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15
Q

What is Non alcoholic fatty liver disease?

A

Non-alcoholic fatty liver disease (NAFLD) is the term for a range of conditions caused by a build-up of fat in the liver. It’s usually seen in people who are overweight or obese.
Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver disease with key stages consisting of hepatic steatosis (NAFL), steatohepatitis (NASH), fibrosis, and eventual cirrhosis
-> Histologically looks like alcoholic liver disease
-> Actually associated with insulin resistance secondary to Diabetes and a raised BMI
-> Being recognised as one of the commonest causes of liver disease, world-wide.

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16
Q

What is autoimmune hepatitis?

A

Active Chronic Hepatitis with Plasma Cells

  • > F>M
  • > Anti-smooth muscle actin antibodies in the serum
  • > Steroid responsive

Autoimmune Hepatitis has VERY ACTIVE INFLAMMATION, flooded with inflammatory cells.

17
Q

How does Alpha-1 Anti Trypsin Deficiency affect the liver?

A

Deficiency of A1AT in the blood

  • > In the hepatocyte there is a gross excess.
  • > These misfolded A1AT damages the hepatocytes.
  • > Chronic Hepatitis – Cirrhosis.
18
Q

Which areas of the liver are predominantly affected by paracetamol toxicity?

A

pale dead areas predominantly at zones 2->3

19
Q

What are examples of benign liver tumours?

A
  • > Liver Cell Adenoma COCP
  • > Bile Duct Adenoma
  • > Haemangioma
20
Q

What are examples of malignant liver tumours?

A

SECONDARY TUMOURS i.e. Mets are most common

Primary Include

  • > Hepatocellular Carcinoma
  • > Hepatoblastoma
  • > Cholangiocarcinoma
  • > Haemangiosarcoma
21
Q

What are cholangiocarcinomas associated with?

A

Ass. With PSC, Worm Infections, Cirrhosis

Can arise from intrahepatic ducts & extra hepatic ducts.

22
Q

What is Wilson’s disease?

A

Accumulation of copper due to failure of excretion by hepatocytes into the bile

  • > Genes on chromosome 13
  • > Accumulates in the liver and CNS (hepato-lenticular degeneration) including Kayser-Fleischer rings
23
Q

What is Primary Biliary Cholangitis?

A

Autoimmune Disease consisting of bile duct loss ass. with chronic granulomatous inflammation

  • > F>M
  • > Anti-mitochondrial antibodies are the Hallmark feature.
24
Q

What is Primary Sclerosing Cholangitis?

A

Periductal bile duct fibrosis leading to its loss
-> Associated with UC
M>F

  • > Bile Duct Imaging is Diagnostic i.e. ERCP, MRCP
  • > Increased risk of Cholangiocarcinoma
25
Q

What is PBC and PSC secondary to?

A

PBC is Bile Duct Loss secondary to Autoimmune Inflammation

PSC is Bile Duct Loss secondary to Fibrosis

26
Q

What is haemochromatosis?

A

Genetically determined increased Gut Absorption leading to iron deposition at multiple organs
-> 1mg extra absorption per day, so it takes a while to reach to reach a critical stage.

Mutation of Chromosome 6; HFE – Hemochromatosis Iron Gene.
Common in Celtic Populations - AR.

27
Q

What is “Bronzed Diabetes”?

A

Iron depositions in haemochromatosis causes bronzing of the skin, and is also deposited in the pancreas.