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Yr 2 Gastrointestinal > Wk 2 - Pathology: Fibrosis, Cirrhosis and Fatty Changes > Flashcards

Wk 2 - Pathology: Fibrosis, Cirrhosis and Fatty Changes Flashcards

1
Q

What is the average weight of the adult liver?

A

1.2-1.5kg

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2
Q

Where does the liver receive blood supply from?

A
  • 20% from hepatic artery (a branch of the coeliac)
  • 80% from the portal vein (formed from splenic vein and SMV)
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3
Q

What does the SMV drain?

A

Small intestine, parts of large intestine, stomach and pancreas

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4
Q

What does the splenic vein drain?

A

Spleen, stomach, pancreas and parts of large intestine

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5
Q

The hepatic artery carries ____ blood while the portal vein carries ______ blood from the ____.

A

The hepatic artery carries oxygenated blood while the portal vein carries nutrient-rich, deoxygenated blood from the gut.

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6
Q

Anatomically, what is the liver divided to?

A
  • Right lobe
  • Left lobe
  • Quadrate lobe
  • Caudate lobe
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7
Q

What divides the left and right lobes?

A

The falciform ligament - connects liver to diaphragm and anterior abdominal wall.

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8
Q

What is the porta hepatis?

A
  • The porta hepatis is the point where the portal vein and hepatic artery enter the liver, and where the bile ducts leave.
  • It is also the point of passage of the hepatic nerve plexus, hepatic ducts and lymphatics.
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9
Q

Explain the structural anatomy of the liver.

A
  • There are 8 segments of liver, each with its own vascular inflow, outflow and biliary drainage
  • The segments are divided by branches of the hepatic vein, and portal vein
  • Clinical relevance - if there is a tumour in one segment, it can be resected without damaging the remaining liver
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10
Q

What is the functional unit of the liver?

A

The functional unit of the liver, the hepatic lobule, is a three-dimensional hexagonal structure

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11
Q

Describe the structure of the hepatic lobule.

A
  • At the edges of the hexagon are portal tracts, comprising branches of the portal vein, hepatic artery and bile duct.
  • Blood flows into the liver from the portal tract, where it is most oxygenated
  • Blood flows from the portal vein in the portal tract, towards the central or central hepatic vein, through the liver sinusoids.
  • As oxygen and nutrients are delivered to the hepatocytes, the deoxygenated blood enters the central vein, finally draining into the inferior vena cava
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12
Q

What are the different hepatic zones?

A
  • The portal tract is also designated as zone 1. The central vein is designated as zone 3. Zone 2 lies between the portal tract and central vein
  • Zone 1 contains the most oxygenated blood whilst zone 3 contains the least
  • Zone 3 is therefore the most susceptible zone to ischaemic injury.
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13
Q

What zone has the most oxygenated blood?

A

Zone 1

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14
Q

What are the functions of the liver?

A
  1. Carbohydrate metabolism includes: production of glycogen by glycogenesis, production of glucose from breakdown of glycogen (glycogenolysis), and production of glucose from lipids and amino acids by gluconeogenesis.
  2. Synthetic function including: production of amino acids, albumin, coagulation factors (fibrinogen, prothrombin, factors V, VII, VIII, IX, X, XI, XIII, protein C and S, cholesterol and bile.
  3. Storage function including: vitamins A, D, B12 and K
  4. Detoxification: Drug metabolism, breakdown of bilirubin, and production of urea from ammonium.
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15
Q

Define cirrhosis.

A

A chronic disease process of the liver characterised by fibrosis and nodular regeneration that leads to impairment in hepatic blood flow and liver function

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16
Q

What happens to hepatocytes in cirrhosis?

A

Nodules of hepatocytes separated by fibrous septa made up of type IV collagen which is highlighted as blue in this picture, with a special stain for collagen called Masson’s trichrome.

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17
Q

List the most common causes of cirrhosis.

A
  • Alcoholic steatohepatitis
  • Non-alcoholic steatohepatitis
  • Chronic viral hepatitis (HBV and HCV)
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18
Q

List other less common causes of cirrhosis.

A
  • Biliary tract obstruction
    • Stones
    • Primary diseases of biliary tract
  • Autoimmune Hepatitis
  • Metabolic disorders
    • e.g. haemochromatosis (iron overload) and Wilson’s disease (copper deposition)
  • Venous outflow obstruction
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19
Q

What are two metabolic disorders that cause cirrhosis?

A
  • Haemochromatosis (iron overload)
  • Wilson’s disease (copper deposition)
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20
Q

Briefly describe the pathogenesis of cirrhosis.

A
  1. Hepatocellular injury and death
  2. Capillarisation and altered vascular resistance
  3. Fibrosis and shunting of blood flow
  4. Nodular regeneration
  5. A final common pathway
21
Q

Describe the liver parenchyma. Draw a diagram to illustrate it.

A
  • Hepatocytes form plates one cell thick
  • Between the plates are sinusoids through which the blood flows
22
Q

List the cells implicated in fibrosis.

A
  1. Hepatic stellate cells
  2. Liver sinusoidal endothelial cells
  3. Kupffer cells
  4. Hepatocytes
  5. Cytokines
23
Q

What is the function of hepatic stellate cells in general?

A

When the liver is in a normal state, the number of HSCs is fewer. These cells store vitamin A, control vascular tone through release of alpha smooth muscle myosin (αSMA), produce extracellular matrix, growth factors and cytokines.

24
Q

What role do hepatic stellate cells have during fibrosis?

A
  • Following liver injury HSCs are activated, where they proliferate, lose their retinol storage function and acquire myofibroblastic properties.
  • They produce and deposit more extracellular matrix (promoting fibrosis) and collagen and have enhanced contractility, contributing to increased vascular resistance and impaired blood flow.
25
Q

What is the general function of liver sinusoidal endothelial cells?

A

Contain fenestrae that act as a filter

26
Q

What happens to liver sinusoidal endothelial cells during liver injury?

A

Roles in fibrosis:

  • Defenestration
  • Subendothelial basement membrane deposition
  • Retinol deficiency
  • HSC activation

Liver injury results in extracellular matrix deposition, leading to defenestration and basement membrane deposition, leading to impaired exchange between sinusoidal blood and hepatocytes.

27
Q

What is the general function of Kuppfer cells?

A

Hepatic macrophages that reside in hepatic sinusoids - normally responsible for phagocytosis of micro-organisms and degenerated mormal cells

28
Q

What happens to liver Kuppfer cells during liver injury?

A

When activated Kuppfer cells activate HSCs through release of pro-inflammatory cytokines

29
Q

What happens to hepatocytes during liver injury?

A

Hepatocytes release Reactive Oxygen Species and fibrogenic mediators that activate HSCs

30
Q

List some causes of fatty liver disease.

A

Fatty change accompanies some types of hepatocellular metabolic derangement:

  • Alcohol
  • Obesity
  • Drugs and toxins
  • Type II diabetes
  • Hypertriglyceridaemia
  • Starvation
31
Q

What is the difference between macro vs microvascular steatosis?

A

Macro:

  • Characterised by large droplets of fat that displace the nucleus to one side - more commonly seen
  • Causes: Alcohol, obesity, DM, Hepatitis C, malnutrition and corticosteroids

Micro (often v sick when presenting + v uncommon):

  • Characterised by fine vacuolations of cytoplasm, with nucleus in centre of cell
  • Causes: Fatty liver of pregnancy, Reye syndrome, alcoholic foamy degeneration, drug toxicity and TPN
32
Q

List some of the complications of fatty liver disease.

A
  • Steatohepatitis
  • Fibrosis
  • Cirrhosis
33
Q

What are the histological features of steatohepatitis.

A
  1. Balloning
  2. Mallory bodies
  3. Fibrosis (special stain - Pericellular fibrosis)
  4. Inflammation
34
Q

List some complication of cirrhosis.

A
  • Liver failure
  • Portal hypertension
  • Hepatocellular carcinoma
35
Q

Explain how cirrhosis leads to liver failure and portal hypertension.

A
36
Q

How is portal hypertension defined clinically?

A
  • Clinically defined by a Hepatic Venous Pressure Gradient equal to or >8mmHg
  • Comparison of pressures between portal vein and IVC
37
Q

What are the common causes of portal hypertension?

A
  • Pre-hepatic: Portal or splenic vein thrombosis
  • Intra-hepatic: Any cause of cirrhosis
  • Post-hepatic: Obstruction of hepatic vein/IVC
38
Q

What are the consequences of portal hypertension?

A
  1. Opening of portal-systemic collateral veins (varices)
  2. Ascites
  3. Splenomegaly
  4. Porto-systemic encephalopathy
39
Q

Why do varices occur?

A

Varices occur due to porto-systemic shunting

40
Q

Where do the varices occur?

A
  • Oesophageal
  • Gastric
  • Splenic
  • Anterior abdominal wall
  • Anal canal
41
Q

What is caput medusae?

A

Engorgement of the paraumbilical veins - key in diagnosing

42
Q

Why do ascites occur?

A

Portal hypertension + reduced oncotic pressure + retention of salt and water = fluid leaks out of blood vessels into abdominal cavity

43
Q

What is splenomegaly and why does it happen?

A
  • Enlargement of spleen
  • Due to backflow of blood from the portal to the splenic vein
44
Q

What causes portosystemic encephalopathy?

A
  • Encephalopathy may occur due to acute or chronic liver failure
  • Caused by build up of ammonia in systemic circulation either due to damaged hepatocytes (unable to metabolise ammonia) or porto-systemic shunting resulting in by-passing of liver
  • Ammonia crosses blood brain barrier, and is taken up by astrocytes, which become swollen
45
Q

What are some of the symptoms and signs of encephalopathy?

A

Symptoms and signs of encephalopathy include: Mild confusion, irritability, amnesia, reversed sleep-wake cycle, liver flap (asterixis)

46
Q

What are some of the symptoms and signs of chronic liver failure?

A
47
Q

What are some of the peripheral physical signs of liver failure?

A

Peripheral physical signs:

  1. Palmar erythema – redness of the palms due to dilated capillaries in the hand. May be related to increased oestrogen levels
  2. Dupytren’s contracture – fibromatosis of the palmar fascia resulting in contracture of one or two fingers
  3. Asterixis – tremor of hands when arms are outstretched and wrists extended
  4. Jaundice
48
Q

Cirrhosis of any kind can predispose to ______.

A

Cirrhosis of any kind can predispose to hepatocellular carcinoma.

Yr 2 Gastrointestinal (37 decks)

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