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SGUL - Physiology 1 > The Liver - An Introduction to Its Function > Flashcards

The Liver - An Introduction to Its Function Flashcards

1
Q

What are the 3 major aspects of the liver’s structure that influence its function?

A
  • vascular system
  • biliary tree
  • 3D arrangement of liver cells with the vascular and biliary systems
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2
Q

What accounts for a majority of blood supply to the liver?

A

Venous blood from the portal vein

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3
Q

Where does the blood in the portal vein come from?

A

Blood returning from the GI, full of digested products

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4
Q

What accounts for a minority of blood supply to the liver?

A

Hepatic artery

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5
Q

How does blood from the liver return to the vena cava?

A
  • Blood from the central veins in the liver lobules drain into the hepatic vein
  • This drains into the vena cava.
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6
Q

What are the four types of liver cells?

A

HEPATOCYTES
KUPFFER CELLS
LIVER ENDOTHELIAL CELLS and STELLATE CELLS.

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7
Q

What are the purpose of hepatocytes?

A

Metabolic functions in liver

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8
Q

What is the functional unit of the liver?

A

Hepatic lobule

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9
Q

Describe the structure of the hepatic lobule.

A
  • Hexagonal plates of hepatocytes around the central hepatic vein.
  • At each of the corners are branches from the portal vein, hepatic artery and bile duct.
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10
Q

Describe blood flow through the liver.

A
  • Enters the lobules through branches of the portal vein and hepatic artery
  • Flows through small channels called sinusoids that are lined with hepatocytes.
  • Blood exits lobule through central vein (hepatic venule)
  • Blood flow is in the opposite direction to the flow of bile.
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11
Q

What do hepatocytes do to blood flowing through the lobule?

A

Remove toxic substances, including alcohol, from the blood

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12
Q

Compare and contrast the oxygen content of blood entering the lobule to blood leaving the lobule.

A
  • Blood entering (at the hepatic artery) is relatively oxygen-rich
  • Blood leaving contains low levels of oxygen (at the terminal hepatic venule)
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13
Q

Why does blood leaving the lobule have low levels of oxygen?

A
  • Hepatocytes along the sinusoids use up much of the available oxygen
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14
Q

How does the biliary system go (in terms of structures)?

A
  • bile is secreted by hepatocytes
  • goes through canalinculi
  • goes to small ducts
  • goes to large ducts
  • anastamose onto common bile duct
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15
Q

How does the liver’s microstructure support its roles?

A
  • massive surface area for exchange of molecules
  • sophisticated separation of blood from bile
  • specific positioning of pumps to achieve specific localisation of materials
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16
Q

What happens to blood as it passes through the intestinal capillaries?

A
  • Picks up bacteria
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17
Q

What are the purpose of Kupffer cells?

A

Cleanse the blood as it passes through the sinusoid

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18
Q

What happens as bacteria come into contact with Kupffer cells?

A
  • Bacterium passes inwards through the wall of the Kupffer cells
  • Permanently lodged in wall till digested.
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19
Q

What is bile?

A

Liquid consisting of a complex mix of water, electrolytes and organic molecules

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20
Q

Give examples of the organic molecules found in bile.

A
  • Cholesterol
  • Bilirubin
  • Phospholipids
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21
Q

Outline what occurs during bile secretion.

A
  • Hepatocytes secrete bile into the canaliculi
  • Bile flows into the bile ducts
  • Modified by water and bicarbonate-rich secretion from epithelial ductal cells.
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22
Q

What does bile do?

A
  • Fat digestion and absorption via emulsification
  • Neutralises gastric juice as it enters the small intestine and aids digestive enzymes.
  • Aids elimination of waste products from the blood
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23
Q

What waste products does bile aid the elimination of?

A
  • Bilirubin
  • Cholesterol
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24
Q

How does bile enter the duodenum?

A

Via the major duodenal papillae (the Sphincter of Odii)

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25
Q

What is the purpose of the Sphincter of Odii?

A

Controls bile entry

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26
Q

How can bile be transported to the gall bladder?

A

Via the cystic duct where it is stored and concentrated

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27
Q

What is bilirubin?

A
  • Yellow pigment formed from the breakdown of haemoglobin
  • Gives bile its colour.
  • Toxic and made in large quantities so has to be eliminated.
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28
Q

Describe the destruction of aged RBCs. PART 1

A
  • Digested by macrophages throughout the body.
  • Fe is recycled.
  • Globin chains are catabolised to various amino acids and then reused.
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29
Q

Describe the destruction of aged RBCs. PART 2

A
  • Haem cannot be recycled so has to be eliminated
  • Haem converted to bilirubin
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30
Q

Describe the formation and elimination of bilirubin. PART 1

A
  • Senescent red cell is broken down into globin, haem and iron
  • Haem is converted into free bilirubin.
  • Bilirubin is released into the plasma and carried around bound to albumin.
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31
Q

Describe the formation and elimination of bilirubin. PART 2

A
  • Albumin-bound bilirubin is then stripped of the albumin and absorbed into hepatocytes, where it is conjugated with glucuronic acid.
  • Conjugated bilirubin then secreted into the bile, where it is metabolised by bacteria of the intestinal lumen.
32
Q

Describe the formation and elimination of bilirubin. PART 3

A
  • Bacteria in the intestinal lumen metabolise bilirubin to other compounds which are eliminated either in faeces or in urine (following reabsorption).
  • Major metabolite of bilirubin in faeces is stercobilin.
  • In the urine, yellow urobilin and urobilinogen.
33
Q

What is increased during hepatocyte damage/hepatitis?

A

Renal excretion of urobilin and stercobilinogen

34
Q

What is jaundice?

A

Excessive quantities of free or conjugated bilirubin accumulate in the ECF

35
Q

What are the symptoms of jaundice?

A

Yellow discolouration of the skin, sclera and mucous membranes is observed

36
Q

What was the rare case of ‘green’ jaundice caused by?

A
  • Mutation of the biliverdin reductase gene
  • Biliverdin not converted to bilirubin and instead built up in the serum
37
Q

What are the consequences of increased haemolysis in neonates?

A

Excess bilirubin that the liver has no capacity to conjugate

38
Q

What cannot be done with unconjugated bilirubin in neonates?

A

Cannot be excreted in the urine and remains in circulation

39
Q

What causes neonatal jaundice?

A
  • Neonates have increased red cell mass for survival in utero.
  • Increased rate of RBC destruction as foetal Hb replaced with adult Hb after birth
  • Liver still immature, so delay in processing.
40
Q

How can light therapy be used to treat neonatal jaundice?

A
  • Isomerisation of bilirubin
  • Transformation into water-soluble compounds that can be excreted via urine and stools.
41
Q

Describe the hepatic causes of jaundice. PART 1

A

Problems with hepatocytes - increase in unconjugated and conjugated serum bilirubin.

42
Q

Describe the hepatic causes of jaundice. PART 2

A

Gilbert’s Syndrome
- Congenital disorder where patients have decreased levels of an enzyme that conjugates bilirubin with glucuronic acid
- Accumulation of unconjugated bilirubin.

43
Q

What hepatocyte problems can cause jaundice?

A
  • Damage to the hepatocytes and biliary tree from cirrhosis
  • Drugs
  • Viral infections like Hep A, B, C,E
44
Q

Describe the post-hepatic causes of jaundice.

A
  • Passage of conjugated bilirubin into the duodenum is blocked and leaks into the circulation and urine
  • Causes itching (pruritus)
45
Q

Describe the liver’s role in biotransformation/detoxification.

A

Metabolises and excretes toxic substances:
- bilirubin
- ammonia
- hormones (eg. all steroid hormones (androgens, cortisol, aldosterone, thyroxine) are inactivated by conjugation and excretion
- drugs and exogenous toxins (such as asprin, paracetamol, ethanol, etc.)

46
Q

In what form are most steroids excreted as?

A

Glucuronide/sulphate conjugates.

47
Q

RECAP TO FPP: Describe Phase 1 of drug metabolism.

A
  • Oxidation via cytochrome P450 enzymes.
  • Substrate becomes more polar which sometimes makes it more active/toxic.
48
Q

RECAP TO FPP: Describe Phase 2 of drug metabolism.

A
  • Conjugation occurs in order to make the drug water-soluble to be eliminated.
  • Conjugated with different groups, such as glucuronyl (the most important), acetyl, methyl, sulphate, etc.
49
Q

RECAP TO FPP: Describe Phase 3 of drug metabolism.

A

Conjugate substance eliminated into the blood or bile using ATPase pumps.

50
Q

Describe what happens during paracetamol overdose.

A
  • Liver enzymes are saturated and glutathione stores are rapidly depleted
  • Leads to liver necrosis and damage to the kidney by toxic metabolites.
51
Q

What is the main treatment for paracetamol overdose?

A

Giving N-acetylcysteine, the precursor to glutathione, which increases its levels.

52
Q

Describe why ethanol metabolism and oxidation is important.

A
  • Alcohol is readily absorbed in GI tract
  • Alcohol cannot be stored, and therefore, must be oxidised, which only happens in liver.
53
Q

What occurs during ethanol metabolism?

A
  • Oxidation of ethanol to acetaldehyde
  • Catalysed by the enzyme alcohol dehydrogenase, containing the coenzyme NAD+.
54
Q

Alcohol oxidation produces high amounts of NADH, which has many uses. Describe some of these uses. PART 1

A

Conversion of pyruvic acid to lactic acid requires NADH.
- Pyruvic Acid + NADH + H+ = Lactic Acid + NAD+

55
Q

How can pyruvic acid conversion lead to hypoglycaemia?

A
  • Pyruvic acid used for conversion into glucose by gluconeogenesis
  • Most get converted to lactic acid
  • Pathway is inhibited from the lack of glucose synthesis.
56
Q

How can pyruvic acid conversion lead to acidosis?

A

Lactic acid accumulation

57
Q

Alcohol oxidation produces high amounts of NADH, which has many uses. Describe some of these uses. PART 2

A

Used as a reducing agent in two pathways involved in lipogenesis - one to synthesise glycerol and the other to synthesise fatty acids.

58
Q

Alcohol oxidation produces high amounts of NADH, which has many uses. Describe some of these uses. PART 3

A

May be used directly in the ETC to synthesis ATP as a source of energy

59
Q

What is the consequence of increased NADH consumption within the ETC? PART 1

A
  • Inhibits normal oxidation of fats in the fatty acid spiral and citric acid cycle.
  • Fats or Acetyl CoA may accumulate, with resulting production of ketone bodies.
60
Q

What is the consequence of increased NADH consumption within the ETC? PART 2

A
  • Accumulation of fat in the liver can be alleviated by secreting lipids into the blood stream.
  • Higher lipid levels in the blood may be responsible for heart attacks.
61
Q

What is the result of excess acetaldehyde?

A
  • Toxic to liver
  • Can cause hepatitis and cirrhosis
62
Q

Describe the alcohol flush reaction.

A
  • Face and/or body experiences flushes or blotches, due to an accumulation of acetaldehyde.
63
Q

What is the alcohol flush reaction caused by?

A
  • Missense polymorphism that encodes acetaldehyde dehydrogenase (ALDH2), normally responsible for breaking down acetaldehyde
64
Q

What are some liver problems caused by alcohol? PART 1

A

FATTY LIVER - alcohol abuse can lead to the accumulation of fat within the liver cells

65
Q

What are some liver problems caused by alcohol? PART 2

A

ALCOHOL HEPATITIS: the excessive use of alcohol can cause acute and chronic hepatitis (inflammation of the liver)

66
Q

What are some liver problems caused by alcohol? PART 3

A

ALCOHOLIC CIRRHOSIS: Degenerative disease where liver cells are damaged and replaced by scar formation.

67
Q

What can cause cirrhosis?

A
  • Excessive alcohol intake
  • Chronic hepatitis B and C infections
  • Intake of certain chemicals and poisons
  • Too much iron or copper
68
Q

How does severe liver disease affect coagulation? PART 1

A
  • Liver activates several factors that are essential in the coagulation cascade, such as fibrinogen, prothrombin, and other factors (eg. V, VI, IX, X, XII).
69
Q

How does severe liver disease affect coagulation? PART 2

A
  • Vitamin K is also essential for the formation of prothrombin and factors II, VII, IX and X.
  • In severe liver disease, excessive bleeding may result due to a lack of these factors.
70
Q

Describe the vitamin storage in the liver.

A
  • Hepatocytes (stellate cells in particular) are involved in storage fat-soluble Vitamin D, K, E and A.
  • With liver dysfunction, we will end up with fat malabsorption, which would lead to a vitamin deficiency.
71
Q

Describe Vitamin B12 storage in the liver.

A
  • Liver stores Vitamin B12
  • Vitamin B12 deficiency leads to anaemia.
72
Q

Why does the liver store folate?

A

Required in early pregnancy

73
Q

Describe iron storage in the liver.

A
  • Stored as ferritin
  • Released when needed (blood-iron buffer).
74
Q

What divides the liver into 2 lobes?

A

Falciform ligament

75
Q

Why is accidental overdose common with paracetamol?

A

Narrow therapeutic index

76
Q

When should paracetamol not be taken?

A

Following alcohol consumption

77
Q

What are the 3 pathways that paracetamol is metabolized by?

A

→ Glucuronidation
→ Sulfation
→ N-hydroxylation & dehydration

SGUL - Physiology 1 (68 decks)

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