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Gastrointestinal > Introduction to the Liver > Flashcards

Introduction to the Liver Flashcards

1
Q

Describe distinguishable features of the liver

A
  • Largest gland (2nd largest organ)

- Numerous functions; impacts all body systems

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2
Q

What is the significance of the livers structure?

A

Major aspects of it’s structure influence it’s functions:

  • vascular system
  • billiary tree

3D arrangement of liver cells with vascular and biliary systems

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3
Q

Describe the structure of the liver

A

Divided into 2 lobes by the falciform ligament

- each lobe has own blood supply

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4
Q

What is the role of the gallbladder?

A

Stores bile (is green sac)

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5
Q

How does bile reach the duodenum?

A

The common bile duct delivers bile into the duodenum

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6
Q

Describe the venous blood supply of the liver

A

majority (75%) of liver blood supply is venous blood from the portal vein, carrying blood returning from GI full of digested products

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7
Q

Describe the arterial blood supply to the liver

A

25% from the hepatic artery

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8
Q

Describe the venous blood flow in the liver

A

Blood from the central veins in the liver lobules drain into the hepatic vein and then into vena cava

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9
Q

What are the 2 primary cells of the liver?

A 
Hepatocytes (60%)
Kupffer cells (30%)
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10
Q

What is the function of hepatocytes?

A

perform most metabolic functions

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11
Q

What is the role of the endothelial kupffer cells?

A

(type of macrophage)

carry out phagocytic activity by removing aged / damaged rbcs, bacteria, viruses and immune complexes

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12
Q

How does the liver deal with toxic substances?

A

Hepatocytes remove toxic substances, including alcohol from the blood
exits lobule through central vein (hepatic venule)

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13
Q

Describe the counter-current flow of blood and bile

A

Blood flows in the opposite direction to bile

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14
Q

What is the functional unit of the liver?

A

Hepatic lobules

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15
Q

What are hepatic lobules?

A

Hexagonal plates of hepatocytes around a central hepatic vein
At each 6 corners there’s a triad of portal vein, hepatic artery and bile duct branches

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16
Q

Describe the flow of bile through the billiary system

A 
Bile secreted by hepatocytes
↓
series of channels between cells (canaliculi)
↓
small ducts
↓
large ducts
↓
anastomose onto common bile duct
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17
Q

What is the benefit of the liver’s micro-structures?

A

Provides large SA for the exchange of molecules

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18
Q

How does the liver remove toxins?

A

Blood enters lobules through branches of the portal vein and hepatic artery, into smaller channels (sinusoid) lined with hepatocytes which pick up any bacteria from the intestine

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19
Q

What is bile?

A

Greenish-yellow liquid consisting of complex mix of water, electrolytes and organic molecules:

  • bile acids
  • cholesterol
  • bilirubin
  • phospholipids
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20
Q

What is the role of bile?

A

Essential for fat digestion & absorption via emulsification

Bile + pancreatic juice neutralises gastric juice as it enters the small intestine aids digestive enzymes

Elimination of waste products from blood in particular bilirubin & cholesterol

500mg of cholesterol converted to bile acids per day

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21
Q

What are the 2 stages of bile secretion?

A
  1. By hepatocytes:
    • Bile salts, cholesterol & other organic constituents
  2. By Epithelial cells lining bile ducts
    • Large quantity of watery Na+ & HCO₃⁻ solution
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22
Q

What causes the secretion of bile?

A

Release stimulated by secretin hormone in response to acid in the duodenum

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23
Q

Describe in detail the flow of bile

A
  1. Initially hepatocytes secrete bile into canaliculi
  2. Flows into bile ducts containing lots of bile salts,
    cholesterol and other organic constituents.
  3. Modified by water and bicarbonate-rich secretion from
    epithelial ductal cells
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24
Q

How does the gallbladder end up storing bile?

A 
Bile from hepatic ducts
↓
common bile duct
↓
duodenum
OR
diverted via cystic duct
↓
GALL BLADDER
↓
concentrated
& stored (30-50ml)
↓
Released by CCK in response to fat in the duodenum
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25
Q

What is the role of the sphincter of Oddi?

A

controls entry of bile into duodenum

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26
Q

What is bilirubin?

A

Yellow pigment formed from breakdown of haemoglobin
Useless & toxic but made in large quantities
(~6g/day) → must be eliminated

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27
Q

What is the average lifespan of RBCs?

A

120 days

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28
Q

What happens to dead / damaged RBCs?

A

Digested by macrophages throughout body:

  • Spleen
  • Liver
  • Red bone marrow etc.
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29
Q

What is the fate of the Fe from breakdown of RBCs?

A

Fe is recycled and stored in liver

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30
Q

What happens to the globin chains after RBC breakdown

A

Globin chains are protein → catabolized into amino acids for protein synthesis

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31
Q

What is the fate of haeme groups after RBC breakdown?

A

Haeme (porphyrin) cannot be recycled → eliminated

32
Q

Explain how haeme is eliminated

A

Haem → bilverdin → bilirubin → liver → incorporated into bile

33
Q

Outline how bilirubin is eliminated

A
  1. Haeme converted into free bilirubin, (intermediate
    product is biliverdin)
  2. Released into plasma; carried around body to liver
    bound to albumin
  3. Free bilirubin absorbed by hepatocytes → conjugated
    with glucoronic acid (to become soluble in bile)
  4. Conjugated bilirubin secreted into bile → metabolised
    by bacteria intestinal lumen & eliminated into faeces /
    urine
34
Q

What pigments cause the colour of urine and faeces?

A

Major metabolite in faeces is Stercobilin – brown colour

In urine – Yellow urobilin & urobilinogen

35
Q

What is jaundice?

A

Excessive quantities of free or conjugated bilirubin accumulated in ECF causing a yellow discoloration of skin, sclera and mucous membranes

36
Q

What is the normal bilirubin content in the plasma?

A

Normal plasma [bilirubin] <17µmol/L (1.0 mg/dl),

37
Q

How much bilirubin is required to cause discolouration?

A

discolouration > 34-51µmol/L (2-3mg/dl)

38
Q

What is the sclera?

A

opaque, white outer layer of the eye

39
Q

What are the 3 types of jaundice that can occur?

A

Pre-hepatic (haemolytic)
Hepatic
Post-hepatic (obstructive)

40
Q

Explain the cause of Pre-hepatic (haemolytic) jaundice

A

Excessive RBC breakdown

Excess conjugated bilirubin not excreted - remains in circulation

41
Q

Give an example of pre-hepatic jaundice

A

e.g. Neonatal jaundice
- baby in anaerobic environment in womb so lungs filled
with fluid
- switch to air when born →lots of RBCs broken down

Treatment: Light therapy (UV)
converts bilirubin→water soluble compound

42
Q

Describe hepatic jaundice and its causes

A

Extensive (>80%) hepatocyte damage caused by:

  • cirrhosis
  • drugs
  • Hepatitis A, B, C, E
  • Gilbert’s syndrome
  • excess (un)conjugated bilirubin
43
Q

Give an example of hepatic jaundice

A

e.g. Gilbert’s Syndrome
- congenital disorder; patients have decreased enzyme to
conjugate bilirubin with glucoronic acid
- increases unconjugated bilirubin

44
Q

What is post-hepatic (obstructive) Jaundice?

A

Excess conjugated bilirubin - enters circulation + urine
(v. dark urine)
Obstruction of passage into duodenum

45
Q

What causes post-hepatic (obstructive) jaundice?

A

gallstones
carcinoma
pancreas/bile ducts

46
Q

Which toxic substances does the liver metabolise?

A 
Bilirubin
Ammonia
Hormones
- e.g. inactivates all steroids:
 (androgens, oestrogen, cortisol, thyroxine, aldosterone)
Drugs + exogenous toxins 
- e.g. aspirin, paracetamol, ethanol
47
Q

What are the 2 phases the liver metabolises drugs and hormones in?

A

Phase 1 - oxidation/reduction
Phase 2 - Conjugation

*not all drugs require both phases

48
Q

Explain what occurs in Phase 1 of metabolism

A

Primarily oxidation / reduction
Occurs in SER
Catalysed mainly by Cytochrome P450 family
=> polar compound formed

49
Q

What happens in stage 2 of liver metabolism?

A

Conjugation to form a water soluble product

Glucoronyl is most prevalent

50
Q

How are metabolised drugs / hormones excreted?

A

Elimination occurs via ATPase pumps

51
Q

What is the chemical name of paracetamol?

A

acetaminophen

52
Q

Why is overdose common with paracetamol?

A

Has a narrow therapeutic index so deliberate/accidental overdose is common

53
Q

What is the maximum dose of paracetamol to be taken?

A

4 g/day or 1 g/dose

*not to be taken after alcohol consumption

54
Q

How does the detoxification of paracetamol occur?

A

Metabolised by 3 pathways:

  1. Glucoronidation
  2. Sulfation (20-30%)
  3. N-hydroxylation and dehydration
    • Intermediate = NAPQI (toxic)
    • detoxified by GSH conjugation
55
Q

What is the effect of Paracetamol overdose?

A

Liver enzymes become saturated
GSH stores are depleted
=> NAPQI builds up

Causes liver necrosis and kidney damage

56
Q

How is paracetamol overdose treated?

A

Via infusion of N-acetyl cysteine (GSH precursor) to conjugate NAPQI

57
Q

What are the 2 effects (phases) of Paracetamol overdose?

A
  • damage not immediate

- effective treatment but given too late

58
Q

Where in the body is alcohol removed from?

A

Only in the liver

59
Q

What happens to alcohol consumed?

A

Alcohol →acetaldehyde (via alcohol dehydrogenase)

=> produces NADH used by pyruvic acid→lactate
=> lactate build up = acidosis

60
Q

How does alcohol consumption lead to hypoglycemia?

A

pyruvic acid is a substrate for gluconeogenesis
=> can develop hypoglycemia after drinking
- reducing BGL

61
Q

What is the fate of the NADH produced from alcohol metabolism?

A

NADH enters fat metabolism to generate FA and glycerol

→FA burnt off as energy→acetyl coA (driven by NADH)
→acetyl CoA→ketone bodies rather than entering tca

62
Q

What happens if FA can’t enter the tca?

A

build up as ketone bodies

form excess lipids and are deposited in adipose tissue

63
Q

What is the fate of acetaldehyde production from alcohol metabolism?

A

Acetaldehyde is toxic - needs removal:

Acetaldehyde→Acetate→circulation
via acetaldehyde dehydrogenase

64
Q

Explain why alcohol flush reaction occurs so commonly among asians?

A

50% of asians have ALDH2 deficiency due to mutation of copy 1 gene → accumulation of acetaldehyde → alcohol flush reaction

65
Q

What are the stages of alcohol induced liver damage?

A

Fatty liver → Liver fibrosis → cirrhosis

66
Q

Describe a fatty liver caused by alcohol

A

Deposits of fat causes liver enlargement

Strict abstinence can lead to a full recovery

67
Q

Describe liver fibrosis

A

Scar tissue forms on liver

Recovery is possible, but scar tissue remains

68
Q

Describe liver cirrhosis

A

Growth of connective tissue destroys liver cells

Damage is irreversible

69
Q

What are the effects of impaired detoxification?

A

Gynecomastia due to alcoholic cirrhosis

70
Q

Name blood clotting factors synthesised in the liver

A

Fibrinogen
Prothrombin
nearly all other factors e.g. V, VI, IX, X, XII

71
Q

What is the significance of vitamin K in coagulation factor synthesis?

A

Vitamin K is essential for prothrombin formation and Factors II, IX VII and X

72
Q

What effect does liver damage have on clotting factors?

A

In severe liver disease, excessive bleeding may result due to a lack of coagulation factors

73
Q

Outline the storage that occurs in the liver

A

Hepatocytes - depots for fat soluble vitamins: K, D, E A

Stores Vit. B12 , folate and Iron as ferritin

74
Q

What is the consequence of liver dysfunction?

A

fat malabsorption→vit. deficiency

75
Q

What is the effect of Vit. B12 deficiency?

A

pernicucus anemia

76
Q

What is the requirement of folate?

A

Required during pregnancy

Gastrointestinal (18 decks)

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