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ESA 3 - Gastrointestinal System > Liver, Biliary Tree and Pancreas > Flashcards

Liver, Biliary Tree and Pancreas Flashcards

1
Q

Into where does the stomach empty chyme?

A

The duodenum

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2
Q

What are the key properties of chyme?

A
  • Acidic
  • Hypertonic
  • Partly digested
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3
Q

How is the acidic nature of chyme corrected?

A

By HCO3- secreted from the pancreas, liver, and duodenal mucosa

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4
Q

When is HCO3- produced?

A

During the production of gastric acid

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5
Q

How is the hypertonicity of chyme corrected?

A

Osmotic movement of water into the duodenum across its wall

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6
Q

How is digestion of chyme completed?

A
  • By enzymes from the pancreas and duodenal mucosa
  • With bile acids from the liver
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7
Q

What components is bile made up of?

A
  • Bile acid dependant
  • Bile acid independant
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8
Q

What is the bile acid dependant component of bile secreted by?

A

Cells lining the canaliculi

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9
Q

What does the bile acid dependant component of bile consist of?

A
  • Bile acids (salts)
  • Cholesterol
  • Bile pigments
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10
Q

Name the two primary bile salts

A
  • Cholic acid
  • Chenodeoxycholic acid
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11
Q

What happens to bile salts in bile?

A

They are conjugated to amino acids and travel as micelles in the bile

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12
Q

Where do bile salts play a major role?

A

In the digestion and absorption of fat

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13
Q

What is the name of the majority bile pigment?

A

Bilirubin

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14
Q

What secretes the bile acid independent component of bile?

A

Cells lining the intra-hepatic bile ducts

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15
Q

What does the bile acid independant component of bile consist of?

A

Alkaline juice (HCO3-) like that form pancreatic duct cells

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16
Q

Label this diagram

A
  • A - Liver lobules
  • B - Interlobular portal triads
  • C - Central veins
  • D - Hepatocytes
  • E - Sinusoids
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17
Q

What supports the livers function?

A

Its microscopic structure

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18
Q

What is the basic functional unit of the liver?

A

A lobule surrounding a central vein

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19
Q

What does the central vein of a liver lobule do?

A

Drains blood from the liver to the systemic veins

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20
Q

Where does blood entering the liver lobule come from?

A

The hepatic portal vein and hepatic arteries

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21
Q

Where does blood entering the lobule from the hepatic portal vein and the hepatic arteries enter the vessels?

A

At the periphery of the lobule

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22
Q

How does blood entering the lobule via the hepatic portal vein and hepatic artery reach the central vein?

A

It flows through sinusoids

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23
Q

What lines sinusoids?

A

Hepatocytes

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24
Q

Where is bile formed?

A

Canaliculi

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25
Q

What happens to bile once it has been produced in canaliculi?

A

It flows towards the periphery into bile ducts

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26
Q

Label this diagram

A
  • A - Deep lymphatic duct receiving lymph from perisinusoidal space
  • B - Blood flowing in sinusoids from interlobular (hepatic) artery and (portal) vein
  • C - Perisinusoidal spaces (of Disse)
  • D - Peribiliary arterial plexus
  • E - Hepatocytes
  • F - Central vein
  • G - Bile flowing from hepatocytes into bile canaliculi, to interlobular biliary ducts, and then to bile ducts in the extrahepatic portal triad
  • H - Bile canaliculi
  • I - Interlobular portal triad
    • ​Ii - Hepatic portal vein
    • Iii - Hepatic artery
    • Iiii - Biliary duct
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27
Q

What are the main functions of hepatocytes?

A
  • Produce bile
  • Detoxify blood
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28
Q

What is the main function of the central vein?

A

Transports clean blood to hepatic vein

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29
Q

What does the duodenum do in response to gastric emptying?

A

Secretes cholecystokinin (CCK)

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30
Q

What effect does CCK have?

A

It stimulates the contraction of the gall bladder

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31
Q

What is the effect of the contraction of the gall bladder?

A

It ejects concentrated bile acids together with enzymes from the pancreas

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32
Q

What organs release alkali for digestion?

A
  • Pancreas
  • Liver
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33
Q

What is alkali released from the pancreas and liver in response to?

A

Secretin

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34
Q

What are bile acids released through?

A

The Ampulla of Vater

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35
Q

What is the role of bile acids?

A

Aid with the digestion and absorption of fats

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36
Q

Where do bile acids go once they have been released?

A

They continue to the terminal ileum

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37
Q

What happens to bile acids in the terminal ileum?

A

They are actively absorbed by the epithelium

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38
Q

What happens once bile acids have been absorbed by the ileum epithelium?

A

Venous return from the gut enters the hepatic portal blood

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39
Q

What happens when bile acids have reached the hepatic portal blood?

A

Hepatocytes actively take up bile acids, and re-secrete them into the Canaliculi

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40
Q

What is the ultimate fate of most bile acids?

A
  • Most are recovered
  • Some are unconjucated by the gut bacteria and lost
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41
Q

How is the loss of unconjugated bile acids dealt with?

A

Hepatocytes subsequently replace them

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42
Q

What happens to bile acids in between meals?

A

They return to the liver

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43
Q

When are bile acids secreted by canaliculi cell walls?

A

A long time before they are next needed

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44
Q

What happens to bile acids that are secreted before they are needed?

A

They are stored in the gall bladder

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45
Q

How is the volume of bile acids that needs to be stored reduced?

A

Bile acids are concentrated by the transport of salt and water across the gall bladder epithelium

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46
Q

What is the clinical importance of the concentration process of bile acids?

A

It increases the risk of precipitation, leading to gall stones

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47
Q

What are the consequences of gallstones?

A

Often asymptomatic, but can cause very painful biliary colic

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48
Q

What causes biliary colic?

A

The movement of gallstones into the neck of the gall bladder of biliary tree

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49
Q

What often follows biliary colic?

A
  • Inflammation
  • Infection of the gall bladder
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50
Q

What is inflammation of the gall bladder called?

A

Cholecystitis

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51
Q

When may pain from gallstones be worse?

A

After eating

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52
Q

Why may pain from gallstones be made worse after eating?

A

The secretion of CCK will cause the gall bladder to contract

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53
Q

What does the exocrine pancreas secrete?

A
  • Alkaline juice (HCO3-)
  • Enzymes
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54
Q

What enzymes does the exocrine pancreas secrete?

A
  • Proteases
    • Trypsin(ogen)
    • Chymotrypsin
    • Elastase
    • Carboxypeptidase
  • Amylases
  • Lipases
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55
Q

What kind of organ is the exocrine pancreas?

A

A gland

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56
Q

What are the main components of the exocrine pancreas?

A
  • Acini
  • Ducts
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57
Q

What do the pancreatic acini do?

A

Secrete enzymes

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58
Q

In what form do the pancreatic acini secrete enzymes?

A

Mostly as inactive precursors

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59
Q

What happens to the enzymes being secreted from the pancreatic acini?

A

Packaged into condensing vacuoles, forming zymogen granules

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60
Q

What happens to zymogen granules?

A

They are secreted by exocytosis

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61
Q

Where are zymogen granules activated?

A

In the intestine

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62
Q

How are zymogen granules activated?

A

By enzymatic cleavage

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63
Q

What do the pancreatic ducts do?

A

Secrete alkaline juice

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64
Q

Why is HCO3- present in the blood at elevated concentrations?

A

Due to gastric acid secretion

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65
Q

How does the cellular mechanism of secretion of HCO3- in the pancreatic duct differ from in other cells?

A

It doesn’t

ha ha trick question i got u

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66
Q

What is the mechanism of secretion of HCO3-?

A
  • Na-K-ATPase sets up a Na+ concentration gradient
  • Hydrogen ions are exported from the duct cell into ECF using the Na+ concentration gradient
  • H+ ions combine with HCO3- to from H2O and CO2, which are taken up into the cell
  • H2O and CO2 reform H+ and HCO3- inside the cell
  • HCO3- is exported into the duct lumen
  • H+ ion is recycled, ‘going round in a circle’ to carry more HCO3- from the ECF to the lumen
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67
Q

What is duct secretion of HCO3- stimulated by?

A

Secretin

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68
Q

What releases secretin?

A

Jejunal cells

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69
Q

What is secretin released from jejunal cells in response to?

A

Low pH

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70
Q

What facilitates secretin’s action?

A

Cholecystokinin (CCK)

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71
Q

What are the two sources of pancreatic secretion?

A
  1. Acinar
  2. Duct
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72
Q

What is pancreatic acinar secretion stimulated by?

A

Cholecystokinin (CCK)

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73
Q

Where is CCK released from?

A

Duodenal APUD cells

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74
Q

What is CCK secretion and thus pancreatic acinar secretion stimulated by?

A
  • Hypertonicity
  • Fats
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75
Q

What stimulates pancreatic duct secretion?

A

Secretin

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76
Q

What is secretin release and thus pancreatic duct secretions stimulated in by?

A

Low pH

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77
Q

What is CCK secreted by the duodenum in reponse to?

A

Gastric emptying

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78
Q

What does CCK stimulate?

A

Contraction of the gall bladder muscle

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79
Q

What is the result of the contraction of the gall bladder muscle?

A

Biliary secretion

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80
Q

Are fats soluble in water?

A

No, relatively insoluble

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81
Q

What is the result of fats being relatively insoluble in water?

A

They tend to aggregate into large globules

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82
Q

What is the result of the aggregation of fats into large globules in water?

A

It prevents the effective action of digestive enzymes

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83
Q

What exacerbates the formation of large globules of fat in the stomach?

A

Acid

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84
Q

What do bile acids enable in the duodenum?

With regards to fats

A

Enable fats to be incorporated into small micelles

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85
Q

How big are the micelles formed with the aid of bile acids in the duodenum?

A

4-6nm

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86
Q

Describe the structure of the micelles that fats are incorporated into in the duodenum?

A
  • Fats in the middle
  • Polar components of the bile acids on the outside
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87
Q

What is the purpose of the bile acid-fat micelles?

A
  • Generate a high surface area for the action of lipases
  • Carry products into the ‘unstirred layer’
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88
Q

What do lipases do to the bile acid-fat micelle?

A

Cleave the fatty acids from glycerol

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89
Q

Where is the ‘unstirred layer’ found?

A

Immediately next to the mucosa

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90
Q

What happens at the ‘unstirred layer’?

A

Fatty acids can be released to slowly diffuse into the epithelial cells

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91
Q

What happens to fatty acids once inside the epithelial cells?

A

They are reconstituted into triacylglycerols, and re-expelled as chylomicrons

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92
Q

What are chylomicrons?

A

Structured small particles made up of lipids covered in phospholipids

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93
Q

What do chylomicrons do?

A

Facilitate the transport of fat in the lymphatic system from the gut to systemic veins

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94
Q

What is steatorrheoa?

A

Fatty faeces

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95
Q

What causes steatorrheoa?

A

Bile acids or pancreatic enzymes not being secreted in adequate amounts, resulting in fat in the faeces

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96
Q

What are the symptoms of steatorrheoa?

A

Faeces that-

  • Pale
  • Float
  • Smell foul
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97
Q

What are bile pigments?

A

Excretory products

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98
Q

What is the most common bile pigment?

A

Bilirubin

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99
Q

When is bilirubin produced?

A

As a product of haemoglobin breakdown

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100
Q

What happens to bilirubin after production?

A

It is conjugated in the liver and secreted in the bile to be excreted in faeces

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101
Q

What happens if bilirubin cannot be excreted?

A

It accumulates in the blood, giving the condition known as jaundice

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102
Q

What is inevitable when ingesting food and water?

A

We also risk ingesting toxins

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103
Q

What toxins are we at risk of ingesting when eating and drinking?

A
  • Chemical
  • Bacteria
  • Viruses
  • Protozoa
  • Nematodes
  • Cestodes
  • Trematodes
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104
Q

What are nematodes?

A

Roundworms

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105
Q

What are cestodes?

A

Tapeworms

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106
Q

What are trematodes?

A

Flukes

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107
Q

How can the defence mechanisms that the GI tract has to deal with toxins be subdivided?

A
  • Innate
  • Adaptive
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108
Q

What are the types of innate immunity?

A
  • Physical
  • Cellular
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109
Q

What physical innate defences are present in the GI tract to deal with toxins?

A
  • Sight
  • Smell
  • Saliva
  • Stomach acid
  • Small intestine secretions
  • Colonic mucus
  • Anaerobic environment
  • Peristalsis
  • Segmentation
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110
Q

How does the sight and smell of food act as a defence?

A

If food looks or smells bad, you don’t eat it

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111
Q

How does memory act as a defence?

A

If food tastes bad, you don’t eat it next time

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112
Q

What pH is saliva?

A

7.0

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113
Q

What does saliva contain?

A
  • Lysozyme
  • Lactoperoxidase
  • Complement
  • IgA
  • Polymorphs
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114
Q

How does saliva act as a defence?

A

It washes toxins down into the stomach

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115
Q

How does stomach acid act as a defence?

A

Low pH kills the majority of bacteria and viruses

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116
Q

What are the small intestine secretions?

A
  • Bile
  • Proteolytic enzymes
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117
Q

How do the small intestine secretions act as a defence?

A
  • Means there is a lack of nutrients
  • Cause the shredding of epithelial cells
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118
Q

What is the purpose of the colonic mucus?

A

Protects the colonic epithelium from it’s contents

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119
Q

What areas in the GI tract have an anaerobic environment?

A
  • Small bowel
  • Colon
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120
Q

What is the normal intestinal transit time?

A

12-18hrs

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121
Q

What happens if peristalsis is slowed?

A

Gut infections are prolonged

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122
Q

Give an example of an infection that can be prolonged by slowed peristalsis?

A

Shigellosis

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123
Q

What cellular innate defences are present in the GI tract to deal with toxins?

A
  • Neutrophils
  • Macrophages
  • Natural killer cells
  • Tissue mast cells
  • Eosinophils
124
Q

What are macrophages called in the liver?

A

Kupffer cells

125
Q

What do NK cells do?

A

Kill virus infected cells

126
Q

When are eosinophils recruited?

A

In parasitic infections

127
Q

Where does all venous blood from the GI tract pass before returning to the systemic circulation?

A

Through the liver - the hepatic portal system

128
Q

What are Kupffer cells?

A

Specialised macrophages in the liver

129
Q

Draw a diagram illustrating blood and bile flow through the hepatic portal system

130
Q

What adaptive defences does the GI tract have to protect against toxins?

A
  • B lymphocytes
  • T lymphocytes
  • Lymphatic tissues
131
Q

What do B lymphocytes do?

A

Produce antibodies, including IgA and IgE

132
Q

What are IgA and IgE particularly effective against?

A

Extracellular microbes

133
Q

What are T lymphocytes directed against?

A

Intracellular organisms

134
Q

What is Mucosal Associated Lymphoid Tissue (MALT) in the GI tract called?

A

Gut Associated Lymphoid Tissue (GALT)

135
Q

How is GALT distributed?

A
  • Diffusely distributed
  • Nodular in three locations-
    • Tonsils
    • Peyer’s patches
    • Appendix
136
Q

What do Peyer’s patches look like?

137
Q

What is reduced salivary flow known as?

A

Xerostomia

138
Q

What can cause xerostomia?

A
  • Severe illness
  • Dehydration
139
Q

What does xerostomia lead to?

A

Microbial overgrowth in the mouth and dental caries

140
Q

What can microbial overgrowth in the mouth and dental caries lead to?

141
Q

What is parotitis?

A

Salivary glands infections

142
Q

What microbe causes parotitis?

A

Staphylococcus aureus

143
Q

What is achlorhydria?

A

Absent or low gastric acid production

144
Q

What can cause achlorhydria?

A
  • Pernicious anaemia
  • Drugs such as H2 antagonists
  • PPIs
145
Q

What are patients with achlorhydria more susceptible to?

A

Shigellosis, cholera, and salmonella infections

146
Q

What is the clinical relevance of patients taking a protein pump inhibitor?

A

In a hospital environment, they are at increased risk of acquired Clostridium difficile

147
Q

Give 3 examples of resistant organisms?

A
  1. Mycobacterium tuberculosis
  2. Some enteroviruses
  3. Helicobacter Pylori
148
Q

What is mycobacterium tuberculosis resistant to?

A

Gastric acid

149
Q

What kind of bacterium is mycobacterium tuberculosis?

A

Acid and alcohol fast bacterium

150
Q

Give 3 examples of enteroviruses that are resistant?

A
  1. Hepatitis A
  2. Polio
  3. Coxsackle
151
Q

What are some enteroviruses resistant to?

A

Gastric acid

152
Q

Why is Helicobacter Pylori resistant?

A

It produces urease, which acts on urea to produce a protective cloud of ammonia

153
Q

What do mast cell granules contain?

154
Q

Which gut infections recruit mast cells?

A

Those that activate complement

155
Q

What does the recruitment of mast cells lead to?

A

The release of histamine

156
Q

What does the release of histamine cause?

A

Vasodilation and increased capillary permeability, which can give massive fluid loss

157
Q

How much fluid is lost per hour in cholera?

A

May get losses of 1litre/hr

158
Q

What is the mortality of cholera if untreated?

159
Q

What is the clinical significace of GALT?

A
  • Tonsillitis
  • Ileocaecal lymphatic tissue
  • Appendicitis
160
Q

What conditions are related to ileocaecal lymphatic tissue?

A
  • Mesenteric adenitis
  • Typhoid fever
161
Q

What is mesenteric adenitis a common cause of?

A

Right iliac fossa pain in children

162
Q

What can mesenteric adenitis be easily mistaken for?

A

Appendicitis

163
Q

What is mesenteric adenitis mostly caused by?

A

Adenovrius or coxsackie virus

164
Q

What does typhoid fever cause?

With respect to Peyer’s patches

A

Inflamed Peyer’s patches in the terminal ileum

165
Q

What is the potential outcome of inflamed Peyer’s patches in typhoid fever?

A

They can perforate and kill patients

166
Q

What do many causes of appendicitis arise from?

A

Lymphoid hyperplasia at the appendix base

167
Q

Why can lymphoid hyperplasia at the appendix base lead to appendicitis?

A

It leads to obstructed outflow.

Stasis leads to infection

168
Q

When is purulent appendictis more common?

A

During epidemics of chickenpox in children

169
Q

How may the appendix be obstructed, other than lymphoid hyperplasia?

A
  • By a faecolith
  • By a worm
170
Q

What is a faecolith?

A

Calcified faecal matter

171
Q

How can faecoliths be visualised?

A

On an X-ray

172
Q

What to the GI tract’s defence mechanism require?

A

The GI tract itself to have an intract blood supply

173
Q

What can intestinal or hepatic ischaemia be due to?

A
  • Arterial disease
  • Systemic hypertension
  • Intestinal venous thrombosis
174
Q

What can intestinal or hepatic ischamia lead to?

A
  • Overwhelming sepsis
  • Rapid death (within hours)
175
Q

What does liver failure increase susceptibility to?

A
  • Infections
  • Toxins
  • Drugs
  • Hormones
176
Q

What chemical will be present in increased amounts in the blood in liver failure?

177
Q

Why is ammonia present in the blood in increased amounts in liver failure?

A

Due to failure of the urea cycle

178
Q

What is ammonia produced by?

A
  • Colonic bacteria
  • Deamination of amino acids
179
Q

What is the clinical significance of an increase blood level of ammonia?

A

Can cause hepatic encephalopathy

180
Q

What are the causes of liver failure?

A
  • Industrial solvents
  • Drugs
  • Viral hepatitis
  • Mushroom poisioning
  • Alcohol
181
Q

What is the main cause of liver failure worldwide?

A

Viral hepatitis

182
Q

What is the main cause of liver failure in the UK?

183
Q

What is hepatic fibrosis also known as?

184
Q

What does hepatic fibrosis lead to?

A

Portal venous hypertension

185
Q

What does portal venous hypertension lead to?

A

Porosytemic shunting

186
Q

What does portosystemic shunting lead to?

A
  • Toxin shunting
  • Oesophageal varices
  • Haemorrhoids
  • Caput medusa
187
Q

What are bile pigments?

A

Excretory products

188
Q

What is the most common bile pigment?

189
Q

What is bilirubin produced as a product of?

A

Haemoglobin breakdown

190
Q

What happens to bilirubin after production?

A

It is conjugated in the liver and secreted in the bile to be excreted in faeces

191
Q

What happens if bilirubin cannot be excreted?

A

It accumulates in the blood

192
Q

What condition is caused by accumulation of bilirubin in the blood?

193
Q

What hormone does the liver notably break down?

194
Q

What are the functions of the liver, in relation to blood proteins?

A
  • Producing albumin
  • Producing coagulation factors
  • Producing thrombopoietin
  • Amino acid synthesis
195
Q

What is the most abudant plasma protein?

196
Q

What is albumin essential for?

A

Maintaining the oncotic pressure needed for proper distribution of body fluids

197
Q

What coagulation factors are produced by the liver?

A
  • I
  • II
  • V
  • VII
  • IX
  • X
  • XI
  • Protein C
  • Protein S
  • Antithrombin
198
Q

What is coagulation factor I also known as?

A

Fibrinogen

199
Q

What is coagulation factor II also known as?

A

Prothrombin

200
Q

What is thrombopoietin?

A

A glycoprotein hormone

201
Q

What does thrombopoietin do?

A

Regulates the production of platelets by bone marrow

202
Q

What aspect of amino acid synthesis is the liver responsible for?

A

Transamination

203
Q

What are the tests for liver function?

A
  • ALT/AST levels
  • Bilirubin levels
  • Alkaline phosphate levels
  • Albumin levels
  • Prothombin time (clotting)
204
Q

What does the presence of ALT or AST in the blood indiciate?

A

Liver damage

205
Q

Why is ALT and AST present in liver damage?

A

In hepatocellular damage, the ruptured membranes will allow aminotransferases into the blood stream

206
Q

What do raised levels of bilirubin or alkaline phosphate indicate?

A

Cholestasis (obstruction of the bile ducts)

207
Q

What happens to bilirubin in cholestasis?

A

Unable to excrete bilirubin, plasma concentration rises

208
Q

What is alkaline phosphatase?

A

An enzyme in cells lining the liver’s biliary ducts

209
Q

What happens to alkaline phosphatase in cholestasis?

A

Plasma levels rise with obstruction

210
Q

What happens to albumin in chronic liver disease?

A

Levels are reduced

211
Q

What does prothrombin time measure?

A

The clotting tendency of blood

212
Q

What kind of tests are those for albumin levels and prothrombin time?

A

Synthetic function

213
Q

Why does liver damage cause jaundice?

A

Damaged hepatocytes have a reduced capacity to excrete bilirubin. This leads to bilirubin accumulating in the blood, giving jaundice

214
Q

What is the name for the clinical condition describing increased levels of bilirubin?

A

Hyperbilirubinaemia

215
Q

What are the symptoms of hyperbilirubinaemia?

A

Yellowish pigmentation of the skin, conjunctival membranes over the scleae and other mucus membranes

216
Q

When is jaundice clinically detectable?

A

At levels >40µmol/L (normal range <22µmol/L)

217
Q

What are the types of jaundice?

A
  • Pre-hepatic
  • Hepatic
  • Post-hepatic
218
Q

What is the underlying pathology of pre-hepatic jaundice?

A

Excessive bilirubin production, and the liver is unable to cope with the excess bilirubin

219
Q

What usually causes excessive bilirubin production in pre-hepatic jaundice?

A

An increased breakdown of red blood cells (haemolysis)

220
Q

What are the lab findings in pre-hepatic jaundice?

A
  • Unconjugated hyperbilirubinaemia
  • Reticulocytosis
  • Anaemia
  • Increased LDH
  • Decreased haptoglobin
221
Q

What are the main causes of pre-hepatic jaundice?

A
  • Inherited
  • Congential hyperbilirubinaemias
  • Acquired
222
Q

What are the inherited causes of pre-hepatic jaundice?

A
  • Red cell membrane defects
  • Haemoglobin abnormalities
  • Metabolic defects
223
Q

What are the congential hyperbilirubinaemias leading to pre-hepatic jaundice?

A
  • Gilbert’s syndrome
  • Criger-Najjar syndrome
  • Dublin-Johnson syndrome
224
Q

How common is Gilbert’s syndrome?

A

Present in 10% of the population

225
Q

How common is Crigler-Najjar syndrome?

226
Q

How common is Dublin-Johnson syndrome?

227
Q

What are the acquired causes of pre-hepatic jaundice?

A
  • Immune
  • Mechanical
  • Acquired membrane defects
  • Infections
  • Drugs
  • Burns
228
Q

Give an example of a mechanical cause of pre-hepatic jaundice?

A

RBC’s running across metal heart valves

229
Q

What is the main pathology of hepatic jaundice?

A

Reduced capacity of liver cells to secrete conjugated bilirubin into the blood

230
Q

What are the lab findings in hepatic jaundice?

A
  • Mixed unconjugated and conjugated hyperbilirubinaemia
  • Increase in the liver enzymes ALT and AST
  • Abnormal clotting
231
Q

What are the main causes of hepatic jaundice?

A
  • Congential
  • Hepatic inflammation
  • Drugs
  • Cirrhosis
  • Hepatic tumours
232
Q

What are the congential causes of hepatic jaundice?

A
  • Gilbert’s syndrome
  • Crigler-Najjar syndrome
233
Q

What are the main causes of hepatic inflammation?

A
  • Viral
  • Autoimmune hepatitis
  • Alcohol
  • Haemochromotosis
  • Wilson’s disease
234
Q

What are the viral causes of hepatic inflammation?

A
  • Hepatitis A, B, C, and E
  • Epstein Barr Virus (EBV)
235
Q

What drugs can cause hepatic jaundice?

A

Paracetamol

236
Q

What are the main causes of cirrhosis?

A
  • Alcohol
  • Chronic hepatitis
  • Metabolic disorders
237
Q

What are the main kinds of hepatic tumours?

A
  • Hepatocellular carcinoma
  • Metastases
238
Q

What is the main pathology of post-hepatic jaundice?

A

Obstruction to the drainage of bile

239
Q

What is the consequence of the obstruction to the drainage of bile?

A

Causes a back up of bile acids into the liver, and so the passage of conjugated bilirubin is blocked

240
Q

What are the types of obstructions to the drainage of bile?

A
  • Intrahepatic
  • Extrahepatic
241
Q

What are the lab findings in post-hepatic jaundice?

A
  • Conjugated hyperbilirubinaemia
  • Bilirubin in the urine (makes urine dark)
  • Increased canalicular enzymes (ALP)
  • Can be incresed liver enzymes (ALT/AST)
242
Q

What are the main causes of intrahepatic post-hepatic jaundice?

A
  • Hepatitis
  • Drugs
  • Cirrohosis
  • Primary biliary colic
243
Q

What are the extrahepatic causes of post-hepatic jaundice?

A
  • Gallstones
  • Biliary stricture
  • Carcinoma
  • Pancreatitis
  • Sclerosig cholangitis
244
Q

What carcinomas can cause post-hepatic jaundice?

A
  • Head of pancreas
  • Ampulla
  • Bile duct
  • Porta hepatis lymph nodes
  • Liver metastases
245
Q

Is there bilirubin in the faeces in post-hepatic jaundice?

A

No, it is pale

246
Q

What is the pathology of alcoholic liver disease

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
247
Q

What is the pathogenesis of fatty liver?

A
  • Alcohol metabolism generates NADH from NAD+. Increased NADH induces fatty acid synthesis, and decreased NAD+ results in a decrease in fatty acid oxidation
  • There is an accumulation of fatty acids in the liver, with glycerol being converted to TAGs
  • TAGs accumulate, giving fatty liver
248
Q

What is alcoholic hepatitis?

A

Inflammation of hepatocytes

249
Q

What happens in cirrhosis?

A

Liver cell necrosis followed by nodular regeneration and fibrosis

250
Q

What is the result of liver cirrhosis?

A
  • Increased resistance to blood flow
  • Derenged liver function
251
Q

What are the potential complications of alcoholic liver disease?

A
  • Hepatocellular carcinoma
  • Liver failure
  • Wericke-Korsakoff syndrome
  • Encephalopathy
  • Dementia
  • Epilepsy
252
Q

What are the causes of liver cirrhosis?

A
  • Alcohol
  • Wilson’s Disease
  • Biliary cirrhosis
  • Haemochromotosis
  • Hepatitis B or C
  • Autoimmune hepatitis
  • α1-antitrypsin deficiency
253
Q

What are the clinical features of liver cirrhosis?

A
  • Liver dysfunction
  • Jaundice
  • Anaemia
  • Bruising
  • Palmar erythema
  • Dupuytren’s contracture
254
Q

What are the results of investigations indicating liver cirrhosis?

A
  • May be increase ALT/AST
  • Increased ALP
  • Increased bilirubin
  • Decreased albumin
  • Deranged clotting
255
Q

What is involved in the management of cirrhosis?

A
  • Stopping drinking
  • Treating complications
  • Transplantation
256
Q

What is portal hypertension defined as?

A

Portal venous pressure >20mmHg

257
Q

What can portal hypertension be caused by?

A
  • Obstruction of the portal vein
  • Obstruction of flow within the liver
258
Q

What are the main causes of obstruction of the portal vein?

A
  • Congenital
  • Thrombosis
  • Extrinsic compression
259
Q

What are the main causes of obstruction of flow within the liver?

A
  • Cirrhosis
  • Hepatoportal sclerosis
  • Schistosomiasis
  • Sarcoidosis
260
Q

What may portal hypertension lead to?

A
  • Ascites
  • Splenomegaly
  • Pathologies related to porto-systemic anastomoses
261
Q

How does portal hypertension cause ascites?

A

The high pressure in the portal venous system means blood is backed up into the abdomen. The increase in hydrostatic pressure in the abdomen means less fluid is reabsorbed into blood vessels at the end of capillary beds

262
Q

What may contribution to the development of ascites if the liver is damaged?

A

Reduced oncotic pressure inside the vessels, due to lack of plasma proteins

263
Q

Why does portal hypertension cause splenomegaly?

A

Due to subsequent increase blood pressure in the spleen

264
Q

How do pathologies related to porto-systemic anatomoses arise with portal hypertension?

A

There are several anastomoses bewteen the hepatic portal and systemic veins. As such, when the pressure is increased in the portal venous system, blood is backed up through these anastomoses, increasing the blood pressure

265
Q

What does increased blood pressure in porto-systemic anatomoses cause?

A
  • Vessels to dilate
  • Vessels to protrude into lumen
  • Rupturing
  • Ulceration
  • Haemorrhage
266
Q

What pathologies can arise due to increased pressure in porto-systemic anastomoses?

A
  • Oesophageal varices
  • Rectal varices
  • Caput Medusae
267
Q

Label this diagram

Include the porto-systemic anastomoses, running from portal to systemic.

A
  • A - Esophageal vein
  • B - Left gastric to Azygous/Oesphageal anastomoses
  • C - Stomach
  • D - Left gastric vein
  • E - Hepatic portal vein
  • F - Splenic vein
  • G - Inferior mesenteric vein (IMV)
  • H - Retroperitoneal veins
  • I - Colon
  • J - Colonic/Splenic/Portal to Retroperitoneal veins of the posterior abdominal wall or diaphragm anastomoses
  • K - Superior rectal vein
  • L - Rectal veins
  • M - Inferior rectal vein
  • N - Anus
  • O - Superior rectal to inferior rectal anastomoses
  • P - Epigastric veins
  • Q - Umbilicus
  • R - Paraumbilical to small epigastric of abdominal wall anastomoses
  • S - Paraumbilical vein
  • T - Superior mesenteric vein (SMV)
  • U - Liver
  • V - Inferior vena cava (IVC)
  • W - Azygous vein
    *
268
Q

What does increased pressure in the left gastric to azygous/oesophageal anastomoses lead to?

A

Oesophageal Varices

269
Q

What does increased pressure in the superior rectal to inferior rectal anatomoses lead to?

A

Rectal varices

270
Q

What does increased pressure in the paraumbilical to small epigastric of abdominal wall anastomose cause?

A

Caput Medusae

271
Q

Where are the portal veins involved in the portal to retroperitoneal veins of posterior abdominal wall or diaphragm located?

A

On the posterior aspects (bare areas) of secondarily retroperitoneal viscera or the liver

272
Q

What happens to bile acids in between meals?

A

They return to the liver

273
Q

What secrete bile acids?

A

Canaliculi cell walls

274
Q

When are bile acids secreted?

A

Long before they are next needed

275
Q

Where are bile acids stored until they are needed?

A

In the gall bladder

276
Q

How is the volume of bile acids that need to be stored reduced?

A

They are concentrated by the transport of salt and water across the gall bladder epithelium

277
Q

What is the problem with the process of concentration of bile acids?

A

It increases the risks of precipitation

278
Q

What does precipitation of bile acids lead to?

A

Gall stones

279
Q

What are the symptoms of gallstones?

A
  • Often asymptomatic
  • Can cause painful biliary colic, or obstruction
280
Q

When do gallstones cause biliary colic?

A

When they move itno the neck of the gall bladder or biliary tree

281
Q

What is biliary colic often followed by?

A
  • Inflammation of the gall bladder (cholecystitis)
  • Infection of the gall bladder
282
Q

When may pain from gallstones be worse?

A

After eating

283
Q

Why may pain from gallstones be worse after eating?

A

The secretion of cholecystokinin (CCK) will cause the gall bladder to contract

284
Q

Label this diagram

Indicate the clinically relevant locations of gallstones, and what they cause

A
  • A - Hepatic ducts
  • B - Common hepatic duct
  • C - Hartmann’s pouch
  • D - Common bile duct
  • E - Pancreatic duct
  • F - Sphincter of Oddi
  • G - Ampulla of Vater
  • H - Duodennum
  • I - Gall bladder
  1. Causing biliary obstruction
  2. Stone causing gallstone pancreatitis
  3. Asymptomatic gallstones
  4. Impacted in cystic duct, causing acute cholecystitis
285
Q

What is pancreatitis?

A

An inflammatory process

286
Q

What causes pancreatitis?

A

Effects of enzymes released from pancreatic acini

287
Q

What are the macroscopic features of chronic pancreatitis?

A
  • Oedema
  • Haemorrhage
  • Necrosis
288
Q

What are the symptoms of acute pancreatitis?

A
  • Severe pain
  • Vomiting
  • Dehydration
289
Q

What will be found in investigations indicating pancreatitis?

A
  • Increased amylase
  • Increase glycaemia
  • Increasde ALP
  • Increased bilirubin
  • Decreased Ca2+
290
Q

What are the macroscopic features of chronic pancreatitis?

A
  • Fibrosis
  • Calcification
291
Q

What are the symptoms of chronic pancreatitis?

A
  • Pain
  • Malabsorption
  • Jaundice
292
Q

What does malabsorption caused by chronic pancreatitis cause?

A
  • Steatorrheoa
  • Decreased albumin
  • Weight loss
293
Q

What are the causes of pancreatitis?

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion bite
  • Hyperlipidaemia
  • ERCP / Iatrogenic
  • Drugs
294
Q

How can gallstones cause pancreatitis?

A

They block the pancreatic duct or Ampulla of Vater

295
Q

How can ethanol cause pancreatitis?

A

Hyper-stimulation of pancreatic secretions

296
Q

What % of pancreatic carcinomas do ductal adenocarciomas account for?

297
Q

What % of cancer deaths do pancreatic carcinomas account for?

298
Q

What is the clinical presentation of pancreatic carcinomas?

A
  • Initially symptomless
  • Then lots of symptoms all at the same time
    • Obstructive jaundice
    • Pain
    • Vomiting
    • Malabsoprtion
    • Diabetes

ESA 3 - Gastrointestinal System (12 decks)

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