Liver, Biliary Tree and Pancreas Flashcards Preview

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

Flashcards in Liver, Biliary Tree and Pancreas Deck (305):
1

Into where does the stomach empty chyme? 

The duodenum

2

What are the key properties of chyme? 

  • Acidic
  • Hypertonic
  • Partly digested

3

How is the acidic nature of chyme corrected? 

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

4

When is HCO3- produced? 

During the production of gastric acid

5

How is the hypertonicity of chyme corrected?

Osmotic movement of water into the duodenum across its wall

6

How is digestion of chyme completed?

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

7

What components is bile made up of? 

  • Bile acid dependant 
  • Bile acid independant 

8

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

 Cells lining the canaliculi

9

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

  • Bile acids (salts)
  • Cholesterol
  • Bile pigments 

10

Name the two primary bile salts

  • Cholic acid
  • Chenodeoxycholic acid

11

What happens to bile salts in bile? 

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

12

Where do bile salts play a major role? 

In the digestion and absorption of fat 

13

What is the name of the majority bile pigment? 

Bilirubin 

14

What secretes the bile acid independent component of bile? 

Cells lining the intra-hepatic bile ducts

15

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

Alkaline juice (HCO3-like that form pancreatic duct cells

16

Label this diagram

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

17

What supports the livers function? 

Its microscopic structure

18

What is the basic functional unit of the liver? 

A lobule surrounding a central vein 

19

What does the central vein of a liver lobule do? 

Drains blood from the liver to the systemic veins 

20

Where does blood entering the liver lobule come from? 

The hepatic portal vein and hepatic arteries 

21

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

At the periphery of the lobule 

22

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

It flows through sinusoids 

23

What lines sinusoids? 

Hepatocytes 

24

Where is bile formed? 

Canaliculi 

25

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

It flows towards the periphery into bile ducts

26

Label this diagram

  • 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

27

What are the main functions of hepatocytes? 

  • Produce bile 
  • Detoxify blood

28

What is the main function of the central vein? 

Transports clean blood to hepatic vein 

29

What does the duodenum do in response to gastric emptying? 

Secretes cholecystokinin (CCK)

30

What effect does CCK have? 

It stimulates the contraction of the gall bladder

31

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

It ejects concentrated bile acids together with enzymes from the pancreas

32

What organs release alkali for digestion? 

  • Pancreas 
  • Liver

33

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

Secretin 

34

What are bile acids released through? 

The Ampulla of Vater

35

What is the role of bile acids? 

Aid with the digestion and absorption of fats 

36

Where do bile acids go once they have been released? 

They continue to the terminal ileum

37

What happens to bile acids in the terminal ileum? 

They are actively absorbed by the epithelium 

38

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

Venous return from the gut enters the hepatic portal blood

39

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

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

40

What is the ultimate fate of most bile acids? 

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

41

How is the loss of unconjugated bile acids dealt with? 

Hepatocytes subsequently replace them 

42

What happens to bile acids in between meals? 

They return to the liver 

43

When are bile acids secreted by canaliculi cell walls? 

A long time before they are next needed 

44

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

They are stored in the gall bladder

45

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

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

46

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

It increases the risk of precipitation, leading to gall stones

47

What are the consequences of gallstones? 

Often asymptomatic, but can cause very painful biliary colic

48

What causes biliary colic? 

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

49

What often follows biliary colic? 

  • Inflammation 
  • Infection of the gall bladder

50

What is inflammation of the gall bladder called? 

Cholecystitis

51

When may pain from gallstones be worse? 

After eating

52

Why may pain from gallstones be made worse after eating?  

The secretion of CCK will cause the gall bladder to contract

53

What does the exocrine pancreas secrete? 

  • Alkaline juice (HCO3-)
  • Enzymes

54

What enzymes does the exocrine pancreas secrete? 

  • Proteases
    • Trypsin(ogen)
    • Chymotrypsin
    • Elastase
    • Carboxypeptidase
  • Amylases
  • Lipases

55

What kind of organ is the exocrine pancreas? 

A gland

56

What are the main components of the exocrine pancreas? 

  • Acini
  • Ducts

57

What do the pancreatic acini do? 

Secrete enzymes

58

In what form do the pancreatic acini secrete enzymes? 

Mostly as inactive precursors 

59

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

Packaged into condensing vacuoles, forming zymogen granules

60

What happens to zymogen granules? 

They are secreted by exocytosis

61

Where are zymogen granules activated? 

In the intestine

62

How are zymogen granules activated? 

By enzymatic cleavage 

63

What do the pancreatic ducts do? 

Secrete alkaline juice

64

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

Due to gastric acid secretion 

65

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

It doesn't 

 

ha ha trick question i got u 

66

What is the mechanism of secretion of HCO3-?

  • Na-K-ATPase sets up a Naconcentration gradient 
  • Hydrogen ions are exported from the duct cell into ECF using the Na+ concentration gradient 
  • Hions 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
  • Hion is recycled, 'going round in a circle' to carry more HCO3- from the ECF to the lumen

67

What is duct secretion of HCO3stimulated by?

Secretin 

68

What releases secretin? 

Jejunal cells 

69

What is secretin released from jejunal cells in response to? 

Low pH

70

What facilitates secretin's action? 

Cholecystokinin (CCK)

71

What are the two sources of pancreatic secretion? 

  1. Acinar
  2. Duct

72

What is pancreatic acinar secretion stimulated by? 

Cholecystokinin (CCK)

73

Where is CCK released from?

Duodenal APUD cells 

74

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

  • Hypertonicity 
  • Fats 

75

What stimulates pancreatic duct secretion? 

Secretin 

76

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

Low pH

77

What is CCK secreted by the duodenum in reponse to? 

Gastric emptying

78

What does CCK stimulate? 

Contraction of the gall bladder muscle 

79

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

Biliary secretion 

80

Are fats soluble in water? 

No, relatively insoluble 

81

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

They tend to aggregate into large globules

82

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

It prevents the effective action of digestive enzymes

83

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

Acid

84

What do bile acids enable in the duodenum?

With regards to fats 

Enable fats to be incorporated into small micelles

85

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

4-6nm

86

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

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

87

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

  • Generate a high surface area for the action of lipases
  • Carry products into the 'unstirred layer'

88

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

Cleave the fatty acids from glycerol 

89

Where is the 'unstirred layer' found? 

Immediately next to the mucosa 

90

What happens at the 'unstirred layer'? 

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

91

What happens to fatty acids once inside the epithelial cells?

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

92

What are chylomicrons? 

Structured small particles made up of lipids covered in phospholipids

93

What do chylomicrons do? 

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

94

What is steatorrheoa? 

Fatty faeces

95

What causes steatorrheoa?

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

96

What are the symptoms of steatorrheoa? 

Faeces that-

  • Pale
  • Float
  • Smell foul

97

What are bile pigments? 

Excretory products

98

What is the most common bile pigment? 

Bilirubin

99

When is bilirubin produced? 

As a product of haemoglobin breakdown 

100

What happens to bilirubin after production? 

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

101

What happens if bilirubin cannot be excreted? 

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

102

What is inevitable when ingesting food and water? 

We also risk ingesting toxins

103

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

  • Chemical
  • Bacteria
  • Viruses
  • Protozoa 
  • Nematodes 
  • Cestodes 
  • Trematodes 

104

What are nematodes? 

Roundworms

105

What are cestodes? 

Tapeworms

106

What are trematodes? 

Flukes

107

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

  • Innate
  • Adaptive

108

What are the types of innate immunity? 

  • Physical
  • Cellular

109

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

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

110

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

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

111

How does memory act as a defence? 

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

112

What pH is saliva? 

7.0

113

What does saliva contain? 

  • Lysozyme
  • Lactoperoxidase 
  • Complement 
  • IgA
  • Polymorphs

114

How does saliva act as a defence? 

It washes toxins down into the stomach

115

How does stomach acid act as a defence? 

Low pH kills the majority of bacteria and viruses

116

What are the small intestine secretions? 

  • Bile 
  • Proteolytic enzymes

117

How do the small intestine secretions act as a defence? 

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

118

What is the purpose of the colonic mucus? 

Protects the colonic epithelium from it's contents 

119

What areas in the GI tract have an anaerobic environment? 

  • Small bowel
  • Colon

120

What is the normal intestinal transit time? 

12-18hrs

121

What happens if peristalsis is slowed? 

Gut infections are prolonged 

122

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

Shigellosis

123

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

  • Neutrophils
  • Macrophages
  • Natural killer cells 
  • Tissue mast cells
  • Eosinophils

124

What are macrophages called in the liver? 

Kupffer cells

125

What do NK cells do? 

Kill virus infected cells 

126

When are eosinophils recruited? 

In parasitic infections

127

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

Through the liver - the hepatic portal system

128

What are Kupffer cells? 

Specialised macrophages in the liver

129

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

130

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

  • B lymphocytes
  • T lymphocytes
  • Lymphatic tissues

131

What do B lymphocytes do? 

Produce antibodies, including IgA and IgE

132

What are IgA and IgE particularly effective against? 

Extracellular microbes 

133

What are T lymphocytes directed against? 

Intracellular organisms

134

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

Gut Associated Lymphoid Tissue (GALT)

135

How is GALT distributed? 

  • Diffusely distributed 
  • Nodular in three locations- 
    • Tonsils
    • Peyer's patches 
    • Appendix 

136

What do Peyer's patches look like? 

137

What is reduced salivary flow known as? 

Xerostomia

138

What can cause xerostomia? 

  • Severe illness
  • Dehydration 

139

What does xerostomia lead to? 

Microbial overgrowth in the mouth and dental caries 

140

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

Parotitis 

141

What is parotitis? 

Salivary glands infections 

142

What microbe causes parotitis? 

Staphylococcus aureus

143

What is achlorhydria? 

Absent or low gastric acid production

144

What can cause achlorhydria? 

  • Pernicious anaemia
  • Drugs such as H2 antagonists
  • PPIs

145

What are patients with achlorhydria more susceptible to? 

Shigellosis, cholera, and salmonella infections 

146

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

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

147

Give 3 examples of resistant organisms? 

  1. Mycobacterium tuberculosis 
  2. Some enteroviruses
  3. Helicobacter Pylori

148

What is mycobacterium tuberculosis resistant to? 

Gastric acid 

149

What kind of bacterium is mycobacterium tuberculosis? 

Acid and alcohol fast bacterium 

150

Give 3 examples of enteroviruses that are resistant? 

  1. Hepatitis A 
  2. Polio
  3. Coxsackle

151

What are some enteroviruses resistant to? 

Gastric acid

152

Why is Helicobacter Pylori resistant? 

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

153

What do mast cell granules contain? 

Histamine 

154

Which gut infections recruit mast cells? 

Those that activate complement 

155

What does the recruitment of mast cells lead to? 

The release of histamine

156

What does the release of histamine cause? 

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

157

How much fluid is lost per hour in cholera? 

May get losses of 1litre/hr

158

What is the mortality of cholera if untreated? 

60% 

159

What is the clinical significace of GALT? 

  • Tonsillitis
  • Ileocaecal lymphatic tissue
  • Appendicitis 

160

What conditions are related to ileocaecal lymphatic tissue? 

  • Mesenteric adenitis 
  • Typhoid fever

161

What is mesenteric adenitis a common cause of? 

Right iliac fossa pain in children

162

What can mesenteric adenitis be easily mistaken for? 

Appendicitis 

163

What is mesenteric adenitis mostly caused by? 

Adenovrius or coxsackie virus

164

What does typhoid fever cause?

With respect to Peyer's patches

Inflamed Peyer's patches in the terminal ileum 

165

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

They can perforate and kill patients 

166

What do many causes of appendicitis arise from? 

Lymphoid hyperplasia at the appendix base 

167

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

It leads to obstructed outflow. 

Stasis leads to infection

168

When is purulent appendictis more common? 

During epidemics of chickenpox in children

169

How may the appendix be obstructed, other than lymphoid hyperplasia

  • By a faecolith 
  • By a worm

170

What is a faecolith? 

Calcified faecal matter

171

How can faecoliths be visualised? 

On an X-ray

 

172

What to the GI tract's defence mechanism require? 

The GI tract itself to have an intract blood supply

173

What can intestinal or hepatic ischaemia be due to? 

  • Arterial disease
  • Systemic hypertension
  • Intestinal venous thrombosis

174

What can intestinal or hepatic ischamia lead to? 

  • Overwhelming sepsis 
  • Rapid death (within hours)

175

What does liver failure increase susceptibility to? 

  • Infections
  • Toxins
  • Drugs
  • Hormones

176

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

Ammonia

177

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

Due to failure of the urea cycle 

178

What is ammonia produced by? 

  • Colonic bacteria
  • Deamination of amino acids

179

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

Can cause hepatic encephalopathy 

180

What are the causes of liver failure? 

  • Industrial solvents 
  • Drugs
  • Viral hepatitis 
  • Mushroom poisioning
  • Alcohol

181

What is the main cause of liver failure worldwide? 

Viral hepatitis 

182

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

Alcohol

183

What is hepatic fibrosis also known as? 

Cirrhosis 

184

What does hepatic fibrosis lead to? 

Portal venous hypertension 

185

What does portal venous hypertension lead to? 

Porosytemic shunting

186

What does portosystemic shunting lead to? 

  • Toxin shunting 
  • Oesophageal varices 
  • Haemorrhoids 
  • Caput medusa 

187

What are bile pigments? 

Excretory products 

188

What is the most common bile pigment?

Bilirubin 

189

What is bilirubin produced as a product of? 

Haemoglobin breakdown 

190

What happens to bilirubin after production? 

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

191

What happens if bilirubin cannot be excreted? 

It accumulates in the blood

192

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

Jaundice 

193

What hormone does the liver notably break down? 

Insulin

194

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

  • Producing albumin
  • Producing coagulation factors 
  • Producing thrombopoietin
  • Amino acid synthesis

195

What is the most abudant plasma protein? 

Albumin

196

What is albumin essential for? 

Maintaining the oncotic pressure needed for proper distribution of body fluids

197

What coagulation factors are produced by the liver? 

  • II
  • V
  • VII
  • IX
  • X
  • XI
  • Protein C
  • Protein S 
  • Antithrombin

198

What is coagulation factor I also known as? 

Fibrinogen 

199

What is coagulation factor II also known as? 

Prothrombin

200

What is thrombopoietin? 

A glycoprotein hormone 

201

What does thrombopoietin do? 

Regulates the production of platelets by bone marrow 

202

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

Transamination

203

What are the tests for liver function? 

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

204

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

Liver damage

205

Why is ALT and AST present in liver damage? 

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

206

What do raised levels of bilirubin or alkaline phosphate indicate? 

Cholestasis (obstruction of the bile ducts)

207

What happens to bilirubin in cholestasis? 

Unable to excrete bilirubin, plasma concentration rises

208

What is alkaline phosphatase? 

An enzyme in cells lining the liver's biliary ducts

209

What happens to alkaline phosphatase in cholestasis? 

Plasma levels rise with obstruction 

210

What happens to albumin in chronic liver disease? 

Levels are reduced

211

What does prothrombin time measure? 

The clotting tendency of blood

212

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

Synthetic function

213

Why does liver damage cause jaundice? 

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

214

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

Hyperbilirubinaemia 

215

What are the symptoms of hyperbilirubinaemia? 

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

216

When is jaundice clinically detectable? 

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

217

What are the types of jaundice? 

  • Pre-hepatic
  • Hepatic
  • Post-hepatic 

218

What is the underlying pathology of pre-hepatic jaundice? 

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

219

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

An increased breakdown of red blood cells (haemolysis)

220

What are the lab findings in pre-hepatic jaundice? 

  • Unconjugated hyperbilirubinaemia 
  • Reticulocytosis
  • Anaemia
  • Increased LDH
  • Decreased haptoglobin

221

What are the main causes of pre-hepatic jaundice? 

  • Inherited 
  • Congential hyperbilirubinaemias
  • Acquired 

222

What are the inherited causes of pre-hepatic jaundice? 

  • Red cell membrane defects 
  • Haemoglobin abnormalities 
  • Metabolic defects 

223

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

  • Gilbert's syndrome 
  • Criger-Najjar syndrome
  • Dublin-Johnson syndrome

224

How common is Gilbert's syndrome? 

Present in 10% of the population

225

How common is Crigler-Najjar syndrome? 

Rare

226

How common is Dublin-Johnson syndrome? 

Rare

227

What are the acquired causes of pre-hepatic jaundice? 

  • Immune
  • Mechanical
  • Acquired membrane defects 
  • Infections
  • Drugs
  • Burns

228

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

RBC's running across metal heart valves

229

What is the main pathology of hepatic jaundice? 

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

230

What are the lab findings in hepatic jaundice? 

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

231

What are the main causes of hepatic jaundice? 

  • Congential 
  • Hepatic inflammation 
  • Drugs
  • Cirrhosis
  • Hepatic tumours 

232

What are the congential causes of hepatic jaundice? 

  • Gilbert's syndrome
  • Crigler-Najjar syndrome

233

What are the main causes of hepatic inflammation? 

  • Viral 
  • Autoimmune hepatitis 
  • Alcohol
  • Haemochromotosis
  • Wilson's disease 

234

What are the viral causes of hepatic inflammation? 

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

235

What drugs can cause hepatic jaundice? 

Paracetamol 

236

What are the main causes of cirrhosis? 

  • Alcohol
  • Chronic hepatitis
  • Metabolic disorders 

237

What are the main kinds of hepatic tumours? 

  • Hepatocellular carcinoma
  • Metastases 

238

What is the main pathology of post-hepatic jaundice? 

Obstruction to the drainage of bile 

239

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

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

240

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

  • Intrahepatic
  • Extrahepatic

241

What are the lab findings in post-hepatic jaundice? 

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

242

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

  • Hepatitis
  • Drugs
  • Cirrohosis 
  • Primary biliary colic

243

What are the extrahepatic causes of post-hepatic jaundice? 

  • Gallstones
  • Biliary stricture 
  • Carcinoma
  • Pancreatitis 
  • Sclerosig cholangitis 

244

What carcinomas can cause post-hepatic jaundice? 

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

245

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

No, it is pale

246

What is the pathology of alcoholic liver disease 

  1. Fatty liver 
  2. Alcoholic hepatitis 
  3. Cirrhosis 

247

What is the pathogenesis of fatty liver? 

  • 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

What is alcoholic hepatitis? 

Inflammation of hepatocytes 

249

What happens in cirrhosis? 

Liver cell necrosis followed by nodular regeneration and fibrosis 

250

What is the result of liver cirrhosis? 

  • Increased resistance to blood flow 
  • Derenged liver function

251

What are the potential complications of alcoholic liver disease? 

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

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What are the causes of liver cirrhosis? 

  • Alcohol
  • Wilson's Disease
  • Biliary cirrhosis
  • Haemochromotosis
  • Hepatitis B or C
  • Autoimmune hepatitis
  • α1-antitrypsin deficiency

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What are the clinical features of liver cirrhosis? 

  • Liver dysfunction 
  • Jaundice 
  • Anaemia 
  • Bruising
  • Palmar erythema 
  • Dupuytren's contracture 

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What are the results of investigations indicating liver cirrhosis? 

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

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What is involved in the management of cirrhosis? 

  • Stopping drinking
  • Treating complications
  • Transplantation

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What is portal hypertension defined as? 

Portal venous pressure >20mmHg

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What can portal hypertension be caused by? 

  • Obstruction of the portal vein 
  • Obstruction of flow within the liver 

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

  • Congenital 
  • Thrombosis 
  • Extrinsic compression

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

  • Cirrhosis
  • Hepatoportal sclerosis
  • Schistosomiasis
  • Sarcoidosis

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What may portal hypertension lead to? 

  • Ascites 
  • Splenomegaly 
  • Pathologies related to porto-systemic anastomoses 

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How does portal hypertension cause ascites? 

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 

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

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

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Why does portal hypertension cause splenomegaly? 

Due to subsequent increase blood pressure in the spleen

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

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

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

  • Vessels to dilate 
  • Vessels to protrude into lumen
  • Rupturing
  • Ulceration
  • Haemorrhage

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

  • Oesophageal varices 
  • Rectal varices 
  • Caput Medusae 

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Label this diagram

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

  • 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
  •  

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

Oesophageal Varices 

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

Rectal varices 

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

Caput Medusae 

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

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

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What happens to bile acids in between meals? 

They return to the liver 

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What secrete bile acids? 

Canaliculi cell walls 

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When are bile acids secreted? 

Long before they are next needed

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Where are bile acids stored until they are needed? 

In the gall bladder 

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

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

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

It increases the risks of precipitation 

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What does precipitation of bile acids lead to? 

Gall stones 

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What are the symptoms of gallstones? 

  • Often asymptomatic 
  • Can cause painful biliary colic, or obstruction

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When do gallstones cause biliary colic? 

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

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What is biliary colic often followed by? 

  • Inflammation of the gall bladder (cholecystitis)
  • Infection of the gall bladder

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When may pain from gallstones be worse? 

After eating 

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Why may pain from gallstones be worse after eating? 

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

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Label this diagram

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

  • 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

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What is pancreatitis? 

An inflammatory process

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What causes pancreatitis? 

Effects of enzymes released from pancreatic acini

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What are the macroscopic features of chronic pancreatitis? 

  • Oedema
  • Haemorrhage
  • Necrosis

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What are the symptoms of acute pancreatitis? 

  • Severe pain 
  • Vomiting
  • Dehydration 

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What will be found in investigations indicating pancreatitis? 

  • Increased amylase
  • Increase glycaemia 
  • Increasde ALP 
  • Increased bilirubin
  • Decreased Ca2+

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What are the macroscopic features of chronic pancreatitis? 

  • Fibrosis 
  • Calcification 

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What are the symptoms of chronic pancreatitis? 

  • Pain 
  • Malabsorption
  • Jaundice 

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What does malabsorption caused by chronic pancreatitis cause? 

  • Steatorrheoa 
  • Decreased albumin 
  • Weight loss 

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What are the causes of pancreatitis? 

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

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How can gallstones cause pancreatitis? 

They block the pancreatic duct or Ampulla of Vater 

295

How can ethanol cause pancreatitis? 

Hyper-stimulation of pancreatic secretions

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What % of pancreatic carcinomas do ductal adenocarciomas account for? 

90%

297

What % of cancer deaths do pancreatic carcinomas account for? 

~5% 

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What is the clinical presentation of pancreatic carcinomas? 

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

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