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MBChB - year 2 > Week 2 GI Lectures > Flashcards

Week 2 GI Lectures Flashcards

1
Q

Where is bile generated and stored?

A

Generated in the liver

Stored in the gallbladder

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2
Q

What are the components of bile?

A 
Bicarbonate
cholesterol
phospholipids 
bile pigments
bile salts
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3
Q

What is the lifespan of a RBC?

A

120days

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4
Q

What is the daily turnover of Hb?

A

6g/day

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5
Q

what are the globin monomers from Hb broken down to?

A

To their constituent amino acids and recycled

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6
Q

What is the porphyrin ring converted to?

A

Bilirubin

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7
Q

What is converted into bilirubin?

A

The porphyrin ring

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8
Q

Why is the porphyrin ring converted to bilirubin?

A

For transport to the liver for modification and excretion

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9
Q

What changes haem into biliverdin?

A

Haem oxygenase

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10
Q

What are the different stages before the final product of bilirubin is made?

A

Haem –> biliverdin –> unconjugated bilirubin –> conjugated bilirubin

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11
Q

How is biliverdin changed into bilirubin?

A

Biliverdin reductase

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12
Q

What colour is bilirubin?

A

An orange/ yellow pigment

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13
Q

What is responsible for conjugating bilirubin?

A

UDP Glucuronyl transferase

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14
Q

What happens when bilirubin become conjugated?

A

It becomes hydrophilic

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15
Q

What are the three things that U-bilirubin can turn into?

A

Mesobilinogen
Stercobilinogen
Urobilinogen

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16
Q

What does Mesobilinogen turn into and how?

A

Intestinal microflora in the large intestine turns it into mesobilin

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17
Q

What does Stercobilinogen

turn into and how?

A

Intestinal microflora in the large intestine turns it into stercobilin

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18
Q

What does Urobilinogen turn into and how?

A

Intestinal microflora in the large intestine turns it into Urobilin

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19
Q

Why are bile salts/acids required?

A

Oil and water don’t mix so they act as biological emulsifiers

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20
Q

What is emulsification?

A

The breakdown of large lipid droplets into small uniformly distributed droplets (1mm or 1000nm) that helps lipase break down triglyceride

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21
Q

What does the hydrophobic portion of bile salts/acid bind to?

A

It binds to and disperses large triglyceride lipid droplets

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22
Q

What does the hydrophobic portion of bile salts/acid prevent?

A

Prevents large droplets reforming

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23
Q

What are the lipid soluble vitamins?

A

A
D
E
K

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24
Q

What are micelles?

A

Very small lipid aggregates with hydrophilic (polar) head groups on the outside and hydrophobic (non-polar) tails pointing in

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25
Q

What are micelles made up of?

A

Bile salts, fatty acids, monoglycerides, phospholipids, cholesterol and fat soluble vitamins

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26
Q

What happens when micelles constantly break down and reform?

A

The contents are released each time and some diffuse across the intestinal lining

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27
Q

Where do TAGs reform?

A

They reform in epithelial cells and are packaged into chylomicrons which enter the blood via the lymph

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28
Q

Where do the bile salts emulsify the fat globules?

A

In the intestines

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29
Q

What does the digestion of the emulsion droplets by lipases form?

A

Free fatty acids (monoglycerides) and bile salts

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30
Q

What do the bile salts do to free fatty acids (Monoglycerides)?

A

Form micelles

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31
Q

What do absorbed free fatty acids form?

A

Triglycerides

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32
Q

What are the free fatty acids that are absorbed and formed into triglycerides packaged into?

A

Packaged into chylomicrons for secretion in lacteals

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33
Q

Is the sphincter of Oddi contracted or relaxed during the Interdigestive period?

A

Contracted

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34
Q

What is the Interdigestive period?

A

The time between meals

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35
Q

What is the sphincter of Oddi?

A

A muscular valve that controls the flow of bile and pancreatic fluid into the duodenum

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36
Q

How is bile concentrated?

A

Epithelial cells reabsorb water and electrolytes

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37
Q

What does fatty acids and amino acids entering the duodenum after a meal stimulate?

A

Enteroendocrine cells to release CCK

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38
Q

What does CCK stimulate?

A

Contraction of the gallbladder smooth muscle and relaxation of the sphincter of Oddi

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39
Q

What does acidic chyme in the duodenum stimulate?

A

Release of secretin fron endocrine cells

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40
Q

What does secretin do?

A

Stimulates duct cells in the liver to release bicarbonate into the bile which neutralises acid and stimulates bile production

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41
Q

Why do bile salts need to be recycled by the enterohepatic circulation?

A

Bile salts in the body are not enough to fully process the fats in a typical meal

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42
Q

Where do transporters move bile salts?

A

From the digestive tract to the intestinal capillaries

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43
Q

Where do bile salts go after they reach intestinal capillaries?

A

Transported to the liver via the hepatic portal vein

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44
Q

What takes up the bile salts from the blood?

A

Hepatocytes

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45
Q

What is hyperbilirubinaemia?

A

Too much bilirubin in the blood

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46
Q

What is jaundice?

A

Yellowing that is most common in the eyes and sometimes the skin caused by elevated levels of bilirubin

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47
Q

What level of total bilirubin may jaundice be visible in the sclera?

A

over 30mmol/L

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48
Q

What level of total bilirubin may jaundice be visible in the skin?

A

Over 100 mmol/L

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49
Q

What is prehepatic jaundice?

A

Jaundice with the cause before the liver (elevated haemolysis)

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50
Q

What is hepatic jaundice?

A

The cause of the jaundice is in the liver (liver damage)

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51
Q

What is post hepatic jaundice?

A

The cause of the jaundice is after the liver (blockage of bile ducts)

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52
Q

What can be used to distinguish between groupings?

A

Proportion of unconjugated: conjugated bilirubin

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53
Q

What can cause pre-hepatic jaundice?

A
  • tropical diseases e.g. yellow fever
  • side effect of quinine based anit-malarial drugs
  • genetic disorders that aare associated with increased haemolysis (e.g. sickle cell)
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54
Q

Why does pre-hepatic jaundice happen?

A

More RBC breakdown
More haemoglobin
More bilirubin produced (unconjugated bilirubin)

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55
Q

What is neonatal jaundice?

A

common and usually harmless jaundice of new-born babies

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56
Q

What causes neonatal jaundice?

A
  • After birth, new-borns must destroy foetal haemoglobin and replace with adult haemoglobin, RBCs have short lifespan
  • Undeveloped liver (with lack of glucuronyl transferase) has insufficient capacity to cope with elevated haemolysis
  • Inhibitors of conjugation in breast milk
  • Bilirubin peaks at 3-5 days and lasts < 14 days
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57
Q

How is neonatal jaundice treated?

A

phototherapy - blue light changes unconjugated bilirubin to a water soluble form that can be excreted

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58
Q

What organ takes up unconjugated bilirubin?

A

The liver takes up unconjugated bilirubin, conjugates it and exports it to the gall bladder

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59
Q

What are the three problems that can cause hepatic jaundice?

A
  • impaired uptake of unconjugated bilirubin
  • impaired conjugation of bilirubin
  • Impaired transport of conjugated bilirubin into bile canaliculi
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60
Q

What causes post hepatic jaundice?

A

Conditions associated with obstruction of hepatic, cystic or common bile duct - prevention of bile being released into the small intestine (cholestasis)

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61
Q

What does the severity of gallstone symptoms depend on?

A

Their location and size, they become increasingly problematic when gallbladder contractions cause stones to move further along the bile ducts

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62
Q

What are the symptoms of gallstones in the cystic bile duct?

A

Painful contractions

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63
Q

What are the symptoms of gallstones in the common bile duct?

A

Steatorrhea, grey faeces, post hepatic jaundice

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64
Q

What are the symptoms of gallstones in the Duodenal papilla?

A

Malnutrition, acute pancreatitis

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65
Q

What is the duodenal papilla?

A

Opening of the pancreatic duct into the duodenum, surrounded by the sphincter of Oddi

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66
Q

What is vitamin K required for?

A

Efficient coagulation

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67
Q

What is GGCX?

A

g-glutamyl carboxylase

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68
Q

What is GGCX required for?

A

To make active coagulation factors II VII IX and X

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69
Q

What is the plasma unconjugated bilirubin like in prehepatic jaundice?

A

Very high

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70
Q

What is the plasma unconjugated bilirubin like in hepatic jaundice?

A

A bit high

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71
Q

What is the plasma unconjugated bilirubin like in post hepatic jaundice?

A

Normal

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72
Q

What is plasma conjugated bilirubin like in pre-hepatic jaundice?

A

Normal or a bit high

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73
Q

What is plasma conjugated bilirubin like in hepatic jaundice?

A

Moderately raised

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74
Q

What is plasma conjugated bilirubin like in post hepatic jaundice?

A

very high

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75
Q

What is the urine conjugated bilirubin like in pre-hepatic jaundice?

A

Normal (absent)

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76
Q

What is the urine conjugated bilirubin like in hepatic jaundice?

A

Slightly raised

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77
Q

What is the urine conjugated bilirubin like in post-hepatic jaundice?

A

Moderately raised

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78
Q

What is the urine urobilinogen/urobilin like in post-hepatic jaundice?

A

absent

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79
Q

What is the urine urobilinogen/urobilin like in hepatic jaundice?

A

Slightly raised

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80
Q

What is the urine urobilinogen/urobilin like in pre-hepatic jaundice?

A

Slightly raised

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81
Q

What is the stercobilin in the faeces like in pre-hepatic jaundice?

A

Slightly raised

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82
Q

What is the stercobilin in the faeces like in hepatic jaundice?

A

normal

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83
Q

What is the stercobilin in the faeces like in post-hepatic jaundice?

A

Absent

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84
Q

What are the steps for measuring direct (conjugated) bilirubin?

A
  1. Add diazo reagent to serum.
  2. Conjugated bilirubin converted to blue/purple diazo derivative of bilirubin (Azobilirubin).
    - NB unconjugated bilirubin bound to albumin as not water soluble so does not react with diazo reagent
  3. Measurement of absorbance @ 530-545 nm proportional to conjugated bilirubin (not unconjugated).
  4. Compare to known standards to calculate concentration
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85
Q

What are the steps for measuring total bilirubin?

A
  1. Add diazo reagent with caffeine to serum.
  2. Caffeine displaces unconjugated bilirubin from albumin.
    - Free unconjugated bilirubin can now react with the diazo reagent
  3. Both conjugated and unconjugated bilirubin converted to blue/purple diazo derivative of bilirubin (Azobilirubin).
  4. Measurement of absorbance @ 530-545 nm proportional to BOTH conjugated and unconjugated bilirubin
  5. Compare to known standards to calculate concentration
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86
Q

Is bile pigment measured in faeces?

A

No - a waste of time/money and visual inspection is easy

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87
Q

Summarise the three types of jaundice

A 
Pre-hepatic = due to elevated haemolysis e.g. Neonatal jaundice 
Hepatic = conditions associated with liver damage e.g Hepatitis 
Post-hepatic = blockage in bile release into the intestines   e.g Gallstones
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88
Q

What are the two areas of the GI tract under voluntary control?

A

Upper oesophageal sphincter and the external anal sphincter

89
Q

What does contraction of the longitudinal muscle allow for?

A

Shortening of the intestine

90
Q

What are the interstitial cells of cajal?

A

Cells that have an intrinsic pacemaker function that helps regulate muscular function

91
Q

Which neurotransmitter does the gut muscle not respond well to?

A

Ach

92
Q

What is the function of the enteric nervous system?

A

Mediates reflex activity in the absence of CNS input (interprandial period)

93
Q

What extrinsic factors is the enteric nervous system influenced by?

A

Vagal control and sympathetic control

94
Q

What effect does the influence of vagal control have on the enteric nervous system?

A

It is excitatory to non-sphincteric muscle

95
Q

What effect does the influence of sympathetic control have on the enteric nervous system?

A

Inhibitory to non-sphincteric muscle

Excitatory to sphincteric muscle

96
Q

What are the neurohormonal influences on the enteric nervous system?

A

Motilin, 5 hydroxy-tryptamine and opioid receptors

97
Q

How is motility function measured in the GI tract?

A

Pressure (circular muscle function) - catheters used to measure how much pressure muscles exert when the muscle is contracted
Transit - radiolabelled isotopes and dynamic contrast radiology used

98
Q

Where is the sympathetic innervation of the oesophagus from?

A

The sympathetic trunk

99
Q

Where is the parasympathetic innervation of the oesophagus from?

A

The vagus nerve

100
Q

Is the upper part of the oesophagus circular or longitudinal muscle?

A

Circular

101
Q

Is the lower part of the oesophagus circular or longitudinal muscle?

A

Longitudinal

102
Q

How is a HRM trace information gathered?

A

A catheter is placed into the nose and all the way down into the stomach. Low pressure shows as blue and high shows as purple

103
Q

Where on a HRM trace should there be tonic pressure?

A

At the upper and lower oesophageal sphincters. These are shown at the top and bottom of the graph respectively

104
Q

What are examples of oesophageal motility?

A
  • Achalasia
  • Nutcracker/jackhammer oesophagus
  • Diffuse oesophageal spasm
  • Oesophageal involvement in scleroderma
105
Q

What is achalasia?

A

The lower oesophageal sphincter doesn’t relax and always stays contracted meaning food can’t get through

106
Q

What is a key feature of a barium swallow of a patient with achalasia?

A

The oesophagus has a birds beak at the end at the lower oesophageal sphincter and the oesophagus is dilated

107
Q

What are the treatment options for achalasia?

A
  • Rigiflex balloon dilatation
  • Laparoscopic Heller’s myotomy
  • POEM
108
Q

What is a laparoscopic Heller’s myotomy?

A

A cut is made in the outer layer of muscle which changes the pressure at the sphincter

109
Q

What is a POEM?

A

Per Oral Endoscopic Myotomy - cut in the mucosa to reach the muscle layer then cut this and seal mucosa back up

110
Q

What happens to the oesophagus in scleroderma?

A

Weak lower oesophageal sphincter with absent peristalsis and severe oesophagitis

111
Q

What is nutcracker oesophagus?

A

It is associated with pain on swallowing. There are no evident therapies.
The patient has a functional swallow and benign prognosis

112
Q

What is diffuse oesophageal spasm?

A

Very rapid contractions of the oesophagus. Very rare condition

113
Q

What is the migrating motor complex?

A

A cyclic contraction sequence that occurs every 90 minutes

114
Q

What are the 4 phases of the migrating motor complex?

A

i) Prolonged period of quiescence
ii) Increased frequency of contractility
iii) A few minutes of peak electrical and mechanical activity
iv) Declining activity merging to next phase I

115
Q

What regulates the migrating motor complex?

A

Motilin

116
Q

What is the function of the migrating motor complex?

A

It acts to cleanse the stomach and intestine in between meals

117
Q

What is motilin and where is it made?

A

Motilin is a polypeptide hormone that is produced by M cells in the small intestine. It is secreted in 90 minute intervals to stimulate the mmc

118
Q

What acts as a motilin agonist?

A

Erythromycin

119
Q

What are the three phases of meal related motility?

A

Cephalic
Gastric
Intestinal

120
Q

What is the cephalic phase?

A

It is a vagally mediated secretory phase. The sight/ smell of food results in increased gastric secretion

121
Q

What mediates the cephalic phase?

A

Vagus nerve

122
Q

How much of gastric secretion occurs during the cephalic phase?

A

20%

123
Q

What happens during the gastric phase?

A

proximal gastric tone reduces and the stomach expands without an increase in pressure

124
Q

What is the MMC replaced by during the gastric phase?

A

contractions of variable amplitude and frequency, allowing mixing and digestion

125
Q

What controls the frequency and direction of gastric muscular contractions?

A

Gastric pacemaker zone within the proximal gastric body

126
Q

How does the Gastric pacemaker zone control the frequency and direction of gastric muscular contractions?

A

The pacemaker generates rhythmic depolarisations at a frequency of 3 cycles per minute which only trigger gastric smooth muscle contractions with additional neurohumoral input

127
Q

What leaves the stomach first solids or liquids?

A

Liquids

128
Q

What is the emptying time for inert liquids?

A

20 minutes

129
Q

What size are digestible food particles when they leave the stomach?

A

2mm

130
Q

How long do solids take to empty completely from the stomach?

A

3-4 hours

131
Q

What happens at the start of gastric emptying of solids?

A

An initial lag phase in which little chyme is released to the duodenum

132
Q

What are disorders of gastric emptying?

A
  • Accelerated gastric emptying (dumping syndrome, diarrhoea)

- Delayed gastric emptying (abdominal pain, vomiting, poorly controlled gastro-oesophageal reflux, malnutrition)

133
Q

What is gastroparesis?

A

delayed gastric emptying

134
Q

What causes gastroparesis?

A
  • Idiopathic
  • Longstanding diabetes with macrovascular disease
  • drugs (opiates)
  • post viral
135
Q

What are the symptoms of gastroparesis?

A
  • abdominal pain
  • nausea and (often delayed) vomiting
  • weight loss
136
Q

How is gastroparesis managed (not medication)?

A
  • dietary (small meals frequently, liquid food better than solid, nutritional support (post pyloric feeding))
  • Attention to the underlying cause (limit use of trigger medication, post viral may improve with time, diabetes - improve diabetic control)
137
Q

How is gastroparesis managed with medication?

A 
- prokinetics 
  5HT4 agonists (cisapride, metoclopramide) 
  D2 antagonists (metoclopramide, doperidone) 
   Motilin agonist (erythromycin)
138
Q

How can gastroparesis be managed surgically?

A
  • endoscopically botulinum toxin is injected to the pyloric sphincter
  • Gastric electrical stimulation - two electrodes on the stomach that release high frequency, low amplitude waves.
139
Q

What provides motility in the small intestine during fasting conditions?

A

the MMC

140
Q

What rate are solids and liquids transported in the small intestine?

A

The same rate but liquids reach the caecum faster because they are released from the stomach first

141
Q

What are some disorders of small bowel transit?

A
  • Chronic intestinal pseudo-obstruction

- Acute post-operative ileus

142
Q

What is chronic intestinal pseudo-obstruction?

A

signs of mechanical obstruction without mechanical occlusion
can be caused by either neuropathic or myopathic aetiology

143
Q

What are symptoms of chronic intestinal pseudo-obstruction?

A
  • chronic abdominal pain
  • constipation
  • vomiting
  • weight loss
144
Q

What is acute post-operative ileus?

A

Constipation and intolerance of oral intake in the absence of mechanical obstruction after a surgery.

145
Q

How long does acute post-operative ileus last in different parts of the GI tract?

A
  • small intestine - 0-24 hours
  • stomach - 24-48 hours
  • colon - 48-72 hours
146
Q

What are risk factors for acute post-operative ileus?

A
  • Open surgery (vs laparoscopic)
  • Prolonged abdominal or pelvic surgery
  • Delayed enteral nutrition
  • Peri-operative complications
  • Peri-operative opiate analgesia
147
Q

What are two disorders of bowel transit?

A
  • Acute colonic pseudo-obstruction (Ogilvie’s syndrome)

- chronic intestinal pseudo-obstruction

148
Q

What is acute colonic pseudo-obstruction (Ogilvie’s syndrome)?

A

A large bowel parasympathetic dysfunction that can occur after surgery, most commonly cardio or spinal surgery.

149
Q

How is acute colonic pseudo-obstruction (Ogilvie’s syndrome) managed?

A
  • gut rest - IV fluids, nasogastric decompression
  • IV neostigmine (acetylcholinesterase inhibitor)
  • colonoscopic decompression
  • surgery
150
Q

What are myopathic causes of chronic intestinal pseudo-obstruction?

A
  • scleroderma

- amyloidosis

151
Q

What is scleroderma?

A

A chronic autoimmune disorder that causes connective tissue in the body to harden

152
Q

What is amyloidosis?

A

An abnormal protein called amyloid builds up in tissues and organs

153
Q

What are neuropathic causes of chronic intestinal pseudo-obstruction?

A

Parkinson’s disease

154
Q

What are endocrine causes of chronic intestinal pseudo-obstruction?

A
  • diabetes

- severe hypothyroidism

155
Q

What are drug related causes of chronic intestinal pseudo-obstruction?

A
  • Phenothiazines

- Anti- parkinsonian drugs

156
Q

What is the management of chronic intestinal pseudo-obstruction?

A
  • Nutritional - enteral and parenteral feeding
  • Antibiotics for small bowel bacterial overgrowth
  • in refractory cases, small bowel transplant
157
Q

What is pacemaker activity like in the colon?

A

There is no typical pacemaker activity

158
Q

What must the colon do?

A
  • mix material without propulsion (for water absorption)
  • act as a storage site
  • cause aboral movement of contents
  • expel faeces
159
Q

How long are the contractions in the colon?

A

A mixture of short and long duration contractions

160
Q

What happens to colonic activity in response to a meal?

A

There is a marked increase (gastrocolic reflex)

161
Q

How long does transit from caecum to rectum take?

A

1-2 days

162
Q

What are the taenia coli?

A

Three distinct strips of longitudinal muscle orientated at 120 degrees from each other in the proximal colon

163
Q

What does the intermittent contraction of circular muscle create?

A

Segments in the colon known as Haustra

164
Q

How is colonic transit measured?

A

Serial x-rays with radio-opaque markers
No markers left = normal transit
Markers in rectosigmoid = pelvic outlet obstruction
Markers scattered throughout = slow transit constipation

165
Q

What drugs reduce colonic motility?

A
  • opiates
  • anticholinergics
  • loperamide
166
Q

What is loperamide?

A

A gut selective opiate mu receptor agonist. It decreases tone and activity of myenteric plexus.
This slows colonic transit leading to increased water absorption Used for symptomatic management of diarrhoea

167
Q

What drugs increase colonic motility?

A
  • Stimulant laxatives
  • prucalopride
  • linaclotide
168
Q

What are stimulant laxatives?

A

Drugs that increase gut motility. They alter gut electrolyte transport.
They have short, dramatic effects

169
Q

What is prucalopride?

A

A gut selective 5HT4 receptor agonist that increases gut motility

170
Q

What is linaclotide?

A

A minimally absorbed guanylate C receptor agonist that increases secretion of chloride and HCO3 into the lumen

  • -> increases intestinal fluid
  • -> speeds colonic transit
171
Q

What is the internal anal sphincter?

A

A smooth muscle sphincter that is under involuntary control. In resting conditions this provides greatest component of contraction

172
Q

What can cause anal sphincter weakness?

A
  • Muscle (sphincter) damage

- Damage to the pudendal nerve

173
Q

What can cause anorectal constipation?

A
  • Hirschrung’s disease
  • Obstructive defecation (paradoxical contraction of puborectalis and external sphincter during defecation)
  • Rectocele
  • Anal fissure (associated pain on defecation)
174
Q

What is Hirschprung’s disease?

A

Failure of the neural crest cells to the distal colon. The affected segment is aganglionic and contracted. The proximal colon is dilated

175
Q

How is Hirschprung’s disease managed?

A

Surgical resection of the affected colon

176
Q

What happens if there is injury to T12 or above?

IN TERMS OF THE COLON

A
  • Reflex bowel
  • Damage to upper motor neurones
  • Reflex arc intact
  • Tonic anal sphincter
  • Bowel opens spontaneously but without control
  • Reflex can be initiated by rectal stimulation (e.g. suppository)
177
Q

What happens if there is injury to the sacral nerve roots?

IN TERMS OF THE COLON

A
  • Lower motor neurone injury
  • “Flaccid bowel”
  • No reflex arc
  • Slow stool propulsion through colon
  • Flaccid anal sphincter –> incontinence
  • Management based on manual evacuation of stool
178
Q

What does the conventional LFTs profile include?

A
  • bilirubin
  • albumin
  • alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST)
  • Alkaline phosphatase
  • gamma glutamyl transferase (γ-GT)
  • total protein
179
Q

What are some reasons LFTs might be done?

A
  • well person screening
  • to investigate unexplained symptoms
  • to investigate symptoms and signs suggestive of liver disease
  • for pre-operative or baseline assessment
  • to monitor the progress of established liver disease and assess the response to treatment
180
Q

What is unconjugated hyperbilirubinaemia?

A

Indirect bilirubin is >85% of total bilirubin.

Occurs with increased bilirubin production or defects in hepatic uptake or conjugation (e.g. gilberts disease)

181
Q

What is conjugated hyperbilirubinaemia?

A

Occurs in inherited or acquired defects in hepatic excretin.

Direct bilirubin is >50% of total bilirubin

182
Q

What does AST stand for?

A

Aspartate

183
Q

What does ALT stand for?

A

Aminotransferase

184
Q

What are the two aminotransferases?

A

AST and ALT

185
Q

What is the function of AST and ALT?

A

They take part in gluconeogenesis by catalysing the transfer of amino groups from aspartic acid or alanine to ketoglutaric acid to produce oxaloacetic acid and pyruvic acid respectively

186
Q

What do the levels of AST and ALT in LFTs show?

A

They are markers of hepatocellular injury

187
Q

What is AST (sGOT)?

A

Glutamate oxalo-acetate transaminase
This is present in cytosolic and mitochondrial isoenzymes.
It is found in in liver, cardiac and skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes and red cells.
It is less specific/sensitive for the liver

188
Q

What Is the plasma half life for AST (sGOT)?

A

48hours

189
Q

What is ALT (sGPT)?

A

Glutamate pyruvate transaminase is a cytosolic enzyme with similar tissue distribution as AST but the activity in extra hepatic tissues is much lower

190
Q

What does an increase of ALT signify?

A

liver disease

191
Q

What is the plasma half life of ALT (sGPT)?

A

18 hours

192
Q

What is GGT?

A

y-glutamyl transferase is a microsomal enzyme that is present throughout the in liver, cardiac and skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes and red cells

193
Q

What is the function of GGT?

A

the transfer of glutamyl groups from gamma-glutamyl peptides to other peptides or amino acids

194
Q

What are the GGT results used for?

A

It has specificity for liver disease but useful to either identify raised ALP of liver origin or chronic alcohol consumption

195
Q

When would plasma activity of GGT be raised?

A

Those with chronic liver disease will have higher plasma GGT activity than those without significant liver disease

196
Q

What is ALP and what is its function?

A

Alkaline phosphatase

Hydrolyses phosphate esters in alkaline solutions

197
Q

Where is the liver derived isoenzyme of ALP found?

A

The exterior surface of the bile canalicular membrane

198
Q

Where does the serum activity of ALP come from?

A

Mainly the liver and bone isoenzymes with some from intestinal (and placental during pregnancy)

199
Q

What does prothrombin time measure?

A

the rate of conversion of prothrombin to thrombin and reflects a vital synthetic function of the liver

200
Q

What are Kupffer cells?

A

macrophages in the liver that act as phagocytes

201
Q

What are hepatocytes?

A

Cells that make up 70% of the volume of the liver. They are regenerative and perform the main functions of the liver

202
Q

Where is zone 1 of the acinus?

A

Closest to the afferent arteriole (centre of the acinus)

203
Q

What are the functions of zone 1 of the acinus?

A
  • respiratory chain
  • citric acid cycle
  • fatty acid oxidation
  • gluconeogenesis
  • urea synthesis
  • bile production
204
Q

What is zone 2 of the acinus?

A

Ill defined area

205
Q

Where is zone 3 of the acinus located?

A

Closer to the terminal hepatic veins (outside of the acinus)

206
Q

What are the functions zone 3 of the acinus?

A
  • glucolysis
  • glutamine synthesis
  • Xenobiotic metabolism
207
Q

What is gluconeogenesis?

A

Synthesis of glucose from other sources, e.g. lactate, pyruvate, glycerol and alanine

208
Q

What are the products fatty acids can be turned into?

A
  • Cholesterol –>steroids
  • prostaglandins
  • Phospholipids
  • Glycolipids
209
Q

What is nitrogen converted to in the liver?

A

Converted into urea and then excreted by the kidneys

210
Q

What is biotransformation and excretion?

A

A process used for detoxification but can generate toxic or carcinogenic metabolites

211
Q

What are the 2 phases of reaction in biotransformation and excretion?

A
  • phase 1 reactions in the smooth endoplasmic reticulum mediated by cytochrome P450 to produce hydroxylated or carboxylated compounds
  • Phase 2 reactions: subsequent conjugation with glucuronic acid, acetyl or methyl radicals or glycine, taurine or sulphate
212
Q

What happens to urobilinogen that is created by intestinal bacteria from conjugated bilirubin?

A
  • 80% - oxidised to stercobilin and excreted in faeces (giving stool its brown colour)
  • 20% - recycled - absorbed by extra-hepatic circulation to be recycled through liver and re-excreted –> enters systemic circulation to be filtered by kidney and excreted in urine
213
Q

What different types of metabolic disorder of the liver can you get?

A
  • of amino acid metabolism
  • of bile acid synthesis and metabolism
  • of carbohydrate metabolism
  • of bile flow and excretion
  • of mitochondrial function
  • of peroxisomal function
  • of copper metabolism
214
Q

What types of mitochondrial damage can you get?

A
  • Inhibition of beta oxygenation of fatty acids
  • -> Leads to micro-vesicular steatosis
  • Interference with oxidative phosphorylation
  • -> Leads to insufficient ATP generation
  • Impairment of the respiratory chain
  • -> Leads to excess ROS with lipid peroxidation
  • Increase in permeability transition
  • -> Leads to apoptosis
215
Q

What are different types of metabolic dysfunction within the liver?

A
  • essential product deficit – e.g. G-6-P deficiency (glycogen storage I)
  • precursor accumulation – e.g. OTC deficiency (hyperammonaemia)
  • Alternative pathway activation – e.g. amino-acidopathy
  • Combinations of above
216
Q

What are different consequences of toxic damage to the liver?

A 
- Mitochondrial damage
	Drugs (antivirals, salicylate, valproate, tetracycline)
	Toxins (hypoglycin, atractyloside) 
- Endothelial damage to hepatic veins
	Drugs (cytotoxic drugs)
	Toxins (Senecio, aflatoxin, pyrrolizidine)
- Glutathione depletion and cell death
	Drugs (paracetamol)
	Hypoxic ischaemia
217
Q

What are mechanisms of centrilobular necrosis?

A
  • Sepsis
  • shock induced ischaemia
  • congestive heart failure
  • toxicity from drugs and poisons
218
Q

What are clinical patterns of metabolic disease involving the liver?

A
  • New-born acute metabolic crisis - mimics sepsis
  • Severe vomiting and failure to thrive
  • Recurrent episodes of vomiting and encephalopathy with acidosis
  • Progressive retardation or seizures with hepatomegaly
  • Hepatomegaly with/without jaundice and failure to thrive/grow normally

MBChB - year 2 (25 decks)

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