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Alimentary System > Revision > Flashcards

Revision Flashcards

1
Q

Where does digestion take place?

A

Stomach

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2
Q

Which cells produce Hcl?

A

Parietal cells

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3
Q

What is the role of Hcl in digestion?

A

Activates pepsinogen to form pepsin which hydrolyses proteins

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4
Q

Where in the GI tract does absorption occur?

A

Small intestine

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5
Q

Name the 4 distinct layers of the alimentary canal

A

Mucosa
Submucosa
Muscularis externa
Serosa/adventitia

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6
Q

What nerve plexus lies between the mucosa and submucosa?

A

Submucosal plexus

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7
Q

What is the mucosa composed of?

A

Epithelium
Lamina propria
Muscularis mucosae

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8
Q

Which nerve plexus lies between the inner and outer layer of the muscular externa?

A

Myenteric plexus

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9
Q

What type of epithelium is present in the oesophagus?

A

Non-keratinised stratified squamous

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10
Q

What type of epithelium is present in the anal canal?

A

Non-keratinised stratified squamous

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11
Q

What type of epithelium is present in the tongue?

A

Keratinised stratified squamous

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12
Q

What type of epithelium is present in the small intestine?

A

Simple columnar

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13
Q

What type of epithelium is present in the stomach?

A

Simple columnar

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14
Q

What is the lamina propria?

A

A loose connective tissue layer that lies below the epithelium

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15
Q

What type of fibres are carried in the submucosal plexus (Meissner’s plexus)?

A

Parasympathetic

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16
Q

Which segment of the small intestine contains payer’s patches?

A

Submucosa of the ileum

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17
Q

Which tunic of the GI tract contains blood, lymph and glands?

A

Submucosa

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18
Q

Which nerves carry parasympathetic innervation to the gut?

A

Vagus nerve (CN X)

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19
Q

Which nerves carry sympathetic innervation to the gut?

A

Splanchnic nerve

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20
Q

What effect would increasing parasympathetic innervation to the gut have?

A

Increases activity of enteric nervous system:
Increased gut motility
Increased gastric secretions (parietal cells and G cells)

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21
Q

What substance do G cells secrete?

A

Gastrin

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22
Q

What effect would increasing sympathetic innervation to the gut have?

A

Decreases activity of enteric nervous system:
Decreased gut motility
Inhibits gastric secretions

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23
Q

Name 3 monosaccharides

A

Glucose
Galactose
Fructose

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24
Q

Glucose + Glucose =

A

Maltose

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25
Q

Glucose + Galactose =

A

Lactose

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26
Q

Glucose + Fructose =

A

Sucrose

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27
Q

Where, in the GI tract, are disaccharides broken down to form monosaccharides?

A

In small intestine by brush border enzymes

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28
Q

What is the action of proteases?

A

Hydrolyse peptide bonds

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29
Q

What is the action of peptidases?

A

Reduce peptides to amino acids

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30
Q

Where is intrinsic factor produced and what does it bind to?

A

Parietal cells

Binds to Vitamin B12 to form complex

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31
Q

Where is vitamin B12 absorbed?

A

Distal ileum

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32
Q

Which protein does iron bind to when it is being stored intracellularly?

A

Ferritin

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33
Q

Which plasma protein does iron bind to?

A

Transferrin

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34
Q

Anaemia is caused by a lack of which iron binding protein?

A

Ferritin

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35
Q

What effect would increased parasympathetic innervation have on salivary secretion?

A

Profuse watery secretions

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36
Q

What effect would increased sympathetic innervation have on salivary secretion?

A

Small volume of serous saliva

High mucus & amylase content

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37
Q

Which type of muscle makes up the upper 1/3 of the muscular externa of the oesophagus?

A

Skeletal muscle

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38
Q

Which type of muscle makes up the lower 1/3 of the muscular externa of the oesophagus?

A

Smooth muscle

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39
Q

Which type of cells in the muscular is externa control peristaltic rhythm?

A

Pacemaker cells

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40
Q

What is the normal frequency of peristalsis in the stomach?

A

3 waves per minute

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41
Q

Which region of the stomach is mainly responsible for mixing/grinding ingested material?

A

Antrum

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42
Q

Which region of the stomach is mainly responsible for producing gastric secretions?

A

Body

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43
Q

What do chief cells secrete?

A

Pepsinogen

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44
Q

What do parietal cells secrete?

A

Hcl and intrinsic factor

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45
Q

Which cells secrete mucus?

A

Mucus neck cells

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46
Q

Where are enterogastrones secreted from?

A

Gland cells in duodenal mucosa

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47
Q

What occurs during the cephalic phase of gastric acid secretion?

A

Food is tasted/smelt
Increased vagus nerve activity
This stimulates G cells to produce gastrin
Gastrin stimulates parietal cells to produce Hcl

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48
Q

What is the role of gastrin in digestion?

A

Stimulates parietal cells to produce Hcl

Stimulates muscle contraction

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49
Q

During gastric phase of gastric acid secretion, distension of the stomach causes?

A

Vagal/enteric parasympathetic nerve to release Acetylchoine

Acetylcholine stimulates parietal cells to produce Hcl

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50
Q

During gastric phase of gastric acid secretion, peptides in the lumen causes?

A

Stimulation of G cells to produce Gastrin

Gastrin stimulates parietal cells to produce Hcl and intrinsic factor

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51
Q

During the intestinal phase of digestion once acid, fatty acids and monoglycerides reach the duodenum, which hormones are released?

A

Enterogastrones:
CCK
Secretin
GIP

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52
Q

What stimulates the release of secretin?

A

Acid in duodenum

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53
Q

What stimulates the release of CCK?

A

Fatty acids in duodenum

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54
Q

What is the role of CCK?

A

Decreases gastric emptying
Increases pancreatic enzyme secretion
Gallbladder contraction
Relaxes sphincter of oddi

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55
Q

What is the role of secretin?

A

Decreases gastric emptying
Decreases gastric acid secretion
Increases pancreatic HCO3 secretion
Increases digestive enzyme secretion

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56
Q

What switches off the production of secretin?

A

When pH rises back to normal

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57
Q

What is the role of gastric mucus?

A

Protects cells from corrosion by Hcl (acts as a buffer)

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58
Q

Which cells secrete pepsinogen?

A

Chief cells

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59
Q

Pepsinogen is the inactive precursor of what?

A

Pepsin

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60
Q

What stimulates pepsinogen activation?

A

Low pH produced by Hcl (from parietal cells)

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61
Q

What do pancreatic duct cells secrete?

A

Bicarbonate

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62
Q

What do pancreatic acinar cells secrete?

A

Digestive enzymes

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63
Q

Name the components of bile

A 
Bile acids
Lecithin
Cholesterol
Bilirubin
Toxic metals
Bicarbonate
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64
Q

Which cells secrete bile acids?

A

Hepatocytes of the liver

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65
Q

Which cells secrete the bilirubin component of bile?

A

Hepatocytes of the liver

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66
Q

Which cells secrete the bicarbonate component of bile?

A

Duct cells of the pancreas

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67
Q

What is bilirubin derived from?

A

Breakdown products of haemoglobin

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68
Q

Which amino acids are bile acids conjugated with to form bile salts?

A

Taurine or Glycine

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69
Q

What is the purpose of conjugating bile acids with amino acids?

A

To improve solubility

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70
Q

Which duct(s) does excess bile drain from the liver to the gall bladder?

A

Common hepatic duct then cystic duct

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71
Q

Which tunic layer is absent in the gallbladder?

A

Submucosa

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72
Q

How does bile move from the gall bladder to the duodenum?

A

It is ejected by contraction of muscular externa of gall bladder
It then moves down cystic duct and common bile duct to sphincter of oddi

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73
Q

What is the function of the gallbladder?

A

Stores and concentrates bile by removing water and sodium

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74
Q

What is the function of the spinchter of oddi?

A

Controls release of pancreatic juice and bile into duodenum

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75
Q

What hormone is responsible for relaxing the sphincter of oddi?

A

CCK

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76
Q

What happens when the sphincter of oddi is contracted?

A

Bile is forced back into gallbladder

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77
Q

Where does iron absorption occur?

A

Duodenum

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78
Q

Where does the majority of nutrient absorption occur?

A

Jejenum of small intestine

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79
Q

What is the function of crypts in the small intestine?

A

Active secretion of Cl

Osmotic secretion of water - keeps chyme in liquid state

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80
Q

Why are digestive enzymes produces in an inactive form? (zymogens)

A

Prevents enzymes from digesting the cells which secrete them

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81
Q

Whilst absorption is occurring in the small intestine, which muscle layer is acting to produce segmentation of chyme?

A

Longitudinal muscle layer of muscular externa

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82
Q

When does peristalsis occur?

A

After absorption has occurred

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83
Q

What triggers the end of peristalsis and beginning of segmentation?

A

Arrival of food

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84
Q

What determines the frequency of segmentation?

A

Basal electrical rhythm (BER)

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85
Q

What is the purpose of segmentation in small intestine?

A

Mixes partially digested food and digestive juices

Brings chyme into contact with intestinal wall to aid absorption

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86
Q

The law of intestine states that if intestinal smooth muscle is distended by a bolus of chyme, smooth muscle on the oral side of the bolus will:

A

Contract

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87
Q

The law of intestine states that if intestinal smooth muscle is distended by a bolus of chyme, smooth muscle on the anal side of the bolus will:

A

Relax

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88
Q

Which layer of the muscular externa is incomplete in the large intestine?

A

Longitudinal layer

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89
Q

What forms the teniae coli of the large intestine?

A

3 bands of longitudinal muscle

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90
Q

What forms the haustra of the large intestine?

A

Contraction of teniae coli

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91
Q

What type of epithelium is present in the mucosa of the large intestine?

A

Simple columnar

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92
Q

What type of muscle is present at the external anal sphincter?

A

Skeletal

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93
Q

What type of muscle is present at the internal anal sphincter?

A

Smooth

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94
Q

What is odonphagia?

A

Painful swallowing

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95
Q

What are some of the main causes of dysphagia?

A 
Malignancy
Mobility disorders
Benign stricture
Eosionophilic oesophagus
Extrinsic compression e.g. lung tumour
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96
Q

Name some substances that can reduce LOS pressure and lead to reflux

A

Nicotine
Alcohol
Dietary xanthines

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97
Q

What is the chronic form of reflux called?

A

GORD

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98
Q

What are the main symptoms of GORD?

A 
Heartburn
Water brash
Sleep disturbance
Cough 
Dysphagia
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99
Q

If a patient presents with GORD symptoms what investigations would you carry out?

A

If under 55 and no ALARM symptoms begin treatment

If over 55 or ALARM symptoms give upper GI endoscopy and manometry

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100
Q

What are ALARM symptoms?

A

Symptoms suggestive of malignancy

Anaemia
Loss of weight
Anorexia
Recent onset
Malena 
Swallowing difficulty
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101
Q

What is the gold standard test for GORD?

A

pH monitoring

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102
Q

What treatment can be given for GORD?

A 
Lifestyle changes
Pharmacological 
- Alaginates (Gaviscon)
- H2RA
- PPI (omneprazole)
Anti reflux surgery
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103
Q

What is Barrett’s oesophagus?

A

Metaplasia in the oesophagus caused by repeated acid exposure as a result of GORD

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104
Q

In Barrett’s oesophagus, what epithelial cell change occurs?

A

Squamous cells become columnar

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105
Q

What type of cancer is likely to occur as a result of Barrett’s oesophagus?

A

Adenocarcinoma

Squamous cell carcinoma is more linked to tobacco smoke

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106
Q

What treatment can be given for Barrett’s oesophagus?

A

Radiofrequency ablation

Endoscopic mucosal resection

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107
Q

Barrett’s oesophagus is most likely to lead to cancer in which part of the oesophagus? (Proximal, Middle or Distal)

A

Distal 1/3

108
Q

Squamous cell carcinoma is most likely to occur in which part of the oesophagus?

A

Proximal and Middle 1/3

109
Q

What are the common symptoms of oesophageal cancer?

A

PROGRESSIVE DYSPHAGIA
Stridor
Weight loss

110
Q

What are the common metastatic sites for oesophageal cancer?

A

Liver
Brain
Lungs
Bone

111
Q

How is oesophageal cancer diagnosed?

A

Endoscopy and biopsy

CT for distant metastases

112
Q

What are the 3 types of oesophageal motility disorder?

A

Hypermotility
Hypomotility
Achalasia

113
Q

What condition is oesophageal hyper motility often mistaken for?

A

Angina

114
Q

How is oesophageal hyper motility diagnosed?

A

Corkscrew appearance on barium swallow

Manometry

115
Q

How is oesophageal hyper motility treated?

A

Smooth muscle relaxants

116
Q

What is achalasia?

A

Degeneration of LOS neurons in myenteric plexus

Prevents LOS from relaxing

117
Q

How is achalasia diagnosed?

A 
Manometry
Barium swallow (shows dilated distal oesophagus)
118
Q

What complication are achalasia patients at risk of?

A

Squamous cell carcinoma due to toxins building up in oesophagus

119
Q

What are the risks of endoscopy?

A

Person must be fasted - if not aspiration can occur
Perforation (1/2000)
Bleeding - must come off anticoagulants

120
Q

When is manometry indicated?

A

Investigation of dysphagia following endoscopy

When motility disorder is suspected

121
Q

What does manometry check?

A

Spinchter tonicity
Relaxation of sphincters
Oesophageal muscle contractions

122
Q

What are the 2 types of hiatus hernia that can occur?

A

Para-oesophageal

Sliding

123
Q

How is achalasia treated?

A

Pharmacological (Nitrates)
Endoscopic (Botox, Balloon dilation)
Surgical (Myotomy)

124
Q

How is staging of oesophageal cancer carried out?

A

Endoscopy + biopsy (T/N stage)

CT of chest and abdomen (M stage)

125
Q

What are the treatment options for an individual diagnosed with oesophageal cancer who is deemed terminal?

A

Stenting to improve dysphagia
Radiotherapy to improve dysphagia
Palliative chemotherapy

126
Q

What are the treatment options for an individual diagnosed with oesophageal cancer who is deemed fit for surgery?

A

Neoadjuvant Chemotherapy + oesophagectomy

127
Q

What are the treatment options for an individual diagnosed with oesophageal cancer who is deemed unfit for surgery?

A

Radiotherapy + chemotherapy

128
Q

What are the risks involved in an oesophagectomy?

A

5-10% mortality risk
Lung needs to be collapsed so surgeon can get into oesophagus
Long recovery period

129
Q

When is anti reflux surgery indicated?

A

When GORD is occurring as result of hiatus hernia

130
Q

What is the most common type of anti reflux surgery?

A

Fundoplication

Carried out laparoscopically - top of stomach is wrapped round oesophagus

131
Q

What complications are associated with fundoplication?

A

Dysphagia
Difficulty belching/vomiting
Gas bloating

132
Q

What are the indications for bariatric surgery?

A

Life threatening obesity
BMI >40 or BMI >35 in patients with hypertension or diabetes
Or if weight loss is needed before life saving surgery

133
Q

What are the common symptoms of dyspepsia?

A

Epigastric pain
Belching
Nausea
Low appetite

134
Q

How should a dyspepsic patient be assessed?

A

History - drugs and lifestyle
If they are >55 or have alarm symptoms - upper Gi endoscopy
If they are <55 test for H.pylori

135
Q

What are the common tests used to diagnose H.pylori infection?

A

Non invasive tests:

  • Serology IgG
  • Urea breath test
  • Stool antigen test

Invasive tests:
- Endoscopy + gastric biopsy

136
Q

What are the outcomes of an infection with H.pylori?

A

80% are asymptomatic
15-20% develop ulcers or metaplasia
<1% develop gastric cancer

137
Q

What treatment is given for H.pylori infection?

A

Triple therapy for 7 days:
Clarithromycin
Amoxicillin
PPI

138
Q

Where does H.pylori colonise?

A

Gastric mucosal epithelium

139
Q

What is the most common cause of peptic ulcers?

A

H.pylori

140
Q

What are the common symptoms of peptic ulcers?

A 
Epigastric pain (often worse at night or when hungry)
Epigastric tenderness
Nausea
Weight loss
Bleeding (haematemesis/malena/anaemia)
141
Q

How are peptic ulcers treated?

A

Stop NSAIDs
Triple therapy for H.pylori infection
PPIs/H2RA
Surgery in complicated cases

142
Q

What are the complications of peptic ulcers?

A

Acute bleeding (haematemesis/malaena)
Chronic bleeding (anaemia)
Perforation (peritonitis)
Strictures

143
Q

How can peptic ulcers eventually lead to gastric outlet obstruction?

A

Stricture formation due to healing by fibrosis can cause outlet to become obstructed

144
Q

What are the common symptoms of gastric outlet obstruction?

A

Vomit lacking bile and containing fermented food
Dehydration due to lack of absorption
Abdominal distension
Early satiety

145
Q

If gastric outlet obstruction is suspected, how should it be investigated?

A

UGIE to identify cause

146
Q

What are the main causes of gastric outlet obstruction?

A

Stricture formation due to ulcers

Cancer

147
Q

What is the pathophysiology behind the formation of peptic ulcers?

A

Imbalance between acid secretion and mucosal barrier

148
Q

What is gastritis?

A

Inflammation of the gastric mucosa

149
Q

What are the main causes of gastritis?

A

Autoimmune
Bacterial (H.pylori) - most common
Chemical (NSAIDs, alcohol)

150
Q

Which type of cancer is most commonly found in gastric mucosa?

A

Adenocarcinoma

151
Q

If you suspected someone may have gastric cancer, which investigations would you carry out?

A

UGIE + biopsy

CT chest and abdomen

152
Q

Autoimmune gastritis is caused by autoantibodies to which cells?

A

Parietal cells - causes decreased acid secretion and loss of intrinsic factor

153
Q

Define functional bowel disorders

A

Disorder of bowel function where structure remains normal

154
Q

Name some examples of functional bowel disorders

A

IBS
Non ulcer dyspepsia
Drug related effects

155
Q

How are functional bowel disorders such as IBS diagnosed?

A
  1. History
  2. Examination
  3. Refer for endoscopy/colonoscopy if alarm symptoms present
  4. Bloods (FBC, blood glucose, thyroid status)
  5. Coeliac serology
156
Q

What are the clinical features of IBS?

A 
Abdominal pain/discomfort relieved by defecting
Bloating
Altered stool passage
Symptoms worse after eating
Mucus in stool
157
Q

If you suspected someone may have IBS, what investigations would you carry out?

A
  1. History
  2. Examination
  3. FBC/blood analysis
  4. Stool culture
  5. Calprotectin

Mainly you are trying to rule out other causes

158
Q

How is IBS treated?

A 
FODMAP
Antispasmodics
Probiotics
Anti motility agents
Laxitives
159
Q

Name some of the functional causes of vomiting

A 
Drugs
Alcohol
Pregnancy
Migraine
Functional bowel disorder
160
Q

Define structural bowel disorders

A

Disorders of the small bowel which have detectable pathology

161
Q

What are the clinical signs of small bowel structural disorders?

A

Symptoms of malabsorption:

Decreased BMI
Vitamin deficiencies
Iron deficiency

162
Q

What are some of the non-specific signs associated with small bowel structural disorders?

A

Clubbing
Scleroderma
Mouth ulcers
Dermatitis herpetiformis

163
Q

Name some of the causes of small bowel malabsorption

A

Inflammation (coeliac)
Infection (Giardia, HIV, Whipples)
Impaired motility

164
Q

What is the pathophysiology of coeliac disease?

A

Gliadin fraction of gluten gets through mucosal barrier and is activated by tissue transglutaminase
Certain genotypes sensitise due to MHCII which leads to inflammation

165
Q

How is coeliac disease diagnosed?

A

Serology:
Anti-tissue transglutaminase antibody
Anti-gliadin in children

Distal duodenal biopsy - gold standard if serology positive

166
Q

What is refractory coeliac disease?

A

When symptoms persist even after antigen (gluten) is removed from diet

167
Q

What is dermatitis herpetiformis?

A

A cutaneous manifestation of coeliac disease due to IgA deposits in skin which causes blistering of scalp, elbows and knees

168
Q

If small bowel malabsorption is found to be due to Giardia, how is this treated?

A

Metronidazole

169
Q

If a patient presents with small intestinal malabsorption, after completing blood tests and stool tests what other investigations can be carried out?

A 
Endoscopy + biopsy 
MRI enterography
White cell scan
CT scan
Capsule enterography
170
Q

Vitamin C malabsorption can cause?

A

Scurvy

171
Q

Vitamin A malabsorption can cause?

A

Night blindness

172
Q

Vitamin K malabsorption can cause?

A

Raised prothrombin time

173
Q

Niacin malabsorption can cause?

A

Unexplained heart failure

174
Q

Name some types of inflammatory bowel disorder

A

Ulcerative colitis
Crohns
Indeterminate colitis
Microscopic colitis (collagenous and lymphocytic)

175
Q

Compare ulcérative colitis and crohn’s disease

A

UC affects females more, Crohn’s M=F

UC only affects colon, Crohn’s affects mouth to anus

UC has no skip lesions, Crohn’s has skip lesions

UC peak incidence is 20-40 years, Crohn’s peak incidence is 20-40 years and >60 years

176
Q

What are the common presenting symptoms of ulcerative colitis?

A

Bloody diarrhoea
Weight loss
Abdominal pain

177
Q

What are the common presenting symptoms of Crohn’s disease?

A 
Diarrhoea
Abdominal pain 
Weight loss
Malabsorption
Mouth ulcers

Depends largely on which areas are affected

178
Q

If you suspected someone may have inflammatory bowel disease, which investigations would you carry out?

A 
Bloods:
ESR and CRP
Increased platelets 
Increased white cell count
Low haemoglobin
Low albumin

Colonscopy with biopsy - gold standard

179
Q

What are the complications associated with inflammatory bowel disease?

A

Ulcerative colitis:
Colonic carcinoma
Sclerosing cholangitis
Toxic megacolon

Crohn’s:
Strictures
Fistulas

180
Q

What is primary sclerosis cholangitis?

A

A disease of the bile ducts of the liver due to multiple strictures, can eventually lead to cirrhosis

181
Q

How is IBD treated?

A

First aim is to induce remission, this can be done using steroids

  1. 5ASAs - anti inflammatory used to induce and maintain remission (1st line in UC)
  2. Corticosteroids
  3. Azathioprine (steroid sparing anti inflammatory but with significant side effects)
182
Q

What are some of the risks involved with taking Azathioprine?

A 
Increased lymphoma risk
Leukopenia
Hepatotoxicity
Pancreatitis
Intolerance
183
Q

What is acute pancreatitis?

A

Inflammation of the pancreas with biochemical associations (increased amylase, increased lipase)

184
Q

What are the main causative agents of acute pancreatitis?

A 
Gallstones
Ethanol (most common)
Trauma
Others: Mumps, HIV, Autoimmune, Carcinoma
Idiopathic (10%)
185
Q

What is the pathogenesis of acute pancreatitis?

A

Primary insult e.g. alcohol causes release of activated pancreatic enzymes (remember pancreatic enzymes are normally released as inactive zymogens)
This causes auto digestion of own pancreas: oedema, inflammation, haemorrhage etc

186
Q

What are the symptoms of acute pancreatitis?

A

Epigastric pain
Anorexia
Nausea/vomiting
Flank bruising

187
Q

If you suspect someone may have acute pancreatitis, what investigations would you carry out?

A
  1. Serum amylase and lipase - This confirms pancreatic inflammation
  2. FBC, urea and electrolytes, Glucose, CRP to indicate prognosis

Now need to determine cause:

  1. Abdominal ultrasound (gallstones)
  2. AXR (excludes pleural effusion)
  3. ERCP
  4. CT
188
Q

What does ERCP image?

A

Allows X-rays to be taken of ducts of pancreas, liver and gallbladder

189
Q

What scoring system is used to determine severity of acute pancreatitis?

A

Glasgow Prognosis Score (3 or more is severe)

190
Q

How would you treat a patient with acute pancreatitis?

A

Initial management:
Analgesia
IV fluids
Oxygen

Then treat underlying cause

191
Q

How would you treat acute pancreatitis caused by gallstones?

A

Consider ERCP or cholecystectomy

192
Q

Name some of the complications of acute pancreatitis

A

Pancreatic necrosis
Abscess
Pseudocyst

193
Q

Define chronic pancreatitis

A

Structural integrity of pancreas is permanently altered as a direct result of chronic inflammation
Characterised by glandular destruction

194
Q

What is the pathology of chronic pancreatitis?

A

Glandular atrophy
Fibrous tissue formation
Dilation of ducts - eventually become strictures
Secretions may calcify

195
Q

What are the main causes of chronic pancreatitis?

A

Alcohol (80%)
Cystic fibrosis (2%)
Congenital abnormalities
Hereditary pancreatitis

196
Q

Name some of the genes associated with hereditary pancreatitis

A

CFTR (cystic fibrosis)
PRSS1
SPINK1

197
Q

What are the main signs of chronic pancreatitis?

A 
Early disease may be asymptomatic
Main symptom is pain! Exacerbated by food and alcohol, may be relieved by sitting forward
Weight loss
Steatorrhoea
Portal hypertension, jaundice
198
Q

If you suspected a patient may have chronic pancreatitis, what investigations would you carry out?

A 
1. Bloods
Serum amylase - usually normal unless acute on chronic attack
FBC
LFTs
Blood glucose
HbA1C
  1. Secretin test (does pancreas respond to secretin?)
  2. Ultrasound
  3. Plain xray or CT (shows calcification)
199
Q

If a patient was diagnosed with chronic pancreatitis, how would you manage them?

A
  1. Pain management
    Avoid alcohol
    Opiate analgesia
  2. Exocrine and endocrine management
    Low fat diet
    Pancreatic enzyme supplements
    Insulin for diabetes
200
Q

What are the clinical signs of pancreatic carcinoma?

A 
Epigastric pain (body and tail tumours)
Painless obstructive jaundice (head tumours)
Weight loss
Steatorrhoea 
Portal hypertensio/ascites
Abdominal mass
Abdominal tenderness
201
Q

What % of patients that present with pancreatic carcinoma are operable?

A

<10%

202
Q

If a patient with pancreatic carcinoma is deemed to be operable, what radical surgery is carried out?

A

Pancreatoduodectomy

203
Q

A Pancreatoduodectomy involves removal of which organs?

A 
Head of pancreas
Gall bladder
Part of duodenum
Pylorus
Lymph nodes near head of pancreas
204
Q

If a patient with pancreatic carcinoma is deemed inoperable, what treatments can be given to them to improve symptoms?

A

Stent - improves jaundice

Opiates for pain control

205
Q

What do raised ALT and AST indicate?

A

Acute liver injury

206
Q

Which enzyme is more specific to liver damage, AST or ALT?

A

ALT

207
Q

An AST:ALT ratio of 2:1 suggests?

A

Alcoholic liver disease

208
Q

Raised albumin is suggestive of?

A

Chronic liver injury

209
Q

Prothrombin time is a measurement of?

A

Time taken for blood to clot

210
Q

Raised prothrombin indicates what?

A

Liver dysfunction

Reduced blood clotting

211
Q

What is the definition of liver failure?

A

Not enough functioning hepatocytes to keep up with liver function

212
Q

What is the most likely outcome of infection with hepatitis C?

A

Chronic liver failure

213
Q

What are the outcomes of infection with hepatitis A?

A

Acute failure or resolution

214
Q

What are the outcomes of infection with hepatitis B?

A

Acute failure or chronic failure

215
Q

What is alcoholic hepatitis?

A

Alcohol causes fat to accumulate in hepatocytes which causes inflammatory response in liver

216
Q

If a patient has continued episodes of alcoholic hepatitis what is the likely outcome?

A

Liver cirrhosis

217
Q

What is the pathology of liver cirrhosis?

A

Loss of hepatocytes

Hepatocytes replaced by fibrous tissue

218
Q

Name some of the causes of liver cirrhosis

A 
Alcohol
Hepatitis B or C
Autoimmune hepatitis
Primary biliary cholangitis
Idiopathic (>50%)
219
Q

What is jaundice?

A

An accumulation of bilirubin

220
Q

What level of bilirubin needs to be present in the serum before jaundice becomes apparent?

A

Around 35umol/L

221
Q

What are the 3 types of jaundice?

A

Pre hepatic
Hepatic
Post hepatic

222
Q

Name a pre hepatic cause of jaundice

A

Hemolytic anaemia (abnormal breakdown of RBCs)

223
Q

Which component of haemoglobin is used to form bilirubin?

A

Heme

224
Q

In hepatocytes, bilirubin is conjugated with what to make it water soluble?

A

Glucuronic acid

225
Q

Name 2 hepatic causes of jaundice

A

Cholestasis

Intrahepatic bile duct obstruction

226
Q

Name 3 causes of intrahepatic bile duct obstruction

A

Primary biliary cholangitis
Primary sclerosis cholangitis
Liver tumours

227
Q

What is cholestasis?

A

Accumulation of bile in hepatocytes of bile calculi

228
Q

What are the causes of cholestasis?

A

Viral hepatitis
Alcoholic hepatitis
Drugs

229
Q

What are the main differences between primary biliary cholangitis and primary sclerosing cholangitis?

A

Primary billiary is an organ specific autoimmune disease
Primary sclerosing is associated with IBD

Primary biliary affects females more than males
Primary sclerosing affects males more than females

Primary biliary is associated with granulomatous inflammation
Primary sclerosing is associated with stricture formation

Both lead to destruction of bile ducts but primary sclerosing leads to cirrhosis quicker

230
Q

A cholangiocarcinoma is a tumour of which tissue?

A

Bile duct epithelium

231
Q

Name the 2 main post hepatic causes of jaundice

A

Gallstones

Common bile duct obstruction

232
Q

What are the risk factors for developing gallstones?

A

Obesity

Diabetes

233
Q

What is acute cholecystitis?

A

Acute inflammation of the gallbladder

234
Q

What is the main cause of acute cholecystitis?

A

Gallstone blocking the cystic duct

235
Q

If a patient has acute cholecystitis, which complication are you most concerned about?

A

Perforation of the gallbladder which can cause empyema

236
Q

What is chronic cholecystitis?

A

Gallbladder damage due to repeated attacks of inflammation - healing and fibrosis occurs
Thickened wall makes it hard to expel bile

237
Q

What are the causes of common bile duct obstruction?

A

Gallstones
Bile duct tumours (cholangiocarcinoma)
Extrinsic tumour compression
Benign stricture

238
Q

If levels of conjugated bilirubin are elevated, what does this suggest?

A

Hepatic or post hepatic cause of jaundice

239
Q

If a patient appears with pain in upper right quadrant and jaundice, what liver function tests would you carry out?

A

ALT:AST
ALP and Gamma GT
Conjugated bilirubin
Prothrombin time

240
Q

What does raised ALP indicate?

A

ALP is an enzyme found in bile ducts and it becomes raised when they are obstructed, however it is not specific so should be measured alongside gamma GT o confirm liver source

241
Q

Would you expect an elevated or lowered platelet count in a patient with cirrhosis?

A

Low

Cirrhosis causes splenomegaly which causes the spleen to destroy platelets

242
Q

If a patient appears with jaundice and upper right quadrant pain, which investigations would you carry out?

A 
LFTs 
Abdominal ultrasound (shows site and cause of obstruction)
Hep B and C serology
Copper test (Wilson's)
ERCP
243
Q

What is ascites?

A

Fluid in peritoneal space

244
Q

How would you investigate a patient with ascites?

A

Examination shows swiftness dullness (>1.5L)
Abdominal ultrasound (100ml)
Diagnostic removal of ascitic fluid for testing

245
Q

How is ascites treated?

A

Paracentesis - needle removal
Shunt
Diuretics
Liver transplant

246
Q

If ascites has a serum albumin gradient of more than 1.1g/dL what does that suggest?

A

Shows portal hypertension so ascites is being caused by cirrhosis and other conditions which cause portal hypertension

247
Q

Define varices

A

Abnormally dilated vessels at porto-systemic anastomoses

248
Q

If varices are present and rupture, how is this dealt with?

A

This is a medical emergency

  1. Resuscitate
  2. Blood transfusion
  3. Emergency endoscopic band ligation
249
Q

What are the 3 stages of alcoholic liver disease?

A
  1. Alcoholic fatty liver disease - reversible (fat in liver cells)
  2. Alcoholic hepatitis
  3. Alcoholic cirrhosis
250
Q

How is alcoholic fatty liver disease diagnosed?

A

AST:ALT >2:1
Raised gamma GT
Low platelet count

Abdominal ultrasound can show fatty liver

251
Q

What are the common presentations of alcoholic hepatitis?

A

Jaundice (cholestasis - intrahepatic cause)

Encephalopathy

252
Q

If you suspect someone may have alcoholic hepatitis, what investigations would you carry out and what results would you expect?

A
  1. History - alcohol
  2. Bloods
    Raised ALP and Gamma GT
    Raised prothrombin time
    Hep B/C screen to rule out viral hepatitis
253
Q

How is alcoholic hepatitis managed?

A 
Support alcohol withdrawal 
Treat infections
Treat encephalopathy 
Nutritional help
Oral steroids if hepatitis score is more than 9
254
Q

How is hepatic encephalopathy treated?

A

Laxitives and antibiotics

255
Q

What is hepatic encephalopathy often preceded by?

A

Constipation or infection

256
Q

What is spontaneous bacterial peritonitis?

A

Infection of fluid in abdomen

257
Q

What are the symptoms of spontaneous bacterial peritonitis?

A

Patient with ascites becomes feverish and has signs of sepsis

258
Q

How would you diagnose spontaneous bacterial peritonitis?

A

Do ascitic tap and check for:
decreased fluid
Increased white cell count

259
Q

What 3 conditions come under the term ‘non alcoholic fatty liver disease’?

A

Simple steatosis
Non alcoholic steatohepatitis
Fibrosis and cirrhosis

260
Q

You suspect a patient has fatty liver disease but you are unsure if it is caused by alcohol or not, what test can you do to determine the answer?

A

AST:ALT
If >2:1 it is alcohol related
If <1:1 is is non alcohol related

261
Q

What are the main causes of non-alcoholic fatty liver disease?

A

Obesity
Diabetes
Hypertension

262
Q

How is non-alcoholic fatty liver disease diagnosed?

A
  1. AST:ALT
  2. Ultrasound to look for fat
  3. Fibroscan
  4. MR spectroscopy (quantifies fat)
263
Q

How is non alcoholic fatty liver disease managed?

A

Diet and weight reduction
Exercise
Insulin sensitisers e.g. Metformin
Weight reduction surgery

264
Q

What are the indications for liver transplantation?

A

Chronic disease with poor predicted outcome or poor quality of life
Hepatocellular carcinoma
Acute liver failure

265
Q

What scoring criteria is used to determine a patient’s eligibility for liver transplantation?

A

Child’s pugh score

MELD score

Alimentary System (3 decks)

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