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Gastroenterology Flashcards

1
Q

Give examples of alarm features (gastro) obtained from a patient history.

A

Dysphagia, bleeding, weight loss, nocturnal symptoms, aged > 45 years, acutely unwell, recent onset.

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2
Q

Give examples of alarm features (gastro) obtained from a patient examination.

A

Jaundice, abdominal mass, lymphadenopathy.

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3
Q

Give examples of alarm features (gastro) obtained from patient lab results.

A

Deranged bloods, positive coeliac serology, raised faecal calprotectin.

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4
Q

What three groups of people do gastrointestinal infections most commonly occur in?

A

Young, old and immunocompromised.

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5
Q

How do gastrointestinal infections commonly present?

A

Nausea + vomiting, diarrhoea, abdominal discomfort and fever.

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6
Q

Define diarrhoea.

A

Three loose stools over 24 hours.

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7
Q

What organism(s) typically cause watery diarrhoea?

A

Enterotoxigenic Escherichia coli.

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8
Q

What organism(s) typically cause bloody diarrhoea?

A

Shigella, Campylobacter.

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9
Q

What is the presentation of traveller’s diarrhoea?

A

Watery diarrhoea, dehydration, abdominal pain.

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10
Q

What organism is responsible for most cases of traveller’s diarrhoea?

A

Enterotoxigenic E. coli

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11
Q

What is the management of traveller’s diarrhoea?

A

Self-limiting condition - provide supportive management (provide oral rehydration). Consider loperamide for mild-moderate diarrhoea.

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12
Q

What is the general management of gastroenteritis?

A

Provide oral rehydration and monitor Na/K. Give prochlorperazine for sickness and loperamide for diarrhoea. Further antibiotic treatment depends on the causative organism.

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13
Q

What antibiotic is used in the treatment of gastroenteritis caused by cholera?

A

Tetracycline antibiotics.

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14
Q

What antibiotic is used in the treatment of gastroenteritis caused by salmonella?

A

Ciprofloxacin.

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15
Q

What antibiotic is used in the treatment of gastroenteritis caused by shigella?

A

Ciprofloxacin.

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16
Q

What is the pathophysiology of clostridium difficile infection?

A

Typically following a hospital stay or course of antibiotics which disrupt the normal gut flora.

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17
Q

What antibiotics are commonly associated with the development of clostridium difficile?

A

Clindamycin, cephalosporins (cefuroxime, ceftriaxone), ampicillin, amoxicillin and fluroquinolones (ciprofloxacin).

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18
Q

What investigations are performed in suspected clostridium difficile?

A

Stool culture and monitor WCC (raised).

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19
Q

What is the non-abx management of clostridium difficile infection?

A

Stop the causative antibiotic immediately and provide intravenous fluids.

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20
Q

What is the abx management of clostridium difficile?

A

First presentation - oral vancomycin. Recurrent (within twelve weeks) - oral fidaxomicin.

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21
Q

What is the management of clostridium difficile if there is a failure to respond to abx therapy?

A

Faecal transplant.

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22
Q

What is the presentation of H. pylori infection?

A

Epigastric pain, weight loss and vomiting.

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23
Q

What investigations are performed in H. pylori infection?

A

Urea breath test and stool antigen testing.

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24
Q

In H. pylori: How is a urea breath test performed?

A

Ask people to consume a drink containing carbon isotope 13 enriched urea. After 30 minutes patient exhales into a glass tube and mass spectrometry is used to identify the presence of carbon 13 CO2.

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25
Q

Explain how a urea breath test can identify presence of H. pylori.

A

Carbon isotope 13 enriched urea is broken down by H. pylori urease (if h. pylori is present) into carbon 13 CO2.

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26
Q

What medications must be stopped before a urea breath test is performed and for how long?

A

Test should not be performed within four weeks of treated with an antibacterial or within two weeks of treatment with an antisecretory (e.g. PPI).

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27
Q

What is gastro-oesophageal reflux disease (GORD)?

A

Common condition in which acidic gastric juices flow up into the oesophagus.

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28
Q

What is a structural cause of GORD?

A

Structurally weak lower oesophageal sphincter (or more frequent transient relaxations) due to obesity, etc.

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29
Q

What are non-structural causes of GORD?

A

Increased gastric pressure (due to obesity). Hyperacidity.

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30
Q

In GORD: what are causes of hyperacidity?

A

Certain foods.
Alcohol excess.
Rebound after prolonged PPI therapy.

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31
Q

What is the characteristic symptom of GORD?

A

Retrosternal chest pain.

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32
Q

What is the primary method of GORD investigation?

A

Endoscopy (more than half will have a normal oesophagus… non-erosive disease).

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33
Q

Other than endoscopy, how else can GORD be investigated?

A

Oesophageal pH testing.

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34
Q

What is the main complication of GORD if left untreated?

A

Barrett’s oesophagus.

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35
Q

How are people with GORD monitored for Barrett’s oesophagus?

A

Surveillance endoscopy.

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36
Q

What is the non-pharmacological management of GORD?

A

Lifestyle (healthy eating, weight loss, smoking cessation, alcohol moderation).

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37
Q

What is the pharmacological management of GORD?

A

Proton pump inhibitor (omeprazole).

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38
Q

What is Barrett’s oesophagus?

A

Metaplasia of the lower oesophageal mucosa.

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39
Q

Barrett’s oesophagus carries an increased risk of which cancer?

A

Oesophageal adenocarcinoma.

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40
Q

What cellular changes are characterised by Barrett’s oesophagus?

A

Squamous epithelium is replaced by columnar epithelium.

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41
Q

How often should patients with Barrett’s oesophagus have endoscopic surveillance with biopsy?

A

Three to five years.

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42
Q

How should Barrett’s oesophagus be treated generally?

A

High-dose PPI (omeprazole).

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43
Q

How should dysplasia of any grade be treated in Barrett’s oesophagus?

A

Endoscopic mucosal resection or radiofrequency ablation.

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44
Q

What is oesophageal achalasia?

A

Failed oesophageal peristalsis and failed relaxation of the lower oesophageal sphincter (LOS).

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45
Q

What is the pathophysiology of oesophageal achalasia?

A

Degenerative loss of ganglia from the Auerbach’s plexus.

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46
Q

What is the presentation of oesophageal achalasia?

A

Dysphagia of liquids and solids. Heartburn and food regurgitation.

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47
Q

What investigations are performed in suspected oesophageal achalasia?

A

Barium swallow.

Oesophageal manometry.

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48
Q

What does barium swallow reveal in individuals with oesophageal achalasia?

A

Grossly expanded oesophagus with characteristic ‘birds beak’ appearance.

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49
Q

What does oesophageal manometry reveal in individuals with oesophageal achalasia?

A

Excess lower oesophageal sphincter tone which doesn’t relax on swallowing.

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50
Q

What is first/second-line treatment of achalasia?

A

Pneumatic (balloon) dilatation. Heller cardiomyotomy can be used if there is recurrent/persistent symptoms.

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51
Q

What is the non-surgical treatment of achalasia?

A

Botulinum toxin injections.

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52
Q

What is the management of functional dyspepsia?

A

PPIs and neuromodulators (low-dose amitriptyline).

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53
Q

Does raised urea indicate upper or lower gastrointestinal bleeding?

A

Upper.

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54
Q

How does urea indicate upper gastrointestinal bleeding?

A

Urea is a breakdown product of digested blood.

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55
Q

What are oesophageal varices?

A

Extremely dilated submucosal vessels in the lower third of the oesophagus.

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56
Q

What is the main complication of oesophageal varices?

A

Severe bleeding.

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57
Q

What causes the development of oesophageal varices?

A

Portal hypertension secondary to liver cirrhosis.

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58
Q

How can oesophageal varices present?

A

Active haemorrhage - haematemesis (large volume fresh blood), epigastric pain and haemodynamic compromise.

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59
Q

What is the management of active haemorrhage in individuals with oesophageal varices?

A

Terlipressin and prophylactic antibiotics.

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60
Q

What is the action of terlipressin in the management of active haemorrhage with oesophageal varices?

A

Induces vasoconstriction.

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61
Q

What surgical procedure can be used for the treatment of oesophageal varices?

A

Endoscopic band ligation.

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62
Q

Following the surgical treatment of oesophageal varices… what medication is used to reduce the risk of further bleeding?

A

Propranolol.

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63
Q

What are gallstones?

A

The formation within the gallbladder out of precipitated bile components (cholesterol, bile pigments, phospholipids).

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64
Q

What are three different types of gallstone?

A

Pigment stone.
Cholesterol stone.
Mixed stone.

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65
Q

What are the three main risk factors for the development of a cholesterol stone?

A

Female.
Fat.
Forty.

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66
Q

What is biliary colic?

A

Symptoms that develop if a gallstone causes cystic duct obstruction.

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67
Q

What is the presentation of biliary colic?

A

Right upper quadrant pain that radiates to the back.

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68
Q

What is the management of biliary colic?

A

Pain relief and rehydration. Elective laparoscopic cholecystectomy.

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69
Q

What is acute cholecystitis?

A

Stone or sludge impaction in the neck of the gallbladder causing cystic duct obstruction.

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70
Q

What is the presentation of acute cholecystitis?

A

Continuous epigastric or right upper quadrant pain with an inflammatory component (fever, vomiting, local peritoneum, palpable mass). Murphy’s sign positive.

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71
Q

How is Murphy’s sign elicited?

A

Palpate the right subcostal area and ask the patient to take and hold a deep breath.

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72
Q

What is positive Murphy’s sign?

A

Pain on inspiration while palpating the right subcostal area.

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73
Q

How may acute cholecystitis progress if a gallstone moves to the common bile duct?

A

Development of obstructive jaundice and cholangitis.

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74
Q

What investigations are performed in suspected cholecystitis?

A

WCC.

Ultrasound.

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75
Q

What does ultrasound reveal in those with acute cholecystitis?

A

Thick-walled gallbladder, dilated common bile duct and hyperechoic stones.

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76
Q

What is the medical management of acute cholecystitis?

A

Pain relief, fluids and antibiotics (co-amox).

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77
Q

What is definitive treatment of acute cholecystitis?

A

Laparoscopic cholecystectomy.

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78
Q

What is diverticulosis?

A

An extremely common disorder characterised by multiple outpouchings of the bowel wall.

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79
Q

Where in the bowel does diverticulosis most commonly occur?

A

Sigmoid colon.

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80
Q

Give two risk factors for diverticulosis.

A

Increasing age.

Low-fibre diet.

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81
Q

Describe the pathophysiology of the development of diverticulosis.

A

Increased intra-colonic pressure along the weaker areas of the bowel wall (such as where the penetrating arteries enter the colonic wall).

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82
Q

What are the two conditions that diverticulosis may present as?

A

Diverticular disease.

Diverticulitis.

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83
Q

What are four possible complications of diverticulosis?

A

Abscess formation.
Peritonitis.
Obstruction.
Perforation.

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84
Q

What is diverticular disease?

A

Symptomatic diverticulosis.

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85
Q

What is the presentation of diverticular disease?

A

Altered bowel habit (constipation or diarrhoea), bleeding, colicky left-sided abdominal pain.

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86
Q

How can diverticular disease be investigated?

A

Colonoscopy, CT colonogram, barium enema.

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87
Q

What is the management of diverticular disease?

A

Increased dietary fibre intake.

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88
Q

What is diverticulitis?

A

Infection of diverticula.

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89
Q

What is the presentation of diverticulitis?

A

Left iliac fossa pain + tenderness, anorexia, nausea + vomiting, diarrhoea, bleeding and fever.

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90
Q

How is a mild attack of diverticulitis managed?

A

Oral antibiotics, liquid diet and appropriate analgesia.

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91
Q

How is a severe attack of diverticulitis managed?

A

Intravenous antibiotics (cephalosporin + metronidazole) with intravenous fluids.

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92
Q

Define constipation.

A

Unsatisfactory defecation because of infrequent stools (< 3 times/week), difficult stool passage (straining) or incomplete defecation.

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93
Q

How can constipation be managed conservatively?

A

Increase fluid intake, increase dietary fibre intake, exercise, regular toileting habits.

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94
Q

How can constipation be managed medically?

A

Provision of ispagula husk, marcogol, Senna.

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95
Q

Ispagula husk is an example of what type of laxative?

A

Bulk-forming laxative.

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96
Q

Macrogol is an example of what type of laxative?

A

Osmotic laxative, such as Movicol.

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97
Q

Senna is an example of what type of laxative?

A

Stimulant laxative.

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98
Q

What is coeliac disease?

A

Sensitivity to the protein gluten.

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99
Q

What is the pathophysiology of coeliac disease?

A

Repeated exposure to gluten results in villous atrophy which in turn causes malabsorption.

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100
Q

What are features of coeliac disease in children?

A

Failure to thrive.

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101
Q

What are features of coeliac disease in adults?

A

Foul-smelling diarrhoea, nausea + vomiting, prolonged fatigue abdominal pain/cramping/distension, weight loss and anaemia.

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102
Q

How is coeliac disease investigated?

A

Presence of tissue transglutaminase antibodies (tTG) indicates coeliac disease.

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103
Q

In investigating coeliac disease: what test must be carried out alongside anti-tTG to exclude a false negative result?

A

Total IgA levels.

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104
Q

In investigating coeliac disease: why are total IgA levels tested alongside anti-tTG?

A

Anti-tTG is an IgA. Patients with IgA deficiency may have falsely negative anti-tTG.

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105
Q

How is coeliac disease investigated other than antibody levels?

A

Jejunal endoscopy + biopsy.

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106
Q

What does jejunal endoscopy + biopsy reveal in coeliac disease?

A

Villous atrophy and crypt hyperplasia.

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107
Q

What is the treatment of coeliac disease?

A

Lifelong gluten-free diet.

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108
Q

What are the neurological features of coeliac disease?

A

Rare: peripheral neuropathy, cerebellar ataxia and epilepsy.

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109
Q

What is enteropathy-associated T cell lymphoma?

A

Possible complication of coeliac disease. Features include fevers, night sweats and bilateral inguinal lymphadenopathy.

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110
Q

What are the features of irritable bowel syndrome?

A

Abdominal pain.
Bloating.
Change in bowel habit.
Remember ABCs.

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111
Q

Give examples of exacerbating and relieving factors of IBS.

A

Symptoms worse after eating and improved by opening bowels.

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112
Q

What investigations should be performed when diagnosing IBS to exclude other pathologies?

A

FBC, ESR and CRP (normal).
Faecal calprotectin negative.
Anti-tTG negative.

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113
Q

What is the non-pharmacological management of IBS?

A

Encourage fluid intake, regular small meals, reduced processed foods, limited caffeine and alcohol.

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114
Q

What is first-line pharmacological management of IBS?

A

Loperamide for diarrhoea.
Laxatives for constipation.
Hyoscine butylbromide for abdominal cramps.

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115
Q

What is the second- and third-line pharmacological management of IBS?

A

Second - tricyclic antidepressants (amitriptyline).

Third - SSRI antidepressants.

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116
Q

What is Crohn’s disease?

A

A form of inflammatory bowel disease that can be seen anywhere in the gastrointestinal tract (from mouth to anus).

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117
Q

What part of the bowel is most commonly affected in Crohn’s disease?

A

Terminal ileum and colon.

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118
Q

What are the features of Crohn’s disease?

A

Weight loss, lethargy, (non-bloody) diarrhoea, abdominal pain.

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119
Q

What are possible extra-intestinal features of Crohn’s disease?

A

Arthritis, osteoarthritis and episcleritis.

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120
Q

How is Crohn’s disease investigated?

A 
Serological investigations (FBC, ESR, CRP, vitamin D, vitamin B12). 
Faecal calprotectin. 
Endoscopy with biopsy.
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121
Q

What does FBC, ESR, CRP, vitamin D and B12 reveal in a patient with Crohn’s disease?

A

Raised inflammatory markers.
Anaemia.
Vitamin B12 deficiency.
Vitamin D deficiency.

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122
Q

What does faecal calprotectin reveal in a patient with Crohn’s disease?

A

Raised.

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123
Q

What is faecal calprotectin?

A

A marker of inflammation in the GI tract. Calprotectin is released as a result of white cell degradation when white cells spill from blood into gut.

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124
Q

What does endoscopy + biopsy reveal in Crohn’s disease?

A

Deep ulcers and skip lesions (cobblestone appearance). Histology reveals inflammation in all layers, increased goblet cells and granulomas.

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125
Q

How is management of Crohn’s disease categorised?

A

Maintenance therapy.

Reliever therapy.

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126
Q

What is first-line in remission induction of Crohn’s disease?

A

Prednisolone.

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127
Q

What is second-line in remission induction of Crohn’s disease?

A

Mesalazine.

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128
Q

What class of drug is mesalazine?

A

5-aminosalicyclic acid.

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129
Q

When is add-on therapy required to reliever therapy of Crohn’s disease?

A

If there are two or more inflammatory exacerbations in a twelve-month period.

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130
Q

What add-on therapy is used in the management of a Crohn’s flare?

A

Azathioprine (immunosuppressant) given alongside prednisolone.

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131
Q

What add-on therapy is used in the management of a Crohn’s flare if azathioprine cannot be tolerated?

A

Methotrexate.

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132
Q

What is the relationship between smoking and Crohn’s disease?

A

Smoking is a risk factor - strongly encourage cessation.

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133
Q

What is first-line in maintenance therapy of Crohn’s disease?

A

Azathioprine or mercaptopurine.

134
Q

What % of Crohn’s disease sufferers will eventually require surgical intervention?

A

80%.

135
Q

What is the most common surgical intervention for Crohn’s disease?

A

Ileocaecal resection.

136
Q

What is ulcerative colitis?

A

A form of inflammatory bowel disease that starts at the rectum and spreads continuously (without skip lesions) and never spreads beyond the ileocaecal valve.

137
Q

At what age is peak incidence of ulcerative colitis?

A

Bimodal - 15-25 years and 55-65 years.

138
Q

What are features of ulcerative colitis?

A

Bloody diarrhoea, urgency, tenesmus, abdominal pain.

139
Q

What are three extra-intestinal features of ulcerative colitis?

A

Arthritis, uveitis, primary sclerosis cholangitis.

140
Q

What is the gold-standard investigation of ulcerative colitis?

A

Endoscopy + biopsy.

141
Q

What does endoscopy + biopsy reveal in a patient with ulcerative colitis?

A

Red, raw mucosa without skip lesions. Histology reveals superficial inflammation (not extending beyond submucosa), depletion of goblet cells and crypt abscesses.

142
Q

What is the management of proctitis and proctosigmoiditis (ulcerative colitis)?

A

Topical/rectal mesalazine (aminosalicyclates). Second line: topical corticosteroid.

143
Q

What is the management of acute severe ulcerative colitis?

A

Intravenous hydrocortisone (corticosteroid).

144
Q

What is the management of acute severe ulcerative colitis if steroids are contraindicated?

A

Intravenous ciclosporin.

145
Q

What are the surgical management options of ulcerative colitis?

A

Panproctocolectomy (complete removal of rectum and large bowel) with permanent end ileostomy or ileoanal anastomosis.

146
Q

What is the difference between endocrine and exocrine?

A

Endocrine - secretion into the circulation.

Exocrine - secretion into a duct to an epithelial surface.

147
Q

What are the pancreas’ endocrine functions (and which cells secrete)?

A

Alpha cells - glucagon.
Beta cells - insulin.
Delta cells - somatostatin.

148
Q

What are the pancreas’ exocrine functions?

A

Pancreatic juice containing bicarbonate (to neutralise stomach acid) and digestive enzymes.

149
Q

What digestive enzymes does the pancreas produce?

A

Proteases, lipases, amylase and elastase.

150
Q

What are the two most common causes of acute pancreatitis?

A

Gallstones and heavy alcohol use.

151
Q

What are the potential causes of acute pancreatitis?

A

Iatrogenic/idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion venom, hypercalcaemia, ERCP, drugs.

152
Q

Describe how gallstones can lead to the development of acute pancreatitis.

A

Obstruction of the common bile duct after the pancreatic duct has joined… duct outflow obstruction results in refluxed biliary-pancreatic secretions and pancreatic duct hypertension… autodigestion by pancreatic enzymes leads to necrosis.

153
Q

What is the presentation of acute pancreatitis?

A

Severe epigastric pain radiating through the back. Vomiting, epigastric tenderness, fever.

154
Q

What are two rare but characteristic signs of acute pancreatitis?

A

Grey-Turner’s sign (flank discolouration). Cullen’s sign (peri-umbilical discolouration).

155
Q

What investigations are performed in suspected acute pancreatitis?

A

Serum amylase.
Serum lipase.
Abdominal ultrasound.

156
Q

What does serum amylase and serum lipase reveal in acute pancreatitis?

A

Raised.

157
Q

What may ultrasound reveal in acute pancreatitis?

A

May reveal gallstones.

158
Q

What is the management of acute pancreatitis?

A

Appropriate fluids and analgesia. Provide enteral nutrition. Acute pancreatitis due to gallstones should undergo early cholecystectomy.

159
Q

What are two complications of acute pancreatitis?

A

Pancreatic necrosis.

Pancreatic pseudocysts.

160
Q

What is chronic pancreatitis?

A

Inflammatory condition that affects both the exocrine and endocrine functions of the pancreas.

161
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol excess.

162
Q

Other than alcohol excess, what are two causes of chronic pancreatitis?

A

Cystic fibrosis and haemochromatosis.

163
Q

What are the clinical features of chronic pancreatitis?

A

Epigastric pain worse 15-30 minutes following a meal, steatorrhoea, diabetes mellitus.

164
Q

What imaging technique is used in the investigation of chronic pancreatitis?

A

CT scan.

165
Q

What is the management of chronic pancreatitis?

A

Pancreatic enzyme supplements and analgesia.

166
Q

What is the most common type of pancreatic cancer and where does it affect?

A

80% are adenocarcinomas which typically occur at the head of the pancreas.

167
Q

Give five risk factors for the development of pancreatic cancer.

A

Aging, smoking, diabetes, chronic pancreatitis and BRCA2 gene.

168
Q

What are the features of pancreatic cancer?

A

Painless jaundice (pale stool, dark urine, pruritus), anorexia, weight loss, epigastric pain.

169
Q

What do LFTs reveal in pancreatic cancer?

A

Cholestatic picture (normal unconjugated bilirubin, raised conjugated bilirubin, raised ALP, raised GGT).

170
Q

What does high-resolution CT reveal in pancreatic cancer?

A

May show double duct sign - dilatation of common bile and pancreatic duct.

171
Q

What management may be offered for those with pancreatic cancer?

A

Whipple’s resection (pancreaticoduodenectomy) with adjuvant chemotherapy.

172
Q

LFTs: What is alanine transaminase (ALT)?

A

A liver enzyme found in high concentrations within hepatocytes - a marker of liver damage.

173
Q

LFTs: What is aspartate aminotransferase (AST)?

A

A liver enzyme found in hepatocytes (as well as heart and skeletal muscle cells).

174
Q

LFTs: What is alkaline phosphatase (ALP)?

A

An enzyme found in high concentrations in the liver and is an indirect marker of cholestasis. Also found in bone.

175
Q

LFTs: What is gamma-glutamyltransferase (GGT)?

A

An enzyme raised in biliary damage, bile flow obstruction and alcohol excess.

176
Q

LFTs: What is bilirubin?

A

A breakdown product of haemoglobin that is taken up by the liver.

177
Q

LFTs: What is albumin?

A

A protein synthesised in the liver and is a marker of liver function.

178
Q

LFTs: What is prothrombin time?

A

Can indicate liver disease due to the liver’s responsibility in the production of clotting factors.

179
Q

LFTs: How can ALT and ALP be compared to distinguish between hepatocellular injury and cholestasis?

A

> 10x rise in ALT and <3x rise in ALP = hepatocellular injury.
<10x rise in ALT and >3x rise in ALP = cholestasis.

180
Q

LFTs: What pathology is suggested if ALT > AST?

A

Chronic liver disease. (A(LT) = long term).

181
Q

LFTs: What pathology is suggested if AST > ALT?

A

Cirrhosis and acute alcoholic hepatitis. (A(ST) = short term).

182
Q

LFTs: What pathology is suggested by raised ALP and raised GGT?

A

Cholestasis.

183
Q

LFTs: What pathology is suggested by raised ALP and normal GGT?

A

Non-hepatobiliary pathology such as bone tumours/metastases, vitamin D deficiency and fractures.

184
Q

LFTs: What pathology is suggested by raised bilirubin and normal ALT/ALP?

A

Pre-hepatic cause of jaundice such as Gilbert’s syndrome, haemolysis.

185
Q

What are the two types of peptic ulcer?

A

Gastric ulcer and duodenal ulcer.

186
Q

What is the most common type of peptic ulcer?

A

Duodenal ulcer.

187
Q

What two processes lead to the development of a peptic ulcer?

A

Breakdown of the protective layer of the stomach and increased stomach acidity.

188
Q

Peptic ulcer: what causes breakdown of the protective layer of the stomach?

A

Medications (steroids and NSAIDs). Helicobacter pylori infection.

189
Q

Peptic ulcer: what causes increased stomach acidity?

A

Stress, alcohol, caffeine, smoking and spicy foods.

190
Q

What are the clinical features of peptic ulcer?

A

Epigastric pain/discomfort, nausea + vomiting, dyspepsia, haematemesis, melaena.

191
Q

What effect does eating have on the presentation of peptic ulcers?

A

Eating worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

192
Q

How are peptic ulcers investigated?

A

Endoscopy + rapid urease test (to check for H. pylori). Consider biopsy to exclude malignancy.

193
Q

How are peptic ulcers managed?

A

High dose PPI (e.g. omeprazole).

194
Q

What are three potential complications of peptic ulcer disease?

A

Bleeding.
Perforation = peritonitis.
Scarring + strictures = pyloric stenosis.

195
Q

What is liver failure?

A

Inability of the liver to perform its normal physiological functions.

196
Q

What are the three types of liver failure?

A

Acute liver failure (previously healthy liver).
Chronic liver failure (background of cirrhosis).
Acute-on-chronic liver failure (decompensation of chronic liver failure).

197
Q

How may liver failure present clinically?

A

Jaundice, hepatic encephalopathy, asterixis, constructional apraxia and ascites. As well as coagulopathy.

198
Q

What is ascites?

A

Accumulation of free fluid within the peritoneal cavity.

199
Q

Liver failure: What are the three processes by which ascites develops?

A

Local inflammation.
Low protein.
Low flow.

200
Q

Liver failure: Describe how ascites develops.

A

Portal hypertension develops due to cirrhosis and fluid leaks out of the vessels. Protein concentration is reduced therefore less able to pull fluid into the intravascular space… fluid accumulates in the peritoneum.

201
Q

What serological investigations are performed in liver failure?

A

LFTs, coagulation factors, glucose, ammonia.

202
Q

What do LFTs reveal in liver failure?

A

Hyperbilirubinaemia, high ALT, high AST.

203
Q

What do blood glucose and blood ammonia reveal in liver failure?

A

Low glucose.

High ammonia.

204
Q

Liver failure: Management of paracetamol overdose.

A

N-acetylcysteine.

205
Q

Liver failure: Management of raised intracranial pressure.

A

Intravenous mannitol.

206
Q

What is the cause of hepatic encephalopathy in liver failure?

A

Build up of nitrogenous waste (ammonia) in the circulation which crosses the blood brain barrier.

207
Q

Describe the two processes whereby ammonia results in hepatic encephalopathy.

A

Ammonia is neurotoxic (it halts the Krebs cycle) causing irreparable cell damage and cell death.
Ammonia is cleared by astrocytes, involving the conversion of glutamate to glutamine. Excess glutamine creates an osmotic gradient resulting in cerebral oedema.

208
Q

How does stage I hepatic encephalopathy present?

A

Altered mood/behaviour, sleep disturbance, dyspraxia, poor arithmetic.

209
Q

How does stage II hepatic encephalopathy present?

A

Increased drowsiness, confusion, slurred speech, liver flap, inappropriate behaviour.

210
Q

How does stage III hepatic encephalopathy present?

A

Incoherent, restless, liver flap, stupor.

211
Q

How does stage IV hepatic encephalopathy present?

A

Coma.

212
Q

Describe the pathophysiology behind liver cirrhosis.

A

Inflammation, matrix deposition, necrosis and angiogenesis lead to fibrosis (and reduced function).

213
Q

How does liver cirrhosis present?

A

Leukonychia (white discolouration on nails), clubbing, palmar erythema, Dupuytren’s contracture, Spider Naevi, xanthelasma, loss of body hair, hepatomegaly, bruising, ankle swelling, abdominal pain.

214
Q

What is the coagulopathy paradox of liver disease?

A

Increased risk of bleeding and increased risk of thrombosis.

215
Q

What do clotting studies reveal in liver disease?

A

All clotting factors low except for factor VIII.

216
Q

Coagulopathy paradox of liver disease: why is there an increased risk of bleeding?

A

Coagulation factors synthesised in hepatocytes (therefore production impaired in liver failure). Reduced circulating coagulation factors leads to increased risk of bleeding.

217
Q

Coagulopathy paradox of liver disease: why is there an increased risk of thrombosis?

A

Factor VIII is synthesised in body endothelial cells. Good hepatic function is required to clear activated factor VIII from the bloodstream therefore factor VIII increases = increased risk of thrombosis.

218
Q

How can ammonia accumulation be managed in liver disease?

A

Give lactulose to promote excretion. Give antibiotics to reduce the number of ammonia-producing intestinal bacteria.

219
Q

What are the four most common causes of liver cirrhosis?

A

Chronic alcohol use.
Non-alcoholic fatty liver disease.
Hepatitis B.
Hepatitis C.

220
Q

Give examples of less common causes of liver cirrhosis.

A 
Primary biliary cirrhosis. 
Autoimmune hepatitis. 
Hereditary haemochromatosis. 
Wilson's disease. 
Alpha-1 antitrypsin deficiency.
221
Q

Describe the pathophysiology of viral hepatitis.

A

Viruses target hepatocytes and cause them to present abnormal proteins via MHC I molecules which are recognised by CD8+ T-cells… resulting in apoptosis and liver damage.

222
Q

What are the clinical features of viral hepatitis?

A

Fever, malaise, nausea. Later… hepatomegaly and abdominal pain.

223
Q

What are the results of LFTs in viral hepatitis?

A

Raised ALT, raised AST. Increase in conjugated + unconjugated bilirubin.

224
Q

What is chronic hepatitis?

A

Prolonged infection (> 6 months). Inflammation mostly in the portal tract.

225
Q

What is Hepatitis A?

A

Benign, self-limiting disease most commonly found in travellers (rarely severe).

226
Q

What is the structure of the hepatitis A virus?

A

RNA virus.

227
Q

What route is hepatitis A virus transmitted via?

A

Faecal-oral route.

228
Q

What are the features of hepatitis A infection?

A

Flu-like prodrome, abdominal pain, tender hepatomegaly, jaundice.

229
Q

Hepatitis A: What is indicated by HAV IgM antibody?

A

Active infection.

230
Q

Hepatitis A: What is indicated by HAV IgG antibody?

A

Recovery or vaccination.

231
Q

What is the typical management of hepatitis A?

A

Prophylactic vaccination.

232
Q

Who is typically given hepatitis A vaccination?

A

Those travelling to areas with high prevalence of Hep A.

Patients with chronic liver disease, haemophilia, intravenous drug users or those with occupational risks.

233
Q

What is the structure of the hepatitis B virus?

A

Double-stranded DNA.

234
Q

What route is hepatitis B virus transmitted via (give examples of transmission)?

A

Infected blood and bodily fluids (childbirth, unprotected sex, intravenous drug use).

235
Q

What is the prognosis of hepatitis B?

A

20% of cases develop into a chronic condition (increased risk of post-necrotic cirrhosis, hepatocellular carcinoma).

236
Q

What three antigens are present in those with hepatitis B?

A

HBsAg (surface antigen).
HBcAg (core antigen).
HBeAg (active infection marker).

237
Q

Hepatitis B: What does HBsAg represent?

A

Present at the onset of infection and in the acute phase and in chronic infection. Not present if infection cleared after exposure.

238
Q

Hepatitis B: What does HBcAg represent?

A

Present during acute or chronic infection, present after exposure but not after immunisation.

239
Q

Hepatitis B: What does HBeAg represent?

A

Secreted by infected cells and indicates active infection, replication and can be used as a marker of infectivity.

240
Q

Hepatitis B: IgM antibodies are produced against which antigens?

A

HBcAg (core antigen).

241
Q

Hepatitis B: IgG antibodies are produced against which antigens?

A

HBsAg (surface antigen).

242
Q

At what age are children immunised for hepatitis B?

A

2, 3 and 4 months.

243
Q

Hepatitis B: What group of people are tested for response to immunisation?

A

Occupational workers (e.g. healthcare) are tested for antibodies.

244
Q

Hepatitis B immunisation response assessment: What is the management if anti-HBs > 100?

A

Adequate response - booster at five years.

245
Q

Hepatitis B immunisation response assessment: What is the management if anti-HBs 10-100?

A

Suboptimal response - one additional vaccine dose.

246
Q

Hepatitis B immunisation response assessment: What is the management if anti-has < 10?

A

No response - further vaccine course (3 doses).

247
Q

What is the prognosis for hepatitis C?

A

60% develop into chronic hepatitis.

248
Q

What is the structure of hepatitis C virus?

A

RNA virus.

249
Q

What route is hepatitis C virus transmitted via (give examples of transmission)?

A

Blood exposure (childbirth, intravenous drug use, unprotected sexual intercourse).

250
Q

What are the clinical features of hepatitis C?

A

Malaise, fatigue, intermittent RUQ pain.

251
Q

How is hepatitis C investigated?

A

HCV RNA investigation of choice.

252
Q

What is the structure of hepatitis D virus?

A

Single stranded RNA.

253
Q

Infection with hepatitis D requires what?

A

Hepatitis B to complete the replication and transmission cycle.

254
Q

What are the two possible processes of hepatitis D infection?

A

Coinfection - hepatitis B and D infection at the same time.

Superinfection - individual +ve HBsAg infected with hepatitis D.

255
Q

Hepatitis E is benign in most people except which group?

A

Pregnant women (20% mortality).

256
Q

What is the structure of hepatitis E virus?

A

RNA virus.

257
Q

Hepatitis E: HEV IgM indicates what?

A

Active infection.

258
Q

Hepatitis E: HEV IgG indicates what?

A

Recovery.

259
Q

What is hepatorenal syndrome secondary to?

A

A consequence of liver cirrhosis.

260
Q

Describe the pathophysiology of hepatorenal syndrome.

A

Hypertension in portal system = dilatation of portal vessels = reduction in circulating blood volume = reduction in blood flow to kidneys = activation of RAAS = renal vasoconstriction = starvation of blood flow to kidneys.

261
Q

What is primary biliary cholangitis?

A

A chronic autoimmune disease of the liver characterised by slow, progressive destruction of the small (interlobular) bile ducts of the liver.

262
Q

What are the complications of primary biliary cholangitis?

A

Cholestasis and liver cirrhosis. Osteoporosis. Malabsorption of fat-soluble vitamins (A, D, E and K).

263
Q

What is the classic presentation of primary biliary cholangitis (and in what group of people)?

A

Itching in the middle-aged female (9x more common in females).

264
Q

What are the clinical features of primary biliary cholangitis?

A

Asymptomatic in most. Itching, fatigue, jaundice, RUQ pain.

265
Q

What serological investigations are performed in suspected primary biliary cholangitis?

A

Anti-mitochondrial antibodies (98% specific).

Raised serum IgM.

266
Q

What is the first-line treatment of primary biliary cholangitis?

A

Ursodeoxycyclic acid.

267
Q

Primary biliary cholangitis: what is the treatment of pruritus?

A

Cholestyramine.

268
Q

Primary biliary cholangitis: what is curative treatment option?

A

Liver transplantation.

269
Q

Primary biliary cholangitis: What’s the ‘M’ rule for PBC?

A

IgM, anti-Mitochondrial antibodies (M2 subtype), Middle-aged females.

270
Q

What is primary sclerosing cholangitis?

A

Chronic liver disorder characterised by inflammation and scarring of the intra- and extra-hepatic bile ducts.

271
Q

Describe the pathophysiology of primary sclerosing cholangitis.

A

Scarring of bile ducts causes narrowing and hardening that results in impaired bile flow… resulting in cholestasis.

272
Q

Primary sclerosing cholangitis is strongly associated with what condition?

A

Ulcerative colitis (80% of patients with PSC have UC).

273
Q

What are the clinical features of primary sclerosis cholangitis?

A

Jaundice, pruritus, RUQ pain and fatigue.

274
Q

What does serological investigation reveal in primary sclerosing cholangitis?

A

Raised bilirubin and raised ALP.

275
Q

What is the standard diagnostic procedure for primary sclerosing cholangitis (and its results)?

A

MRCP (magnetic resonance cholangiopancreatography). Beaded appearance of biliary strictures.

276
Q

What does autoantibody testing reveal in primary sclerosing cholangitis?

A

p-ANCA may be positive.

277
Q

Primary sclerosing cholangitis: what is the treatment for pruritus?

A

Cholestyramine.

278
Q

What is the management of end-stage primary sclerosing cholangitis?

A

Liver transplantation.

279
Q

What group of people are typically affected by primary sclerosing cholangitis?

A

Young men.

280
Q

What is alcoholic liver disease?

A

Liver damage as a result of long-term excessive consumption of alcohol

281
Q

What are the current recommendations for alcohol intake?

A

No more than 14 units per week. No more than 5 units per day.

282
Q

What are the three stages of progression of alcoholic liver disease?

A

Alcohol related fatty liver.
Alcoholic hepatitis.
Cirrhosis.

283
Q

What are the elements of the CAGE questionnaire for alcoholic liver disease?

A

C - cut down? (ever thought you should cut down?)
A - annoyed? (ever been annoyed about someone asking about your drinking?)
G - guilty? (ever feel guilty about your drinking?)
E - eye opener? (ever need a drink in the morning to help hangover/nerves?)

284
Q

What are the clinical features of alcoholic liver disease?

A

Jaundice, hepatomegaly, spider naevi, palmar erythema, gynaecomastia, bruising, ascites, caput medusae, asterixis.

285
Q

Describe the pathophysiology behind the development of spider naevi in alcoholic liver disease?

A

Spider naevi are dilated blood vessels. Liver disease reduces the clearance/metabolism of oestrogen… which causes vasodilation of the arterioles.

286
Q

What does FBC reveal in alcoholic liver disease?

A

Macrocytosis / raised MCV.

287
Q

What do LFTs reveal in alcoholic liver disease?

A

Raised ALT, raised AST, raised GGT, raised ALP, low albumin, elevated bilirubin.

288
Q

What imaging is performed in the investigation of alcoholic liver disease?

A

Ultrasound.

CT / MRI.

289
Q

What does ultrasound reveal in alcoholic liver disease?

A

Fatty changes, increased echogenicity.

290
Q

How is alcoholic liver disease managed?

A

Stop alcohol consumption immediately and permanently. Consider detox regime and give nutritional support (thiamine).

291
Q

What is non-alcoholic fatty liver disease?

A

Metabolic syndrome relating to processing and storage of energy. Characterised by fat deposits in the liver which interfere with functioning cells.

292
Q

What are the four stages of NAFLD progression?

A

Non-alcoholic fatty liver disease.
Non-alcoholic steatohepatitis.
Fibrosis.
Cirrhosis.

293
Q

What are risk factors for NAFLD?

A

Obesity, poor diet, T2DM, high cholesterol, ageing, smoking, hypertension.

294
Q

What is the management of NAFLD?

A

Weight loss, exercise, stop smoking, diabetes control, avoid alcohol.

295
Q

What is Wilson’s disease?

A

Inherited disease characterised by excessive copper deposition in tissue.

296
Q

What is the inheritance pattern of Wilson’s disease?

A

Autosomal recessive.

297
Q

What are the three main groups of symptoms in Wilson’s disease?

A

Hepatic problems.
Neurological problems.
Psychiatric problems.

298
Q

Wilson’s disease: What are the hepatic problems?

A

Cirrhosis signs (clubbing, hepatomegaly, spider naevi, etc).

299
Q

Wilson’s disease: What are the neurological problems?

A

Impaired coordination/concentration, dysarthria, dystonia, Parkinsonism.

300
Q

Wilson’s disease: How is Parkinsonism different from Parkinson’s disease?

A

Develops symmetrically (as opposed to unilaterally in Parkinson’s).

301
Q

Wilson’s disease: What are the psychiatric problems?

A

Risk of depression and psychosis.

302
Q

Wilson’s disease: What is the characteristic eye sign?

A

Kayser-Fleischer rings (copper deposition in cornea).

303
Q

What investigations are performed in Wilson’s disease?

A

Serum caeruloplasmin, serum copper, liver biopsy.

304
Q

What are the results of serum caeruloplasmin and serum copper in Wilson’s disease?

A

Serum caeruloplasmin low. Serum copper low.

305
Q

What are the results of liver biopsy in Wilson’s disease?

A

High copper content.

306
Q

What is the treatment of Wilson’s disease?

A

Copper chelating agents (penicillamine).

307
Q

What is hereditary haemochromatosis?

A

An inherited disorder of iron absorption and metabolism resulting in iron accumulation.

308
Q

What mutation results in hereditary haemochromatosis?

A

Mutations in HFE gene on both copies of chromosome 6.

309
Q

What are the clinical features of hereditary haemochromatosis?

A

Fatigue, arthralgia, erectile dysfunction, bronze skin pigmentation.

310
Q

What are the potential complications of hereditary haemochromatosis?

A

Diabetes mellitus, liver disease, heart disease and arthritis.

311
Q

What investigations are performed in hereditary haemochromatosis?

A

Transferrin saturation is considered the most useful marker. Ferritin. Total iron binding capacity.

312
Q

What is the first line management of hereditary haemochromatosis?

A

Venesection. Monitor transferrin saturation (should be < 50%) and serum ferritin (<50 ug/l)

313
Q

What is the second line management of hereditary haemochromatosis?

A

Desferrioxamine (chelating agent that binds to free iron and enhances its elimination).

314
Q

What is Gilbert’s syndrome?

A

Condition of defective bilirubin conjugation due to deficiency of UDP glucuronosyltransferase.

315
Q

What are clinical features of Gilbert’s syndrome?

A

Jaundice during illness, exercise or fasting.

316
Q

What is revealed on investigation of Gilbert’s syndrome?

A

Unconjugated hyperbilirubinaemia.

317
Q

What is the management of Gilbert’s syndrome?

A

No treatment required.

318
Q

What is alpha-1-antitrypsin deficiency?

A

Inherited condition of abnormal alpha-1-antitrypsin (a protease inhibitor).

319
Q

What is the inheritance pattern of alpha-1-antitrypsin deficiency?

A

Autosomal recessive.

320
Q

What are the two groups of features in alpha-1-antitrypsin deficiency?

A

Liver.

Lung.

321
Q

What is the function of A1AT?

A

A1AT is produced in the liver and is responsible for inhibiting elastase (an enzyme secreted by neutrophils which digests connective tissue).

322
Q

Describe the pathophysiology of A1AT deficiency that leads to lung disease?

A

Deficiency leads to an excess in protease enzymes which attack the connective tissue of the lungs to cause bronchiectasis and emphysema.

323
Q

Describe the pathophysiology of A1AT deficiency that leads to liver disease?

A

Mutated alpha-1-antitrypsin gets trapped in the liver, builds up and causes liver damage… leads to cirrhosis.

324
Q

What investigations are performed in the diagnosis of A1AT deficiency?

A

Serum alpha-1-antitrypsin
Liver biopsy.
Genetic testing.

325
Q

A1AT deficiency: what does serum alpha-1-antitrypsin reveal?

A

Low.

326
Q

A1AT deficiency: what does liver biopsy reveal?

A

Cirrhosis + acid-Schiff-positive staining globules.

327
Q

What is the management of A1AT deficiency?

A

Stopping smoking, symptom management and organ transplant.

328
Q

What is Budd-Chiari syndrome?

A

Condition characterised by obstruction to hepatic venous outflow.

329
Q

Give examples of causes of Budd-Chiari syndrome?

A

Underlying haematological or procoagulant condition (antiphospholipid syndrome). Physical obstruction (tumour).

330
Q

What are the features of Budd-Chiari syndrome?

A

Sudden onset severe abdominal pain, ascites, tender hepatomegaly.

331
Q

What is the preferred method of investigation of Budd-Chiari syndrome?

A

Ultrasound with Doppler flow studies.

Finals (11 decks)

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