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1 - MSRA > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is achalasia

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter due to degenerative loss of ganglia from Auerbach’s plexus

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2
Q

Demographic achalasia

A

Typically presents in middle age
Equally common in men and women

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3
Q

Features achalasia

A

Dysphagia of liquid and solids
Typically variation in severity of symptoms
Heartburn
Regurgitation of food, may lead to cough, aspiration pneumonia

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4
Q

Most important diagnostic test achalasia

A

Oesophageal manometry

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5
Q

Findings oesophageal manometry in achalasia

A

Excessive LOS tone which doesn’t relax on swallowing

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6
Q

Findings barium swallow in achalasia

A

Grossly expanded oesphagus with fluid level
Birds beak appearance

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7
Q

CXR findings achalasia

A

Wide mediastinum
Fluid level

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8
Q

First line treatment achalasia

A

Pneumatic (balloon) dilation

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9
Q

Advantage of pneumatic dilatation over surgery in achalasia

A

Less invasive, quicker recovery time than surgery

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10
Q

Why do patients need to be low surgical risk for pneumatic dilatation achalasia

A

Surgery may be required if complications occur

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11
Q

Surgical options achalasia

A

Heller cardiomyotomy

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12
Q

When to consider Heller cardiomyotomy in achalasia

A

Recurrent or persistent symptoms

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13
Q

Options for high surgical risk patients in achalasia

A

Intra-sphincteric injection of botulinum toxin

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14
Q

Drugs used in achalasia

A

Nitrates
Calcium channel blocker

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15
Q

Limitations of drug therapy in achalasia

A

Limited by side effects

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16
Q

Causes of acute liver failure

A

Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy

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17
Q

Features acute liver failure

A

Jaundice
Coagulopathy - raised prothrombin time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure (hepatorenal syndrome)

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18
Q

Oesophageal causes haematemesis

A

Oesophageal varices
Oesophagitis
Cancer
Mallory Weiss tear

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19
Q

Gastric causes haematemesis

A

Gastric ulcer
Gastric cancer
Dieulafoy lesion
Diffuse erosive gastritis

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20
Q

What is Dieulafoy lesion

A

Arteriovenous malformation

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21
Q

Presentation Dieulafoy lesion

A

Often no prodromal features
May produce quite considerable haemorrhage
May be difficult to detect endoscopically

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22
Q

Presentation diffuse erosive gastritis

A

Usually haematemesis and epigastric discomfort
Large volume haemorrhage may occur with considerable haemodynamic compromise

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23
Q

Duodenal causes haematemesis

A

Duodenal ulcer
Aorto-enteric fistula

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24
Q

Where are duodenal ulcers usually sited

A

Posteriorly

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25
Q

Complications of posteriorly sited duodenal ulcers

A

May erode the gastroduodenal artery

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26
Q

Presentation duodenal ulcers

A

Haematemesis
Melena
Epigastric discomfort

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27
Q

Gastric vs duodenal ulcer presentation

A

Duodenal ulcer pain occurs several hours after eating

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28
Q

Who gets aortic-enteric fistulas

A

Patients with previous abdominal aortic aneurysm surgery

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29
Q

What risk assessment for haematemesis at first assessment

A

Glasgow-Blatchford score

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30
Q

Purpose of Glasgow-Blatchford score in haematemesis

A

Help decide if patients can be managed as outpatients or not

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31
Q

Risk assessment to be done after endoscopy in haematemesis

A

Rockall score

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32
Q

Purpose of Rockall score

A

Provides percentage risk of rebleeding and mortality

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33
Q

Things in Rockall score

A
  • Age
  • Features of shock
  • Co-morbidities
  • Aetiology of bleeding
  • Endoscopic stigmata of recent haemorrhage
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34
Q

Things in Blatchford score

A
  • Urea
  • Haemoglobin
  • Systolic BP
  • Pulse
  • Presentation with melaena
  • Presentation with syncope
  • Hepatic disease
  • Cardiac failure
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35
Q

What Blatchford score can be considered for early discharge

A

0

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36
Q

Use of platelet transfusion in haematemesis

A

If active bleeding and platelets less than 50

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37
Q

Use of FFP in haematemesis

A

Fibrinogen less than 1g/L, or
Prothrombin time or APTT greater than 1.5x normal

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38
Q

Use of prothrombin complex in haematemesis

A

Patients taking warfarin and actively bleeding

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39
Q

Timeframe for endoscopy in haematemesis

A

Immediately after resuscitation in severe bleeding
All patients within 24 hours

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40
Q

Who has PPIs haematemesis

A

Patients with non-variceal bleeding and sigmata of recent haemorrhage on endoscopy

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41
Q

Management of variceal bleeding before endoscopy

A

Terlipressin
Prophylactic antibiotics

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42
Q

Management variceal bleeding at endoscopy

A

Band ligation for oesophageal varices
Injections of N-butyl-2-cyanoacrylate for patients with gastric varices

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43
Q

Management variceal bleeding not controlled by endoscopy

A

Transjugular intrahepatic portosystemic shunts (TIPS)

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44
Q

Screening questionnaires used for problem alcohol drinking

A

AUDIT
FAST
CAGE

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45
Q

How many questions in AUDIT

A

10

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46
Q

Minimum, maximum, and problem scores AUDIT

A

Minimum = 0
Maximum = 40
8+ in men/7+ in women = strong likelihood of hazardous/harmful alcohol consumption
15+ in men/13+ in women = alcohol dependence

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47
Q

What is AUDIT-C

A

Abbreviated form of audit consisting of 3 questions

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48
Q

Minimum and maximum scores in FAST and problem score

A

Minimum = 0
Maximum = 16
Hazardous drinking = 3

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49
Q

What is first question of FAST, and how to interpret

A

“How often do you have 8 (men)/6 (women)+ drinks on on occasion”

If answer never, not misusing alcohol
If answer is weekly, daily, or almost daily, patient is hazardous, harmful, or dependent drinker

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50
Q

How is CAGE interpreted

A

4 questions, 2 or more positive answers considered ‘positive’ result

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51
Q

Diagnostic criteria alcohol problem drinking

A

Need 3+:
- Compulsion to drink
- Difficulties controlling alcohol consumption
- Physiological withdrawal
- Tolerance to alcohol
- Neglect of alternative activities to drinking
- Persistent use of alcohol despite evidence of harm

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52
Q

Government recommendations alcohol

A

Men and women should drink no more than 14 units per week
If drinking as much as 14 units per week, spread evenly over 3 days or more

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53
Q

How much is one unit of alcohol

A

Equal to 10ml pure ethanol, e.g.
- 25ml spirits
- 1/3 pint of peer
- half 175ml glass of red wine

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54
Q

How to calculate units in a drink

A

(Millilitres x ABV)/1000

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55
Q

What is alcohol ketoacidosis

A

A non-diabetic euglycaemic form of ketoacidosis

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56
Q

What causes alcohol ketoacidosis

A

Alcoholics often not eat regularly and may vomit food they do eat, leading to episodes of starvation → malnourishment → body breaks down fat, producing ketones

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57
Q

Presentation alcohol ketoacidosis

A

Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

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58
Q

Treatment alcoholic ketoacidosis

A

Infusion of saline and thiamine

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59
Q

Purpose of thiamine in alcoholic ketoacidosis

A

To avoid Wernicke encephalopathy/Korsakoff psychosis

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60
Q

Investigation findings alcoholic liver disease

A

Elevated gamma-GT
Ratio of AST:ALT >2 (>3 strongly suggestive of acute alcohol hepatitis)

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61
Q

Management acute episodes of alcoholic hepatitis

A

Glucocorticoids, e.g. prednisolone
Pentoxyphylline - not as good as glucocorticoids

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62
Q

How to determine who would benefit from glucocorticoids

A

Maddrey’s discriminat function, calculated using prothrombin time and bilirubin concentration

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63
Q

Mechanism 5-ASA

A

Released in colon and not absorbed, acts locally as anti-inflammatory, mechanism not understood but may inhibit prostaglandin synthesis

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64
Q

Examples aminosalicylates

A

Sulphasalazine
Mesalazine
Olsalazine

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65
Q

What is in sulphasalazine

A

Sulphapyridine (a sulphonamide) and 5-ASA

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66
Q

Side effects sulphasalazine caused by sulphapyridine

A
  • Rashes
  • Oligospermia
  • Headache
  • Heinz body anaemia
  • Megaloblastic anaemia
  • Lung fibrosis
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67
Q

SEs all aminosalicylates

A

GI upset
Headache
Agranulocytosis
Pancreatitis
Interstitial nephritis

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68
Q

What is mesalazine

A

Delayed release form of 5-ASA

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69
Q

Investigation unwell patient on aminosalicylates

A

FBC

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70
Q

Risk of pancreatitis sulphasalazine vs mesalazine

A

Pancreatitis 7 times more common in patients taking mesasalazine

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71
Q

What is angiodysplasia

A

Vascular deformity of GI tract, predisposes to bleeding and iron deficiency anaemia

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72
Q

Associations angiodysplasia

A

Aortic stenosis (debated)

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73
Q

Demographic angiodysplasia

A

Generally seen in elderly patient

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74
Q

Features angiodysplasia

A

Anaemia
GI bleeding - if upper GI, melena. If lower GI, brisk, fresh PR bleeding

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75
Q

What does ascites with SAAG (serum ascites albumin gradient) >11g/L indicate

A

Portal hypertension

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76
Q

Liver causes ascites with SAAG >11g/L

A

Cirrhosis/alcoholic liver disease
Acute liver failure
Liver metsL

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77
Q

Cardiac causes ascites with SAAG >11g/L

A

Right heart failure
Constrictive pericarditis

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78
Q

Other causes ascites with SAAG >11g/L

A

Budd-Chiari syndrome
Portal vein thrombosis
Veno-occlusive disease
Myxoedema

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79
Q

Causes ascites with SAAG <11g/L

A

Hypoalbuminaemia, e.g. nephrotic syndrome, severe malnutrition
Peritoneal carcinomatosis
Tuberculous peritonitis
Pancreatitis
Bowel obstruction
Biliary ascites
Post-op lymphatic leak
Serositis in connective tissue disease

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80
Q

Conservative management ascites

A

Reduce dietary sodium
Fluid restriction if sodium <125mmol/L

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81
Q

Medical management ascites

A

Aldosterone antagonists, e.g. spironolactone +/- loop diuretics
Prophylactic antibiotics to reduce risk of SBP

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82
Q

Prophylactic antibiotics ascites

A

Oral cipo or nofloxacin

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83
Q

Who is offered prophylactic antibiotics in ascites

A

People with cirrhosis and ascites with ascitic protein 15g/L or less

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84
Q

Invasive management ascites

A

Drainage if tense
Transjugular intrahepatic portosystemic shunt in some patients

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85
Q

What is required for large volume paracentesis for treatment of ascites

A

Albumin

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86
Q

Complications paracentesis for ascites

A

Circulatory dysfunction if large volume (>5L)
Hepatorenal syndrome
Dilution hyponatraemia
Asciters recurrence

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87
Q

Associations autoimmune hepatitis

A

Other autoimmune disorders
Hypergammaglobulinaemia
HLA B8
HLA DR3

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88
Q

Type 1 autoimmune hepatitis antibodies

A

ANA and/or SMA

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89
Q

Demographic T1 autoimmune hepatitis

A

Adults and children

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90
Q

Type 2 autoimmune hepatitis antibodies

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

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91
Q

Demographic T2 autoimmune hepatitis

A

Children

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92
Q

Type 3 autoimmune hepatitis antibodies

A

Soluble liver-kidney antigen

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93
Q

Demographic type 3 autoimmune hepatitis

A

Adults in middle age

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94
Q

Presentation autoimmune hepatitis

A

Acute hepatitis - fever, jaundice (25%)
Amenorrhoea

May present with chronic liver disease

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95
Q

Immunoglobulins in autoimmune hepatitis

A

Raised IgG levels

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96
Q

Liver biopsy autoimmune hepatisi

A

Inflammation extending beyond limiting plate
Piecemeal necrosis
Bridging necrosis

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97
Q

Management autoimmune hepatitis

A

Steroids
Other immunosuppressants, e.g. azathioprine
Liver transplantation

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98
Q

What is Barrett’s oesophagus

A

Metaplasia of lower oesophageal mucosa, with usual squamous epithelium being replaced by columnar epithelium

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99
Q

Management Barrett’s oesophagus

A

High dose PPI

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100
Q

Management Barrett’s oesophagus with metaplasia

A

Endoscopy surveillance with biopsies every 3-5 years

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101
Q

Management Barrett’s oesophagus with dysplasia

A

Endoscopic intervention - radio frequency ablation first line, endoscopic mucosal resection second line

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102
Q

Cause of primary bile-acid malabsorption

A

Excessive production of bile acid

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103
Q

Secondary causes bile acid malabsorption

A

Ileal disease, e.g. Crohns
Cholecystectomy
Coeliac disease
Small intestinal bacterial overgrowth

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104
Q

Features bile acid malabsorption

A

Steatorrhoea
Vitamin ADEK malabsorption

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105
Q

Investigation bile acid malabsorption

A

SeHCAT - nuclear medicine test, scans done 7 days apart to assess retention/loss of radio labelled SeHCAT

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106
Q

Management bile acid malabsorption

A

Bile acid sequestrates, e.g. cholestyramine

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107
Q

What is Budd-Chiari syndrome

A

Hepatic vein thrombosis

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108
Q

Cause Budd-Chiari syndrome

A

Polycythaemia rubra vera
Thrombophilia
Pregnancy
COCP

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109
Q

Features Budd-Chiari syndrome

A

Abdominal pain - sudden onset, severe
Ascites → abdominal distention
Tender hepatomegaly

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110
Q

Investigation Budd-Chiari syndrome

A

Ultrasound with Doppler flow studies

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111
Q

When do carcinoid tumours cause carcinoid syndrome

A

Usually when mets present in liver → release serotonin into systemic circulation
May also occur with lung carcinoid - mediators not cleared by the liver

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112
Q

Features carcinoid syndrome

A

Flushing
Diarrhoea
Bronchospasm
Hypotension
Right heart valvular stenosis

Other molecules e.g. ACTH and GHRH may be secreted
Pellagra

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113
Q

Cause pellagra in carcinoid syndrome

A

Dietary tryptothan diverted to serotonin by the tumour

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114
Q

Investigation carcinoid syndrome

A

Urinary 5-HIAA
Plasma chromogranin A yMa

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115
Q

Management carcinoid syndrome

A

Somatostatin analogues, e.g. octreotide

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116
Q

Management diarrhoea caused by carcinoid syndrome

A

Cyproheptadine

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117
Q

What kind of bacteria is C diff

A

Anaerobic gram positive rod

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118
Q

Risk factors C diff

A

Second and third gen cephalosporins
Clindamycin
PPI

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119
Q

Transmission C diff

A

Faecal-oral route by ingestion of spores

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120
Q

Features C diff

A
  • Diarrhoea
  • Abdominal pain

Severe toxic megacolon may develop

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121
Q

Characteristic investigation findings C diff

A

Raised WCC

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122
Q

Criteria mild C diff

A

Normal WCC

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123
Q

Criteria moderate C diff

A

Raised WCC
Typically 3-5 loose stools/day

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124
Q

Criteria severe C diff

A

Raised WCC, or acutely raised creatinine (>50% baseline), or temp >38.5
Evidence of severe colitis, e.g. abdominal or radiological signs

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125
Q

Criteria life threatening C diff

A

Hypotension
Partial or complete ileus
Toxic megacolon
CT evidence of severe disease

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126
Q

Diagnostic criteria C diff

A

Detection of C difficult toxin in stool

C. diff antigen = exposure, not current infection

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127
Q

First line C diff

A

Oral vancomycin 10 days

Stop other antibiotic therapy if possible

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128
Q

Second line C diff

A

Oral fidaxomicin

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129
Q

Third line C diff

A

Oral vancomycin +/- IV metronidazole

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130
Q

Management recurrence C diff within 12 weeks of symptom resolution

A

Oral fidaxomicin

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131
Q

Management recurrence C diff after 12 weeks of symptom resolution

A

Oral vancomycin or fidaxomicin

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132
Q

Treatment life threatening C diff infection

A

Oral vancomycin and IV metronidazole
Specialist advice - surgery may be considered

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133
Q

Other treatment options C diff

A

Bezlotoxumab (not supported by NICE)
Faecal microbiota transplant

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134
Q

When is faecal microbiota transplant considered in C diff

A

Patients with 2 or more previous episodes

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135
Q

Liver failure clotting factors

A

All clotting factors are low except VIII (can be high)

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136
Q

Gene associations coeliac disease

A

HLA-DQ2
HLA-DQ8

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137
Q

Signs/symptoms that need screening for coeliac

A
  • Chronic or intermittent diarrhoea
  • Failure to thrive/faltering growth
  • Persistent or unexplained GI symptoms, inc N&V
  • Prolonged fatigue
  • Recurrent abdo pain, cramping, distention
  • Sudden/unexpected weight loss
  • Unexplained anaemia
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138
Q

Conditions that need screening for coeliac

A
  • Autoimmune thyroid disease
  • Dermatitis herpetiformis
  • IBS
  • T1DM
  • First degree relative with coeliac
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139
Q

Complications coeliac

A
  • Anaemia
  • Hyposplenism
  • Osteoporosis, osteomalacia
  • Lactose intolerance
  • Enteropathy-associated T-cell lymphoma of small intestine
  • Subfertility, unfavourable pregnancy outcomes
  • Oesophageal cancer
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140
Q

Cause of anaemia in coeliac disease

A

Iron deficiency
Folate deficiency
Vitamin B12 deficiency

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141
Q

How long before testing for coeliac does patient need to reintroduce gluten if stopped eating

A

6 weeks

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142
Q

Diagnosis of coeliac

A

Serology + endoscopic intestinal biopsy

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143
Q

Serology tests coeliac

A

Tissue transglutaminase (TTG)
Endomyseal antibody

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144
Q

Why is endomyseal antibody testing needed in coeliac

A

To look for selective IgA deficiency, which would give false negative coeliac result

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145
Q

Who needs endoscopic intestinal biopsy to look for coeliac disease

A

All patients with suspected coeliac disease

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146
Q

Where is biopsied suspected coeliac

A

Traditionally duodenum, but jejunal biopsies sometimes done

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147
Q

Findings on biopsy coeliac disease

A
  • Villous atrophy
  • Crypt hyperplasia
  • Increase in intraepithelial lymphocytes
  • Lamina propria infiltration with lymphocytes
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148
Q

Forms of inherited colon cancer

A

Hereditary non-polyposis colorectal cancer (Lynch syndrome) HNPCC
Familial adenomatous polyposis FAP

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149
Q

Inheritance HNPCC

A

Autosomal dominant

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150
Q

Features of colorectal cancer in HNPCC

A
  • Often proximal colon
  • Poorly differentiated
  • Highly aggressiveW
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151
Q

Second most common cancer associated with HNPCC

A

Endometrial cancer

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152
Q

Inheritance FAP

A

Autosomal dominant

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153
Q

Management FAP

A

Total proctocolectomy with ileal pouch anal anastomosis in 20’s

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154
Q

What other tumours FAP patients at risk of

A

Duodenal

Variant Gardner’s syndrome - osteomas of skull and mandible, retinal pigmentation, thyroid carcinoma, epidermoid cysts on skin

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155
Q

Presentation Crohn’s disease

A

Non-specific symptoms e.g. weight loss, lethargy
Diarrhoea - can be bloody
Abdominal pain
Perianal disease, e.g. skin tags, ulcers

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156
Q

Bloods Crohn’s disease

A

Raised inflammatory markers
Anaemia
Low B12 and vitamin D

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157
Q

Which extra-intestinal manifestations of Crohn’s and UC are related to disease activity

A

Pauciarticular asymmetric arthritis
Erythema nodosum
Episcleritis
Osteoporosis

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158
Q

Which extra-intestinal manifestations of Crohn’s and UC are unrelated to disease activity

A

Polyarticular symmetric arthritis
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing

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159
Q

Episcleritis UC vs Crohns

A

More common in Crohns

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160
Q

Primary sclerosing cholangitis UC vs Crohns

A

Much more common in UC.

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161
Q

Uveitis UC vs Crohns

A

More common in UC

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162
Q

Smoking and Crohn’s

A

Patients should be strongly advised to stop smoking

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163
Q

First line for inducing remission in Crohns

A

Glucocorticoids - ora, topical, or IV

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164
Q

Second line for inducing remission in Crohns

A

5-ASA, e.g. mesalazine

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165
Q

Role enteral feeding with elemental diet in inducing remission in Crohns

A

May be used in addition to or instead of other measures to induce remission, particularly if concerns about side effects of steroids e.g. in young children

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166
Q

Drugs used as add-on therapy in inducing remission in Crohn’s

A

Azathioprine
Mercaptopurine
Methotrexate

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167
Q

Role of infliximab inducing remission in Crohn’s

A

Refractory disease/fistulating Crohn’s

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168
Q

Role metronidazole inducting remission in Crohn’s

A

Often used for isolated perianal disease

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169
Q

First line maintenance of remission Crohn’s

A

Azathioprine or mercaptopurine

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170
Q

Second line maintenance of remission Crohn’s

A

Methotrexate

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171
Q

Surgical options Crohn’s

A
  • Ileocaecal resection
  • Segmental small bowel resections
  • Stricturoplasty
  • Surgery for perianal fistula or abscess
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172
Q

When is ileocaecal resection done in Crohn’s

A

Stricturing terminal ileal disease

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173
Q

Investigation perianal fistulae in Crohn’s

A

MRI

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174
Q

Purpose of MRI in perianal fistulae in Crohn’s

A
  • Determine presence of fistula or abscess
  • Determine if fistula is simple (low fistula) or complex (high fistula that passes through or above muscle layers)
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175
Q

Medical treatment perianal fistula in Crohns

A
  • Oral metronidazole
  • Anti-TNF agents, e.g. infliximab
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176
Q

Surgical treatment complex fistula in Crohns

A

Draining seton

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177
Q

Treatment perianal abscess in Crohns

A

Incision and drainage with antibiotic therapy
Draining seton if tract is identified

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178
Q

Complications Crohn’s

A

Small bowel cancer
Colorectal cancer
Osteoporosis

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179
Q

What should be checked before offering azathioprine or mercaptopurine in Crohns

A

TPMT activity

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180
Q

Presentation cyclical vomiting syndrome

A

Severe nausea and vomiting lasting hours to days
Prodromal intense sweating and nausea
Well in between episode

May also have weight loss, reduced appetite, abdominal pain, diarrhoea, dizziness, photophobia, headache

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181
Q

Prophylaxis cyclical vomiting syndrome

A

Amitriptyline
Propanolol
Topiramate

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182
Q

Acute treatments cyclical vomiting syndrome

A

Ondansetron
Prochlorperazine
Triptans

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183
Q

When is stool culture required in diarrhoea

A
  • Systemically unwell needing hospital admission
  • Blood or pus in stool
  • Immunocompromised
  • Recent ABx, PPI, or hospital admission
  • Recent foreign travel
  • Public health indication - diarrhoea in high risk people, suspected food poisoning
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184
Q

Blood findings diarrhoea

A

AKI
Hypokalaemia
Hyponatraemia

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185
Q

Presentation diverticulitis

A

Left iliac fossa pain and tenderness
Anorexia, nausea, and vomiting
Diarrhoea
Features of infection - pyrexia, raised WCC and CRP

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186
Q

Management diverticulitis

A

Mild attacks treated with oral antibiotics
More significant episodes - NBM, IV fluids, IV antibiotics

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187
Q

IV antibiotics in severe diverticulitis

A

Cephalosporin + metronidazole

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188
Q

Complications diverticulitis

A

Abscess formation
Peritonitis
Obstruction
Perforation

189
Q

Drugs causing hepatocellular picture of liver disease

A

Paracetamol
Sodium valproate, phenytoin
MAOIs
Halothene
Anti-tuberculosis - isoniazid, rifampicin, pirazinamide
Statins
Alcohol
Amiodarone
Methyldopa
Nitrofurantoin

190
Q

Drugs causing cholestatic picture of liver disease

A

COCP
Antibiotics - fluclox, co-amox, erythromycin
Anabolic steroids, testosterones
Phenothiazines - chlorpromazine, prochlorperazine
Sulphonylureas
Fibrates

191
Q

Drugs causing liver cirrhosis

A

Methotrexate
Methyldopa
Amiodarone

192
Q

2WW referral dyspepsia (oesophageal/stomach)

A
  • Dysphagia
  • Upper abdominal mass consistent with stomach cancer
  • Aged ≥55 with weight loss + any of upper abdo pain, reflux, dyspepsia
193
Q

Non-urgent referral for dyspepsia

A

Haematemesis
≥55 with;
- Treatment resistent dyspepsia
- Upper abdominal pain with low haemoglobin levels
- Raised platelet count with any of: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
- Nausea and vomiting with any of: weight loss, reflux, dyspepsia, upper abdominal pain

194
Q

Treatment for dyspepsia not needing referral

A
  • Review medications
  • Lifestyle advice
  • Trial full dose PPI for 1 month, or ‘test and treat’ approach for H pylori
195
Q

Testing method for H pylori at initial diagnosis

A

Carbon-13 urea breath test or stool antigen test

196
Q

Test of cure H pylori

A

Not required if symptoms resolved
If repeat testing required, carbon-13 urea breath test

197
Q

Investigation dysphagia

A

Urgent endoscopy in all cases

198
Q

Features of CREST syndrome

A
  • Calcinosis
  • Raynaud’s phenomenon
  • Oesophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
199
Q

Features globus hystericus

A
  • History of anxiety
  • Symptoms intermittent and relieved by swallowing
  • Usually painless
200
Q

Role of ferritin

A

Intracellular protein that binds iron and stores it to be released in a controlled fashion at sites where iron is required

201
Q

Definition increased ferritin levels

A

> 300 in men/post menopausal women
200 in premenopausal women

202
Q

Causes of raised ferritin without iron overload

A
  • Inflammation (ferritin is acute phase reactant)
  • Alcohol excess
  • Liver disease
  • CKD
  • Malignancy
203
Q

Causes of raised ferritin with iron overload

A

Primary iron overload, e.g. hereditary haemochromatosis
Secondary iron overload, e.g. repeated transfusion

204
Q

Investigation to determine if iron overload present

A

Transferrin saturation

205
Q

Normal transferrin saturation

A

<45% in women
<50% in men

206
Q

Cause reduced ferritin

A

Iron deficiency anaemia (as iron and ferritin bound)

207
Q

Presentation gallstones

A

Colicky RUQ occuring after meals
Symptoms worst following fatty meal

208
Q

Investigation gallstones

A
  • Abdominal ultrasound
  • Liver function tests
209
Q

Investigation suspected CBD stones

A

MRCP
Intraoperative imaging

210
Q

Management biliary colic

A

Laparoscopic cholecystectomy

211
Q

Features acute cholecystitis

A

RUQ pain
Fever
Murphys sign
Occasionally midly deranged LFTs, esp Mirizzi syndrome

212
Q

Management acute cholecystitis

A

Cholecystectomy, ideally within 48 hours of presentation

213
Q

Features gallbladder abscess

A

Usually prodromal illness and RUQ pain
Swinging pyrexia
Patient may be systemically unwell
Generalised peritonism not present

214
Q

Imaging gallbladder abscess

A

USS +/- CT

215
Q

Management gallbladder abscess

A

Ideally surgery (subtotal cholecystectomy may be needed if Calot’s triangle is hostile)
In unfit patients, percutaneous drainage

216
Q

Features cholangitis

A

Patients severely unwell and septic
Jaundice
RUQ pain

217
Q

Management cholangitis

A

Fluid resuscitaiton
Broad spectrum IV antibiotics
Correct coagulopathy
Early ERCP

218
Q

Features gallstone ileus

A

Small bowel obstruction, may be intermittent

219
Q

Management gallstone ileus

A

Laparotomy and removal of gallstone from small bowel - enterotomy must be made proximal to site of obstruction, not at site of obstruction
Do not interfere with fistula between gallbladder and duodenum

220
Q

Features acalculous cholecystitis

A
  • Incurrent illness, e.g. diabetes, organ failure
  • Systemically unwell
  • Gallbladder inflammation in absence of stones
  • High fever
221
Q

Management acalculous cholecystitis

A

If patient fit, cholecystectomy
If unfit, percutaneous cholecystostomy

222
Q

Management asymptomatic gallstones

A

Leave unless causing problems

223
Q

Treatment biliary colic in very frail patient

A

Ultrasound guided cholecystostomy

224
Q

Risks of ERCP

A

Bleeding
Duodenal perforation
Cholangitis
Pancreatitis

225
Q

Most common type of gastric cancer

A

Gastric adenocarcinoma

226
Q

Risk factors gastric cancer

A

H pylori infection
Pernicious anaemia, atrophic gastritis
Diet high in salt or nitrates
Japanese or Chinese
Smoking
Blood group A

227
Q

Features gastric cancer

A
  • Abdominal pain - typically vague, epigastric, may present as dyspepsia
  • Weight loss and anorexia
  • Nausea and vomiting
  • Dysphagia
  • Overt upper GI bleeding in minority of patients
228
Q

Features gastric cancer with lymphatic spread

A

Virchow’s node (left supraclavicular node)
Sister Mary Joseph’s nodule (periumbilical nodule)

229
Q

Initial investigation gastric cancer

A

Oesophago-gastric-duodenoscopy with biopsy

230
Q

Characteristic biopsy finding gastric cancer

A

Signet ring cells - high numbers = worse prognosis

231
Q

Staging investigation gastric cancer

A

CT CAP

232
Q

Management gastric cancer

A

Surgery - endoscopic mucosal resection, partial or total gastrectomy
Chemotherapy

233
Q

Indications for endoscopy in GORD

A

Age >55
Symptoms >4 weeks or persistent symptoms despite treatment
Dysphagia
Relapsing symptoms
Weight loss

234
Q

Investigations if endoscopy negative in GORD

A

Consider 24-hour oesophageal pH monitoring

235
Q

What is Gilberts syndrome

A

Condition of defective bilirubin conjugation due to deficiency of UDP glucuronosyltransferase

236
Q

Inheritance Gilbert’s syndrome

A

Autosomal recessive

237
Q

Features Gilbert’s syndrome

A

Unconjugated hyperbilirubinaemia - may only be seen during intercurrent illness, exercise, or fasting

238
Q

Investigation Gilbert’s syndrome

A

Rise in bilirubin following prolonged fasting or IV nicotinic acid

239
Q

Treatment Gilbert’s syndrome

A

No treatment required

240
Q

What is haemochromotosis

A

Autosomal recessive disorder of iron absorption and metabolism → iron accumulation

241
Q

Inheritance haemochromotosis

A

Autosomal recessive

242
Q

Early features of haemochromotosis

A

Fatigue
Erectile dysfunction
Arthralgia

243
Q

Later features of haemochromotosis

A

Bronze skin pigmentation
Diabetes mellitus
Liver signs - stigmata of chronic liver disease, hepatomegaly, cirrhosis
Cardiac failure
Hypogonadism

244
Q

Cause of cardiac failure in haemochromotosis

A

Dilated cardiomyopathy

245
Q

Cause of hypogonadism in haemochromotosis

A

Cirrhosis and pituitary dysfunction

246
Q

Reversible complications of haemochromotosis

A

Cardiomyopathy
Skin pigmentation

247
Q

Irreversible complications of haemochromotosis

A

Liver cirrhosis
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

248
Q

Screening for haemochromatosis in the general population

A

Transferrin saturation

249
Q

Screening for haemachromatosis in family members

A

Genetic testing for HFE mutation

250
Q

Typical iron study profile in patient with haemochromatosis

A

Transferrin saturation >55% in men or >50% in women
Raised ferritin and iron
Low TIBC

251
Q

Further tests in haemochromatosis

A

Liver function tests
Molecular genetic testing for C282Y and H63D mutations
MRI

252
Q

Purpose of MRI in haemochromatosis

A

Quantify liver and/or cardiac iron

253
Q

Role of liver biopsy in haemochromatosis

A

Now generally only used if suspected hepatic cirrhosis

254
Q

First line treatment haemochromatosis

A

Venesection

255
Q

Monitoring of adequacy of venesection in haemochromatosis

A

Transferrin saturation should be kept below 50%, and serum ferritin concentration below 50ug/L

256
Q

Second line treatment haemochromatosis

A

Desferrioxamine

257
Q

H pylori gram +ve or -ve

A

-ve

258
Q

What conditions can H pylori cause

A

Peptic ulcer disease - 95% of duodenal ulcers, 75% of gastric uulcers
Gastric cancer
B cell lymphoma of MALT tissue
Atrophic gastritis

259
Q

H pylori and GORD

A

Association clear, no role in GORD for H pylori eradication

260
Q

Management H pylori

A

Eradication with 7 days of PPI + amox + clari or metronidazole

If pen allergic, PPI + metronidazole + clari

261
Q

How is urea breath test done?

A

Patients consume drink containing carbon isotope 13 enriched urea. After 30 minutes, patient exhales into glass tube.

262
Q

When can urea breath test be done re. medications

A

Not within 4 weeks of treatment with an antibacterial, or within 2 weeks of anti-secretory drug

263
Q

What happens in rapid urease test (CLO test)

A

Biopsy sample mixed with urea and pH indicator, colour change if H pylori urease activity

264
Q

Disadvantage of serum antibody testing for H pylori

A

Remains positive after eradication

265
Q

Use of culture of gastric biopsy for H pylori

A

Provides information on antibiotic sensitivity

266
Q

What test is used to check for H pylori eradication

A

Breath test

267
Q

Features hepatic encephalopathy

A

Confusion, altered GCS
‘Liver flap’ - arrhythmic negative myoclonus with frequency of 3-5Hz
Constructional apraxia - inability to draw a 5-pointed star

268
Q

EEG findings hepatic encephalopathy

A

Triphasic slow waves

269
Q

Grading hepatic encephalopathy

A

Grade I - irritability
Grade II - confusion, inappropriate behaviour
Grade III - incoherent, restless
Grade IV - coma

270
Q

Factors precipitating hepatic encephalopathy

A

Infection, e.g. SBP
GI bleed
Post TIPS
Constipation
Drugs
Hypokalaemia
Renal failure
Increased dietary protein

271
Q

Drugs precipitating hepatic encephalopathy

A

Sedatives
Diuretics

272
Q

First line treatment hepatic encephalopathy

A

Lactulose

273
Q

Secondary prophylaxis hepatic encephalopathy

A

Rifaximin

274
Q

Interpretation of positive HBsAg hepatitis B serology

A

Usually acute disease
If present for >6 months, implies chronic disease

275
Q

Interpretation positive anti-HBs hepatitis B serology

A

Immunity - exposure or immunisation

Negative in chronic disease

276
Q

Interpretation positive anti-HBc hepatitis B serology

A

Previous or current infection

IgM anti-HBc appears during acute or recent (6 months) hep B infection. IgG anti-HBc persists

277
Q

Interpretation HbeAg hepatitis B serology

A

Current infection

278
Q

Most common cause hepatocellular carcinoma worldwide

A

Chronic hepatitis B

279
Q

Most common cause hepatocellular carcinoma in Europe

A

Chronic hepatitis C

280
Q

Risk factors hepatocellular carcinoma

A

Liver cirrhosis (most important)
Alpha-1 antitrypsin deficiency
Hereditary tyrosinosis
Glycogen storage disease
Aflatoxin
Drugs
Porphyria cutanea tarda
Male sex
Diabetes mellitus, metabolic syndrome

281
Q

Drugs risk factors for hepatocellular carcinoma

A

OCP
Anabolic steroids

282
Q

Presentation hepatocellular carcinoma

A

Jaundice
Ascites
RUQ pain
Hepatomegaly
Pruritis
Splenomegaly

283
Q

How to screen hepatocellular carcinoma

A

Ultrasound +/- alpha-fetoprotein

284
Q

Who to screen hepatocellular carcinoma

A

Patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
Men with liver cirrhosis secondary to alcohol

285
Q

Management options hepatocellular carcinoma

A

If early disease - surgical resection
Liver transplantation
Radiofrequency ablation
Transarterial chemoembolisation
Sorafenib

286
Q

Features type 1 hepatorenal syndrome

A

Rapidly progressive
Doubling of serum creatinine to >221, or halving of creatinine clearance to less than 20ml/min over a period of less than 2 weeks
Very poor prognosis

287
Q

Features type 2 hepatorenal syndrome

A

Slowly progressive
Prognosis poor, but patients may live for longer

288
Q

Management hepatorenal syndrome

A

Vasopressin analogues, e.g. terlipressin
Volume expansion - 20% albumin
Transjugular intrahepatic portosystemic shunt

289
Q

Presentation features more common in Crohns vs UC

A

Weight loss
Upper GI symptoms, mouth ulcers
Perianal disease
Abdominal mass in RIF

290
Q

Presentation features more common in UC vs Crohn’s

A

Bloody diarrhoea
Abdo pain LLQ
Tenesmus

291
Q

Extra-intestinal manifestations more common in Crohn’s vs UC

A

Gallstones
Oxalate renal stones

292
Q

Extra-intestinal manifestations more common in UC vs Crohn’s

A

Primary sclerosing cholangitis

293
Q

Complications more common in Crohn’s vs UC

A

Obstruction
Fistula

294
Q

Complications more common in UC vs Crohn’s

A

Colorectal cancer

295
Q

Histology features of Crohn’s

A

Inflammation in all layers from mucosa to serosa
Increased goblet cells
Granulomas

296
Q

Histology features UC

A

No inflammation beyond submucosa (unless fulminant disease)
Neutrophils migrate through walls of glands to form crypt abscesses
Depletion of goblet cells and mucin from gland epithelium
Granulomas infrequent

297
Q

Endoscopy Crohn’s

A

Deep ulcers
Skip lesions → cobblestone appearance

298
Q

Endoscopy UC

A

Widespread ulceration with preservation of adjacent mucosa - pseudopolyps

299
Q

Small bowel enema finding Crohn’s

A

Strictures - ‘Kantor’s string sign’
Proximal bowel dilatation
‘Rose thorn’ ulcers
Fistulae

300
Q

Barium enema findings Crohns

A

Loss of haustrations
Superficial ulceration, pseudopolyps
In longstanding disease, colon narrow and short - drainpipe colon

301
Q

Inherited causes unconjugated jaundice

A

Gilbert’s syndrome
Crigler-Najjar syndrome

302
Q

Inherited causes conjugated jaundice

A

Dubin-Johnson syndrome
Rotor syndrome

303
Q

Inheritance pattern of inherited jaundice conditions

A

All autosomal recessive

304
Q

Crigler-Najjar syndrome prognosis

A

Type 1 do not survive to adulthood
Type 2 less severe

305
Q

Treatment Crigler-Najjar syndrome type 2

A

Phenobarbital

306
Q

Features Dubin-Johnson syndrome

A

Relatively common in Iranian jews
Results in grossly black liver
Benign

307
Q

Cause in rise in TIBC

A

IDA
Pregnancy, oestrogen

308
Q

How to calculate transferrin saturation

A

Serum iron / TIBC

309
Q

Blood results anaemia of chronic disease

A

Normochromic/hypochromic normocytic anaemia
Reduced serum and TIBC
Normal or raised ferritin

310
Q

Diagnostic criteria IBS

A

Abdominal pain relieved by degeceation, or associated with altered bowel frequency, in addition to 2/4 of:
- Altered stool passage - straining, urgency, incomplete evacuation
- Abdominal bloating, distention, tension, or hardness
- Symptoms made worse by eating
- Passage of mucus

311
Q

Red flag features suggesting not IBS

A

Rectal bleeding
Unexplained/unintentional weight loss
Family history of bowel or ovarian cancer
Onset after 60y/o

312
Q

Suggested primary care investigations IBS

A

FBC
ESR/CRP
Coeliac disease screen

313
Q

First line IBS treatment predominant pain

A

Antispasmodic agents

314
Q

First line IBS treatment predominant constipation

A

Laxatives (avoid lactulose)

315
Q

First line IBS treatment predominant diarrhoea

A

Loperamide

316
Q

Second line treatment constipation IBS

A

Linaclotide

317
Q

When to consider linaclotide IBS

A

Optimal or maximum tolerated doses of previous laxatives from different classes have not helped, and had constipation for at least 12 months

318
Q

Second line treatment (all symptoms) IBS

A

Low dose TCA

319
Q

When to consider psychological intervention IBS

A

If symptoms do not response to pharmacological treatments after 12 months - CBT, hypnotherapy, psychological therapy

320
Q

Predisposing factors bowel ischaemia

A

Increasing age
AF (particularly mesenteric ischaemia)
Other causes of emboli - endocarditis, malignancy
CVS risk factors - smoking, hypertension, diabetes
Cocaine

321
Q

Presentation bowel ischaemia

A

Abdo pain - sudden onset, severe, out of keeping with exam findings
Rectal bleeding
Diarrhoea
Fever

322
Q

Investigation of choice bowel ischaemia

A

CT

323
Q

Cause acute mesenteric ischaemia

A

Typically embolism resulting in occlusion of artery supplying small bowel e.g. superior mesenteric artery

324
Q

Management acute mesenteric ischaemia

A

Urgent surgery

325
Q

Presentation chronic mesenteric ischaemia

A

Colicky, intermittent abdominal pain

326
Q

What is ischaemic colitis

A

Acute but transient compromise in the blood flow to large bowel → inflammation, ulceration, haemorrhage

327
Q

Where in bowel ischaemic colitis more likely to occur

A

‘Watershed’ areas, e.g. splenic flexure, that are located at borders of territory supplied by superior and inferior mesenteric arteries

328
Q

Investigation findings ischaemic colitis

A

Thumbprinting on AXR due to mucosal oedema/haemorrhage

329
Q

Management ischaemic colitis

A

Usually supportive
Surgery may be required in minority of cases if conservative management fails

330
Q

Indications for surgery ischaemic colitis

A

Generalised peritonitis
Perforation
Ongoing haemorrhage

331
Q

Presentation malabsorption

A

Diarrhoea
Steatorrhoea
Weight loss

332
Q

Intestinal causes of malabsorption

A

Coeliac disease
Crohn’s disease
Tropical sprue
Whipple’s disease
Giardiasis
Brush border enzyme deficiencies, e.g. lactase insufficiency

333
Q

Pancreatic causes of malabsorption

A

Chronic pancreatitis
Cystic fibrosis
Pancreatic cancer

334
Q

Biliary causes malabsorption

A

Biliary obstruction
Primary biliary cirrhosis

335
Q

Other causes of malabsorption

A

Bacterial overgrowth, e.g. systemic sclerosis, diverticulae, blind loop
Short bowel syndrome
Lymphoma

336
Q

What is melanosis coli

A

Disorder of pigmentation of bowel wall - pigment laden macrophages on histology

337
Q

Cause melanosis coli

A

Laxative abuse, esp anthraquinone compounds e.g. senna

338
Q

Mechanism metoclopramide

A

D2 receptor antagonist

339
Q

Uses metoclopramide

A

Mainly used in management of nausea
GORD
Gastroparesis (prokinetic action)
Migraine

340
Q

Why is metoclopramide useful in migraine

A

Migraine attacks result in gastroparesis, slowing absorption of analgesics

341
Q

Adverse effects metoclopramide

A

Extrapyramidal effects - acute dystonia e.g. oculogyric crisis
Diarrhoea
Hyperprolactinaemia
Tardive dyskinesia
Parkinsonism

342
Q

Use of metoclopramide in bowel obstruction

A

Should be avoided in bowel obstruction, but may be helpful in paralytic ileus

343
Q

Risk factors NAFLD

A

Obesity
T2DM
Hyperlipidaemia
Jejunoileal bypass
Sudden weight loss/starvation

344
Q

Features NAFLD

A

Usually asymptomatic
Hepatomegaly

345
Q

Bloods NAFLD

A

ALT>AST

346
Q

USS NAFLD

A

Increased echogenicity

347
Q

Further investigation if NAFLD found

A

Enhanced liver fibrosis blood test - check for advanced fibrosis
Used in combo with hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1

348
Q

What to do if testing shows NAFLD with advanced fibrosis

A

Refer to liver specialist - biopsy for more accurate staging

349
Q

Management NAFLD

A

Lifestyle changes, particularly weight loss and monitoring

350
Q

Most common type oesophageal cancer

A

Adenocarcinoma

351
Q

Location oesophageal adenocarcinoma

A

Lower third

352
Q

Location oesophageal SCC

A

Upper 2/3

353
Q

Risk factors oesophageal adenocarcinoma

A

GORD
Barrett’s oesophagus
Smoking
Obesity

354
Q

Risk factors oesophageal SCC

A

Smoking
Alcohol
Achalasia
Plummer-Vinson syndrome
Diets rich in nitrosamines

355
Q

Features oesophageal cancer

A

Dysphagia
Anorexia and weight loss
Vomiting
Odynophagia
Hoarseness
Melaena
Cough

356
Q

Diagnosis oesophageal cancer

A

Upper GI endoscopy

357
Q

Investigation for staging oesophageal cancer

A

Endoscopic ultrasound for locoregional staging
CT CAP - FDG-PET CT for occult mets if not seen on initial CT
Laparoscopy sometimes to detect occult peritoneal disease

358
Q

Treatment oesophageal cancer

A

Operable disease (T1N0M0) - surgical resection
Chemotherapy

359
Q

Main complication surgical resection oesophageal cancer

A

Anastomotic leak → mediastinitis

360
Q

What is Plummer-Vinson syndrome

A

Triad of:
Dysphagia secondary to oesophageal webs
Glossitis
Iron deficiency anaemia

361
Q

Treatment Plummer-Vinson syndrome

A

Iron supplementation
Dilation of webs

362
Q

What is Boerhaave syndrome

A

Severe vomiting → oesophageal rupture

363
Q

Most common type of pancreatic cancer

A

Adenocarcinoma

364
Q

Risk factors pancreatic cancer

A

Increasing age
Smoking
Diabetes
Chronic pancreatitis
Hereditary non-polyposis colorectal carcinoma
Multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation

365
Q

Classic presentation pancreatic cancer

A

Painless jaundice - pale stools, dark urine, pruritis, cholestatic liver function tests

366
Q

Abdominal masses in pancreatic cancer

A

Hepatomegaly - due to mets
Gallbladder
Epigastric mass - from primary tumour

367
Q

Courvoisiers law

A

In presence of painless obstructive jaundice, palpable gallbladder unlikely to be due to gallstones

368
Q

Other symptoms pancreatic cancer

A

Non specific presentation - anorexia, weight loss, epigastric pain
Loss of exocrine function eg steatorrhoea
Loss of endocrine function eg diabetes
Atypical back pain
Trousseau sign

369
Q

What is Trousseau sign

A

Migratory thrombophlebitis

370
Q

Investigation pancreatic cancer

A

High resolution CT scanning

371
Q

Imaging pancreatic cancer

A

‘Double duct’ sign - simultaneous dilatation of common bile duct and pancreatic ducts

372
Q

Treatment resectable pancreatic cancers

A

Whipple (pancreaticoduodenectomy) + adjuvant chemotherapy

373
Q

SEs Whipple

A

Dumping syndrome
Peptic ulcer disease

374
Q

Palliation pancreatic cancer

A

ERCP with stenting

375
Q

What is pernicious anaemia

A

Autoimmune disorder affecting gastric mucosa resulting in vitamin B12 deficiency

376
Q

Other causes of B12 deficiency (other than pernicious anaemia)

A

Atrophic gastritis (secondary to H pylori)
Gastrectomy
Malnutrition, e.g. alcoholism

377
Q

Risk factors pernicious anaemia

A

Female
Middle to old age
Other autoimmune disorders - thyroid disease, T1DM, Addison’s, rheumatoid, vitiligo
Blood group A

378
Q

Features pernicious anaemia

A

Anaemia features - lethargy, pallor, dyspnoea
Neurological features
Mild jaundice
Atrophic glossitis → sore tongue

379
Q

Neurological features pernicious anaemia

A
  • Peripheral neuropathy - pins and needles, numbness, typically symmetrical, legs > arms
  • Subacute combined degeneration of spinal cord - progressive weakness, ataxia, paresthesia → spasticity and paraplegia
  • Neuropsychiatric features - memory loss, poor concentration, confusion, depression, irritability
380
Q

FBC in pernicious anaemia

A

Macrocytic anaemia
Hypersegmented polymorphs on blood film
Low WCC and platelets

381
Q

Antibodies in pernicious anaemia

A

Anti-intrinsic factor antibodies (highly specific)
Anti-gastric parietal cell antibodies (low specificity)

382
Q

Management pernicious anaemia

A

IM vitamin B12 - if no neuro features, 3 injections/week for 2 weeks → 3 monthly. More frequent if neuro features
Folic acid supplements

383
Q

Malignancy increased risk in pernicious anaemia

A

Gastric cancer

384
Q

Inheritance Peutz-Jeghers syndrome

A

Autosomal dominant

385
Q

Features Peutz-Jeghers syndrome

A

Hamartomatous polyps in GI tract, mainly small bowel → SBO due to intussusception, GI bleeding
Pigmented lesions on lips, oral mucosa, face, palms, soles

386
Q

What is primary biliary cholangitis

A

Chronic liver disorder - autoimmune. Interlobular bile ducts damaged by chronic inflammatory process → progressive cholestasis → cirrhosis

387
Q

Associations primary biliary cholangitis

A

Sjorgen’s syndrome (80%)
RA
Systemic sclerosis
Thyroid disease

388
Q

Presentation primary biliary cholangitis

A

Fatigue
Pruritis
Cholestatic jaundice
Hyperpigmentation, esp over pressure points
RUQ pain
Xanthelsmas and xanthomata
Clubbing
Hepatosplenomegaly

389
Q

Blood tests primary biliary cholangitis

A

AMA antibodies
Raised serum IgM

390
Q

First line management primary biliary cholangitis

A

Usodeoxycholic acid - slows progression and improves symptoms

391
Q

Treatment pruritis in primary biliary cholangitis

A

Cholestyramine

392
Q

Other treatments in primary biliary cholangitis

A

Liver transplant
Fat-soluble vitamin supplementations

393
Q

Complications primary biliary cholangitis

A

Cirrhosis → portal hypertension → ascites, variceal haemorrhage
Osteomalacia and osteoporosis
Significantly increased risk of hepatocellular carcinoma

394
Q

What is primary sclerosing cholangitis

A

Biliary disease characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

395
Q

Associations primary sclerosing cholangitis

A

UC (80%)
Crohn’s
HIV

396
Q

Features primary sclerosing cholangitis

A

Cholestasis - jaundice, pruritis
RUQ pain
Fatigue

397
Q

Diagnostic investigation primary sclerosing cholangitis

A

ERCP or MRCP

398
Q

Findings ERCP/MRCP primary sclerosing cholangitis

A

Multiple biliary strictures giving beaded appearance

399
Q

Antibody in primary sclerosing cholangitis

A

pANCA

400
Q

Findings liver biopsy primary sclerosing cholangitis

A

Fibrous, obliterative cholangitis often described as onion skin

401
Q

Complications primary sclerosing cholangitis

A

Cholangiocarcinoma
Increased risk of colorectal cancer

402
Q

Adverse effects PPIs

A

Hyponatraemia, hypomagnaseaemia
Osteoporosis → increased risk of fractures
Microscopic colitis
Increased risk of C.diff

403
Q

Risk factors small bowel bacterial overgrowth syndrome

A

Neonates with congenital GI abnormalities
Scleroderma
Diabetes mellitus

404
Q

Presentation small bowel bacterial overgrowth syndrome

A

Chronic diarrhoea
Bloating, flatulence
Abdominal pain

405
Q

Diagnosis small bowel bacterial overgrowth syndrome

A

Hydrogen breath test
Small bowel aspiration and culture

406
Q

Management small bowel bacterial overgrowth syndrome

A

Rifaximin treatment of choice

Co-amox or metro effective in majority

407
Q

Diagnosis spontaneous bacterial peritonitis

A

Paracentesis - neutrophil >250

408
Q

Most common organism causing SBP

A

E. coli

409
Q

Management SBP

A

IV cefotaxime

410
Q

Criteria for prophylaxic antibiotics in patients with ascites

A
  • Prev episode fo SBP
  • Fluid protein <15g/L, and either Child-Pugh score of at least 9 or hepatorenal syndrome
411
Q

Prophylactic antibiotic in ascites

A

Oral cipro or norfloxacin

412
Q

Presentation UC

A

Bloody diarrhoea
Urgency
Tenesmus
Abdominal pain, esp left lower quadrant
Extra-intestinal features

413
Q

Diagnostic investigation UC

A

Colonoscopy and UC

In patients with severe colitis, avoid colonoscopy due to risk of perf - flexi sig instead

414
Q

Scope findings UC

A

Red, raw mucosa, bleeds easily
No inflammation beyond submucosa (unless fulminant disease)
Widespread ulceration with preservation of adjacent mucosa (pseudopolyps)
Inflammatory cell infiltrate in lamina propria
Crypt absses
Depletion of goblet cells and mucin

415
Q

Barium enema findings UC

A

Loss of haustrations
Superficial ulceration, pseudopolyps
If longstanding, colon narrow and short

416
Q

Criteria mild UC

A

<4 stools/day, small amount of blood

417
Q

Criteria moderate UC

A

4-6 stools/day, varying amount of blood, no systemic upset

418
Q

Criteria severe UC

A

> 6 bloody stools/day
Features of systemic upset - pyrexia, tachycardia, anaemia, raised inflammatory markers

419
Q

First line treatment mild/moderate UC with proctitis

A

Rectal aminosalicylate (mesalazine)

420
Q

Second line treatment mild/moderate UC with proctitis

A

If remission not achieved in 4 weeks, add oral aminosalicylate

421
Q

Third line treatment mild/moderate UC with proctitis

A

Add topical or oral corticosteroid

422
Q

First line treatment mild/moderate UC with proctosigmoiditis and left sided disease

A

Rectal aminosalicylate

423
Q

Second line treatment mild/moderate UC with proctosigmoiditis and left sided disease

A

If remission not achieved in 4 weeks, add high-dose oral aminosalicylate and topical corticosteroid

424
Q

Third line treatment mild/moderate UC with proctosigmoiditis and left sided disease

A

Stop topical treatments, offer oral aminosalicylate and oral corticosteroid

425
Q

First line treatment mild/moderate UC extensive disease

A

Topical (rectal) aminosalicylate and high dose oral aminosalicylate

426
Q

Second line treatment mild/moderate UC extensive disease

A

If remission not achieved in 4 weeks, stop topical treatment and offer high dose oral aminosalicylate and oral corticosteroid

427
Q

First line treatment severe UC

A

Hospital admission
IV steroids (IV ciclosporin if steroids CI)

428
Q

Second line treatment severe UC

A

If no improvement after 72 hours, consider adding IV ciclosporin or consider surgery

429
Q

Maintaining remission following mild/moderate UC flare with proctitis/proctosigmoiditis

A

Rectal aminosalicylate (daily or intermittent) +/- oral aminosalicylate
Or oral aminosalicylate (not as effective)

430
Q

Maintaining remission following mild/moderate UC flare with left-sided and extensive disease

A

Low maint dose of oral aminosalicylate

431
Q

Maintaining remission following severe relapse or ≥2 exacerbations in past year

A

Oral azathioprine or oral mercaptopurine

432
Q

First line acute treatment variceal haemorrhage

A

Terlipressin
Prophylactic IV antibiotics
Endoscopy - band ligation (superior) or sclerotherapy

433
Q

What IV antibiotics given in acute variceal haemorrhage

A

Quinolones

434
Q

Second line treatment acute variceal haemorrhage

A

Sengstaken-Blakemore tube

435
Q

Third line treatment acute varicael haemorrahge

A

TIPSS

436
Q

Complication TIPSS

A

Exacerbation of hepatic encephalopathy

437
Q

Prophylaxis variceal haemorrhage

A

Propanolol
Endoscopic variceal band ligation
TIPSS if above measures unsuccessful

438
Q

How is endoscopic variceal band ligation carried out as prophylaxis for variceal haemorrhage

A

Should be performed at two weekly intervals until all varices have been eradicated
PPI cover to prevent EVL-induced ulceration

439
Q

Who should be offered prophylactic endoscopic variceal band ligation

A

People with cirrhosis who have medium to large oesophageal varices

440
Q

Presentation vitamin A deficiency

A

Night blindness

441
Q

Vitamin A fat or water soluble

A

Fat

442
Q

Vitamin B1 aka

A

Thiamine

443
Q

Vitamin B1 fat or water soluble

A

Water

444
Q

Causes B1 (thiamine) deficiency

A

Alcohol excess
Malnutrition

445
Q

Conditions associated with B1 (thiamine) deficiency

A

Wernicke’s encephalopathy
Korsakoffs syndrome
Dry beriberi
Wet beriberi

446
Q

Features Wernicke’s encephalopathy

A

Nystagmus
Opthalmoplegia
Ataxia

447
Q

Features Korsakoffs syndrome

A

Amnesia
Confabulation

448
Q

Features dry beriberi

A

Peripheral neuropathy

449
Q

Features wet beriberi

A

Dilated cardiomyopathy

450
Q

Vitamin B12 aka

A

Cobalamin

451
Q

Causes B12 deficiency

A

Pernicious anaemia
Diphyllobothrium latum infection
Crohn’s

452
Q

Consequences B12 deficiency

A

Macrocytic, megaloblastic anaemia
Peripheral neuropathy

453
Q

B12 water or fat soluble

A

Water

454
Q

Vitamin B6 aka

A

Pyridoxine

455
Q

B6 water or fat soluble

A

Water

456
Q

Causes of B6 deficiency

A

Isoniazid therapy

457
Q

Consequences B6 deficiency

A

Peripheral neuropathy
Sideroblastic anaemia

458
Q

What is Whipple’s disease

A

Rare multi-system disorder caused by Tropheryma whipellii infection

459
Q

Risk factors Whipples disease

A

Middle aged men
HLA-B27

460
Q

Features Whipple’s disease

A

Malabsorption - diarrhoea, weight loss
Large joint arthralgia
Lymphadenopathy
Hyperpigmentation, photosensitivity
Pleurisy, pericarditis
Neurological symptoms - opthalmoplegia, dementia, seizures, ataxia, myoclonus

461
Q

Investigations Whipple’s disease

A

Jejunal biopsy - deposition of macrophages containing Periodic acid-Schiff granules

462
Q

Management Whipple’s disease

A

Oral co-trimoxazole for a year
Sometimes preceded by IV penicillin

463
Q

Inheritance pattern Wilson’s

A

Autosomal recessive

464
Q

Onset of symptoms Wilson’s disease

A

10-25

465
Q

Features Wilson’s disease

A

Hepatitis, cirrhosis
Neurological features
Kayser-Fleischer rings
Renal tubular acidosis
Haemolysis
Blue nails

466
Q

Neurological features Wilsons’ disease

A

Basal ganglia degeneration
Speech, behavioural, and psychiatric problems - often first manifestations
Asterixis
Chorea
Dementia
Parkinsonism

467
Q

Investigation findings Wilsons

A

Reduced serum caeruloplamin
Reduced total serum copper, increased free serum copper
Increased 24hr urinary copper excretion

468
Q

Confirmation of diagnosis Wilsons

A

Genetic testing ATP7B

469
Q

First line Wilsons

A

Penicillamine (chelates copper)

1 - MSRA (23 decks)

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