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GI Passmedicine Flashcards

1
Q

What are the two most common causes of acute GI bleeds?

A

Peptic ulcers

Oesophageal varices

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2
Q

What risk assessment scores can you use to assess acute GI bleeds?

A

Blatchford score at first assessment

Full Rockall score after endoscopy

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3
Q

What features are assessed using the Blatchford score?

A 
Urea
Hb
Systolic BP
Pulse
Presentation with malaena
Presentation with syncope
Hepatic disease
Cardiac failure
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4
Q

Patients with what Blatchford score may be considered for early discharge?

A

0

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5
Q

What is involved in resus in acute GI bleed?

A

ABC, wide bore IV access

In some pts: FFP, platelets, prothrombin complex

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6
Q

What GI bleed pts would you give platelets to?

A

Those actively bleeding + with platelet count <50x10^9/l

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7
Q

What acute GI bleed pts would you give FFP to?

A

Fibrinogen level <1g/L or PT/APTT >1.5x normal

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8
Q

What acute GI bleed pts would you give prothrombin complex to?

A

Those actively bleeding and taking warfarin

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9
Q

What is the management of acute GI bleed?

A

Resus

Endoscopy

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10
Q

In what time period should those with an acute GI bleed have an endoscopy?

A

Within 24h

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11
Q

How is non-variceal acute GI bleed managed?

A

PPIs after endoscopy

If further bleeding - repeat endoscopy, interventional radiology and surgery

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12
Q

How is variceal acute GI bleeding managed at presentation?

A

Teripressin and prophylactic antibiotics

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13
Q

What is the treatment of oesophageal varices?

A

Band ligation

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14
Q

What is the treatment of gastric varices?

A

N-butyl-2-cyanoacrylate

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15
Q

Is band ligation/N-butyl-2-cyanoacrylate fails to control variceal bleeding what is the next measure implemented?

A

Transgular intrahepatic portosystemic shunts

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16
Q

What will you see on the blood results will you see in someone with an acute GI bleed?

A 
Raised urea (upper GI bleed)
Marginal normocytic anaemia
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17
Q

Why do patients with an acute upper GI bleed get a raised urea?

A

RBCs in the stomach are broken down into urea (blood acts as a protein meal)

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18
Q

What drugs can increase the risk of having a GI bleed?

A

NSAIDs without gastroprotection (peptic ulcers –> bleeding)
Prednisolone (upper GI bleed)
Alcohol excess

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19
Q

What receptor does metoclopramide act on?

A

D2 receptor antagonist

also a 5HT3 receptor antagonist/5HT4 receptor agonist

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20
Q

What is the main use of metoclopramide?

A

Anti-nausea drug

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21
Q

What are other causes of metoclopramide?

A

GORD
Prokinetic action useful in gastroparesis in diabetic neuropathy
Migraine (migraine –> gastroparesis which slows absorption of analgesics)

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22
Q

What adverse effects are associated with metoclopramide?

A

EPS: oculogyric crisis
Hyperprolactinaemia
Tardive dyskinesia
Parkinsonism

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23
Q

In which condition is metoclopramide CI?

A

Bowel obstruction

PD

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24
Q

Which group of patients are most at risk of developing extrapyramidal side effects from use of metoclopramide?

A

Children, young adults

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25
Q

What is the mechanism of action of metoclopramide in combating nausea?

A

Antagonism of D2 receptor in CTZ

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26
Q

What is the mechanism of action of ondansteron?

A

Antagonism of 5HT3 serotonin receptor

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27
Q

What is the most common acute abdominal condition requiring surgery?

A

Acute appendicitis

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28
Q

Describe the pain of acute appendicitis

A

Peri-umbilical –> RIF (migration of pain strong indicator of appendicitis)

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29
Q

What causes the peri-umbilical pain in acute appendicitis?

A

Visceral stretching of appendix lumen

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30
Q

What causes the RIF pain in acute appendicitis?

A

Localised parietal peritoneal inflammation

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31
Q

What may make the pain worse in acute appendicitis?

A

Cough, going over speed bumps

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32
Q

What are the clinical features of acute appendicitis?

A 
Pain
Vomiting (usually not persistent)
Mild pyrexia 
Anorexia 
Diarrhoea rare
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33
Q

When might patients with acute appendicitis get generalised peritonitis?

A

If perforation has occurred/local peritonism

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34
Q

What sign may be seen in acute appendicitis?

A

Rovsing’s sign

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35
Q

What is Rovsing’s sign?

A

Palpation in LIF causes pain in RIF

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36
Q

What things justify an appendiectomy?

A

Typical raised inflammatory markers, with compatible hx and ex

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37
Q

What is the most common blood test finding found in appendicitis?

A

Neutrophil predominant leucocytosis

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38
Q

Why might you want to do urine analysis in a person presenting with suspected appendicitis?

A

Rule out pregnancy in women, renal colic and UTI

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39
Q

What urine analysis result may you find in someone with appendicitis?

A

Mild leucocytosis

NO nitrates

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40
Q

What US finding should raised your suspicion of acute appendicitis?

A

Free fluid

nb not always able to see appendix on USS

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41
Q

What are the two types of appendiectomy?

A

Laparoscopic (preferred)

Open

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42
Q

What should be given pre-operatively in an appendiectomy to reduce risk of wound infection?

A

IV prophylactic antibiotics

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43
Q

What does a perforated appendix often need?

A

Copious abdominal lavage

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44
Q

What is McBurneys point?

A

Site of maximum pain in appendicitis

It is one third of the distance from the ASIS to the umbilicus

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45
Q

What is the triad of symptoms seen in Plummer-Vinson syndrome?

A

Dysphagia (secondary to oesophageal webs)
Glossitis
Iron deficiency anaemia

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46
Q

What is the treatment of Plummer-Vinson syndrome?

A

Iron supplementation and dilation of webs

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47
Q

What is Mallory-weiss syndrome?

A

Severe vomiting –> painful mucosal lacerations in the gastro-oesphageal junction –> haematemesis

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48
Q

Who is Mallory-weiss syndrome most common in?

A

Alcoholics

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49
Q

What is Boerhaave sydnrome?

A

Severe vomiting –> oesophageal rupture

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50
Q

What is Gilbert’s syndrome?

A

Autosomal recessive condition of defective bilirubin conjugation due to deficiency of UDP glucuronosyltrasnferase

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51
Q

What kind of hyperbilirubinaemia do you get in Gilbert’s syndrome?

A

Unconjugated

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52
Q

What is the main feature of Gilbert’s syndrome?

A

Jaundice during periods of intercurrent illness, exercise or fasting

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53
Q

How is Gilbert’s syndrome investigated?

A

See rise in bilirubin after prolonged fasting/IV nicotonic acid

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54
Q

How is Gilbert’s syndrome treated?

A

No treatment req.

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55
Q

What is the most common type of oesophageal cancer?

A

Adenocarcinoma

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56
Q

Patients with a history of what are more likely to get adenocarcinoma of the oesophagus?

A

GORD/Barrett’s

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57
Q

Where are adenocarcinomas of the oesophagus most commonly found?

A

GO junction

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58
Q

Where are SSCs of the oesophagus most commonly found?

A

Middle third of oesophagus

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59
Q

What are RFs for oesophageal cancer?

A 
Smoking
Alcohol
GORD
Barrett's oesophagus
Achalasia
Plummer-Vinson syndrome
SSC linked to diets rich in nitrosamines
Rare: coeliac, scleroderma
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60
Q

What are the clinical features of oesophageal cancer?

A

Dysphagia
Anorexia
Wt loss
Vomiting

Others: odynophagia, hoarseness, melaena, cough

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61
Q

What is the most common presenting symptom of oesophageal cancer?

A

Dysphagia

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62
Q

What is the first line test for suspected oesophageal cancer?

A

Upper GI Endoscopy

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63
Q

How is oesophageal cancer staged?

A

CT chest, abdo, pelvis
If overt mets –> further imaging unnecessary
If no mets –> local stage assessed by endoscopic USS to assess for peritoneal disease
PET CT performed if laparoscopy negative

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64
Q

How is oesophageal cancer managed?

A

Best if operable -resection

Adjuvant chemo

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65
Q

What is the biggest risk with resection for oesophageal cancer?

A

Anastomotic leak

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66
Q

How does the dysphagia from oesophageal cancer tend to present?

A

Progressive dysphagia - first solids then liquids (suggests growing obstruction)

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67
Q

How does achalasia tend to present?

A

Inability to swallow liquids and solids from onset

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68
Q

How to PPIs work?

A

Irreversibly block H+/K+ ATPase of the gastric parietal cells

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69
Q

Give 2 examples of PPIs

A

Omeprazole

Lansoprazole

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70
Q

What adverse effects are associated with PPIs?

A

Hyponatraemia, hypomagnasaemia (–> muscle weakness)
Osteoporosis + inc. risk of fractures
Microscopic colitis
Increased risk of c. diff infectiosn

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71
Q

What is niacin AKA?

A

Vitamin B3

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72
Q

Is niacin water or fat soluble?

A

Water soluble

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73
Q

What is niacin a precursor to?

A

NAD+ and NADP+

It therefore plays an essential metabolic role in cells

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74
Q

What two conditions can lead to niacin deficiency?

A

Hartnup disease: hereditary disorder which reduces absorption of tryptophan

Carcinoid syndrome: increased tryptophan metabolism into serotonin

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75
Q

What is niacin deficiency called?

A

Pellagra

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76
Q

What are the triad of symptoms in pellagra?

A

Dermatitis
Dementia
Diarrhoea

Can lead to Death

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77
Q

What kind of bacteria is c. diff?

A

Gram +ve rod

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78
Q

What condition does c. diff cause?

A

Pseudomembranous colitis

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79
Q

How does c. diff cause pseudomembranous colitis?

A

By releasing an endotoxin

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80
Q

What drugs are associated with c. diff infections?

A

Antibiotics - the c’s: cephalosporins, clindamycin etc.

PPIs

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81
Q

What are the clinical features of a c. diff infection?

A

Diarrhoea
Ab pain
Raised WCC

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82
Q

If you get a really severe c. diff infection what can result?

A

Toxic megacolon

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83
Q

How do you diagnose a c. diff infection?

A

Detecting c. diff toxin in the stool

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84
Q

Why can’t you use c. diff antigen for diagnosis of a c. diff infection?

A

Antigen positively only indicates exposure to bacteria rather than infection

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85
Q

What is the pathophysiology of a c. diff infection?

A

Normal gut flora is suppressed, e.g. due to broad spectrum antibiotics

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86
Q

What is the first line management of c. diff infection?

A

Oral metronidazole 10-14d

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87
Q

If you have a severe c. diff infection or do not respond to metronidazole what antibiotic should be used?

A

Oral vancomycin

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88
Q

What is the 3rd line antibiotic for c. diff infections?

A

Fidaxomicin

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89
Q

How should life-threatening c. diff infections be treated?

A

Oral vancomycin + IV metronidazole

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90
Q

What is a pharyngeal pouch?

A

Posteromedial diverticulum through Killian’s dehiscence

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91
Q

What is Hillian’s dehiscence?

A

Triangular area in the wall of the pharynx between the thyropharyngeus and cricopharyngeus muscles

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92
Q

In which gender is a pharyngeal pouch more common?

A

Men

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93
Q

In which age group is a pharyngeal pouch more common in?

A

Elderly patients

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94
Q

What are the features of a pharyngeal pouch?

A 
Dysphagia
Regurgitation 
Aspiration 
Neck swelling which gurgles on palpation 
Halitosis
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95
Q

How is pharyngeal pouch managed?

A

With surgery

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96
Q

What kind of cancers do carcinoid syndrome tend to occur with?

A 
Liver mets (which release serotonin into systemic ciruclation)
Lung carcinoid (as mediators are not cleared by the liver)
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97
Q

What are the features of carcinoid syndrome?

A 
Flushing
Diarrhoea
Bronchospasm
Hypotension
Right heart valvular stenosis
Other molecules, e.g. ACTH and GHRH can be secreted leading to cushings for e.g.
Pellagra
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98
Q

Why can pellagra develop in carcinoid syndrome?

A

Dietary trytophan is diverted to serotonin by the tumour

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99
Q

What is usually the first symptom of carcinoid syndrome?

A

Flushing

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100
Q

What investigations should be done for suspected carcinoid syndrome?

A

Urinary 5-HIAA

Plasma chromogranin A y

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101
Q

How is carcinoid syndrome managed?

A

Somatostatin analogues, e.g. octreotide

Diarrhoea - cyproheptadine

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102
Q

What molecules can be released by carcinoid tumours?

A

Vasoactive amines - serotonin, noradrenaline, dopamine
Peptides - e.g. bradykinin
Prostaglandins

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103
Q

Why can you only get GI carcinoid syndrome with liver mets?

A

These vasoactive substances produced are inactived by the liver

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104
Q

What is the aetiology of autoimmune hepatitis?

A

Unknown

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105
Q

Who commonly gets autoimmune hepatitis?

A

Young females

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106
Q

What things are associated with autoimmune hepatitis?

A

Other autoimmune diseases
Hypergammaglobulinaemia
HLA B8, DR3

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107
Q

How many types of autoimmune hepatitis are there?

A

3

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108
Q

What are the types of autoimmune hepatitis?

A

1
2
3

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109
Q

Who does type 1 autoimmune hepatitis affect?

A

Adults + children

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110
Q

What antibodies are present in type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

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111
Q

Who does type 2 autoimmune hepatitis affect?

A

Only children

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112
Q

What antibodies are present in type 2 autoimmune hepatitis?

A

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

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113
Q

What antigen is present in type 3 autoimmune hepatitis?

A

Soluble liver-kidney antigen

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114
Q

Who does type 3 autoimmune hepatitis affect?

A

Adults in middle age

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115
Q

What are features of autoimmune hepatitis?

A

Signs of chronic liver disease
Acute hepatitis: fever, jaundice etc. (25% present in this way)
Amenorrhoea is common

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116
Q

What might you see in the liver biopsy of someone with autoimmune hepatitis?

A

Inflammation extending beyond limiting plate ‘piecemeal necrosis’ bridging necrosis

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117
Q

How is autoimmune hepatitis managed?

A

Steroids, immunosupressants, e.g. azathioprine

Liver Tx

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118
Q

What liver markers are most likely to be raised in autoimmune hepatitis?

A

ALT/AST

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119
Q

What are common symptoms of viral hepatitis?

A

N+V, anorexia
Myalgia
Lethargy
RUQ pain

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120
Q

What are clues in a hx that someone may have viral hepatitis?

A

RFs e.g. IVDA, foreign travel

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121
Q

What is congestive hepatomegaly commonly a consequence of?

A

Congestive heart failure

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122
Q

What can occur in severe cases of congestive hepatomegaly?

A

Cirrhosis

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123
Q

How does biliary colic tend to present?

A

RUQ pain, intermittent usually begins abruptly and subsides gradually
Nausea common

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124
Q

When do attacks of pain in biliary colic typically happen?

A

After eating

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125
Q

What patients are known to typically get biliary colic?

A

Female, fat, fair, forties

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126
Q

What causes the pain in biliary colic?

A

A gallstone temporarily blocking the bile duct

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127
Q

What is ascending cholangitis?

A

Infection of the bile ducts commonly secondary to gallstones

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128
Q

What is the triad of symptoms seen in ascending cholangitis?

A

Fever (+rigors)
RUQ pain
Juandice

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129
Q

What is gallstone ileus?

A

Small bowel obstruction due to impacted gallstone

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130
Q

What causes gallstone ileus?

A

Fistula develops between a gangrenous gallbladder + duodenum

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131
Q

What are common symptoms seen in gallstone ileus?

A

Ab pain, distension, vomiting

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132
Q

How does cholangiocarcinoma tend to present?

A

Persistent biliary colic, anorexia, jaundice, wt loss
Palpable mass in RUQ
Sister mary joseph nodes
Virchow node

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133
Q

What is Courvoisier sign?

A

Palpable mass in RUQ

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134
Q

What are sister mary joseph nodes?

A

Periumbilical lymphadenopathy

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135
Q

What is a virchow node?

A

Left supraclavicular adenopathy

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136
Q

What tends to be the cause of acute pancreatitis?

A

Alcohol, gallstones

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137
Q

How does acute pancreatitis tend to present?

A

Severe epigastric pain

Vomiting

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138
Q

What might you see on Ex in acute pancreatitis?

A

Tenderness, ileus + low grade fever

Periumbilical discolouration, flank discolouration (rare)

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139
Q

What is Cullen’s sign?

A

Periumbilical discolouration

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140
Q

What is Grey-Turner’s sign?

A

Flank discolouration

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141
Q

What is the ‘classical presentation’ of pancreatic cancer?

A

Painless jaundice

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142
Q

What is another v. common symptom of pancreatic cancer?

A

Pain

NB anorexia, wt loss are common too

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143
Q

What symptoms are associated with an amboeic liver abscess?

A

Malaise, anorexia, wt loss
Mild RUQ pain

Jaundice rare

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144
Q

How is Wilson’s disease inherted?

A

AR

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145
Q

What is Wilson’s disease?

A

Condition characterised by excessive copper deposition in tissues

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146
Q

Why is there increased copper in those with wilson’s disease?

A

Metabolic abnormalities –> increased copper absorption from small intestine, decreased hepatic copper excretion

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147
Q

A mutation in what gene on what chromosome leads to wilson’s disease?

A

ATP7B gene on chromosome 13

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148
Q

When is the onset of symptoms in wilson’s disease usually?

A

10-25Y

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149
Q

How do children tend to present with wilson’s disease?

A

Liver disease

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150
Q

How do young adults tend to present with wilson’s disease?

A

Neurological disease

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151
Q

Where is copper especially deposited in wilson’s disease?

A

Brain
Liver
Cornea

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152
Q

Deposition of copper in the liver in wilson’s disease leads to what?

A

Hepatitis

Cirrhosis

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153
Q

Deposition of copper in the brain in wilson’s disease leads to what?

A

Basal ganglia degeneration
Speech, behavioural, psychiatric problems
Asterixis, chorea, dementia, parkinsonism

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154
Q

What can you often see in the cornea of those with wilson’s disease?

A

Kayser-Fleischer rings (due to deposition of copper in cornea)

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155
Q

What are other features (not liver, neuro, cornea) of wilson’s disease?

A

Renal tubular acidosis (esp. Fanconi syndrome)
Haemolysis
Blue nails

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156
Q

How do you diagnose Wilson’s disease?

A

Reduced serum caeruloplasmin
Reduced serum copper
Inc. 24h urinary copper excretion

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157
Q

Why does copper deposition in tissues lead to damage to the tissues?

A

Copper reacts with hydrogen peroxide to produce free radicals which can damage the tissues

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158
Q

How is wilson’s disease managed?

A

Penicillamine

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159
Q

How does penicillamine work for Wilson’s disease?

A

Chelates copper

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160
Q

What is an alternative treatment option for wilson’s disease?

A

Trientine hydrochloride

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161
Q

Define refeeding syndrome

A

Metabolic abnormalities which occur on feeding a person following a period of starvation

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162
Q

When can refeeding syndrome occur?

A

After an extended period of catabolism ends abruptly switching to carb metabolism

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163
Q

What are the metabolic consequences of refeeding syndrome?

A

Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

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164
Q

What can hypomagnesaemia predispose to?

A

Torsades de pointes

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165
Q

What can the metabolic abnormalities in refeeding syndrome lead to?

A

Organ failure

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166
Q

Patients are considered at high risk of refeeding syndrome if they have 1+ of the following:

A

BMI <16
Unintentional wt loss >15% over 3-6m
Little nutritional intake >10d
Hypokalaemia, hypophosphataemia, or hypomagnesaemia prior to feeding

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167
Q

Patients are considered at high risk of refeeding syndrome if they have 2+ of the following:

A

BMI <18.5
Unintentional wt loss >10% over 3-6m
Little nutritional intake >5d
Hx: alcohol abuse, drug therapy incl. insulin, chemotherapy, diuretics, antacids

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168
Q

How do you avoid refeeding syndrome?

A

If a patient has not eaten for >5 days aim to re-feed at no more than 50% of requirements for the first 2 days

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169
Q

Define diarrhoea

A

> 3 loose/watery stools per day

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170
Q

Define acute diarrhoea

A

<14 days

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171
Q

Define chronic diarrhoea

A

> 14 days

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172
Q

What symptoms are classical of diverticulitis?

A

LLQ pain, diarrhoea, fever

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173
Q

What would be a typical history of a patient with constipation causing overflow diarrhoea?

A

Hx of alternating diarrhoea + constipation

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174
Q

What are the most common features of IBS?

A

Abdominal pain
Bloating
Change in bowel habit

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175
Q

What are the two types of IBS?

A

Constipation predominant

Diarrhoea predominant

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176
Q

What additional features may be seen in IBS?

A

Lethargy
Nausea
Backache
Bladder symptoms

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177
Q

What are the clinical features of UC?

A 
Bloody diarrhoea
Crampy abdominal pain 
Wet loss
Faecal urgency 
Tenesmus
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178
Q

What are the clinical features of CD?

A 
Cramp ab pain + diarrhoea
Malabsorption, wt loss, lethargy
Mouth ulcers
Perianal disease (skin tags, ulcers)
Intestinal obstruction
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179
Q

What symptoms can you get with colorectal cancer?

A 
Depends on site of lesion 
Diarrhoea
Rectal bleeding
Anaemia
Constitutional symptoms, e.g. wt loss, anorexia
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180
Q

What are clinical features of coeliac disease in children?

A

FTT
Diarrhoea
Abdominal distension

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181
Q

What are clinical features of coeliac disease in adults?

A

Lethargy
Anaemia
Diarrhoea
Wt loss

Other autoimmune dx may be present

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182
Q

What conditions may be associated with diarrhoea?

A

Thyrotoxicosis
Laxative abuse
Appendicitis
Radiation enteritis

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183
Q

What is diverticulosis?

A

Multiple out pouchings of the bowel

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184
Q

Where is the most common places to get diverticulae in diverticulosis?

A

Sigmoid colon

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185
Q

What is the difference between diverticulosis and diverticular disease?

A

Diverticulosis = diverticula present

Diverticular disease = symptomatic disease

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186
Q

What are risk factors for diverticulosis?

A

Increasing age

Diet low in fibre

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187
Q

What is the two ways in which diverticulosis can present?

A

Painful diverticular disease

Diverticulitis

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188
Q

How does painful diverticular disease present?

A

Altered bowel habit, colicky left sided ab pain

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189
Q

What is the recommended management of painful diverticular disease?

A

Diet high in fibre to minimise symptoms

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190
Q

What is diverticulitis?

A

A diverticula becomes infected

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191
Q

What is the classical presentation of diverticulitis?

A

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

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192
Q

How are mild attacks of diverticulitis managed?

A

Oral antibiotics

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193
Q

How are more severe episodes of diverticulitis managed?

A

In hospital

Nil by mouth, IV fluids, IV antibiotics

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194
Q

What IV antibiotics are given for more severe episodes of diverticulitis?

A

Cephalosporin + metronidazole

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195
Q

What are complications of diverticulitis?

A

Abscess formation
Perionitis
Obstruction
Perforation

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196
Q

Where is the most common place to get diseased bowel in CD?

A

Terminal ileum

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197
Q

What inflammatory marker correlates well with disease activity in CD?

A

CRP

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198
Q

What is the investigation of choice in CD?

A

Colonscopy

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199
Q

What features may you see during colonscopy in CD?

A

Deep ulcers

Skip lesions

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200
Q

What can you see on histology in CD?

A

Transmural inflammation
Goblet cells
Granulomas

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201
Q

What sign might you see on small bowel enema in CD?

A

Kantor string sign (from strictures in terminal ileum so it appears narrow)

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202
Q

What signs may you see on barium enema in someone with CD?

A 
Strictures
Proximal bowel dilatation
Rose thorn ulcers
Fistulae
Crypt abscesses
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203
Q

In what patients is spontaneous bacterial peritonitis seen in?

A

Usually those with ascites secondary to liver cirrhosis

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204
Q

What are the clinical features of spontaneous bacterial peritonitis?

A

Ascites
Abdominal pain
Fever

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205
Q

What is a common finding with spontaneous bacterial peritonitis on paracentesis?

A

Neutrophil count >150cells/ul

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206
Q

What is the most common organism found in the ascitic fluid in spontaneous bacterial peritonitis?

A

E. coli

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207
Q

How is spontaneous bacterial peritonitis managed?

A

IV cefotaxime

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208
Q

What patients with ascites should be given prophylaxis for spontaneous bacterial peritonitis?

A

Those who:
Have had a prev. SBP
With fluid protien <15g/l + either Child Pugh score 9+ or hepatorenal syndrome

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209
Q

What antibiotic is given for prophylaxis in spontaneous bacterial peritonitis?

A

Oral ciprofloxacin or norfloxacin

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210
Q

What medications should be withheld in c. diff infections (besides the offending antibiotic)?

A

Antimotility + antiperistalsis medications, e.g. opioids

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211
Q

Why should antimotility/antiperistalsis medications be withheld in c. diff infections?

A

By slowing clearance of c. diff infection they predispose to toxic megacolon

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212
Q

What is Barrett’s oesophagus?

A

Metaplasia of the lower oesophageal mucosa (with normal squamous epithelium being replaced with columnar)

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213
Q

What does Barrett’s oesophagus carry an increased risk of?

A

Oesophageal adenocarcinoma

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214
Q

What is the screening programme for Barrett’s oesophagus?

A

There is not one

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215
Q

What are the two subtypes of Barrett’s oesophagus?

A

Short <3cm

Long >3cm

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216
Q

What does the length of the affected segment in Barrett’s oesophagus correlate with?

A

The chances of identifying metaplasia

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217
Q

What is the strongest RF for developing Barrett’s oesophagus?

A

GORD

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218
Q

What are other RFs for Barrett’s oesophagus?

A

Male gender
Smoking
Central obesity

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219
Q

Is alcohol consumption a RF for Barrett’s oesophagus?

A

It is not an independent RF, although it is associated with oesophageal cancer and GORD

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220
Q

What are the clinical features of Barrett’s oesophagus?

A

Barrett’s oesophagus itself is asymptomatic but clearly pt will have sx of GORD

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221
Q

How is Barrett’s oesophagus investigated?

A

Endoscopic surveillance + biopsies

pH and manometry

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222
Q

How is Barrett’s oesophagus managed?

A

PPIs

Endoscopic surveillance to monitor if metaplasia is occurring

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223
Q

For patients with metaplasia (but no dysplasia) how often is endoscopic surveillance recommended?

A

Every 3-5y

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224
Q

Once in Barrett’s oesophagus the metaplasia –> dysplasia what treatment is offered?

A

Endoscopic mucosal resection

Radiofrequency ablation

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225
Q

What is melanosis coli?

A

Disorder of pigmentation of the bowel

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226
Q

What do you see on histology in melanosis coli?

A

Pigment laden macrophages

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227
Q

What is melanosis coli associated with?

A

Laxative abuse esp. anthraquinone compounds e.g. senna

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228
Q

Ischaemia to the lower GI tract can lead to a variety of conditions. What re the 3 main conditions it can cause?

A

Acute mesenteric ischaemia
Chronic mesenteric ischaemia
Ischaemic colitis

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229
Q

What are common predisposing factors for ischaemia to the lower GI tract?

A 
Increased age
AF (esp. mesenteric ishcaemia)
Emboli: endocarditis, malignancy
CV RFs: smoking, HTN, DM
Cocaine (ischaemic colitis sometimes seen in young people after cocaine use)
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230
Q

What are some common features that can be seen following ischaemia to the lower GIT?

A 
Ab pain 
Rectal bleeding
Diarrhoea
Fever
Elevated WCC and lactic acidosis
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231
Q

What is the investigation of choice in ischaemia to the lower GIT to reach a diagnosis?

A

CT

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232
Q

What tends to cause acute mesenteric ischaemia?

A

Embolism resulting in occlusion of an artery that supplies the small bowel, e.g. SMA

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233
Q

Patients with acute mesenteric ischaemia classically have what condition?

A

AF

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234
Q

What is typical of the abdominal pain experienced in acute mesenteric ischaemia?

A

It is very severe, of sudden onset and out of keeping with physical signs

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235
Q

How is acute mesenteric ischaemia managed?

A

Urgent surgery

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236
Q

What is the prognosis of acute mesenteric ischaemia?

A

Very poor

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237
Q

What is chronic mesenteric ischaemia?

A

Intestinal angina

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238
Q

What is the pain in chronic mesenteric ischaemia like?

A

Colicky, intermittent

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239
Q

What is ischaemic colitis?

A

Acute transient compromise in blood flow to the large bowel which may lead to inflammation, ulceration and haemorrhage

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240
Q

Where are the most common places for ischaemic colitis?

A

Watershed areas, e.g. splenic flexure (where borders of territory are supplied by the IMA and SMA)

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241
Q

What might you see on AXR in ischaemic colitis?

A

Thumbprinting due to mucosal oedema/haemorrhage

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242
Q

How is ischaemic colitis managed?

A

Usually supportive

Surgery if conservative measures fail, or generalised peritonitis, perforation or ongoing haemorrhage

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243
Q

What pattern do you see on ABG in ischaemia of the lower GIT?

A

LACTIC ACIDOSIS

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244
Q

Where does the inflammation in UC always start?

A

Rectum

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245
Q

Where is UC said never to spread past?

A

Ileocaecal valve

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246
Q

Is UC continuous or are there skip lesions?

A

Disease usually continuous

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247
Q

What is the peak age for developing UC?

A

15-25y

second peak at 55-65y

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248
Q

What symptoms do you tend to get in UC?

A 
Bloody diarrhoea
Urgency
Tenesmus
Ab pain (esp LLQ)
Extra-intestinal features
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249
Q

What are extra-intestinal features of IBD?

A 
Arthritis - CD + UC
Episcleritis - UC
Erythema nosodum 
Osteoporosis
Uveitis - UC
PSC - UC
Clubbing
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250
Q

What layers of the bowel are affected by UC?

A

Mucosa only

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251
Q

What does UC look like on endoscopy?

A

Pseudopolyps
Red, raw mucosa, contact bleeding
Wide spread ulceration
Neutrophils migrate through walls of glands to form crypt abscesses
Depeleted goblet cells + mucin from gland epihelium

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252
Q

What can you see on barium enema in UC?

A

Loss of haustrations
Superficial ulceration, pseudopoyps
Long standing disease - drainpipe colon (colon narrow + short)

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253
Q

Are crypt abscesses seen more commonly in UC or CD?

A

CD

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254
Q

What is coeliac disease?

A

Autoimmune condition caused by sensitivity to protein gluten

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255
Q

What is the prevalence of coeliac disease?

A

1%

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256
Q

Why do you get malabsorption in coeliac disease?

A

Repeated exposure to gluten leads to vilous atrophy

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257
Q

What conditions are associated with coeliac disease?

A

Dermatitis herpetiformis

Autoimmune dx e.g. T1DM, autoimmune hepatitis

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258
Q

What is dermatitis herpetiformis?

A

A vesicular, pruritic skin eruption

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259
Q

What HLA allele is coeliac disease associated with?

A

HLA-DQ2 and HLA-DQ8

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260
Q

Patients with what conditions should be screened for coeliac disease?

A 
Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
T1DM
First degree relatives with coeliac disease
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261
Q

What symptoms/signs may lead to you test for coeliac disease?

A

Chronic/intermittent diarrhoea
FFT/faltering growth in kids
Persistent/unexplained GI symptoms (incl. NV)
Prolonged fatigue
Recurrent ab pain, cramping, distension
Sudden/unexplained wt loss
Unexplained iron deficiency anaemia/other anaemia

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262
Q

What are complications of coeliac disease?

A 
Anaemia (Fe, folate, B12)
Hyposplenism
Osteoporosis, osteomalacia
Lactose intolerance
Subfertility
Rare: oesophageal cancer, other malignancies
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263
Q

What malignancy is associated with coeliac disease?

A

Enteropathy-associated T cell lymphoma of small intestine

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264
Q

What is primary sclerosing cholangitis?

A

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

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265
Q

Which condition has the strongest association with PSC?

A

UC

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266
Q

What other conditions are associated with PSC?

A

CD

HIV

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267
Q

What are the clinical features of PSC?

A

Cholestasis - jaundice, pruritus
RUQ pain
Fatigue

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268
Q

What investigations are diagnostic in PSC?

A

ERCP or MRCP

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269
Q

What do you see on ERCP/MRCP in PSC?

A

Multiple biliary strictures giving a beaded appearance

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270
Q

What does ERCP stand for?

A

Endoscopic retrograde cholangiopancreatography

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271
Q

What does MRCP stand for?

A

Magnetic resonance cholangiopancreatography

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272
Q

There is a limited role for liver biopsy in PSC but what might you see if you do it?

A

Fibrous obliterative cholangitis (‘onion skin’)

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273
Q

What are complications of PSC?

A 
Acute bacterial cholangitis
Cholangiocarcinoma
Increased risk of colorectal cancer
Cirrhosis + liver failure
Deficiencies in fat soluble vitamins
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274
Q

What antibody may be +ve in PSC?

A

pANCA

ANA and and aCL can also be up

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275
Q

What is the function of the bile ducts?

A

Taking the bile from where its made in the liver into the small intestine

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276
Q

What is meant by a stricture?

A

Narrowing

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277
Q

What is meant by fibrosis?

A

Hardening

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278
Q

What does the stricturing + fibrosis of the bile ducts in PSC lead to?

A

Obstruction of bile –> back pressure of bile –> liver –> inflammation (hepatitis) –> fibrosis of liver –> cirrhosis

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279
Q

What might you see on the LFTs of someone with PSC?

A

Cholestatic picture - high ALP, bilirubin and GGT

Then other ALT and AST will become more derranged as disease progresses to cirrhosis

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280
Q

What is the only definitive management of PSC?

A

Liver transplant

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281
Q

What is the management of PSC if liver transplant cannot be done?

A

ERCP - dilate and stent strictures
Ursodeoxycholic acid
Colestryamine - bile acid sequestrate (reduces pruritus)

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282
Q

What does ERCP involve?

A

Inserting camera into duodenum, through sphincter of Oddi, ampulla of vater
Can dilate and stent stricture if find any

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283
Q

What is Budd-Chiari also known as?

A

Hepatic vein thrombosis

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284
Q

Where is Budd-Chiari usually seen in the context of?

A

Underlying haematological disease or other procoagulant conditions

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285
Q

What are causes of Budd-Chiari syndrome?

A

Polycythaemia rubra vera
Thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C and S deficiencies
Pregnancy
COCP

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286
Q

What is the classic triad of clinical features seen in Budd-Chiari syndrome?

A

Ab pain - sudden, severe
Ascites
Tender hepatomegaly

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287
Q

How is Budd-Chiari syndrome diagnosed?

A

USS with doppler flow studies

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288
Q

Does Budd-Chiari syndrome cause portal hypertension?

A

Yes

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289
Q

What SAAG indicates portal hypertension is the cause of an ascites?

A

> 11g/L

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290
Q

What are the three types of colon cancer?

A

Sporadic 95%
HNPCC
FAP

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291
Q

What does HNPCC stand for?

A

Hereditary non-polyposis colorectal cancer

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292
Q

What does FAP stand for?

A

Familial adenomatous polyposis

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293
Q

What is thought to cause sporadic colon cancer?

A

A series of genetic mutations
E.g. loss of APC gene, then activation of a K-ras oncogene or deletion of p53/DCC tumour supressor genes to lead to an invasive carcinoma

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294
Q

What is the mode of inheritance of HNPCC?

A

AD

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295
Q

Where is the commonest place to develop colon cancer in HNPCC?

A

Proximal colon

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296
Q

Do the colon cancers in HNPCC tend to be aggressive or slow growing?

A

Aggressive

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297
Q

What % of people with HNPCC will develop a colon cancer?

A

90%

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298
Q

Currently ___ mutations causing HNPCC have been identified, which can affect genes involved in ________ leading to _______.

A

7

Genes involved in DNA mismatch repair leading to microsatellite instability

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299
Q

What are the two most common genes involved in HNPCC?

A

MSH2 and MLH1

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300
Q

What is the second most common cancer after colon cancer for people with HNPCC to get?

A

Endometrial cancer

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301
Q

What criteria is used to aid the diagnosis of HNPCC?

A

Amsterdam critera

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302
Q

What is the amsterdam criteria?

A

At least 3 family members with colon cancer
Cases span at least 2 generations
At least 1 case diagnosed before age 50

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303
Q

What is FAP?

A

AD condition which leads to the formation of hundreds of polyps before age 30-40

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304
Q

Do patients with FAP tend to go on to develop carcinoma?

A

Yes

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305
Q

What is FAP due to?

A

Mutation in tumour supressor gene called adenomatous polyposis coli gene located on chromosome 5

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306
Q

How can FAP be diagnosed?

A

Via genetic testing by analysis DNA from a pts WBCs

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307
Q

What tends to be the management for FAP?

A

Total colectomy with ileo-anal pouch formation

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308
Q

A variant of FAP is Gardener’s syndrome which also features what?

A

Osteomas of the skull and mandible
Retinal pigmentation
Thyroid carcinoma
Epidermioid cysts on the skin

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309
Q

What are patients with FAP also at risk of?

A

Duodenal tumours

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310
Q

What is the most common inheritable form of colorectal cancer?

A

HNPCC

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311
Q

Define malnutrition

A

BMI <18.5 OR
Unintentional wt loss >10% within last 3-6m OR
BMI <20 and unintentional wt loss >5% in last 3-6m

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312
Q

What is the best screening tool for malnutrition?

A

MUST

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313
Q

When should MUST screening be used?

A

On admission to care/nursing homes and hospital or if there is concern

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314
Q

If a pt is high risk of malnutrition what i the management?

A

Dietician input
Food-first approach with clear instructions rather than just prescribing for e.g. ensure
Oral nutritional supplements should be taken between meals rather than instead of meals

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315
Q

What is achalasia?

A

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

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316
Q

At what age does achalasia tend to occur?

A

Middle age

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317
Q

What are the clinical features of achalasia?

A

Dysphagia of SOLIDS and LIQUIDS from the start
Variation in severity of symptoms
Heartburn
Regurg (may lead to aspiration pneumonias)

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318
Q

How is achalasia investigated?

A

Oesophageal manometry

Barium swallow

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319
Q

What do you see on oesophageal manometry in achalasia?

A

Excessive LOS tone which doesn’t relax on swallowing

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320
Q

What do you see on barium swallow in achalasia?

A

Grossly expanded oesophagus, fluid level , bird’s beak appearance (due to narrowing of LOS)

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321
Q

What are the treatment options for achalasia?

A

Intra-sphincteric injection of botox
Heller cardiomyotomy
Pneumatic (balloon) dilation

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322
Q

Name 3 of the commonest causes of hepatomegaly

A

Cirrhosis
Malignancy
R heart failure

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323
Q

What does a cirrhotic liver feel like?

A

Non-tender, firm liver

Remember later liver decreases in size

324
Q

What does a malignant liver feel like?

A

Hard, irregular liver edge

325
Q

What does hepatomegaly due to R heart failure feel like?

A

Firm, smooth, tender liver edge

Pulstaile

326
Q

What are other causes of hepatomegaly?

A 
Viral hepatitis
Glandular fever
Malaria 
Abscess - pyogenic/amoebic
Hydatid disease
Haematological malignancies
Haemochromatosis
PBC
Sarcoidosis, amyloidosis
327
Q

Why can hepatomegaly due to R heart failure be pulsatile?

A

Due to back up of blood in liver

328
Q

Who tends to be at more risk of pernicious anaemia?

A

Elderly females

329
Q

What is the pathophysiology of pernicious anaemia?

A

Autoimmune disease caused by antibodies to the gastric parietal cells/intrinsic factors

330
Q

Pernicious anaemia is a deficiency in…

A

B12

331
Q

What conditions are associated with pernicious anaemia?

A

Thyroid disease, DM, Addison’s, RA, vitiligo

332
Q

What can pernicious anaemia predispose to?

A

Gastric carcinoma

333
Q

What are the features of pernicious anaemia?

A

Lethargy, weakness
Dyspnoea
Paraesthesia (loss of vibration sense in feet)
Mild jaundice (LEMON TINGE), diarrhoea, sore tongue

334
Q

What are possible signs of pernicious anaemia?

A

Retinal haemorrhages, mild splenomegaly, retrobulbar neuritis

335
Q

How is pernicious anaemia managed?

A

3mnthly injections of B12

Folic acid supplements may also be req.

336
Q

What causes a lemon tinge in pernicious anaemia?

A

Pallor (anaemia) + mild jaundice (due to haemolysis)

337
Q

Over 80% of pancreatic cancers are…

A

Adenocarcinomas

338
Q

Where do pancreatic cancers tend to occur?

A

Head of pancreas

339
Q

What things are associated with pancreatic cancer?

A 
Increased age
Smoking
DM
Chronic pancreatitis
HNPCC
MEN
BRCA2 mutation
340
Q

How does pancreatic cancer classically present?

A

Painless jaundice

341
Q

What is Courvoisier’s law?

A

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

342
Q

How do a majority of patients with pancreatic cancer actually present?

A

Non-specific symptoms, e.g. anorexia, wt loss, epigastric pain

May have loss of exocrine function - steatorrhoea, loss of endocrine function - DM, atypical backpain often seen 
Migratory thrombophlebitis (Trousseau sign)
343
Q

What is the investigation of choice for diagnosing pancreatic cancer?

A

High resolution CT

344
Q

What sign might you see on imaging in pancreatic cancer?

A

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

345
Q

What procedure is performed for resectable pancreatic cancer?

A

Whipple’sresection (pancreaticoduodenectomy) + adjuvant chemo

346
Q

What are side effects of Whipple’s procedure?

A

Dumping syndrome and peptic ulcer disease

347
Q

What procedure can be used for palliation in pancreatic cancer?

A

ERCP with stenting

348
Q

How is UC usually classified?

A

Mild
Moderate
Severe

349
Q

Define mild UC

A

<4 stools/day, only a small amount of blood

350
Q

Define moderate UC

A

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

351
Q

Define severe UC

A

> 6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

352
Q

How do you induce remission in mild-to-moderate UC proctitis?

A

Topical (rectal) aminosalicylate (mesalazine)
No remission in 4w - add oral aminosalicylate
If no remission still - add topical/oral corticosteroid

353
Q

How do you induce remission in someone with mild-to-moderate UC proctosigmoiditis + left sided UC?

A

Topical (rectal) aminosalicylate
No remission in 4w - add high dose oral aminosalicylate OR switch to high dose oral aminosalicylate + topical corticosteroids
No remission still - stop topical treatments and offer oral aminosalicylate + oral corticosteroid

354
Q

How put EXTENSIVE mild-to-moderate UC into remission?

A

Topical (rectal) aminosalicylate + high dose oral aminosalicylate
No remission in 4w - stop topical treatments and offer high dose oral aminosalicylate + oral corticosteroid

355
Q

Should you admit someone with a severe flare UC?

A

Yes

356
Q

What is the first line treatment for severe flare of UC?

A

IV steroids

If steroids CI - IV ciclosporin

357
Q

If you admit someone with a severe flare of UC to hospital and give IV steroids and this does not cause improvement within 72h what should you do?

A

Consider adding IV ciclosporin to IV corticosteroids OR consider surgery

358
Q

How do you maintain remission following a mild to moderate UC flare in someone who had proctitis or proctosigmoiditis?

A

Rectal aminosalicylate alone OR oral + reacl aminosalicylate OR oral aminosalicylate alone

Treatment can be daily or intermittent

359
Q

How do you maintain remission following a mild to moderate UC flare in someone who had left sided or extensive UC?

A

Low dose of oral aminosalicylate

360
Q

What therapy is given to someone who has had a severe relapse of UC or >= 2 exacerbation in the last year?

A

Oral azathioprine or oral mercaptopurine

361
Q

What kinds of drugs are azathioprine and mercaptopurine?

A

Thiopurines

362
Q

What are the most common organisms causing pyogenic liver abscesses in kids?

A

Staph aureus

363
Q

What are the most common organisms causing pyogenic liver abscesses in adults?

A

E. coli

364
Q

What is the management of a pyogenic liver abscess?

A

Drainage + antibiotics

365
Q

What kind of drainage is usually done for pyogenic liver abscesses?

A

Imaged guoded percutaneous

366
Q

What antibiotics are usually given for pyogenic liver abscesses?

A

Amoxicillin + ciprofloxacin + metronidazole

if penicillin allergic: ciprofloxacin + clindamycin

367
Q

At what age is there a peak of gastric cancers?

A

70-80yos

368
Q

What cells might you see in a gastric cancer?

A

Signet ring cells

369
Q

What do signet ring cells look like?

A

Large vacuole of mucin which displaces the nucleus to one side

370
Q

In gastric cancer a higher number of signet cells is associated with what?

A

A worse prognosis

371
Q

What things are associated with gastric cancer?

A 
H. pylori infection 
Blood group A
Gastric adenomatous polyps
Pernicious anaemia
Smoking
Diet - salty, spicy, nitrates
Maybe be negatively associated with duodenal ulcer
372
Q

What are features of gastric cancer?

A

Dyspepsia
NV
Anorexia, wt loss
Dysphagia

373
Q

How do you diagnose gastric cancer?

A

Endoscopy with biopsy

374
Q

How do you stage a gastric cancer?

A

1st line: CT chest, abdo, pelvis
Laparoscopy to identify occult peritoneal disease
PET CT

375
Q

What staging system is used to stage gastric cancer?

A

TNM staging

376
Q

How many types of cancers of the gastro-oesophageal junction are there?

A

3

377
Q

What is type 1 gastro-oesophageal cancer?

A

True oesophageal cancer (may be assoc. with Barrett’s)

378
Q

What is type 2 gastro-oesophageal cancer?

A

Carcinoma of the cardia, arising from cardiac type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction

379
Q

What is type 3 gastro-oesophageal cancer?

A

Subcardial cancers that spread across the junction

380
Q

What are the options for treatment of gastric cancer?

A 
Subtotal/total gastrectomy
Oesophagogastrectomy
Endoscopic submucosal resection 
Lymphadenectomy 
Pre/post-op chemo for most pts
381
Q

What patients may receive a subtotal gastrectomy for their gastric cancer?

A

If they have proximally sited disease greater than 5-10cm from OG junction

382
Q

What patients may receive a total gastrectomy for their gastric cancer?

A

If the tumour is <5cm from OG junction

383
Q

What patients may receive a oesphagogastrectomy for their gastric cancer?

A

Type 2 junctional tumours (extending into oesophagus)

384
Q

What patients may receive endoscopic submucosal resection for their gastric cancer?

A

If they have an early gastric cancer confined to the mucosa

385
Q

What is the cause of hepatic encephalopathy?

A

Liver disease

386
Q

What is the aetiology of hepatic encephalopathy?

A

Excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut

387
Q

How might the presentation of hepatic encephalopathy differ in acute vs chronic liver failure?

A

In chronic may develop subtle symptoms (e.g. MCI) first

388
Q

What are features of hepatic encephalopathy?

A 
Confusion, altered GCS
Asterix
Constructional apraxia
Raised ammonia level 
Triphasic slow waves on EEG
389
Q

What is asterix?

A

Liver flap

Arrythmic negative clonus

390
Q

What is constructional apraxia?

A

Inability/difficult to build, assemble or draw objects

E.g. unable to draw 5 pointed star when asked

391
Q

What are the grades of hepatic encephalopathy?

A

1 - irritability
2 - confusion, inappropriate behaviour
3 - incoherent, restless
4 - coma

392
Q

What factors may precipitate hepatic encephalopathy?

A 
Infection, e.g. SBP
GI bleed
Post transgular intrahepatic portosystemic shunt
Constipation 
Drugs, e.g. sedatives, diuretics
Hypokalaemia
Renal failure
Increased dietary protein
393
Q

How do you manage hepatic encephalopathy?

A

Rx underlying cause

1st line: lactulose + rifaximin for 2ndary prophylaxis of HE

394
Q

How does lactulose work in treating hepatic encephalopathy?

A

Promotes excretion of ammonia and inhibits production of ammonia in the intestine

395
Q

How does rifaximin work in treating hepatic encephalopathy?

A

Antibiotics like rifaximin modulate gut bacteria resulting in decreased ammonia production

396
Q

What advice should be given to patients with crohn’s disease re their lifestyle?

A

Stop smoking

397
Q

How do you induce remission in CD?

A

Glucocorticoids/budesonide
Enteral feeding with an elemental diet can be used in children
2nd line: 5ASA
Azathiopurine/mercaptopurine may be used as add on therapies but not alone
Methorexate can be used instead of azathioprine
Infliximab useful in refractory disease + fistulating CD
Metronidazole often used for isolated peri-anal disease

398
Q

What drugs are used first line in CD to maintain remission?

A

Azathioprine/mercaptopurine

399
Q

What drug are used second line in CD to maintain remission?

A

Methorexate

Consider 5ASA if pt has had prev. surgery

400
Q

Around what % of CD patients will eventually have surgery?

A

80%

401
Q

What is the commonest pattern of CD?

A

Stricturing terminal ileal disease

402
Q

What surgical treatments may be offered to those with CD?

A

Segmental resections

Stricturoplasty

403
Q

CD is notorious for forming fistulae - where might these form?

A

Between rectum + skin (perianal), or small bowel + skin or between loops of bowel

404
Q

What can fistulae in CD result in?

A

Bacterial overgrowth + malabsorption

405
Q

What conditions are patients with CD at more risk of?

A

Small bowel cancer
Colorectal cancer
Osteoporosis

406
Q

What MUST you do before offering azathioprine/mercarptopurine?

A

Assess thiopurine methyltransferase activity

Those with TMPT deficiency may get severe SEs from conventional doses of thiopurines

407
Q

List some foods in which vitamin C is found

A 
Citrus fruits
Tomatoes
Potatoes
Brussel sprouts
Cauliflower
Broccoli
Cabbage
Spinach
408
Q

What is vitamin C deficiency AKA?

A

Scurvy

409
Q

What does scurvy lead to?

A

Impaired collagen synthesis + disordered connective tissue

410
Q

Why does vitamin C deficiency lead to impaired collagen synthesis?

A

Absorbic acid is a cofactor for enzymes used in the production of proline and lysine

411
Q

Who is prone to scurvy?

A

Those with severe malnutrition, drug/alcohol abuse, living in poverty

412
Q

What are signs/symptoms of scurvy?

A

Follicular hyperkeratosis + perifollicular haemorrhage
Ecchymosis, easy bruising
Poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
Oedema
Arthalgia
Impaired wound healing
Generalised symptoms, e.g. weakness, malaise, anorexia, depression

413
Q

Should you always endoscopy someone with new onset dysphasia?

A

Yes - this is a red flag symptom

414
Q

What would be a typical history of someone with oesophageal cancer?

A

Dysphagia + wt loss, anorexia, vomiting whilst eating

PMH Barrett’s, GORD, excessive smoking/alcohol use

415
Q

What would be a typical history of someone with oesophagitis?

A

Hx heartburn

Odynophagia, no wt loss + systemically well

416
Q

What would be a typical history of someone with oesophageal candidiasis?

A

Hx HIV/other RF e.g. steroid inhaler use

417
Q

What would be a typical history of someone with achalasia?

A

Dysphagia of solids + liquids from the start
Heartburn
Regurg of food (may lead to cough/aspiration pneumonia etc.)

418
Q

What are typical symptoms in pharyngeal pouch?

A

Dysphagia, regurg, aspiration, chronic cough

Halitosis

419
Q

What are the features of CREST syndrome?

A 
Calcinosis
Raynauds
Oesophageal dysmotility (+ LOS pressure is decreased)
Scleroderma
Telangiectasia
420
Q

What would be a typical history of myasthenia gravis presenting with dysphagia?

A

Other symptoms like extraocular muscle weakness/ptosis

Dysphagia with liquids + solids

421
Q

What would be a typical history of someone with globus hystericus?

A

Hx anxiety
Sx intermittent + relieved by swallowing
Usually painless

422
Q

What is a good way to image oesophageal motility disorders?

A

Barium swallow

423
Q

What study may be used in the investigation of GORD/achalasia?

A

pH and manometry studies

424
Q

What are neurological causes of dysphagia?

A 
CVA
PD
MS
Brainstem pathology
Myasthenia gravis
425
Q

What is the classical triad of symptoms experienced in intestinal angina?

A

Severe, colicky, post-prandial abdominal pain
Wt loss
Abdominal bruit

426
Q

What is the commonest cause of intestinal angina?

A

Atherosclerotic disease in the arteries supplying the GIT

427
Q

What is the most common cause of HCC (hepatocellular carcinoma) worldwide?

A

Chronic Hep B

428
Q

What is the most common cause of HCC (hepatocellular carcinoma) in Europe?

A

Chronic Hep C

429
Q

What is the main risk factor for HCC?

A

Liver cirrhosis, e.g. secondary to hep B/C, alcohol, haemachromatosis, PBC

430
Q

What are other RFs for HCC?

A 
Alpha-1-antitrypsin deficiency
Hereditary tyrosinosis
Glycogen storage disease
Aflatoxin
COCP, anabolic steroids
Pophyria cutanea tarda
Male
DM, metabolic syndrome
431
Q

Does HCC tend to present early or late?

A

Late

432
Q

What are the features of HCC?

A

Features of liver cirrhosis/failure

May present as a decompensation in pt with chronic liver disease

433
Q

What are features of liver cirrhosis/failure?

A

Jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly

434
Q

What screening is done for high risk groups for HCC?

A

USS +/- AFP

435
Q

What groups are considered at high risk of HCC?

A

Pts with liver cirrhosis secondary to hep B and C/haemachromatosis
Men with liver cirrhosis secondary to alcohol

436
Q

What are management options for HCC?

A 
Early disease - resection
Liver Tx
Radiofrequency ablation
Transarterial chemoembolisation
Sorafenib (multikinase inhibitor)
437
Q

What is AFP more used for in HCC?

A

To monitor for recurrence

438
Q

What are the criteria for a mild flare of UC?

A

<4 stools a day w/wo blood
No systemic disturbance
Normal ESR/CRP

439
Q

What are the criteria for a moderate flare of UC?

A

4-6 stools a day

Minimal systemic disturbance

440
Q

What are the criteria for a severe flare of UC?

A

> 6 bloody stools a day
Systemic disturbance, e.g. fever, tachycardia, abdominal tenderness, distension, reduced bowel sounds, anaemia, hypoalbuminaemia

441
Q

What is the pattern of inheritance of haemochromatosis?

A

AR

442
Q

What is haemachromatosis?

A

Disorder of iron absorption and metabolism leading to iron accumulation

443
Q

Where is the mutation in haemochromatosis?

A

HFE gene on both copies of chromosome 6

444
Q

How should you screen for haemochromatosis in the general population?

A

Transferrin saturation + ferritin (but ferritin usually normal in early stages)

445
Q

How should you screen for haemochromatosis in those with affected family members?

A

Genetic testing for HFE mutation

446
Q

What are the diagnostic tests for haemachromatosis?

A

MOlecular genetic testing for C282Y and H63D mutations

Liver biopsy - Perl’s stain

447
Q

What is the typical iron study profile in a pt with haemochromatosis?

A

Transferrin saturation > 55% in men or > 50% in women
Raised ferritin (e.g. > 500 ug/l) and iron
Low TIBC

448
Q

What is the first line treatment of haemachromatosis?

A

Venesection

449
Q

How should people with haemochromatosis on venesection monitor their treatment?

A

Transferrin sat should be kept below 50%

Serum ferritin conc below 50microg/L

450
Q

What might you see if you X-ray the joints of someone with haemochromatosis?

A

Chrondocalcinosis

451
Q

Is h. pylori gram positive or negative?

A

Negative

452
Q

What is h. pylori principally associated with?

A

Peptic ulcer disease

453
Q

Is h. pylori infection associated with duodenal or gastric ulcers more?

A

Duodenal

454
Q

What other associations does h. pylori have?

A

Gastric cancer
B cell lymphoma of MALT tissue
Atrophic gastritis

455
Q

How do you eradicate h. pylori?

A

PPI + amoxicillin + clarithromycin OR PPI + metronidazole + clarithromycin

456
Q

How is the cause of ascites categorised?

A

SAAG <11g/L or >11g/L

457
Q

What does a SAAG >11g/L indicate in ascites?

A

Portal hypertension

458
Q

What are causes of ascites with a SAAG <11g/L?

A 
Cirrhosis
Alcoholic hepatitis
Cardiac ascites
Mixed ascites
Massive liver mets
Fulminant hepatic failure
Budd-Chiairi syndrome
Portal vein thrombosis
Veno-occlusive disease
Myxoedema
Fatty liver of pregnancy
459
Q

What are causes of ascites with a SAAG >11g/L?

A 
Peritoneal carcinomatosis
Tuberculous peritonitis
Pancreatic ascites
Bowel obstruction 
Biliary ascites
Post-op lymphatic leak 
Serositis in connective tissue diseases
460
Q

How do you manage ascites?

A 
Reduce dietary Na
?Fluid restrict
Aldosterone antagonist, e.g. spirnolactone +/- loop diuretic
?Drainage
Prophylactic antibiotic 
TIPS in some patients
461
Q

What patients with ascites may need to fluid restrict?

A

If the sodium is <125mmol/L

462
Q

What kind of ascites may you need to drain?

A

Tense ascites

463
Q

What ‘cover’ does large volume paracentesis require?

A

Albumin to reduce risk of paracentesis induced circulatory dysfunction

464
Q

What can paracentesis induced circulatory dysfunction cause?

A

Hepatorenal syndrome, dilutional hyponatraemia

There is a high mortality rate

465
Q

Why do you offer patients with ascites prophylactic antibiotics?

A

To reduce risk of spontaneous bacterial peritonitis

466
Q

What does TIPS stand for?

A

Transjugular intrahepatic portosystemic shunt

467
Q

What is alcoholic ketoacidosis?

A

Non-diabetic euglycaemic form of ketoacidosis that occurs in people who drink large volumes of alcohol

468
Q

Why can alcoholics go into ketoacidosis?

A

Often alcoholics will not eat regularly + vomit food –> periods of starvation
Once they become malnourished, after an alcohol binge the body breaks down fat producing ketones

469
Q

What do you see on ABG in a alcoholic ketoacidosis?

A

Elevated anion gap metabolic acidosis

470
Q

What do you see on testing the blood/urine of someone in an alcoholic ketoacidosis?

A

Elevated serum ketones

Normal/low glucose conc.

471
Q

How is alcoholic ketoacidosis managed?

A

Infusion of saline + thiamine

472
Q

Why are patients with alcoholic ketoacidosis given thiamine?

A

To prevent Wernicke’s/Korsakoffs

473
Q

Lists drugs that are toxic to the liver

A 
Paracetamol
Na valproate, phenytoin
MAOIs
Halothane
Anti-TB antibiotics
Statins
Alcohol
Amiodarone 
Methyldopa
Nitrofuratoin
474
Q

What drugs can cause cholestasis (+/- hepatitis)?

A

COCP
Antibiotics - flucloxacillin, co-amoxiclav, erythromycin
Anabolic steroids, testosterones
Phenothiazines: chlorpromazine, prochlorperazine
SUs
Fibrates
Nifedipine

475
Q

What drugs are linked with liver cirrhosis?

A

Methotrexate
Methyldopa
Amiodarone

476
Q

What tests can be used to test for H. pylori infection?

A 
Urea breath test
Rapid urease test (CLO test) 
Serum antibody
Culture of gastric biopsy
Gastric biopsy
Stool antigen test
477
Q

The urea breath test involves drinking what?

A

Urea with carbon isotope 13

478
Q

Why does the urea breath test work?

A

Urea is broken down by H. pylori

479
Q

What are the four regions of the stomach?

A

Fundus
Cardia
Body
Pylorus

480
Q

What are the two parts of the pylorus?

A

Antrum

Pyloric canal

481
Q

What are the four layers of the stomach?

A

Mucosa
Submucosa
Muscularis
Serosa

482
Q

What are the three layers of the mucosa of the stomach?

A

Epithelial layer
Lamina propria
Muscularis mucosa

483
Q

What does the epithelial layer of the stomach do?

A

Absorbs and secretes mucus and digestive enzymes

484
Q

What does the lamina propria of the stomach contain?

A

Blood + lymph vessels

485
Q

The epithelium of the stomach extends down into the lamina propria to create what?

A

Gastric pits

486
Q

What do the foveolar cells in the stomach produce?

A

Mucus

487
Q

What is the role of mucus lining the epithelium of the stomach?

A

Protects it from digestive enzymes and hydrochloric enzymes

488
Q

What do parietal cells secrete?

A

HCl

Intrinsic factor

489
Q

What do chief cells in the stomach secrete?

A

Pepsinogen to help digest proteins

490
Q

What do G cells in the stomach secrete?

A

Gastrin

491
Q

How does h. pylori protect itself from the harsh acidic environment of the stomach?

A

It has urease an enzyme which breaks urea down into CO2 and ammonia which can neutralise the stomach acid

492
Q

What symptoms might someone with a H. pylori infection get?

A

Usually asymptomatic
Heartburn, SoB, loss of apetite, pain in abdomen
Chronic infection –> chronic anaemia (bacteria eat iron)

493
Q

How is a urea breath test conducted?

A

Patient consumes urea with carbon isotope 13
After 30m exhales into gas tube
Mass spectrometry analysis calculates amount of 13C CO2

494
Q

When can a urea breath test not be conducted?

A

Within 4 weeks of an antibiotic/anti-secretory drug, e.g. PPI

495
Q

What is the only test to check for h. pylori eradication?

A

Urea breath test

496
Q

How does a rapid urease test work?

A

Biopsy sample mixed with urea + pH indicator

Colour change if H. pylori urease activity

497
Q

How is coeliac disease diagnosed?

A

Immunological tests + duodenal biopsy

498
Q

Does vilous atrophy/immunology reverse on a gluten free diet in coeliac disease?

A

Yes

Patients should be asked to reintroduce gluten 6 w before testing

499
Q

What is the first choice immunological test for coeliac disease?

A

Serum TTG and IgA

500
Q

What other immunological tests might you do in coeliac disease?

A

Endomyseal antibody (IgA) - needed to look for selective IgA deficiency which would given false negative coeliac result

501
Q

What do you see on duodenal biopsy in coeliac disease?

A

Villous atrophy
Crypt hyperplasia
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes

502
Q

What are early symptoms of haemochromatosis?

A

Fatigue
Erectile dysfunction
Arthalgia (often hands)

503
Q

What are later features of haemochromatosis?

A

Bronze skin pigmentation
DM
Liver - stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition
Cardiac failure (2ndary to dilated cardiomyopathy)
Hypogonadism (2ndary to cirrhosis and pituitary dysfunction)

504
Q

What features of haemochromatosis are reversible with treatment?

A

Liver cirrhosis
DM
Hypogonadotrophic hypogonadism
Arthropathy

505
Q

Define GORD

A

Symptoms of oesophagitis secondary to refluxed gastric contents

506
Q

How should endoscopically proven oesophagitis be treated?

A

Full dose PPI 1-2m
If response - low dose Rx as req.
No response double PPI for 1m

507
Q

How should endoscopically negative reflux disease be treated?

A

Full dose PPI 1m
If response offer low dose Rx possuble as req.
No response - H2RA or prokinetic for 1m

508
Q

What are complications of GORD?

A 
Oeosphagitis
Ulcers
Anaemia
Benign strictures
Barrett's oesophagus
Oesophageal carcinoma
509
Q

What heart problems does carcinoid syndrome cause?

A

Pulmonary stensis

Tricuspid insufficiency

510
Q

What is Zollinger-Ellison syndrome?

A

Condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour in the duodenum/pancreas

511
Q

What condition is associated with Zollinger-Ellison syndrome?

A

MEN 1

512
Q

What are the features of Zollinger-Ellison syndrome?

A

Multiple duodenal ulcers
Diarrhoea
Malabsorption

513
Q

What is the best screening test for Zollinger-Ellison syndrome?

A

Fasting gastrin levels

514
Q

What other test can you do to diagnose Zollinger-Ellison syndrome?

A

Secretin stimulation test

515
Q

What drug is used to control the symptoms of Zollinger-Ellison syndrome?

A

PPIs

516
Q

What are the features of MEN 1?

A

Hyperparathyroidism
Pituitary adenomas
Pancreatic tumours - insulinomas, gastrinoma
Also - adrenal/thyroid tumours

517
Q

What is the action of the hormone gastrin?

A

Stimulates secretion of HCl by parietal cells

Aids in gastric motility

518
Q

What is small bowel bacterial overgrowth syndrome?

A

Disorder characterised by excessive amounts of bacteria in teh small bowel –> GI symptoms

519
Q

What are risk factors for SBBOS?

A

Neonates with congenital GI abnormalities
Scleroderma
DM

520
Q

What are the features of SBBOS?

A

Chronic diarrhoea
Bloating, flatulence
Abdominal pain

521
Q

What tests are used to diagnose SBBOS?

A

Hydrogen breath test
Small bowel aspiration + culture
Trail of antibiotics

522
Q

How do you manage SBBOS?

A

Correct underlying disorder

Antibiotics - rifaximin (alt: co-amoxiclav, metronidazole)

523
Q

What group of drugs are first line to treat pain in IBS?

A

Antispasmodics

524
Q

What group of drugs are first line to treat constipation in IBS?

A

Laxatives

525
Q

What laxative should you avoid in IBS?

A

Lactulose

526
Q

What drug is first line to treat diarrhoea in IBS?

A

Loperamide

527
Q

If IBS patients are not responding to conventional laxatives what can you try?

A

Linaclotide (consider if optimal/max dose of prev. laxatives from diff classes haven’t worked or if they have had constipation >12m)

528
Q

What other group of drugs may be useful (2nd line) in the treatment of IBS?

A

Low dose TCAs

529
Q

What psychological therapies may be useful in IBS?

A

CBT, hypnotherapy, psychological therapy

530
Q

What IBS patients might you consider referring for psychological therapies?

A

Those not responding to pharmacological therapy after 12m and who develop a continuing symptom profile

531
Q

What advice should you give re eating habits to someone with IBS?

A

Have regular meals
Take time to eat
Avoid missing meals/having long gaps between eating
Limit high fibre foods
Reduce intake of resistant starch (found in processed foods)
Limit fresh fruit to 3 portions/day
Increase intake oats/linseeds

532
Q

What advice should you give re drinking habits to someone with IBS?

A

At least 8 cups fluid/day
Restrict tea/coffee to 3 cups/day
Reduce alcohol and fizzy drink intake

533
Q

For those with IBS-d what product should you advise them to avoid?

A

Sorbitol

534
Q

Is ferritin raised or decreased in inflammatory disorders?

A

Raised

535
Q

What kind of anaemia do you get in anaemia of chronic disease?

A

Normochromic/hypochromic normocytic anaemia
Reduced TIBC
Normal/raised ferritin

536
Q

What is the recommended treatment of severe alcoholic hepatitis?

A

Prednisone 40mg

537
Q

What are common causes of liver cirrhosis?

A

Alcoholism
NAFLD
Viral hepatitis (B and C)

538
Q

How did we used to diagnose cirrhosis?

A

Liver biopsy

539
Q

How is liver cirrhosis usually diagnosed now?

A

Transient elastography or acoustic radiation force impulse imaging

540
Q

What is the brand name for transient elastography?

A

FibroScan

541
Q

What does a fibroscan involve?

A

50MHz wave passed into liver from small transducer on end of a USS probe
Measures stiffness of liver which is a proxy for fibrosis

542
Q

Who should be offered a fibroscan?

A

People with Hep C infection
Men drinking >50 units/wk, women drinking >35units/week for several months
People diagnosed with ARLD

543
Q

What investigations should be done in those diagnosed with cirrhosis?

A

At time of diagnosis - UGIE to check for varices

Liver USS every 6m (+/- AFP) to check for hepatocellular cancer

544
Q

What are RFs for peptic ulcers?

A

H. pylori infection
Drugs - NSAIDs, SSRIs, corticosteroids, bisphosphonates
Zollinger-Ellison syndrome

545
Q

What are features of peptic ulcers common to both gastric and duodenal ulcers?

A

Epigastric pain

Nausea

546
Q

What are features specific to gastric ulcers?

A

Epigastric pain worsened by eating

547
Q

What are features specific to duodenal ulcers?

A

Epigastric pain when hungry and relieved by eating

548
Q

What investigation should you do in peptic ulcer disease?

A

Urea breath test/stool antigen test to check for h. pylori

549
Q

How do you manage peptic ulcer disease?

A

H. pylori +ve –> H. pylori erradication therapy

H. pylori -ve –> PPIs until ulcer has healed

550
Q

Is there any benefit from differentiating gastric ulcers from duodenal ulcers?

A

Yes, gastric ulcers are more likely to be malignant

551
Q

What is the incubation period of Hep A?

A

2-4 weeks

552
Q

What is a typical hx of hep A infection?

A

Flu like prodrome
Nausea, arthalgia
Can progress to hepatosplenomegaly + jaundice
Seafood consumption

553
Q

How is hep A spread?

A

Faecal oral

554
Q

What kind of virus is hep D?

A

Single stranded RNA virus

555
Q

How is hep D transmitted?

A

Parenterally

556
Q

What does D require to complete its replication + transmission cyle

A

Hep B surface antigen

557
Q

In relation to hep D terminology:

What does co-infection mean?

A

Hep B and D infection at the same time

558
Q

In relation to hep D terminology:

What does superinfection mean?

A

Hep B surface antigen +ve patient subsequently develops a hep D infection

559
Q

What is Hep D superinfection associated with?

A

High risk of fulminant hepatitis, chronic hepatitis status and cirrhosis

560
Q

How do you diagnose a hep D infection?

A

Reverse polymerase chain reaction of hep D RNA

561
Q

How do you treat hep D infection?

A

Interferon

562
Q

What is the characteristic iron study profile in haemochromatosis?

A

Raised transferrin saturation, and ferritin and low TIBC

563
Q

What is transferrin?

A

The main protein iron binds to for transport in the blood

564
Q

What is ferritin?

A

Intracellular storage of iron, with a small amount usually found in blood

565
Q

What is TIBC a measure of?

A

Available binding sites on transferrin

566
Q

Why is TIBC low in haemochromatosis?

A

Lots of irons take up the binding sites on transferrin so there is less capacity to bind more

567
Q

What is the recommended alcohol consumption for women?

A

Do not exceed >14 units a week

568
Q

What is the recommended alcohol consumption for men?

A

Do not exceed >14 units a week

569
Q

If you decide to drink 14 units a week, what is the recommendation regarding spreading it over a certain no of days?

A

Spread evenly over 3 days or more

570
Q

What advice is giving to pregnant women re drinking?

A

Avoid

571
Q

One unit of alcohol is = ____ml pure ethanol.

A

10

572
Q

How is the strength of an alcoholic drink determined?

A

Alcohol by volume (ABV)

573
Q

What is 1 unit in spirits?

A

25ml single measure

574
Q

What is 1 unit in beer?

A

1/3rd pint

575
Q

What is 1 unit in wine?

A

Half of a 175ml (standard) glass of red wine *ABV 12%)

576
Q

How can you calculate the number of units in a drink?

A

No of ml x ABV/1000

577
Q

How is Peutz-Jeghers syndrome inhertied?

A

AD

578
Q

What is Peutz-Jeghers syndrome characterised by?

A

Numerous hamartomatous polyps in the GI tract
Pigmented freckles on lips, face, palms and soles

(Others: intestinal obstruction, e.g. intussception, GI bleeding)

579
Q

Do the polyps in Peutz-Jeghers syndrome have malignant potential?

A

NO

But 50% of pts will have died of another GI cancer by age 60

580
Q

Mutations in what genes are responsible for Peutz-Jeghers syndrome?

A

Serine threonine kinase LKB1 or STK11

581
Q

How is Peutz-Jeghers syndrome managed?

A

Conservatively

Manage complications

582
Q

List indications for an UGIE in GORD

A 
Age >55
Symptoms >4w or persistent symptoms despite Rx
Dysphagia
Relapsing symptoms
Wt loss
583
Q

If endoscopy in GORD is negative what is the next step?

A

Consider 24hr oesophageal pH monitor (which is actually the gold standard test for diagnosis)

584
Q

What drugs (if any) should be stopped before an UGIE and why?

A

PPIs (2w before) so pathology can be identified during the procedure

585
Q

How does cholangiocarcinoma present?

A

Jaundice, wt loss, pruritus, persistent biliary symptoms

586
Q

What is hepatorenal syndrome?

A

Thedevelopment of renal failure in those with severe liver disease in the absence of any other identifiable cause of renal pathology

587
Q

What is the pathophysiology of HRS?

A

Vasoactive mediators –> splanchnic vasodilation –> reduced SVR –> underfilling of hte kidneys
Juxtaglomerular apparatus then activates RAAS –> renal constriction which is not enough to counterbalance the effects of splanchnic vasodilation

588
Q

How many types of HRS are there?

A

2

589
Q

What is type 1 HRS?

A

Rapidly progresssive
Doubling of serum creatinine to >221micromol/L/having creatinine clearance to less than 20ml/min over <2 weeks
V poor prognosis

590
Q

What is type 2 HRS?

A

Slowly progressive

Poor prognosis but pts live for longer

591
Q

What are management options for HRS?

A

Vasopressin analogues, e.g. terlipressin
Volume expansion with 20% albumin
TIPS

592
Q

How do vaspressin analogues work in treating HRS?

A

They cause vasoconstriction of the splanchnic circulation

593
Q

List red flag symptoms for gastric cancer that merit an UGIE

A 
New onset dyspepsia in >55y
Unexplained persistent vomiting
Unexplained wt loss
Progressively worsening dysphagia/odynophagia
Epigastric pain
594
Q

A transjugular intrahepatic portosystemic shunt procedure connects which two vessels?

A

Portal vein and hepatic vein

595
Q

What is the main aim of a TIPS procedure?

A

Treat portal hypertension by making a route for blood to flow from the portal to the systemic circulation bypassing the liver

596
Q

How do you manage an acute variceal haemorrhage?

A 
ABC
Correct clotting (FFP, vit K)
Vasoactive agents
Prophylactic anibiotics
Endoscopy with band ligation 
Sengstaken Blakemore tube if uncontrolled haemorrhage
TIPSS if all above fails
597
Q

What vasoactive agent is licensed for variceal haemorrhage?

A

Terlipressin

598
Q

What prophylactic antibiotics are generally given for variceal haemorrhage?

A

Quinolones

599
Q

What is involved in the prophylaxis of variceal haemorrhage?

A

Propanolol

Endoscopic variceal band ligation

600
Q

How should endoscopic variceal band ligation be done?

A

Every 2 weeks until all varices have been erradicated

601
Q

What drug should be given whilst a patient is getting endoscopic variceal band ligation and why?

A

PPI cover to reduce risk of EVL-induced ulceration

602
Q

Carcinoid tumours usually produce bradykinin and serotonin. What other hormones can they produce?

A

Pituitary hormones, e.g. ACTH –> cushingoid features

603
Q

Define increased ferritin level

A

> 300microg/L in men/postmenopausal women

>200microg/L in premenopausal women

604
Q

What is the issue with interpreting a raised ferritin level?

A

Ferritin is an acute phase protein + may be synthesised in increased quantities in infalmmation

605
Q

How can we split the causes of increased ferritin?

A

Without iron overload

With iron overload

606
Q

What are causes of increased ferritin without iron overload?

A 
Inflammation 
Alcohol excess
Liver disease
CKD
Malignancy
607
Q

What are causes of increased ferritin with iron overload?

A

Primary iron overload - haemochromatosis

Secondary iron overload - repeated transfusions

608
Q

What is the best test to see whether iron overload is present?

A

Transferrin saturation

609
Q

What values of transferrin saturation rule out iron overload?

A

<45% in F

<50% in M

610
Q

What test can be used to differentiate between IBS and IBD in primary care?

A

Faecal calprotectin

611
Q

Where is calprotectin released from?

A

Inflamed bowel

612
Q

What does a positive faecal calprotectin mean?

A

Doesn’t indicate definite IBD but patients should be referred to secondary care for further investigation

613
Q

Do c. diff patients need to be isolated?

A

Yes until the diarrhoea has been resolved for at least 48h

614
Q

What does HBsAg indicate?

A

First marker to appear
Causes production of anti-HBs
Implies acute disease (present for 1-6m)
If present >6m implies chronic disease

615
Q

What does anti-HBs indicate?

A

Immunity (either exposure/vaccination)

616
Q

What does anti-HBc indicate?

A

Previous/current infection
IgM anti-HBc appears during acute or recent hep B infection + is present for about 6m
IgG anti-HBc persists

HBc = Caught

617
Q

What is HbeAg?

A

Results from breakdown of core antigen in infected liver cells

618
Q

What does HbeAg indicate?

A

Infectivity

619
Q

Is vitamin B6 water or fat soluble?

A

Water

620
Q

What is vitamin B6 converted to in the body?

A

Pyridoxal phosphate (PLP)

621
Q

What is PLP a cofactor for?

A

Many reactions inclyding transmination, deamination, decarboxylation

622
Q

What are causes of B6 deficiency?

A

Isoniazid therapy

623
Q

What are consequences of B6 deficiency?

A

Peripheral neuropathy

Sideroblastic anaemia

624
Q

What drug is usually co-prescribed with isoniazid to prevent B6 deficiency?

A

Pyridoxine hydrochloride

625
Q

Which vitamin if taken in high doses can be teratogenic?

A

Vitamin A

Pregnant women should be advised to avoid it and foods high in it, e.g. liver

626
Q

Is vitamin A fat or water soluble?

A

Fat

627
Q

What are the functions of vitamin A?

A

Converted into retinal, an important visual pigment
Important in epithelial cell differentiation
Antioxidant

628
Q

When should biologic therapy be considered for treatment of an acute flare of CD?

A

When symptoms don’t improve after 5 days of IV hydrocortisone

629
Q

What biologics may be used in CD?

A

Anti-TNFa agents, e.g. infliximab or adalimumab

630
Q

All patients with suspected upper GI bleed should have what within 24h of admission?

A

Endoscopy

631
Q

Which patients with dyspepsia should have an urgent referral (i.e. within 2 weeks) for endoscopy?

A

Those with:
Dysphagia
Upper abdominal mass consistent with stomach cancer
Those 55+ with wt loss + any of: upper abdominal pain, reflux, dyspepsia

632
Q

Which patients with dyspepsia should have an non-urgent referral for endoscopy?

A

Those with haematemesis
Those 55y+ with treatment resistant dyspepsia or upper abdominal pain with low Hb levels or raised platelet count + any of: N, V, wt loss, reflux, dyspepsia, upper abdominal pain
NV + any of: wt loss, reflex, dyspepsia, upper abdominal pain

633
Q

How do you manage patients who don’t the criteria for referral for dyspepsia?

A

Review medications for causes of dyspepsia
Lifestyle advice
Trail full dose PPI 1m or test + treat for h. pylori

634
Q

What structures do you transverse in a midline incision?

A

Linea alba, transversalis fascia, extraperitoneal fat, peritoneum

635
Q

What is a paramedial incision?

A

Parallel to the midline (about 3-4cm)

636
Q

Where is Kocher’s incision?

A

Incision under right subcostal margin

637
Q

What operation uses a Kocher’s incision?

A

Open cholecystectomy

638
Q

Where is a Lanz incision?

A

Incision in RIF, e.g. for appendiectomy

639
Q

Where is a Gridiron incision?

A

Oblique incision over McBurneys point (less cosmetically acceptable than Lanz)

640
Q

What is a gable incision?

A

Rooftop incision

641
Q

Where is a Pfannenstiel incision?

A

Transverse suprapubic (used for pelvic surgery)

642
Q

Where is a McEvedy’s incision?

A

Groin incision, e.g. for emergency repair of a strangulated femoral hernia

643
Q

Where is a Rutherford Morrison incision?

A

Extraperitoneal approach to LLQ/RLQ

644
Q

What does a Rutherford Morrison incision give really good access to?

A

Iliac vessels

645
Q

What is the incision of choice for first time renal transplantation?

A

Rutherford Morrison incision

646
Q

What kin of incision is used for a pancreatectomy?

A

Rooftop

647
Q

What kind of incision is used for an emergency c-section?

A

Pfannensteil

648
Q

What would your investigations in CD show?

A

Raised inflammatory markers
Increased faecal calprotectin
Anaemia
Low vit B12 and vitamin D

649
Q

What is the most common symptom of CD in kids?

A

Abdominal pain

650
Q

What is the most common symptom of CD in adults?

A

Diarrhoea

651
Q

What is the most common type of gallstone?

A

Mixed

652
Q

What is the most common cause of a CBD stone in the western world?

A

Migration

653
Q

What are the classical symptoms of gallstones (‘biliary colic’)?

A

Colicky RUQ pain occuring post-prandially

Worse following fatty meals

654
Q

Why is the pain of gallstones worse following a fatty meal?

A

Cholecystokinin levels are higher so gallbladder contraction is maximal

655
Q

What is the diagnostic work up of gallstones?

A

Abdominal USS

LFTs

656
Q

What imaging should be done for suspected CBD stone?

A

MRCP and intraoperative imaging

657
Q

How is biliary colic managed?

A

If imaging shows gallstones –> laparoscopic cholecystectomy

658
Q

What is a typical presentation of acute cholecystitis?

A

RUQ pain
Fever
Murphys sign
May have derranged LFTs

659
Q

How is acute cholecystitis managed?

A

USS imaging and cholecystectomy (within 48h presentation)

660
Q

How does a gallbladder abscess tend to present?

A

Prodromal illness
RUQ pain
Swinging pyrexia
Systemically unwell

661
Q

How should you image a suspected gallbladder abscess?

A

USS +/- CT

662
Q

How is a gallbladder abscess managed?

A

Subtotal cholecystectomy may be req. if Calot’s triangle is hostile
If unfit - percutaneous drainage may be considered

663
Q

What is cholangitis?

A

Infection of the biliary tree

664
Q

How does cholangitis tend to present?

A

Patient septic and v. unwell
Jaundice
RUQ pain

665
Q

How is cholangitis managed?

A

Fluid resus
Broad spectrum IV antibiotics
Correct coagulopathies
Early ERCP

666
Q

How is gallstone ileus managed?

A

Laparotomy, removal of gallstone from small bowel

Do not interfere with fistula between duodenum and gallbladder

667
Q

What is acalculous cholecystitis?

A

Inflammation of the gallbladder without gallstones/cystic duct obstruction

668
Q

Who does acalculous cholecystitis tend to occur in?

A

Those with intercurrent illness, e.g. DM, organ failure

669
Q

How should acalculous cholecystitis be managed?

A

Fit - cholecystectomy

Unfit - percutaneous cholecystostomy (drainage of gallbladder)

670
Q

Should asymptomatic gallbladder stones be treated?

A

No

671
Q

Should asymptomatic stones in the CBD be managed?

A

Consider it as there is a risk of cholangitis/pancreatitis

672
Q

How should you treat symptomatic gallstones?

A

Cholecystectomy via laparoscopic route

673
Q

In a very frail patient with symptomatic gallstones what other treatment should be considered?

A

US guided cholecystostomy

674
Q

What are risks of ERCP?

A

Bleeding
Duodenal perforation
Cholangitis
Pancreatitis

675
Q

What are RFs for developing gallstones?

A 
Increasing age
Family history
Sudden wt loss
Loss of bile salts, e.g. ileal resection/terminal ileitis
DM
Oral contraception
676
Q

What are opioid agonist antidiarrhoea agents?

A

Loperamide

Diphenoxylate

677
Q

How does loperamide work in treating diarrhoea?

A

u-opioid receptor agonist which does not have systemic effects as it is not absorbed through the gut
It reduces peristalsis of the intestines

678
Q

What is the initial investigation that should be done in a case of suspected gallstones?

A

USS

679
Q

What does type 1 HRS typically follow?

A

An acute event, e.g. upper GI bleed

680
Q

What is type 2 HRS generalyl associated with?

A

Refractory ascites

681
Q

What do you typically see on a plain AXR in gallstone ileus?

A

Small bowel obstruction and air in the biliary tree

682
Q

Achalasia increases the risk of SCC or adenocarcinoma of hte oesophagus?

A

SCC

683
Q

Barrett’s/GORD increases the risk of SSC or adenocarcinoma of the oesophagus?

A

Adenocarcinoma

684
Q

What sections of the oesophagus are associated with adenocarcinoma + what sections are associated with SCC?

A

Upper 2/3rd –> SCC

Lower 1/3rd –> adenocarcinoma

685
Q

What is acute liver failure?

A

Rapid onset of hepatocellular dsyfunction leading to a variety of systemic complications

686
Q

What are causes of acute liver failure?

A

Paracetamol OD
Alcohol
Viral hep (usually A or B)
Acute fatty liver of pregnancy

687
Q

What are the features of acute liver failure?

A 
Jaundice
Fetor hepaticus (sweet faecal breath)
Coagulopathy (prolonged PT)
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure (HRS)
688
Q

What is the commonest causes of acute liver failure in the UK?

A

Paracetamol OD

689
Q

What is haematochezia?

A

Passage of fresh blood per rectum

Usually occurs in a lower GI bleed

690
Q

What 2 scores are used to assess the severity of liver cirrhosis?

A

Child-Pugh

MELD (Model for End-Stage Liver Disease)

691
Q

What parameters does the Child-Pugh score take into account?

A 
Bilirubin
Albumin
PT prolonged by
Encephalopathy
Ascites
692
Q

How are Child-Pugh scores graded?

A

A, B or C based on summation of scores

693
Q

What is Child-Pugh score A?

A

<7

694
Q

What is Child-Pugh score B?

A

7-9

695
Q

What is Child-Pugh score C?

A

> 9

696
Q

What factors does MELD take into account?

A

Bilirubin, creatinine, INR

It uses a formula to predict create a score that correlates with mortality

697
Q

What is a typical history of traveller’s diarrhoea?

A

Diarrhoea, abdominal cramps, nausea following travel

698
Q

What is the most common cause of traveller’s diarrhoea?

A

Enterotoxigenic E. coli

699
Q

Should PPIs be given in an acute GI bleed prior to endoscopy?

A

No as they can mask the site of leeding

700
Q

How is coeliac disease managed?

A

Gluten free diet

701
Q

What foods contain gluten?

A

Wheat - bread, pasta, pastry
Beer
Rye
Oats

702
Q

What are good carbs for coeliac patients to eat that are gluten free?

A

Potatoes
Corn
Rice

703
Q

What blood test can be used to check compliance with a gluten free diet in coeliac disease?

A

Tissue transglutaminase (TTG)

704
Q

Why do patients with coeliac disease require extra vaccinations?

A

They have a degree of functional hyposplenism

705
Q

What vaccines are those with coeliac disease advised to recieve?

A

Pneumococcal vaccine with booster every 5 years

Annual flu vaccine

706
Q

What is the gold standard procedure for diagnosing PSC?

A

MRCP

ERCP only if unable to tolerate MRI e.g. metal implants

707
Q

When should a diagnosis of IBS be suspected?

A

In a patient with the following for at least 6 months:

  • Ab pain +/or
  • Bloating +/or
  • Change in bowel habit
708
Q

When should a positive diagnosis of IBS be made?

A

If patient has abdominal pain relieved by defaecation or associated with altered bowel frequency or stool form + 2 of:
- Altered stool passage (straining, urgency, incomplete evacuation)

709
Q

When should a positive diagnosis of IBS be made?

A

If patient has abdominal pain relieved by defaecation or associated with altered bowel frequency or stool form + 2 of:

  • Altered stool passage (straining, urgency, incomplete evacuation)
  • Ab bloating, distension, tension, hardness
  • Symptoms made worse by eating
  • Passage of mucus
710
Q

What are red flag symptoms in IBS that should be enquired about?

A

Rectal bleeding
Unexplained/unintentioanl wt loss
FH of bowel/ovarian cancer
Onset >60y

711
Q

What are suggested primary are investigations for suspected IBS?

A

FBC
ESR/CRP
Coeliac disease screen (TTG Abs + IgA)

712
Q

Which of UC and CD carry a higher risk of colorectal cancer?

A

UC

713
Q

Which of UC and CD carry a higher risk of obstruction and fistula formation?

A

CD

714
Q

In which of UC and CD do you see increased goblet cells?

A

CD

715
Q

In which of UC and CD do you more commonly see crypt abscesses?

A

UC

716
Q

In which of UC and CD do you more commonly see granulomas?

A

CD

717
Q

What do you see on endoscopy in CD?

A

Deep ulcers

Skip lesions - cobblestone appearance

718
Q

What do you see on endoscopy in UC?

A

Widespread ulceration with preservation of adjacent mucosa –> pseudopolyps

719
Q

What do you see on small bowel enema in CD?

A

Strictures –> Kantor’s string sign
Proximal bowel dilatation
Rose thorn ulcers
Fistulae

720
Q

What do you see on barium enema in UC?

A

Loss of haustrations
Pseudopolyps
Long standing disease - colon is narrow + short (drainpipe colon)

721
Q

What is the second most common causative organism causing SBP?

A

Klebsiella

722
Q

What organisms commonly cause a gram positive SBP?

A

Strep pneumoniae
Strep viridians
Staph

723
Q

What is PBC?

A

Chronic disease of the small intrahepatic bile ducts that is characterised by progressive bile duct damage, cholestasis and may eventually lead to cirrhosis

724
Q

What is the aetiology of PBC?

A

Autoimmune

725
Q

Who is PBC typically seen in?

A

Middle aged women

726
Q

What is the classical presentation of PBC?

A

Itching in a middle aged woman

727
Q

What are some early features of PBC?

A

May be asymptomatic (e.g. raised ALP on routine LFTs)

Or fatigue, pruritus

728
Q

What are some later features of PBC?

A 
Cholestatic jaundice
Hyperpigmentation, esp. over pressure joints
May have RUQ pain 
Xanthelasmas, xanthomata
Clubbing, hepatomegaly
729
Q

What are complications of PBC?

A

Malabsorption - osteomalacia, coagulopathy
Sicca syndrome
Portal HTN - ascites, variceal haemorrhage
Hepatocellular cancer

730
Q

By how much does PBC increase your risk of hepatocellular cancer?

A

20x

731
Q

What conditions is PBC associated with?

A

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

732
Q

What factors are used to help diagnose PBC?

A

AMA M2 subtype present in 98%
SMA
Raised serum IgM

733
Q

What drug is used to help itching in PBC?

A

Cholestyramine

734
Q

Apart from cholestyramine, what else is involved in the management of PBC?

A

Fat soluble vit supplements
Ursodeoxycholic acid
Liver transplant, e.g. if bilirubin >100

735
Q

Name 3 aminosalicylate drugs

A

Sulphasalazine
Mesalazine
Olsalazine

736
Q

Where is 5ASA released from in the body and what is its action?

A

The colon

It is not absorbed but it has anti-inflammatory actions (may inhibit prostaglandin synthesis)

737
Q

What is sulphasalazine a combination of?

A

Sulphapyridine (a sulphonamide) and 5ASA

738
Q

What are SEs of sulphasalazine?

A 
Rashes
Oligospermia
Headache
Heinz body anaemia
Megaloblastic anaemia
Lung fibrosis
\+ SEs of mesalazine
739
Q

What is mesalazine?

A

Delayed release form of 5ASA

740
Q

What are the SEs of mesalazine?

A

GI upset, headache, agranulocytosis, pancreatitis, interstitial nephritis

741
Q

What is the structure of olsalazine?

A

2 molecules of 5ASA linked by a diazo bond which is broken by colonic bacteria

742
Q

Is pancreatitic more common in mesalazine or sulphasalazine?

A

Mesalazine

743
Q

What is the first line serological test for coeliac disease?

A

TTG Abs

744
Q

What are infective causes of acute abdomen?

A 
Gastroenteritis
Appendicitis
Diverticulitis
Pyelonephritis
Cholecystitis
Cholangitis
PID
Hepatitis
Pneumonia
745
Q

What are inflammatory causes of acute abdomen?

A

Pancreatitis

Peptic ulcer disease

746
Q

What are vascular causes of acute abdomen?

A

Ruptured abdominal aortic aneurysm
Mesenteric ischaemia
MI

747
Q

What are traumatic causes of acute abdomen?

A 
Ruptured spleen
Perforated viscus (e.g. oesophagus, stomach, bowel)
748
Q

What are metabolic causes of acute abdomen?

A

Renal/ureteric stone

DKA

749
Q

How can you differentiate biliary colic from acute cholecystitis?

A

No fever

Normal inflammatory markers

750
Q

What is acute cholecystitis?

A

Inflammation/infection of the gallbladder secondary to impacted gallstones

751
Q

What is Murphy’s sign?

A

Arrest of inspiration on palpation of the RUQ

752
Q

Where is the pain in biliary colic?

A

RUQ

753
Q

Where is the pain in acute cholecystitis?

A

RUQ

754
Q

What is ascending cholangitis?

A

Bacterial infection of the biliary tree

755
Q

What is the most common predisposing factor for ascending cholangitis?

A

Gallstones

756
Q

What triad of symptoms do you see in ascending cholangitis?

A

Charcot’s triad:
RUQ pain
Fever
Jaundice

757
Q

What are the two most common causes of acute pancreatitis?

A

Alcohol, gallstones

758
Q

Where is the pain in acute cholangitis?

A

RUQ

759
Q

Where is the pain of acute pancreatitis?

A

Epigastrium
May radiate through to back
Very severe!!

760
Q

What do you often see on examination in acute pancreatitis?

A

Tenderness, ileus and low grade fever

761
Q

Where is the pain in acute diverticulitis? What is the character of the pain in acute diverticulitis?

A

Colicky LLQ

762
Q

What do you see on the bloods in acute diverticulitis?

A

Raised inflammatory markers and WCC

763
Q

Apart from pain what are other symptoms of diverticulitis?

A

Fever

Diarrhoea (sometimes bloody)

764
Q

Where is the pain of intestinal obstruction?

A

Central

765
Q

What might you hear if you listened to the abdomen of someone with intestinal obstruction?

A

Tinkering bowel sounds

766
Q

What are features of bowel obstruction?

A

Absolute constipation

Vomiting

767
Q

What are urological causes of acute abdomen?

A

Renal colic
Acute pyelonephritis
Urinary retention

768
Q

Where is the pain of renal colic? What is the character of the pain?

A

Loin to groin pain

Intermittent but severe

769
Q

What other feature may you see (despite the pain) in renal colic?

A

Visible/non-visible haematuria

770
Q

Where is the pain of acute pyelonephritis?

A

Loin pain

771
Q

What are the features of acute pyelonephritis?

A

Fever, rigors, vomiting

Loin pain

772
Q

Where is the pain from urinary retention?

A

Suprapubic

773
Q

What should all women of reproductive age who present with abdominal pain be considered until proven otherwise?

A

Pregnant

774
Q

Where is the pain of an ectopic pregnancy?

A

R or LIF

775
Q

How does ectopic pregnancy typically present?

A

Pain + Hx of amenorrhoea for past 6-9 weeks

Vaginal bleeding may be present

776
Q

What are vascular causes of acute abdomen?

A

Ruptured AAA

Mesenteric ischaemia

777
Q

Where is the pain in ruptured AAA?

A

Central abdominal radiating to the back

778
Q

How can ruptured AAA present?

A

Sudden collapse or persistent central abdominal pain with developing shock (hypotension, tachycardic)

Hx CVdx

779
Q

Where is the pain of mesenteric ischaemia?

A

Central

780
Q

What are other features of mesenteric ischaemia?

A

Hx AF/CVdx
Diarrhoea, rectal bleeding may be seen
Metabolic acidosis due to dying tissue

781
Q

When should you diagnose toxic megacolon?

A

When the transverse colon is >6cm diameter and the patient is systemically unwell

782
Q

How is toxic megacolon managed?

A

Aggressive medical therapy for 24-72h, if no signs of improvement then colectomy

783
Q

Which of UC or CD is more likely to have a palpable mass in the RIF?

A

CD

784
Q

What should be used instead of ferritin as a marker of iron stored in the body during an acute infection?

A

Transferrin saturation

785
Q

What is the first line treatment for NAFLD?

A

Weight loss

786
Q

What part of the bowel is most affected by UC?

A

Rectum

787
Q

What is the most sensitive and specific lab finding for diagnosing liver cirrhosis in those with chronic liver disease?

A

Thrombocytopenia

788
Q

What examination should you always do in a male with acute abdomen and why?

A

Scrotal examination to rule out testicular problems, e.g. torsion

789
Q

What features of a c. diff infection would indicate it is severe and hence requires treatment first line with vancomycin?

A

ITU admission
Shock
WCC >15
Acutely rising blood creatinine (e.g. >50% increase above baseline)
Temperature >38.5°C
Evidence of severe colitis (abdominal signs, radiology)

790
Q

Who should be offered serological testing for coeliac disease?

A

Persistent unexplained abominal/GI symptoms
Faltering growth
Prolonged fatigue
Unexplained wt loss
Severe/persistent mouth ulcers
Unexplained iron, vit B12, folate deficiency
T1DM at diagnosis
Autoimmune thyroid disease at diagnosis
IBS in adults
First degree relatives of those with coeliac disease

791
Q

From what vertebral level does the IMA arise from?

A

L3

792
Q

Where does the IMA supply?

A

Hindgut

793
Q

What is a typical history of acute fatty liver of pregnancy?

A

Jaundice following abdominal pain and pruritus in pregnancy

794
Q

What is the normal LFT pattern in hepatocellular disease?

A

ALT raised at least 2x
ALP normal
ALP/ALP 5+ normal

795
Q

What is the normal LFT pattern in cholestatic disease?

A

ALT normal
ALP raised at least 2x
ALP/ALP <2

796
Q

What is the normal LFT pattern in mixed disease?

A

ALT and ALP raised at least 2x

ALT/ALP 2-5

797
Q

What triad of symptoms are seen in acute liver failure?

A

Encephalopathy
Jaundice
Coagulopathy

798
Q

What is ischaemic hepatitis?

A

Diffuse hepatic injury resulting from acute hypoperfusion (liver shock)

799
Q

How do you diagnose ischaemic hepatitis?

A

In the presence of an initiating event (e.g. cardiac arrest) + marked increases in aminotransferase levels

800
Q

What does ischaemic hepatitis often occur in conjuction with?

A

AKI (tubular necrosis) or other end organ dysfunction

801
Q

Bilirubin is a breakdown product of what?

A

Heme

802
Q

Describe how heme –> bilirubin

A

Heme is processed in macrophages and oxidised to form biliverdin + iron
Biliverdin reduced to form unconjugated bilirubin which enters the blood stream

803
Q

What is UC bilirubin carried by in the blood? Where does it end up?

A

Albumin

Hepatocytes

804
Q

Where is UC bilirubin conjugated?

A

Hepatocytes

805
Q

What is the key difference between conjugated and unconjugated bilirubin?

A

Conjugated bilirubin is water soluble unconjugated is not

GI (8 decks)

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