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Gastrointestinal > MedEd > Flashcards

MedEd Flashcards

1
Q

what does dyspepsia indicate

A

an upper GI problem

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2
Q

what are symptoms of dyspepsia

A 
epigastric pain or burning or discomfort
early satiety and post-prandial fullness
belching
bloating
nausea
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3
Q 
A 47 year old man presents to clinic with a 3 month history of epigastric dull abdominal pain. He states that the pain is worse at night and is relieved on eating. On direct questioning, there is no history of weight loss. He is not anaemic. 
Duodenal ulcer 
Zollinger-Ellison Syndrome
Gastric ulcer 
Gastro-oesophageal reflux disease 
Non-ulcer dyspepsia
A

Duodenal ulcer

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4
Q 
2. A 59 year old man presents with severe retrosternal burning pain. Upper GI endoscopy  shows ‘metaplastic changes within the epithelium’. 
Gastric ulcer 
Gastric carcinoma 
Oesophageal carcinoma
Gastro-oesophageal reflux disease 
Barrett’s oesophagus
A

Barrett’s oesophagus

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5
Q 
3. A 41 year old man is referred to gastroenterology outpatients  out patients with a 3 month history of worsening epigastric pain and dyspepsia. Upper GI endoscopy confirms multiple ulcers in the stomach and duodenum. Serum gastrin is elevated. 
Duodenal ulcer 
Zollinger-Ellison Syndrome
Gastric ulcer 
Gastric carcinoma 
Gastro-oesophageal reflux disease
A

Zollinger-Ellison Syndrome

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6
Q 
4. A 40 year old woman presents with a 2 month history of burning upper abdominal pain which is worse on eating. On examination there is mild tenderness to palpation of the epigastric region. 
Duodenal ulcer 
Zollinger-Ellison Syndrome
Gastric ulcer 
Gastric carcinoma 
Gastro-oesophageal reflux disease
A

Gastric ulcer

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7
Q

what is Zollinger-Ellison Syndrome

A

rare condition in which one or more tumours form in the pancreas or duodenum
these gastrinomas secrete large amounts of gastrin causing increased stomach acid production

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8
Q 
5. A 37 year old overweight woman presents to the GP with burning upper abdominal pain. She says it is especially bad when she goes to bed. She also complains of a tickly cough and a funny taste in her mouth.  
Zollinger-Ellison Syndrome
Gastric ulcer 
Oesophageal carcinoma
Gastro-oesophageal reflux disease 
Non-ulcer dyspepsia
A

Gastro-oesophageal reflux disease

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9
Q

def of peptic ulcer disease

A

a break in the superficial epithelial lining of either the stomach or duodenum

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10
Q

what sort of peptic ulcer is more common, gastric or duodenal

A

duodenal

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11
Q

what is a common cause of PUD in developing countries

A

h. pylori

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12
Q

what is a common cause of PUD in developed countries

A

NSAID use

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13
Q

what are the two most important risk factors for PUD

A

h. pylori

NSAIDs

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14
Q

how do NSAIDs increase risk of PUD

A

NSAIDs inhibit COX which leads to decreased prostaglandins and this can lead to mucosal damage

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15
Q

what are rare associations with PUD

A

increased gastrin (zollinger-ellison)

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16
Q

what sort of organism is h.pylori

A

gram-negative flagellate

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17
Q

how common is h.pylori

A

very common in developing countries

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18
Q

what does h. pylori infection lead to

A

gastritis
peptic ulcers
gastric cancer

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19
Q

what sort of pain is PUD associated with

A

recurrent epigastric pain which is a burning and knawing pain

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20
Q

what does pain in PUD commonly occur

A

related to eating a meal (dyspepsia)

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21
Q

what symptoms are associated with PUD

A

N+V
getting full very quickly
weight loss or anorexia

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22
Q

what are the signs of PUD on examination

A

epigastric tenderness
‘pointing sign’
PR blood

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23
Q

when does pain from duodenal ulcers occur

A

hours after eating

can wake patients up in the night

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24
Q

when does pain from gastric ulcers occur

A

immediately after eating

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25
Q

what relieves the pain of duodenal ulcers

A

eating

antacids

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26
Q

what relieves the pain of gastric ulcers

A

minimal relief with antacids

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27
Q

what is pointing sign

A

in PUD

patient can point to site of pain with one finger (specific area of pain)

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28
Q

A 40 year old woman presents with a 2 month history of burning upper abdominal pain which is worse on eating.
You suspect she has a gastric ulcer. What is the most appropriate investigation?
Upper GI endoscopy
Full blood count
Abdominal X-Ray
H.Pylori Breath Test
Trial of Proton Pump inhibitor

A

H.Pylori Breath Test

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29
Q

what are the indications for a h.pylori breath test or antigen test

A

<55yrs and NO alarm symptoms

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30
Q

what are the indications for 2wk UGI endoscopy

A

> 55yrs or alarm (red flag) symptoms or no response to treatment

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31
Q

if an ulcer is present after a UGI endoscopy, what must be done

A 
1 histology (neoplasia?)
2 h. pylori testing (biopsy urease testing?)
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32
Q

if a gastric ulcer is present after after a UGI endoscopy and is treated, what must be done as follow up?

A

repeat endoscopy after 6-8wks to rule out malignancy

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33
Q

what are red flag symptoms

A 
weight loss
bleeding
anaemia
vomiting
dysphagia
early fullness on eating
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34
Q

what is the treatment for h.pylori

A

triple therapy
1PPI
2xantibiotics

for example
1lansoprazole/omeprazole
2xamoxicillin + clarithromycin

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35
Q

what is the treatment for PUD if h.pylori negative

A

PPI or H2 antagonist

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36
Q

what complications are associated with PUD

A

haemorrhage
perforation
malignancy

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37
Q

what is GORD

A

reflux of stomach contents into the oesphagus

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38
Q

risk factors for GORD

A

obesity
smoking
pregnancy
haitus hernia

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39
Q

what foods are associated with GORD

A

large fatty meals

coffee or alcohol

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40
Q

what conditions are associated with GORD

A

achalasia

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41
Q

what symptoms are associated with GORD

A

burning retrosternal pain related to good

a sour taste in the mouth

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42
Q

what makes GORD better and worse

A

better - anatacids

worse - bending or lying flat

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43
Q

what are the extra-oesophageal features of GORD

A

nocturnal asthma
chronic cough
laryngitis (hoarseness)

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44
Q 
A 37 year old overweight woman presents to the GP with burning upper abdominal pain. She says it is especially bad when she goes to bed. She also complains of a tickly cough and a funny taste in her mouth.  
She has no other significant symptoms and you suspect she has GORD. 
What is the most appropriate next step?
UGI endoscopy
Start her on a proton pump inhibitor
Barium Swallow study 
Start her on a H2 antagonist 
Oesophageal manometry
A

Start her on a proton pump inhibitor

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45
Q

what investigations are completed for GORD

A

a clinical diagnosis generally

however a trial of PPI is often diagnostic and therapeutic

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46
Q

what is the conservative management for GORD

A

lose weight
avoid precipitants (large fatty meals and coffee and alcohol before bed)
elevate bed for sleeping
stop smoking

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47
Q

what is the medical management for GORD

A

PPIs

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48
Q

what is the MOA of PPIs

A

inhibits H+/K+ ATPase pump

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49
Q

what drugs affect oesophageal tone and could lead to GORD

A

nitrates and CCBs

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50
Q

how does GORD lead to oesophageal adenocarcinoma

A

GORD leads to oesophagitis which leads to barretts this leads to dysplasia and oesophageal adenocarcinoma

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51
Q

what changes occur for oesophagitis to turn into barretts oesophagus

A

squamous to columnar (metaplasia)

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52
Q

what history is associated with oesophageal stricture

A

intermittent progressive dysphagia

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53
Q

how should barretts oesophagus be treated

A

1 surveillance (regular endoscopy + biopsy)
2 treatment
-high grade dysplasia with radiofrequency ablation and PPI
-nodule with endoscopic mucosal resection and PPI or oesophagectomy

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54
Q

what is zollinger ellison syndrome

A

gastrin-secreting tumour of the pancreas

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55
Q

what endocrine condition is ZE syndrome associated with

A

MEN1

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56
Q

how does ZE syndrome cause gastric ulcers

A

increased gastrin from gastrinomas
hypertrophy of the gastric mucosa and stimulation of acid secreteing cells
this leads to damaged mucosa and ulceration

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57
Q

how does ZE syndrome cause malabsorption

A

damage of GI mucosa and inactivation of pancreatic enzymes

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58
Q

when should ZE syndrome considered

A

with multiple ulcers

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59
Q

what are symptoms of ZE syndrome

A

abdominal pain (similar to PUD)
diarrhoea
heartburn

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60
Q

what are symptoms of ZE syndrome when associated with MEN1

A

PPP
pituitary
parathyroid
pancreatic

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61
Q

what are the investigations for for ZE syndrome

A

fasting serum gastrin

serum calcium

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62
Q

what is the management for ZE syndrome

A

PPIs

surgical resection

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63
Q

what are common DDx for dyspepsia

A

GORD
PUD
cancer
non-ulcer dyspepsia

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64
Q 
1) A 29 year old woman presents with 2 week history of passing bloody diarrhoea with mucus up to 12 times a day. This is associated with lower abdominal, cramp like pain and malaise. On examination she looks pale and generally unwell and there is some tenderness in the left iliac fossa. 
a gastroenteritis
b crohns disease
c IBS
d hyperthyroidism
e UC
A

e UC

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65
Q 
2) A 55 year old woman with diabetes presents with weight loss, diarrhoea and angular stomatitis. Blood tests reveal presence of tTG antibodies. 
a hyperthyroidism
b colorectal carcinoma
c IBS
d coeliacs
e CD
A

d coeliacs

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66
Q 
3) A 16 year old boy is brought to paediatric out patients by his mother with a 9 month history of weight loss, abdominal pain and diarrhoea. On examination, he is on the 10th centile for height and weight, having been on the 50th centile previously. tTG antibodies are negative. 
a gastroenteritis
b coeliacs
c UC
d hyperthyroidism
e CD
A

CD

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67
Q 
4) A 28 year old medical student returns from his elective in Thailand with a short history of severe lower abdominal cramps and passage of blood diarrhoea. 
a gastroenteritis
b pseudomembranous colitis
c UC
d hyperthyroidism
e CD
A

gastroenteritis

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68
Q 
5) A 24 year old woman gives a long history (several years) of intermittent diarrhoea and constipation. She also complains of abdominal bloating and left iliac fossa pain. The pain and bloating are made worse by eating and are relieved by defecation. 
a gastroenteritis
b coeliacs
c IBS
d hyperthyroidism
e CD
A

IBS

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69
Q

what is IBD

A

a group of chronic disorders which cause inflammation to the GI tract

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70
Q

def of UC

A

a relapsing and remitting inflammatory disorder of the colonic mucosa

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71
Q

how is UC classified

A

by location

by severity

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72
Q

who does US commonly affect

A

adolescents or young adults

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73
Q

def of CD

A

a chronic inflammatory condition which may affect any part of the GI tract from mouth to anus

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74
Q

who does CD commonly affect

A

bimodal peak of onset
1 adolescents and young adults
elderly

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75
Q

where does UC affect

A

starts distally and spreads proximally (no further than ileocaecal valve)
mucosa and submucosa

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76
Q

where does CD affect

A

any part of the GI tract from mouth to anus

transmural

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77
Q

what sort of inflammation is typical in UC and CD

A

UC - continuous

CD - discontinuous (skip lesions)

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78
Q

what does non-caseating granulomas indicate

A

CD

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79
Q

what are symptoms of UC

A

bloody diarrhoea
tenesmus
diffuse abdomen pain

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80
Q

what are symptoms of CD

A

diarrhoea
steatorhoea (when the ileum is affected)
weight loss and generally more ill than in UC

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81
Q

what is p anca associated with

A

IBD

  • positive in UC
  • negative in CD
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82
Q

what does UC increase risk of

A

PSC
cholangiocarcinoma
colorectal cancer

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83
Q

what are granulomas

A

collections of immune cells which leads to inflammation

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84
Q

what does non-caseating mean

A

no area of central necrosis

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85
Q

what is cobblestone mucosa associated with

A

CD

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86
Q

what is rose thorn appearance associated with

A

UC

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87
Q

what are extra GI features of IBD

A

mouth ulceration
erythema nodusum
pyoderma gangrenosum

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88
Q

what is episcleritis

A

uncomfortable red eye with no loss of vision

associated with IBD

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89
Q

what is scleritis

A

painful red eye with no loss of vision

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90
Q

what is uveitis

A

painful red eye with loss of vision

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91
Q

what is an acute severe UC attack

A

12x a day

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92
Q

how is IBD diagnosed?

A

stool sample

-faecal calprotectin

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93
Q

what is coeliacs disease

A

a chronic autoimmune disease of small intestine which leads to intolerance to dietary gluten
this leads to villous atrophy and malabsorption

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94
Q

who does coeliacs commonly affect

A

infants and middle aged

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95
Q

what are symptoms of coeliacs

A

N+V+D
weight loss
abdominal pain + distension

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96
Q

what are signs of coeliacs

A

aphthous ulcers
angular stomatitis
anaemia with pallor
dermatitis herpetiformis

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97
Q

what causes angular stomatitis

A

B12/iron deficient

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98
Q

what antibodies indicate coeliacs

A

tissue transglutaminase antibodies
anti-endomysial antibody
anti-gliadin

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99
Q

what is found on endoscopy and duodenal biopsy

A

villous atrophy
crypt hyperplasia
intraepithelial WBCs

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100
Q

what is the treament for coeliacs

A

gluten free diet

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101
Q

what is gastroenteritis

A

acute gastrointestinal infection

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102
Q

who is at risk of gastroenteritis

A

young and old

travellers

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103
Q

is bacterial or virla gastroenteritis more common

A

bacterial

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104
Q

what is dysentry

A

bloody diarrhoea

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105
Q

pathology of diarrhoea

A

toxins or bacteria sticking to gut mucosa

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106
Q

pathology of dysentry

A

pathogens penetrate the intestinal mucosa and epithelial cells are destroyed
this leads to bloody diarrhoea and abdominal pain

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107
Q

what pathogen causes diarrhoea and dysentry

A

campylobacter
c. difficile
salmonella

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108
Q

what pathogens cause diarrhoea

A

s aureus
vibrio cholera
e coli
bacillus cereus

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109
Q

what pathogens cause dysentry

A

haemorrhagic e.coli
entamoeba histolytica
shigella

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110
Q

name an antidiarrhoeal

A

codeine phosphate

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111
Q

how is gastroenteritis investigated

A

stool microscopy and culture

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112
Q

how is gastroenteritis treated

A

oral rehydration therapy

antibiotics (if systemically unwell, elderly, suppressed)

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113
Q

what is IBS

A

mixed group of abdominal symptoms with no obvious cause

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114
Q

who does IBS commonly affect

A

women>men

onset in <40yrs

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115
Q

which set of criteria is used to diagnose IBS

A

ROME II/III

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116
Q

what are features of ROME II/III

A 
chronic (>6months) abdo pain:
-relieved by defaecation
-associated with altered stool form or bowel frequency
and 2 of:
-urgency
-tenesmus
-abdo bloating/distension
-mucuous
-symptoms worse after food
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117
Q

how is IBS diagnosed

A

diagnosis of exclusion

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118
Q

what are features of colorectal carcinoma history

A

elderly

‘red flags’

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119
Q

what are features of a pseudomembranous colitis history

A

c diff infection after recent antibiotic treatment

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120
Q

what are infective causes of diarrhoea

A

gastroenteritis

pseudomembranous colitis

121
Q

what are inflammatory causes of diarrhoea

A

IBD

122
Q

what are malignant causes of diarrhoea

A

colorectal carcinoma

123
Q

what are autoimmune causes of diarrhoea

A

coeliacs disease

124
Q

what is used to classify severity of UC

A

Truelove and Witts severity index

125
Q

what are features of a mild UC

A

<4 bowel movements/day
no blood in stools
ESR <30mm/hr

126
Q

what are features of moderate UC

A

4-6 bowel movements/day
minimal blood in stools
ESR <30mm/hr

127
Q

what are features of severe UC

A 
>6 bowel movements/day
with at least one systemic feature:
-obvious blood in stools
-pyrexia
-HR>90bpm
-anaemia
ESR >30mm/hr
128
Q

how is mild and moderate UC flare ups treated with proctitis (inflammation of rectum and anus) or proctosigmoiditis (inflammation of from anus to sigmoid colon)

A

topical 5-ASA
+/- oral 5-ASA

(to induce remission)

129
Q

give an example of a topical ASA

A

mesalazine

130
Q

give an example of a oral ASA

A

sulfasalazine

131
Q

how is mild and moderate UC flare ups treated with left sided and extensive colitis

A

high dose oral 5-ASA
+/- topical 5-ASA
or oral beclomethasone

(to induce remission)

132
Q

what should be given to mild or moderate UC if no improvement

A

oral prednisolone

and if no response to this oral tacrolimus

133
Q

how is severe UC flare ups treated

A

admit
1 IV corticosteroids + IV fluids
2 consider IV ciclosporin or surgery if no improvement or worsening in 72hrs

(to induce remission)

134
Q

how is remission maintained in proctitis (inflammation of anus and rectum) or proctosigmoiditis (inflammation from anus to sigmoid colon)

A

topical or oral 5-ASA

or both

135
Q

how is remission maintained in left sided or extensive colitis

A

oral 5-ASA

136
Q

when should oral azathioprine or oral mercatopurine be considered

A

with exacerbations

137
Q 
1. A 20 year old man presents with diarrhoea. He is passing stool 3 times a day. He is generally well with no fever. After a number of investigations he is diagnosed with Ulcerative Colitis, confined to the rectum. What treatment should be given first?
Oral prednisolone 
IV corticosteroid 
Oral tacrolimus
Topical 5-ASA 
High dose oral 5-ASA
IV ciclosporin
A

Topical 5-ASA

138
Q 
2.  A 20 year old man presents with diarrhoea. He is passing bloody stool 7 times a day. He looks unwell and on examination he is tachycardic and has a fever. After a number of investigations he is diagnosed with Ulcerative Colitis. What treatment should be given first?
Oral prednisolone 
IV corticosteroid 
Oral tacrolimus
Topical 5-ASA
High dose oral 5-ASA
IV ciclosporin
A

IV corticosteroid

139
Q

does smoking make UC or CD better

A

UC better

CD worse

140
Q

what are the medical treaments for inducing remission in active CD

A

1 corticosteroids
2 5-ASA
3 immunosuppressants (azathioprine or mercaptopurine)
4 infliximab or adalimumab (anti-TNF)

141
Q

what is the medical treatment for maintaining remission in CD

A

monotherapy with azathioprine or mercaptopurine

142
Q

5-ASA, steroids, immunosuppressants are for which IBD

A

UC

143
Q

steroids, immunosuppressants, anti-TNF are for which IBD

A

CD

144
Q

what are the two main functions of the liver

A

synthetic function

metabolic function

145
Q

what does the liver synthesise

A

clotting factors

albumin

146
Q

what does the liver metabolise

A

bilirubin
oestrogens
ammonia

147
Q

what happens to the synthetic function of the liver with disease

A

reduced synthesis of:
clotting factors
albumin

148
Q

what is a sign of reduced clotting factor synthesis

A

bruising

149
Q

what are signs of reduced albumin synthesis

A

ascites

leukonychia

150
Q

what happens to the metabolic function of the liver with disease

A

reduced breakdown, so increased:
bilirubin
oesotrogen
ammonia

151
Q

what is a sign of increased bilirubin levels

A

jaundice

152
Q

what are signs of increased oestrogen levels

A

palmar erythrema
spider naevae
gynaecomastia

153
Q

what are signs of increased ammonia

A

confusion

asterixis

154
Q

what are true measures of liver function

A

bilirubin
albumin
INR (clotting factors or PTT)

155
Q

what are markers of acute liver injury

A

ALT
AST
ALP
GGT

156
Q

A 19-year-old male is admitted following an alcohol binge. His friends report he has vomited several times and fell over. You notice some bruises on his hands.

Which of the following is likely to be most elevated?

AST
ALT
GGT
ALP
All of the above
A

GGT

raised GGT in isolation is common after recent alcohol consumption

157
Q

A 42-year-old female is admitted with severe RUQ pain that is worse on eating fatty foods. After obtaining her LFTs, you notice a remarkably high ALP.

What is the most likely diagnosis?

Viral hepatitis
Alcoholic hepatitis
Short-term alcohol abuse
Biliary tract obstruction
Gilbert’s syndrome
A

Biliary tract obstruction

158
Q

A 45-year-old chronic alcoholic presents with jaundice, bruising and abdominal pain. His stools and urine are of normal colour. His bilirubin and AST are raised.

What other marker is likely to be abnormal?

ALT
Albumin
ALP
Haemoglobin
GGT
A

ALT

159
Q

what does a AST:ALT ratio of >2.5:1 indicate

A

alcoholic liver disease

160
Q

what does a AST:ALT ration of <1:1 indicate

A

viral hepatitis

161
Q

what causes a rise in ALP

A

BLIP

Bone
Liver
Intestines
Placenta

162
Q

what are the important markers of liver injury

A

AST

ALT

163
Q

what are the important markers of biliary duct injury

A

ALP

GGT

164
Q

what does an isolated GGT indicate

A

acute alcohol intake

165
Q

A 38-year old woman presents with vague, colicky right-sided abdominal pain. She reports it is got worse 6 hours ago after eating an Indian take-out. On examination her sclera appear icteric, and her abdomen is soft and non-tender. Select the investigation needed to confirm her diagnosis:

Liver function tests
Ultrasound of the biliary tree
Split bilirubin ratio
ERCP
Liver biopsy
A

Ultrasound of the biliary tree

166
Q

While waiting for her cholecystectomy, the same woman falls more unwell. She feels feverish, has vomited twice and reports that the pain initially felt colicky, but now is constant in her RUQ. She also feels dull pain in her right shoulder. On examination, she displays rebound tenderness in her RUQ and a positive Murphy’s sign. Select the likely diagnosis:

Biliary colic
Primary Biliary Cholangitis
Ascending Cholangitis
Acute Cholecystitis
Cholangiocarcinoma
A

Acute Cholecystitis

167
Q

A 48-year old obese man presents to A&E in agony. He is shivering visibly, clutching his right upper quadrant. You notice his hands are yellow and there are excoriations on his arms. His bloods show a raised white cell count and CRP. Select the likely diagnosis:

Biliary colic
Primary Sclerosing Cholangitis
Primary Biliary Cholangitis
Viral hepatitis
Ascending Cholangitis
A

Ascending Cholangitis

168
Q

2 hours later, the same man has deteriorated whilst waiting for a hospital bed. His BP is 87/45, HR is 128 and RR is 35. He is drowsy, responding only to pain. Select the likely cause of shock:

Septic shock
Hypovolaemic shock due to low albumin
Neurogenic shock
Hypovolaemic shock due to blood loss
Cardiogenic shock
A

Septic shock

169
Q

what are risk factors for gallstones

A 
4Fs
Fat
Female
Fertile
Forty
170
Q

what is a classical presentation of gallstones

A

colicky RUQ pain

worse on eating fatty foods

171
Q

what investigation is gold standard for gallstones

A

USS of biliary tree

172
Q

what would you see on LFTs with a gallstone

A

a raised ALP (and GGT)

173
Q

why are women more prone to gallstones

A

increased oestogen causes an increase in the cholesterol content of the bile, this makes cholesterol gallstone formation much more likely

174
Q

what sort of gallstones show up on AXR

A

calcium bilirubinate

175
Q

what is the management for a gallstone in the gallbladder

A

cholecystectomy

176
Q

what is the management for a gallstone in the common bile duct

A

cholecystectomy

bile duct clearance

177
Q

how is bile duct clearance completed

A

ERCP

US lithotripsy

178
Q

what can a gallstone in the common bile duct progess into

A

a gallstone in the common bile duct leads to bile stasis
bacteria from the gut can move into the bile ducts
this is ascending cholangitis

179
Q

what can a gallstone in the gallbladder or cystic duct progress into

A

a combination of bile stasis, inflammation and bacterial infection can lead to acute cholecystitis

180
Q

how does acute cholecystitis present

A

constant RUQ pain which radiates to the R shoulder and scapula
associated with fever, N+V

181
Q

what sign is indicative of acute cholecystitis

A

murphys sign

182
Q

what would be found O/E of acute cholecystitis

A

jaundice (if CBD stone)
rebound tenderness
murphys sign

183
Q

what investigations would be used to diagnose acute cholecystitis

A

FBC (raised WCCs)
LFTs (raised ALP + GGT)
imaging (USS, CT/MRI)

184
Q

what is the management for acute cholecystitis

A

cholecystectomy <1wk

185
Q

what is charcots triad associated with

A

ascending cholangitis

186
Q

what is ascending cholangitis

A

bacterial infection of the biliary tract due to obstruction

187
Q

what is charcots triad

A

RUQ pain
jaundice
fevers

188
Q

how does a gallstone in the biliary tract lead to bacterial infection

A

bile stasis (reduced bile out of the common bile duct) therefore bacterial from the duodenum ascends the biliary tract and causes infection

189
Q

what does reynolds pentad indicate

A

acute suppurative cholangitis (more severe ascending cholangitis)
which is pus in the biliary ducts

190
Q

what is reynolds pentad

A 
RUQ pain
jaundice
fevers
hypotension
confusion
191
Q

how does ascending cholangitis become acute suppurative cholangitis

A

bacteria enters the bloodstream

192
Q

what are the 2 main forms of autoimmune biliary disease

A

PBC

PSC

193
Q

what antibody is classic of PBC

A

AMA

194
Q

what antibody is classic of PSC

A

pANCA

195
Q

why is primary biliary cholangitis also called primary biliary cirrhosis

A

autoimmune damage to small bile ducts leads to intrahepatic cholestasis
stasis of bile leads to liver damage

196
Q

how is PBC diagnosed

A

biopsy

197
Q

how is PSC diagnosed

A

ERCP

198
Q

what is PBC associated with

A

RA
thyroid disease
sjogrens

199
Q

what is PSC associated with

A

UC

200
Q

what is the pathology of PBC

A

autoimmune damage to small bile ducts which leads to intrahepatic cholestasis

201
Q

what is the pathology of PSC

A

autoimmune damage to intra and extrahepatic bile ducts which causes inflammation, scarring and narrowing

202
Q

A 53-year old man staggers into A&E having vomited 6 times in 2 hours. He is intoxicated and jaundiced. His friend said his vomit was initially “normal”, but after the first couple of episodes has had fresh blood in it. What is the likely diagnosis?

Ruptured oesophageal varices
Mallory-Weiss tear
Ruptured peptic ulcer
Boerhaave syndrome
Oesophagitis
A

Mallory-Weiss tear

203
Q

what is a mallory-weiss tear

A

tear in the mucosal layer of the oesphagus

204
Q

what is associated with a mallory-weiss tear

A

common after many episodes of severe vomiting

vomiting always precedes bleeding

205
Q

what does the blood look like in mallory-weiss tear

A

blood is streaked in vomit

206
Q

where does the tear occur in MW

A

gastro-oesophageal junction

207
Q

how quickly does a MW tear resolve

A

1-2days

208
Q

what is boerhaaves syndromes

A

more severe MWT

complete rupture of oesphageal wall

209
Q

how is boerhaaves syndrome diagnosed

A

CXR and CT scan

-pneumediastinum

210
Q

what are the 2 main causes of oesophageal varices

A

liver cirrhosis

chronic alcohol use

211
Q

how does liver cirrhosis cause oesophageal varices

A

1 decreased clotting factors which increases bleeding risk

2 increased extrahepatic blood shunting which leads to portal HTN

212
Q

how does chronic alcohol use lead to oesophageal varices

A

oesophageal irritation

213
Q

how does oesophageal varices present

A

PMH of liver cirrhosis +/ chronic alcohol use

large volume of fresh blood

214
Q

what investigations can confirm oesophageal varices

A

FBC (macrocytic anaemia)
LFTs (raised GGT from alcohol, low albumin from cirrhosis)
UEs (raised urea)

215
Q

how is oesophageal varices managed

A

ABCDEFG
IV fluids and reduce portal HTN
endoscopy (band ligation is first line)

216
Q

what is used to reduced portal HTN

A

terlipressin

217
Q

what is the first line management of oesophageal varices

A

band ligation

218
Q

how does ruptured peptic ulcer present

A

PMH of PUD, NSAID use, H.pylori

a “coffee ground” vomit +/ meleana

219
Q

what investigations confirm ruptured peptic ulcer

A

decreased BP

220
Q

management of ruptured peptic ulcer

A

1 endoscopy
-IM adrenaline at site of ulcer
2 omeprazole
3 triple therapy (with H.pylori)

221
Q

A 76-year old retired greengrocer visits her GP with difficulty swallowing solids. She says this has been getting progressively worse over 1 month. There is no coughing, choking or heartburn. She reports food getting “stuck” 2-3 seconds after swallowing. She attributes her weight loss to not eating properly, and also thinks this has caused loose, brown-black stools. Bloods show a microcytic anaemia. Select the likely diagnosis:

Stroke
Oesophageal cancer
Pharyngeal pouch
Plummer-Vinson syndrome
Benign stricture
A

Oesophageal cancer

222
Q

what is plummer-vinson syndrome

A

rare disease characterized by difficulty in swallowing, iron deficiency anemia, glossitis, cheilosis and esophageal webs

223
Q

A 27-year old lawyer presents with a 2-year history of mild dysphagia to both solids and liquids. She has no weight loss. She has symptoms of heartburn and nocturnal cough, but PPIs and bronchodilators haven’t helped. She is systemically well, and her examination is unremarkable. A “bird’s beak” appearance is noted on barium swallow. Select the diagnosis:

Achalasia
Benign stricture
Plummer-Vinson syndrome
Oesophageal spasm
Stroke
A

Achalasia

224
Q

A 45-year old man presents with a 6-week history of dysphagia. This is associated with pain in his fingers, with him noting that he sees the colour vary from red, to white, to blue. He also has several red, vascular marks on his face. Select the diagnosis:

Plummer-Vinson syndrome
Ortner’s syndrome
Pharyngeal pouch
Limited cutaneous scleroderma
Oesophageal spasm
A

Limited cutaneous scleroderma

225
Q

what are functional causes of high dysphagia

A

stroke

parkinsons

226
Q

what are functional causes of low dysphagia

A

achalasia
oesophageal spasm
CREST

227
Q

what are structural causes of high dysphagia

A

pharyngeal pouch

228
Q

what are structural causes of low dysphagia

A

cancer
benign stricture
plummer vinson
ortners syndrome

229
Q

when is a barium swallow indicated

A

high (functional or structural) or low dysphagia (achalasia)

230
Q

when is endoscopy indicated

A

first line for low dysphagia

231
Q

when is videofluoroscopy indicated

A

functional high dysphagia

232
Q

when is manometry indicated

A

differentiate between motility disorders

233
Q

what cancer commonly occurs in the middle third of the oesphagus

A

squamous cell carcinoma

234
Q

what cancer commonly occurs in the lower third of the oesophagus

A

adenocarcinoma

GORD to oesophagitis to barretts (metaplasia) to adeoncarcinoma (dysplasia

235
Q

how does achalasia lead to dysphagia

A

absence of ganglion cells in the myenteric plexus (auerbachs plexus)
this causes a failure of relaxation fo the LOS and aperistalsis

236
Q

what sort of dysphagia is oesophageal cancer and achalasia

A

oesophageal cancer is structural dysphagia

achalasia is functional dysphagia

237
Q

who does oesophageal cancer commonly affect

A

elderly

238
Q

who does achalasia commonly affect

A

young people

239
Q

what investigations are used for oesophageal cancer

A

OGD

240
Q

what investigations are used for achalasia

A 
barium swallow (birds beak)
manometry
241
Q

what causes neurological dysphagia

A

stroke

parkinsons

242
Q

what symptoms are present with neurological dysphagia

A

coughing immediately on swallowing

choking which implies a problem with the swallowing process

243
Q

what are features of pharyngeal pouch

A

coughing up food
halitosis (bad breath)
gurgling/dysphonia

244
Q

what are features of plummer-vinson syndrome

A

iron deficiency anaemia (signs of severe IDA such as cheilosis, atrophic glossitiis, koilonychia)
oesophageal webs
dysphagia

245
Q

what are features of limited cutaneous scleroderma

A 
CREST
1 calcinosis
2 raynauds
3 esophageal dysmotility
4 sclerodactyly
5 telangiectasia
246
Q

what antibodies are associated with limited cutaneous scleroderma

A

ANA and anti-centromere

247
Q

what is calcinosis

A

calcium deposits on the skin

248
Q

what is sclerodactyly

A

abnormal build up of fibrous tissue in the skin can cause the skin to tighten so severely that the fingers curl and lose their mobility

249
Q 
A 32 year old woman returns from a holiday in India. She started getting diarrhoea after eating at a seafood restaurant on the last night. She is feverish, nauseous and is sore all over. The whites of her eyes are yellow. 
Hepatitis A 
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
A

Hepatitis A

250
Q 
A 29 y/o male comes to the GP with fever, fatigue, joint pain and urticaria-like skin rash. He had unprotected anal sex a month ago. He comes back a week later for a blood test, which shows raised ALT and AST. Now, he complains of feeling sick, RUQ pain and looks a bit yellow. 
Hepatitis A 
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
A

Hepatitis B

251
Q 
A 67 year old man is investigated under the two-week wait for jaundice, tender hepatomegaly, ascites and anorexia. His blood tests show a raised aFP. He mentions that he was diagnosed with hepatitis years ago. What virus(es) are likely? 
Hepatitis A 
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
A

Hepatitis B + C

252
Q 
Which hepatitis virus requires another virus to be present for it to successfully infect?
Hepatitis A 
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
A

Hepatitis D

253
Q

what is the triad of symptoms which applies to all hepatitis

A

1 fever
2 jaundice
3 raised ALT and AST

254
Q

what are faeco-oral hepatitis’

A

Hepatitis A + E

“the vowels which hit your bowels”

255
Q

what are features of hepatitis A

A

Asymptomatic (usually)

Acute

256
Q

what are features of hepatitis E

A

Enteric
Epidemics (water)
Expectant mothers

257
Q

how is hepatitis A spread

A

when faecal matter containing viral hep A is ingested

258
Q

what is a characteristic history of hepatitis B

A 
prodromal symptoms
-non-specific flu like symptoms
-rash
-lymphadenopathy
followed by symptoms of acute infection
-RUQ pain
-N+loss of appetite
-jaundice
259
Q

what is the prognosis of hep B

A

majority recovery

few develop chronic infection

260
Q

what is the management for acute hep B

A

supportive

261
Q

what is the management for chronic hep B

A

peginterferon alpha or tonofovir

262
Q

what is the most common risk factor for developing hepatocellular carcinoma

A

hepatitis

263
Q

how does hep B increase risk of hepatocellular carcinoma

A

virus integrates into host chromosome

acts as an oncogene

264
Q

how does hep C increase risk of hepatocellular carcinoma

A

causes chronic inflammation

mutations accumulate

265
Q

what hepatitis must be present for hepatitis D to occur

A

hepatitis B

266
Q

why does hepatitis D require hepatitis B

A

hepatitis D enters hepatocytes via hep B surface antigens

267
Q 
A 41 year old man is brought into A&amp;E by police after being found wandering the streets seemingly confused. He is completely disorientated and is unable to give a history. As part of your neurological assessment, you examine his eyes and notice the following:  Which of the following is characteristic of this patient’s condition:
A) High serum caeruloplasmin
B) Low serum copper
C) High serum iron
D) Low total iron binding capacity
E) Low transferrin saturation
A

B) Low serum copper

268
Q 
A 56-year-old man, diagnosed with emphysema, presents with a one-month history of jaundice and ascites.  Your registrar tells you that the man has had breathing problems for the majority of his life. 
What is the most likely diagnosis 
Sickle Cell Disease
COPD 
Epstein-Barr Virus 
Idiopathic Pulmonary Fibrosis 
Alpha-1 Antitrypsin Deficiency
A

Alpha-1 Antitrypsin Deficiency

269
Q

why is there a low serum copper in wilsons diseases

A

copper incorporation into caeruloplasmin in hepatocytes and its excretion in bile is impaired
therefore copper is deposited

270
Q

where is copper deposited in wilsons disease

A

firstly liver
then basal ganglia
eyes

271
Q

what sort of genetic disorder is wilsons disease

A

autosomal recessive

272
Q

what does wilsons disease present with

A

1 ataxia
2 tremor
3 dysarthria

273
Q

what is seen in the eyes of wilsons disease patients

A

kayser fleischer rings

274
Q

what sort of genetic disorder is alpha-1 anti-trypsin deficiency

A

autosomal recessive

275
Q

what is the pathology of A1AT deficiency

A

A1AT is genetically mutated leading to it being prevented from release from hepatocytes
this causes a loss of its protective function in the lungs against elastase, leading to emphysema occurs and a build up in the liver leading to destruction an liver disease

276
Q

how does A1AT deficiency normally present

A

emphysema in a young non-smoker with late onset liver signs

277
Q

what are the stages of liver failure

A

1 healthy
2 fatty liver
3 liver fibrosis
4 cirrhosis

278
Q 
A 63-year-old woman stumbles into A+E. She looks unwell with a flushed face. An F1 mentions that when she presented last week, examination of her upper limbs suggested a sensory polyneuropathy. 
Cytomegalovirus 
Primary Biliary Cirrhosis 
Paracetomal Overdose
Alcoholic Liver Disease 
Primary Sclerosis Cholangitis
A

Alcoholic Liver Disease

279
Q 
A 65 year old presents with suspected liver failure.  Which of the following tests would NOT be included in a liver screen for liver failure 
Alpha-1 Antitrypsin 
Caeruloplasmin
HIV Screen
Anti-GBM Antibody 
Aspartate Aminotransferase
A

Anti-GBM Antibody

280
Q

A 56-year-old man with a long history of alcohol abuse presents to the emergency department with abdominal pain. On examination he has a distended abdomen with shifting dullness and has a temperature of 38.2°C.
What is the most likely diagnosis?
A Bowel obstruction
B Liver cirrhosis
C Mallory–Weiss syndrome
D Perforated peptic ulcer
E Spontaneous bacterial peritonitis (SBP)

A

E Spontaneous bacterial peritonitis (SBP)

281
Q 
A 66-year-old man presents to his GP with increasing weight loss, lethargy and fever over the last 3 months. He has also noticed pale stools and dark urine.
Crigler-Najjar Syndrome
Gilberts Syndrome 
Opiate Overdose
Pancreatic Carcinoma
Haemolysis
A

Pancreatic Carcinoma

282
Q 
A 50-year-old man comes to you because he is worried about his skin which occasionally turns yellow. On further questioning you notice that these episodes are particularly bad during periods of stress or illness. He is otherwise well.
Gilbert’s Syndrome 
Hepatic Metastases 
Megaloblastic Anaemia 
Hepatitis A 
Dubin-Johnson Syndrome
A

Gilbert’s Syndrome

283
Q

how is conjugated bilirubin formed

A

haem is converted to unconjugated bilirubin which is then converted to conjugated bilirubin in the liver by UDP glucuronyltransferase

284
Q

how is bilirubin excreted

A

as urobilinogen in the urine

as stercobilin in the stools

285
Q

how does bilirubin cause the yellow colour in our urine

A

bilirubin is converted to urobilinogen which is converted to urobilin giving the distinct yellow colour

286
Q

how does bilirubin cause the brown colour in our stool

A

bilirubin is converted to stercobilin

287
Q

what causes jaundice

A

excess bilirubin

288
Q

what are the causes of jaundice split up into

A

pre-hepatic
hepatic
post-hepatic

289
Q

aetiology of pre-hepatic jaundice

A

dysfunctional transport from spleen to liver

290
Q

what sort of bilirubin is increased in pre-hepatic jaundice

A

unconjugated

291
Q

what are causes of pre-hepatic jaundice

A 
1 haemolysis (low Hb, malaria, haemolytic anaemias)
2 inherited disorders of bilirubin metabolism (gilberts)
292
Q

aetiology of hepatic jaundice

A

dysfunctional hepatocytes

abnormal conjugation/excretion

293
Q

what sort of bilirubin is increased in hepatic jaundice

A

conjugated or unconjugated

294
Q

what are causes of hepatic jaundice

A

VADAM

Viruses - hep A/B/C/E, EBV, CMV
Alcohol
Drugs - paracetomal, isoniazid, rifampicin
Autoimmune - PBC PSC
Metabolic
295
Q

aetiology of post-hepatic jaundice

A

obstructive jaundice

296
Q

what sort of bilirubin is increased in post-hepatic jaundice

A

conjugated bilirubin

297
Q

why is there dark urine and pale stools in obstructive jaundice

A

flow of bilirubin into GI tract is blocked
1 bilirubin is forced into renal system where it is converted to urobilinogen and from there to urobilin (yellow) which in excess causes dark urine
2 less bilirubin in the GI system means less stercobiln (brown) so pale stools

298
Q

what are causes of obstructive jaundice

A

1 stones in common bile duct (biliary colic)
2 carcinoma at head of pancreas
3 stricture

Gastrointestinal (62 decks)

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