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Gastroentrology > 2: GORD, Barrats Oesophagus, Oesophageal Carcinoma, Achalasia, Plummer-Vinson > Flashcards

2: GORD, Barrats Oesophagus, Oesophageal Carcinoma, Achalasia, Plummer-Vinson Flashcards

1
Q

Define gastroesophageal reflux

A

reflux of gastric acid from the stomach into the oesophagus

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2
Q

Define GORD

A

when reflux of gastric acid into the oesophagus causes symptoms

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3
Q

How does the incidence of GORD change with age

A

increases with age

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4
Q

In which gender is GORD more common

A

males (2:1)

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5
Q

What are the four mechanisms contributing to GORD

A
  • Reduced LOS tone
  • Gastric acid hypersecretion
  • Dysmotility
  • Delayed gastric emptying
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6
Q

What factors increasing intra-abdominal pressure may contribute to GORD

A

Obesity

Pregnancy

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7
Q

What factors lowering oesophageal sphincter tone may contribute to GORD

A

Alcohol
Caffeine
Smoking
Medications: TCA, anticholinergics

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8
Q

What are two other factors that are thought to contribute to GORD

A
  • Stress

- Hiatus hernia

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9
Q

Give 5 symptoms of GORD

A
  • Retrosternal chest pain worse following meals and on lying down
  • Water-brashing
  • Odynophagia
  • Belching
  • Nocturnal cough
  • Asthma
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10
Q

In investigating for GORD: if an individual is over 55 or has ALARM symptoms what should be done

A
  • Upper GI endoscopy
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11
Q

What are the ALARMS symptoms

A 
Anaemia 
Loss of weight 
Anorexia 
Recent change in Sx
Melena/haematemesis 
Swallowing difficultly
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12
Q

Over what age with GORD are patients offered an upper GI endoscopy immediately

A

55 years

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13
Q

If patients are not over 55 and have no ALARMS symptoms how should they be immediately managed

A
  • Lifestyle Changes
  • Medication review
  • OTC Antacids
  • Review in 4W
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14
Q

What antacids are offered

A

Magnesium Tricillate

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15
Q

If individuals improve on: medication review, lifestyle changes, OTC antacid what is the next step

A

No further intervention

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16
Q

If individuals do not improve on: medication review, lifestyle changes, OTC antacid what is the next step

A

Test for H.Pylori

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17
Q

If H.pylori test is negative what is offered

A

Trial or H2 antagonist (ranitidine) or PPIs for 4W

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18
Q

If individuals do not improve on ranitidine or H2 blocker what is done

A

Continue on low-dose treatment and offer upper GI endoscopy

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19
Q

If individuals test positive for H.pylori what should be done

A

H.pylori treatment and review in 4W

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20
Q

After 4W of H.pylori treatment what is performed to check it is eradicated

A

Urea breath test

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21
Q

What is the gold-standard investigation for GORD

A

24h pH monitoring

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22
Q

When is 24h pH monitoring for GORD indicated

A

considering surgical intervention

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23
Q

What is 24h pH monitoring often performed with and why

A

oesophageal manometry to exclude oesophageal dysmotility

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24
Q

What are 5 pieces of lifestyle advice for someone with GORD

A
  1. Weight Loss
  2. Smoking Cessation
  3. Small regular meals
  4. Reduce alcohol
  5. Reduce hot drinks
  6. Reduce citrus, tomatoes, fizzy drinks, spicy food, caffeine
  7. Avoid over-eating 3h before bed
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25
Q

What is first-line medical therapy for someone with GORD

A

Antacids - magnesium trisillicate. Alginates - gaviscon

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26
Q

What are there 3 indications for surgical management of GORD

A
  1. Poor response to medical therapy
  2. Complication of GORD
  3. Patient request - does not want to take long-term meds
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27
Q

What is the main surgical method for managing GORD

A

Fundoplication

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28
Q

What is Nissen’s fundoplication

A

The fundus of the stomach is wrapped around the LOS posteriorly 360’

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29
Q

If GORD is prolonged what 4 complications may it lead to

A
  1. Oesophagitis
  2. Barret’s oesophagus
  3. Oesophageal stricture
  4. Anaemia
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30
Q

What is the most serious risk associated with GORD

A

Metaplasia-dysplasia sequence

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31
Q

Explain metaplasia-dysplasia sequence of GORD

A
  • Chronic inflammation of the oesophagus can cause metaplasia of oesophageal squamous epithelium to columnar epithelium. This is called Barret’s oesophagus
  • 0.1-0.4% of Barrett’s oesophagus transforms to oesophageal carcinoma
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32
Q

What is Barret’s oesophagus

A

Metaplasia of squamous epithelium in the oesophagus to simple columnar epithelium

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33
Q

What causes barrett’s oesophagus

A

Chronic GORD

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34
Q

Which gender is Barrett’s oesophagus more common

A

Male (7:1)

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35
Q

Which ethnicity is Barrett’s more common

A

Caucascian

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36
Q

Which age group is Barrett’s seen in

A

> 50’s

37
Q

What are 4 risk factors for Barrett’s oesophagus

A

Smoking
FH
Obesity
Hiatus Hernia

38
Q

Explain association between alcohol GORD, Barret’s and oesophageal carcinoma

A

Alcohol is a risk factor for both GORD and Oeseophageal carcinoma. It is not a risk factor for Barrett’s

39
Q

How will Barrett’s oesophagus present clinically

A

Prolonged symptoms of GORD

40
Q

What histological change occurs in Barrett’s oesophagus

A

Squamous epithelium to simple columnar epithelium

41
Q

What is first-line investigation for Barrett’s oesophagus

A

OGD and biopsy

42
Q

How will Barrett’s oesophagus present on OGD

A

The distal oesophagus opposed to appearing white, will appear red

43
Q

What is required to make a diagnosis of Barrett’s oesophagus

A

Biopsy

44
Q

What classification system is used to determine length of Barrett’s

A

Prague’s classification

45
Q

What medication should all patients with Barret’s oesophagus be started on

A

PPI

46
Q

What is the mainstay management of Barret’s oeseophagus and why

A

Frequent surveillance OGDs due to risk of oesophageal carcinoma

47
Q

If individual on biopsy has no dysplasia, how often should they receive an OGD for Barrett’s oesophagus

A

2-5 years

48
Q

If individual on biopsy has low-grade dysplasia, how often should they receive an OGD for Barrett’s oesophagus

A

every 6 months

49
Q

If low-grade dysplastic barret’s oesophagus is flat how is it managed

A

endoscopic radio frequency ablation (ERA)

50
Q

If low-grade dysplastic barret’s oesophagus is nodular how is it managed

A

endoscopic mucosal resection (EMR)

51
Q

how frequent should high-grade dysplastic barret’ s oeseophagus receive OGD

A

every 3 months

52
Q

if high-grade barret’s oesophagus is flat how is it managed

A

endoscopic radio frequency ablation (ERA)

53
Q

if high-grade barret’s oesophagus is nodular how is it managed

A

endoscopic mucosal resection (EMR)

54
Q

what is the definitive treatment for high-grade barrett’s

A

oeseophagectomy

55
Q

what is the main risk with barret’s oesophagus

A

0.1-0.4% transform to oesophageal adenocarcinoma

56
Q

what are the two types of oeseophageal carcinoma

A

Squamous cell carcinoma

57
Q

which anatomical part of the oesophagus does oesophageal SCC occur

A

Upper 1/3

58
Q

which anatomical part of the oesophagus does oesophageal adenocarcinoma occur

A

Lower 1/3

59
Q

in which country is SCC more common

A

Developing

60
Q

in which country are adenocarcinomas more common

A

Developed countries

61
Q

how do majority of oesophageal adenocarcinomas form

A

Dysplasia-Metaplasia sequence

62
Q

what are 5 risk factors for oesophageal squamous cell carcinoma

A
  • Achalasia
  • Vitamin A deficiency
  • Smoking
  • Alcohol
  • IDA
63
Q

What are 6 risk factors for oeseophageal adenocarcinoma

A
  • Smoking
  • Alcohol
  • GORD/Barret’s
  • Achalasia
  • Plummer-Vinson
  • Obesity
64
Q

What is plummer-vinson syndrome

A

Individual forms webs in the oeseophagus which causes dysphagia

65
Q

What is the most common symptom of oesophageal carcinoma

A

Dysphagia - usually solids then liquids.

66
Q

what are 3 other symptoms of oesophageal cancer

A

Weight Loss
Vomiting
Melena
Anorexia

67
Q

what is first-line investigation for individuals with suspected oesophageal cancer

A

OGD

68
Q

if oesophageal cancer what is used to look for metastses

A

CT-CAP

69
Q

if no metastses are found on CT-CAP investigation is used and why

A

Endoscopic US - able to look for local metastses and assess tumour depth (T)

70
Q

What investigation may also be offered for junctional oesophageal carcinomas

A

Laparoscopy to look for metastses

71
Q

if no metastses found on laparoscopy what investigation is used for oesophageal cancer

A

PET-CT

72
Q

outline investigations for oesophageal cancer

A
  1. OGD in 2W
  2. CT CAP: to stage
  3. Endoscopic US: assess tumour depth and local metastses
  4. Laproscopy for junctional tumours
  5. PET-CT if laparoscopy negative
73
Q

how are 70% of patients with oesophageal cancer managed and why

A

Palliative due to patient’s presenting at advanced stages

74
Q

how are oesophageal SCC managed

A

Chemoradiotherapy

75
Q

how are oesophageal adenocarcinomas managed

A

Oeseophagectomy with Neo-adjuvant CRT

76
Q

how are oesophageal carcinoma patients palliatid

A
  • Oesophageal stenting
  • Chemoradio to reduce size
  • Gastrotomy to bypass obstruction
  • Nutritional support- thickened fluids
77
Q

why is overall prognosis of oesophageal adenocarcinoma poor

A

Due to patients presenting late

78
Q

what is overall survival rate of oesophageal adenocarcinoma

A

5-10%

79
Q

Define achalasia

A

Disrupted oesophageal peristalsis and failure of LOS to relax due to absence of ganglia in auerbachs plexus

80
Q

Which age-group is achalasia more common

A

Middle-age

81
Q

Which gender is achalasia more common

A

Male and Females

82
Q

How will achalasia present clinically

A
  • Dysphagia of both solids and liquids

- Regurgitation of food could lead to cough and aspiration pneumonia

83
Q

What is first line investigation of achalasia

A

Manometry

84
Q

What will be seen on mamometry in achalasia

A

Increase LOS tone

85
Q

what will be seen on barium swallow in achalasia

A

Dilation of the oesophagus with a fluid-level giving a ‘birds-beak appearance’

86
Q

what will be seen on CXR in achalasia

A

Widened mediastinum with fluid-level

87
Q

how may achalasia be managed

A
  • intersphenteric botox injections
  • heller cardiomyopathy
  • pneumatic balloon dilation
88
Q

what is Plummer Vinson syndrome

A

Rare disease characterised by formation of oesophageal webs that lead to dysphagia

89
Q

What is the triad of symptoms in Plummer Vinson syndrome

A
  1. Dysphagia
  2. IDA
  3. Glossitis

Gastroentrology (18 decks)

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