Barretts oesophagus Flashcards

(77 cards)

1
Q

What is Barrett’s oesophagus?

A

Condition where metaplastic columnar epithelium replacing the normal stratified squamous epithelium of the distal oesophagus

Develops in response to chronic exposure to gastro-oesophageal reflux and predisposes to adenocarcinoma of the oesophagus.

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2
Q

What are the types of metaplastic columnar epithelium in Barrett’s oesophagus?

A
  • Gastric-fundic type
  • Cardiac type
  • Intestinal type

Australian guidelines require the presence of intestinal type metaplasia for the diagnosis of BE.

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3
Q

What does SIM stand for in the context of Barrett’s oesophagus?

A

Specialised Intestinal Metaplasia

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4
Q

What is the global prevalence of Barrett’s oesophagus?

A

Globally prevalence low (<5%)

Higher in select groups such as those with GORD (>15%).

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5
Q

How does ethnicity affect the prevalence of Barrett’s oesophagus?

A

Prevalence varies by ethnicity, with <1% in the Asian population.

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6
Q

Which gender is more commonly affected by Barrett’s oesophagus?

A

More common in males

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7
Q

What was the prevalence of Barrett’s oesophagus in the Swedish study of 3000 people?

A

1.6% despite GORD rate of 40% and 15% with oesophagitis.

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8
Q

What percentage of people with Barrett’s oesophagus had no reflux symptoms in the preceding 3 months in the Swedish study?

A

44%

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9
Q

What percentage of people with reflux had Barrett’s oesophagus according to the Swedish study?

A

2.3%

Not statistically different from baseline rate.

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10
Q

True or False: Other studies have shown increased prevalence of Barrett’s oesophagus with a history of reflux.

A

True

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11
Q

What are the non-modifiable risk factors for Barrett’s?

A

Age, Male Sex, Family hx

Family hx refers to family history of Barrett’s or related conditions.

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12
Q

List the modifiable risk factors for Barrett’s.

A

GORD, Central Obesity, Smoking

GORD stands for Gastroesophageal Reflux Disease.

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13
Q

True or False: Smoking is a non-modifiable risk factor for Barrett’s.

A

False

Smoking is classified as a modifiable risk factor.

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14
Q

Fill in the blank: _______ is a modifiable risk factor for Barrett’s associated with weight distribution.

A

Central Obesity

Central obesity refers to excess fat around the stomach area.

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15
Q

Which gender is identified as a non-modifiable risk factor for Barrett’s?

A

Male Sex

Males are at a higher risk for developing Barrett’s compared to females.

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16
Q

What are the major non-modifiable risk factors for Barrett’s oesophagus?

A

Age, Male Sex, Family hx

Family hx refers to family history of related conditions.

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17
Q

What are the major modifiable risk factors for Barrett’s oesophagus?

A

GORD, Central Obesity, Smoking

GORD stands for gastro-oesophageal reflux disease.

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18
Q

What is the potential protective effect of past infection with H. pylori?

A

Atrophic gastritis causes reduction in acid production and reduced acid exposure.

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19
Q

Is there evidence that alcohol or dietary factors influence the risk of Barrett’s oesophagus?

A

No evidence.

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20
Q

What pathological change occurs in Barrett’s oesophagus due to chronic exposure to reflux?

A

Metaplasia occurs as a maladaptive response to inflammation from chronic reflux oesophagitis.

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21
Q

What is the reason for reflux in Barrett’s oesophagus?

A

Loss of mechanisms that prevent reflux.

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22
Q

How is mucosal damage from reflux typically repaired in most patients?

A

By regeneration of more squamous cells.

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23
Q

What replaces squamous cells in some patients with Barrett’s oesophagus?

A

Metaplastic columnar cells.

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24
Q

What predisposes Barrett’s patients to develop adenocarcinoma?

A

Accumulation of genetic mutations leading to progressive dysplastic changes.

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25
Does Barrett's oesophagus cause any symptoms?
No symptoms.
26
With which condition is Barrett's oesophagus commonly associated?
GORD - heartburn and regurgitation.
27
What complications can arise from Barrett's oesophagus?
Bleeding from erosions, dysphagia from strictures.
28
How does Barrett’s oesophagus appear endoscopically?
As salmon pink mucosa extending above the GOJ into the tubular oesophagus.
29
What classification is used to describe Barrett’s oesophagus?
Prague Classification C&M criteria.
30
In the Prague Classification, what does 'C' stand for?
Maximum extent of circumferential disease.
31
In the Prague Classification, what does 'M' stand for?
Maximum proximal extent.
32
What defines a short segment of Barrett's oesophagus?
Short Segment >3cm.
33
What defines a long segment of Barrett's oesophagus?
Long Segment <3cm.
34
When should Barrett's be suspected?
When Z-line is more than >1cm proximal to OGJ and has a salmon pink color with a velvet-like texture compared to squamous epithelium's pale, glossy appearance ## Footnote The Z-line is the junction between the squamous epithelium and columnar epithelium of the esophagus.
35
What criteria are used to assess the extent of Barrett's?
Prague C & M criteria ## Footnote The GOJ is the key anatomical landmark defined as the proximal extent of gastric folds.
36
What defines the short segment vs long segment of Barrett's?
Short segment: less than or equal to 3cm; Long segment: greater than 3cm ## Footnote If the Z-line is <1cm with non-circumferential tongues, it's called an irregular Z-line.
37
What is the Seattle Protocol for biopsy in Barrett's?
4 quadrant biopsies every 2cm and a separate biopsy from the anatomic cardia ## Footnote If dysplasia is present, biopsies should be taken at 1cm intervals.
38
What is the minimum number of biopsies required for histological confirmation of Barrett's?
Minimum 8 biopsies required ## Footnote Only 4 biopsies result in Barrett's esophagus being confirmed in 34.7% of cases.
39
What is required for the diagnosis of Barrett's?
Histological diagnosis from biopsies on endoscopy ## Footnote US guidelines require intestinal metaplasia (IM) to diagnose Barrett’s, while British guidelines only require columnar lined mucosa (CLM).
40
What percentage of patients with endoscopically suspected Barrett's had no histological confirmation?
42% had no endoscopic or histologic evidence of Barrett's esophagus ## Footnote 46% had endoscopic appearances consistent with Barrett's but no histologic evidence.
41
What confers the highest known risk of cancer development in Barrett's?
Intestinal metaplasia (IM) ## Footnote In patients with long segment Barrett's (>3cm), IM is almost always found.
42
What is the established role of screening for Barrett's?
No established role ## Footnote Long-segment Barrett's esophagus is found in 3 to 5 percent of patients with chronic GERD symptoms.
43
What factors determine the management of Barrett's?
Presence and degree of dysplasia, length of Barrett's esophagus ## Footnote The absolute risk of esophageal adenocarcinoma in patients with GERD symptoms is low.
44
True or False: Screening patients with GERD symptoms reliably identifies all individuals at high risk for esophageal adenocarcinoma.
False ## Footnote More than 40 percent of patients with esophageal adenocarcinoma have no history of heartburn.
45
What is the incidence of oesophageal cancer in Barrett's esophagus?
0.4-3% incidence per year ## Footnote Barrett's esophagus confers a 30x risk compared to the general population.
46
What is the main goal of managing Barrett's esophagus?
Prevent progression, eradicate disease burden, and avoid development of esophageal cancer.
47
What is the role of PPIs in Barrett's esophagus management?
No strong evidence that treatment reduces risk of progression of IM to HGD or cancer, but one meta-analysis showed an odds ratio of 0.29.
48
What did a randomized trial show regarding H2-blockers in Barrett's esophagus?
Regression with twice daily PPI, no regression in H2-blocker group.
49
What was the outcome of the Celecoxib vs placebo study?
No difference in progression to HGD or cancer.
50
What is the current evidence regarding antireflux surgery in Barrett's esophagus?
No high-quality evidence to support its use to prevent progression.
51
What is the recommended surveillance for no dysplasia in Barrett's esophagus?
Surveillance scope in 2-3 years (>3cm) or 3-5 years (<3cm).
52
What should be done if indefinite dysplasia is found?
Re-scope in 6 months; 60% had no dysplasia at follow-up.
53
How often should low-grade dysplasia be monitored?
Repeat endoscopy every 6-12 months with 1cm biopsies.
54
What is the role of RFA in low-grade dysplasia?
May be useful to prevent progression to HGD (0.8% vs 6.6%).
55
What is the management for high-grade dysplasia?
Repeat endoscopy as soon as possible, with high-resolution endoscopy and 1 cm biopsies.
56
What was traditionally offered to patients with high-grade dysplasia?
Oesophagectomy.
57
What is the current indication for oesophagectomy?
Reserved for T1b disease, multifocal carcinoma, or lesions not amenable to endoscopic resection.
58
What are the types of endoscopic resection?
EMR or ESD.
59
What is RFA and how is it applied?
Uses radiofrequency energy applied via a coiled electrode array to ablate the mucosal epithelium.
60
What is the re-scoping timeline after RFA?
12 weeks later, with PPI and EtOH abstinence.
61
What is the eradication rate of HGD using RFA compared to sham?
81% vs 19%.
62
What is the cancer rate in RFA treatment compared to sham?
1.2% vs 9.3%.
63
What is the pooled adverse reaction rate for RFA?
8.8%.
64
What is the disadvantage of photodynamic therapy compared to RFA?
Inferior to RFA.
65
What does endoscopic surveillance aim to reduce?
Deaths from oesophageal adenocarcinoma.
66
Is there high-quality evidence that surveillance is effective?
No high-quality evidence.
67
What do several small studies suggest about surveillance?
5-year survival is higher in those diagnosed by surveillance compared to those who present with symptoms.
68
What percentage of patients have eradicated specialized intestinal metaplasia (SIM) at 5 years post RFA?
90% ## Footnote RFA stands for radiofrequency ablation.
69
What is the progression rate of Barrett's esophagus (BE) with no dysplasia to high-grade dysplasia or adenocarcinoma in Denmark?
2.2-2.6/1000 person years ## Footnote This rate reflects the risk of progression in a specific population.
70
What is the progression rate of Barrett's esophagus (BE) with no dysplasia to high-grade dysplasia or adenocarcinoma in the UK?
3/1000 person years ## Footnote Indicates a slightly higher risk compared to Denmark.
71
What is the annual progression rate for non-dysplastic Barrett's esophagus?
0.3% per year
72
What is the annual progression rate for short segment Barrett's esophagus?
0.1% per year
73
What is the annual progression rate for low-grade dysplasia in Barrett's esophagus?
1% per year
74
What is the annual progression rate for high-grade dysplasia in Barrett's esophagus?
6-7% per year
75
What are some risk factors for progression of Barrett's esophagus?
* Patient factors (age, sex, obesity, smoking) * Endoscopic appearance (greater segment length, type of Barrett’s, aneuploidy)
76
What effect do regular use of PPI, NSAIDs, and statins have on Barrett's esophagus progression?
May have lower rates of progression
77
How much more likely are patients with Barrett's esophagus to die of other causes than oesophageal adenocarcinoma?
10x more likely