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Oesophageal disorders Flashcards

1
Q

Define Achalasia

A

failure of esophageal peristalsis and failure of the lower esophageal sphincter to relax with swallowing

  • difficulty swallowing solids and liquids
  • may be associated with chest pain and regurgitation
  • thought to be due to degeneration of the myenteric plexus resulting in loss of inhibitory neutrons in the lower oesophageal sphincter
  • rare: 1/100,00
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2
Q

How is Achalasia diagnosed

A

Barium swallow shows “birds beak” appearance
- initial test
Manometry is gold standard - esophageal aperistalsis and incomplete (or absence of) relaxation of the lower esophageal sphincter with wet swallows

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3
Q

How is Achalasia managed?

A

Surgical release of LOS with myotomy - often complicated by GORD which may require Nissen fundoplication
- most effective
Balloon dilatation
Botox injection to LOS - lasts 6-9 months
Calcium channel blockers and nitrites - short term management

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4
Q

What are some common causes of infectious oesophagitis and their treatments?

A

Candida - dysphagia, white plaques on endoscopy
- treat with Fluconazole

HSV - multiple superficial ulcers
- treat with Acyclovir

CMV - isolated oesophageal ulcers, CMV inclusion bodies on histology
- treat with IV Gancyclovir

  • all usually in immunocompromised individuals
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5
Q

What medications commonly cause “pill induced oesophagitis” ?

A 
Tetracyclines
Iron
Bisphosphonates
NSAIDs
Potassium
Quinidine
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6
Q

How is eosinphilic oesophagi’s defined?

A

eosinophilic infiltration of the esophageal mucosa
greater than 15 eosinophils/hpf on esophageal endoscopic biopsy and by exclusion of GORD (must trial PPI prior to diagnosis)
- typically presents with solid-food dysphagia and food impaction

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7
Q

What is the epidemiology of eosinophilic oesophagitis?

A

Usually presents in adults
incidence is increasing in parallel to increased rates of asthma and allergy
- high rates of asthma in those with eosinophilic oesophagi’s
54 per 100,000 in the United States
M > F

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8
Q

What is the management of eosinophilic oesophagitis?

A

initial treatment is with swallowed aerosolized corticosteroids
- often requires repeated treatment
Patients with refractory disease may need a combination of esophageal dilation, systemic corticosteroids, or a food elimination diet

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9
Q

What are the alarm symptoms of GORD?

A

dysphagia, anemia, vomiting, or weight loss

  • suggests complications from mucosal injury
  • this should prompt investigation with endoscopy
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10
Q

What is the gold standard investigation fro GORD?

A

Ambulatory pH monitoring

- performed if no response to PPI with normal endoscopy

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11
Q

What is the treatment algorithm for GORD?

A

symptoms without alarm features - trial PPI, lifestyle modification
if no response to PPI then refer for gastroscopy
- H2 blockers may be used in patients who are intolerant of or allergic to PPIs. Tachyphylaxis may occur with H2 blockers.

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12
Q

Name two associated diseases thought to be increased by PPI use.

A

Pneumonia
C. diff
* increased cardiovascular events on Clopidogrel + PPI is questionable

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13
Q

When is surgery considered in GORD?

A

Refractory reflux
Confirmed with ambulatory pH studies
PPI allergies

Nissen fundoplication is about as effective as PPI
- small but significant rate (10% to 15%) of dysphagia, bloating, and diarrhea after successful antireflux surgery

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14
Q

What is Barrett’s Oesophagus?

A

a premalignant complication of gastroesophageal reflux disease in which the normal squamous epithelium of the distal esophagus is replaced by specialized columnar epithelium normally found in the stomach

  • it is most common in white patients with long-standing, severe GORD
  • Approximately 10% of patients with chronic GERD symptoms have BE on endoscopy
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15
Q

What is the risk of malignancy with Barrett’s Oesophagus?

A

30-50 fold increase risk of adenocarcinoma of the oesophagus

Annual incidence of 0.5%

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16
Q

How is the diagnosis of Barrett’s Oesophagus made?

A

Endoscopically suggested and confirmed with histology

  • presence of specialized intestinal metaplasia with acid-mucin–containing goblet cells in the oesophagus
  • short segment 3cm
17
Q

What is the progression of Barrett’s Oesophagus to adenocarcinoma?

A

no dysplasia - metaplasia - low grade dysplasia - high grade - invasive adenocarcinoma

  • suveillance is recommended in those with Barrett’s to detect early changes and initiate therapy
  • surveillance table on MKSAP

The progression of Barrett metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure. The oncosuppressor gene TP53 and various oncogenes, particularly erb -b2, have been studied as potential markers

  • If BE is identified on histology, surveillance endoscopy with multiple biopsies should be performed at diagnosis and at 1 year to detect any prevalent dysplasia that was missed on the first endoscopy. If no dysplasia is found, further surveillance can be deferred for 3 years
18
Q

What are the signs/symptoms of oesophageal carcinoma?

A

Solid food dysphagia - most common
weight loss, anorexia, anaemia
- many patients do not have significant reflux symptoms despite association with GORD and BE

More common in males in 5th-6th decade of life

19
Q

What are the common types of oesophageal carcinoma?

A

Squamous cell carcinoma
- decreasing incidence
- assoc: smoking, alcohol, nitrosamine exposure, corrosive injury to the esophagus, dietary deficiencies (zinc, selenium), achalasia, tylosis (keratosis of the palms and soles), and HPV
Adenocarcinoma
- increasing incidence
- assoc: smoking, obesity, GORD, Barrett’s Oesophagus

20
Q

What is the prognosis of oesophageal cancer?

A

Depends on staging but as most cases are diagnosed at advanced stages this is often poor
- 5 year survival rates

21
Q

How is oesophageal cancer diagnosed?

A

Endoscopy

  • SCC tends to affect the proximal oesophagus
  • Adenocarcinoma affects the distal oesophagus
22
Q

How is oesophageal cancer staged?

A

CT staging scan
Endoscopic USS
- most sensitive test for T and N staging
PET

23
Q

What is the treatment for oesophageal cancer?

A

Stage I – Consideration for endoscopic therapy (eg, mucosal resection or submucosal dissection), particularly for Tis and T1aN0 by EUS; consideration for initial surgery for T1b and any N
Stages II-III – Consideration for chemoradiation followed by surgery (trimodality therapy)
Stage IV – Chemotherapy or symptomatic and supportive care

  • Neoadjuvant therapy consists of a combination of radiotherapy (approximately 45 Gy) and chemotherapy with cisplatin and 5-fluorouracil
  • No benefit with post-op chemo/RT
24
Q

What is the staging system for oesophageal cancer?

A

TNM staging system

25
Q

What are the indications for surgical treatment of oesophageal cancer?

A

Diagnosis of esophageal cancer in a patient who is a candidate for surgery
High-grade dysplasia in a patient with Barrett esophagus that cannot be adequately treated endoscopically

26
Q

What diagnosis does a corkscrew oesophagus on barium swallow suggest?

A

Diffuse oesophageal spasm

On manometry, multiple simultaneous contractions are seen
Treatment is with calcium channel blockers

27
Q

What would be indications for enteric feeding?

A

Loss of more than 10% of body weight, evidence of malnutrition on examination and laboratory evaluation, and inability to maintain caloric intake

28
Q

What are the typical features of oropharyngeal dysphagia and what is the diagnostic test?

A

choking, coughing
aspiration pneumonia

test: video fluoroscopy

29
Q

What is the most effective treatment for Barrett’s with high grade dysplasia?

A

endoscopic resection with radio frequency ablation

  • need several sessions of RFA to treat all areas
  • most common side effect is oesophageal stricture ~5%
30
Q

What is the annual rate of progression to adenocarcinoma from Barrett’s oesophagus with low grade dysplasia?

A
  1. 8%

- management is with close surveillance (6 month OGD) or endoscopic ablation

31
Q

What is the annual rate of progression to adenocarcinoma from Barrett’s oesophagus with high grade dysplasia?

A

10%

- treatment is oesophagectomy vs endoscopic resection with RFA

32
Q

What is the most common reason for GORD?

A

transient relaxation of the lower oesophageal sphincter

33
Q

What features of dysphagia suggest that the underlying pathology is malignant?

A 
shorter duration of dysphagia
solids > liquids
constant and progressive
older age group
accompanying red flags e.g. weight loss
34
Q

What features of dysphagia suggest that the underlying pathology is benign?

A 
long duration of symptoms
liquids and solids
intermittent and unpredictable symptoms
younger patients usually
alarm symptoms e.g. weight loss occur later in disease
35
Q

What % of people with reflux symptoms have oesophagi’s?

A

approximately half

- symptoms severity does not correlate with erosions

36
Q

What is the role of H. pylori testing in GORD?

A

There is no role for H. pylori testing in GORD

- does not cause oesophageal symptoms

37
Q

What are the more common causes for infectious oesophagitis?

A

candida
HSV
CMV

others include: human papillomavirus, Trypanosoma cruzi, Mycobacterium tuberculosis, and Treponema palladium

  • all more common in immunocompromised
38
Q

How does CMV oesophagi’s appear on OGD and how is diagnosis confirmed?

A

isolated oesophageal ulcers
biopsy from ulcer base
treat with Ganciclovir

39
Q

How does HSV oesophagitis appear on OGD and how is diagnosis confirmed?

A

multiple superficial ulcers
biopsy from the ulcer edge
treat with Aciclovir

Gastro (11 decks)

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