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Oesophagus stuff Flashcards

1
Q

What epithelium lines the oesophagus?

A

Stratified squamous epithelium

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2
Q

What are the muscle layers of the oesophagus?

A

Inner - circular / outer - longitudinal

Upper 1/3 striated muscles, lower 2/3 smooth

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3
Q

Possible causes of dysphagia

A

Structural lesions

  • stricture (benign or malignant)
  • esophageal ring (Schatski ring - narrowing of lower oesophagus caused by ring of mucosal tissue), webs, pouch

Neuromuscular

  • pharyngeal - bulbar palsy, myasthenia gravis
  • motility disorders

Inflammation
- reflux esophagitis, eosinophilic oesophagitis

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4
Q

Achalasia

  • what is it?
  • what causes it?
  • presentation
  • complications
  • treatment
A

(1) Failure of LOS relaxation
(2) Absence of peristalsis
“LOS contracted, oesophagus above dilated”

Degenerative lesion of oesophageal innervation - loss of ganglia from Auerbach’s plexus

Presentation

  • dysphagia
  • weight loss
  • chest pain
  • difficulty swallowing food and liquids equally
  • may have regurgitation
  • XRAY - “bird beak” appearance

Complications
- may progress to oesophageal dilatation and respiratory complications

Treatment

  • Nifedipine
  • botox
  • dilatation
  • surgical myotome
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5
Q

Disorders of oesophageal motility

A

Primary:

  • GORD
  • Disorders of impaired LOS relaxation (achalasia, oesophagogastric junction outflow obstruction,
  • Disorders of peristalsis (absent contractility, distal oesophageal spasm)

Secondary

  • systemic sclerosis
  • myasthenia graves
  • pseudoachalasia (not caused by primary denervation like achalasia)
  • drugs
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6
Q

GORD

- pathophysiology

A
  • caused by reflux of gastric contents into oesophagus

Impaired oeseophageal clearance

  • Defective oeseophageal peristaltic activity
  • Primary abnormality – persists after oesophagitis has healed
  • Leads to increased acid exposure time

Mucosal defence

Hiatus hernia

  • 30-50% population
  • On its own sliding hiatus hernia does not cause symptoms
  • Pressure gradient between abdominal and thoracic cavities is lost
  • Oblique angle between cardia and oesophagus disappears
  • Contribution anti-reflux barrier
  • May contribute to severity of reflux
  • Common in people who develop oesophagitis, Barrets, or peptic strictures

Sphincter incompetence - Lower esophageal sphincter (LOS) function

  • LOS tonically contracted under normal circumstances , relaxes during swallowing
    (1) Reduced tone - Allowing reflux into oesophagus when intra-abdominal pressure is high
    (2) Inappropriate sphincter relaxation

Duodeno gastric reflux

Impaired gastric emptying

Predisposing factors: obesity, pregnancy (increased intra-abdominal pressure – pressure may push gastric contents up), large meals, lying position, alcohol and some drugs (anticholinergics, Ca channel blockers, nitrates, opioids, beta-blockers → favour relaxation of sphincter)

Diet: fat, chocolate, alcohol, tea, coffee -> relax LOS

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7
Q

GORD presentation

A 
Overweight.
May be woken at night by choking as refluxed fluid irritates larynx.
Chest pain – mimic angina.
Hoarseness – acid laryngitis.
Recurrent chest infectinos.
Chronic cough
Asthma

Heart burn

Acid regurgitation - Provoked by bending, straining, lying down

Waterbrash - Salivation due to reflex salivary gland stimulation as acid enters gullet

Odynophagia/ dysphagia

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8
Q

GORD complications

A

Oesophagitis
- Endoscopy: mild redness, bleeding ulceration, stricture formation

Peptic stricture

Barrett’s oesophagus

Adenocarcinoma

Benign oesophageal stricture

  • Fibrous stirctures may develop due to long-standing oesophagitis
  • Esp. in elderly, poor oesophageal peristaltic activity
  • Presentation: dysphagia that is worse for solids
  • Diagnosis = endoscopy – biopsy stricture to exclude malignancy
  • Endoscopic balloon dilatation or bouginage
  • PPI – reduce risk of recurrent oesophagitis and stricture formation

Gastric volvulus

  • Massive intrathoracic hiatus hernia may twist → complete oesophageal or gastric obstruction
  • Severe chest pain, vomiting, dysphagia
  • Diagnosis: Chest XRAY (air bubbles in chest) & barium swallow
  • Most resolve spontaneously, recurrence common
  • Surgery advised after acute episode treated by nasogastric deompression
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9
Q

GORD risk factors

A

COCOA qHS

Chocolate
Obesity
Caffeine
Outlet obstruction
Alcohol
q (qHS: eating before bed)
Hiatal hernia
Smoking
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10
Q

GORD diagnosis

A

Based on symptoms

  • Young, typical symptoms,
  • NO dysphagia, weight loss, anaemia
  • Treat empirically

Investigate if >50 years old; atypical symptoms; complication suspected

(1) Endoscopy
- Exclude other upper GI disease, identify complications

Oesophageal pH monitoring

  • 24 hour
  • Indicated if unclear diagnosis or surgical intervention being considered
  • Tether catheter with terminal radiotelemetry pH- sensitive probe above gastro-oesophageal junction
  • Intraluminal pH recorded, while patient undergoes normal activities
  • Episodes of symptoms noted and related to pH
  • pH <4 for more than 6-7% = diagnostic
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11
Q

GORD treatment

A 
Lifestyle measures (smoking, alcohol, diet – avoid late and large meals, wait 3 hours before lying down, weight reduction)
- Avoid chocolate, citrus juice, tomato-based food

Mechanical (posture, clothing, elevate bed-head)

Drugs

  • Antacid +/- alginate
  • Aluminium hydroxide, magnesium carbonate, calcium carbonate
  • OTC – Rennies, Settlers, Tums
  • Combined with alginates – Peptac, Gaviscon

Neutralise gastric acid

  • Alginates – swell when mix with gastric juice, forming ball clot above gastric juice
  • Effective for mild symptoms – rarely achieve healing

SE: Mg → laxative; Al→ Constipating; Ca→ hyperCa,

PPI

  • Lansoprazole, pantoprazole, esomeprazole
  • Blocks final step in H+ ion secretion by H+/K+ ATPase enzyme system in gastric parietal cell 

  • Indications: GORD -1st line
  • Administration 
– 20 mg once daily by mouth for 4 weeks 

  • May require lifelong treatment at lowest possible dose
  • SE: reduced absorption of iron, B12, Mg, small increased risk of osteoporosis, diarrhoea, GI upset but well tolerated long-term

Acid suppression (PPI, H2RA)

Prokinetics

Surgical (or endoscopic?) antireflux procedure

  • Fundoplication
  • Failure of medical treatment, reflux stricture, Barrett’s ulcer?
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12
Q

Histamine 2 receptor antagonists

A

Cimetidine, ranitidine, famotidine, nizatidine

MOA

  • reduced H2 receptor stimulation in gastric parietal cells
  • Decreased acid secretion, gastric volume and H+ concentrations
  • Heals mild oesophagitis in 70-80% patients with GORD

Indication

  • Relieve symptoms without healing oesophagitis
  • Maintenance therapy to prevent relapse

Administration: 400mg 6hourly by mouth 4-8 weeks

SE:

  • Diarrhoea & GI upset, confusion
  • Cimetidine inhibits cytochrome P450 + has important interactions (warfarin, phenytoin, theophylline)
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13
Q

Barrett’s Oesophagus

  • what is it?
  • incidence?
  • RF
A
  • 1.5-5% of population
  • Premalignant condition: Low grade dysplasia; High grade dysplasia; Adenocarcinoma

Relative risk of cancer increased 40-120 fold, absolute risk still low (0.5% per year)

Squamous lining of lower oesophagus replaced by columnar mucosa
- May have areas of intestinal metaplasia

Adaptive response to chronic GORD

Prevalence increasing; Males; obese; >50 y/o; Weak association smoking

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14
Q

Barrett’s Oesophagus Pathophysiology

A

Molecular events
- Inactivation of tumour suppressor protein p16 by loss of heterozygosity or promoter hypermethylation = key event

Followed by somatic inactivation of TP53 → promotes aneuploidy and tumour progression

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15
Q

Barrett’s Oesophagus

  • presentation
  • diagnosis
  • management
A

Often asymptomatic

Diagnosis: multiple systematic biopsies to maximise chance of detecting intestinal metaplasia and/or dysplasia

Management
Acid suppression & anti-reflux surgery do NOT stop progression/induce regression

Treat symptoms of reflux and complications – e.g. stricture

Endoscopy therapies

  • Only used for those with dysplasia or intramucosal cancer
  • Radiofrequency ablation
  • Photodynamic therapy

Surveillance vs ablation

  • Barrets & intestinal metaplasia but no dysplasia
  • Undergo endoscopy 3-5 yearly intervals if length of barrettic segment <3cm and 2-3 yearly if >3cm
  • Low grade dysplasia – endoscopy 6 monthly intervals

High grade dysplasia or intramucosal carcinoma
- Oesophagectomy or endscopic therapy (resection of abnormal areas and radiofrequency ablation of remaining Barrett’s mucosa

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16
Q

Eosinophilic oesophagitis

  • presentation
  • diagnosis
  • treatment
A

Presentation: Food bolus obstruction, dysphagia
- May have chest pain, vomiting

More common in children but also young adults, M>F
Prevalence 50/100,000
History of atopy (asthma, hay fever)

Endoscopy usually normal
- May have furrows, rings (may require endoscopic dilatation), exudates, strictures

Biopsy for diagnosis

Treatment
- Diet – elimination (egg, wheat, milk, nuts, soya, fish)  - esp. children
- Drugs
1.	PPI
2.	Topical steroid
       8-12 week course
        Fluticasone, betamethasone
       Metered-dose inhaler – spray into mouth    &amp; swallow –NOT inhale

Dilatation – for strictures

17
Q

Oesophageal cancer presentation

A

Adenocarcinoma and squamous cell carcinoma

Presentation: progressive painless dysphagia for foods, weight loss, chest pain, anaemia, epigastric mass
- May present acutely due to food bolus obstruction
- Chest pain or hoarseness → mediastinal invasion?
- Fistulation between oesophagus and trachea or bronchial tree → coughing after swallowing, pneumonia, pleural effusion
- Advanced disease – hepatomegaly and ascites
- Rarer but suggests metastatic disease
Left supraclavicular lymph node (Virchow)
Infiltration of umbilicus (Sister Joseph’s nodule)

Short progressive history suspicious

Often advanced stage at presentation; Poor prognosis unless detected early

18
Q

Why may oesophageal cancer present with hoarseness?

A

Laryngeal nerve damage

19
Q

Two most common types of oesophageal cancer

- which one is most common?

A

Adenocarcinoma -> MORE COMMON

Squamous cell carcinoma

20
Q

Oesophageal Adenocarcinoma

  • distribution
  • who it affects
  • incidence
  • RF
A

Lower third oesophagus
younger

Incidence rising

RF:

  • Reflux (Barretts’s)
  • Obesity

Approx. 0.3% p.a
Commonest type of oesophageal carcinoma in UK
- Higher than cancer risk in UC, familial breast cancer
- Older men have higher risk of progression
- Early resection – 90% - 5 year survival
- Late resection - <25% - 5 year survival
- Overall 5 year survival = 13%

21
Q

Oesophageal Squamous cell carcinoma

  • distribution
  • who it affects
  • RF
A

Mid/upper oesophagus
Older

Incidence declining but commonest type world-wide

RF:

  • smoking
  • alcohol
  • chewing betel nuts or tobacco
  • achalasia
  • coeliac
  • post-cricoid web
  • post-caustic stricture
  • tylosis (familial hyperkeratosis of palms and soles)
22
Q

Oesophageal cancer treatment

A

Surgery = mainstay of curative treatment

Balance of risk re-possible benefit


T1-3 N0-1 M0 generally offered if fit


Consider pre-op chemo to downstage

Radical radiotherapy occasionally for SCC

23
Q

Oesophageal cancer palliative treatment

A

Radiotherapy

Chemotherapy

Endoscopic therapy

  • Laser
  • Argon plasma
  • Stent
24
Q

Nutcracker oesophagus

A

Average oesophageal peristaltic pressure > 2 standard deviations above well documented normal range in distal oesophagus (>180mmHg)

Associated: Hypertonic LOS; Peristaltic waves of long duration

Symptoms:
 Chest pain, dysphagia

Endoscopy / barium swallow, Manometry

Treatment: reassurance, nitrates,
calcium channel blockers

GI (7 decks)

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