Oesophagus stuff Flashcards
What epithelium lines the oesophagus?
Stratified squamous epithelium
What are the muscle layers of the oesophagus?
Inner - circular / outer - longitudinal
Upper 1/3 striated muscles, lower 2/3 smooth
Possible causes of dysphagia
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
Achalasia
- what is it?
- what causes it?
- presentation
- complications
- treatment
(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
Disorders of oesophageal motility
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
GORD
- pathophysiology
- 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
GORD presentation
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
GORD complications
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
GORD risk factors
COCOA qHS
Chocolate Obesity Caffeine Outlet obstruction Alcohol q (qHS: eating before bed) Hiatal hernia Smoking
GORD diagnosis
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
GORD treatment
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?
Histamine 2 receptor antagonists
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)
Barrett’s Oesophagus
- what is it?
- incidence?
- RF
- 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
Barrett’s Oesophagus Pathophysiology
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
Barrett’s Oesophagus
- presentation
- diagnosis
- management
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
