GORD Flashcards

1
Q

GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)

A

• Between swallowing, Oesophageal muscles are relaxed except for Sphincters; Lower
Oesophageal Sphincter (LOS) relaxes when swallowing is initiated; Transient LOS Relaxations
(TLESR) occur as part of normal physiology but is more frequent in GORD patients
o Cause of all reflux in normal patients, and 2/3 of GORD patients
• The LOS has a strong resting tone, and increases in response to increased intraabdominal
pressure and intragastric pressure
o Other Antireflux mechanisms include the Intraabdominal Oesophagus which acts as a
flap valve; Mucosal folds of forming a rosette, and the contraction of the Crural
Diaphragm acts as a pinchcock to prevent acid reflux (disrupted in Hiatus Hernia)
o The Oesophagus is also rapidly cleared of refluxate by Secondary Peristalsis, Gravity
and Salivary Bicarbonate

• Failure of anti-reflex mechanisms leads to acidic gastric contents coming in contact with
Lower Oesophageal Mucosa, leading to mucosal damage and Metaplasia
• Risk Factors – Pregnancy/Obesity, Specific Foods (Fat, Chocolate, Coffee, Alcohol), Large
meals, Smoking, Drugs (Antimuscarinics, CCBs, Nitrates), Hiatus Hernia, Systemic Sclerosis or
treatment for Achalasia (E.g. Dilatation)

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2
Q

Presentation of GORD

A

• Heartburn – Aggravated on bending, stooping or lying down (increases acid exposure);
Relieved by oral Antacids; Pain on drinking hot liquids or alcohol
o Poor correlation between degree of pain and Oesophagitis; Psychosocial factors
• Patients might be asymptomatic even with severe Oesophagitis; May present as
Haematemesis or Iron Deficiency Anaemia from chronic blood loss
• Differentiation of Cardiac and Oesophageal pain can be difficult; Trial of PPI worthwhile
• Regurgitation can occur, especially if bending or lying flat; Aspiration pneumonia is unusual
without an accompanying stricture; Cough and Asthma can occur, responds slowly (1 – 4
months) to PPI treatment
• Peptic Strictures – Far less common with PPI therapy; Occur in 60+ with Intermittent
Dysphagia for solid foods, worsens gradually over long period; Treat with PPI, if severe might
require endoscopic dilatation and long-term PPI therapy; Surgery if medical therapy fails

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3
Q

Diagnosis and Investigations for GORD

A

• Clinical Diagnosis, unless alarm signs (especially Dysphagia in under 45)
• Endoscopy – Presence of Oesophagitis/Barrett’s Oesophagus confirms GORD
• Intraluminal Monitoring – 24-hour Intraluminal pH monitoring, or Impedance combined with
Manometry if no response to PPI; Always confirm reflux before surgery
o Excessive reflux – pH <4 for >4% of the time

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4
Q

Treatment of GORD

A

• Simple Antacids, Weight Loss, Raising head of bed during sleep; Avoidance of precipitating
factors, Dietary measures, Alcohol/Caffeine reduction and Smoking Cessation
• Alginate-containing Antacids – Forms “gel raft” with gastric contents to reduce reflux
• Magnesium-containing Antacids – Tend to cause Diarrhoea; Aluminium-containing Antacids
tend to cause Constipation
• H2 Receptor Antagonists – Acid suppression if Antacids fail
• Proton Pump Inhibitors (PPI) – Inhibit gastric H+

/K+ ATPase; Reduce Gastric Acid Secretion by

up to 90%; Drug of choice for all but mild cases
o Once Oesophageal sensitivity is normalised, lower dose for maintenance
o Nonresponsive to Antacids/PPI with normal Endoscopy = Non-Erosive Reflux Disease
(NERD); Usually female and symptoms are functional, or Hypersensitive Oesophagus
• Endoluminal Gastroplication – Plications (Pleats) made below Gastro-Oesophageal Junction
• Laparoscopic Nissen Fundoplication – Return of Gastro-Oesophageal
Junction below Diaphragm, Mobilisation of Fundus, Closure of
Diaphragmatic Crura and Short Tendon-free Fundoplication
o Most common cause of failure is recurrence
o Indications – Intolerance to medical therapy, Freedom from
medication, Expense of therapy and concern of Long-Term SE
o Not indicated for patients with Oesophageal Dysmotility, Patients with no response to
PPI and patients with underlying Functional Bowel Disease

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5
Q

Barrett’s Oesophagus

A

• Normal Squamous Epithelium is replaced by Metaplastic Columnar Mucosa to form
(Columnar Lined Oesophagus); Hiatus Hernia is almost always present
• Diagnosis made by Endoscopy – Proximally displaced Squamo-Columnar Junction and Biopsy
o May be seen as a continual circumferential sheet or finger-like projections, or islands
of Columnar Mucosa; Prague Classification – C (CLO length), M (Maximal length)
o Long segment (>3cm) and Short segment (<3cm)
• Most common in Middle-aged Obese Males (Obesity increase risk 4×)
• 0.12-0.5% of Barrett’s Oesophagus patients develop Oesophageal Adenocarcinoma per year
through gradual transformation of Intestinal Metaplasia to Dysplasia
o 2-yearly Gastroscopy with Biopsy from all quadrants of CLO; Not good evidence base
• Removal by Endoscopic Mucosal Resection (EMR) or Submucosal Dissection preventing the
need for Oesophagectomy
• Treatment with PPI; Endoscopic Ultrasound to stage patients to exclude cancer and
Lymphadenopathy; RF Ablation for treatment of Dysplasia

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6
Q

Urgent Referral for Endoscopy

A
  • Age – Typically >55yrs plus constitutional symptoms (Weight Loss especially)
  • Dyspepsia or Reflux Symptoms 2ww if >55yr with weight loss
  • Dysphagia 2ww regardless of age
  • Non-urgent if – Treatment resistant, >55yrs; Raised Platelet count, N+V
  • Change in Bowel Habit >60yrs, or with bleed >50yrs 2ww
  • Upper Abdominal Pain with Weight Loss 2ww, especially if signs of bleeding
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7
Q

Benign Oesophageal Stricture

A

• Peptic stricture secondary to reflux most common cause
• Physical/Chemical causes – Ingestion of Corrosives, Radiotherapy
• Sclerosis of Oesophageal Varices, Prolonged NG intubation
• Other causes – Oesophageal Webbing (Most post-cricoid, might occur as part of Plummer
Vinson =Chronic IDA, Glossitis, Angular Stomatitis), Oesophageal Rings (Mucosal =Schatzki B
at Squamocolumnar junction, or Muscular A rings, morelproximally)
• Management might involve Endoscopic Dilatation, although some might require surgery

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8
Q

Drugs that affect GI motility

A
  • Gastric Prokinetic Agents – Metoclopramide, Domperidone
  • Constipatory – Opioids, Antimuscarinics, Calcium Channel Blockers, Iron, TCAs
  • Bulk Forming Laxatives – Fibre, Methylcellulose, Ispaghula
  • Stimulant Laxatives (Increase Motility and Secretion) – Bisacodyl, Docusate
  • Osmotic Laxatives – Magnesium Sulfate, Lactulose, Macrogo
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