GERD
• Gastroesophageal reflux disease (GERD) is a prevalent gastrointestinal disorder.
• Stats show that up to 15% of individuals have heartburn and/or regurgitation at least once a
week.
• Symptoms are caused by backflow of gastric acid and other gastric contents into the
esophagus due to incompetent barriers at the gastroesophageal junction.
◦ Content from the stomach goes back up and irritates the esophagus.
Anatomy of the Esophagus
• The esophagus can be divided into the upper two-thirds and lower third.
◦ The upper 2/3 of the esophagus contains stratified skull skeletal muscles.
◦ The lower third contains all smooth muscle and so it is not under voluntary control.
• The mucosal surface of the upper 2/3 is non-keratinized stratified squamous epithelial cells.
◦ The lower third has transitional or stratified squamous epithelium to simple columnar
epithelium.
◦ The squamocolumnar junction has a zigzag appearance, thus sometimes referred to as
the Z line.
* The Z line is a change from the squamous epithelium to the columnar epithelium.
• The esophageal sphincter is a barrier for food and acid from going backwards from the
stomach up to the esophagus.
◦ When the sphincter is incompetent, GERD results.
Basic Physiology of Acid Production in the Stomach
• The stomach is made up of pits which houses many different cells.
◦ Cells of the stomach include mucus cells, parietal cells, enterochromaffin cells and
some other hormone cells.
◦ Parietal cells produce hydrochloric acid.
* There are two important channels for these cells:
* The proton pump which is an antiporter pumping hydrogen ions out in exchange for potassium ion.
* A symporter which pumps both potassium and chloride.
* With hydrogen and chloride in the lumen, this forms hydrogen chloride which helps in digestion of
food.
• Many things can stimulate parietal cell activity and thus stimulate acid production.
◦ Enterochromaffin cells release histamine.
◦ Histamine binds onto histamine receptors on parietal cells stimulating hydrochloric
release.
• "When the lower gastroesophageal sphincter is compromised due to a variety of factors,
gourd results or reflux disease results."
◦ Factors include things that increase intragastric volume pressure:
* Chronic coughing, large meals and delays in gastric emptying.
◦ Other factors include things that decrease the esophageal sphincter tone:
* Alcohol, certain medications or drugs such as tricyclic antidepressants, peptic strictures, previous
surgeries and idiopathic causes.
◦ Scleroderma is also another important cause of lower esophageal symptoms.
* Scleroderma is a condition characterized by thickening of tissue.
Pathological Features of GERD
• GERD is further complicated by reflux esophagitis which develops when the mucosal defenses
are unable to counteract the damage done by acid pepsin and bile.
◦ This causes inflammation of the esophagus.
• Esophageal strictures or peptic strictures result from fibrosis that causes luminal constriction.
◦ These strictures occur in 10% of patients with untreated GERD and also present in the
distal esophagus near the squamocolumnar junction.
Clinical Presentation
• Classic signs and symptoms of GERD/Reflux disease is a classic heartburn, an angina type pain,
worse after meal and worse lying down.
Symptoms and Diagnosis of GORD
• GORD is characterized by:
◦ Acid or water brash
◦ Odynophagia (pain when swallowing)
◦ Reflux into the pharynx, larynx, and tracheobronchial tree, potentially causing chronic
cough, laryngitis, sinusitis, and morning hoarseness.
• Diagnosis is easily made by history alone.
• Diagnostic studies are indicated for patients with persistent symptoms, complications, or
those who don't respond to therapy.
• For patients under 45, a trial of proton pump inhibitors (PPIs) is given if GORD is suspected.
• Investigations are warranted for people greater than 45 years old and have reflux.
• A gastroscopy can be performed to visualize changes in the esophagus.
◦ "Although endoscopy is sensitive for diagnosis of esophagitis, it can miss causes of
reflux since some patients have symptomatic reflux without esophagitis."
• A less invasive investigation is a barium swallowing study.
• A 24-hour ambulatory pH monitor is the most sensitive test for diagnosing GORD.
◦ "Again, the most sensitive test for diagnosis of gord is a 24 hour ambulatory ph
monitoring."
Treatment of GORD
• The goal of treatment is to provide symptom relief, heal erosive esophagitis, and prevent
complications.
• Management of mild cases includes lifestyle changes:
◦ Weight loss
◦ Smoking cessation
◦ Eating small, regular meals
◦ Avoiding meals before sleep
◦ Avoiding certain foods and drinks (fizzy drinks, alcohol, coffee, citrus fruits, and spicy
foods).
• Pharmacological management is first-line for suspected GORD and is used with lifestyle
modifications.
◦ Aims to reduce acid production.
◦ Includes proton pump inhibitors (PPIs), antacids, and histamine receptor antagonists.
• Surgical management (Nissen's operation/fundoplication) is considered when medical
management fails or for patients requiring long-term high-dose PPIs.
◦ "In this operation the gastric fundus is wrapped around the esophagus fundoplication
and this increases the lower esophageal sphincter pressure."
Complications of GORD
• Complications include esophagitis, which can cause dysphagia and metaplasia (Barrett's
esophagus).
• Barrett's esophagus is characterized by changes of squamous cells to columnar cells as well as
increased number of goblet cells in the area.
◦ Increases the risk of esophageal adenocarcinoma.
◦ "Barrett's esophagus is important because people with Barrett's esophagus are at a 30
to 125 time risk of developing esophageal adenocarcinoma than the general population."
• Other complications include stricture formation, ulcers, erosive esophagitis, and iron
deficiency (if bleeding occurs