GASTROESOPHAGEAL REFLUX DISEASE
• DEFINITIONS
• GASTROESOPHAGEAL REFLUX: GER
• Effortless movement of gastric contents from stomach to esophagus
PHYSIOLOGIC, very frequent during day and night, post prandial
with no symptoms or tissue injury.
• GASTROESOPHAGEAL REFLUX DISEASE: GERD
Damage to the esophageal mucosa inducing symptoms and
esophageal inflammation.

EPIDEMIOLOGY
• ALL AGES, peak prevalence 35 – 45 years
• In USA 44% of adults once a month
7% of adults once a week

PATHOPHYSIOLOGY
Contact of the noxius refluxate with the esophageal mucosa
during enough time to produce damage
IMBALANCE BETWEEN: OFFENSIVE FACTORS
DEFENSIVE SYSTEM
OFFENSIVE FACTORS: HCL acid – PEPCIN (their secretion is not
increased but they are in the wrong place)
DEFENSIVE SYSTEM: Antireflux Barrier
Esophageal Clearance
Tissue Resistance

PATHOPHYSIOLOGY
1. Antireflux Barrier:
Lower Esophageal Sphincter: LES
The right crus of the diaphragm
• High pressure zone of 2-3 cm between 2 low
pressure zones (esophagus-stomach)

Pathophysiology
• In GERD
• Low tone LES
• Transiant LES relaxation episodes :TLESR
• 80% of GERD episodes
• Vagaly mediated non cholinergic inhibitory reflex
induced by gastric stimulation (distention , inflammation

Substances Influencing LES Pressure
Increases LES pressure Decreases LES pressure
Hormones Gastrin Secretin
Motilin Cholecystokinin
Substance P Glucagon
Somatostatin
Gastric inhibitory polypeptide
Vasoactive inhibitory polypeptide
Progesterone
Medications Metoclopramide Theophylline
Domperidone Prostaglandins E2 and I2
Cisapride Serotonin
Histamine Morphine
Antacids Meperidine
Prostaglandin F2α Calcium channel blockers
Diazepam
Food Protein Fat
Chocolate
Ethanol
Oil of peppermint
Neural agents α-Adrenergic agonists α-Adrenergic antagonists
β-Andrenergic antagonists β-Adrenergic agonists
Cholinergic agonists Cholinergic antagonists

PATHOPHYSIOLOGY
2. Esophageal acid clearance:
Washes down acid/pepsin
• Abnormal peristaltis: low amplitude non propagating
contractions
• Non reducible hiatal hernia: trapping acid and propelling
it back
• Impaired bicarbonate secretion by salivary and
esophageal glands to neutralize acid

PATHOPHYSIOLOGY
3. Tissue resistance: Stops H+ back diffusion
• Preepithelial: Bicarbonate secretion, weak defense
• Epithelial: Cell membrane
Intercellular tight junction
Intracellular H+ Buffering
• Post epithelial: Blood supplies Bic, Oxygen, Nutrients
and removes H and CO2

Epithelial defense mecanism

In summary
• TLESR allow acid/pepsin to come in
contact with the mucosa,the impared
clearance increases contact time so noxius
agente overcome the normal tissue
resistance

Impaired
mucosal
defence
de Caestecker, BMJ 2001; 323:736–9.
Johanson, Am J Med 2000; 108(Suppl 4A): S99–103.
salivary HCO3
Hiatus hernia
Impaired LOS
(smoking, fat, alcohol)
– transient LOS
relaxations
– basal tone
H+
Pepsin
Bile and
pancreatic
enzymes
oesophageal
clearance of acid
(lying flat, alcohol,
coffee)
acid output
(smoking, coffee)
intragastric pressure
(obesity, lying flat)
bile reflux gastric emptying (fat)
Pathophysiology of GORD

CLINICAL FEATURES
A. ESOPHAGEAL SYMPTOMS
• HEART BURN
• Regurgitation
• Dysphagia – Odynophagia
• Pain – “Non cardiac chest pain”
B. EXTRA ESOPHAGEAL SYMPTOMS
• Pulmonary: Bronchospasm, cough, bronchitis, pneumonia, Asthma.
• Oral: Gingivitis, tooth decay, waterbrach.
• Throat: Hoarsness, laryngitis, globus sensation.
• Ear: Pain.

THE SPECTRUM OF GERD
NERD EROSIVE ESOPHAGITIS BARRETT
ESOPHAGUS
60% 30% <10%

Spectrum of GERD
Symptomatic GERD – the real world
60%+ 35% 5%
NERD Esophagitis
Complicated
erosive reflux
disease

THE SPECTRUM OF GERD
NON EROSIVE REFLUX DISEASE:
• No Endoscopic Lesions
• Histological Alterations: - Mucosal infiltration by granulocytes
- Basal cell hyperplasia
- Dermal pegs elongation

Normal esophagus

THE SPECTRUM OF GERD
EROSIVE ESOPHAGITIS:
Endoscopic findings: erythema, erosions, ulcers, strictures.
BARRETT ESOPHAGUS:
Squamous epithelium replaced by columnar epithelium

LA classification for esophagitis
Grade A Grade
B
Grade C Grade
D

stricture

DIAGNOSIS
A. CLINICAL DIAGNOSIS
B. DOCUMENTATION OF mucosal injury:
• Barium swallow: Normal in NERD and Barrett.
May show Reflux episodes, oesophagitis, ulcers , strictures and
Hiatal Hernia
• Esophago gastro duodenoscopy:Normal in NERD but gold
standard in esophagitis and Barrett
• Bernestein test:esophageal infusion of HCl
C. Quantification of reflux:
24 hour PH monitoning

pH Recording

Scoring system to characterize patterns of reflux
Parameters Evaluated During pH Monitoring
Percentage of recording time when intraesophageal pH was below 4.0 in the upright position or recumbent position
Percentage of recording time with pH below 4.0 for the total 24-hour period
Total number of reflux episodes
Number of episodes longer than 5 minutes
Duration of longest episode

BARRETT’S ESOPHAGUS
• Healing process: colomnar epithelium
• 3 types of cells: cardial, junctionnal, intestinal
• Goblet cell epithelium
• Prevalence of Barrett: < 10%
• Risk of cancer only in Goblet cell type:
1/200 patient/year
30 – 120 times more than the normal
population
Higher in long segment >3cm
 Endoscopy is gold standard + biopsies

Barrett‘s esophagus

Carcinoma of the esophagus

Esophageal stent

OTHER TYPES OF ESOPHIGITIS
• Infectious esophagitis:
Mainly in immunocompromised individuals : neutropenic, cancer
patients, diabetics ,steroid treatment …
Symptoms:Odynophagia, dysphagia , bleeding …
- Viral: HSV 1, VZV, CMV, HIV
- Bacterial: Mycobacterium tuberculosis, Cryptosporidium …
- Candida: Normal oral flora but becomes pathogenic in
immunocompomised patients
Endoscopy: Ulcerations , vesicules in viral causes, white/yellow
pseudomembranes in candida

• Radiation: cancer therapy
Early damage:erythema ,erosions, bleeding
Late damage: strictures by ischemic changes
• Corrosive: acid, alkali
• Pill induced, drug induced: Tetracyclines, NSAId’s, KCL
• Other: Pemphigus vulgaris, Stevens Johnson, GVH,
crohn,Behcet