The document provides a comprehensive overview of gastroesophageal reflux disease (GERD), including its definition, anatomy, pathophysiology, risk factors, clinical presentations, complications, investigations, differential diagnoses, and management strategies. GERD is characterized by the retrograde flow of stomach contents into the esophagus, leading to symptoms such as heartburn and complications like Barrett's esophagus and adenocarcinoma. Management includes lifestyle modifications, medication (antacids and proton pump inhibitors), and, in severe cases, surgical options.

1. Gastroesophageal Reflux Disease
(GERD)
Presenter; Dr Sajaad Othman
ILALA AFYA CENTRE

2. Plan
1. Definition of GERD
2. Anatomy of GEJ
3. Pathophysiology of GERD
4. Risk factors of GERD
5. Clinical presentation of GERD
6. Complications of GERD
7. Investigations
8. Differential diagnosis
9. Management of GERD

3. 1:Definition of GERD
Gastroesophageal reflux disease (GERD) is a
condition that develops when there is a
retrograde flow of stomach contents back into
the oesophagus.
It can present as non-erosive reflux disease or
erosive esophagitis.

4. 2.Anatomy of Gastroesophageal junction
• The oesophagus is the part of the digestive tract that
extends between the pharynx and the stomach.
• It passes through the oesophageal hiatus (opening) of
the diaphragm and ends at the stomach. The oesophagus
transports food from the pharynx to the stomach.
• It has 2 sphincters ;upper oesophageal sphincter and a
lower esophageal sphincter,LES.
Oesophageal mucosa
• is made up of stratified squamous epithelium.
• No effective defence mechanisms against acid.
• Protected by LES ,preventing acid reflux from stomach.

5. STRATIFIED SQUAMOUS EPITHELIAL
CELLS
Eg Oesophageal mucosa
SIMPLE COLUMNAR EPITHELIAL
CELLS
Eg Stomach mucosa

6. Lower oesophageal sphincter, LES
• The LES is normally found at the level where the
oesophagus leaves the thorax and enters the abdomen
through the diaphragmatic hiatus.
• During the swallowing process peristalsis is initiated in
the striated muscle and continues down through the
smooth muscle with a coordinated temporary relaxation
of the lower oesophageal sphincter.
• The LES and the muscular fibers of the diaphragm
together form a functional entity that serves as a
protection against gastroesophageal reflux.

7. 3:Pathophysiology of GERD
• Occasional episodes of gastro-oesophageal reflux are common in health. Reflux is
normally followed by oesophageal peristaltic waves which efficiently clear the gullet,
alkaline saliva neutralises residual acid, and symptoms do not occur.
• GERD develops when the pressure of LES gets lower for some reason, oesophageal
mucosa is exposed to gastroduodenal contents for prolonged periods of time, resulting
in local inflammation(oesophagitis),if becomes more prolonged,may lead to strictures.
• Also if continously damaged,esophageal stratified squamous epithelium is gradually
replaced with columnar cells(metaplasia) in response to adaptation of acidic
environment,this finally results to Barret’s oesophagus which is a pre malignant lesion
for oesophageal adenocarcinoma.

9. 4:Risk factors of GERD
•Obesity
•Fatty meals
•Heavy meals
•Spicy food
•Cigarette smoking
•Tight fitting garments
•Emotional stress
•Coffee,tea,chocolates
•Pregnancy
•Medications eg CCB
•Reclining after eating

10. Types of Hiatus hernia

11. Retrocardiac opacity with
air-fluid filled

12. 5:Clinical presentation of GERD
Symptoms
Oesophageal:
• Heartburn (burning, retrosternal discomfort after meals,
lying, stooping, or straining, relieved by antacids);
• belching; acid brash (acid or bile regurgitation);
• waterbrash (Hypersalivation);
• Odynophagia (painful swallowing, eg from oesophagitis or
ulceration).
Extra-oesophageal:
• Nocturnal asthma,
• chronic cough,
• Pharyngitis,laryngitis (hoarseness, throat clearing),
• sinusitis.
• Recurrent Otitis media

13. 6:Complications of GERD
• Oesophagitis
• Iron deficiency anaemia (consequence of chronic insidious blood loss from long-standing
oesophagitis)
• Benign oesophageal stricture (consequence of longstanding oesophagitis,presenting with
dysphagia).
• Barrett’s oesophagus.
• Oesophageal adenocarcinoma.

14. Barrett’s oesophagus
• Is a pre-malignant condition in which the normal squamous lining of the
lower oesophagus is replaced by columnar mucosa (columnar lined
oesophagus; CLO) containing areas of intestinal metaplasia .
• It occurs as an adaptive response to chronic gastro-oesophageal reflux .
• CLO is a major risk factor for oesophageal adenocarcinoma .
• Regular endoscopic surveillance can detect dysplasia and malignancy at an
early stage and may improve survival.
• It is recommended that patients with CLO without
dysplasia should undergo endoscopy every 2–3 years and those with low-
grade dysplasia at 6–12-monthly intervals.
• Oesophagectomy is widely recommended for those with high-grade
dysplasia (HGD).

15. 7:Investigations and Diagnosis
• Diagnosis of GERD is based on clinical symptoms and therapeutic trial.
• Young patients(<55years ) who presents with typical symptoms of gastro-oesophageal reflux, without worrying
features such as dysphagia, weight loss or anaemia, can be treated empirically without investigations.
• Investigation is advisable if patients Age > 55 years, if symptoms are atypical or if a complication is suspected.
• Endoscopy (investigation of choice);to
 excluding other upper gastrointestinal diseases which can mimic gastro-oesophageal reflux,
 identifying complications.
• Other investigations to be done for excluding differentials for epigastric pain if suspected:eg
 ECG
 Test for H pylori

16. • 24-hour pH monitoring (most accurate test )
indicated only
 if the diagnosis is unclear or
surgical intervention is under consideration.

17. Who to scope?
Dyspepsia+ Age > 55 or ALARM Symptoms or Treatment refractory dyspepsia
ENDOSCOPY
A;Anemia,
L;Loss of weight:
A;Anorexia;
R;Recent onset/progressive symptoms,
M:Melena/Heamatemesis,
S;Swallowing difficulty

18. 8:Differentials
• Oesophagitis from corrosives, NSAIDS, herpes, Candida;
• Duodenal or gastric ulcers or cancers;
• Non-ulcer dyspepsia;
• Oesophageal spasm;
• Cardiac disease;eg Angina,MI,pericarditis

19. 9:Management
1. Lifestyle modifications: (Avoiding risk factors)
• Weight loss
• Smoking cessation
• Avoiding alcohol consumption
• Small regular meals
• Reduce fizzy drinks, spicy and fatty foods, caffeine,chocolates.
• Avoid eating <3h before bed.
• Raise the bed head in those with nocturnal symptoms.

20. 2.Medications:
• Antacids mixture or alginates, eg Gaviscon® relieve symptoms.
• Proton Pump Inhibitors PPI(reduce acid production), eg Omeprazole 20mg
• Avoid drugs
affecting oesophageal motility (nitrates, anticholinergics, Ca2+ channel
blockers—relax the lower oesophageal sphincter)
or that damage mucosa (NSAIDS, K+ salts, bisphosphonates)

21. 3.Surgery:
Laparoscopic Nissenfundoplication,
• aim to increase resting lower
oesophageal sphincter pressure.
• Consider in severe GERD (confirmed by
pH-monitoring)or if drugs are not
working.

22. THANK YOU