In this presentation I have tried to explain in brief about gastro esophageal Reflux Disease (GERD), its etiology, risk factors, diagnosis, and its management via pharmacotherapy.

1. By: Dr. Ankit Gaur
Pharm.D, M.Sc, RPh

2.  Definition of GERD
 Epidemiology of GERD
 Pathophysiology of GERD
 Clinical Manisfestations
 Diagnostic Evaluation
 Treatment
 Complications

3.  Symptoms OR mucosal damage
produced by the abnormal reflux of
gastric contents into the esophagus
 Often chronic and relapsing
 May see complications of GERD in
patients who lack typical symptoms

4.  Physiologic GERD
Postprandial
Short lived
Asymptomatic
No nocturnal sx
 Pathologic GERD
Symptoms
Mucosal injury
Nocturnal sx

5.  GERD occurs in all ages but, most common
in those older than 40 years of age.
 About 10-20% of people in western countries
suffer from GERD symptoms on a weekly
basis
 About 7% have symptoms daily.
 Except for NERD and pregnancy , no much
difference in incidence between men and
women.
 But for Barrett’s esophagus, prevalence is
more in males particularly white adult
males.

6.  Primary barrier to gastro esophageal reflux is the
lower esophageal sphincter
 LES normally works in conjunction with the
diaphragm
 If barrier disrupted, acid goes from stomach to
esophagus
May be due to
 Spontaneous transient LES relaxations
 Transient increase in intra abdominal pressure
 An atonic LES

7.  Drugs that reduce LES tone include calcium
channel antagonists (e.g., nifedipine,
verapamil, diltiazem), nitrates,
anticholinergic agents(e.g.,tricyclic
antidepressants , antihistamines), and oral
contraceptives and estrogen.
 Foods that reduce LES tone include
chocolate, fatty foods , onions, peppermint,
and garlic
 Smoking(nicotine) reduces LES tone.

8. 2)DISRUPTION OF ANATOMICAL BARRIERS
 Associated with hiatal hernia
 The size of hiatal hernia is proportional to the frequency of
LES relaxations
 Hypotensive LES pressures and large hiatal hernia- more
chance of GERD following abrupt increase in intra abdominal
pressure
3) ESOPHAGEAL CLEARANCE
 The GI acid produced spent too much time in contact with
the esophageal mucosa
 Normally swallowing contributes to esophageal clearance by
increasing salivary flow
 Saliva decreases with increasing age, so more often seen
with elderly.

9. 4)MUCOSAL RESISTANCE
 The mucus secreated by the mucus secreting glands
involves in the protection of esophagus
 The bicarbonates moving from the blood to the lumen
can neutralize acidic refluxate in the esophagus. On
repeated exposure to the refluxate or due to some
defect in normal mucosal defenses hydrogen ions
diffuse into the mucosa, leading to cellular
acidification and necrosis leading to esophagitis.
5)DELAYED GASTRIC EMPTYING
 An increase in gastric volume may increase both the
frequency of reflux and the amount of gastric fluid
available to be refluxed
 Physiologic Postprandial Gastro esophageal reflux
occurs

10. 6)COMPOSITION OF REFLUXATE
 If the pH of the refluxate is less than 2, esophagitis may
develop secondary to protein denaturation
 Also pepsinogen activated to pepsin at this pH may cause
esophagitis.

11. Pathogenesis
• Amount of esophageal damage seen
dependent on:
– Composition of refluxed material
– Volume of refluxed material
– Length of contact time
– Natural sensitivity of esophageal mucosa
– Rate of gastric emptying

12. Complications
• Esophagitis
• Esophageal strictures and ulcers
• Hemorrhage
• Perforation
• Aspiration
• Development of Barrett’s esophagus
• Precipitation of an asthma attack

13.  Erosive esophagitis
Erosive esophagitis is a condition in which areas of
the esophageal lining are inflamed and ulcerated. The
most common cause of erosive esophagitis is chronic
acid reflux.
 Responsible for 40-60% of GERD symptoms
 Severity of symptoms often fail to match severity of
erosive esophagitis.

14.  Esophageal stricture
A benign esophageal stricture,
or peptic stricture, is a narrowing
or tightening of the esophagus
that causes swallowing
difficulties.
 May need dilation
 Common in the distal
esophagus and are
generally 1 to 2 cm in
length.

15.  Barrett’s Esophagus
 Columnar metaplasia of the esophagus,i.e
replacement of the squamous epithelial lining of
the esophagus by specialized columnar- type
epithelium
 Associated with the development of
adenocarcinoma
 Have a greater chance (30%) of developing
esophageal stricture

16.  Barrett’s Esophagus
 Acid damages lining of
esophagus and causes
chronic esophagitis
 Damaged area heals in a
metaplastic process (change
in form) and abnormal
columnar cells replace
squamous cells.
 This specialized intestinal
metaplasia can progress to
dysplasia (the enlargement of
an organ or tissue by the
proliferation of cells of an
abnormal type, as an early
stage in the development of
cancer)and adenocarcinoma

17. GERD can lead to the reflux of fluid into the
lungs; this can result in choking, coughing, or
even pneumonia. In some patients, reflux may
worsen asthma symptoms. Treating GERD may
help improve asthma symptoms in these
people. And GERD can be worsened by asthma
and by some of the medicines that are used to
treat asthma.
GERD can also lead to chronic hoarseness,
sleep disturbance, laryngitis, halitosis (bad
breath), growths on the vocal cords, a feeling
as if there is a lump in your throat.
Asthma

18.  3 CLASSES OF SYMPTOMS
 TYPICAL SYMPTOMS
May be aggravated by activities that
worsen gastroesophageal reflux such as
recumbent position, bending over, or
eating a meal high in fat.
 Heartburn— retrosternal burning
discomfort (behind the breastbone)
 Regurgitation (spitting up of food)—
effortless return of gastric contents into
the pharynx without nausea, retching, or
abdominal contractions
 Water brash (hyper salivation)
 Belching

19. ATYPICAL SYMPTOMS
In some cases, these extra esophageal symptoms may be
the only symptoms present, making it more difficult to
recognize GERD as the cause, especially when
endoscopic studies are normal.
 Nonallergic asthma
 Hoarseness
 Pharyngitis
 Chest pain
 Dental erosions
 Cough

20. ALARM SIGNS/SYMPTOMS
These symptoms may be indicative of
complications of GERD such as Barrett’s
esophagus, esophageal strictures, or
esophageal cancer
 Dysphagia (difficulty swallowing )
 Early satiety (feeling full)
 GI bleeding
 Odynophagia (painful swallowing)
 Vomiting
 Unexplained Weight loss
 Iron deficiency anemia
 Choking
 Continual pain

21.  Barium swallow
 Endoscopy
 Ambulatory pH monitoring
 Acid perfusion (Bernstein test)
 Esophageal manometry

22.  An esophagram or barium swallow is an
X-ray imaging test used to visualize the
structures of the esophagus. The patient
swallows liquid barium while X-ray
images are obtained. The barium fills and
then coats the lining of the esophagus so
that it can diagnose anatomical
abnormalities such as tumors.
 Useful first diagnostic test for patients
with dysphagia
Stricture (location, length)
Mass (location, length)
Hiatal hernia (size, type)
Limitations
Detailed mucosal exam for
erosive esophagitis, Barrett’s
esophagus

23.  Indications
 Alarm symptoms
 Empiric therapy failure
 Preoperative evaluation
 Detection of Barrett’s
esophagus

24. Warning Signs
If present, consider an endoscopy:
• Dysphagia
• Bleeding
• Unexplained weight loss
• Choking
• Chest pain

25.  Upper endoscopy, also known as EGD, is a procedure
in which a thin scope with a light and camera at its tip is
used to look inside the upper digestive tract -- the
esophagus, stomach, and first part of the small intestine,
called the duodenum.
 Endoscopy (with biopsy if needed)
 In patients with alarm signs/symptoms
 Those who fail a medication trial
 Those who require long-term tx
 Absence of endoscopic features does not exclude a
GERD diagnosis
 Allows for detection, stratification, and management of
esophageal manisfestations or complications of GERD

26. A 24-hourpH study is often done in conjunction
with the oesophageal manometry to monitor the
levels and changes in acid content in the
oesophagus over a 24-hour period, while the
patient conducts his or her normal daily activities.
It is used to diagnose gastro-oesophageal reflux
disease (GERD – digestive acid passing from the
stomach, up into the oesophagus), to determine
the effectiveness of medications that are given to
prevent acid reflux and to determine if episodes of
acidic reflux are causing chest pain.

27.  24-hour pH monitoring-----Physiologic study
 Frequently performed for diagnosing GERD or reflux
esophagitis.
 Determines the amount of gastroesophageal acid
reflux .
Accepted standard for establishing or
excluding presence of GERD for those
patients who do not have mucosal changes
Trans-nasal catheter or a wireless, capsule
shaped device

28. Ambulatory 24 hr. pH MonitoringAmbulatory 24 hr. pH Monitoring
NormalNormal
GERDGERD

29. The test is done in a gastroenterology laboratory. A
nasogastric (NG) tube is passed through one side of
your nose and into your esophagus. Mild hydrochloric
acid will be sent down the tube, followed by salt water
(saline) solution. This process may be repeated several
times.
You will be asked to tell the health care team about
any pain or discomfort you have during the test.
Onset of symptoms after ingestion of dilute
hydrochloric acid and saline is considered positive
Differentiate between cardiac and non cardiac
chest pain

30. Esophageal Manometry
• Assess LES pressure,
location and relaxation
– Assist placement of
24 hr. pH catheter
• Assess peristalsis
– Prior to antireflux
surgery
Limited role in GERDLimited role in GERD

31.  If classic/typical symptoms like heartburn and
regurgitation exist in the absence of “alarm
symptoms” the diagnosis of GERD can be made
clinically and treatment can be initiated

32.  H2RA or PPI
 Expect response in 2-4 weeks
 If no response
 Change from H2RA to PPI
 Maximize dose of PPI
 If PPI response inadequate despite maximal
dosage
 Confirm diagnosis
 EGD(Esophagogastrodudenoscopy)
 24 hour pH monitor

33. Patient with heartburn
Iniate tx with H2RA or PPI
H2RA taken
BID
Good response
Frequent relapses
On demand tx
PPI taken QD
Good response
Maintenance therapy
with lowest effective dose
Symptoms persist
Consider EGD if
risk factors present
(> 45, white, male
and > 5 yrs of sx)
Increase to
max dose QD
or BID
Good response
Confirm diagnosis
EGD, ph monitor
No
Yes Yes
No
Yes
Yes
No
No

34.  Goals of therapy
 Alleviate or eliminate the patients symptoms.
 Decrease the frequency or recurrence and
duration of gastro esophageal reflux.
 Promote healing of the injured mucosa.
 Prevent the development of complications.

35.  Lifestyle modifications
 Avoid large meals
 Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate,
onions, garlic, peppermint
 Decrease fat intake
 Avoid lying down within 3-4 hours after a meal
 Elevate head of bed 4-8 inches
 Avoid meds that may potentiate GERD (CCB, alpha agonists,
theophylline, nitrates, sedatives, NSAIDS)
 Avoid clothing that is tight around the waist
 Lose weight
 Stop smoking

36.  Antacids
 Over the counter acid
suppressants and antacids
appropriate initial therapy
 Approx 1/3 of patients with
heartburn-related symptoms use
at least twice weekly
 More effective than placebo in
relieving GERD symptoms

37.  Histamine H2-Receptor Antagonists
 Competitively block the histamine receptors in
gastric parietal cells, thereby preventing acid
secretion
 More effective than antacids for relieving
heartburn in patients with GERD
 Faster healing of erosive esophagitis
 Can use regularly or on-demand

38. AGENT DOSAGE
Cimetadine 400-800mg twice daily
Cimetidine(tab),Zydus Cadila
Famotidine 20-40mg twice daily
Famocid(tab), Sun
Nizatidine 150mg twice daily
Axid
Ranitidine 150mg twice daily
Aciloc(tab), Cadila

39.  Proton Pump Inhibitors
 Effective not only with patients having erosive
esophagitis or complications(Barret’s esophagus),
but also with non erosive GERD who have
moderate to severe symptoms.
 Act by decreasing the basal and stimulated
gastric acid secretion through inhibition of the
final step of acid secretion by the parietal cell-
the H+/K+ ATPase proton pump.
 Better control of symptoms with PPIs vs H2RAs
and better remission rates
 Faster healing of erosive esophagitis with PPIs vs
H2RAs

40. AGENT DOSAGE
Esomeprazole 20-40mg daily
Esomac(tab), Cipla
Omeprazole 20mg daily
Lomac(cap), Cipla
Lansoprazole 15mg daily
Lan(Cap), Intas
Pantoprazole 40mg daily
Pan-OD(tab), Burgeon
Rabeprazole 20mg daily
Rabeloc(tab), Cadila

41.  H2RAs vs PPIs
12 week freedom from symptoms
 48% vs 77%
12 week healing rate
 52% vs 84%
Speed of healing
 6%/wk vs 12%/wk

42.  Antireflux surgery
 Failed medical management
 Patient preference
 GERD complications
 Medical complications attributable to a large
hiatal hernia
 Atypical symptoms with reflux documented on
24-hour pH monitoring

44. Laparoscopic

45.  Ant. partial
fundoplication
 Thal/Dor procedure
 Post. partial
fundoplication
 Toupet procedure

46.  Postsurgery
 10% have solid food dysphagia
 2-3% have permanent symptoms
 7-10% have gas, bloating, diarrhea, nausea, early
satiety
 Within 3-5 years 52% of patients back on
antireflux medications

47.  Endoscopic treatment
Relatively new
No definite indications
Select well-informed patients with well-
documented GERD responsive to PPI therapy
may benefit
 Three categories
Radiofrequency application to increase LES
reflux barrier
Endoscopic sewing devices
Injection of a nonresorbable polymer into LES
area