GASTROESOPHAGEAL REFLUX DISEASE

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 bicarbonate s 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.  Erosive esophagitis
 Responsible for 40-60% of GERD symptoms
 Severity of symptoms often fail to match severity
of erosive esophagitis

12.  Esophageal stricture
 Result of healing of
erosive esophagitis
 May need dilation
 Common in the distal
esophagus and are
generally 1 to 2 cm in
length.

13.  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

14.  Barrett’s Esophagus
 Acid damages lining of
esophagus and causes
chronic esophagitis
 Damaged area heals in a
metaplastic process and
abnormal columnar cells
replace squamous cells
 This specialized intestinal
metaplasia can progress to
dysplasia and
adenocarcinoma

15.  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
 Regurgitation—effortless return of gastric
contents into the pharynx without nausea,
retching, or abdominal contractions
 Water brash (hyper salivation)
 Belching

16. 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

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

18.  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

19.  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

20.  Endoscopy (with biopsy if
needed)
 In patients with alarm
signs/symptoms
 Those who fail a medication trial
 Those who require long-term
treatment
 Important in distinguishing
between esophagitis and Barret’s
metaplasia
 Absence of endoscopic features
does not exclude a GERD
diagnosis
 Confirmation can be achieved by
provocative tests such as an acid
perfusion test(Bernstein test),
standard acid reflux test etc.

21.  24-hour pH monitoring
 Helps in establishing the presence of acid above
the LES as the cause of symptoms or esophageal
damage.
 Documents the amount of time the esophageal
pH is low.
 Useful in patients who have not responded or
who have had an incomplete response to empiric
therapy, have symptoms with out evidence of
mucosal injury, or have atypical symptoms.
 Trans-nasal catheter or a wireless, capsule
shaped device

22. 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

23.  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.

24.  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

25.  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

26.  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

27. 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

28.  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

29. 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

30.  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

31.  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

32.  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

33.  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

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

35. ?QUESTIONS?