GERD is common, affecting 10-20% of people in western countries weekly. It occurs most commonly in those over age 40. The pathophysiology involves decreased LES pressure, disruption of anatomical barriers like hiatal hernia, impaired esophageal clearance, and impaired mucosal resistance. Clinical manifestations include typical symptoms of heartburn and regurgitation, as well as atypical symptoms. Diagnostic evaluation includes endoscopy and pH monitoring. Treatment involves lifestyle changes, antacids, H2 blockers, PPIs, and sometimes surgery. Complications include erosive esophagitis, stricture, Barrett's esophagus, and cancer.

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

3. Esophagus
Lower Esophageal
<§> hrt&dicine H'vT-Qom 2004
Gastroesophageal Reflux
Lower Esophagus
Sphincter Closed

4. m»©L©(§E V!
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. mWOlPWSDOLOO
1) Decreased lower esophageal sphincter
PRESSURE
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. ,tricycUc
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 Gl 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)MLCOSAL 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. M1nl©IP!rOTiG©L©@¥ (CONTOo)
Pathophysiology of GERD
Gastric acid: Pei»m 11 seeret ioii;
it opium I/fh ised
Impaired e/iophiigeid
cle»rn rice
11 iatal heriiia
Transient, triHjipropriatc
Ft* I hXh 1i u i i S‘ of Les
Pyloric
i i■ico e itpe1 ence;
di ii odein ogastrie
reflux
resting
pressure of EES
111ipnired salivary
fi i riel ion
Impcii red
esophageal
mucosal
defense
K Delayed gastric
emptying

11. Erosive esophagitis
Responsible for 40-60% of GERD symptoms
Severity of symptoms often fail to match severity
of erosive esophagitis

12. WMFOCATOM
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.
Narrowing of
the esophagus

13. ewmcow
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

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
hagcal reflux such as recumbent
osition, bending over, or eating a meal high in
at.
Heartburn—retrosternal burning
discomfort
Regurgitation-effortless return of gastric
contents into the pharynx without nausea
retching, or abdominal contractions
Water brash (hyper salivation)
fetching

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 JsIGNS/SYMPTOMS
These symptoms may be indicative of
complications of GERD such as Barrett’s
esophagus, esophageal strictures, or
esophageal cancer
Dysphagia
Early satiety
Gl bleeding
Odynophagia
Vomiting
Unexplained Weight loss
Iron deficiency anemia
Choking
Continual pain
WARNING
UNHOLY EXPERIMENT
IN PROGRESS

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.
Interior of Stomach ■
bgM-
Siomaoh Lining
Intenor oF Stomach
Endos«p«
BtolW Samplo
Slonucfi Lining

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

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, MSAIDS)
Avoid clothing that is tight around the waist
Lose weight
Stop smoking

25. Antacids
Over the counter acid
suppressants and antacids
appropriate initial therapy I
Approx 1 / 3 of patients witn
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. WATMT
AGENT
Cimetadine
Cimetidine(tab),Zydus Cadila
Famotidine
Famocidttab), Sun
Nizatidine
Axid
Ranitidine
Aciloc(tab), Cadila
DOSAGE
400-800mg twice daily
20-40mg twice daily
150mg twice daily
150mg twice daily

28. Parietal Cell
AcetyIchpline Gastrin
Proton Pump
Inhibitor
(PPI)
Proton Pump
Histamine

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

30. WTMT
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. Anti reflux 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
are
guaranteed in
life;
Answers
aren't.