Gastroesophageal Reflux Disease

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Transcript Gastroesophageal Reflux Disease

GERD and
Peptic ulcer disease
August 29, 2011
Peptic Physiology
Peptic Physiology
•Intrinsic factor
•Hydrochloric acid
•Stimulated by gastrin, ach, H+
•Mucus
•Bicarbonate
•Pepsinogen
•Stimulated by gastrin
•Primarily in antrum
Gastroesophageal Reflux Disease
Epidemiology
About 44% of the US adult population
have heartburn at least once a month
 14% of Americans have symptoms weekly
 7% have symptoms daily

Physiologic vs Pathologic

Physiologic GERD
 Postprandial
 Short
lived
 Asymptomatic
 No nocturnal sx

Pathologic GERD
 Symptoms
 Mucosal
injury
 Nocturnal sx
Pathophysiology

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Primary barrier to
gastroesophageal reflux
is the lower esophageal
sphincter
LES normally works in
conjunction with the
diaphragm
If barrier disrupted, acid
goes from stomach to
esophagus
Clinical Manifestations

Most common symptoms
 Heartburn—retrosternal burning
discomfort
 Regurgitation—effortless return of
gastric contents into the pharynx
without nausea, retching, or
abdominal contractions
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Dysphagia—difficulty swallowing
Other symptoms include:

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Chest pain, globus sensation,
odynophagia, nausea
Extraesophageal manifestations

Asthma, laryngitis, chronic cough
Diagnostic Evaluation
 If
classic symptoms of heartburn and
regurgitation exist in the absence of “alarm
symptoms” the diagnosis of GERD can be
made clinically and treatment can be initiated
Alarms
Dysphagia
 Early satiety
 GI bleeding
 Odynophagia
 Vomiting
 Weight loss
 Iron deficiency
anemia

Trial of Medications

H2RA or PPI
 Expect
response in 2-4 weeks
 If no response
Change from H2RA to PPI
 Maximize dose of PPI

Trial of Medications

If PPI response inadequate despite
maximal dosage
 Confirm
diagnosis
EGD
 24 hour pH monitor

EGD

Endoscopy (with biopsy if
needed)

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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 manifestations or
complications of GERD
24-hour pH monitoring
 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
Patient with heartburn
Initiate tx with H2RA or PPI
H2RA taken
BID
PPI taken QD
No
Good response
Good response
Yes
Yes
No
Yes
Frequent relapses
No
On demand tx
Increase to
max dose QD
or BID
Maintenance therapy
with lowest effective dose
Yes
Symptoms persist
Good response
No
Consider EGD if
risk factors present
(> 45, white, male
and > 5 yrs of sx)
Confirm diagnosis
EGD, ph monitor
Treatment

Goals of therapy
 Symptomatic
relief
 Heal esophagitis
 Avoid complications
Lifestyle modifications

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Avoid large meals
Avoid acidic foods (citrus/tomato), alcohol, caffeine,
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
Medical Treatment

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
Medical Treatment

Histamine H2-Receptor Antagonists
 More
effective than placebo and antacids for
relieving heartburn in patients with GERD
 Faster healing of erosive esophagitis when
compared with placebo
 Can use regularly or on-demand
Medical Treatment
AGENT
EQUIVALENT
DOSAGES
DOSAGE
Cimetadine
Tagamet
400mg twice daily
400-800mg twice daily
Famotidine
Pepcid
20mg twice daily
20-40mg twice daily
Nizatidine
Axid
150mg twice daily
150mg twice daily
Ranitidine
zantac
150mg twice daily
150mg twice daily
Medical Treatment

Proton Pump Inhibitors
 Better
control of symptoms with PPIs vs
H2RAs and better remission rates
 Faster healing of erosive esophagitis with
PPIs vs H2RAs
Treatment
AGENT
EQUIVALENT
DOSAGES
DOSAGE
Esomeprazole
Nexium
40mg daily
20-40mg daily
Omeprazole
Prilosec
20mg daily
20mg daily
Lansoprazole
Prevacid
30mg daily
15-10md daily
Pantoprazole
Protonix
40mg daily
40mg daily
Rabeprazole
Aciphex
20mg daily
20mg daily
Treatment

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
Treatment

Antireflux surgery candidates
 EGD
proven esophagitis
 Normal esophageal motility
 Partial response to acid suppression
Treatment

Antireflux surgery
 Tenets
of surgery
Reduce hiatal hernia
 Repair diaphragm
 Strengthen GE junction
 Strengthen antireflux barrier via gastric wrap
 75-90% effective at alleviating symptoms of
heartburn and regurgitation

Nissen Fundoplication
Upper GI Study
Treatment

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 nonabsorbable polymer into LES area
Complications
Erosive esophagitis
 Stricture
 Barrett’s esophagus

Complications

Erosive esophagitis
 Responsible
for 40-60% of GERD symptoms
 Severity of symptoms often fail to match
severity of erosive esophagitis
Complications

Esophageal
stricture
 Result
of healing
of erosive
esophagitis
 May need dilation
Complications

Barrett’s Esophagus
 Columnar
metaplasia of
the esophagus
 Associated with the
development of
adenocarcinoma
Complications

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
Complications

Barrett’s Esophagus
 Manage
in same manner as GERD
 EGD every 3 years in patient’s without
dysplasia
 In patients with dysplasia annual to shorter
interval surveillance
 Many patients with Barrett’s are asymptomatic
Complications

Esophageal dysplasia/cancer

Cancer
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High-grade dysplasia
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Esophagectomy
Esophagectomy or ablation
Low-grade dysplasia
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Treat GERD
EGD surviellence
Peptic Ulcer Disease
Peptic Ulcer Disease

Symptoms
 Pain
 Bleeding
 Perforation
 Obstruction
Peptic Ulcer Disease
Duodenal Ulcer
Usually within 2 cm of the pylorus
 Pain cyclical

 1-2

hours after breakfast, lunch and at night
Etiology
H
pylori - 90%
 NSAIDs – 10%
 Increased vulnerablity of mucosa to acid and
pepsin
Duodenal Ulcer

Eridicate H pylori
 Triple

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therapy
PPI – twice daily for 2 weeks
Amoxicillin - 1g twice daily for 2 weeks
Clarithromycin – 500mg twice daily for 2 weeks
Surgery for complications
 Bleeding
 Perforation
 Obstruction
Duodenal Ulcer
Zolliger-Ellison Syndrome
(Gastrinoma)

Very rare

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MEN-1
Tumor of islet cell

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Produce gastrin – lab levels extreme
Typically in wall of duodenum or pancreas
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Ulcers

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Gastrinoma Triangle
Usually multiple
In 2nd-3rd portion of duodenum
Treatment


PPI
Surgical resection
Gastric Ulcer

Types
 Type I
 Most common
 Lesser curve
 H pylori
 Type II
 Pre pyloric
 Associated with duodenal ulcers
 Type III
 Antrum
 NSAIDs
Gastric Ulcer

Need to rule out malignancy

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EGD
Biopsy
Treatment

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Stop NSAIDs
PPI
Treat H pylori
Repeat EGD to check for healing
Surgery
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Malignancy
Bleeding
Perforation
Obstruction
Questions?