Gastroesophagea

l of Reflux
Disease (GERD)

Blok Nutrisi dan Sistem Digesti, 15 April 2009 [7]

Overview of GERD
Definition

Symptoms or mucosal damage produced

by the abnormal reflux of gastric contents
into the esophagus
Classic

symptom is frequent and

persistent heartburn
44 % of Americans experience
heartburn at least once per month
7 % have daily symptoms

Normal Function
Esophagus

Transports food from mouth to stomach through

peristaltic contractions
Lower

esophageal sphincter (LES)/lower

esophageal sphincter
Relaxes, on swallowing, to allow food to enter
stomach and then contracts to prevent reflux

Normal

to have some amount of reflux

multiple times each day (transient relaxation
of LES not associated with swallowing)

http://www.gerd.com/intro/noframe/grossovw.htm

Mekanisme defense dan faktor offense esofagus

berhubungan dengan heartburn (sumber: Siepler & Trudeau,
2004)
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Pathogenesis
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lines of defense must be impaired

for GERD to develop
LES

barrier impairment

Relaxation

of LES
Low resting LES pressure
Increased gastric pressure
Decreased

clearance of refluxed
materials from esophagus
Decreased esophageal mucosal
resistance

Pathophysiology

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

Contributing Factors
Decrease

pressure

LES

Chocolate

Alcohol

meals
Coffee, cola, tea
Garlic
Onions
Smoking

Directly irritate the gastric

mucosa

Fatty

Tomato-based products
Coffee
Spicy foods
Citrus juices
Meds: NSAIDS, aspirin, iron,
KCl, alendronate

Stimulate acid secretions

Soda
Beer
Smoking

Contributing Factors
Drugs

that decrease LES pressure

Alpha-adrenergic

agonists
Anti-cholinergic agents (e.g. TCAs, antihistamines)
Beta-adrenergic agonists
Calcium channel antagonists (nifedipine most
reduction)
Diazepam
Dopamine
Meperidine
Nitrates/Other vasodilators
Estrogens/progesterones (including oral
contraceptives)
Prostaglandins
Theophylline

Lines of Defense
Clearance

of refluxed materials from

esophagus
Primary

peristalsis from swallowing

increases salivary flow
Secondary peristalsis from esophageal
distension
Gravitational effects
Esophageal
Mucus

mucosal resistance

production in esophagus
Bicarbonate movement from blood to mucosa

Pathogenesis
Amount of esophageal damage seen dependent

on:

Composition of refluxed material

Which

is worse: acid or alkaline refluxed material?

Volume of refluxed material

Length of contact time
Natural sensitivity of esophageal mucosa
Rate of gastric emptying

Typical Symptoms
Common symptoms most common when

pH<4

Heartburn
Belching and regurgitation
Hypersalivation

May be episodic or nocturnal

May be aggravated by meals and

reclining position

Atypical Symptoms
Nonallergic asthma
Chronic cough
Hoarseness
Pharyngitis
Chest pain (mimics angina)
May be only symptoms omeprazole

test

Complications
Esophagitis
Esophageal strictures and ulcers
Hemorrhage
Perforation
Aspiration
Development of Barretts esophagus
Precipitation of an asthma attack

Complications
Erosive

esophagitis

Responsible for 40-60% of GERD

symptoms
Severity of symptoms often fail to match
severity of erosive esophagitis

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Complications
Esophageal

stricture

Result of healing
of erosive
esophagitis
May need
dilation

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Barretts Esophagus
Highest prevalence in adult Caucasian males
Histologic change

Lower esophageal tissue begins to resemble the

epithelium in the stomach lining

Predisposes to esophageal cancer (30-60x) and

esophageal strictures (30-80% increased risk)
Odds ratio for development (compared with GERD < 1
yr.)
Patients with GERD 1-5 years 3.0
Patients with GERD > 10 years 6.4

More frequent, more severe, and longer-lasting the

symptoms of reflux, the > the risk of cancer

Complications
Barretts

Esophagus

Columnar metaplasia
of the esophagus
Associated with the
development of
adenocarcinoma

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Complications

Barretts 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

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Therapy Goals
Alleviate or eliminate symptoms
Diminish the frequency of
recurrence and duration of
esophageal reflux
Promote healing if mucosa is
injured
Prevent complications

Therapy
Therapy is directed at:

Increasing LES pressure

Enhancing esophageal acid clearance
Improving gastric emptying
Protecting esophageal mucosa
Decreasing acidity of reflux
Decreasing gastric volume available
to be refluxed

Treatment
Three phases in treatment

Phase I: Lifestyle changes 2 weeks

Lifestyle modifications
Patient-directed therapy with OTC
medications

Phase II: Pharmacologic intervention

Standard/high-dose antisecretory therapy

Phase III: Surgical intervention

Patients who fail pharmacologic treatment or

have severe complications of GERD
LES positioned within the abdomen where it
is under positive pressure

Treatment Selection
Mild intermittent heartburn (Phase I)
Treat with lifestyle changes plus
antacids AND/OR low dose OTC H2receptor antagonists (H2RAs) as needed

Symptomatic relief of mild to

moderate GERD (Phase II)
Treat with lifestyle changes plus
standard doses of H2RAs for 6-12
weeks OR proton pump inhibitors
(PPIs) for 4-8 weeks

Treatment Selection
Healing of erosive esophagitis or
treatment of moderate to severe GERD
(Phase II)
Lifestyle modifications plus PPIs for 8-16
weeks OR high dose H2RAs for 8-12 weeks
PPIs preferred as initial choice due to more
rapid symptom relief and higher rate of healing

May also add a prokinetic/promotility agent

Treatment Considerations
Prokinetic agents are an alternative
to H2RAs
Efficacy similar to prescription dose
H2RAs
Used as a single agent only in mild to
moderate, nonerosive GERD
May be more expensive and use is
limited by side effects

Treatment Considerations
Maintenance therapy may be needed
Large % of patients experience
recurrence within 6-12 months after DC
of therapy
Goal is to control symptoms and prevent
complications
May use antacids, PPIs or H2RAs
In patients with more severe symptoms, PPI
most effective

Lifestyle Modifications
Elevate the head of the bed 6-8 inches
Decrease fat intake
Smoking cessation
Avoid recumbency for at least 3 hours postprandial
Weight loss
Limit alcohol intake
Wear loose-fitting clothing
Avoidance of aggravating foods
These changes alone may not control symptoms

Esophageal
clearance:
Cisapride

Esophageal mucosal
resistance:
Alginic acid, Sucralfate

Gastric emptying:
Metoclopramide
Cisapride

LES pressure:
Metoclopramide
Cisapride

Gastric acid:
Antacids
H2RAs
PPIs
http://www.gerd.com/intro/noframe/grossovw.htm

Drug Therapy - PPIs

Proton Pump Inhibitors
Used to treat moderate to severe GERD
More effective and faster healing than
H2RAs

May be used to treat esophagitis refractory to

H2RAs

All agents effective

Drug Therapy - PPIs

May give higher doses bid for

Patients with a partial response to standard

therapy
Patients with breakthrough symptoms
Patients with severe esophageal dysmotility
Patients with Barretts esophagus

Always give second dose 30 minutes prior

to evening meal

Treatment
AGENT

EQUIVALENT
DOSAGES

DOSAGE

Esomeprazole
Nexium

40mg daily

20-40mg daily

Omeprazole
Prilosec

20mg daily

20mg daily

Lansoprazole
PROSOGAN FD

30mg daily

15-10md daily

Pantoprazole
Protonix

40mg daily

40mg daily

Rabeprazole
Aciphex

20mg daily

20mg daily

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Drug Therapy - Prokinetics

Prokinetic Agents -- MOA

Enhances motility of smooth muscle from

esophagus through the proximal small bowel

Accelerates gastric emptying and transit of

intestinal contents from duodenum to ileocecal
valve

Drug Therapy - Prokinetics

Prokinetic Agents

Results of therapy

Improved gastric emptying

Enhanced tone of the lower esophageal sphincter
Stimulated esophageal peristalsis (cisapride only)

Terima kasih

Helai ilalang jadi pena, dan lautan jadi tinta, takkan cukup untuk menulis ilmuMU

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