gastroesophageal reflux disease

2.  Reflux is a very common problem presenting as
‘heartburn’, acid eructation, sensation of stomach
contents coming back in the foodpipe, especially after a
large meal, aggravated by stooping or lying flat. Some
cases have an anatomical defect (hiatus hernia) but
majority are only functional,
 where in there is relaxation of lower esophageal
sphincter (LES) in the absence of swallowing. Repeated
reflux of acid gastric contents into lower 1 / 3rd of
esophagus causes esophagitis, erosions, ulcers, pain
on swallowing, dysphagia, strictures, and increases the
risk of esophageal carcinoma.There may also be
extraesophageal complications.

3.  The primary barrier to reflux is the tone of LES
which can be altered by several influences:
Inherent tone: of sphincteric smooth muscle.
 Hormonal: gastrin increases, progesterone
decreases (reflux is common in pregnancy).
 Neurogenic: vagus is motor to the sphincter,
promotes esophageal peristalsis.
 Dietary: fats, alcohol, coffee, chocolates
decrease, while protein rich foods increase LES
tone.
 Drugs: anticholinergics, tricyclic
antidepressants, Ca2+ channel blockers,
nitrates reduce LES tone.
 Smoking: relaxes LES.

4.  Delayed gastric emptying and increased
intragastric pressure may overcome the LES
barrier to reflux. GERD is a wide spectrum of
conditions from occasional heartburn
(majority of cases) to persistent
incapacitating reflux which interferes with
sleep and results in esophageal,
laryngotracheal and pulmonary
complications.
 Severity of GERD may be graded as:

5.  Stage 1: occasional heartburn (<3 episodes/
week), mostly only in relation to a
precipitating factor, mild symptoms, no
esophageal lesions.
 Stage 2: > 3 episodes/week of moderately
severe symptoms, nocturnal awakening due
to regurgitation, esophagitis present or
absent.

6.  Stage 3: Daily/chronic symptoms, disturbed
sleep,
esophagitis/erosions/stricture/extraesophage
al symptoms like laryngitis, hoarseness, dry
cough, asthma. Symptoms recur soon after
treatment stopped.

7.  Though GERD is primarily a g.i. motility
disorder, acidity of gastric contents is the
most important aggressive factor in causing
symptoms and esophageal lesions. The
functional abnormality is persistent; though
short-term remissions do occur. Dietary and
other lifestyle measures (light early dinner,
raising head end of bed, weight reduction
and avoidance of precipitating factors) must
be taken. Treatment of GERD is
individualized according to severity and
stage of the disorder.

8.  These are the most effective drugs, both for symptomatic
relief as well as for healing of esophageal lesions.
Intragastric pH >4 maintained for ~18 hr/day is considered
optimal for healing of esophagitis. This level of acid
suppression can be consistently achieved only by PPIs.
Therefore, PPIs are the drugs of choice for patients with all
stages of GERD, particularly stage 2 and 3 cases. Symptom
relief is rapid and 80–90% esophageal lesions heal in 4–8
weeks. Dose titration is needed according to response in
individual patients. Some patients, especially stage 2 and 3
cases, need twice daily dosing. Prolonged (often indefinite)
therapy is required in chronic cases because symptoms
recur a few days after drug stoppage. PPIs have no effect
on LES tone.

9.  They reduce acidity of gastric contents and have no
effect on LES tone. H2 blockers cause less complete
acid suppression than PPIs, viz elevate intragastric
pH to >4 for less than 8 hours in 24 hours with the
conventional doses given twice daily. Adequate
symptom relief is obtained only in mild cases;
healing of esophagitis may occur in 50–70%
patients. H2 antagonists are indicated in stage-1
cases, or as alternative to PPIs in stage 2 or 3
cases. The daily dose should be divided into 2–3
portions for better response.

10.  Their use in GERD is limited to occasional or
intercurrent relief of heartburn because they
act within few minutes. Antacids are no
longer employed for healing of esophagitis,
which they are incapable of.
(a) Systemic: Sodium bicarbonate, Sod. citrate
(b) Nonsystemic: Magnesium hydroxide, Mag. trisilicate,
Aluminium hydroxide gel, Magaldrate, Calcium carbonate

11.  It forms a thick frothy layer which floats on
the gastric contents like a raft may prevent
contact of acid with esophageal mucosa. It
has no effect on LES tone. Combination of
alginate with antacids may be used in place
of antacids alone, but real benefit is
marginal.

12.  Metoclopramide, cisapride and other
prokinetic drugs may relieve regurgitation
and heartburn by increasing LES tone,
improving esophageal clearance and
facilitating gastric emptying, but do not affect
gastric acidity or promote healing of
esophagitis.

13.  Symptom control afforded by prokinetic
drugs is much inferior to that by PPIs/H2
blockers. Their use in GERD has declined.
Prokinetidrugs are often coprescribed with
PPI/H2 blocker therapy, but whether this
improves outcome is not clear.

14. THANK YOU