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GASTROESOPHAGEAL REFLUX DISEASE
1.
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
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
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
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
--distinction between normal and GERD is blurred because some degree of reflux is physiologic is all folks Physiologic—postprandially, short lived, asymptomatic, not during sleep Pathologic—symptoms or mucosal injury and often with nocturnal symptoms
--At level of diaphragmatic hiatus—main deterrant to reflux --disruption due to –review slide--multifactorial
--black arrow squamo-columnar jxn—Z-line --Z-line has undulating smooth contours --green arrow—gastric columnar epithelium above round black sphincter --red arow—pink white esophageal squamous epithelium --ulcerations in 2-7%
4-20% of patients
--1950—Norman Barrett --10-15% --black arrow squamo-columnar jxn—Z-line --Z-line has undulating smooth contours --green arrow—gastric columnar epithelium above round black sphincter --red arow—pink white esophageal squamous epithelium --RFs—male, smoker, age, obese
Adenoca with barretts 0.5%/yr--------without barretts 0.07%/yr
--gerd related chest pain may mimic angina—squeezing/burning, substernal, radiates to back, neck, jaw, arms. Minutes to hours. After meals, awakens patient from sleep, exacerbated by emotional stress --water brash—hypersalivation—heartburn and regurg of sour fluid or tasteless saliva into mouth --globus—lump in throat irrespective of swallowing --odynophagia—esophageal ulcer --nausea—infrequent --hrt burn 70-85%//regurg 60%//dysphagi 15-20%//angina 33%//asthma 15-20%
--need further eval if any present—egd--
--heartburn +/- regurgitation high specificity, low sensitivity
Once established h&p dx and no alarm symptoms can proceed with dx/therapeutic trial of tx.
--if trial of med did not work or if alarm symptoms or long term 5yrs need egd 1a evidence—dysphagia/early satiety/gi bleed/odynophagia/vomiting/wt loss/anemia --50-70% of patient’s with gerd will have a neg egd.
--Transnasal catheter or a wireless capsule shaped device affixed to distal esophagus --cather positioned 5cm above manometrically defined upper limit of les --capsul attached 6cm proximal to endoscopically defined squamocolumnar jxn --if mucosal changes—have dx and do not need 24hph.
--Tums, rolaids, maalox --$1 billion in yearly expenditures --aluminum/calcium—constipation Mag--diarrhea
--otc dose uniformly half of standard lowest prescription dose --similar clinical efficacy
--no significant differences in symptomatic tx of GERD or healing of erosive esophagitis 1a evidence --works only on active pumps—take 30-60min prior to meals --long-term tx generally benefits outweigh risks
candidacy --esophagitis—by egd --need normal manometry/motility --partial response to acid suppression --reduce hh, repair diaphragm, strengthen ge jxn—antireflux barrier --75-90% effective at alleviating hrtburn/regurg --better at helping with hrtburn/regurg than atypical sx