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

Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagus

Often chronic and relapsingMay see complications of GERD in

patients who lack typical symptoms

Physiologic GERDPostprandialShort livedAsymptomaticNo nocturnal sx

Pathologic GERDSymptomsMucosal injuryNocturnal sx

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.

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

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.

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.

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

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.

Erosive esophagitisResponsible for 40-60% of GERD symptomsSeverity of symptoms often fail to match

severity of erosive esophagitis

Esophageal strictureResult of healing of

erosive esophagitisMay need dilationCommon in the distal

esophagus and are generally 1 to 2 cm in length.

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

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

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

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 asthmaHoarsenessPharyngitisChest painDental erosions

ALARM SIGNS/SYMPTOMSThese 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

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

H2RA or PPIExpect 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

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.

24-hour pH monitoringHelps 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

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 therapywith lowest effective dose

Symptoms persist

Consider EGD if risk factors present(> 45, white, maleand > 5 yrs of sx)

Increase tomax dose QD or BID

Good response

Confirm diagnosisEGD, ph monitor

No

Yes YesNo

Yes

Yes

No

No

Goals of therapyAlleviate 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.

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

AntacidsOver 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

Histamine H2-Receptor AntagonistsCompetitively 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 esophagitisCan use regularly or on-demand

AGENT DOSAGE Cimetadine 400-800mg twice

dailyCimetidine(tab),Zydus Cadila

Famotidine 20-40mg twice daily

Famocid(tab), Sun

Nizatidine 150mg twice dailyAxid

Ranitidine 150mg twice dailyAciloc(tab), Cadila

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

AGENT DOSAGE Esomeprazole 20-40mg

dailyEsomac(tab), Cipla

Omeprazole 20mg dailyLomac(cap), Cipla

Lansoprazole 15mg dailyLan(Cap), Intas

Pantoprazole 40mg daily

Pan-OD(tab), Burgeon

Rabeprazole 20mg daily

Rabeloc(tab), Cadila

H2RAs vs PPIs12 week freedom from symptoms

48% vs 77%12 week healing rate

52% vs 84%Speed of healing

6%/wk vs 12%/wk

Antireflux surgeryFailed medical managementPatient preferenceGERD complicationsMedical complications attributable to a

large hiatal herniaAtypical symptoms with reflux documented

on 24-hour pH monitoring

Postsurgery10% have solid food dysphagia2-3% have permanent symptoms7-10% have gas, bloating, diarrhea, nausea,

early satietyWithin 3-5 years 52% of patients back on

antireflux medications

Endoscopic treatmentRelatively newNo definite indicationsSelect well-informed patients with well-

documented GERD responsive to PPI therapy may benefit

Three categoriesRadiofrequency application to increase

LES reflux barrierEndoscopic sewing devices Injection of a nonresorbable polymer into

LES area

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

?QUESTIONS?