Gastro Esophageal Reflux Disease (GERD)

Dr. Abhimanyu ParasharPharm D

Asst. Professor

What is GERD?

“Symptomatic clinical condition or

histopathological alteration resulting from

episodes of reflux of acid, pepsin and

occasionally bile from stomach to esophagus”

Why GERD?

Multiple factors are involved in acid reflux such as, Transient LES relaxations, Reduced tone of LES,

Hiatus hernia &

Abnormal esophageal acid clearance

Why GERD?. . .

Pregnancy:Enlarged uterus

Increased abdominal pressure

Reflux of gastric contents up to esophagus

Why GERD?. . .

Increased progesterone levels in pregnancy

Decreased resting LES pressure &Slow gastric emptying

Why GERD?. . .

Mixed connective tissue disorder (Scleroderma):

Impaired esophageal function

Decreased peristalsis in smooth muscle segment of esophagus

Decreased LES pressure

Why GERD?. . .

Gastro paresis Changes gastricIntestinal Pseudo obstruction emptyingCollagen vascular disorders

increased risk of GERD

ZES (Hypersecretory condition)

Abnormality in Q&Q of refluxate

How GERD?

Esophageal damage as a result of reflux of noxious gastric contents like gastric acid, pepsin, bile acids & pancreatic enzymes

Not associated with hepersecretion but acid produced remains in contact with esophageal mucosa for longer duration

Defective LES pressure causes spontaneous LES relaxations, increases intraabdominal pressure

How GERD?

Transient LES relaxation- most common mechanism that causes reflux

Decreased resting LES tone < 10 mmHg (10-30 mmHg)

Prolonged esophageal acid clearance time leads to esophagitis

Duration of time that the esophageal mucosa remains acidified (PH < 4) after an episode of gastric acid reflux

How GERD? Bicarbonates & growth factors present in saliva enhances

mucosal repair

Periods of diminished salivation like sleep reduces acid neutralization & is associated with more frequent reflux events

Substances that increases salivation like oral lozenges, chewing gum/ bethenechol chloride increases acid clearance

Smoke prolongs acid clearance time & causes hyposalivation

Decreased lower esophageal sphincter pressure due to foods like fatty meals, chocolate, coffee, cola

Foods like spicy food, orange juice and medications like iron supplements, aspirin and NSAID’s, narcotics, anticholinergics, theophylline etc causes direct irritation to the esophageal mucosa

H.pyroli may inhibit or exacerbate the acid reflux

RISK FACTORSDemographic factors:

- Cross sectional studies showed no association with age.-Higher risk in males.

Life style factors:-Obesity, smoking, alcohol, coffee and fatty food

reduce the tone of the sphincter.

Genetic factors:-Higher rates for dizygotic twins

Clinical features

Heart burn

Acid regurgitation

Dysphagia

Waterbrash

Belching

Reflux esophagitis

Atypical symptoms

Non-allergic asthma

Chronic cough

Hoarseness

Pharyngitis

Dental erosion

Chest pain

Diagnostic tools

• Endoscopy

• Barium radiography

• 24 hr ambulatory PH monitoring

The endoscopic classification of Esophagitis using Savary and Miller grading scale

Grade 0 normal esophageal mucosa

Grade 1 erythematic or diffusely red mucosa and edema causing accentuated folds.

Grade 2 isolated round or linear erosions extending from the gastro esophageal junction upwards, not involving the entire circumference.

Grade 3 confluent erosions extending around the entire circumference or superficial ulceration without stenosis.

Grade 4 complicated cases; erosions as above, plus deep ulcerations, strictures, or columnar epithelium-lined esophagus

Non-Pharmacological management

Avoidance of precipitating factors

Head end bed elevation

Weight reduction

Avoiding smoking & alcohol consumption

Avoiding eating or drinking at bed time

Antireflux surgery:to avoid long term therapy with PPIspoor control of symptoms

Interventional approaches.- Anti reflux surgery: done mainly when patients fail to

respond to medications or suffer from complications.- The goal is to position the lower esophageal sphincter

within the abdomen and close any associated hiatal defect.

- Endoluminal therapy:Includes endoscopic suturing.Endoluminal applications of radio frequency heat

energy.Endoscopic injection of a bi polymer known as

enteryx into the junction.

2. Pharmacologic therapy:

a. Step up approach: Starting with life style modification and patient directed therapy-pharmacologic management or interventional approach.

b. Step down approach: Starting with proton pump inhibitor-lowest degree of acid suppression needed to control symptoms.

Pharmacological management

For mild & intermittent disease:

Mg + Al hydroxide preparations 10-20mL POOrAntacid + alginate preparation 10-20 mL PO qidOrH2 rec antagonist

cimetidine 400 mg, famotidine 20 mg,nizatidine 150 mg, ranitidine 150 mg

Pharmacological management. . .

Disease requiring regular therapy:

For patients who have symptoms on most daysPPI for 4 wks

esomeprazole 40 mg, lansoprazole 30 mg,omeprazole 20 mg, pantoprazole 40 mg,rabeprazole 20 mg

If response is inadequate CST for 8 wks

Antacids

Prokinetic agents

Standard dose H2 rec antagonist

Half dose PPI

Standard dose PPI

High dose PPI

Pharmacological management. . .

Antacids: immediate relief of symptoms

Antacids with algenic acid: form a viscous solution that floats on the surface of

gastric content, serves as protective barrier for esophagus against reflux gastric contents

Prokinetic agents:Increases LES pressure in a dose related manner &

accelerates gastric emptying

Phase1Intermittent,mild heart burn

A: Lifestyle changes PLUSB: Antacids•Mg. OH 30 mL as needed or after meals and at bedtime.•Calcium carbonate(500mg) 2-4 tablets as needed. AND/ORC: Low dose H2receptor antagonists(each taken up to twice daily)•Cimetidine 200mg•Famotidine 10mg•Ranitidine 75mg OR proton pump inhibitor (taken once daily)•Omeprazole 20mg

Phase llSymptomatic relief of GERD

A:Lifestyle modifications PLUSB:Standard doses of H2-receptors antagonists for 6-12 weeks.

•Cimetidine 400mg twice daily•Famotidine 20mg twice daily•Ranitidine 150mg twice daily

ORB:Proton pump inhibitors for4-8 weeks.all are given once daily.

•Esomeprazole 20mg•Lansoprazole 15mg•Omeprazole 20mg •Pantoprazole 40mg•Rabeprazole 20mg

Healing of erosive esophagitis or treatment of patients presenting with moderate to severe symptoms or complications

A:Lifestyle modifications. PLUSB:Proton pump inhibitors for 4-6 weeks (up to twice daily)•Esomeprazole 20-40 mg daily•Lansoprazole 30 mg daily•Omeprazole 20 mg daily •Rabeprazole 20 mg daily•Pantoprazole 40 mg daily ORB:High-dose H2-receptor antagonist for 8-12 weeks

•Cimetidine 400mg 4 times daily or800 mg twice daily•Famotidine 40mg twice daily•Ranitidine 150mg 4 times daily

Phase lll Interventional therapies(antireflux surgery or endoluminal therapies)

PROKINETIC AGENTS

• These are drugs which promote gastric motility.• Used as adjuvant therapy along H2RAs.• Due to severe side effects they are withdrawn from the

market.• Cisapride induced arrhythmias and metoclopramide induced

tachyphylaxis.• This combination is appropriate in patients suspected with

motility disorder or who has failed high dose PPI therapy.• In case of motility disorder Cisapride 10mg tid or 20mg bid for

12 weeks is given.• Metoclopramide oral 10mg 4 times daily in 2-4 divided doses.

MAINTAINANCE THERAPY• Omeprazole 20 mg daily alone or in

combination with cisapride 10 mg 3 times daily.

• It was more effective in preventing recurrence of erosive GERD and also complicated form (grades 3 and 4) of esophagitis.

• Omeprezole and lansoprezole in doses of 20 mg and 30 mg daily respectively decreased relapse rates.

GERD IN CHILDREN• In infants less than 6 months, regurgitation is very

common.

• A formal evaluation such as 24 hours esophageal PH monitoring and biopsies is required.

• Simple measures like sleeping or feeding, slight elevation of the head or feeds can be thickened.

• If this attempt fails then pharmacological therapy is justified.

• Ranitidine 2-3 mg/kg orally 3 times daily. Omeprazole 20mg (child <2yrs: 5mg, 2-8yrs: 10mg orally daily).