GERD John Hopkins Modules By Tamara Mansy PGY1

GERD John Hopkin’s Modules By: Tamara Mansy PGY-1 Sep/14/2017

Epidemiology of GERD • It is common disorder with surveys showing it affects 20% of adult US population at least once/wk, & 61 million experience it at least monthly • GERD has significant impact on quality of life, 30% reports decreased work productivity, and associated higher sx severity, often due to disrupted sleep

Definitions of upper GI terms • Dyspepsia: upper abdominal discomfort often associated with bletching, nausea &/or bloating, & sometimes associated with food intake • Heartburn: a common sx of gastroesophageal reflux, retrosternal burning pain, sometimes accompanied by a bitter taste at the back of the mouth • Gastroesophageal reflux (GER): entry of gastric contents into the esophagus, could by symptomatic or asymptomatic. • GERD: presence of GER sx (including but not limited to heart burn and regurge

Pathophysiology • Pressure of stomach > LES pressure (transient or chronic): leading to reflux of stomach contents into the esophagus • GERD is more likely to occur when: • Gastric vol is increased (after a big meal) • Gastric pr is increased and gastric contents are nearer to LES, such as in bending over or recumbent.

Symptoms • Typical hallmark sx are heartburn &/or regurgitation. • Heartburn: burning retrosternal sensation sometimes accompanied by bitter taste at the back of the mouth • Chest pain that can be confused with angina (atypical sx) • Atypical sx: sore throat, laryngitis/hoarseness, chronic cough, refractory asthma, atypical chest pain, burning tongue and excessive salivation, Globus (sensation of fullness in the back of throat) • Alarm sx: Bleeding, Odynophagia, Dysphagia, Anorexia, Wt. loss, Signs of systemic illness • P/E: eroded dental enamel, aphthus ulcer

Causes • Idiopathic • Secondary causes: Ascites, Eosinophilic gastritis, Obesity (or recent wt. gain), Pregnancy, Scleroderma, Surgical destruction of LES, & Tobacco use • Medications: Anticholinergics, Benzodiazipines, BB, CCB, Nitrates, PG, Sildenafil, & TCA • Food triggers: Alcohol, Chocolate, Coffee, High-fat foods, Orange/Citrus, Peppermint or spearmint, Tomato products

The Gerd. Q Questionnaire

Differential Dx • Esophageal dysmotility: cold liquid/emotional distress/hurried eating • • leading to dysphagia, chest pain, and regurgitation Esophageal spasm: dysphagia and chest pain Scleroderma (SSc vs CREST): Raynaud’s phenomenon, stiffness of fingers and knees and skin thickening Dyspepsia: upper abdominal discomfort associated with bletching, nausea &/or bloating, & sometimes associated with food intake Duodenogastroesophageal reflux: esophageal reflux of duodenal contents that may include biliary secretions, pancreatic enz, and HCO 3 (GERD that do not respond to acid lowering treatments)

• Eosinophilic esophagitis: typically young patient with atopy. Reactions to allergens, foods, acid reflux resulting in infiltration of eosinophils in esophageal lining. Dysphagia, food impaction, central chest pain, persistent heartburn, upper abdominal pain and regurg.

Evaluation The need for further testing is invoked in 3 scenarios 1. To avert misdiagnosis (high index of suspicion for other possible Dx, such as cardiac and pulmonary causes of chest discomfort) 2. Identify complications 3. Evaluation of empirical treatment failure

Evaluation • For patients with classic GERD, no red flag sx, and sx easily controlled no need for further evaluation • Refractory GERD (treatment failure): taking a PPI 4 -8 weeks once daily 30 minutes before meal. Followed by trying another 4 -8 weeks BID or switching to a different PPI. • Referral for GI Alarm sx, treatment failure, and > 5 years duration of GERD

Treatment v Life Style modifications v Pharmacotherapy v Surgery and endoscopic therapy

Life style modifications Ø Recommended to all patients regardless severity Ø Elevation of the head of the bed or a foam wedge placed under the head and upper thorax Ø Avoid recumbency for 2 -3 hours postprandially Ø smoking cessation Ø Avoiding trigger foods: alcohol, carbonated beverages, chocolate, coffee, high-fat content foods, oranges, peppermint and tomato Ø Decreased fat intake in general Ø Wt loss

Pharmacotherapy q Mild: intermittent sx precipitated by dietary indiscretions OTC antacids. Long term trials have shown they are effective in 20% of patients who use them q Mild-Moderate, intermittent (<2 episodes/wk), & treatment naive H 2 RA are first line, in standard doses (ranitidine 150 mg BID), achieve symptomatic relief in 60% and endoscopic resolution of documented esophagitis in 50% Promotility agents (metoclopramide) are no longer recommended unless there is documented gastric motility abnormality

Pharmacotherapy q PPI: 1. Severe sx or Persistent (> 2 episodes/wk) 2. Not effective treatment with H 2 RA 3. GERD with complications (ulcerative or erosive esophagitis, barrette esophagus or stricture) Patients with severe erosive gastritis may not respond to conventional doses of PPI and may require doubling or tripling of the dose. Optimization of the dose 30 -60 min prior to meals

SE of PPI

Side Effects of Medications • Theoretical risk of cancer due to chronic acid suppression that lead to increased levels of circulating gastrin with parietal cell hyperplasia and gastric hypertrophy. No evidence of increased cancer risk in studies. • Long term PPI Decreased bone density and increased risk of fracture due to decreased Ca absorption. Will recommend to use Ca supplement at meal time to facilitate absorption of Ca. • Hypomagnesemia: in PPI. Check Mg level prior to initiate therapy and periodically after that

Side Effects • C. Diff infection: PPI and H 2 RA. Discontinuation of PPI should be considered with C. Diff Dx • CAP and HAP through unclear mech: PPI and H 2 RA • Kidney Injury (interstitial nephritis): PPI • Virologic rebound in patients taking nelfinavir for HIV: long term PPI (but not with short term) patients on PI should be counseled to avoid OTC PPI and should not have PPI prescribed for them without careful monitoring • Increased risk of dementia

Treatment Algorithm for GERD

Management suspected GERD

Management Algorithm with atypical sx

Complications of GERD • Ulcerative esophagitis, esophageal stricture formation, Barrett’s esophagus and esophageal adenocarcinoma • Barret’s esophagus: screening interval for cancer after the diagnosis depends on the degree of dysplasia in the biopsy specimens • In patients with Barret’s esophagus, treatment should focus on relief of GERD sx, NOT normalization of Esophageal p. H.

Screening for cancer in Barret’s esophagus

Barret’s Esophagus • Occur with prolonged exposure of esophageal mucosa to gastric acid • Squamous cell injury promotes metaplasia to columinar epith that is more resistant to acid damage. Increased risk of dysplasia and adenocarcinoma • Risk factors: prolonged GERD, male sex, white or Hispanic race, advanced age, smoking and obesity • ACG recommends treatment of barret’s with antireflux therapy that should only be prescribed in doses high enough to achieve healing of esophagitis or ulcers and to control sx , BUT NORMALIZATION OF ACID MUCOSA

H. Pylori • Pathophys: bacteria colonizes the mucous layer of the gut, producing urease which allow it to survive in low p. H and penetrate the mucous layer to adhere to epithelial cells. • Epidemiology: 50% of world’s population (highest in low SES) • Mode of transmission: water-borne, and oral fecal route. Most individuals are infected in childhood

H. Pylori and GERD • No association is found between H. Pylori and GERD the Dx of GERD should not prompt H. Pylori testing • The prevalence of H. pylori in western countries is declining and Barret’s esophagus and esophageal adenocarcinoma is increasing • Theory being investigated that H. pylori may be protective against GERD, perhaps due to chronic gastritis and decreased acid production

Testing for H. Pylori

Non-invasive diagnosis of H. pylori • Urea breath test: sensitivity and specificity >95% and can be used for f/u eradication therapy, 4 weeks after completing the treatment • Stool antigen tests: sensitivity 86 -96% and a specificity >90%. Patients should be off acid suppression therapy for at least 2 weeks prior to stool testing. Note: Serologic testing is not adequately sensitive or specific to diagnose H. pylori in low prevalence areas

Treatment of H. Pylori

summary v. Patients <45 with sx of dyspepsia or >45 with new dyspepsis, unexplained IDA, recurrent ITP, or a first degree relative gastric cancer should be tested for H. Pylori v. Diagnosis of GERD should not prompt testing for H. pylori v. Always treat H. pylori infection to prevent PUD, MALToma, and gastric CA v. Patients who have been treated for H. pylori should have follow up eradication testing (urea-breath test or stool antigen test) 4 weeks after treatment and after being off of acid-suppression treatment for at least 2 weeks.

Thank you