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

2. 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

3. 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

4. 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.

5. 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

6. 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

7. The GerdQ Questionnaire

8. 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 HCO3 (GERD that do not respond to acid lowering treatments)

9. Eosinophilic esophagitis: typically young patient with atopy
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.

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

11. 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

12. Treatment Life Style modifications Pharmacotherapy
Surgery and endoscopic therapy

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

14. Pharmacotherapy
Mild: intermittent sx precipitated by dietary indiscretions  OTC antacids. Long term trials have shown they are effective in 20% of patients who use them
Mild-Moderate, intermittent (<2 episodes/wk), & treatment naive  H2RA are first line, in standard doses (ranitidine 150mg 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

16. Pharmacotherapy PPI: Severe sx or Persistent (> 2 episodes/wk)
Not effective treatment with H2RA
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 min prior to meals

17. SE of PPI

18. 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

19. Side Effects
C. Diff infection: PPI and H2RA. Discontinuation of PPI should be considered with C. Diff Dx
CAP and HAP through unclear mech: PPI and H2RA
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

20. Treatment Algorithm for GERD

21. Management suspected GERD

22. Management Algorithm with atypical sx

23. 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 pH.

24. Screening for cancer in Barret’s esophagus

25. 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 NOT NORMALIZATION OF ACID MUCOSA

26. H. Pylori
Pathophys: bacteria colonizes the mucous layer of the gut, producing urease which allow it to survive in low pH 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

27. 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

28. Testing for H. Pylori

29. 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

30. Treatment of H. Pylori

31. summary
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
Diagnosis of GERD should not prompt testing for H. pylori
Always treat H. pylori infection to prevent PUD, MALToma, and gastric CA
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.

32. Thank you