Gastroenterology - 01. Gastroesophageal Reflux Disease (Courses in Therapeutics and Disease State Management)

Gastroenterology:
Gastroesophageal Reflux Disease

Courses in Therapeutics and Disease State Management
Author: Monica L. Skomo, B.S., Pharm.D., BCACP, CTTS; Assoc. Prof. of Pharmacy Practice; Dir. of Assessment and Educational Strategies; Duquesne University School of Pharmacy
http://accesspharmacy.mhmedical.com/LearningModuleGroup.aspx?id=8
Copyright © 2017 McGraw-Hill Education. All rights reserved
Learning Objectives (Slide 1 of 2)
• Define GERD and describe the various stages of disease severity
• Describe the etiology of GERD and risk factors associated with the
disease
• Discuss typical symptoms, atypical symptoms, alarm symptoms,
aggravating factors and complications associated with GERD
• Describe how GERD is diagnosed and the role of endoscopy
• Discuss the various pharmacologic approaches for the treatment of
GERD
Learning Objectives (Slide 2 of 2)
• Review the roles of the H2-antagonists and proton pump inhibitors in the
treatment of GERD and prevention of its recurrence
• Describe non-pharmacologic and lifestyle measures that may be
beneficial in the reduction of symptoms of reflux disease
• Given a GERD patient history, be able to recommend appropriate
pharmacologic and nonpharmacologic therapies and explain the rationale
behind your decision
• Discuss drug adverse effects and monitoring parameters for drugs and
GERD
Required and Recommended Reading
May D, Thiman M, Rao SC. Gastroesophageal Reflux
Disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells
BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic
Approach, 10e New York, NY: McGraw-Hill; 2017.
GERD Definitions
• GERD (Gastroesophageal Reflux Disease)
– A condition that occurs when refluxed stomach contents lead to troublesome symptoms and/or
complications
– Episodic pyrosis (heartburn) that is not frequent enough or painful enough to be considered
bothersome by the patient is not included in the above consensus GERD definition
• Pyrosis frequency of more than 2 times per week is sometimes used as a criteria for GERD
• Chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents
into the esophagus.
• Symptoms of GERD vary in severity, duration, and frequency.
• When the esophagus is repeatedly exposed to refluxed material for prolonged periods of
time, inflammation of the esophagus (esophagitis) occurs, and in some cases it can progress
to erosion of the squamous epithelium of the esophagus (erosive esophagitis) and may lead
to other complications.
Epidemiology (Slide 1 of 2)
• Heartburn is the most frequent clinical complaint
– Reported to occur at least once daily in 10%
– 20% weekly;
– 44% monthly of U.S. adults
– $5 billion for OTC/Rx per year
• Most frequently occurs in adults over 40 years of age
• Incidence in similar between men and women
Epidemiology (Slide 2 of 2)
• About 50% of pregnant women will experience GERD
• Can also occur in infants
• Prevalence depends on geographic region but is highest in
Western countries
Risk Factors
• Obesity (BMI ≥ 30)
• Alcohol use
• Smoking
• Excessive caffeine intake
• Respiratory diseases
Key Factors in the Development of GERD (Slide 1
of 2)
• A decrease in lower esophageal sphincter (LES) pressure
• Decreased clearance of gastric contents from the esophagus
• Decreased mucosal resistance in the esophagus
Key Factors in the Development of GERD (Slide 2
of 2)
• Composition of reflux contents “extra acidic”
– Gastric fluid that has a pH < 4 is extremely caustic to the esophageal
mucosa.
• Decreased gastric emptying (increased gastric emptying time)
• Certain anatomic features
– Most commonly a hiatal hernia
Pathophysiology of GERD (Role of the Lower
Esophageal Sphincter)
• Link: Figure of comparison of esophageal high-resolution

manometry
• Link: Figure of pathophysiology of esophageal reflux disease

(LES, lower esophageal sphincter)
Hiatal Hernia
• A hiatal hernia occurs when a portion of the stomach protrudes
through the diaphragm into the chest
– Causes a disruption in the normal anatomic barriers between the
stomach and the esophagus
• Link: Figure of radiographic anatomy of the gastroesophageal
junction
GERD Symptoms
• GERD symptoms are often grouped in 3 categories
– Typical or “classic” esophageal symptoms
– Alarm or complicated symptoms
• May be indicative of GERD complications
– Atypical or extraesophageal symptoms
Typical or “Classic” Symptoms
• Pyrosis (heartburn)
– Hallmark symptom
– A substernal feeling of warmth or burning rising up from the abdomen
that may radiate to the neck
• Regurgitation/Belching
• Acid brash/Hypersalivation
• Chest pain (non cardiac in nature)
Alarm (Complicated) Symptoms
• Any of these symptoms warrant immediate referral for testing
– Dysphagia
– Odynophagia
– Bleeding
– Unexplained weight loss
– Choking
– Chest pain (if could be cardiac in nature)
Extraesophageal Symptoms/Manifestations (Atypical
Symptoms)
• These symptoms have an association with GERD but causality
should only be considered if a concomitant esophageal
symptoms are present
– Chronic cough
– Asthma-like symptoms
• About 50% of those with asthma have GERD
– Laryngitis/Hoarseness
– Recurrent sore throat
– Dental enamel erosion
GERD
• GERD is often described on either esophageal symptoms or
esophageal tissue injury
– Symptom-based GERD syndromes (with or without esophageal tissue
injury)
– Tissue injury-based GERD syndromes (with or without esophageal
symptoms)
• Extraesophageal GERD syndromes may also occur
• GERD is also sometimes described in terms of the absence or
presence of esophageal erosions
– Non-erosive reflux disease (NERD)
– Erosive reflux disease (ERD)
Symptom-Based GERD Syndromes
• May or may not have esophageal tissue injury
• Have typical or “classic” esophageal symptoms
• May have alarm symptoms particularly if GERD complications
(see next section) are present
Tissue-Injury Based GERD Syndromes
• Examples of esophageal tissue injury include the presence of any of
the following:
– Esophagitis (inflammation of the esophagus)
– Erosions (erosion of the squamous epithelium of the esophagus)
– Strictures
– Barrett’s esophagus
– Esophageal adenocarcinoma
• May present with alarm symptoms particularly if have GERD
complications
• May or may not have typical or classic symptoms
Extraesophageal GERD Syndromes
• Present with extraesophageal or atypical symptoms
• May or may not have typical esophageal symptoms
• Extraesophageal symptoms have an association with GERD, but
causality should only be considered if a concomitant esophageal
GERD syndrome is also present
• Extraesophageal manifestations of GERD are being recognized with
increasing frequency.
• GERD may be either a causative or exacerbating factor in up to
50% of patients who experience these symptoms.
Aggravating Factors
• Recumbency
• Increased intra-abdominal pressure
• Reduced gastric motility
• Decreased LES tone or pressure
• Direct mucosal irritation
Decrease in LES Pressure
• Examples of foods that decrease LES pressure
– Fatty foods, peppermint, spearmint, chocolate, coffee, cola, tea, garlic,
onions, chili peppers
• Examples of medications that decrease LES pressure
– Anticholinergics, barbiturates, benzodiazepines, caffeine,
dihydropyridine calcium channel blockers, dopamine, estrogen,
ethanol, narcotics, nicotine, nitrates, progesterone, theophylline
Direct Mucosal Irritation
• Examples of foods that are direct irritants to the esophageal
mucosa
– Spicy foods, orange juice, tomato juice, coffee
• Examples of medications that are direct irritants to the
esophageal mucosa
– Oral bisphosphonates, aspirin, iron, NSAIDs, quinidine, potassium
Foods and Medications that May Worsen GERD Symptoms
Foods/Beverages Medications
Decreased Lower Esophageal Sphincter Pressure
Fatty meal Anticholinergics
Carminatives (peppermint, spearmint) Barbiturates
Chocolate Caffeine
Coffee, cola, tea Dihydropyridine calcium channel blockers
Garlic Dopamine
Onions Estrogen
Chili peppers Nicotine
Alcohol (wine) Nitrates
Progesterone
Tetracycline
Theophylline
Direct Irritants to the Esophageal Mucosa
Spicy foods Aspirin
Orange juice Bisphosphonates
Tomato juice Nonsteroidal antiinflammatory drugs (NSAIDs)
Coffee Iron
Tobacco Quinidine
Potassium chloride
Complications of GERD
• Esophagitis
– Link: Figure of EGD demonstrating linear red streaks with a central white
streak extended up the esophagus in peptic regurgitant esophagitis
• Erosions and ulceration of the esophageal mucosa
• Strictures of the esophagus
– Secondary to fibrous tissue deposition after long standing erosion
• Barrett’s esophagus
– Present in about 10% of those with GERD
– Most prevalent in white males in Western countries
• Esophageal adenocarcinoma
Barrett’s Esophagus (Slide 1 of 2)
• Barrett’s esophagus occurs when the normal squamous cell
epithelium in the esophagus converts to a columnar cell
epithelium (intestinal-type epithelium)
• More common in men than women
• Barrett’s esophagus does not cause specific symptoms but the
reflux does
Barrett’s Esophagus (Slide 2 of 2)
• Those with Barrett’s esophagus develop adenocarcinoma of the
esophagus at a rate of 0.12% per year
– Gender ratio for esophageal adenocarcinoma is 8:1 (male:female)
• Patients must be monitored via endoscopy to evaluate changes
in cell type and conversion to adenocarcinoma
Complications of GERD (Photos)
Link: Photos of endoscopic appearance of peptic esophagitis, a

peptic stricture, Barrett’s metaplasia, and adenocarcinoma
GERD Diagnosis/Diagnostic Tests (Slide 1 of 4)
• Clinical History
– Patient’s description of typical or classic GERD symptoms such as
pyrosis, is often enough to consider GERD as an initial diagnosis
(uncomplicated GERD)
• Empiric trial of proton pump inhibitor (PPI) therapy
– ACG (American College of Gastroenterology) guidelines state that it
is reasonable to assume a GERD diagnosis in patients who respond to
appropriate therapy
• Endoscopy
– Endoscopy is the technique of choice to identify complications of GERD
such as ulcerations, erosions, Barrett’s esophagus, etc.
– Biopsy of the esophageal tissue is needed to identify and diagnose Barrett’s
esophagus and esophageal adenocarcinoma
– Many patients with GERD (presenting with typical or atypical symptoms)
will have normal appearing esophageal mucosa on endoscopy
– Usually not part of the work-up except in certain subsets of patients (alarm
symptoms, those refractory to treatment, etc.)
• Ambulatory pH Monitoring
– Identifies patients with excessive esophageal acid exposure and helps
determine if symptoms are acid related
– Useful in patients not responding to acid-suppression therapy
• Barium Radiography
– Not routinely used to diagnose GERD due to a lack of sensitivity and
specificity
– Can detect hiatal hernia
• Patients presenting with extraesophageal or atypical symptoms
should be reviewed on a case-by-case basis to be considered for
testing
• Alarm symptoms always warrant further testing
Therapeutic Approach to GERD
• The initial treatment used is determined by the patient’s
condition:
– Frequency of symptoms
– Degree of symptoms
– Presence and/or degree of esophagitis
– Presence of complications
Goals of Treatment
• Alleviate or eliminate acute symptoms
• Decrease frequency of recurrence
• Promote healing if esophageal tissue injury is present
• Prevent complications
General Treatment Approach
• Initial therapy in patients who present with typical GERD symptoms should
include patient-directed (self-care) therapy (antacids, OTC H 2-antagonist,
or OTC PPIs) and lifestyle modifications
• Those who do not respond to patient-directed therapy and lifestyle
modifications after 2 weeks should seek medical attention and are usually
started on empiric therapy consisting of an acid suppression agent such as a
proton pump inhibitor (PPI)
• Those who do not respond to empiric acid suppression therapy or have
alarm symptoms should undergo testing such as an endoscopy
Nonpharmacologic Therapies
• Lifestyle modifications
– Should be incorporated into the management of GERD regardless of the severity
of disease
– Lifestyle modifications should be tailored to an each individual patient’s needs
• Anti-reflux surgery
– Used as a last resort option in select patients
• When long-term pharmacologic therapy is undesirable
• Who have refractory GERD
• Have complications
• Endoscopic therapies
– Results have been disappointing and hence are not usually recommended
Lifestyle Modifications (Slide 1 of 2)
• Weight loss (if the patient is overweight or obese)
• Elevation of the head of the bed 6 to 8 inches
• Eat smaller, more frequent meals (as opposed to larger meals
less frequently)
• Include protein-rich meals in diet (increases LES pressure)
Lifestyle Modifications (Slide 2 of 2)
• Avoid eating 3 hours prior to sleeping or lying down
• Avoid foods or medications that exacerbate GERD
• Avoid alcohol
• Tobacco cessation
Endoscopic Interventions
• Stretta Procedure
– Stretta is an endoscopically guided radiofrequency (RF) energy delivery system.
The device is guided down the esophagus and RF energy is delivered to tissues
via catheters/needles. RF energy is thought to improve GERD symptoms by
increasing collagen deposition at the LES, increasing muscle wall thickness and
reconstituting the barrier to the reflux of gastric contents.
• LINX Reflux Management System (FDA approved March 2012)
– A series of titanium beads each with a magnetic core connected together with a
wire to form a ring shape.
– Implanted in the LES
– The force of the magnetic beads provides additional strength to a keep a weak
LES closed.
Therapeutic Interventions in the Management of
GERD
Link: Figure of therapeutic interventions in the management of

gastroesophageal reflux disease
Pharmacologic Agents Used in the Treatment of
GERD
• Antacids and alginic acid products
• H2-receptor antagonists (HRA)
• Proton pump inhibitors (PPIs)
• Promotility agents
Antacids (Slide 1 of 2)
• MOA
– Neutralize hydrochloric acid in the stomach, which results in an increase in
gastric pH
• Agents
– Magnesium hydroxide
– Aluminum hydroxide
– Calcium carbonate
• Adverse effects
– Diarrhea (magnesium hydroxide)
– Constipation (aluminum hydroxide and calcium carbonate)
– Alterations in mineral metabolism
– Acid-base disturbances
Antacids (Slide 2 of 2)
• Monitoring
– Periodic calcium and phosphate levels if on chronic antacid therapy
• Patient counseling
– Antacids can decrease the levels of numerous other drugs including
tetracyclines, digoxin, iron supplements, fluroquinolones, and
ketoconazole.
• Patients should separate antacids and other medications by at least 2 hours
– Patients with renal impairment should not use aluminum or magnesium
containing antacids unless directed by their physician
– Onset of relief is less than 5 minutes and duration of relief is 20 to 30
minutes
Composition and Acid Neutralizing Capacities of Popular Antacid Preparations
ACID NEUTRALIZING
PRODUCT Al(OH)3a Mg(OH)2a CaCO3a SIMETHICONEa
CAPACITYb
Tablets
Gelusil 200 200 0 25 10.5
Maalox Quick Dissolve 0 0 600 0 12
Mylanta Double Strength 400 400 0 40 23
Riopan Plus Double Magaldrate, 1080 20 30

Strength
Calcium Rich Rolaids 80 412 0 11
Tums EX 0 0 750 0 15
Liquids
Maalox TC 600 300 0 0 28
Milk of Magnesia 0 400 0 0 14
Mylanta Maximum Strength 400 400 0 40 25
Riopan Magaldrate, 540 0 15

a
Contents, milligrams per tablet or per 5 ml.
b
Acid neutralizing capacity, milliequivalents per tablet or per 5 ml.
The U.S. marketplace for antacids is fluid. The current trend of "reusing" well-known brand names to introduce new products that contain an active ingredient different from expected is a source of confusion that can
present a danger to patients. Medication safety experts encourage clinical practitioners to refer to the active ingredient(s) in conjunction with the proprietary (brand) name when selecting OTC products.
Antacid-Alginic Acid Combination
• MOA
– The antacid neutralizes stomach acid and the alginic acid is a foaming
agent that creates a viscous solution that floats on top of the stomach
contents and may be protect the esophagus from refluxed stomach
acid
• Agents
– Aluminum hydroxide/Magnesium carbonate/Alginic acid (Gaviscon)
H2-Receptor Antagonists (Slide 1 of 2)
• MOA
– Competitive inhibition of histamine at H2 receptors of gastric parietal
cells which inhibits gastric acid secretion
• Agents
– Cimetidine (Tagamet)
– Famotidine (Pepcid)
– Nizatidine (Axid)
– Ranitidine (Zantac)
H2-Receptor Antagonists (Slide 2 of 2)
• Adverse effects
– Headache, somnolence, fatigue, dizziness, constipation, diarrhea
• Monitoring
– Monitor for CNS effects (rare) in those over 50 years old or in those with
renal or hepatic impairment
– If taking once a day, it is preferable to take the dose at bedtime
– Onset of relief is 30 to 45 minutes and duration of relief is 4 to 10 hours
Proton Pump Inhibitors (PPIs) (Slide 1 of 3)
• MOA
– Blocks acid secretion by inhibiting gastric H+/K+ adenosine triphosphatase found on the
secretory surface of gastric parietal cells
– Results in a long-lasting anti-secretory effect that can maintain gastric pH levels above 4
• Agents
– Dexlansoprazole (Dexilant)
– Esomeprazole (Nexium)
– Lansoprazole (Prevacid)
– Omeprazole (Prilosec)
– Omeprazole/sodium bicarbonate (Zegerid)
– Pantoprazole (Protonix)
– Rabeprazole (Aciphex)
• Common adverse effects
– Headache, dizziness, somnolence, diarrhea, constipation, flatulence,
abdominal pain, nausea
• Serious adverse effects
– Increased risk of Clostridium difficile infections
– Increase risk of community-acquired pneumonia
• Long-term adverse effects (> 1 year)
– Hypomagnesemia
– Bone fractures
– Vitamin B12 deficiency
• Monitoring
– Appearance of diarrhea (frequency and type of diarrhea episodes)
– Periodic magnesium levels (if long-term therapy)
– Routine bone density studies (DXA scans)
• If other risk factors for osteoporosis or bone fractures present
– Preferable to take a PPI 30 to 60 minutes before a meal (mainly breakfast)
– If a second dose is needed, take prior to the evening meal
– Onset of relief is 2 to 3 hours and the duration of relief is 12 to 24 hours
Evaluate the Risks versus Benefits of
Long-Term PPI Use (Slide 1 of 2)
• Long-term PPI use has been associated with increased risk of:
– Fractures
– Infections such as C. Diff and pneumonia (expand)
– Hypomagnesemia
– Vitamin B12 deficiency
Evaluate the Risks versus Benefits of
Long-Term PPI Use (Slide 2 of 2)
• Long-term PPI use MAY BE associated with increased risk of:
– Dementia
– Renal disease
– Cardiovascular disease
Promotility Agents
• Promotility agents, such as metoclopramide and bethanechol,
have been used as adjunct therapy to acid suppression agents
such as PPIs in patients who have a known motility defect
• However, they are not generally recommended to be used for
GERD treatment due to their limited effectiveness and
undesirable adverse effect profiles
Pharmacologic Therapy (Slide 1 of 3)
• Patient directed therapy (Self-care) is appropriate for
intermittent, mild pyrosis and is managed using over-the-
counter products such as antacids, OTC H 2-receptor
antagonists, and OTC proton pump inhibitors (PPIs)
• Link: Table on Therapeutic Approach to GERD in Adults
Pharmacologic Therapy (Slide 2 of 3)
• Symptomatic relief of uncomplicated GERD is treated with
prescription H2-receptor antagonists or prescription PPIs at the
following doses and durations:
• Refer to Link: Table on Therapeutic Approach to GERD in
Adults
Pharmacologic Treatment (Slide 3 of 3)
• Healing of erosive esophagitis or treatment of patients
presenting with moderate to severe symptoms or complications
• Refer to Link: Table on Therapeutic Approach to GERD in
Adults
PPIs v. H2-Receptor Antagonists
• Symptomatic improvement as well as endoscopic healing rates
are higher for the PPIs compared to the H 2-receptor antagonists
• PPIs are therefore preferred over H2-receptor antagonists in
patients with erosive disease, moderate to severe symptoms, or
with complications
Maintenance Therapy (Slide 1 of 2)
• What patients should receive maintenance therapy?
– Those with symptomatic relapse following discontinuation of the drug
or a decrease in dose.
• If NERD/uncomplicated GERD, try to manage with on-demand or intermittent
PPI therapy or H2-receptor antagonists
Maintenance Therapy (Slide 2 of 2)
• What patients should receive maintenance therapy?
– Those with a history of complications (e.g. Barrett’s esophagus,
strictures, hemorrhage, ulcerations, etc.)
• Long-term maintenance therapy with PPIs at the lowest possible dose
– Can consider intermittent or on demand PPI therapy in some circumstances
PPIs and Rebound Acid Secretion (Slide 1 of 2)
• There have been reports of rebound acid secretion when PPIs
are abruptly discontinued.
– This can happen when PPIs are used for as little as 2 months (and of
course when they are used longer)
– These hyperacidity symptoms include dyspepsia and heartburn
• Often attributed to a relapse of the disorder (e.g. GERD), but it can even
happen in patients who didn’t have these symptoms to start with
PPIs and Rebound Acid Secretion (Slide 2 of 2)
• Tapering strategies for patients experiencing rebound acid
secretion
– (1) Taper PPI over 4 to 6 weeks
• First lower the dose of the PPI
• Then extend the PPI dosing interval to every other day then every 3rd day
• An H2-antagonist or antacid can be used for symptoms on “off days” as
needed
– (2) Suggest a switch to an H2-antagonist with antacids used as needed
for several weeks then discontinue
Patients with Extraesophageal (Atypical) GERD
(Slide 1 of 2)
• GERD can be considered as a potential co-factor in patients
with asthma, chronic cough, or laryngitis
– Careful evaluation of non-GERD causes should be undertaken in all
of these patients
• Patients with atypical symptoms may need higher doses of acid
suppression therapy with longer treatment duration compared
to those patients with typical symptoms
Patients with Extraesophageal (Atypical) GERD
(Slide 2 of 2)
• A PPI trial is recommended to treat extraesophageal symptoms
in patients who have typical GERD symptoms as well
• Reflux monitoring should be considered before a PPI trial in
patients with extraesophageal symptoms who do not have
typical GERD symptoms
Pediatric Patients (Slide 1 of 2)
• A suspected cause of reflux in infants is a developmentally
immature LES
• Many infants have reflux with little or no clinical consequence
– This uncomplicated reflux usually manifests as regurgitation or
spitting up
– Usually responds to supportive therapy
• Chronic vomiting associated with GERD must be carefully
evaluated and distinguished from other causes
Pediatric Patients
• Careful consideration should be given before a medication is
recommended
• When a medication is deemed necessary, ranitidine dosed at 2 to
4mg/kg twice a day is often used
• PPIs are increasing being used in children older than 1 year
– Lansoprazole, esomeprazole, and omeprazole are indicated for treating
symptomatic and erosive GERD in children > 1 year old
– See next slide for dosing ranges
• Omeprazole has been used off-label in children less than 1 year old
at a dose of 1mg/kg/day
PPIs in Children > 1 year of age
• Lansoprazole
– 15mg per day is recommended for children weighing < 30kg
– 30mg per day is recommended for children weighing > 30kg
• Esomeprazole
– Dosed 10 to 20mg a day for children 1 to 11 years old
– Dosed at 20 to 40mg a day for children 12 to 17 years old
• Omeprazole
– 5mg daily in children weighing between 5 and 10kg
– 10mg daily in children weighing between 10 and 20kg
– 20mg daily in children weighing ≥ 20kg
Elderly Patients
• Many elderly patients have decreased defense mechanisms
such as decreased saliva production
• PPI therapy may be warranted for those > 60 years of age with
symptomatic GERD
– They have superior efficacy and have once a day dosing
– Long-term risk of bone fractures is a concern and elderly patients
should be monitored appropriately
• Elderly are at higher risk of being sensitive to possible CNS
effects of H2-receptor antagonists
Patients with Refractory GERD
• Refractory GERD should be considered in patients who have not
responded to a standard course of twice a day PPI therapy
• The majority of patients with refractory symptoms experience
nocturnal acid breakthrough
• Switching to a different PPI may be effective in some patients
• Adding an H2-receptor antagonist at bedtime for nocturnal
symptoms is reasonable but the effect may decrease over time due
to tachyphylaxis with H2-receptor antagonists
References (Slide 1 of 3)
• May D, Thiman M, Rao SC. Gastroesophageal Reflux Disease. In: DiPiro
JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey
L. eds. Pharmacotherapy: A Pathophysiologic Approach, 10e New York,
NY: McGraw-Hill; 2017.
• Mills JC, Stappenbeck TS. Gastrointestinal Disease. In: Hammer GD,
McPhee SJ. eds. Pathophysiology of Disease: An Introduction to Clinical
Medicine, Seventh Edition. New York, NY: McGraw-Hill; 2013.
• Kahrilas PJ, Hirano I. Diseases of the Esophagus. In: Kasper D, Fauci A,
Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison's Principles of
Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015.
• Wallace JL, Sharkey KA. Pharmacotherapy of Gastric Acidity,
Peptic Ulcers, and Gastroesophageal Reflux Disease. In: Brunton
LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The
Pharmacological Basis of Therapeutics, 12e. New York, NY:
McGraw-Hill; 2011.
• Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and
management of gastroesophageal reflux disease. Am J Gastroenterol
2013; 108: 308-328.
• Schoenfeld AJ, Grady D. Adverse effects associated with proton
pump inhibitors. JAMA Internal Medicine 2016; 176(2): 172-174.
• Micromedex Solutions. Truven Health Analytics, Inc. Ann
Arbor, MI. Accessed October 15, 2016.
• Lexicomp Online®, Lexi-Drugs®, Hudson, Ohio: Lexi-Comp,
Inc. Accessed October 15, 2016.

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Gastroenterology:

Gastroesophageal Reflux Disease

• Link: Figure of comparison of esophageal high-resolution

• Link: Figure of pathophysiology of esophageal reflux disease

Link: Photos of endoscopic appearance of peptic esophagitis, a

Link: Figure of therapeutic interventions in the management of

Gelusil 200 200 0 25 10.5

Maalox Quick Dissolve 0 0 600 0 12

Mylanta Double Strength 400 400 0 40 23

Riopan Plus Double Magaldrate, 1080 20 30

Calcium Rich Rolaids 80 412 0 11

Maalox TC 600 300 0 0 28

Milk of Magnesia 0 400 0 0 14

Mylanta Maximum Strength 400 400 0 40 25

Riopan Magaldrate, 540 0 15

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