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1 GERD: What you don’t know about reflux Bruce D. Askey, MS, ANP-BC Associate Lecturer Fitzgerald Health Education Associates, Inc. North Andover, MA Adult Nurse Practitioner Dept. of Hepatology/Gastroenterology Guthrie Clinic Sayre, Pa/Ithaca, NY Objectives • Having completed the learning activities, the participant will be able to: – Describe the mechanism of gastroesophageal reflux disease. – Describe alarm symptoms that would prompt an endoscopy. – Describe the pharmacologic and non- pharmacologic management of gastroesophageal reflux disease. Fitzgerald Health Education Associates, Inc. 2 Gastroesophageal Reflux Disease (GERD) • Backward movement of gastric contents resulting from an incompetent lower esophageal sphincter 3 Fitzgerald Health Education Associates, Inc.

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Page 1: Objectives activities, the participant will be able to

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GERD: What you don’t know about reflux

Bruce D. Askey, MS, ANP-BCAssociate Lecturer

Fitzgerald Health Education Associates, Inc.North Andover, MA

Adult Nurse PractitionerDept. of Hepatology/Gastroenterology

Guthrie ClinicSayre, Pa/Ithaca, NY

Objectives

• Having completed the learning activities, the participant will be able to: – Describe the mechanism of

gastroesophageal reflux disease.– Describe alarm symptoms that would

prompt an endoscopy.– Describe the pharmacologic and non-

pharmacologic management of gastroesophageal reflux disease.

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Gastroesophageal Reflux Disease (GERD)

• Backward movement of gastric contents resulting from an incompetent lower esophageal sphincter

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Endoscopic View: Normal Anatomy of the Esophagus

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Terms

• Gastroesophageal reflux disease – Backward movement of stomach contents

into the esophagus

• Esophagitis– Inflammation of the esophagus

• Heartburn– Substernal burning radiating upward

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Symptoms of GERD

• Substernal burning radiating toward neck• NOT associated with

– Shortness of breath– Dizziness – Diaphoresis– Exercise

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Symptoms of GERD (continued)

• Generally occurs 1 hour after a meal or within 2 hours of lying flat.

• “Globus” sensation: A sensation of having a “lump in my throat.”

• May not experience heartburn!

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Case Study

• 57-year-old male presents with a several week history of substernal burning radiating to his neck.

• PMH significant for– Diabetes– Hypertension– Obesity– Hyperlipidemia

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• He smokes 2 packs per day and has done so for the past 40 years.

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Case Study (continued)

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• Is this GERD?• What other questions should be asked?

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Case Study (continued)

Symptoms of GERD (continued)

• Esophageal spasm• Stricture

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Dysphagia

• Tumor• Eosinophilic esophagitis• Achalasia

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Dysphagia

• Difficulty swallowing– Oropharyngeal (transfer)– Esophageal

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Oropharyngeal Dysphagia

• Impaired transfer from the mouth to the esophagus

• Neurologic and muscular disorders• Symptoms

– Nasal regurgitation– Cough with eating

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• Diagnostics– Modified barium swallow with speech therapist– Endoscopy

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Oropharyngeal Dysphagia (continued)

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Esophageal Dysphagia

• Sensation of food/water “getting stuck” • Fixed lesion (solids > liquids)

– Tumor (within esophagus, mediastinal)– Stricture (Schatzki’s ring)

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• Motor disorder (solids = liquids)– Esophageal spasm– Achalasia– Scleroderma

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Esophageal Dysphagia (continued)

Diagnostics

• Upper endoscopy• Barium swallow (esophagram)• Esophageal manometry• Computerized tomography (CT)

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Extraesophageal Manifestations of GERD

• Cough• Clearing throat• Hoarse voice• Asthma

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Diagnosis of GERD

• Generally a clinical diagnosis• Upper endoscopy may be normal but can

rule out Barrett’s esophagus• Ambulatory pH monitoring

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Alarm Symptoms Requiring Upper Endoscopy

• Dysphagia• Melena• Anemia• Weight loss

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Treatment of GERD

• Phase 1 lifestyle modifications– Weight loss– Smoking cessation– Avoid lying flat after eating– Avoid chocolate/peppermint– Avoid acid foods

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Pharmacologic Management of GERD

• Antacids (neutralize acid)– Simethicone (Mylanta®)– Simethicone (Maalox®)– Calcium carbonate (Tums®)– Calcium carbonate (Rolaids®)

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• H2 Blockers – Block histamine receptors on gastric parietal

cells resulting in decreased acid production• Cimetidine (Tagamet®)• Famotidine (Pepcid®)• Nizatidine (Axid®)• Ranitidine (Zantac®)

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Pharmacologic Management of GERD

(continued)

• Proton pump inhibitors (PPIs)– Inhibit the hydrogen pumps in the gastric

parietal cell• Omeprazole (Prilosec®)• Lansoprazole (Prevacid®)• Omeprazole/sodium bicarb (Zegerid®)• Pantoprazole (Protonix®)• Rabeprazole (AcipHex®)• Esomeprazole (Nexium®)• Dexlansoprazole (Kapidex®, Dexilant®)

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Pharmacologic Management of GERD

(continued)

PPIs: Life savers or heartbreakers?

• Interaction with clopidogrel (Plavix®) • Hip fractures• Pneumonia• Increased risk of C. difficile

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PPIs: Life savers or heartbreakers? (continued)

• Interaction with clopidogrel (Plavix®)– Clopidogrel is metabolized to its active

metabolite by cytochrome P450 enzymes. • Primarily CYP2C19

Laine, L. American Journal of Gastroenterology. 2010; 105: 34-41.http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProvider

s/DrugSafetyInformationforHeathcareProfessionals/PublicHealthAdvisories/ucm190825.htm

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• Interaction with clopidogrel (Plavix®) (cont.)– PPIs are also metabolized by CYP2C19 and may

competitively inhibit the conversion of clopidogrel (Plavix®) to its active metabolite.

Laine, L. American Journal of Gastroenterology. 2010; 105: 34-41.http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/Dr

ugSafetyInformationforHeathcareProfessionals/PublicHealthAdvisories/ucm190825.htm

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PPIs: Life savers or heartbreakers? (continued)

• Interaction with clopidogrel (Plavix®) (cont.)– The FDA has issued a public health advisory

warning against the concomitant use of omeprazole and clopidogrel.

http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/PublicHealthAdvisories/ucm190825.htm

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PPIs: Life savers or heartbreakers? (continued)

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• Hip fractures– It is theorized that acid suppression results

in decreased calcium absorption leading to bone demineralization and hip fractures.

– There is conflicting data.

Laine, L. The American Journal of Gastroenterology. 2009; 104 (supplement 2): S21-S26.Moayyedi, M. The American Journal of Gastroenterology. 2008; 103:2428-2431.

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PPIs: Life savers or heartbreakers? (continued)

• Pneumonia– It is theorized that gastric acid suppression

allows increased colonization of the upper GI tract.

– Those at highest risk for community-acquired pneumonia are those who have started a PPI in the past 30 days.

Sarkar, M. Annals of Internal Medicine. 2008.;149(6): 391-400.

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PPIs: Life savers or heartbreakers? (continued)

• Increased risk of C. difficile– It is theorized that gastric acid plays a role

in eradicating C. difficile and neutralizing its toxin.

Howell, M. Archives of Internal Medicine. 2010; 170(9): 784-790.

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PPIs: Life savers or heartbreakers? (continued)

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Indications for Surgery

• Failure of medical management

• Complications of medical management

• Treatment of “extra-esophageal” reflux disease

• Alternative to medical management

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Barrett’s Esophagus

• A change in the lining of the distal esophagus – Squamous epithelium changes to columnar tissue

similar to that seen in the small intestine– Result of long-standing esophageal exposure to

gastric juiceAGA medical position statement on the management of Barrett’s esophagus. Gastroenterology. 2011;140

(3):1084-1091.

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Barrett’s Esophagus (continued)

• A change in the lining of the distal esophagus (cont.)– Potentially pre-malignant

• The major risk factor for esophageal adenocarcinoma in the US

AGA medical position statement on the management of Barrett’s esophagus. Gastroenterology. 2011;140 (3):1084-1091

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Demographics

• 1.6% of population has Barrett’s• >40-years-old• Male • Caucasian• Long-standing GERD (>13 years)• Obesity

Wang, K. American Journal of Gastroenterology. 2008;103:788-797.

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Diagnosis

• EGD (upper endoscopy)– Biopsy to confirm diagnosis – Screen for dysplasia– Currently the only accurate method to

detect Barrett’s esophagus

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Dysplasia

• Abnormal cells– Early transition toward cancer– Inflammation from acid injury

• Low grade– Aggressive management with PPI – Repeat EGD with biopsies in 6-12 monthsAGA medical position statement on the management of Barrett’s esophagus.

Gastroenterology. 2011;140 (3):1084-1091

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Dysplasia (continued)

• High grade– Aggressive management with PPI– Repeat EGD in 3 months– Endoscopic mucosal resection

AGA medical position statement on the management of Barrett’s esophagus. Gastroenterology. 2011;140 (3):1084-1091

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Surveillance for Barrett’s

• Increased survival if cancers detected via endoscopic biopsy rather than development of symptoms– Dysphagia– Weight loss– Melena/iron deficiency anemia– Fevers/chills/night sweats

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• Barrett’s with no dysplasia– EGD in 3-5 years

AGA medical position statement on the management of Barrett’s esophagus. Gastroenterology. 2011;140 (3):1084-1091

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Surveillance for Barrett’s (continued)

Management of Barrett’s

• Phase 1 life-style modifications• Weight loss• Aggressive PPI therapy (BID)• Endoscopic mucosal resection

Wang, K. American Journal of Gastroenterology. 2008;103:788-797.

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Management of Barrett’s (continued)

• BARRX: Ablation of malignant tissue• Esophagectomy for persistent high grade

dysplasia or the development of adenocarcinoma

Wang, K. American Journal of Gastroenterology. 2008;103:788-797.

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Eosinophilic Esophagitis

• Eosinophilic infiltration of the esophageal mucosa identified via biopsy during upper endoscopy– >15 eosinophils/high-power field

Dellon, E, et al. ACG clinical guideline: Evidence based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). American Journal of Gastroenterology 2013; 108: 679-692.

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Eosinophilic Esophagitis: Symptoms

• Dysphagia and food impaction are often the presenting symptoms.– Chest pain/GERD

• Typically affects males (3:1) when compared to females

• Childhood and 3rd to 4th decadeDellon, E, et al. ACG clinical guideline: Evidence based approach to the diagnosis and

management of esophageal eosinophilia and eosinophilic esophagitis (EoE). American Journal of Gastroenterology 2013; 108: 679-692.

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Eosinophilic Esophagitis: Endoscopic Findings

• Esophageal rings are noted at the time of endoscopy.

• Furrows• Exudates• Edema

Dellon, E, et al. ACG clinical guideline: Evidence based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). American Journal of Gastroenterology 2013; 108: 679-692.

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Eosinophilic Esophagitis: Pathophysiology

• Eosinophils release proinflammatory cytokines

• Cytokines cause tissue damage and result in fibrosis

• Major basic protein causes esophageal smooth muscle contraction→ 

dysphagia/impactionSwoger, J. Mayo Clinic Proc. 2007; 82 (12): 1541-1549.

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• Often seen with coexisting inhalant allergies• Food allergies• Eczema• 50% of adults and 80% of children have an

allergic disorder

Swoger, J. Mayo Clinic Proc. 2007; 82 (12): 1541-1549.

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Eosinophilic Esophagitis: Pathophysiology

(continued)

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End of PresentationThank you for your time and attention.

Bruce D. Askey, MS, ANP-BCWebsite: www.fhea.com E-mail: [email protected]

Reference

• Kahrilas, P, et al. American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease. Gastroenterology. 2008: 135(4): 1383-1391.

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All websites listed active at the time of publication.

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