objectives activities, the participant will be able to
TRANSCRIPT
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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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