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Gastroesophageal Reflux Disease (1).pptx
1. Gastroesophageal Reflux Disease
• Definition
condition in which the stomach contents (most
characteristically acid) moves backwards from the stomach
into the esophagus .
2. Etiology
• inappropriate transient relaxations of LES – most common
cause
• low basal LES tone (especially in scleroderma)
• contributing factors include: delayed esophageal clearance,
delayed gastric emptying, obesity, pregnancy, acid
hypersecretion (rare) from Zollinger-Ellison syndrome (gastrin-
secreting tumor)
• hiatus hernia worsens reflux, does not cause it.
3. Clinical Features
• “heartburn” (pyrosis) and acid regurgitation (together are 80%
sensitive and specifc for refux) ± sour regurgitation; less sensitive and
less specifc: water brash, sensation of a lump in the throat (globus
sensation), and frequent belching
• non-esophageal symptoms are increasingly recognized of being poor
predictors of refux.
4.
5.
6. investigations
• usually, a clinical diagnosis is sufficient based on
symptom history and relief following a trial of
pharmacotherapy (PPI: symptom relief 80% sensitive for
refux)
gastroscopy indications
absolute indications
◆ heartburn accompanied by red-fags (bleeding, weight
loss, etc.)
7. ◆ persistent refux symptoms or prior severe erosive
esophagitis afer therapeutic trial of 4-8 wk of PPI 2x daily
◆ history suggests esophageal stricture especially
dysphagia
◆ high risk for Barrett’s (male, age >50, obese, white,
tobacco use, long history of symptoms)
8. •repeat endoscopy after 6-8 wks of PPI therapy indicated
if: severe esophagitis because it can mask Barrett’s
esophagus or symptoms
• esophageal manometry (study of esophageal motility)
• done to diagnose abnormal peristalsis and/or decreased
LES tone, but cannot detect presence of refux; indicated
before surgical fundoplication to ensure intact
esophageal function
9. • 24 h pH monitoring: most accurate test for refux, but not
required or performed in most cases
■ most useful if PPIs do not improve symptoms
10. Treatment
1. PPIs are the most efective therapy and usually need to be
continued as maintenance therapy
2. on-demand: antacids (Mg(OH)2, Al(OH)3, alginate), H2-
blockers, or PPIs can be used for NERD
3. diet helps symptoms, not the disease; avoid alcohol,
cofee, spices, tomatoes, and citrus juices
4. only benefcial lifestyle changes are weight loss (if obese)
and elevating the head of bed (if nocturnal symptoms)
5. symptoms may recur if therapy is discontinued
11.
12. Complications
1. esophageal stricture disease – scarring can lead to
dysphagia (solids)
2. ulcer
3. bleeding
4. Barrett’s esophagus and esophageal adenocarcinoma –
gastroscopy is recommended for patients with chronic
GERD or symptoms suggestive of complicated disease
(e.g. anorexia, weight loss, bleeding, dysphagia)
13. Barrett’s Esophagus
• Definition
• metaplasia of normal squamous esophageal epithelium
to abnormal columnar epithelium containing type
intestinal mucosa (intestinal metaplasia)
14. Etiology
• thought to be acquired via long-standing GERD and
consequent damage to squamous epithelium
15. Epidemiology
• in North America and Western Europe, 0.5-2.0% of adults
are thought to have Barrett’s esophagus
• up to 10% of GERD patients will have already developed
BE by the time they seek medical attention
• more common in males, age >50, Caucasians, smokers,
overweight, hiatus hernia, and long history of reflux
symptoms
16. Pathophysiology
• endoscopy shows erythematous epithelium in distal
esophagus; diagnosis of BE relies on biopsy
demonstrating the presence of specialized intestinal
epithelium of any length within the esophagus
• BE predisposes first to premalignant changes
characterized as low or high-grade dysplasia, which then
progresses to adenocarcinoma
17. significance
• rate of malignant transformation is approximately 0.12% per yr for all
BE patients prior to dysplasia
• risk of malignant transformation in high-grade dysplasia is
significantly higher; studies have reported a 32-59% transformation
rate over 5-8 yr of surveillance
• increased gastric acid secretion is more frequently associated with
Barrett’s esophagus as opposed to reflux alone
18. Treatment
• acid suppressive therapy with high-dose PPI indefinitely (or surgical
fundoplication)
• endoscopy every 3 yr if no dysplasia
• high grade dysplasia: regular and frequent surveillance with
intensive biopsy, endoscopic ablation/ resection, or esophagectomy
produce similar outcomes; however, evidence increasingly favoring
endoscopic ablation with mucosal resection or radiofrequency
ablation
• if low grade dysplasia, both surveillance and endoscopic
ablation/resection are satisfactory options
20. Esophageal Motor Disorders
Clinical Features
• dysphagia with solids and liquids
• chest pain (in some disorders)
Diagnosis
• motility study (esophageal manometry)
• barium swallow sometimes helpful
Causes
• idiopathic
• achalasia (painless)
• scleroderma (painless)
• DM
• DES: rare and can be difficult to diagnose due to intermittent presentation
21.
22. Esophageal Diverticula
• Definition
outpouchings of one or more layers of the esophageal tract
• Clinical Features:
commonly associated with motility disorders, dysphagia,
regurgitation, retrosternal pain, intermittent vomiting, may be
asymptomatic
23. classification
classified according to location:
• pharyngoesophageal (Zenker’s) diverticulum
• most frequent form of esophageal diverticulum
• posterior pharyngeal outpouching most often on the left side, above
cricopharyngeal muscle and below the inferior pharyngeal constrictor
muscle
◆ symptoms: dysphagia, regurgitation of undigested food, halitosis
◆ treatment: endoscopic or surgical myotomy of cricopharyngeal
muscle ± surgical excision of sac
24. ■ mid-esophageal diverticulum
• secondary to mediastinal inflammation (“traction” diverticulae),
motor disorders
◆ usually asymptomatic; no treatment required
■ just proximal to LES (pulsatile type)
◆ usually associated with motor disorders
◆ usually asymptomatic, no treatment require
25. Peptic Stricture (from Esophagitis)
• presents as dysphagia alongside a long history of reflux
symptoms, but reflux symptoms may disappear as
stricture develops
• diagnosed with endoscopy or barium study if endoscopy
contraindicated or unavailable
28. Webs and Rings
• web = partial occlusion (upper esophagus)
• ring = circumferential narrowing (lower esophagus)
29. Clinical Features
• asymptomatic with lumen diameter >12 mm, provided peristalsis is
normal
• dysphagia with large food boluses
• Schatzki ring
■ mucosal ring at squamo-columnar junction above a hiatus hernia
■ causes intermittent dysphagia with solids
■ treatment involves disrupting ring with endoscopic boogie
31. • Risk Factors
• DM
• chemotherapeutic agents
• immunocompromised states
• Clinical Features
• characteristically odynophagia, less often dysphagia
• diagnosis is via endoscopic visualization and biopsy
32. • Appearance
• Candida (most common): whitish-yellow plaques without
visible ulceration or inflammation
• Herpes (second most common), CMV: focal ulcers
• Investigations
• diagnosis via endoscopic visualization and biopsy
33. Treatment
• Candida: nystatin swish and swallow, ketoconazole,
fluconazole
• Herpes: often self-limiting; acyclovir, valacyclovir,
famciclovir
• CMV: IV ganciclovir, famciclovir, or oral valganciclovir