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Gastro-Esophageal Reflux Disease.

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Presentation on theme: "Gastro-Esophageal Reflux Disease."— Presentation transcript:

1 Gastro-Esophageal Reflux Disease

2 Gastro-Esophageal Reflux Disease (GERD):
Definitions Gastro-Esophageal Reflux Disease (GERD): It is a chronic disorder which describes any symptomatic or histopathologic alteration resulting from episodes of gastro-esophageal reflux into the esophagus and/or adjacent organs

3 ERD NERD Erosive Reflux Disease Non Erosive Reflux Disease 2/3
Definitions ERD Erosive Reflux Disease 1/3 NERD Non Erosive Reflux Disease 2/3

4 Typical: Symptoms Heartburn Acid regurgitation > 2x/week
> 4 to 8 weeks

5 Symptoms-Atypical Esophageal: Pulmonary: Non-cardiac chest pain
Non-obstructive dysphagia Globus hystericus Pulmonary: Asthma Chronic cough Hemoptysis Bronchitis Broncheictasis Recurrent pneumonia

6 Symptoms-Atypical Otorhinolaryngological: Oral
Hoarseness Throat cleaving laryngitis Sinusitis Otolagia Oral Etching of dental enamel Halitosis

7 Epidemiolgy

8 Shubbar & Taka

9 Increasing Prevalence:
% %

10 Pathogenesis Transient lower esophageal sphincter (LES) relaxation
Hypotensive LES Delayed Esophageal clearance Delayed gastric emptying Salivary function Tissue resistance

11 Diagnosis

12 1-History Age Alarm features Nocturnal reflux Dysphagia Odynophagia
Weight loss GI bleeding Nausea &/or vomiting Family history of cancer Nocturnal reflux

13 -ve endoscopy is seen in 2/3 of GERD
Useful in: Grading Hiatus hernia Ulcer or stenosis Barrett’s Esophagus Indications: Age over 40 years-old Alarm features Atypical symptoms -ve endoscopy is seen in 2/3 of GERD

14 24 hrs pH Recording Indications: Atypical symptoms
NERD who do not respond to PPI When esophagitis is not demonstrated in the pre-operative endoscopic examination

15 Management

16 Symptoms Antacids/Alginates Proton pump inhibitor Full dose Poor response Consider pH Monitoring Reconsider diagnosis Normal Fundoplication Maintenance dose Good response H2 receptor Antagonists Antacids

17 Behavioral modifications in the treatment of GERD
Special care with at risk medications: anticholinergics, theophylline, tricyclic antidepressants, Ca channel blockers, B-Adrenergic agonists, alendronate. Avoidance of lying down for 2 hrs after meals Avoidance of large meals Drastic reduction in, or cessation of, smoking. Reduction of body weight if overweight

18 Surgical treatment Indications:
No response to medical treatment including atypical symptoms. Continuous maintenance treatment is required especially in patients younger than 40 year old. Financial impediment

19 Complications Barrett’s esophagus Stenosis Ulcer Bleeding

20 Barrett's Esophagus is the condition in which an abnormal columnar epithelium that is predisposed to malignancy replaces the stratified squamous epithelium that normally lines the distal esophagus. Barrett's esophagus is a consequence of chronic gastroesophageal reflux disease (GERD), which damages the esophageal squamous epithelium and causes it to heal through a metaplastic process in which columnar cells replace reflux- damaged squamous cells. The columnar-lined esophagus causes no symptoms, and the condition has clinical importance only because it is a risk factor for esophageal adenocarcinoma, a tumor whose frequency has increased more than six-fold over the past several decades. Barrett's esophagus is diagnosed by endoscopic examination, and two criteria must be fulfilled. First, the endoscopist must ascertain that columnar-appearing epithelium lines the distal esophagus( Endoscopically, columnar epithelium has a reddish color and velvet- like texture that can be distinguished readily from normal esophageal squamous epithelium, which is pale and glossy). Second, biopsy specimens of that columnar-appearing epithelium must show evidence of metaplasia.

21 Achalasia Achalasia is characterized by impaired LES relaxation with swallowing, and aperistalsis in the smooth muscle esophagus. The resting LES pressure is elevated in about 60% of cases. If there are nonperistaltic, spastic contractions in the esophageal body, the disease is referred to as vigorous achalasia or, more recently, spastic achalasia. Clinical manifestations of achalasia may include dysphagia starting for fluid then solid, regurgitation, chest pain, hiccups, halitosis, weight loss, aspiration pneumonia, and heartburn. All patients have solid food dysphagia; the majority of patients also have variable degrees of liquid dysphagia. The onset of dysphagia is usually gradual, with the duration of symptoms averaging two years at presentation. Characteristic barium swallow findings are proximal esophageal dilatation with the tapering of distal esophagus at the gastroesophageal junction. ENDOSCOPY and Esophageal Manometry help dx, Rx: Pharmacologic treatments, calcium channel blockers, are not very effective, making them more appropriate as temporizing maneuvers than definitive therapies. The definitive treatments of achalasia are disruption of the LES either surgically (Heller myotomy) or with a pneumatic dilator.


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